Understanding Depression

UNDERSTANDING DEPRESSION
Second Edition
ALSO BY PAUL R. ROBBINS
AND FROM MCFARLAND
Coping with Stress:

Commonsense Strategies (2007)
The Psychology of Dreams (1988; paper 2005)
Anger, Aggression and Violence:

An Interdisciplinary Approach (2000)
Adolescent Suicide (1998)
Romantic Relationships: A Psychologist

Answers Frequently Asked Questions (1996)
UNDERSTANDING
DEPRESSION
Second Edition
Paul R. Robbins
McFarland & Company, Inc., Publishers

Jefferson, North Carolina, and London
LIBRARY OF CONGRESS CATALOGUING-IN-PUBLICATION DATA
Robbins, Paul R. (Paul Richard)
Understanding depression / Paul R. Robbins.— 2nd ed.
p. cm.
Includes bibliographical references and index.
ISBN 978-0-7864-3542-5
softcover : 50# alkaline paper
¡. Depression, Mental — Popular works. I. Title.

RC537.R58 2009
6¡6.85'27 — dc22 2008023087
British Library cataloguing data are available
©2009 Paul R. Robbins. All rights reserved
No part of this book may be reproduced or transmitted in any form

or by any means, electronic or mechanical, including photocopying
or recording, or by any information storage and retrieval system,
without permission in writing from the publisher.
Cover art by Boris Zaysev (iStockphoto). Front cover by TG Design
Manufactured in the United States of America
McFarland & Company, Inc., Publishers

Box 6¡¡, Je›erson, North Carolina 28640
www.mcfarlandpub.com
To the memories of Maurice and Edith Robbins
and Marguerite Horyna
Acknowledgments
The author would like to thank Sharon Hauge and Herschel Shosteck for
their continued interest in and many contributions to the manuscript. He
would also like to thank Linda Lewin for her contribution, Allison Nugent of
the National Institute of Mental Health for her helpful explanations concern-
ing the genetic research now going on at the Institute, Lynn Nelson for shar-
ing his knowledge about medieval medicine, Donald Jewell for providing a case
study of the psychotherapeutic treatment of depression, Karen Kraft for pro-
viding information about the Depression and Bipolar Support Alliance and
Leroy Resnick and George Winfield for help in preparing the final version of
the manuscript.
Grateful acknowledgment is made to the following for permission to
reprint excerpts from their copyrighted materials: Plenum Publishing Corpo-
ration for S. D. Hollon and P. C. Kendall, “Cognitive self-statements in depres-
sion: Development of an automatic thoughts questionnaire,” Cognitive Therapy
and Research, 4 (1980): 383–95, and J. D. Safran, M. Vallis, Z. V. Segal, and B. F.
Shaw, “Assessment of core cognitive processes in cognitive therapy,” Cognitive
Therapy and Research 10 (1986): 509–26; Clinical Psychology Publishing Co.,
Inc., Brandon, VT 05733, for P. R. Robbins, and J. F. Nugent, III, “Perceived
consequences of addiction: A comparison between alcoholics and heroin-
addicted patients,” Journal of Clinical Psychology 31 (1975): 367–69; Farrar,
Straus and Giroux, for J. Anouilh, The Restless Heart, in Jean Anouilh Five Plays,
Volume 2, copyright 1959 by Hill and Wang.
vi
Table of Contents
Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . vi
Preface to the Second Edition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
1. Depressed Mood and Depression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7

2. Depression in the United States . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26
3. The Biological Bases of Depression . . . . . . . . . . . . . . . . . . . . . . . . . . 46
4. A Psychological Perspective on Depression . . . . . . . . . . . . . . . . . . . . 60
5. The Roots of Depression: A Look at Childhood Experiences . . . . . 75
6. Stress and Depression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 88
7. Depression, Alcohol and Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97
8. Coping with Depressed Feelings . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109
9. Some Counsel for the Family and Friends of a Depressed
Person . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127
10. Seeking Professional Help: Changing Patterns . . . . . . . . . . . . . . . . 134
11. Antidepressant Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 138
12. Psychotherapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 151
13. Hospitalization for Depression and the Use of
Electroconvulsive Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 167
14. Alternative Treatments for Depression . . . . . . . . . . . . . . . . . . . . . . 172
15. The Problem of Recurrence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 185
16. Concluding Remarks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 192
Chapter Notes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 197

Bibliography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 209
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 231
vii
This page intentionally left blank
Preface to the
Second Edition
When I had nearly completed my perusal of the recent scientific literature

on depression, and was about to commence writing the second edition of Under-
standing Depression, I took some time to reflect on the history of the subject.
While it was clear that the disorder had been a source of distress from the early
days of recorded history, our reliable knowledge about the nature of depres-
sion and how to treat it could be collapsed into our own era, into a lifetime or
even half a lifetime. Given the rudimentary knowledge that existed over the
centuries, the progress that has been made during recent years strikes me as
rather remarkable.
In the literature of the ancient world one finds examples of the expression
of a lingering sadness ritualized into lamentations. These lamentations may be
found in the Bible or even earlier in the writings of the Sumerians— lament-
ing the fall of the ancient city of Ur. Ritualized sadness also comes down to us
in the plays of the ancient Greeks, such as Aeschylus’ The Persians. Clinical
depression as we conceive of it today shares some core common elements with
these ancient lamentations— particularly prolonged sadness and guilt and self-
reproach.
The earliest descriptions of depression that have come down to us may be
those found in ancient Egyptian writings and later in the work of the inspired
Greek physician, Hippocrates. Hippocrates described a condition called melan-
cholia which he believed was caused by an excess of one of four hypothesized
bodily fluids called black bile. Melancholia was characterized by a number of
depressive-like symptoms including long lasting despondency.
In the dark ages of Europe following the destruction of the Roman Empire,
much of Greek teaching was lost leaving a vacuum of knowledge for most Euro-
peans that persisted for centuries. The Greek theories about bodily humors,
however, survived and found their way into medieval medicine. The idea that
depression was a disease was also present in the Arab civilizations that devel-
oped in North Africa, Spain and the Middle East in the wake of the spread of
Islam.
1
2 Preface to the Second Edition
We know next to nothing about how ordinary men and women through
the dark ages and the early medieval period conceived depressive symptoms or
what anyone could do about the condition. Perhaps, some people might have
believed that the malaise was the work of demons, the evil-eye, or some malev-
olent spirit that needed casting out. In my novel, Medieval Summer, one of the
characters, a monk, Brother Peter, went into a prolonged depression. The
Abbott of the monastery reacted by relieving him of his duties, and when the
illness lingered sent him off to the mother house of the order — a kind of benign
exile. The concept of exiling people with mental or emotional disorders became
institutionalized centuries later in western countries. These places of exile were
known as insane asylums. And unlike Brother Peter’s fate, such exile was not
benign; often, insane asylums were little more than the brutal warehousing of
sick people. In mid–twentieth century, Albert Deutsch wrote a riveting book
complete with photographs describing the overcrowded, sometimes squalid
conditions of American mental hospitals where treatment was almost nonexis-
tent. The photographs showed women strapped to beds and even more appalling
scenes when viewed from our contemporary mental health perspective.
The first rays of sunlight that came into this rather bleak picture of treat-
ment for mental disorders were the insights of Sigmund Freud. Freud treated
people who were depressed using the new approach to treatment he developed
for emotional and mental disorder: psychoanalysis. Based on his clinical obser-
vations, he offered theoretical contributions to the understanding of depres-
sion highlighting the role of loss and self-directed anger. While Freud was a
brilliant thinker and clinician, he was not a research psychologist in any sense
of the word and had no way of testing his theories in an objective and replic-
able way. This had to wait until both psychiatry and psychology matured which
was well into the 20th century.
Psychiatry began to assume its modern form with the work of pioneers
such as Emil Kraepelin who made a careful study of the symptoms of mental
patients and developed a system of classification of mental disorders. One of
the important disorders recognized was manic-depressive psychosis now known
as bipolar disorder.
For its part, psychology evolved rather tentatively, initially focusing on
problems that were easily measurable like calculating reaction times and stud-
ies of memory, and then under the influence of the behaviorists analyzing behav-
ior of rats in mazes and later Skinner Boxes. It was well into the post–World
War II years before psychologists began to apply their developing research tech-
niques to study serious problems such as depression. With research funds com-
ing through the National Institute of Mental Health, psychiatrists and
psychologists began to study depression in earnest, slowly at first and then in
a more accelerated manner. By the time I wrote the first edition of Understand-
ing Depression in 1993, researchers had developed both a very respectable sci-
ence base and new methods for treating the disorder.
Preface to the Second Edition 3
With the continued influx of new information about depression, it seemed

a propitious time to write a second edition of Understanding Depression. Since
the publication of the first edition of the book, there have been important
changes in both our understanding of the disorder and in our approach to treat-
ment. The new edition reflects these new realities. In particular, I have given
increased emphasis to recent studies highlighting the biological foundations of
depression, the development of and wide use of antidepressant drugs, the shift
in the means of dispensing these drugs from mental health professionals to pri-
mary care physicians, the development of alternative medicine approaches to
the treatment of depression, and the critical need to find ways to prevent the
recurrence of the disorder.
Introduction
Most people “get depressed” now and then. It’s a sad feeling, being in the
dumps. The feeling is usually transient, vanishing in hours or days, like the
proverbial dark clouds that give way to sunshine. We think of such short-lived
depressed states as depressed moods, not to be confused with the often chronic,
severe problem called clinical depression.
Transient depressed moods may be as common as the cold. My colleague
Roland Tanck and I carried out a series of studies on college students in which
we asked the students to fill out a special type of diary before they went to bed
for a period of ten nights. The diary included the question “Did you feel depressed
today?” There were very few students who did not answer the question yes at
some time during the ten-day period, and many students said yes repeatedly.
Going to college is not easy. There are major adjustments that must be
made in being away from home. Problems in relationships develop with fre-
quent disappointments. Term papers are due and examinations generate a great
deal of stress. One might expect to observe depressed moods in students, and
one finds them in abundance. Still, most of the students do not stay depressed.
They get over romantic disappointments, pass their exams, and continue to
study and go about their daily lives. Brief periods of depressed mood give way
to more pleasant moods. Good times are often right around the corner.
In clinical depression there is a sharp contrast. Often, the clinically
depressed person doesn’t see a corner. He or she may not even see that there is
a possibility of a corner. Clinical depression is something like being in a black
hole. The person feels trapped and the future may appear hopeless.
This perception of hopelessness is often accompanied by deep feelings of
sadness, loss of interest in what had previously made life meaningful and some-
times thoughts of suicide. The depressed person often has slowed reactions,
trouble concentrating and remembering, difficulty in sleeping and sometimes
a marked weight loss. When such problems persist over time, we are talking
about an emotional illness that merits careful evaluation and appropriate ther-
apy. I shall have much to say about the options for treatment that are available
and I hope the discussion will prove useful if seeking professional help is under
consideration.
5
6 Introduction
Between the occasional blue moods of everyday life and a severe clinical
depression, there are millions of people who experience periods of mild to
moderate depressed mood. They may experience some of the same symptoms
of the clinically depressed person, such as difficulties in sleeping and feelings
of sadness. Such people enjoy life much less than they would like. At times, their
daily routine seems like drudgery, but they continue to function, going to
school, working and taking care of their children. The depressed state dimin-
ishes the quality of life, but life goes on.
There is a lot that such depressed people can do to create a happier, more
rewarding life for themselves. In this book I shall present some ideas and infor-
mation that I hope will assist them in moving toward this goal. However, the
book is not intended as a substitute for professional treatment if that is what
is needed. For many people who experience chronic low levels of depression,
getting good professional help can make a world of difference in their lives. I
believe that this book will also be helpful to those who know or live with peo-
ple who are prone to depression. The information that shall be presented may
help these people better understand what is happening to their friend or loved
one.
To fulfill these objectives, I shall present in the first seven chapters of the
book a wide-ranging picture of what is currently known about depressed moods
and depression. We shall look at how depression is currently defined, examine
its demographic, biological, and psychological aspects, consider its antecedents
in childhood experiences, examine the role of stress in bringing on depression,
and look at its relation to alcohol and drug abuse. Then, I shall offer some ideas
about how to prevent depressed moods and how to cope with these moods
when they occur. The later part of the book will be devoted to the treatment of
depression, with a discussion of antidepressant medicines, psychotherapy, elec-
troconvulsive therapy and alternative treatments for depression. We will con-
clude with a discussion of the very troublesome issue of the recurrence of
depression, presenting some current views about how to lessen this risk.
1. Depressed Mood
and Depression
A grief without a pang, void, dark, and drear

A stifled, drowsy, unimpassioned grief,
Which finds no natural outlet, no relief,
In word, or sigh, or tear...
— Samuel Taylor Coleridge, “Dejection: An Ode”
Your mood colors the way you perceive your environment, the people
about you and yourself. If you are in a happy mood, you tend to look at oth-
ers and yourself through rose-colored glasses. Everything seems right with the
world. There is, indeed, some truth in the feeling that when you’re happy, the
whole world seems happy, too. People may not be happy in reality but if you’re
happy, it may not matter that much.
When you are feeling in a sad mood, you tend to look at things with a
negative perspective. Gone are the rose-colored glasses. Now you are wearing
very dark ones. And this overflow of bleak mood can affect the way you look
at yourself. An interesting experiment demonstrates how mood may influence
judgment. Before describing the experiment, I should state that researchers
have developed techniques that can be used to alter the mood of normal sub-
jects.
One of these mood induction techniques is hypnosis. Another compara-
tively simple technique that has been widely used is to ask the subject to read
a set of standardized phrases that are sad in content.1 An example would be,
“The way I feel now, the future looks boring and hopeless.” It has been repeat-
edly demonstrated that when people read these phrases and feel the mood as
they do so— they become more depressed. In contrast, reading happy phrases
tends to elevate mood. Mood can be that sensitive to change!
The experiment I am going to describe was carried out by Joseph Forgas
and his colleagues.2 For the experiment, the subjects were first interviewed for
a while on a variety of topics. These interviews were videotaped with the sub-
7
8 Understanding Depression
jects’ consent. On the following day, the subjects were given a mood induction
technique to make them feel either happier or sadder about themselves. The
subjects were then asked to make judgments about their own videotapes. The
subjects in the positive mood judged their performance as competent, confident
and socially skilled. The subjects who had been put in a negative mood saw their
previous performances as incompetent, clumsy and unskilled. Objective judges
did not see any difference in the two sets of interviews. It was all in the minds
of the subjects.
If depressed mood can make you think more negatively, it is equally true
that negative thoughts can depress your mood. Drawing on this observation,
Aaron T. Beck has developed one of the most influential theories about the
cause of depression, as well as an effective form of therapy, called cognitive ther-
apy.3 When mood and thinking patterns are negative, you may also see changes
in behavior, such as slowed reactions and a loss of interest in your usual activ-
ities. Moreover, there may be changes in the way you feel physically. A person
may have a variety of physical complaints and not sleep or eat as well as before.
Instead of a simple depressed mood, what we now have is a more complex sit-
uation — a mixture of symptoms. This group of symptoms is called depression.
The clinical description and understanding of depression has become
refined in recent years, but as we indicated in the preface, the notion that peo-
ple can become saddened and immobilized goes back a long way. Hippocrates
and Aretaeus, physicians of ancient Greece, wrote about people who suffered
from a form of depressive illness and advanced a naturalistic, biologically based
theory to explain it.4 Although the theory was inaccurate, their views of depres-
sion remain a testament to careful observation and the importance of building
testable explanatory models in scientific inquiry.
The world’s literature has its share of characters who appear depressed.
One finds depressed people in literary works ranging from the tales of, “A Thou-
sand and One Nights” to the writings of the German poet and dramatist Johann
Wolfgang von Goethe.5 Remember the despondent figure of King Lear in Shake-
speare or the guilt-ridden Lady Macbeth?
Among historical figures, Abraham Lincoln was described as a melancholy
man. He wrote to his law partner, John Stuart, “I am now the most miserable
man living. If what I feel were equally distributed to the whole human family,
there would not be one cheerful face on earth. Whether I shall ever be better,
I cannot tell: I awfully forebode I shall not. To remain as I am is impossible. I
must die or be better....”6
In her carefully documented book Touched with Fire: Manic-depressive Ill-
ness and the Artistic Temperament, Kay Redfield Jamison presents a long list of
well known poets, novelists, composers, and painters who may have been
afflicted with one form or another of depressive illness including bipolar dis-
order.7 This list includes poets Lord Byron, Emily Dickinson, T. S. Eliot, John
Keats, Edgar Allan Poe, Sara Teasdale, and Walt Whitman, novelists Charles
1. Depressed Mood and Depression 9
Dickens, Ernest Hemingway, F. Scott Fitzgerald, Herman Melville, and Leo

Tolstoy, composers Hector Berlioz, George Frederick Handel, Robert Schu-
mann, and Peter Tchaikovsky, painters Michelangelo, Vincent van Gogh, Paul
Gauguin, Jackson Pollock, and Georgia O’Keeffe. Jameson’s list includes some
of the major artistic talents in the history of Western civilization. Is there indeed
a link between depressive illness and artistic creativity? Jamison’s bibliographic
work suggests that this is the case.
While the concept of depression has its roots in early times, the attempt
to clearly define it as a clinical-disorder had to await the development of psy-
chiatry in the nineteenth century. The description and classification of men-
tal and emotional disorders gained great impetus during the latter half of the
nineteenth century, much of it resulting from the pioneering efforts of Ger-
man psychiatrist Emil Kraepelin. In eight editions of his Textbook of Psychia-
try, he distinguished between different types of mental illness, using such terms
as manic-depressive disorder, which remain part of psychiatric language today.8
The attempts to describe and classify what appeared to be different types
or shadings of depression have continued since Kraepelin’s time. Various
descriptive terms have entered the psychiatric literature, proving more-or-less
useful, including involutional melancholia, endogenous depression, reactive
depression, neurotic depression, and dysthymic disorder. Dysthymic disorder may
be the least familiar of these names, but is a term in current favor that refers
to depression which is typically not severe but is long lasting, the type of prob-
lem that may linger for years. Despite this formidable sounding list of diag-
nostic categories, the problem of meaningfully distinguishing between varieties
of depressive problems is not fully settled. The American Psychiatric Associa-
tion, through its task forces and committees, has been wrestling with the prob-
lem. The Association’s current thinking is embodied in its Diagnostic and
Statistical Manual of Mental Disorders.9 While there is some uncertainty con-
cerning the subtypings of depression, there is general agreement about the typ-
ical symptoms of depression. I shall now describe these symptoms.
Symptoms of Depression
As a starting point it is important to recognize that the diagnosis of depres-
sion is based almost entirely on the patient’s report of symptoms. The physi-
cal exam that is often essential in making a diagnosis of a physical illness is of
little help in making a diagnosis of depression nor are there yet laboratory tests
which are specific to depression. The diagnosis is based on what the patient
reports. In making the diagnosis, the physician or psychotherapist relies on a
list of nine symptoms. The rule of thumb is that if a patient reports five of these
symptoms and they have persisted for a period of time (at least two weeks) the
patient is diagnosed as experiencing major depression. Among the five symp-
toms, the patient must report either feeling sad or having lost interest in his or
her usual activities. So among the nine symptoms, these two can be viewed as
being particularly diagnostic.
Here then is a short list of the nine symptoms used in diagnosing depres-
sion.
1. Depressed mood
2. Diminished interest or pleasure in usual activities
3. Weight loss or gain
4. Insomnia, or excessive sleep
5. Psychomotor agitation or retardation
6. Fatigue
7. Feelings of worthlessness, guilt
8. Diminished concentration or indecisiveness
9. Suicidal thoughts
Let’s take a look at these symptoms in more detail.
One of the clearest signs of depression is mood. A sad, blue mood that per-
sists is usually a dead giveaway that something is wrong. Sadness is sometimes
visible in facial expressions. Depressed people may look glum and downcast.
Using the electromyograph to measure activity of the muscles, one can study
the facial muscles of depressed people. For example, electrodes can be placed
near the eyes to monitor the corrugator muscles, which pull the eyebrows down.
EMG readings for these muscles tend to be higher in depressed people and may
be even higher when depressed people think unhappy thoughts.10
There are times in life when sadness is a normal, expected response to
unhappy or tragic events. Bereavement is such a time and we expect a period
of grief and mourning as part of a psychological healing process. But protracted
sadness under any circumstances is something to be concerned about.
A second sign that a person is depressed is a loss of interest and pleasure
in his or her usual activities and pursuits. The person may simply go through
the motions or even stop the activities altogether. An example would be Arlene,
once an enthusiastic gardener, interested in cooking and entertaining, active
in her church. Her enthusiasm for all of these activities has dwindled. When
her friends asked her about this, she replied, “I don’t care anymore.” What was
important and fulfilling in her life had lost its meaning.
Changes in appetite and significant weight loss or gain can be a sign of
depression. Because changes in weight can also reflect a variety of medical prob-
lems (e.g., anorexia nervosa, cancer) as well as changes in living arrangements
and circumstances (e.g., leaving home for college, marriage, joining the army,
going on a diet to lose excess weight), one should be circumspect in applying
this criterion. If, however, you hear such statements as, “I’ve totally lost my
appetite, I don’t care about food anymore,” it certainly has the ring of depres-
sion.
Trouble in sleeping is another possible indication of depression. Obvi-

ously, not everybody who has trouble sleeping is depressed, but so many peo-
ple who are depressed have difficulty sleeping that this problem is often a
tell-tale sign. Sometimes the problem is what is called sleep onset insomnia. The
person goes to bed at night and can’t fall asleep. Instead of lapsing into sleep,
the person may begin to rethink and replay the events of the day or troubling
unresolved problems. As the person lies in bed, these thoughts may repeat
themselves over and over, something like a phonograph record that is stuck in
a groove. When we ask a depressed patient what he or she was thinking about
while struggling to sleep, we often gain a pretty good encapsulation of what
some of the person’s major problems are.
Overeating and oversleeping are signs of what has been called atypical
depression. Some depressed patients appear to be restless and agitated. In con-
trast, others have slowed reactions. They seem both slow in sizing up a situa-
tion and in responding. While it is difficult to separate these two components
of reaction in real life, efforts have been made to do so in laboratory experi-
ments. Research has shown that compared to normal controls, depressed
patients are slower in making physical reactions.11
The slowed reaction times which one finds in many depressed people can
show themselves in a variety of everyday activities including driving. In an
interesting demonstration of this tendency, Canadian researchers compared the
driving behavior of 18 non-medicated patients diagnosed with major depres-
sive disorder with a group of control subjects.12 Using a driving simulator which
took all of the subjects through a trip on a country road, the researchers
reported that the depressed patients showed slower steering reaction times and
were more likely to veer out of their lanes and/or collide with other vehicles.
We would need a large-scale study of the driving safety records of people who
are clinically depressed to see what kind of implications, if any, these findings
might have in the real world.
When people are extremely depressed, their body movements may have a
uniform, monotonous, limited character. Picture in your mind the graceful move-
ments of a dancer, then imagine what the opposite of that might be like. In a
metaphorical sense, it is as if the restriction in the patients’ movements mirror
the restriction in their current lives. When depressed patients begin to improve,
constricted body motion begins to become more mobile, complex and dynamic.
Chronic fatigue is yet another sign of possible depression. While all of us
get tired at times, depressed people often feel tired and lethargic. To get out of
bed in the morning may seem like a tremendous task. For some depressed peo-
ple, the day seems to drag like a clock going in slow motion and the person
may feel about as energetic as the clock. The combination of dysphoric mood
and fatigue can be immobilizing. Allison, a writer and teacher who was in the
midst of a depressive episode described this lethargic state well. “I began to feel
immobilized. I did not want to get out of bed. I remember needing to move
my car to keep from getting a parking ticket, but it felt like a major undertak-
ing to get up, get dressed, walk a couple of blocks and do it.”
When a person reports chronic fatigue and there is no clear physiological
basis for it, one must be alert to the possibility of an underlying depression.
Another sign of depression is excessive self-reproach. Therapists who have
worked with depressed patients have observed that many depressed patients are
overly self-critical. Freud described depressed patients in the following way:
“The patient represents his ego to us as worthless, incapable of any effort, and
morally despicable; he reproaches himself, vilifies himself and expects to be cast
out and chastised.”13 Depressed people may feel responsible for events they
really have no control over. They are often overly concerned with their own
faults, shortcomings and failings. The message may boil down to “I’m no good.”
The flip side of this conclusion is often, “I deserve to be punished.”
Many depressed people carry with them a large burden of guilt, a painful
feeling that they have violated the standards of what is right and wrong, what
is acceptable and unacceptable. These standards have strong emotional roots
in childhood learning experiences and particularly in the moral teachings of
parents. To feel you have violated these expectations can be a wrenching expe-
rience.
In addition to the substantial clinical observation that feelings of self-
reproach and guilt are often part of a depressive picture, there is some exper-
imental evidence that activating guilt may deepen the depressed mood, and
that this may happen on an unconscious level.14 The process may take place
without any awareness. The experimental procedure used in these studies is
interesting, though controversial, as it utilized the not-fully-understood tech-
nique of subliminal perception. Depressed subjects viewed short sentences or
phrases at such rapid speeds of exposure that they were unable to make out
what they were looking at. What the subjects saw was something like a flash or
a blur. When researchers used phrases like, “leaving Mom is wrong” or “I have
been bad,” the subject’s mood after the experiment became more depressed.
The effect was clearest in subjects who seemed more guilt-prone on psycho-
logical testing.15 Diminished ability to concentrate is also a possible sign of
depression. Patients will often complain of this problem in their jobs or school
work. A task that normally goes easily may not go along at all. Experimental
studies suggest that attention and learning may be particularly compromised
if the matter at hand stirs up unpleasant emotions.16
In the most recent edition of the Diagnostic and Statistical Manual of Men-
tal Disorders, indecision has been coupled with difficulties in concentration. I
have been puzzled by this coupling because focusing attention and decision-
making seem like quite different phenomena. Indecision often flows from
conflicts. While wrestling with choice — playing Hamlet — may be a sign of
depression in some people, why it should be included in a category with trou-
bles in focusing escapes me.
Thoughts of suicide are another sign of depression. Sometimes these

thoughts are expressed in verbal statements that are direct and unmistakable.
Sometimes the idea of suicide is expressed obliquely and not easily recogniza-
ble. The possibility of suicide in depression must be taken very seriously. Esti-
mates are that the lifetime risk of suicide in persons with serious depression
runs on the order of 15 percent while it is only about 1 percent for the general
population.17
Researchers have been carrying out studies to better understand the risk
factors that increase the chances of suicidal behavior in depressed patients.
Recent data suggest that among the classic symptoms of depression, some of
the ones to look out for are loss of appetite and weight, insomnia, and feelings
of guilt and worthlessness, and as one might expect, thoughts of suicide. Per-
sonality tendencies of impulsivity and aggressiveness are other signs to watch
out for. A concomitant problem of alcohol or drug abuse, and even as one study
suggests, heavy smoking — any such substance abuse could be indicators of
increased risk. Previous attempts at suicide are a marker for possible future acts,
and lack of a partner may also contribute to the risk.18
In addition to these nine symptoms that currently serve as the basis for
diagnosing depression, there are other characteristics which one often finds in
people who are depressed. These include difficulties with memory, a tendency
to ruminate about one’s problems, and the development of physical complaints.
Difficulties in memory may reflect difficulties in paying attention. People
who are having trouble concentrating and focusing may not absorb and remem-
ber what they are insufficiently attending to. And, indeed experimental stud-
ies of the memory of depressed people for verbal materials have found that
their memory was not as good as that of control subjects. In an early review of
these studies, Mark Johnson and Peter Magaro stated, “Given the frequent com-
plaints of memory impairment reported by depressed patients, a number of
investigators have attempted to verify this phenomena experimentally. The
majority of these investigations have examined memory processes in depressed
inpatient samples. Most have demonstrated some memory impairments when
depressed patients are compared with normal nonpsychiatric control groups.”19
Generally speaking, the more severe the depression is, the greater the problems
with memory. A recent study carried out in Norway suggests that the negative
impact of depression on memory may not be evident with patients who are
mildly to moderately depressed.20
One possible explanation for the difficulties in memory experienced by
many people who are depressed is that they are often very preoccupied with
their own problems. This self-focusing may interfere with their ability to con-
centrate on the external world and communications coming from others. It is
hard to remember things when it is a challenge to pay attention to what is going
on about you.
Many depressed people have a tendency to ruminate about their prob-
lems. Sometimes, they think about what is bothering them to the point it
becomes obsessive. And what often happens is that their thoughts and conclu-
sions are quite negative in nature which may only deepen the depression.
When a person has been feeling in a depressed mood — even in a mild
one — she or he will often report more physical complaints. As an illustration
of this pattern, consider some research Roland Tanck and I carried out using
our student diaries. We asked the students whether they were feeling depressed
during the day. We also asked them whether they had been experiencing any
physical symptoms during the day. To assist the students in recording these
symptoms, we provided a list of physical complaints such as headaches, nau-
sea, dizziness, weakness and diarrhea, and asked the students to check off any
of the complaints they had experienced. The students who reported feeling
higher levels of depressed mood reported more physical complaints.21
Depressed mood has a relation with physical symptoms. It is not, how-
ever, easy to establish what is cause and what is effect. It is possible that the
depressed mood may cause physical problems. However, it is also possible that
a person may react to physical problems by becoming depressed.
In exploring the symptoms the patient reports in a clinical interview, the
mental health professional will often gain enough information to go beyond
the basic diagnosis of major depression. He or she may be able to add some
“specifiers” to the diagnosis, asking such questions as is this a first-time event
or as frequently happens, a recurrent problem? Is the level of depression, mild,
moderate, or severe? Does the patient’s depression have atypical features? For
example, instead of experiencing insomnia, the patient reports sleeping too
much.
While the approach we have outlined to diagnosing depression has been
widely accepted for a number of years, a number of people working in the field
have raised questions about it. For example, some researchers have asked, do
all of these nine symptoms contribute to the diagnosis of depression? Perhaps
some of them do not and may be irrelevant in making a diagnosis. Recent stud-
ies carried out by Martin Zimmerman and his colleagues suggested that leav-
ing out weight loss or gain and indecisiveness would do little to change a
diagnosis of depression.22
Some psychologists have gone beyond making attempts to refine the cur-
rent approach to making a diagnosis of depression; they have raised funda-
mental questions about the the nature of depression, itself. They have asked,
is depression really a diagnostic category like tuberculosis or asthma that peo-
ple either have or don’t have or is it more like a dimension that ranges from a
little (most of us have times in which we feel depressed) to a lot. In the dimen-
sional view, what we call depression is really being high on this depression con-
tinuum (scale), somewhere beyond an arbitrary cutoff point. These differing
views of depression —categorical verses dimensional are clearly quite different
and these differences have implications for the way we think about depression,
treat depression, and the way we carry out research on depression. If we were
inclined to follow the dimensional model we would be more attuned to study
levels of depression rather than simply compare two groups of people, one of
which is categorized as depressed and the other as not depressed. While the
views of the mental health profession seem currently firmly rooted in the cat-
egorical camp, there has been some research which seems to support the dimen-
sional view.23 As it is a hallmark of science to change its models and theories
when data contradicts currently held views, it seems important to keep an open
mind about this question. It is possible that further research may cause us to
revise our thinking about the nature of depression.
Measuring Depression
These, then, are some of the typical symptoms of depression. How do we
measure depression as a practical matter? How do we say that this person has
a mild depression or that person has a more serious problem? The best method
we have to date for diagnosing a person as depressed is a clinical interview con-
ducted by trained psychiatrists or psychologists using a set of benchmark cri-
teria similar to the symptoms we have described. The most widely used guide
for such clinical interviews—considered the gold standard for diagnosing
depression is the Hamilton Depression Rating Scale.24
A good deal of research has demonstrated that one can get a reasonably
good estimate of what the clinicians would find in their interviews by using
questionnaires in which people report their own symptoms. One of the most
widely used of these self-report measures is a 21-item inventory developed by
Aaron Beck and his colleagues.25 Another inventory used in community stud-
ies on depression was developed by the National Institutes of Health’s Center
for Epidemiological Studies.26
The scale developed by Beck and his colleagues generally referred to as the
Beck Depression Inventory (BDI) has been revised twice since its original devel-
opment in the early 1960s. The BDI uses a dimensional approach with scores
ranging from zero (no indication of depression) to a theoretical maximum
score of 63. Beck and his colleagues have suggested cutoff points for the scores
indicating various levels of depression such as mild, moderate, and severe.
Because the BDI is self-administered and in my experience easily understood
by those using it, it has been a workhorse for psychological research on depres-
sion over the years. I have used it myself in a number of studies, exploring
problems such as the relation of depression level and recall for very early mem-
ories.27 The BDI has been translated into a number of languages ranging from
Japanese to Arabic and has proven useful to researchers abroad as it has in the
United States. While I will not reproduce any of the items from published inven-
tories such as the BDI, I would like to give you an idea of the types of ques-
tions that are used in self report measures of depression. The following are
some questions that are similar to those used in depression inventories:
1. Have you experienced extended periods of sadness during the past few
weeks?
2. Have you been having problems sleeping?
3. Has your appetite been poor lately?
4. Have you been more withdrawn from people in recent weeks?
5. Have you felt tired a lot of the time?
6. Have you noticed that you have little enthusiasm about doing things?
7. Have you been down on yourself lately?
8. Do you find that you are getting much less satisfaction from your
usual activities than you used to?
9. Have you recently been troubled by feelings of guilt?
10. Do you often feel like crying?
11. Have you been experiencing feelings of deep pessimism?
12. Have you recently been troubled by physical symptoms such as
headaches, nausea, or dizziness?
13. Have you noticed a decline in your desire for having a sexual experience?
14. Have you been feeling that you are very much alone in life?
15. Have you noticed you have had difficulty lately in concentrating on
your work?
16. Do you find yourself sluggish in your reactions?
17. Do you have feelings that nothing in life seems worthwhile?
18. Have you been feeling overwhelmed by the problems you have been
facing in life?
19. Have you been thinking that you are a failure in life?
20. Have people been telling you that you seem depressed?
The sample of preceding questions is a collection of items, not a psycho-
logical test. We would have to show by research that a score based on the
responses to such items is a reliable and valid measure before we could inter-
pret the results with any precision. Having said this, if you answered the ques-
tions and found that you had only a few “yes” answers, it seems unlikely that
you would have a serious depressive problem. On the other hand, if you
answered most of the questions yes, you might want to consider consulting a
mental health professional to discuss the things that are bothering you.
As we have indicated, most of us experience times in which our mood is
sad or blue and we may experience some of the symptoms of depression. What
makes these symptoms more serious or less serious is how intense they are and
how long they persist. Take mood for example. You can feel a little blue or you
can feel just terrible. It is the latter condition you worry about. There is no
absolute rule of thumb for how long depressed feelings persist before you should
begin to feel concerned, but certainly a couple of weeks of intense symptoms
is more than enough time to recognize that you ought to do something about
it. The American Psychiatric Association’s Diagnostic and Statistical Manual
suggests that two weeks of intense symptoms is enough to classify what is hap-
pening as a major depressive episode.
While we are discussing measurement, let’s consider the measurement of
mood. In contrast to the measurement of depressed states which may require
use of a variety of questions to explore a number of different symptoms such
as sleep and appetite disturbances— the measurement of mood seems straight-
forward. We are able to assess a person’s mood in surprisingly easy ways. One
such technique is to use the Adjective Check List.
Let’s say a researcher is trying to find out what your mood is like at this
moment. To do this, he or she might ask you to respond to a list of words that
describe various moods. The list will have been refined with the aid of statis-
tical procedures so that the researcher can derive scores to represent the inten-
sity of different moods, such as anger, anxiety or depression. To give you an
idea how these techniques work, we have drawn up a list of words that are sim-
ilar to those used in standardized adjective check lists. As was true for our ques-
tions about depression, this is not a psychological test, simply a way of showing
how researchers study mood.
If you are interested, try responding to the list of words using the follow-
ing procedure. Look at each word in the list in turn. If you don’t feel in the
mood described at all, check the box on the left. If you feel a little bit in the
mood described, check the box in the center. If you definitely feel that way, check
the box on the right.
Not at All A Little Bit Definitely

Affectionate 0 0 0
Alert 0 0 0
Angry 0 0 0
Anxious 0 0 0
Blue 0 0 0
Cheerful 0 0 0
Dejected 0 0 0
Distraught 0 0 0
Downhearted 0 0 0
Energetic 0 0 0
Fearful 0 0 0
Friendly 0 0 0
Glad 0 0 0
Gloomy 0 0 0
Happy 0 0 0
Irritable 0 0 0
Jittery 0 0 0
Joyful 0 0 0
Kindly 0 0 0
Lethargic 0 0 0
Merry 0 0 0
Optimistic 0 0 0
Pessimistic 0 0 0
Pleasant 0 0 0
Relaxed 0 0 0
Restful 0 0 0
Sad 0 0 0
Sociable 0 0 0
Suspicious 0 0 0
Thoughtful 0 0 0
Tired 0 0 0
Worried 0 0 0
Look at the words for which you checked “Definitely.” What kinds of
moods do these words suggest? Look at the words you checked “Not at All.”
What kinds of moods do these words suggest? Do you see any patterns? Now,
take a closer look at the words Blue, Dejected, Distraught, Downhearted,
Gloomy, Pessimistic and Sad. If you checked “Definitely” for several of these
words, chances are that your mood at the moment is depressed. Mood changes:
If you check this list again tomorrow, you might find a different pattern. When
depressed mood persists, however, there is a problem.
Mood Swings
It would be a very rare person indeed whose moods are constant. Some of
us have moods like shifting winds. We react to changes in body chemistry, to
events in our environment and to our thought processes consciously, and in
the psychoanalytic view, unconsciously as well. As we have indicated, it is pos-
sible to induce a depressed mood by simply reading and trying “to feel” a list
of depressive phrases.
If you think about it, you can probably recall books that you have read or
movies you have seen that left you feeling depressed. Try listening to the last
movement of Tchaikovsky’s Pathétique Symphony (No. 6). It can be a real
downer.
The other side of this process is mood elevation. Try thinking of people,
parties, music, vacations, books, sporting events— good times that have elevated
your mood, producing a sense of well being.
We mentioned that body chemistry can influence mood. A good example
of this is the premenstrual syndrome (PMS) experienced by many women.
These women may feel depressed, anxious and irritable during the premenstrual
phase of the menstrual cycle. It is a little difficult to estimate how many women
experience premenstrual depression because many women who have this prob-
lem also experience intermittent depression at other times during the month.
However, there are studies which suggest that about 40 percent of the women
who report PMS depression experience an increase in depressed mood only in
the premenstrual period and return to a normal mood after menstruation
ceases.28
What kind of variation in mood do you experience during a day? Are you
more likely to be bursting with enthusiasm during the day and dropping off as
the day ends? Or are you a grumbler in the morning and a free spirit in the
evening? Are you a night person?
Roland Tanck and I were interested in the problem of mood swings within
the day and used our diaries to obtain some information from college stu-
dents.29 The results might surprise you. If you feel brighter during the day and
your mood deteriorates somewhat as evening falls, you are not alone.
In reflecting upon their day’s experiences, most of the students reported
that typically the downside of mood was in the evening. The students felt best
during various times of the day, but by evening, the day’s activities seem to have
taken a toll on them and their mood deteriorated. A night’s sleep seemed to
clear things up and they were ready to go in the morning.
We found fewer instances of the reverse pattern, of “night people” stu-
dents who felt more depressed in the morning and peaked in the evening.
Some students in our sample reported having periods of depressed mood
that persisted right through the day with little evidence of mood swing. It was
these students with stretches of rather constant depressed mood who were more
likely to report the typical symptoms of depression such as a plethora of phys-
ical complaints.
Mood Swings in Clinical Depression

SEASONAL AFFECTIVE DISORDER
Over 100 years ago during an early exploration into Antarctica, the expe-
dition physician, Frederick Cook noted that during the darkness of winter,
members of the expedition became markedly depressed. He wrote that, “The
curtain of blackness which has fallen over the outer world of icy desolation has
descended upon the inner world of our souls. Around the tables, in the labo-
ratory, and in the forecastle, men are sitting about sad and dejected, lost in
dreams of melancholy from which, now and then, one arouses with an empty
attempt at enthusiasm.”30 Writing in the American Psychologist, Lawrence Palin-
kas noted that Cook endeavored to treat the symptoms by having, “Crew mem-
bers sit in front of large blazing fires” and this may have been the “First recorded
attempt to use light therapy to treat symptoms of winter depression, or sea-
sonal affective disorder.”31
In recent years scientific studies carefully carried out in laboratories in

both the Arctic and Antarctica have confirmed the general thrust of Cook’s
observations. Prolonged exposure to a dark environment has a deleterious effect
on mood and behavior. In reviewing these studies, Palinkas concluded that,
“When viewed collectively, therefore, these results suggest that behavior in
Antarctica is influenced by patterns of exposure to daylight associated with
time of year and latitude.”32
Cook’s observations were telling and his choice of therapy astute. But, I
would imagine that long before his time the depressing impact on humans of
the darkened days of winter could not help be noticed. Shakespeare employed
the idea metaphorically in one of his plays chronicling the War of the Roses in
England, the struggle of the houses of Lancaster and York to control the English
throne. In the opening of the play Richard the Third, Shakespeare penned the
lines, “Now is the winter of our discontent made glorious summer by this sun
of York.”33
My first exposure to Seasonal Affective Disorder occurred during my early
years of private practice before the disorder had found its way into the estab-
lished listing of mental disorders, the Diagnostic and Statistical Manual of Men-
tal disorders. The patient, a man in his late 20s came to see me reporting some
of the usual symptoms of depression such as a sad mood, loss of energy, and a
loss of interest in his usual activities. Interestingly, he told me that his life
seemed so “draggy” in the winter, but how he felt so much better in the sum-
mer when he played tennis and softball. I thought part of the problem might
be the recent holiday season and we talked about the feelings he experienced
in being alone and away from home during Christmas. Still, this did not seem
to be the crux of the problem. During therapy he alluded several times to the
feeling that everything seemed so dark and dreary in the winter. I suggested
that he try lighting up his apartment with bright lights and see if that might
help. I don’t know whether he thought going to a therapist who offered such
simple-minded advice was a poor investment, but he ceased coming soon after-
wards.
Some years later, I began to read of a new concept called seasonal affective
disorder. Patients report they feel OK in the sunlit days of summer but feel ter-
rible during the dark days of winter. Norman Rosenthal and his colleagues have
been largely responsible for developing the idea.34 Among the therapies that
seem effective in treating this mid-winter case of the blahs are very bright
lights. Interestingly, artificial light therapy seems to work best when it is car-
ried out in the morning. Perhaps it mimics the pleasant sensation of awaken-
ing on a bright summer day. In any event, I was delighted to learn that my
off-the-cuff suggestion to a patient was not idiotic after all. To feel less cheer-
ful, less happy and energetic in the dark days of winter is a common experi-
ence. A telephone survey carried out in Montgomery County, Maryland, a state
in which the winters are not especially severe, almost everyone surveyed (92
percent) noticed seasonal changes in their moods. About a quarter of those

surveyed reported that these seasonal changes presented a problem and for
about four to 10 percent of the sample, the problem was severe enough to sug-
gest Seasonal Affective Disorder (SAD).35
Between the nuisance level of mild winter blahs and the frank depression
of SAD, there is a category which has the imposing name of Subsyndromal Sea-
sonal Affective Disorder. One might think of this category as “almost, but not
quite” SAD. It is difficult to estimate the prevalence of SAD and its subclinical
variety because if we are correct in our thinking, the prevalence of these prob-
lems should vary with latitude and climate. And indeed a study carried out in
the mid 1984 found this to be true. The title of the study could not be more
explicit in this regard, “Seasonal Affective Disorder: prevalence varies with lat-
itude and climate.”36 Go to northern lands and you would expect to encounter
more SAD.
There have been reports that seasonal depression may work the other way
as well-feeling OK in the winter and depressed in the summer. This seems
somewhat harder to explain than its counterpart. A case of this atypical pat-
tern of seasonal depression was described by Thomas Wehr and his colleagues:
Ms. A, a 66-year-old married retired secretary, had had recurrent sum-
mer depressions, beginning in March-April and ending in August–October,
for at least 15 years. When depressed, she was indecisive, had negative thoughts,
and scarcely spoke. She had frequent crying spells and suicidal thoughts.
Because of lethargy, lack of motivation, and difficulty concentrating, she
engaged in no activity voluntarily and tried to sleep as much as possible. In the
fall and winter she was energetic and outgoing. She required less sleep, was talk-
ative and had racing thoughts. Her clinical state appeared to be influenced by
changes in climate and weather. Her depressions began earlier than usual dur-
ing spring vacations in Florida, and remissions occurred during midsummer
vacations in New England.... We observed a temporary remission when an
unusual cold front reduced the temperature to 39° F in June. Furthermore, she
appeared to improve after an experimental cold treatment, as just described.37
Researchers have been studying people reporting seasonal depression, com-
paring them with people whose depression is not seasonal. One interesting
observation is that the seasonal depressives do not have difficulties in getting
enough sleep. They often sleep too much. In addition, they may have very good
appetites— and often have a tendency to crave carbohydrates. This pattern is
very reminiscent of what has been called atypical depression.
Since the behavior of animals as well as humans is affected by seasonal
changes— one thinks of the hibernation of bears, it is no great leap to look for
the causes of SAD in our biology. Among the prime suspects are our circadian
rhythms (our biological internal clocks) which seem to shift with the seasons
and the action of melatonin, a hormone secreted by the pineal gland in the
brain. Melatonin influences the sleep-wake cycle and when administered as a
drug can alter the sleep-wake cycle. The neurotransmitter, serotonin, of which
we will have much to say about in later chapters is an almost automatic sus-
pect in any depressive illness and has been linked to the craving of carbohy-
drates which is a characteristic of SAD. Psychological vulnerabilities to
depression can also play a role in transforming normal unenthusiastic reactions
to long dark days into SAD. We shall consider these causes in later chapters.
Bipolar Disorder
The clinical disorder of bipolar disorder is characterized by pronounced
shifts in mood. The disorder was recognized in the mid nineteenth century by
a physician named J. P. Falret, who published descriptions of manic excitement
and depression and used the term circular insanity to describe the phenome-
non.38 This legalistic and pejorative term never received much currency and was
replaced by the diagnostic labels of manic depressive disorder and bipolar disor-
der, which have essentially the same meanings. The key elements in bipolar
disorder are dramatic swings in mood. At times the patient may be very
depressed, reporting many of the symptoms in our earlier description of clin-
ical depression. However, at other times, the patient will be in a hyperelated
state, which has been termed mania or hypomania, depending on severity. The
patient may engage in a whirlwind of activities, thoughts firing rapidly from
one idea to the next and speech difficult to interpret. The need for sleep seems
to vanish. Self-esteem becomes inflated. Prudence may disappear and the
patient may do some very rash things.
In a manic state the patient may make all kinds of plans, look up old
friends— sometimes calling them in the middle of the night — go on buying
sprees, even drive recklessly. This state of euphoric mood and hyperexcitement
seems like it is 180 degrees away from the patient’s depressed state. Hence the
term bipolar disorder.
In their booklet, A Story of Bipolar Disorder, the National Institute of Men-
tal Health included a very useful checklist of signs of mania presented in the
form of first person statements.39 The statements provide a good sense of what
mania is like.
I feel like I’m on top of the world

I feel powerful. I can do anything I want, nothing can stop me.
I have lots of energy.
I don’t seem to need much sleep.
I feel restless all the time.
I feel really mad.
I have a lot of sexual energy.
I can’t focus on anything for very long.

I sometimes can’t stop talking and I talk really fast.
I’m spending lots of money on things I don’t need and can’t afford.
Friends tell me that I’ve been acting differently. They tell me that I’m
starting fights, talking louder, and getting more angry.
These signs are indicative of bipolar disorder. If the symptoms are clear
enough to call it a manic episode, then the condition is classified as bipolar
disorder Type I. If the symptoms of manic behavior are less severe — what we
call hypomanic, the condition is called bipolar disorder Type II. People who
are hypomanic might exhibit some of the same behaviors as people who are
manic; they may appear to be very energetic, even euphoric, but their thoughts
and behavior are not as erratic and disorganized as people who are clearly
manic.
People who have bipolar disorder typically go through cycles with manic
episodes, depressive episodes and normal periods. A revealing study carried
out by Richard Depue and his colleagues tells us a good deal about the behav-
ior of people with bipolar depressive problems.40 The subjects in the study had
bipolar problems but were not at that time impaired enough to require hospi-
talization. They reported increased and decreased energy patterns, uneven pat-
terns of productivity, mental confusion, high and low sociability patterns, high
and low interest patterns, increased and decreased sleep patterns, and highs and
lows in sexual interest.
Depue reported that typically depressed episodes lasted from three to six
days. The duration of manic episodes was about the same — two to six days.
About two-thirds of his subjects had between two and six depressed episodes
per year with about the same numbers holding for manic episodes. The impres-
sion one gets from these statistics is that the outbreaks of bipolar symptoms
were fairly frequent, but time limited. For Depue’s sample of people whose
problems were not serious enough to require hospitalization, the episodes
seemed to run their course.
The researchers described a case that illuminates some of the clinical fea-
tures of bipolar disorder. The subject, Ms. S, was an 18-year-old college stu-
dent. The researchers first described some of the behaviors of her hypomanic
phase. The following are some excerpts:
Mood. Feeling clearly higher or happier than is usually the case, “as if I have a
different personality, I feel hyper, and I fool around a great deal, laughing and
joking all the time.” Other people notice the change in mood and comment to
her about it.
Energy and need for excitement. She has greatly increased energy that “goes with
the high feelings.” People comment on this, usually saying that she “ought to slow
down” or that she is “wearing them out.” She participates in many more sports
activities, goes more places than usual (“to see people, stores, bars, anywhere”),
and does other activities that she might not ordinarily do. During these active
times she can get so excited that she is unable to sit still, and she jumps from one
activity to another.
She reports an intense need for excitement, and begins new activities with lots
of enthusiasm and then quickly loses interest in them. For instance, in one recent
phase, she started skiing lessons, two new embroidery works, needlepoint lessons,
learning a new complicated card game, and she joined a women’s group, but
dropped all of them at the end of her 2-week hypomanic period....
Thoughts, speech and distractibility. During these phases her thoughts race so
fast that she “can say about one half of a thought and then it is gone.” Also, her
attention jumps rapidly from one thought to another so that she loses her “train
of thought totally” At these times, she talks very fast, and stumbles over words,
and others complain that they cannot hold a conversation with her....
Irresponsible behavior. She spends money she cannot afford or other people’s
money.... [S]he is sexually active with new male friends, which leads to trouble
with her steady boyfriend; she gets into a lot of verbal, and sometimes physical,
fights; she frequents bars more and drinks more when she goes to bars; she drives
recklessly (goes through red lights and stop signs) and faster than usual (more
than 10 miles over the speed limit, whereas this is not usual for her).
The authors then describe the behaviors of her depressive phases.

Mood. Both depression and irritability, but mainly the former. Others always
tell her she looks sad or depressed during “lows,” and the feeling is described as
“painful.” Nonverbal cues of depression are apparently evident in facial expres-
sion, since others always comment on her depression, and she has frequent cry-
ing spells, without understanding why, and has an almost constant urge to cry....
Energy and motor activity. During “lows” she feels very tired and worn out.
She does not do school work (“couldn’t if I tried”). She could manage to go
out, but she “wouldn’t go out on my own initiative.” She reports that she is
“slowed down” and that “moving is more difficult.”
Concentration. Her concentration is poor; it is “difficult or impossible to read.”
Somatic complaints. Her somatic complaints are frequent during “lows” (head-
aches, blurred vision, constipation; vacillates between feeling too hot and too
cold)....
Cognitions. She reports a range of negative cognitions, including indecision
over small matters, pessimism about present and future, being a burden to her
family, that she would be better off dead....
Ms. S had been experiencing hypomanic and depressive periods since her
first year of junior high school. It was reported that she might experience four
phases in a year, each of which would last for at least two continuous weeks.
With four manic and depressive episodes a year, Ms. S would meet the
minimal criteria for what is called “rapid cycling.” Four or more manic or
depressive episodes in a year is a benchmark for rapid cycling and it is not at
all uncommon for bipolar patients to reach this benchmark. In a recent study
carried out in the Netherlands, nearly 40 percent of a large group of bipolar
patients studied were classified as rapid cyclers. In the study, it was found the
rapid cyclers were more likely to be diagnosed as bipolar type I than bipolar
type II, were likely to have experienced abuse as a child, and to have abused
drugs.41 A long-term follow-up study carried out in Italy suggests that for many
patients, rapid cycling can become a way of life — a pattern that continues over
the years.42
There are some patients who experience very rapid cycling — a complete
turn around in only 48 hours, and some patients who cycle even more rapidly
than that. One can imagine how bewildering that must be, not only to the
patient but to his or her friends and family.43
What are bipolar patients like when they are in a non episodic, normal
state? Do they have characteristic features of personality, and if so, how would
they differ from unipolar patients? A large-scale study using a variety of person-
ality tests found some interesting differences between bipolar type I, bipolar
type II, and unipolar depression patients when they were in a recovered state.
The unipolar patients tended to be insecure and introverted. The bipolar type
I patients were surprisingly most nearly normal on the tests while bipolar type
II patients were very conscious of experiencing dramatic, uncomfortable
changes in mood. They were the ones who saw themselves as emotionally unsta-
ble. It may be that the Type I bipolar patients in the study (who actually expe-
rienced more pronounced manic episodes) were going through a process of
denial when it came to viewing themselves and their symptoms during recov-
ery.44
As is true for their counterparts with unipolar depression, people who
have bipolar disorder tend to perform less well than control subjects on tests
of attention and memory. Recent studies have reported contradictory results
as to whether bipolar type I or bipolar type II patients experience these deficits
more severely, but it seems clear that such deficits are a part of the picture of
both types of bipolar disorder.45
Thoughts of suicide and attempted suicide are characteristic of patients
with bipolar disorder. Studies carried out in Finland indicated that about half
of the bipolar patients studied had at some time in their lives made a suicide
attempt.46 Bipolar patients are a relatively high risk group for suicidal behav-
ior. During depressive episodes, if the patient reports feeling hopeless, this should
be taken very seriously.
2. Depression in the
United States
We shall now turn to the questions of how prevalent depression is in the

United States and who appears most vulnerable. In pursuing our inquiries, we
are going to put on the hat of an epidemiologist–the statistically trained scien-
tist who collects and analyzes data on diseases. In this role, we will ask such
questions as: How many people in this country suffer from depression and
which groups in the population seem to be at higher risk of becoming depressed?
Are men or women more likely to become depressed? Does being in a minor-
ity group increase one’s vulnerability? Does it make a difference whether one
lives in an urban area or in the countryside? And what relation does the onset
of depression bear to one’s age? The answers to such questions will help us bet-
ter understand the scope of the problem of depression in this country and iden-
tify groups of people at greater risk.
How does one estimate the number of people who suffer from depression?
The problem is more difficult than it may seem. One possible approach would
be to survey the nation’s mental health centers, psychotherapists in private
practice and family physicians, asking how many people are being treated for
depression and who these people are. The problem with this approach is that
a very large number of people who are depressed do not seek professional treat-
ment. Moreover, the people who do seek treatment are not likely to be repre-
sentative of the entire population of depressed people; they are likely to be
more affluent and better educated. Minority groups will be underrepresented.
Probably the only way to estimate how many people are depressed in the
United States is to go knocking on doors in our cities, towns and farms, to sur-
vey representative samples of our population and to ask questions that will
accurately tell whether a person is depressed. And you have to do this in a way
so that people will not slam the door in your face. After all, information about
emotional health is sensitive.
In the 1980s The National Institute of Mental Health (NIMH) made the
first concerted effort to address the problem. Researchers working under the
auspices of NIMH developed an interview guide — a series of questions that
26
2. Depression in the United States 27
enables one to identify with reasonable accuracy people with different mental
and emotional disorders. The technique was validated by comparing the results
obtained using the interview guide with the results from clinical evaluations.
The interview guide was found to be acceptable for community surveys. Hav-
ing said this, the technique should be viewed as a screening instrument and
not as an ideal measure of depression. Like any other self-report measure of
depression, it will classify some people who are actually clinically depressed as
not depressed and some people who are not depressed as depressed. There is
an error rate.1
In large scale studies, researchers used the interview guide in selected com-
munities in Connecticut, North Carolina, California, Maryland and Missouri.
Thousands of people were interviewed in their homes. The results from these
surveys indicated that about 5 percent of the adult population have suffered at
one time or another from a major depression and 3 percent have experienced
a protracted period of moderate depression (dysthymic disorder).2 Translating
these percentages into raw numbers, something like 9 million adult Americans
were thought to have experienced a major depression and 5 million dysthymic
disorder. At any given point in time, the number of persons experiencing
depression would be less, though still numbering well into the millions.
A large majority of the cases of depression uncovered in the 1980 surveys
were cases of unipolar depression. While the rates for experiencing a major
depression were about five in one hundred, only one out of one hundred peo-
ple interviewed reported ever experiencing a manic episode. Bipolar disorder
was clearly less prevalent than unipolar depression.
Studies carried out using the NIMH interviewing technique suggested that
the chances of a person becoming depressed in the 1980s were higher than they
were in past generations. This conclusion is based on the findings that people
who were in their twenties were much more likely to report having experienced
a depressive illness in their relatively short lives than people who were senior
citizens. If this was indeed the case, it was a provocative observation.
There are, of course, problems in making comparisons between people at
very different age ranges with different memories. One may raise questions
about how reliable the memories of older people are about emotional troubles
experienced many years earlier. Still, the apparently large increase in the rate
of depression cannot be easily dismissed.
Other more recent straws in the wind buttress the possibility that the
prevalence of depression in the population has been on the rise. Two recent
large scale surveys of the prevalence of depression in the American population
indicate that the figure now is substantially higher than was estimated from the
studies carried out during the 1980s. In one of these studies, “The National
Comorbidity Survey Replication,” carried out between 2001 and 2003, a nation-
ally representative sample of American households was surveyed using profes-
sional interviewers of the University of Michigan School of Social Research. In
this study over 9000 people were interviewed. It was found that the lifetime
prevalence of major depressive disorder — the percent of people who have expe-
rienced such depression at some time in their lives was not of the order of 5
percent as was reported in the 1980s, but more than three times as large — nearly
17 percent.3 In an even larger study, “The National Epidemiologic Survey on
Alcoholism and Related Conditions,” over 43,000 people were interviewed.
The prevalence of depression in this study was 13 percent.4 In discussing their
results, the researchers noted that their data suggested a higher prevalence of
depression than was noted in earlier studies. In both of the recent studies the
highest lifetime prevalence of depression had shifted from younger people to
middle-aged people.
As was true for the previous analysis, one cannot rule out the possibility
that the differences between the findings of the 1980s and the more recent
findings may be the result of artifacts rather than represent real differences. For
example, there were differences in the samples used; the more recent studies
used nationally representative samples while the earlier studies sampled selected
geographical areas. However, it seems unlikely that these different sampling
procedures would have produced such dramatic differences in the findings.
Another line of explanation involves possible changes in public attitudes about
depression. With the extensive flow of public information about depression in
recent years and the heavy advertising of the pharmaceutical industry promot-
ing antidepressant medicines, it seems likely that people today are both more
knowledgeable about depression and more open about revealing the problem
than they might have been 20 years earlier. Perhaps, the earlier estimates for
major depressive disorder were on the low side because the people interviewed
may have been more reluctant to admit having the problem.
Given these cautionary notes, we still cannot dismiss the possibility that
the data means exactly what it says, that there has been a substantial increase
in the prevalence of major depressive disorder in the United States over the last
several decades. If this is indeed the case, it is an intriguing question as to why
this would be so.
Why should people today be more prone to being depressed than people
of past generations? While this is a tantalizing question, there are so many dif-
ferences between the lifestyles of today and earlier generations, that it is difficult
to ascribe the apparent increase in depression to any one reason. One would
be comparing an era of smaller communities to sprawling cities and suburbs,
to jobs using manual typewriters and card filing systems to those using high
speed computers and ever more sophisticated information technology. If I were
forced to pick one reason to explain the apparent increase in depression, my
candidate would be the breakdown of social support systems and most impor-
tantly, the family. The family has traditionally provided the individual with
meaning and security. However, there has been a large increase in the number
of families experiencing divorce and separation. Moreover, one is less likely to
have one’s extended family — aunts, uncles, cousins and grandparents— within
hailing distance as might have been the case in the past. Today’s lifestyle tends
to scatter families. An individual may feel isolated, even rootless. In times of
trouble and emotional stress, there may be no one close to turn to.
The idea that family ties, or to use a broader sociological term, social inte-
gration, has a relation to depressive behavior, is not a new one. One of the
founding fathers of sociology, Emile Durkheim, reported in nineteenth-cen-
tury France that persons who were more integrated into the society (e.g., mar-
ried persons, persons coming from larger families) had lower suicide rates than
those who were less integrated.5 I shall return to this theme — that social sup-
port has protective value against depression in later chapters.
Sex Differences in Depression

When we compare groups of men and women we usually find that women
are more likely to be depressed. It should be stated that this is not always the
case. For example, I once studied a sample of over 200 college students using
the well-respected Beck Depression Inventory to assess depression and found
no difference between the male and female students. However, when we exam-
ine the case records in treatment centers such as mental hospitals and outpa-
tient clinics, we typically find that more of the cases diagnosed as depressed
are women. Moreover, in all of the major household surveys undertaken, we
find that more women than men report being depressed. This is a very robust
finding.
A number of explanations have been offered to account for the higher rates
of depression found in women. One theory is that women may be more bio-
logically vulnerable to depression. It has been suggested that this vulnerability
may relate in part to the reproductive system in women. Many women expe-
rience depressed reactions during the premenstrual phase of the menstrual
cycle. When such distress is pronounced, it may be given the name of premen-
strual dysphoric disorder. Moreover, many women experience depressed reac-
tions following the birth of a child. This postpartum depression is a widespread
phenomenon, with a mix of biological and social elements. In Western soci-
eties estimates are that about one in 10 new mothers will experience this prob-
lem.6 A recent study of over 4000 American women reported a figure of nearly
18 percent with depressive symptoms.7 Postpartum depression has been reported
in such widely differing societies as Hong Kong, Dubai of the United Arab Emi-
rates, Turkey, and India.8
Researchers have carried out studies trying to ascertain what factors tend
to be associated with postpartum depression. It was thought that the method
of childbirth — vaginal verses cesarean might make a difference in this regard —
that cesarean delivery might be associated with postpartum depression but a
recent meta analysis of existing research casts doubt on such a linkage.9 Hav-
ing a history of depression is a risk factor for postpartum depression as is smok-
ing.10 Poor relationships with partners and negative feelings about pregnancy
are probably not helpful.
Postpartum depression has implications for child care. Research suggests
that women who develop postpartum depression are less likely to play with
and talk to their infant children and more likely to use harsh punishment.11
The influence of biology in promoting depression may be most evident
when a girl enters puberty. Prior to that time, research shows that boys and
girls do not differ in the likelihood of their being depressed. When girls reach
the age of about 13, all that changes. The frequency of depression increases
markedly for girls. Not so for boys, at least not yet. But, for girls, mid-puberty
is the time in which depressive symptoms tend to increase, and the difference
between males and females in the report of depression begins to emerge.12
Studies attempting to tie ovarian hormone levels directly to the experi-
ence of depression in both adolescent and adult females have produced some
positive and quite a few negative results. For example, a study reported by
Brooks-Gunn and Warren found no relation between levels of depressive symp-
toms and any of five hormones tested.13 If, as this study suggests, it is not the
hormonal changes themselves that are directly associated with depression, then
it seems plausible that it is the way girls deal with these changes in their every-
day lives that may influence vulnerability to depression. The onset of puberty
may place a girl into a new status within her family and among her friends,
with new expectations and challenges. Going into the teen years is a major
adjustment which for many girls can be difficult and threaten their self-esteem.
Because many girls tend to internalize problems, they may react by feeling low
and dispirited.
A second type of explanation for the gender differences in the report of
depression emphasizes such psychological vulnerabilities. Studies show the girls
tend to experience more negative events during childhood and adolescence
than boys.14 Such negative events, by themselves, can promote depressed feel-
ings. Negative mindsets can exacerbate the meaning of these events, making
them seem worse than they actually are and there is some evidence that girls
may be more likely than boys to have such mindsets.15 Girls tend to place more
emphasis on social relationships than boys and may be more likely to experi-
ence personal rejection in the insensitivities that often characterize these rela-
tionships. Finally, girls tend to place a great deal of importance on their personal
attractiveness and studies show that a large majority of young adolescent girls
are dissatisfied with their body image.16
A third, more sociological type of explanation is that the role of women
in our society often places them at a disadvantage, both economically and psy-
chologically, leaving them in situations that increase their vulnerability to
depressive reactions. Let’s illustrate this idea with two case examples.
Tracy tells a story of being in an unhappy marriage. She was married

shortly after high school graduation and had three children over the next six
years. In the last two years her relationship with her husband has deteriorated,
and he has been physically abusive. Tracy would like to leave him, but feels she
can’t. She has small children to support and sees no way of doing it. She feels
dependent and powerless.
Denise is a single mother. She has near total responsibility for bringing in
money from a job, keeping up the house and raising two children. This triple
responsibility puts her in a perpetual time squeeze that creates high levels of
stress, particularly when something goes wrong, like sickness in the children
or herself. While both Tracy and Denise are vulnerable to depression, because
of their circumstances, I suspect that it is Tracy who may be the most vulner-
able of the two for Denise can make adjustments to reduce the stress load in
her life; while Tracy faces a very difficult road.
A fourth type of explanation is that the cultural definition of being female
permits women to more easily admit having emotional problems. From early
on, males in our society are raised to be self-reliant and not to appear weak.
The need to project a strong image may deter some men from admitting that
they have a depressive problem and from seeking the help they need. Accord-
ing to this theory, men may have a higher rate of depression than is believed,
but it is simply not reported.
Many men feel that if they express the fact that they are depressed to oth-
ers, they may not only feel a loss of self-esteem, they may experience rejection.
Constance Hammen and Stefanie Peters ran an experiment that suggests such
fears are not groundless.17 Try the experiment on yourself. Read the following
description of a young woman:
Susan is 18 years old and a freshman in college. She was a good student in high
school, well-adjusted, and got along well with her schoolmates. However, a cou-
ple of problems have developed since she started college. She is finding the course
work quite a bit more difficult than she had expected, and lately it seems like her
boyfriend from high school is losing interest in her.
For the past few weeks, Susan has been feeling pretty down. She’s feeling really
miserable about what’s been happening in her life and can’t imagine that things
will ever get any better. When she goes out with her friends or her boyfriend,
she can’t seem to shake her gloomy feelings and enjoy herself. Susan’s been try-
ing to keep up with her schoolwork, but she’s falling farther and farther behind
because most of the time she gets so discouraged and pessimistic that she gives
up. The other day one of Susan’s friends asked her if she wanted to get together
for lunch, but Susan said “no” because she hasn’t really felt like eating lately and
found that she had no appetite at all. Often she feels like there’s no point in even
getting up in the morning, and, in fact, Susan has been staying in bed longer and
longer every morning. It seems like she just doesn’t have any energy left for any-
thing.
Now ask yourself the following questions: How much would you like to
have this person as an acquaintance? How much would you like her as a co-
worker on a task? How much would you like her as a close friend?
Now go back and read the description of the person again, only this time,
substitute a name like Bill or Jack for Susan, and girlfriend for boyfriend. When
you finish, ask yourself the same three questions.
The subjects in the study carried out by Hammen and Peters were more
likely to reject the person described when identified as a male than when
identified as a female.
Urban and Rural Comparisons

One can make a case that the atmosphere of many cities is more turbu-
lent than that of small towns and rural areas. Many big cities have serious prob-
lems with crime and drugs. They are congested, noisy and seem impersonal.
In these respects, the stress-arousing potential of the city seems higher than that
of rural areas. At the same time, the stress buffering potential of family and
close friends often found in integrated small communities may be diminished
in the city. One might expect that these conditions could lead to higher rates
of depression in urban areas.
The idea that one might find less depression in low-stress environments
receives some support from research conducted in close-knit, less technolog-
ically advanced communities. For example, researchers studying a preliterate
society in New Guinea in 1984 found little evidence of depression or suicide.
A study of the Amish people in Lancaster County, Pennsylvania, also found low
rates of unipolar depression.18 In a systematic study, researchers compared rates
of depression in several urban and rural American communities. The research
team surveyed five counties in North Carolina. One of the counties (Durham
County) was part of a major urban center containing several well-known uni-
versities and an industrial park. The four rural counties contained no major
industries and were described as representative of the rural South.
Carefully chosen samples of people in these communities were interviewed
using the NIMH interview guide. The results? Reports of current major depres-
sive episodes were three times as frequent in the urban county. When the
researchers controlled statistically for a number of important social and demo-
graphic factors, such as sex, education, race and selective migration, they con-
tinued to find a substantial difference in the rates of depression between the
urban and rural areas. The results indicated that urban life is associated with
a higher risk of depression.19
The tendency observed in the North Carolina study for residents of urban
areas to more frequently report being depressed than residents of rural areas
has been observed in other countries. Several studies carried out in the United
Kingdom as well as studies carried out in Canada have reported this tendency
and there is some suggestive data along these lines that was collected in Nige-
ria. There appears to be elements in urban living which increase vulnerability
to depressive reactions.20
There is another interesting pattern which may tie in here, if only loosely.
Studies have found that some groupings of people who immigrate to the United
States are less depressed than their counterparts who were born in this coun-
try and reside here. This is particularly true for white immigrants, presumably
coming in the main from Europe and English-speaking countries and is also
the case for Mexican immigrants.21 If a person moves here from such countries,
the data suggest that he or she is not as likely to be depressed as their counter-
parts who have become acculturated to our society.
One possible explanation for this difference is that the lifestyle of the coun-
try of orgin and particularly the routines of the workplace may be more relaxed
than what we find here in America. Lower levels of stress tend to be reflected
in lower levels of depression. The individual choosing to immigrate to Amer-
ica may come here to take advantage of the economic opportunities that this
country offers. However, as the immigrant becomes acclimated to America, he
or she may find that the workplace is very competitive, and as studies have
shown generates high level of stress.22Living with such increased levels of stress,
we might hypothesize that, in time, the immigrant’s level of depression would
increase and eventually match that of his or her native born counterparts. And,
as we have noted, there may be a link, here, to the observation that people liv-
ing in urban areas tend to have higher rates of depression than people living
in rural areas.
Depression in Members of Minority Groups

Let’s turn our attention to the question of whether depression is more
likely to occur among members of minority groups. Our focus will be on
three of America’s largest minority groups: Asian, Hispanic and African Amer-
icans.
In considering the potential risk for depression among these minority
groups, we might start with the observation that African Americans and His-
panics are likely to be economically poorer than non–Hispanic whites. These
groups have a higher chance of living in poorer, more crime-ridden neighbor-
hoods. They may also be subjected to prejudice based on racial and ethnic bias.
In addition, African Americans have a higher rate of single parent families than
other groups, which brings additional burdens. All of these factors might lead
one to speculate that at least some minority groups are exposed to relatively
high levels of environmental stressors, which might be reflected in higher rates
of depression.
Is this deduction correct? Let’s look at the research, beginning with stud-
ies of depression among African Americans. In the large National Comorbid-
ity Survey Replication we cited earlier, comparisons were made between
Non-Hispanic whites and African Americans in terms of whether they had ever
experienced a major depressive disorder. The data revealed that lifetime preva-
lence rates for African Americans were not higher than for whites; rather, they
were far lower (African Americans 11 percent, non–Hispanic whites 18 per-
cent). The figures for dysthymic disorder were about the same for African Amer-
icans and whites, while the figures for bipolar disorder were higher for African
Americans (5 percent versus 3 percent). In regard to the other psychiatric cat-
egories used in the survey, lifetime prevalence rates for anxiety disorders were
lower for African Americans. African Americans and whites were generally
similar in the report of impulse control disorders while African Americans had
lower figures for alcohol abuse and dependency.23 It seems fair to conclude
from this study that the added stresses that were traditionally experienced by
African Americans in this country do not show themselves in increased rates
of unipolar depression or most other major psychiatric categories. This is an
interesting, in some ways counterintuitive finding and raises the intriguing
question as to what it is in the African American experience that protects against
the development of such emotional disorders. The important role of the church
in the African-American community has been suggested as a factor. It would
be interesting to see studies looking at the possible influence of the patterns of
social relationships in the African-American community as well as studies of
attitudes and beliefs that might be protective against the onset of depression.
Hispanic Americans have a diverse history in this country. Mexicans
resided in California and the Southwest long before people from the eastern
United States settled there in large numbers. Puerto Ricans have been living in
such cities as New York for generations. Recall the wonderful Leonard Bern-
stein-Stephen Sondheim musical West Side Story. Many Cubans immigrated to
Florida following the establishment of Fidel Castro’s regime. And more recently
immigrants have come from Central America and the Caribbean islands. While
Hispanic Americans share a common language and for the most part a com-
mon religion, household surveys which place all Hispanics under the same
rubric may obscure important differences between groups of Hispanics.
The National Comorbidity Survey Replication provides us with an
overview comparison of non–Hispanic whites and Hispanics for the lifetime
prevalence of depression. Because the survey used only English speaking peo-
ple, it probably excluded many Hispanics whose command of English would
not permit them to participate in the survey. The sample would be non-repre-
sentative in this respect. With this caveat, the bottom line is that the survey
found that for both major depressive disorder and dysthymic disorder, Hispan-
ics have lower lifetime prevalence figures. For major depressive disorder the
figures are 14 percent for Hispanics versus 18 percent for non–Hispanic whites.
For Dysthymic disorder the figures are 2 percent versus 4 percent. There were
no differences for bipolar disorder. Interestingly, the difference in lifetime preva-
lence for depression applies only to the younger people sampled (age 43 or
younger). For the older people sampled, Hispanics and non–Hispanic whites
did not differ.24
In regard to specific groups of Hispanic Americans, probably the best avail-
able data is on Mexican Americans. The National Epidemiological Survey on
Alcoholism and Related Conditions found that the risk of psychiatric problems
among Mexican-Americans was lower than among non–Hispanic whites. This
was also reported in an earlier version of the National Comorbidity Survey.25
A particularly revealing study on depression was carried out on Mexican
Americans living in two Los Angeles communities. As was true for the national
household surveys, the lifetime prevalence of major depressive episodes was
lower for Mexican Americans than for non–Hispanic whites. There were some
very interesting findings reported for Hispanic women. In the younger age range
Hispanic women were much less likely to be depressed than young non–His-
panic white women. However, when the researchers looked at Hispanic women
over 40, they found a relatively large number of women who reported long-
lasting, moderate levels of depression.26 This finding seems to jibe with the
findings from the more recent national survey which found that the lower rates
of depression (dysthmic disorder) for Hispanics was limited to the younger
people sampled.
One wonders what it was about growing up in these Mexican American
families that offered young women protection against depressive reactions? Was
it the protection of a close-knit, extended family, where one has many links to
other people? Was it the immersion in religion that often assumes a predomi-
nant place in Hispanic culture? Was there more certainty in the future roles of
young women, with less pressure toward career achievement? One also won-
ders what happens in later life that breaks down this early protection leaving
these Mexican American women more vulnerable toward a protracted malaise.
For purposes of statistical analysis, “Asian Americans” are often grouped
together, but Chinese Americans, Japanese Americans, Vietnamese Americans
and Americans whose origins are in the Indian subcontinent have diverse lan-
guages and cultures. A recent study carried out in California showed that the
use of mental-health services by people categorized as Asian Americans varied
considerably, with people whose origin was in East Asia more likely to use the
services than people coming from South East Asia, the Philippines or other
areas.27
There are some difficulties in obtaining a clear answer to the question of
the prevalence of depression in Asian Americans. For many Asian Americans
and in particular recent immigrants there may be a language problem in
answering questions phrased in English. The use of interpreters can lead to
misleading conclusions because of the subtlety of the language used in the
description of psychological states. An example of the error resulting from the

use of a translator is provided in an article by Luis Marcos.
A clinician wanted information from a Chinese-speaking patient. He
asked, “What kinds of moods have you been in recently?” The interpreter
turned to the patient and asked, “How have you been feeling?” The patient
replied to the interpreter, “No, I don’t have any more pain, my stomach is now
fine, and I can eat much better since I take the medication.” The interpreter
said to the clinician, “He says that he feels fine, no problems.”28
A second problem that may affect the validity of the data obtained is a feel-
ing held by many Asian Americans that being treated for a mental illness such
as depression carries with it a stigma. People who feel this way may be unwill-
ing to reveal having the disorder. In writing about mental illness in Asian Amer-
icans, David and Stanley Sue observed that the, “amount of stigma or shame
associated with emotional difficulties is probably much greater among Asian
American groups. Mental illness in a family member is considered a failure of
the family system itself. For Eastern more than for Western families, the fail-
ure or weakness of an individual is considered a disgrace to the family unit....
[Researchers] reported that the stigma of mental illness in Asian Americans
remains so great that, even among individuals of the third and fourth genera-
tion, there is hesitation to admit to psychological problems.”29 A recent study
of a sample of depressed Asian Americans drawn from Internet users suggests
the observation voiced by David and Stanley Sue continues to hold true. Com-
pared to whites, Asian Americans more strongly felt that being treated for
depression carried a stigma.30
Researchers have reported that Asian Americans seem willing to describe
their problems in terms of bodily complaints— headaches, fatigue, insomnia,
dizziness and heart palpitations, but are reluctant to admit to demoralized psy-
chological states. This denial of an emotional problem may even persist into
treatment. Given this cultural tradition, which would lead to underreporting
of the problem, there is a need for caution in interpreting the findings from
household surveys which assess the prevalence of depressive problems among
Asian Americans.
Here are some findings from two large-scale studies. The first study
reported in 1999 surveyed over 18,000 people from a number of selected sites.
It was found that Asian-Americans had lower rates of bipolar disorder than
whites.31 The second study called the Chinese American Psychiatric Epidemi-
ological Study was carried out in Los Angeles and reported in 1998. The sam-
ple consisted of over 1700 Chinese-Americans who spoke either English,
Mandarin, or Cantonese. The variety of languages used in the study was at
remedy for the problems caused by an unfamiliar language and helped keep
the sample of Chinese Americans representative. Lifetime prevalence estimates
for both major depressive disorder and dysthymic disorder were considerably
lower than the figures for whites reported in the two recent national surveys.32
Age at Onset of Depression

At what age do people become depressed? Is it likely to begin in early child-
hood? Adolescence? Young adulthood? Some preliminary answers to this ques-
tion were suggested by a study carried out in Oregon. Over 2,000 people who
had shown some evidence of depression on psychological screening tests were
interviewed in detail about current and past episodes of depression.33 About
1,000 of the people were diagnosed as having at least one current or past episode
of unipolar depression. During the interviews, the researchers tried to ascer-
tain the time at which the first episode of depression occurred. They found that
the risk of developing depression in childhood was very low. Before we accept
this conclusion as gospel, however, we must point out that there have been real
difficulties in diagnosing depression in children. As we shall see, we really can’t
estimate these numbers very well.
As an anchoring point in what has been an area of controversy, we should
note that children are being treated today in psychiatric hospitals for depres-
sion. Using the benchmarks described in the American Psychiatric Associa-
tion’s Diagnostic and Statistical Manual, children have been diagnosed as having
major depressions and are being treated using psychotherapy and antidepres-
sant drugs.
What is a young child who is diagnosed as having a major depression like?
Here are some excerpts from a case study presented by Javad Kashani and his
colleagues.34
The depressed child, a five-year-old boy named Mike, became a matter of
considerable concern to his teacher, “when he told her that he wanted to ‘kill
himself and die.’ The teacher found him to be sad, worried, overactive, rest-
less and irritable. He had feelings of self-reproach, self-blame, and hopeless-
ness about the future and had difficulty in concentrating and following rules.”
Mike had physical complaints such as stomach aches and pains in his legs and
arms. He was also fatigued. His mother reported that he had crying spells, was
irritable and had a poor appetite.
When Mike was interviewed by the researcher, he did not smile, but
appeared solemn. He said he didn’t like himself and that nobody liked him.
When he was asked what was going to happen to him when he became a big
man, he replied, “I’ll be dead.”
Mike is a depressed child, not difficult to recognize as such. So, too, are
other children in psychiatric hospitals being treated with drugs and psychother-
apy. When we move away from such severe cases, however, the problem
becomes murkier. It is hard to say how many children in this country should
be considered depressed.
One of the reasons for this uncertainty is that the clinicians and researchers
who have studied depression in children have disagreed about the very nature
of childhood depression. In describing the disorder, some writers have included
symptoms that go well beyond those listed in the Diagnostic and Statistical Man-
ual for adults. They have interpreted a number of troublesome behaviors in
children as “masking depression,” behaviors that disguise an underlying depres-
sion. Behaviors as wide-ranging as hyperactivity, aggressiveness, delinquency,
temper tantrums, boredom and restlessness have been cited as evidence of
depression. In a paper on childhood depression, Monroe Lefkowitz and Edward
Tesiny observed that such a “catalogue of symptoms must, at one time or
another, encompass all children.”35
At the other extreme, it has been argued that much of what has been called
depression in childhood is really transitory problems in development–prob-
lems that often disappear as children grow up. An example would be poor
appetite, a symptom of depression in adults. One study identified a number of
children at age six with poor appetites. By age nine the problem in most of the
children had disappeared.36 It would be stretching things to infer that these
children had been depressed.
How do we identify children who are depressed? Parents and teachers are
usually in the most strategic positions to recognize that something is troubling
the young child and that he or she appears to be depressed. Research suggests
that by around the age of nine, the children themselves can be good reporters
of their own moods.37 Child behavioral checklists are available for researchers
and clinicians to help in evaluating depression. And there are self-report meas-
ures for children which measure depression. These self report measures of
depression for children, somewhat similar to those used to assess depression
in adults, probably increase in usefulness and accuracy as the child grows older.
The Children Depression Inventory (CDI), developed in 1981 and com-
mercially published in 1992 has been the principal self report measure used for
assessing depression in children.38 The inventory consists of 27 items that sam-
ple various aspects of depression in children such as self-blame, suicidal
thoughts, feelings of sadness, and feelings of loneliness. The scale is internally
consistent and has shown a moderate correspondence with the ratings of cli-
nicians. The scale has been translated into foreign languages and used both in
this country and abroad.
While the Children’s Depression Inventory has shown itself useful in a
variety of research studies, its value as a reliable instrument in diagnosing
depression in children has been questioned. A recent study carried out in Bel-
gium concluded that the test was a useful diagnostic instrument, but earlier
studies have not always found this to be the case.39 In one study, for example,
researchers used the measure to try to distinguish between children in a clinic
diagnosed as depressed and children diagnosed as having “conduct” disorders
such as truancy or over aggressiveness. The test misclassified about two-thirds
of the children. The researchers concluded, “The level of discrimination
achieved from the CDI factor scores falls far short of the necessary level of dif-
ferentiation required of a diagnostic tool. Thus, the use of the CDI as the sole
criterion for the selection of depressed youths for treatment or research pur-
poses is not recommended.”40
In another example, researchers administered the test to children in the
schools of four rural communities. To estimate the prevalence of depression,
the researchers used “cutoff ” scores suggested by the developers of the instru-
ment. A score above a certain number was thought to indicate the likelihood
of depression. Using these recommended cutoff scores for identifying depres-
sion, the researchers would have come up with the astonishing figure that 46
percent of the children in the community were depressed.41 This figure, of
course, is ludicrous and just emphasizes the fact that we do not yet have accu-
rate ways of identifying depression in young children that can be applied to
large, heterogeneous samples with confidence.
The difficulty of identifying children with subclinical (less than full-blown)
levels of depression was highlighted in a study carried out by Reed Larson and
his co-workers. They monitored the moods and behavior of 483 fifth-and ninth-
graders for a week, comparing the behavior of children who scored high on a
measure of childhood depression with those who did not. They reported, “In
general, we were struck by how few associations there were between depres-
sion and how children and young adolescents experienced the different con-
texts of their lives. Outwardly, the daily patterns of depressed children and
adolescents are quite like those of nondepressed peers.”42
In reviewing the state of the art, Mary Kerr and her colleagues likened
attempts to conceptualize and measure depression in children to the story of
the blind man examining the elephant.43 Because of these troublesome prob-
lems in definition and measurement, I think it is fair to say that we do not as
yet have a trustworthy estimate of the number of children who are depressed
in this country. While it seems likely that the prevalence of depression in young
children is a good deal less than what we find in adolescence, to provide pre-
cise estimates of the prevalence of depression in children, and particularly
younger children would be a very difficult undertaking. As we have suggested,
depression in children is not always easy to recognize. It is not difficult to spot
a “problem child” who bullies his playmates, has recurrent nightmares or sets
fires at home, but a child who seems lonely or sad may not be viewed as being
all that unusual. The child may be described as “quiet” or “shy,” rather than
depressed. The parents or teacher may not identify a depressive problem for
what it is, and young children should not be expected to diagnose themselves.
While we may not often recognize depression in young children either
because it occurs infrequently, as suggested by the Oregon study, or because
we are not sophisticated enough to identify it when it does occur — the situa-
tion is quite different for adolescents. Depression in adolescence is a wide-
spread problem. Suicide among teenagers, for example, has received a great
deal of publicity and for good reason. Suicide is the second leading cause of
death among people in the 15 to 24 age range. Surveys carried out on teenagers
reveal that large numbers of them have thought about committing suicide at
some time during their lives. Many of these teenagers feel that they would find
it difficult to tell their parents or teachers about these thoughts.44
How extensive is depression among adolescents? In an early study William
Reynolds surveyed high schools using a battery of self-report measures of
depression and reported that he found levels of moderate to severe depression
running in about 11 to 17 percent of the students.45 A more recent self report
survey carried out on a large number of French high school students reported
figures in the 10 percent range for boys and more than twice as high for girls.46
Correcting for the possibility that self-report inventories may overestimate the
extent of depression when compared to interviews conducted by trained clini-
cians, it still looks as if depression in adolescents is a widespread problem.
As is true for unipolar depression, the prevalence of bipolar depression
tends to increase sharply during adolescence. If you examine graphs showing
the age of onset of bipolar disorder, you will see a pronounced spike in the late
teens extending into the early twenties. While bipolar disorder can occur at
almost anytime, this is the time of life that bipolar disorder very frequently
begins.47
Psychologists studying “loneliness” have found that these very unpleasant
feelings, which often coincide with depression, frequently are at high levels
during the teenage years. Adolescents are noted for their gregariousness but
frequently feel lonely and sometimes alienated. The experience of loss such as
the divorce of one’s parents sometimes precedes the onset of a major depres-
sive disorder in adolescence. Tensions within the family have been linked to
the longer lasting dysthymic disorder.
Studies carried out in Finland where SAD might be expected to be a par-
ticular problem indicates that the disorder is especially prevalent in young
women.48
Turning to college students, Roland Tanck and I included in our diary the
questions, “Did you feel depressed today? And if yes, what do you think was
causing these depressed feelings?” In perusing the students’ responses, we
noticed that while on occasion the students were at a loss to identify the cause
of their depressed moods, they usually offered a reason, and often a specific
event. Frequently, the students attributed their depressed feelings to problems
relating to school work. A few examples of such responses were, “I feel very
behind in my school work as though I will never catch up,” “Without a doubt-
the chemistry exam,” and “Big test that I did poorly on.”
The students pointed to relationships as another source of depressed feel-
ings. Sometimes, the depressed feelings were caused by problems in a roman-
tic relationship. For example, “He is interested in someone else more than me,”
or “A problem with a boyfriend.” Sometimes there was friction in a relation-
ship. Some examples are, “A fight with a friend,” or “An unpleasant conversa-
tion with the girl upstairs.” And sometimes there was the possibility of a
breakup of relationships: “I thought too much about two good friends who are
transferring next semester.”
At times, the students identified the source of their depressed feelings not
as events, but as their own thought processes. Sometimes the students spent
time looking within themselves, questioning their own performance. “My lack
of motivation to do things,” or “I’m wasting too much time.” Sometimes they
thought about the future and felt uncertain about where they were going: “I
was wondering where my life is leading.” And occasionally, there was a vague
feeling of concern, such as, “I was worrying about life in general.”
Reading through our collection of student diaries leaves one with the
impression that a great many college students experience periods of mild to
moderate depression. Using the Beck Depression Inventory, we estimated that
about 14 percent of the students in our research project were moderately
depressed.
The data, then, suggests that the risk of becoming depressed increases
sharply in the late adolescent and young adult years. A case example would be
Allison who I briefly mentioned in the proceeding chapter. Allison has suffered
from recurrent depression for many years. She experienced her first episode as
a young adult and interestingly had no clear understanding of what was hap-
pening to her during this first episode. She related, “As far as the history of my
depression, it began at age 20, when I was between my junior and senior years
of college. I began feeling strange and did not know why. I did not know it was
depression. Then I decided to try committing suicide. I told my brother and
he drove me to the doctor who put me in the hospital overnight until they
arranged for me to go to a clinic for treatment. While I was at the clinic I had
no inkling of what was bothering me and I did not know what to talk about
with the psychiatrist. I was cut off from my feelings....”
Even with the wide dissemination of information about depression in
recent years, I can still see how the first episode of depression may not only be
very unsettling, but confusing and in many cases bewildering both to the patient
and the family.
The recent National Epidemiological Survey on Alcoholism and Related
Conditions indicates that the highest lifetime risk of becoming depressed occurs
in middle age.49 Interestingly, the Oregon study suggests that period of high
risk may occur somewhat earlier for males than for females. For males, the risk
is significant by the early twenties and remains so until it begins to decline in
the later years of life. The years of higher education, of starting a career, of devel-
oping relationships, of marriage, and starting and raising a family — these years
of ever increasing responsibility are the years when depression is most likely to
occur in men.
Kevin, a young musician whose career ambitions had been sidetracked by
the pressures of an early marriage, is an example of this age related risk in men.
From an early age, Kevin had hoped to become a pianist. In his second year of
college, he met Julie, an art student, fell in love, married and within a year
became a father. His musical studies slipped into the background as he took
jobs that were unrelated to music in order to support his family. He waited on
tables, tried selling real estate, then took a job as a bank teller. The birth of his
second child made it still harder to seriously resume his studies. The press of
responsibilities and the fading of his dreams posed an emotional strain to both
Kevin and his wife. Kevin became irritable and difficult to talk to. He became
morose and withdrawn. Eventually, he entered therapy for depression.
The Oregon researchers reported that the risk of becoming depressed for
women did not reach its highest point until well into middle age. This differ-
ence in peak age of onset of depression indicated in the study may reflect tra-
ditional differences in sex roles. For example, society has placed a higher
premium on physical attractiveness in women than in men and the fading of
physical beauty may have more of an emotional impact on women. In addi-
tion, the responsibilities and satisfactions that come with childrearing tradi-
tionally provide a great deal of meaning in the lives of women, and when these
diminish as children leave home, many women experience an emotional let-
down and a sense of emptiness in their lives.
Women differ greatly in the way they adapt to these role transitions. Many
women find that diminished family responsibilities and increased time for
themselves provide an opportunity to fulfill longstanding ambitions. Janice,
for example, always wanted to write children’s books and now has the time to
do so. Ellen always wanted to travel and decided to take a tour of Europe with
her husband. In contrast, Rose, who was a housewife for many years, found
herself with few meaningful things to do after the children were gone. She did
not want to incur the risks involved with reentering the job market and was at
loose ends. She was caught in what has been called the “empty nest syndrome”
and would appear to be the most vulnerable of the three women.
As is true for men, there is a decline in the onset of depression in women
during the later years of life. In reflecting on these trends, it appears that the
most likely times for the onset of a depressive illness are the prime years of life.
What may be some of one’s best years in terms of drive, earning capability and
fulfilled relationships may also be one’s most vulnerable years for becoming
depressed.
Depression Among the Elderly

Some years ago I was a member of an organization of volunteers, physi-
cians, nurses, psychologists and social workers, which provided free health
services to people who did not have easy access to medical services. My assign-
ment along with another psychologist was to offer therapy to the residents of
a large public housing project for the elderly. Many of the residents came to
our weekly evening clinic, but only a few people ever asked for an appointment
with a therapist.
At the time I was surprised by the apparently low prevalence of emotional
problems among the residents. In reading articles on aging, I was struck by all
of the things that can go wrong: chronic illness, slowdown in mental acuity,
financial deprivation, widowhood, loss of friends, and so on. Given these con-
ditions, I expected to encounter a lot of emotional problems, particularly
depression. However, in the senior citizens’ apartment complex, that did not
seem to be the case.
The senior citizens’ housing complex offered a wide range of social and
recreational activities. The complex was not just a roof over one’s head; it was
a place to live and socialize. Perhaps it was these opportunities for an active
lifestyle that helped keep psychological distress to a minimum.
Consider a contrasting situation. I once acted as a consultant to another
senior citizens’ facility, a very large metropolitan nursing home. The residents
were not as well off physically as the residents in the housing complex, nor did
they enjoy the same quality of life in terms of housing, social life and recre-
ational activities. With the aid of the institution’s nursing staff, we carried out
a study of psychological problems among the residents of the nursing home
and found evidence that about 15 percent of the residents experienced at least
one depressive episode during a six-week observational period.
These two isolated observations point to a conclusion that is buttressed
by considerable research. The physical health and social environment of sen-
ior citizens can make a difference in whether they are likely to experience
depression. A study carried out in Canada indicated that the factors promot-
ing depression in the elderly might vary somewhat depending on whether the
people lived in rural or urban areas, but in general living alone or lacking com-
panionship, inadequate financial resources, poor physical health, and declin-
ing mental functioning tended to relate to depression in the elderly.50
The impact of these factors in promoting depression in the elderly is illus-
trated by Kathy Biggs, an elderly, retired librarian. Kathy led a quiet, fairly soli-
tary life in a suburban community. She read a great deal, worked in her garden
and spent a lot of time with a lifelong friend, Joan. Joan died suddenly and unex-
pectedly. It was a terrible blow to Kathy. The loss, coupled with increasing
physical disabilities of her own, left Kathy alone and isolated. Her quiet, com-
fortable world had been turned upside down and she had no one to turn to.
She began to experience many of the symptoms of depression.
When we pose the question “What is the prevalence of depression in the
elderly?” we encounter some difficulties. A significant number of elderly peo-
ple suffer from brain disorders such as Alzheimer’s disease and unless some care
in diagnosis is made, it is possible to confuse some symptoms of depression
with brain dysfunction. Another problem is that elderly people all too often
learn of the death of family members and close friends and experience the grief
that comes with such loss. Grief and depression are not the same, but may
appear similar and can easily be confused. It is quite possible that when the
researcher looks for the symptoms of depression, he or she may find them, even
though the person is not clinically depressed. All of these considerations then
lead to some caution in making hard and fast estimates of the prevalence of
depression in the elderly. The Oregon study suggested that depression is rela-
tively infrequent in older people. Findings from the National Comorbidity Sur-
vey Replication indicated that the percentage of cases of major depressive
disorder that have their onset after the age of 56 or so is not that large, less than
10 percent.51
A long term study of elderly depressed people carried out in Amsterdam
in the Netherlands indicated that the depression was more likely to persist than
to clear up. In about 40 percent of the people studied, the depression had an
unfavorable although fluctuating course while in another 32 percent the depres-
sion had a severe chronic course. Remission occurred in only 23 percent of the
people studied.52
When an older person becomes depressed, it can foreshadow poorer health
and overall functioning in the future. Researchers at the National Institutes of
Health assessed older persons on a measure of depression and tested them on
a variety of physical performance measures such as a timed walk and a timed
test of five repetitions of rising from a chair. Four years later the older people
were retested on the performance measures. The elderly subjects who were
assessed as more depressed at the original assessment had a higher risk of expe-
riencing physical decline.53
Because of the risks presaged by depression in the elderly for an overall
decline in health, it is important to treat depression in the elderly when it
occurs. Too often, however, depression in older people is ignored. Both the
individual who is depressed and his or her family may not recognize depres-
sion for what it is, believing that what they see is only a normal part of aging.
In the limited time that physicians have to spend with individual patients, the
physician may not recognize the depression, either. The problem may remain
untreated. A research study reported in the late 1980s suggested that there may
be a need for more emphasis in medical education in identifying depression in
the elderly. In the study of a sample of elderly patients at a Veterans Adminis-
tration Hospital, only 2 of 23 depressed elderly patients were correctly identified
by the house staff as depressed.54
Some studies, though not all, indicate that the risk of depression is higher
among seniors in the less affluent stratas of society. Being caught in a daily
economic squeeze and not being able to do much about it can create constant
psychological pressures, which may lead to depressed reactions.
In this chapter I have presented some statistics about the prevalence of
depression in the United States. The figures presented depend on the methods
used to obtain the information, and these methods are far from perfect. Still,
it is very clear that the problem of depression is widespread and probably

increasing in scope. We are talking about many millions of adults who have
experienced moderate to severe levels of depression and a problem that hap-
pens to all of the groups that make up our society. And we are talking about a
problem that is likely to arise in the best years of our lives.
3. The Biological Bases
of Depression
I remember looking through a textbook on abnormal psychology written

for undergraduate students in the 1950s and being struck by the effort to explain
the causes of mental illness in purely psychological terms. Manic depressive dis-
order and schizophrenia were viewed as exaggerations of normal psychologi-
cal tendencies. Little attention was given to biological bases for these emotional
and mental disturbances. One of the reasons for this approach was that scien-
tists looking for biological links to these disorders had not yet been able to find
much. The paucity of biological findings reflected the lack of sophisticated
technologies to adequately research the problem.
In recent years, the situation has changed drastically. There have been dra-
matic improvements in technology that allow researchers to both obtain images
of the different regions in the brain and using positron emission tomography
(PET) and functional magnetic resonance imaging (fMRI) to measure activity
levels within these regions.1 The discovery that many clinically depressed peo-
ple have imbalances in the neurotransmitters in the brain has spurred inten-
sive interest in the biological bases of depression. The pendulum has swung so
far that people talk about depression as a biological illness.
With the perspective that increasingly sophisticated research provides, it
now seems likely that both biological and psychological factors play major roles
in depressive disorders. The task that lies ahead for scientists will be to inte-
grate the findings from both disciplines to provide a comprehensive model that
will best explain depression.
What I will attempt to do in this chapter is to present thumbnail sketches
of some of the important findings showing biological bases for depression. We
will look first at the influence of heredity on depression. Then we will consider
structural differences in the brains of depressed patients, the role of the neu-
rotransmitters in depression, the possibilities for a laboratory test for depres-
sion, the links between depression and physiological measures of sleep, and the
impact of depression on the immune system. We shall conclude with a discus-
sion of the search for genes that may underlie depression.
46
3. The Biological Bases of Depression 47
Many diseases “run in families.” Some examples that come to mind are
allergies, hypertension, Alzheimer’s disease and schizophrenia. When we say
that an illness “runs in families” we simply mean that someone in a family in
which one person has been afflicted is more likely to develop the problem than
someone in a family where there is no history of the disease. It does not mean
that everyone in the family will develop the problem or that the onset of the
disorder is inevitable. We are saying that the risk is higher.
When we observe such family patterns, we often suspect that there is some
genetic basis for what we see. This may not always be the case, for environ-
mental conditions can trigger both physical and emotional problems and mem-
bers of a family are usually exposed to a similar environment. A high level of
stress, a pattern of poverty, or destructive parenting practices can affect all
exposed persons. Still, the possibility of a hereditary basis for an illness is an
obvious place to start looking when we observe familial patterns of illness.
Depression has some tendency to run in families. If someone in a family
is clinically depressed, a very close relative — such as a sister or brother has
about twice the risk of developing the problem then someone in the general
population. For children of parents with major depressive disorder — the risks
of developing depression are even higher — perhaps over a threefold increase.
For close relatives of depressed people the onset of such a depression is likely
to be relatively early. Some research suggests that the problem might initially
present itself as an anxiety disorder.2
When we move away from very close relatives to more distant relatives
such as aunts, uncles, cousins and grandparents, the risk of depression decreases
appreciably.3
The fact that depression does run in families suggests the possibility of a
genetic basis for the disorder. Is this the case? One of the best ways to establish
that heredity plays a role in a disorder is to carry out studies that use the twin
study method. In such studies, one compares the concordance of depression in
identical twins (monozygotic twins) and fraternal twins (dizygotic twins). The
reasoning behind such studies goes something like this: Monozygotic twins
have exactly the same heredity, coming from the same fertilized ovum. Dizy-
gotic twins happen to be born at the same time and share a common environ-
ment, but come from different fertilized ovums. Such twins have the same
hereditary makeup as any other pair of siblings. If heredity plays a role in
depression, we would expect to find more cases among monozygotic twins than
dizygotic twins in which when one of the twins becomes depressed, the other
also becomes depressed. And this is just what we find in research.
An example of this type of study was carried out by a research team in
Australia. The team, led by Kenneth Kendler, mailed questionnaires to people
listed on the Australian Twin Register. They received about 4,000 replies from
both members of twin sets. The questionnaire included items that asked about
depressive symptoms. The researchers found much more similarity in the
responses of the monozygotic twins to these items than in the responses of the
dizygotic twins.4
Kendler as well as other researchers have carried out additional twin stud-
ies to estimate the extent to which depression is genetically based. Two large-
scale twin studies reported in 1999 estimated that major depressive disorder is
about 40 percent “heritable.”5 So, while the studies indicate that genes play a
major role in the development of depression, one’s environment and unique
experiences also play a significant role, probably larger than heredity. While
twin studies clearly support the important role of heredity in unipolar depres-
sion, it is equally clear that heredity is not totally determinative. If it were, both
members of identical twins would invariably come down with depression if
one were afflicted and this is simply not the case.
These two major twin studies yielded conflicting results as to whether
heredity plays a more significant role for males or females in the development
of depression. One study found that heredity played a less important role for
males, the other did not. This question needs further study.
What we have in some people is a genetic vulnerability that increases the
risk of becoming depressed should environmental conditions develop that pro-
mote depression. The interplay of genetic and environmental factors needs to
be clarified by further research.
While heredity appears to play a significant, but probably not dominat-
ing role in the development of unipolar depression, the influence of heredity
on bipolar depression appears to be very considerable. Two recent twin stud-
ies in which a twin had bipolar illness yielded very high heritability estimates,
in the 80 to 90 percent range.6 Bipolar illness would seem to be an attractive
target to search for implicated genes.
Magnetic Resonance Imaging (MRI) provides a powerful tool for meas-
uring the size of various regions in the brain. Using this technique researchers
have been able to compare regions in the brains of people who are clinically
depressed with those of people who are not. Much of the attention of researchers
has been focused on two structures in the brain which are known to be involved
in emotions. These structures are the hippocampus and the amygadala.
The hippocampus, named for its shape which resembles a sea-horse lies
in the medial temporal lobe of the brain. Researchers believe that the hippocam-
pus plays an essential role in the development of new memories. Damage to
the hippocampus can produce amnesia.
A number of studies have been carried out which compare the size of the
hippocampus in depressed subjects with that of control subjects. A meta-analy-
sis examining the overall trend of these studies indicated that in patients with
long standing depressive illness, the hippocampus appears reduced in size. This
brain structure has appeared to atrophy.7
It is believed that the diminished size of the hippocampus in depressed
patients may reflect a decline in the number of neurons (nerve cells). One of
the reasons for this decline may be the high level of stress many depressed peo-
ple have experienced. Studies using animals have demonstrated that stress has
a negative effect on the production of new nerve cells. As the duration of the
illness appears to be a factor in the reduced size of the hippocampus, it may be
that the depressive process, itself, contributes to this decline in the genesis of
new nerve cells. Interestingly, there is research on animals which suggests that
the action of antidepressant treatments may reverse this tendency towards
decline.8
The amygadala is an almond shape mass located in the anterior portion
of the temporal lobe of the brain. Many studies have shown that it plays a
significant role in emotion, particularly in the genesis of fear reactions. Some
studies have found that the amygadala in depressed subjects are enlarged when
compared with control subjects. However, other studies have not reported this
finding. While the question of amygadala enlargement in depressed patients
remains unsettled, there is some suggestion that patients with a short-term ill-
ness are more likely to show this enlargement than patients who have been
depressed for a long time.9
In an interesting study carried out in Germany, patients with major depres-
sive disorder who have an enlarged amygadala tended to have difficulties in pro-
cessing emotional materials (photographs of fearful, surprised, and disgusted
faces) into memory. Their ability for dealing with these materials appears to
have been compromised.10
Some MRI studies of the brain have been carried out on patients with
bipolar disorder. A review of the studies concluded that for adult bipolar dis-
order patients, the brain regions studied appeared heterogeneous in volume;
there were no clear indications that the regions studied were either larger or
smaller than those of controls. In contrast, in the fairly rare form of bipolar
disorder called early onset bipolar disorder in which the disorder strikes chil-
dren and adolescents, there appeared to be volumetric differences between
patients and controls. Several studies have reported that the amygadala and
probably the hippocampus as well were reduced in size and the total cerebral
volume seemed also smaller in patients with early onset bipolar disorder. To
fully understand the meaning of these findings, we need to follow early onset
bipolar disorder over time to see whether these differences persist or tend to
normalize as the child matures into an adult.11
The Neurotransmitters
The search for biological bases for depression has opened up another rich
vein of ore in the study of the action of the neurotransmitters. To appreciate
the important role neurotransmitters play in our functioning, keep in mind
that there are billions of nerve cells (neurons) in the brain. These nerve cells
are separated by small gaps called synapses. Electrical messages transmitting sig-
nals within the brain and relaying instructions to various parts of the body
cross these gaps through the action of certain chemicals. When nerve cells
release these chemicals, they seep across the gaps to a receptor in an adjacent
nerve cell, transmitting the message to “fire” or “not fire.” These chemicals are
called neurotransmitters.
Now, an interesting thing happens to some of the neurotransmitters as
they are discharged from the terminal of a neuron to stimulate the adjacent neu-
ron. Some of these neurotransmitters do not complete their appointed rounds;
instead, they are reabsorbed back into the transmitting neuron. In this reab-
sorption process called reuptake, there is less availability of the chemical to do
what it is doing. Reuptake reduces the active levels of the neurotransmitter
which as we shall see has important implications for the pharmacological treat-
ment of depression.
Researchers have identified a sizable number of neurotransmitters. Two
of these neurotransmitters, serotonin (5HT and norepinephrine (NE) have
especially interested researchers for the role they play in depression. To date,
serotonin has attracted the most attention. Serotonin, an organic compound
synthesized from the amino acid tryptophan was discovered about 60 years ago
and was initially recognized as a vasoconstrictor in blood serum. Subsequently,
serotonin was found to be involved in emotions, sleep, and memory, all of
which can be part of the depressive picture. The recognition that serotonin
might be involved in depression led to considerable research that has substan-
tiated the hypothesis. In addition, the development of drugs that acted to inhibit
the reuptake of this neurotransmitter, thereby increasing the availability of
active serotonin have proven effective in ameliorating symptoms in many
depressed people.
If, as we believe, serotonin levels influence the development of depres-
sion, a classic approach to demonstrate this would be (1) to increase serotonin
levels in depressed people to see if the depressive symptoms are ameliorated
and (2) decrease serotonin levels in normal people to see if depressive symp-
toms develop. There are obvious ethical concerns that have to be addressed in
carrying out the latter procedure.
Now serotonin cannot be used directly in such experiments because sero-
tonin cannot cross the blood-brain barrier. However the precursor of sero-
tonin, the amino acid tryptophon can be used in such research. Richard
Wurtman and his collaborators found that tryptophan controls the amount of
serotonin the brain produces. They found that injecting tryptophan solution
into laboratory animals increased the level of brain serotonin.12 Tryptophan is
sold as a food supplement and its effects have been studied on depressed peo-
ple. There is some evidence that increasing the amount of tryptophan in the
diet can have an antidepressant effect. Indeed, in some countries, tryptophan
has been marketed as an anti-depressant.
What happens when tryptophan is depleted in people who are not

depressed? Does this bring on depressive symptoms? The answer appears to
be no. The procedure that has been used is to give the subjects capsules con-
taining all the essential amino acids the body requires with the exception of
tryptophan. This procedure depletes the amino acid to a fraction of its usual
concentration in plasma. Several studies including a recent investigation at
the National Institute of Mental Health showed that tryptophan depletion did
not induce depressive symptoms in normal people.13 Nor did brain imaging
(PET) show increased brain activity in suspected areas of the brain. However,
if you try this experiment with people who have suffered major depression dis-
order and are now in remission, you are likely to find that some of these patients
will experience transient returns of depressive symptoms. Moreover, they may
show increased activity in a number of areas of the brain including the
orbitofrontal cortex, the medial thalamus, and the anterior and posterior cin-
gulate cortices.
The findings that tryptophan depletion has depressive effects on people
who have been clinically depressed but not on controls points to the conclu-
sion that while serotonin is clearly involved in depression, there is much more
to the story. Clearly individual differences in vulnerability to depression are
very important and that is likely to reflect both genetic and experiential fac-
tors.
One of the interesting findings concerning serotonin is a link to suicide.
Autopsies of suicide victims have revealed low levels of serotonin activity, par-
ticularly when the victim’s suicide was a violent act.14
Norepinephrine, also known as noradrenaline, may be more familiar in
its role as a stress hormone that when released into the blood helps prepares
the body to react to emergencies. You know the feeling, the “fight or flight”
reaction. Your heart races, you feel alert, primed, and sometimes acutely anx-
ious. Norepinephrine is also synthesized within the brain and is used in the
transmission of signals within the brain. So, norepinephrine has a dual capac-
ity, as a stress hormone and as a neurotransmitter.
As is the case for serotonin, norepinephrine, as a neurotransmitter is sub-
ject to the reuptake process. Researchers have developed norepinephrine reup-
take inhibitors in a manner analogous to the serotonin reuptake inhibitors.
These drugs have been used alone or combined with serotonin reuptake
inhibitors. Both types of drugs have been shown to be effective in the treat-
ment of depression. It seems possible that the unique profiles of the two types
of neurotransmitters might lead to drugs with somewhat different types of
effects on depression. J. M. Gorman and his colleagues at Columbia Univer-
sity suggested that influencing norepinephrine might be useful in relieving
energy and interest deficits in depressed patients.15
It now seems clear that in many depressed people there are problems in
the way these neurotransmitters are working. At this point, the dynamics of
these abnormalities in the neurotransmitters in depressed people are not fully

understood. Some researchers have questioned whether the abnormalities are
simply a matter of too low an activity level. They have raised the question of
whether these neurotransmitters are regulated correctly, suggesting that these
systems may be out of kilter. It would be something like the thermostat in your
house or automobile was malfunctioning.
Researchers have used the term dysregulation to describe some of the
abnormalities observed in these biological systems. In elucidating the concept
of dysregulation, Larry Siever and Kenneth Davis discussed such ideas as
impaired mechanisms, erratic output, disruption in normal periodicities, less
selective response to environmental stimuli, and slower return to basal levels.
These ideas conjure up an image of an engine that is out of sync.16
A Possible Biological Test for Depression

When a person is confronted with stress-provoking situations (stressors),
the body reacts in a number of ways. We have already mentioned the role of
norepinephrine in activating the sympathetic nervous system. Another hor-
mone that is released into the bloodstream as a response to stressors is corti-
sol. Cortisol has a multiplicity of effects. It helps regulate blood pressure and
the way the body uses its sources of energy; the brain receives more glucose
and fat cells are released into the muscles.
The release of cortisol in the body involves the action of the HPA axis
which includes the hypothalamus, the pituitary gland, and the adrenal glands.
Briefly, the hypothalamus, based deeply within the brain releases a hormone
called CRH that stimulates the pituitary gland located in the base of the skull,
which, in turn secretes a hormone, ACTH, which regulates the actions of the
adrenal cortex, located in the chest cavity next to the kidneys. The adrenal cor-
tex then secretes a hormone, cortisol into the bloodstream. Cortisol secretion
as a response to stress seems to be greater when people are in situations in
which they feel they are being evaluated and when the stress-provoking situa-
tion appears to be uncontrollable.17
Now what does this mean for depression? HPA system dysfunction is
frequently found in depressed patients. In a large number of depressed patients,
perhaps as many as 60 percent, one finds evidence of hypersecretion of corti-
sol. Researchers have attempted to capitalize on this observation to develop
a test that would be a biological marker for depression. A procedure that
has generated a lot of interest is called the Dexamethasone Suppression Test
(DST).18
For most people, the chemical dexamethasone suppresses the secretion of
cortisol for a period of at least 24 hours. Under the influence of this agent,
plasma levels of cortisol measured by standardized laboratory procedures are
low. While this suppressive effect is found in most normal people, it is not
found in many people who are depressed. In many depressed patients, corti-
sol levels continue to remain high even after taking dexamethasone. The fail-
ure to suppress cortisol, then, could be an indication for depression.
The procedure for the DST may go something like this: dexamethasone is
administered at 11:00 P.M. During the following morning, afternoon and eve-
ning, blood samples are taken from the patient to check the level of plasma cor-
tisol concentration. An elevation of cortisol in any of the blood samples
indicates a failure of the expected suppression activity of the drug, and is con-
sidered a positive test result.
How accurately will positive results on the DST identify persons with diag-
noses of major depression? After several thousand people had been tested, the
provisional answer to this question is that the test picks out about half (45 per-
cent) of individuals with major depression. About one out of ten normal sub-
jects also test positively on the DST.19
You can see from these figures that the DST is not as accurate as one would
like as a technique for identifying persons with major depression. It would be
something like a lie detector test that could pick out people who actually lied
about half of the time, although it was reasonably good at clearing people who
were telling the truth.
With the evidence mounting that the DST was not a definitive biological
marker for depression, researchers have looked for other possibilities. The
abnormalities in the HPA axis observed in many depressed patients still seemed
like a good bet for further study and there are alternative ways of looking
at these abnormalities. In pursuing this objective, researchers devised a new
test to assess HPA system functioning.
The test which combines the usual DST procedure with a second proce-
dure, that of corticotropin releasing hormone stimulation, is called the DEX/
CRH test. In this combined procedure, the usual procedure for the DST is fol-
lowed and then on the following day corticotropin releasing hormone is admin-
istered to the subject. Blood samples to determine plasma cortisol are taken at
intervals over the next few hours. This new test appears to be more sensitive
in identifying people with depressive disorders than the DST procedure when
used alone. Interestingly, research studies have found that the test is more likely
to show abnormalities in patients with major depressive disorder when the
patients are in the acute state of the disorder then when depression becomes
chronic.20
A study carried out in Japan found that the DEX/CRH test results appear
more normalized after treatment for depression.21 In contrast, in bipolar dis-
order patients, research indicates that the test results are abnormal both when
the patients are symptomatic and when the dis-order appears to be in remis-
sion.22 The combined DEX/CRH test shows promise as a neuroendrocinolog-
ical tool in the assessment of depression.
Depression and Sleep Patterns

We know that difficulty in sleeping is one of the more common symptoms
of depression. Apart from the fact that people who are depressed have trouble
falling asleep and may wake up frequently, there are physiological differences
in the sleep patterns that distinguish depressed and nondepressed individuals.
These differences have been identified in sleep laboratories.
Sleep laboratories were developed as controlled scientific settings to mon-
itor sleep and dream activity. While subjects sleep, their breathing and heart
rates are monitored, their brain waves are recorded by an electroencephalo-
graph (EEG), and the movements of their eyes that take place during sleep are
recorded with the aid of electrodes pasted on the scalp.
Using this equipment, researchers are able to monitor the various phases
of sleep, including the periods of jerky rapid eye movements (REM) during
which dreams are most likely to occur.
When persons diagnosed as having a major depression are compared with
nondepressed controls in terms of these instrument recordings, a number of
differences emerge. For example, there are periods in the sleep cycle in which
the EEG pens mark out a pattern of slow, high amplitude waves. This slow wave
sleep, called delta sleep, is usually characterized by deep sleep. When people
are experiencing depression, they tend to get less delta sleep than nondepressed
controls. There is also a tendency for delta sleep to be shifted back further into
the night’s sleep.
Differences have also been observed for REM sleep. One of the findings
that has been reported is that depressed patients tend to have shorter REM
sleep latencies (the interval of time between the beginning of sleep and the first
period of REM activity). There is also increased eye movement density (num-
ber of eye movements per period of REM sleep).23
In a paper reviewing these and other findings on sleep research, Cindy
Ehlers, Ellen Frank and David Kupfer pointed out that about 90 percent of
patients with major depression have at least one indicator of sleep abnormal-
ity. Subsequent studies put this figure a bit lower, but still quite sizeable. Ehlers
and her colleagues suggested that these disruptions in sleep rhythms could be
an important clue in the understanding of depression.24
These researchers also looked at depression as a state in which there is a
dysregulation or disruption of certain biological processes. These processes
include both the neuroendocrine system, which we have already discussed, and
the sleep-wake cycle. In the latter instance, it is as if one’s biological clock is
out of kilter, something like a case of perpetual jet lag. There is a possible tie-
in of this view to one particular type of depression — seasonal affective disor-
der, the depressed state that typically sets in during winter and abates in spring.
This tie-in is based on circadian rhythms.
All of us—for that matter — all animals— have circadian rhythms (approx-
imately 24 hours cycles) wired into our biology. These rhythms inform us when
to sleep and when to wake. The master biological clock in mammals is located
in a specialized group of cells in the hypothalamus. Destruction of these cells
results in destruction of the sleep-wake cycle.
Now the rhythms controlled by this pacemaker may fall out of sync with
the sleep wake cycle. In winter, for example, daybreak occurs later in the morn-
ing; it is dark outside, and awakening may be delayed while the clock ticks on
the bedside table well past the usual time of opening one’s eyes and letting out
that morning yawn. Research suggests that when the circadian rhythms are not
synchronized with respect to the clock and the sleep-wake cycle — this may be
a factor in promoting the symptoms characteristic of seasonal affective disor-
der. Bright light therapy immediately upon awakening is effective for many
people with SAD in ameliorating symptoms. This therapy may be effective, in
part, because it can correct the disconnect between the circadian rhythms and
the sleep-wake cycle.25
Extending the theory of dysregulation into the realm of social interaction,
Ehlers and her colleagues note that environmental events can affect biological
rhythms. They point to the commonplace observation of how one’s sleeping
and eating habits are affected by living with others. Think of life before and
after marriage.
The biological desynchronization that takes place in depression and the
influence of social and environmental causes in producing this condition are
important ideas to keep in mind as we pursue our inquiries in subsequent
chapters, particularly when we consider the effects of stress in triggering depres-
sive reactions.
The effects of antidepressant medicines upon sleep are interesting. Sleep
disturbances such as insomnia, poor quality of sleep and over sleeping are com-
mon symptoms of depression. One would expect that anti-depressant medi-
cines would be effective in diminishing these symptoms, but paradoxically they
sometimes make the problem worse, at least in the initial phase of treatment.
The drugs may cause daytime sleepiness and promote night time insomnia.26
Antidepressant drugs have noticeable effects on REM parameters, increas-
ing REM latencies and reducing the amount of REM sleep. These drugs tend
to reverse the abnormalities observed in untreated depressed patients and can
even swing the pendulum in the other direction. One class of anti-depressant
drugs, MAO inhibitors wipes out our REM sleep altogether for an extended
period of time. An antidepressant drug which appears to be particularly prom-
ising in the treatment of depressive-related sleep problems is agomelatine. This
drug demonstrates electroencephalograph changes which seem consistent with
patterns of more normal sleep. Patients with depressive related sleep problems
have responded favorably to this antidepressant drug.27
We know from much research that REM sleep is associated with dream-
ing, and we also know that the REM patterns of persons with major depres-
sion are atypical. These observations raise questions about the dreams of peo-
ple who are depressed — what are they like?
My own research carried out on normal subjects indicated that when peo-
ple are in a depressed mood, they tend to have better dream recall than when
their mood is more positive. This better recall may simply reflect a tendency
for people not to sleep as well when they are troubled; nocturnal awakenings
help one remember one’s dreams. In contrast to normal subjects, people who
are very depressed tend to have rather poor dream recall. Their dreams are
usually short and banal. During the height of depression, recall for dreams,
many of which can arouse uncomfortable feelings, seems to be at a low point.
There may be some kind of psychological or biological mechanism operating
to reduce stress.28
Researchers working out of the University of Alberta have carried out
some intriguing studies on the dreams of bipolar disorder patients. They found
that the latency of REM tended to increase in bipolar patients as their moods
improved. The researchers did not find this to be true for their unipolar patients.
Generally, the dream reports of the patients collected in the morning tended
to reflect their moods. The researchers noted that bipolar patients frequently
reported dreams about death, and most interestingly, these death dreams pre-
saged an upward shift in mood. In ancient times, dreams were widely thought
to predict the future. A dream of death might have been viewed as an omen of
catastrophe. For the moods of bipolar disorder patients, however, the opposite
might sometimes be true.29
A final note about sleep. Depressed mood is sometimes associated with
sleep-related respiratory disturbance, a condition characterized by loud and dis-
ruptive snoring. In the sleep laboratory, researchers have reported that in eld-
erly males, this sleep respiratory problem was associated with depressed mood.30
Depression and the Immune System

We have noted that when people feel depressed, they are more likely to
experience stress-related physical complaints such as headaches, dizziness, nau-
sea and diarrhea. Moreover, there are reports that when people are clinically
depressed, they have higher rates of infections,.31 These observations have led
researchers to ask the question: Does depression lower the body’s resistance to
fighting off disease? And more specifically, is there a relation between depres-
sion and the functioning of the body’s immune system?
Because of inconsistencies in research findings, one must be cautious about
drawing conclusions about these questions. These inconsistencies were high-
lighted in a 1992 review carried out by Carol Weisse of 23 studies looking at
the relation of depression to immune system function.32 Weisse cited over a half
dozen studies which found that depressed patients had lowered immune
responses using in vitro response to mitogins as a measure. Included in these

depressed counts were lower numbers of T-cells and T-helper cells. A number
of other studies reported that depressed patients had lower numbers and per-
centages of leucocytes. If we were to judge solely from these studies, we would
have the proverbial slam dunk: depression is associated with lowered immune
function. The problem, however, is that a fair number of other studies found
nothing — no evidence of lowered immune function.
What do we make of it all? It seems to me that there is clear evidence of
some relation between depression and immune function. Too many studies
have found positive results. But the conditions under which this effect is likely
to happen needs to be further specified. We know, for example, that stress is
associated with lowered immune function so it seems likely that depressed
patients with a high stress component in their clinical picture might be partic-
ularly vulnerable to immune system decrements. In her review, Weisse noted
that hospitalized unipolar depressed patients may be particularly vulnerable to
immune system alterations.
If we successfully treat depressed patients with lowered immune system
function, we should expect to see an improvement in immune system func-
tioning. Some studies have reported this to be the case, although there is a need
for additional research to be more certain of this.33
The Search for Genes That Underlie Depressive Disorders

The family and twin studies on major depressive disorder and bipolar dis-
order pointed to a substantial basis in heredity for the former and an even more
substantial basis for the latter. These findings raise the question: Can we iden-
tify the genes that underpin these disorders? To date, this has proven to be a
challenging undertaking. For one thing as we currently understand it, depres-
sion is a complex entity, a constellation of a variety of disparate symptoms
ranging from fatigue to suicide. One would not expect to find a single gene
underlying such a disorder. In addition, there are a very large number of genes
in the human genome. Given the complexity of the disorder and the number
of genes to choose from, the task of linking specific genes to the development
of depression is inherently difficult.
One of the approaches that researchers are currently using to better tar-
get their search for genes is to break down depression into its psychological
and biological components and then try to link these components to genes. For
example, a researcher might be interested in looking at the psychological aspects
of depression which relate clearly to brain function such as memory and atten-
tion deficits or the biological aspects of brain function such as dysfunctions in
the neurotransmitter systems. The researcher might use measures of these
deficits as intervening variables and try to link these to genotypes. The hope
is that these intervening measures which are termed endophenotypes may pro-
vide simpler clues to the underpinning genes. The best bets for fruitful
endophenotypes are thought to be those which are associated with candidate
genes or gene regions and have shown significant heritability in family and
twin studies.34
Within this targeted approach, researchers have been examining the poten-
tial role of a number of genes. Here is an example. We know from a variety of
studies that serotonin is involved in depression. We, also, know that the reup-
take process that diminishes the concentration of serotonin in the synapse plays
an important role in whether a person vulnerable to depression experiences
depressive symptoms. Inhibiting reuptake of serotonin often ameliorates symp-
toms. Researchers are learning a great deal about the reuptake process. As a
neurotransmitter, serotonin’s action is regulated by a transporter (5HTT), a
molecule located in the plasma membrane of the presynaptic (firing) neuron.
This serotonin transporter returns serotonin to the presynaptic cell where it
may be recycled or degraded. Now, here is where the genes come into the story.
This serotonin transporter is under the regulation of a gene, and in the regu-
lator promoter area of the gene (designated 5-HTTLPR) two distinct forms are
encoded — a short variant (S) and a long variant (L).35 Researchers have uncov-
ered a number of differences in the action of these two variants which, though
not fully understood lead to the conclusion that the short variant is associated
with a relative loss of transporter function. Current thinking is that the short
variant may not regulate serotonin activity in a way that is as optimal for the
person as the longer variant and under certain circumstances such as exposure
to stressors, this can lead to differences in the processing of emotion, particu-
larly anxiety and depression.36
As part of the effort to link these genotypes to anxiety, researchers have
been studying the possibility that people who carry the short variant of the
transporter gene will score higher on personality measures of anxiety and related
states. The findings, so far, appear unclear with both positive and negative
results.37 While the data seems equivocal as to whether people carrying the
short variant have a trait-like propensity to experience anxiety in many life sit-
uations, there is accumulating evidence from brain imaging studies that they
may have a tendency to react strongly to potentially threatening situations.
Consider a study carried out by using reactivity of the amygdala as a bench
mark. Recall that the amygdala plays a major role in fear reactions. The study
carried out by Ahmad Hariri and his colleagues compared people carrying the
short variant with those carrying the long variant on a perceptual task of match-
ing anxious and angry faces while the subjects were being monitored by brain
imaging for amygdala activity. The people carrying the short variant showed
much greater reactivity. It was reported that the difference in amygdala activ-
ity between the two groups was nearly fivefold.38 The suggestion from these and
other findings is that people carrying the short variant might experience hyper-
activity of the amygadala when confronted with unsettling situations. People

who are prone to phobias or suffer from panic reactions might have particu-
larly strong reactions.
Let’s consider depression. A very intriguing study carried out in England
found that people carrying the short variant showed more depressive symp-
toms in response to stressful life events than people carrying the long variant.39
Studies have also linked the short variant along with another recently recog-
nized variant called L(G) to severity of depression in a clinical sample.40 How-
ever, the role these variants play in depression is still far from understood.
Recall the study carried out at the National Institute of Mental Health in which
remitted depressed patients were given the tryptophan depletion procedure.
While tryptophan depletion increased depressive symptoms in all genotypes,
the largest increase in depressive symptoms occurred in the patients carrying
the long variant.41 This surprising result tells us that much remains to be learned
about the complex links between genes, neurotransmitter activity and depres-
sion.
One of the areas of research that could have important implications for
patient care will be comparisons between patients carrying the long variant and
the short variant in terms of response to various antidepressant drugs. One can
envision the use of genetic typing as a factor in choosing drugs for patients.
The studies combining genetic assessment, neuroimaging and exposure
to stress are exciting, groundbreaking research, often calling for a team of
researchers coming from several disciplines. Because of the complexity of the
procedures required, the sample sizes used are sometimes small. This under-
scores the importance of replication of findings.
It is clear from these thumbnail sketches that our biology plays a very
important role in depression. One can envision a time in which people who
are clinically depressed will be asked to take a variety of laboratory tests which
may help in both diagnosis and the formulation of a treatment plan. However,
it is also clear that biological factors are only a part of the picture. We can
already see that stress plays a large role in depression and we shall see that the
way people interpret the situations in life that cause stress and react to these
situations can make an important difference in whether the person becomes
depressed. This brings us to the consideration of psychological factors in depres-
sion and an array of ideas that underpin the psychotherapeutic treatment of
depression.
4. A Psychological
Perspective on Depression
People who feel depressed tend to have different views of themselves and
the world about them than people who are not depressed. These differences have
been identified by clinical observation of depressed patients and confirmed by
subsequent research. Some theorists like Aaron Beck have proposed that these
beliefs or thought patterns play a large role in bringing on depressed mood,
assuming that these thought patterns give rise to the sadness experienced in
depression.1
This theory is an interesting one because it leads to the idea that if you
can change thinking patterns, you may be able to alter depressed states. This
is the basis for cognitive therapy for depression (the word cognitive coming from
cognitions or ideas). In cognitive therapy, the therapist tries to help the patient
change his or her depressive beliefs. The good news is that many studies have
found this approach is helpful.
How do the world and the self look to the person who has become
depressed? Let’s consider two people whose moods have recently become
depressed. Debbie is a housewife. She stays at home and looks after two school-
aged children. Her husband, Tom, works long hours at his job and is usually
tired when he comes home. Tom is a good provider, nice with the children
when he has the time, quiet spoken, never abusive — but he doesn’t give Deb-
bie the attention she feels she needs. She feels the spark has gone out of their
marriage. The romance of courtship and the early days of marriage seem like
a distant memory. Now her life seems like an endless series of chores— shop-
ping, cooking, cleaning, and chauffeuring. She feels people expect things from
her all the time and she feels little sense of accomplishment or fulfillment. Lately
she feels trapped. She’s taken to watching soap operas and fantasizing about
having affairs. But the idea leaves her very uncomfortable and it remains only
a fantasy. She has been drinking a lot and sleeping badly. Occasionally she
“blows up,” giving some hint of the resentment that has been building. Most
of the time, however, she just goes through the motions. When her best friend
asked her what was wrong, she only replied, “What’s the use?”
60
4. A Psychological Perspective on Depression 61
Alan is a 20-year-old sophomore student at a suburban community col-

lege. His mood plummeted after his first day of class in economics. During the
class, the professor had outlined what she was planning to cover in the course.
When the class was over, Alan sat down on a bench on the campus and pic-
tured in his mind what lay ahead. The course outline sounded difficult. He
didn’t understand some of the things the professor had said. The student in the
class who asked questions seemed very sharp. Alan wondered whether he could
compete. During the previous semester he had had a bad experience in a math
class, and didn’t economics involve math? Maybe the best thing was not to take
the risk. Better to drop the course than fail again. Alan felt a sense of defeat, a
sense of giving up that he had experienced before, both in school and out of
school.
There is a pattern running through these cases. In both instances, the indi-
vidual looks at her or his situation in life in a negative way and feels pessimistic
about the possibility of change. The outlook boils down to this: “My situation
is bad and I cannot do anything to make things better.” A tendency to view
one’s situation in a negative way and a feeling of powerlessness to do anything
about it are important cornerstones of a depression related mind-set.
The Negative Perspective

In a bit of whimsy, or perhaps in a flight of cynicism, someone once sug-
gested that the only things that are certain in life are death and taxes. I would
expand on this short list with the notion that there are a lot of other negative
events, which while not as certain to occur as these two, are nonetheless very
likely to happen. Such negative events may begin in early childhood with a
spanking, sitting in the corner, or some other form of disciplinary measure,
and continue right on through the school years with getting a bad grade on a
test, or not being chosen for the team, through adolescence and young adult-
hood with rejection by a sought-for romantic interest, not getting accepted
into the college of one’s choice, not getting the job you interviewed for, and so
forth and so on. Sporadic losses, disappointments, and failures are part of almost
everybody’s life experiences. The question is not so much will you experience
such negative events; rather it is, when you do, what will you make of them.
How do you evaluate them, how do you interpret them, where do you see the
fault lies, and what kind of context do you place them in? People who become
depressed tend to take a more profoundly negative view of such events when
they occur. Moreover, this mind-set often generalizes to interpret events which
are not particularly negative as more negative than they are, and to downplay
or even dismiss positive events as not being all that meaningful and significant.
Whether this negative perspective rises to the level of a cause of depression is
not entirely clear, but it is certainly closely linked to depression and in any event
is not helpful and can well exacerbate the problem. Researchers have shown
that negative mind-sets are predictive of depression, the severity of its course
and the probability of recurrent episodes.2
When we talk about having a negative perspective, we are talking about a
tendency to view events in a negative rather than positive light. It is a mind-
set in which you evaluate yourself and the world you live in unfavorably. Con-
sider the proverbial glass that may be seen as half full or half empty; the negative
perspective views it as half empty.
This negative perspective shows itself not only in the evaluation of events,
but can even influence what would seem to be straightforward perceptions.
Almost everyone can recognize a happy face. This is a near universal experi-
ence that transcends cultures. But as research suggests, if you show a picture
of a happy face to a person who is depressed, they may not see it as such. The
facial expression may have to look really happy before they recognize it as such.
However, when researchers showed depressed people pictures of sad faces, they
more readily identified them correctly as sad than they were able to do for other
emotions such as anger.3
Aaron Beck, who has been one of the principal architects of the negative
thinking pattern approach to depression, sees this negative perspective apply-
ing to one’s view of oneself, the world about one and the future. It’s a “triple
whammy.” In therapy, we often listen to patients describe their lives as unpleas-
ant. They may relate grim details about their job and find little appealing in
their home lives. Their worlds appear unpromising and unrewarding.
Now, there may be a good deal of truth in what the depressed person points
out. In therapy, the patient may complain, “I’m not getting anywhere in life,”
and this may be true. The job situation and home life may present real prob-
lems. However, depressed people, like everyone else, have a tendency towards
selective perception. To varying degrees, people see what they want to see and
hear what they want to hear. It is something like what happens during a polit-
ical campaign. You may listen to a candidate on a television program who says
things you agree with, but turn off one who says things you disagree with. The
depressed person may present a reasonably accurate picture as far as it goes,
but it is likely to be selective. He or she may be ignoring things that could make
the overall picture seem a good deal brighter than it appears.
While some persons with tendencies toward depression engage in bouts
of self-analysis and reason themselves into negative conclusions, negative think-
ing processes often have an almost automatic character. Such thoughts seem
to chase across the depressed person’s stream of consciousness something like
the spots or floaters that chase across people’s eyes when a section of vitreous
in the eye becomes detached. At times, these depressive thought patterns have
an almost obsessive quality.
In his book Cognitive Therapy and the Emotional Disorders, Aaron Beck
related how he first became sensitized to these automatic thoughts while he was
doing psychoanalytic therapy. When he became convinced of the importance

of these automatic thoughts, he began to ask his patients to pay particular atten-
tion to them and to report them to him. He told his patients that when they
experienced unpleasant feelings, to try to recall the thoughts they had prior to
the feelings.4
Beck observed that automatic thoughts were typically discrete and specific,
resembling a kind of shorthand. The patients did not try to initiate the thoughts;
they simply occurred. Once the thought appeared in the patient’s conscious-
ness, it was hard for the patient to get rid of it. These thoughts could not be
easily turned off like water from a faucet.
Beck reported that while outside observers might consider the negative
ideas of depressed patients to be farfetched, the patients felt they were reason-
able and true. In talking with a patient, one might be able to persuade her or
him that these thoughts didn’t make a lot of sense, but in a short period of time,
the patient might soon revert to believing the ideas as strongly as ever. The neg-
ative thoughts that may preoccupy the mind of a depression-prone person can
be resilient.
The tendency for depressed people to view their own performance nega-
tively has been demonstrated in experiments. Here is an example. Depressed
and nondepressed subjects took part in an individualized learning experiment.
The subjects had to learn to associate particular numbers with particular words.
Each time the subject responded, the experimenter would say whether she or
he was right or wrong. At a point in the learning experiment, the researchers
asked the subjects to estimate what percentage of their prior responses were
correct. The depressed subjects were more likely to underestimate how often
they had been told they were correct than the nondepressed subjects.5
There is an increasing body of research that suggests that the negative eval-
uations of depressed people are only part of the equation. People who are not
depressed may have a tendency to inflate how well they have performed in
experimental studies.6 People who are not depressed may have some degree of
illusion about their performance. As we shall speculate later, this positive, opti-
mistic perspective may act as a kind of protective shield against depressive reac-
tions.
Powerlessness
Powerlessness is a belief that you are at the mercy of external events and
there is little or nothing you can do to change things. Like negative thought
patterns, feeling powerless is associated with depression.
Researchers have studied one aspect of the relation of powerlessness and
depression at length, and that is the extent to which people view the sources of
gratification in their life as being under the control of external forces or under
their own control. The hypothesis is that the former (external) view would be
associated with depression. In testing this idea, researchers have used psycho-
logical tests to measure a person’s perception of internal vs. external control.
How might such a test look? Suppose someone presented you with pairs of
items like “getting somewhere in life is a matter of hard work,” and “the most
important thing about achieving success is being lucky,” and asked you to check
the item that is closer to your way of thinking. If you checked many items like
the second, you would receive a high external score.7
After examining studies exploring the relation between perceived locus of
control and measures of depression, Victor Benassi and his colleagues con-
cluded, “We found strong support for the hypothesis that greater externality is
associated with greater depression.”8
One facet of powerlessness is a belief that the world you live in is com-
posed of immovable obstacles that will prove resistant to anything you try to
do. No matter what you try to do, the result will be something like running
into a stone wall. The outcome of such a view is likely to be, “I won’t be able
to do anything, so what’s the use of trying.” Martin Seligman has referred to
reactions like this as learned helplessness. The idea is that your experiences have
led you to conclude that your own efforts have no clear effect on outcomes and
events. Life appears something like a slot machine — a one-armed bandit that
doesn’t payoff.9
The belief that what you do is not going to make any difference is some-
thing that may be learned from repeated frustrations. Imagine an experiment
in which the subject is exposed to an unpleasant condition like loud noise. The
subject presses a button in an attempt to turn the noise off, but finds that push-
ing the button doesn’t stop the noise. The subject gives up. When put into a
similar situation where pushing a new device (a knob) would actually turn off
the noise, the subject is less likely to even try it. He or she may sit passively and
remain uncomfortable while the noise blasts away.10
Perhaps an even more debilitating form of powerlessness than believing
that the environment is stacked against you is the feeling that you are incom-
petent and can’t do anything. This was the feeling Alan had in response to his
poor grades in school. Believing the environment is the problem at least offers
some protection for your self-esteem. Believing that you are incompetent
doesn’t leave you many “outs” psychologically.
Feelings of inadequacy — the idea that “I can’t do it” or “I won’t measure
up”— may be viewed as another form of learned helplessness. This belief typ-
ically has its roots in childhood, in frustrating, unsuccessful experiences, and
in disparaging messages communicated from parents, peers and teachers.
Repeated experiences of nonrewarded performance and derision erode self-
confidence and lead to the conclusion, “I’m not capable.”
Janet Altman and J. R. Wittenborn gave out questionnaires to a group of
women who had once experienced a serious depression and to a group of non
depressed controls. There were consistent differences between the groups in

reported confidence, perceived competence and self-esteem. The women who
had been depressed were more likely to respond that it was hard to credit them-
selves with good, doubted that they deserved praise, were uncomfortable with
responsibility, often failed unnecessarily, and were not good enough to try for
the top.11
The consequence of learned helplessness and feelings of powerlessness are
likely to include a passive lifestyle. A person is less likely to take risks when the
thought of failure looms large and is more willing to tolerate an unpleasant state
of affairs— a cramped and limited lifestyle — if it seems secure. The chances are
higher that he or she may fall into a dependency relationship with someone per-
ceived as more competent.
The tendency to view oneself and one’s environment in a negative way, in
conjunction with a perception that one is powerless to change things, may ulti-
mately lead to a feeling of hopelessness, that one is boxed into a miserable life.
Things haven’t worked out well to date, and there’s no prospect that they ever
will. When problems seem insolvable and when a feeling of hopelessness
becomes lodged in one’s consciousness, suicidal thoughts may develop. The
playwright Jean Anouilh described the feeling aptly in his play Restless Heart
when he spoke of “the farthest limits of his pain” and “the far end of despair.”12
The feeling of hopelessness casts a bleak shadow over one’s daily experi-
ence. The depressed person often feels that time lingers, that the day is inter-
minable. If put to a test of estimating how much time has actually elapsed
between two settings on the clock, people who are in a depressed mood are likely
to do as well as anyone else — it is the subjective evaluation of experience that
is different.13 Life seems to have little movement and vitality. In some ways, it
is as if the depressed person is cast in a mental prison.
A person looking from the outside with a more objective perspective can
see that the depressed person’s view of his or her own situation is often not a
true assessment of the way things are or could be. Except for a terminal illness
for which all remedies have been exhausted, there are very few things in life
that are hopeless. Separation or divorce is an antidote to a very bad marriage.
One can change jobs. Joining a club is a step toward ending loneliness. Few bad
situations are unalterable. But the depressed person has to alter his view to see
that this mental prison is more apparent than real and that some things can be
done.
Some Depressive Thought Patterns

Let’s turn our attention to some of the thought patterns often found in
depressed people that contribute to the feeling of hopelessness. One of these
patterns is a tendency to overgeneralize. It is the classic case of 2 + 2 = 5, or
perhaps even 50. Take Liz, who works in a large office in an insurance com-
pany. Every week Liz has contacts with about 20 other employees. One of these
employees, Barbara, had a nasty argument with Liz and now walks right past
Liz without speaking to her. Another woman, Judy, is also unfriendly to Liz,
but Judy is unfriendly to just about everyone in the office. What has Liz con-
cluded? That no one likes her at the office, and worse, that she is unlikable. One
could point out to Liz that if she listed all of the people in the office, and went
through the names one by one, she would find there were many people in her
office who are in fact friendly to her. But Liz, like many people who become
depressed, has overgeneralized from a few incidents and drawn a sweeping con-
clusion.
Overgeneralization may take the form that if some things are wrong in life,
then everything is wrong. And if things are bad in the foreseeable future, they
will always be bad. The tendency for depressed people to overgeneralize has been
demonstrated in psychological experiments. For example, in an experiment in
which the subjects had been told they had done poorly in a “social perceptive-
ness test,” the subjects who were more depressed tended to magnify and over-
generalize their failure. As the authors Richard Wenzlaff and Sherilyn Grozier
described their results, “the failure feedback had more far-reaching effects on
depressed subjects’ self-perceptions than on those of nondepressed subjects.
After learning they had done poorly on a test of social perceptiveness, depressed
subjects not only lowered their estimates of their social perceptiveness, but also
believed they were generally less proficient.”14 The subjects also tended to mag-
nify the importance of what they had been tested on.
Charles Carver and Ronald Ganellen developed a questionnaire measure
of the tendency to overgeneralize, using such items as, “When even one thing
goes wrong I begin to feel bad and wonder if I can do well at anything at all,”
and “How I feel about myself overall is easily influenced by a single mistake.”15
The researchers found that people who scored high on this measure were more
likely to score high on a measure of depression.
Perfectionism and black and white categorization are other forms of think-
ing that may contribute to depression. When one hears the phrase, “he’s a per-
fectionist,” one thinks of a person who has a very high level of aspiration. His
goals are not only high, they may be out of sight. He may pay inordinate atten-
tion to details, imposing exacting standards that everything must be “just so.”
If it isn’t right, you do it again. There is an obsessive striving to attain a stan-
dard that may not be reachable. What might be seen as reasonable progress by
another person may be seen only as failure.
An example of problems that come with perfectionist thinking is the stu-
dent who is hung up on grades. If only an A grade will do and she doesn’t get
an A, where is she? Disappointed, maybe depressed.
In therapy, I have often heard statements like “My father said, if you can’t
do it right, don’t do it at all.” This overly demanding standard didn’t help the
people who consulted me and I wonder how much good it did for their fathers
and mothers. If the only standard one can accept is perfection, then who can
possibly meet it? The consequence of perfectionist thinking is often not being
happy with what you do or not being willing to try anything because of the
belief it may not turn out good enough. Both of these tendencies can contribute
to a depressed mood.
Psychologists interested in the measurement of perfectionism have
identified a number of aspects of this tendency. Of these, socially prescribed
perfectionism, concern over mistakes, and self criticism seem to be particu-
larly correlated with depressive symptoms.16 Very high standards foisted on
others accompanied by criticism for not meeting them can make the recipients
feel miserable. Excessively high standards accompanied by self-criticism can
do a number on oneself. Interestingly, in a study of people who suffer from
chronic insomnia, it was found that these people were very concerned about
mistakes. In addition, they were the recipients of frequent parental criticism.17
Longitudinal studies on patients being treated for depression have found
that perfectionism is a predictor of how well these people respond to therapy.
Depressed patients with perfectionist dependencies don’t seem to do as well.
Part of the problem may be difficulties in establishing a working relationship
with the therapist.18
Trying to do as well as one can is an admirable characteristic. But self-
acceptance is also important. Being a perfectionist in life almost inevitably gen-
erates frustration and discontent and can set one up for a depressive reaction.
Black and white categorization is a tendency to evaluate things in an
extreme way — as being either “super” or “lousy”— and to not see what is in
between. One often finds some intolerance with this perspective, a predilec-
tion to classify people as wonderful or terrible and not as the mix of strengths
and frailties that they really are. With this outlook, one can come down very
hard on people — and pretty soon one may find oneself with few friends. Being
without friends often translates into feeling lonely, which in turn may trans-
late into depressed mood.
Albert Ellis, writing from the perspective of rational-emotive therapy,
developed a list of “irrational beliefs” that are related to depression. Ellis
included such beliefs as a need to excel in everything one does to feel worth-
while as a person, the idea that it is terrible when things are not going the way
one would like them to go, and that one cannot overcome the effects of past
history. 19 Aaron Beck developed a similar sounding list of attitudes that he
believed predisposes people to sadness or depression. These attitudes contain
elements of perfectionist and absolutist thinking, as well as a tendency to view
events in one’s life as being under external control.20
As these researchers suggest, many depression-prone people apply exces-
sively demanding standards to themselves. Freud would have talked about a
demanding superego. Imagine that your life is being run by a permanent drill
sergeant who tolerates no excuses, sees no extenuating circumstances and sees

no shades of gray in life. With this mental makeup, it’s not a big step to arrive
at a conclusion that one has fallen short of almost everything and to find one’s
self-esteem deflated.
People can further tear down their self-esteem and drive themselves deeper
into the mental prison of depression by frequently comparing themselves with
others who seem to be doing better. Comparing oneself with others on occa-
sion is not unusual, but many depressed people have a habit of doing this, and
they do so in a way that deepens their feelings of inadequacy. The comparisons
emphasize their shortcomings, not their strong points. If you think about it,
you can always find someone who seems smarter or better looking, or makes
more money or has nicer furniture, or is a better athlete, or whatever else is
important to you. Measuring oneself by the accomplishments (or perceived
accomplishments) of others can leave one chronically frustrated and discon-
tented.
Many people who become depressed spend a lot of time thinking about
themselves. Attention is focused inwardly rather than on things to do in the
external world. While occasional self-monitoring can be a good thing, it is not
usually helpful to make a career out of it. Moreover, the problem is com-
pounded by the tendency of depressed people to have a negative bias in their
thinking. Excessive inward attention may simply be multiplying negatives. Con-
stantly turning over the question of, “What’s wrong with me?” is unlikely to
make a person feel positive about anything.21
Resentment and Anger

When we accumulate these psychological patterns— a focus on the nega-
tive, a feeling of powerlessness, overgeneralization, perfectionist thinking, and
the tendency to come down hard on oneself — one can see why self-esteem takes
a beating and mood is likely to plummet. The person may become paralyzed
in this mental prison and rendered inactive and ineffectual. He or she may also
become angry.
Anger sometimes takes the form of a deep sense of resentment. We are talk-
ing about people who may become frustrated by what is happening in their lives.
They may be frustrated by not being able to do what they want, or their view
of reality may be so negatively skewed that they are not able to enjoy what they
are accomplishing. When this happens, the person may feel like a “victim,”
looking at the world about her or him as unfair. Developing resentment may
be directed against one’s family and friends, or turned inwardly against one-
self.
In psychoanalytic theory, the concept of anger turned inward occupies a
central place in the causation of depression. The idea has its roots in a semi-
nal essay of Sigmund Freud’s entitled Mourning and Melancholia.22 Freud was
struck by some of the similarities between mourning following the death of a
loved one and depression. He believed that depression, too, was based upon
the experience of loss, but that the dynamics of what happened were more com-
plex. Freud wrote that in depression the relationship between the person who
becomes depressed and the lost loved one is not a straightforward positive one;
rather, the depressed persons’ feelings are characterized by marked ambiva-
lence, that is, the presence of both positive and negative feelings. The negative
feelings often arise from incidents in the relationship in which the person was
disappointed, hurt and neglected. Freud wrote of an ensuing struggle in the
person’s unconscious in which feelings of love and hostility wrestle with each
other. The struggle resolves itself not by the anger being overtly expressed
towards the person who “provoked” it, or by the person giving up his or her
love; rather, the anger is displaced, turned inwardly against the self. The per-
son describes himself or herself as worthless, rather than describing the lost
loved one, the one who rejected him or her, as such. In this process, a degree
of revenge is often exacted as the depressive illness provides a means of tor-
menting the person who injured the depressed person’s feelings.
It is an intriguing scenario, a testament to Freud’s ingenuity and remark-
able powers of clinical observation. And, indeed, one often sees elements of
the scenario in depressed patients, the experience of loss, anger and remorse.
The patient’s resentment toward others, however, may be anything but buried
in the unconscious. Resentment may be simmering on the surface, if not boil-
ing. My distinct impression is that anger toward others may coexist with anger
toward the self.
Roland Tanck and I were interested in the formulation that anger directed
against oneself is associated with increased feelings of depression. In one of our
studies, we asked university students to fill out diaries for a period of 10 nights.
During each night they responded to the questions, “Did you feel angry or
annoyed today?” “And, if yes, what was it that made you feel angry?” The stu-
dents who reported instances in which their angry feelings resulted from their
own missteps, failures and shortcomings scored higher on several measures of
depression than the students who attributed their angry feelings to other
sources.23
When we work with depressed patients, we often see self-reproach as part
of the clinical picture. In interpreting this, one must keep in mind the psycho-
analytic view that some of these negative feelings toward the self have as their
true target someone else. A man might feel very angry toward his wife or boss,
but may be unable to express these feelings, and eventually this resentment
comes home to roost. It is not clear, however, that self-reproach is always an
unconscious process of displaced anger. An individual may begin to recognize
his own shortcomings and failures in dealing with his problems and react in
self-disgust. One can picture a sequence of thoughts, “I can’t do it ... I’m no
good ... Damn it!” Perhaps both conscious and unconscious processes are at
work in directing anger inwardly.
If self-directed anger plays a role in the depressive process, we should
expect to see less of this as the patient improves in therapy. There is some
research that indicates that this is the case.
The Measurement of Mind-Sets

We have discussed a number of mind-sets, attitudes and personality ten-
dencies that seem to promote depressive reactions. Psychologists have been
developing instruments to measure the various mind-sets. We have already
mentioned questionnaires that assess perceived external vs. internal control of
reinforcement and a tendency to overgeneralize. Other self-report measures
that have been developed are questionnaires that assess the frequency of auto-
matic thoughts, typical styles for interpreting negative experiences and the ten-
dency to hold irrational beliefs. All of these techniques have been used by
researchers in trying to more clearly understand the role of psychological fac-
tors in depression.
Let’s look at a few of these techniques, beginning with a measure to assess
automatic thoughts, appropriately called the Automatic Thoughts Question-
naire. Imagine a list of very short statements in front of you, such as “My future
is bleak,” “Something has to change,” “I’m a failure,” “I wish I were somewhere
else,” “No one understands me,” “I’m so disappointed in myself,” and “I feel
so helpless.” Your instructions are to indicate, on a five-point scale ranging
from “not at all” to “all the time,” how frequently these thoughts occurred to
you over the last week.24 You can readily see that if you often had such thoughts,
you would qualify for a depressive mind-set.
A second measure called the Dysfunctional Attitudes Scale developed by
Myrna Weisman and Aaron Beck is based on Beck’s thinking about mindsets
associated with depression.25 The scale, which includes items sampling such
concepts as perfectionistic standards, concern about the judgments of others,
and imperatives that one must follow, is presented on a seven point scale, rang-
ing from totally agree to totally disagree. The Dysfunctional Attitude Scale
yields a total score which has been used by researchers as a measure of belief
patterns that are linked to depression. In a recent study, for example, researchers
use the measure to explore how such belief patterns might play a role in post-
partum depression.26
A third approach to measuring cognitions that relate to depression is the
Attribution Style Questionnaire that followed from the thinking of Martin
Seligman, Lyn Abramson and their colleagues who were interested in the
attributions people made about the events that occurred in their lives.27 Peo-
ple are asked to look for causes of these events: Were they something attri-
butable to one’s own actions (internal) or caused by external forces. Would

they view them as stable or transitory? Global in scope or narrowly confined?
Researchers drew up a list of commonly experienced events, some negative,
some positive, and asked the subject to imagine them and to make ratings
about them on the dimensions of internal-external, global-specific, and sta-
ble-unstable. While, the resulting measure, the Attribution Style Question-
naire has been modified over the years in various ways, such as substituting
real events for hypothetical events, the basic format has remained the same
with the overall score representing an attributional style of viewing events
as internally caused, stable, and global. When such an attributional style is
applied to negative events, the assumption that is usually made, either explic-
itly or implicitly, is that this is a factor in increasing vulnerability to depres-
sion. And, indeed, meta-analyses looking at the relation of attribution style
and measures of depression have found positive associations for both children
and adults.28
Here is an informal exercise you might want to try. Think back to some
of the more stressful or disappointing experiences of recent months and con-
sider the way you interpreted them. For example, think about a disappoint-
ment in a romantic relationship or a stressful problem that happened on your
job or at school. Take a moment and go over the situation in your mind.
What was your reaction like?
How did you evaluate the situation?
Did you tend to put the worst light on the situation by thinking, “My
whole life is in shambles” or “Things will never get any better”?
Did you go through a period of time in which you blamed yourself for
what happened?
Did you conclude you were not a worthwhile person?
Now go back a little further in time to another incident in which you expe-
rienced stress or disappointment. Once again take some time and think about
how you felt and what was going through your mind. Ask yourself the same
set of questions.
If you answered yes to most of the questions for both incidents, think back
to other episodes and again ask yourself the questions. Is this typical for you?
Is this your characteristic way of reacting to stressful and disappointing situa-
tions? If it is, then you could well have the type of mind-set that makes you
vulnerable to depression, a concern you may want to address.
The psychological factors we have profiled for depression probably don’t
work in isolation from one another; most likely they augment one another pro-
ducing a cumulative effect. Perfectionist tendencies, for example, are likely to
increase the chances of self-reproach. A description of this interaction, offered
in a theoretical paper by H. A. Meyersburg and his colleagues noted that guilt
is often tied to failures in perfectionistic expectations. When perfectionism
becomes an absolute, all-or-nothing issue, even, falling slightly short of the

mark may be interpreted as total failure. The tighter the perfectionistic system,
the more one feels a sense of inadequacy when things don’t go well and the
greater the chance of triggering a depressogenic process.”29
Meyersburg and his colleagues believed that in the face of severe stress
coming with loss and disappointment, a constellation of psychological fac-
tors— impulsivity, perfectionism, guilt and self-punitiveness interact with one
another as a kind of reverberating mechanism, escalating anxiety to the point
where it becomes overwhelming. The reverberating mechanism can turn a
difficult situation into a psychological debacle.
Mind-sets, attitudes and personality tendencies act as a kind of filtering
system between the stressors of the world — the things that can go wrong and
often do— and our reactions as human beings. These psychological factors play
an important role in determining whether a person becomes seriously
depressed. While persons with depressive mind-sets have heightened vulner-
ability, it is important to recognize that attitudes and mind-sets can be changed
and, as we shall see, this often takes place in therapy.
The Protective Shield

Frustration and disappointments are near universals in life. Even the best
job and the most wonderful family will have their share of unpleasant times.
And the less than super job that many of us have and the more typical family
will engender problems aplenty. The person who is relatively free from depres-
sion seems to have a kind of protective shield against these daily stresses. He
or she is able to tolerate frustrations and disappointments without experienc-
ing sustained periods of depressed mood.
While part of what we call a protective shield is clearly biological and
genetically based, there are important psychological components as well.
The idea of a protective shield was suggested in part from unexpected
findings in psychological experiments carried out with depressed and nonde-
pressed subjects. The following is an example of one of these experiments:
Imagine you have been recruited to take part in the study. You were told that,
“The investigators were interested in learning more about how people who are
strangers relate to one another.30 You find yourself in a room with four or five
other people. You don’t know that some of the people are being treated for
depression at the university psychology clinic.
All of the people in the group are asked to give three-minute introduc-
tory statements about themselves. Then everybody makes conversation for
another twenty minutes. At the end of the session, you fill out a rating form
asking about your perceptions of the behavior of the other people and your-
self during the session. The rating form includes a number of positive descrip-
tions, such as friendly, warm, communicates clearly, interested in other peo-

ple, socially skillful, and so on. While you take part in this conversational exer-
cise, observers watch you and the other participants through one-way vision
screens. They can see you; you can’t see them. These observers make the same
ratings that you do. Three additional sessions are held at later times.
As the researchers expected, the participants who were clinically depressed
evaluated their own performance more negatively than the other subjects. What
was not expected, however, was that the nondepressed subjects had a more
favorable view of their own performance than was given them by the outside
observers.
When the depressed patients improved during treatment, they began to
rate themselves more favorably than the outside observers did, just like
the nondepressed subjects were doing. In speculating about their findings, the
researchers, Peter Lewinsohn and his colleagues, stated, “It is tempting to
conjecture that a key to avoiding depression is to see oneself less stringently
and more favorably than others see one.” 31 The authors use such terms as
an “illusory glow in their self-perceptions” to describe the nondepressed sub-
jects.32
This study, as well as a number of other studies with similar results, sug-
gests that one of the ways of resisting the stressors that promote depression is
to have an optimistic, positive attitude, a tendency to put the best face on cir-
cumstances and to believe that one can bring events under control.
As an example, consider possible reactions to an unsuccessful undertak-
ing, such as doing badly on a test at school. One could look at one’s perform-
ance in a very negative way or one could frame the event in such a way as to
protect one’s self-esteem. These “reframing maneuvers,” as C. R. Snyder called
them, make things seem not as bad. As Snyder put it, they soften, bleach and
repackage the act that may generate self-blame and diminish self-esteem.33
One may soften the poor mark on the test with explanations such as, “Most
people would not have done any better,” “The test was extremely difficult,” “I
was preoccupied with others things that were bothering me and couldn’t con-
centrate,” “The test really wasn’t that important, anyway,” or “I wasn’t at my
best — I’m not a machine.” While one can’t make a living by perpetually ration-
alizing away disappointments, protecting one’s ego from a debacle when one
experiences failure has the decided advantage of allowing one to pick oneself
up and regroup, and to try again without going through a protracted malaise.
The concept of a psychological shield protecting a person against the
storms of reality is reminiscent of Charles Dickens’ character Mr. McCawber,
who was able to cope with the most miserable circumstances with an outlook
that, “something is bound to turn up!” The outlook is something like seeing
that half full glass, three-quarters full. Or to use the cliché— to look at life
through rose-colored glasses.
Such an attitude may be clearly unrealistic at times, but a strong dose of
optimism may act as a deflector, bouncing off stressors like force fields repelling
attackers in a science fiction story.
This notion of a psychological protective shield bears a resemblance to the
concept of the defense mechanisms postulated by psychoanalytic theories.
Defense mechanisms act to protect the ego from being overwhelmed.
We are not suggesting that we should all become Pollyannas or dismiss real-
ity. Perhaps you remember the character Ilya in the classic movie Never on Sun-
day? When she related the grim story of Medea, she concluded not with the
story’s horrible blood bath, but with everyone going for an outing to the beach.
We are not suggesting that people follow her example. We are, however, sug-
gesting that optimistic thinking has value in warding off depression.
5. The Roots of Depression:
A Look at Childhood
Experiences
It is axiomatic that one’s past experiences influence what one is today. The
influence of childhood experiences seems particularly important, for that is
where formative personality patterns are laid down. It seems reasonable to
search for long-range causes of adult depression in child development and espe-
cially in the pattern of parent-child relationships.
Some patients enter therapy with this idea in mind; they assume that there
are deep underlying causes for their depressed feelings and anticipate that the
therapist will spend considerable time delving into their childhood recollec-
tions trying to unearth these causes. The thinking may be that when these
causes are uncovered, the depressive symptoms will disappear. This can be a
somewhat romanticized view of therapy, for there are usually pressing prob-
lems that confront patients in their daily lives that demand attention in ther-
apy, problems that are currently having an impact on the patient’s well being.
Nonetheless, these patients do have a point. Understanding one’s past often puts
the depressive problem into a much clearer perspective.
As an illustration of this, a young woman, Alexandra, entered therapy. She
was experiencing considerable anxiety and depression, and had serious prob-
lems relating to self-confidence. A failure in her most recent job had plunged
her self-esteem to a low level. Alexandra’s therapist explored her past history.
She learned that Alexandra had previous experiences of failure and when new
opportunities presented themselves, she had an expectation of failure. Alexan-
dra and her therapist traced the idea that she couldn’t succeed back through
her school years to her early relationships with her parents and to her Aunt Josie,
with whom she used to spend her summers in the country. Her mother — who
had been widowed when her husband died in an automobile crash — was over-
protective, not letting Alexandra play in the street with other children. She was
careful to see that Alexandra “wouldn’t get hurt.” Her mother was always say-
75
ing “Don’t do this” and “Don’t do that.” For her part, Josie was usually criti-
cal of the things Alexandra did and left her with the feeling that she couldn’t
do anything right. When Alexandra tried to help Josie in the kitchen or with
her garden, she was left with the feeling that she was a klutz. During the course
of therapy, Alexandra began to understand that these early experiences had
thwarted the building of self-confidence. She realized that her current depres-
sion had a long history underlying it and was better able to understand her
problem.
Theories of child development often make the assumption, implicitly if
not explicitly, that successful experiences in an earlier phase of human devel-
opment will increase the chances of successful experiences in later phases of
development. Think of making a structure out of building blocks; if the lower
blocks are placed correctly, the growing structure will be well supported. If the
supporting blocks are badly placed, the structure may crumble. If the child fails
to adapt well in early phases of development, there is an increased likelihood
of trouble down the line. Obviously, there are many things that can happen in
later experiences to mitigate the effects of early problems; there is no inevitabil-
ity that developmental difficulties will lead to depression or other psychologi-
cal problems. Nonetheless, a bad start is just that and could leave the child with
handicaps in the race of life that lies ahead.
When we observe emotional difficulties in children, we consider a variety
of possible causes. Among the chief suspects are parent-child relationships, for
these relationships are of prime importance in providing the skills and under-
standing the child needs to negotiate the world about her or him. When there
are failures in these all-important relationships, one may anticipate a greater
chance for future problems.
The Concept of Attachment

In discussing parent-child relationships, let’s begin with the very early
days, the first year of life. One of the fundamental processes that occurs at this
time is attachment. Attachment has been defined by such theorists as John
Bowlby as any type of behavior in which an individual maintains closeness
(usually physical nearness) with another individual who is perceived as more
capable of dealing with the world.l One can see immediately that for the infant,
attachment is all important as the infant is helpless, totally dependent on oth-
ers for survival. Attachment in the infant is more than being fed, cleaned or
clothed; it includes the physical comfort of being held and cuddled and the
sense of security that comes with this contact.
The importance of cuddly contact was underscored by Harry Harlow’s
ingenious experiments with infant chimps. In these experiments, Harlow used
different types of mechanical “surrogate mothers.” One of the mothers was soft
5. The Roots of Depression 77
and cloth covered, but provided no nursing; the other was simple wire mesh
with a bottle. Given a choice, the infant chimps preferred the cloth mother
without feeding to the wire mesh mother with feeding.2
Observations by Rene Spitz, John Bowlby and others in England during
and following the Second World War also pointed to the importance of attach-
ment and the hazards of prolonged separation from the mother for the normal
emotional development of the child. Children who experienced prolonged sep-
aration from their mothers went through a sequence of distress reactions. The
infants began by protesting; they were angry. Later, they began to show despair.
Finally, they became detached and did not seek the comfort of adults. The nor-
mal attachment bonds, which offer a secure base for dealing with the world,
had been severely damaged.
The writings of Bowlby were very influential in stimulating interest in
attachment. Researchers have confirmed Bowlby’s observations that separation
from parents has a negative effect on attachment bonds. For example, a recent
study compared children from divorced families with those from intact fami-
lies and found that the children from divorced families had less secure attach-
ments.3
Following in Bowlby’s footsteps, researchers have delineated several phases
in the process of attachment. In the beginning there is a preattachment phase,
which lasts for the first eight to twelve weeks of life. By the age of two or three
months, the infant begins groping for attachments, usually developing a pref-
erence for being close to the mother. Around the age of six months, a primary
pattern of attachment is well established; the young child uses this relationship
as a base from which to explore and test his or her environs. It is something
like a safe port in uncharted seas. Eventually, as the child develops more under-
standing and capabilities, the child becomes less dependent.4
Mary Ainsworth, who has made singular contributions to the study of
attachment, provided us with a descriptive analysis of this early attachment
process.
“At birth, the infant is equipped with a repertoire of species-characteris-
tic behaviors that promote proximity to a caregiver. Most conspicuous among
these are signaling behaviors, such as crying, that operate to activate caregiv-
ing behavior, attracting the caregiver to come near. At first, these attachment
behaviors are simply emitted, rather than being directed toward any specific
person, but gradually the baby begins to discriminate one person from another
and to direct attachment behavior differentially.
At about the middle of the infant’s first year, a new phase of development
may be identified. A number of important changes occur more or less simul-
taneously. These include the emergence of locomotion and directed reaching
and grasping, which enable proximity-keeping behavior to become more active,
effective, and “goal-oriented.” Furthermore, the baby forms his or her first
inner representation of the principal caregiver, having attained some capacity
for believing that the caregiver exists even when not present to perception, and
with this achievement comes the onset of separation distress when the care-
giver leaves the infant. At this point, the baby is capable of attachment and is
very likely to have become attached not only to his or her mother figure, but
to one or a few other familiar persons as well.”5
The implications of attachment and separation for the child’s emotional
health have been systematically studied in the psychological laboratory using
a procedure developed by Ainsworth and her colleagues, called the strange sit-
uation. The procedure consists of a number of episodes that last about three
minutes each. In the beginning segments, the mother and her infant child go
into an unfamiliar room. There, they are joined by a woman who is a stranger
to them. The mother leaves the infant with the woman. After a few minutes
the mother returns and the stranger leaves. Then the mother departs also, leav-
ing the infant alone. While these sequences take place, the infant’s reactions
are monitored. Researchers note how the infant reacts both to the separation
from the mother and to the reunion with her. The researchers note whether the
infant seeks contact with the mother and the stranger, whether there is avoid-
ance and whether the infant engages in searching behavior while separated. The
observers evaluate the attachment relationship as to whether it is “secure” or
“insecure” in various ways. For the great majority of children, the relationship
is evaluated as secure.
Attachment theorists believe that the way a mother behaves toward her
child affects the security of the child’s attachment. In observing the mother’s
behavior, they ask such questions as, How responsive is she to the child’s cry-
ing? Does she spend time being close to the child? Does she hold the child when
the child expresses this desire? Is she affectionate? Does she appear positive
when she talks to the child? Using the child’s behavior in the strange situation
as a basis for measurement, researchers have found that as the theorists antic-
ipated, the attachment relationships of infants of responsive, sensitive moth-
ers tend to be more secure. While the mother’s caretaking behavior is not the
only factor that makes a difference in the security of the child, it is significant.
The early research carried out on childhood attachment was very intriguing
and raised a number of questions. Do children with insecure attachments as
infants have more difficulties in interpersonal relationships as they grow up?
Do they tend to show less self-confidence and self-reliance? Do attachments
styles persist over the years? And, do insecure attachment styles make individ-
uals more vulnerable to experience emotional difficulties and particularly
depression?
Researchers have carried out studies which shed some light on these ques-
tions. To offer a broad generalization about the results of these studies, inse-
cure attachments in early childhood are simply not helpful. It is something like
beginning the adventure of life with a called “strike one.” Some of the effects
of insecure attachment can be seen rather early. Eighteen to 24 month old tod-
dlers were observed in playgrounds. Children judged in the strange situation

to form insecure attachments received more negative reactions to even their
positive behaviors from other children. At this tender age, there was already
the suggestion of interpersonal difficulties, if not rejection.6
One may wonder what the long-range significance of mother-infant behav-
ior monitored in the strange situation is. Can one make predictions about what
the child will be like a number of years later when she or he is well along in
school? A longitudinal study carried out over many years on children born into
economically, disadvantaged families suggests that early attachment ratings can
be harbingers of future behavior.7 In this study, researchers observed over 200
mothers and their infant children in the strange situation developed by
Ainsworth, making assessments at both l2 and 18 months. Then, they followed
these children through childhood, adolescence, and into adulthood. During
childhood, they observed the behavior of the children in the nursery school
and later in summer camps. Children evaluated as secure in their early attach-
ments in the strange situation were judged to be far more self-reliant; they
seemed much less dependent on their teachers. The children with secure attach-
ment histories were consistently judged to show more self-confidence and more
self-esteem and were thought to be better able to bounce back after dealing with
stressors. They were more curious and exploring in their behavior. Both in the
preschool classroom and on the playground, they were judged to be more suc-
cessful in their interpersonal relationships; they were likely to be actively
involved in the peer group and less frequently isolated. When followed into
adolescence and beyond, those who had been evaluated in infancy as having
secure attachment experienced fewer emotional problems. The researchers
made the important point that while attachment was critically important in that
it was the process that initiated many of the events that followed, childhood
development is a very complex process and that attachment was only one of
the factors involved. While parent-child attachments do not relate inexorably
to any particular outcome, the suggestion from this study is that a secure early
attachment between mother and child promotes positive emotional develop-
ment in the child.
The mother-child attachment remains important with both continuities
and changes as the child grows and develops. This ongoing, powerful dynamic
continues to influence the child in many ways. For example, a recent study of
9 to 11 year old children which utilized children’s current views of their attach-
ments with their mothers found that children who felt insecurely attached
reported less positive moods and were judged by their teachers to have less abil-
ity to tolerate frustration; they seemed to have less emotional control.8
Attachment continues to be an important part of the human experience
as the child matures into an adolescent and then into an adult. The focus of
attachment, of course, begins to shift from the initial bonds with parents, first
to friends and later to romantic partners. The ability to bond without undue
strain to another person can be a critical part of our emotional development,

enabling us to fulfill our needs, adding gratification and security to our exis-
tence. Researchers have found that adults with insecure patterns of attachments
are more likely to experience depression.9 Fear of rejection can be an impor-
tant component of an insecure attachment style and this can be a particularly
difficult issue for many women. Researchers have linked this fear of rejection
to both the severity of depression in a clinically depressed sample of women
and to depressive tendencies in a normal sample of women.10
Troublesome Patterns in Parent-Child Relationships

An influential view in the child development literature was articulated in
the 1970s by Sidney Blatt who observed that two patterns of parent-child rela-
tions seem particularly related to the development of depressive tendencies. The
first pattern followed from the research on attachment and separation. In this
scenario, the child develops a fear of abandonment by the mother and of not
being loved by her. Such fears may lead to exaggerated dependency on others
for support and satisfaction in life, to feelings of helplessness and fears of being
on one’s own. Depression with these characteristics has been termed anaclitic
depression.11
Following through on this idea, we might deduce that if separation from
parents in childhood increases vulnerability to later depression, the death of a
parent would be particularly linked to subsequent depression in the child and
perhaps in the adult as well. Researchers examining biographical information
and depression inventory scores of adults have found an association between
the death of a parent during the patient’s childhood and current levels of depres-
sion.12 The chances of the loss of a parent being followed by depression in the
children seems to be higher if the loss occurred relatively early in the child’s
life rather than in later childhood or when the child is in adolescence. Inter-
estingly, depression may happen more frequently when children experience the
loss of a parent through the separation of divorce than through the parent’s
death.13
The second pattern of parent-child relationships that seems to foster
depression is one in which the relationship is characterized by excessive nega-
tive parental control. In this pattern, parents are often hostile and deprecatory
and inconsistent in offering affection. Under these conditions, the child learns
to feel unworthy and unlovable and may develop a strong sense of guilt and a
pattern of self-criticism. The child may feel that she or he has not lived up to
expectations and may develop a need for super-striving in order to prove her-
self or himself. In a recent study the recollections of parents as rejecting and
overprotective were related to feelings of self-hating self-criticism. If you tie
this in with my own research which found that anger directed against the self
was related to scores on the Beck Depression Inventory, you can see how this
pattern of parent-child relationships could become depressogenic.14 Depression
that emphasizes these problems has been called introjective depression.
In the late 1970’s, researchers combined the ideas of a lack of warmth and
caring from parents with over-control (for example, criticism, intrusiveness)
and termed the concept “affectionless control.” To measure this construct, a
team of Australian researchers led by G. Parker devised a self report instrument
called the Parental Bonding Instrument in which people assessed these char-
acteristics of their parents.15 The availability of the instrument has led to a spate
of interesting research. For example, affectionless control by parents in child
rearing has been linked to both dysfunctional attitudes and low self-esteem in
the children — both of which can promote subsequent depression.16
Researchers have also studied the relation of affectionless control in par-
enting with measures of depression in their children. In an early study Parker
administered the Parental Bonding Instrument to a group of people diagnosed
with neurotic depression and to a group of control subjects. He found that
when analyzed separately, the parental care component of the scale fared bet-
ter than the excessive control component in picking out the depressed people
from the control subjects. Using both components of the instrument together
to provide an index of affectionless control, Parker reported that 67 percent of
the depressed people characterized one or both of their parents’ behaviors this
way as against 37 percent of the controls.17 A recent review of studies conducted
on the relation of affectionless control and depression reported by Lauren Alloy
and her colleagues confirmed these early results. Their review concluded that
depressive symptoms were associated both with a lack of care and too much
control. Lack of warmth and caring appeared to be the more important of the
two components.18
When adult depressed patients are asked about their memories of the way
their parents reared them, their reports often include both elements of affec-
tionless control — lack of warmth and over-control. In reflecting on the stud-
ies of parenting and depression, Edward McCranie and Judith Bass wrote,
“Considered together, these studies suggest that depression proneness in gen-
eral is influenced by parental child-rearing practices that combine elements of
rejection, inconsistent expressions of affection, and strict control. Such parental
behaviors could be expected to hinder the development of normal self-esteem
in the child, resulting in an increased vulnerability to generalized feelings of
helplessness and failure.”19
To cite an illustrative study, women who had experienced depression and
women who had not were asked to agree or disagree with a number of state-
ments describing their mothers. The women who had experienced depressive
problems more often endorsed statements that portrayed their mothers as crit-
ical and demanding, such as, “Mother wanted me to be different,” “Mother felt
many things about my performance should be corrected,” “I couldn’t live up
to Mother’s expectations,” “Mother honored my brothers’ and sisters’ requests

more than mine.”20
We must introduce a note of caution here because these studies use ret-
rospective accounts, memories of what things were like in childhood. Like per-
ception, memory is selective; we remember some things and not others. And
there are many studies that show that depressed emotion can influence what
one recalls. People who are depressed often show a bias toward recalling what
is unpleasant. This bias poses an obvious problem in interpreting retrospec-
tive accounts.
There is yet another problem with retrospective studies, particularly con-
cerning early childhood. Many people have difficulty remembering very much
about this period. In conducting research on this problem, Roland Tanck and
I found that recall is often very poor. For the first three years of life, about half
of our college student subjects couldn’t remember anything. About one in ten
subjects couldn’t recall anything through age six.21 To appreciate the difficul-
ties that might be involved in retrospective accounts, think back to your very
early memories. How much do you recall?
With this limitation in mind, researchers set about the more difficult,
time-consuming task of carrying out prospective studies. In these studies, meas-
ures of parenting style were obtained, sometimes by observing parents and
their children together in an interaction task, sometimes by conducting inter-
views with mothers and their children, and sometimes using the Parental Bond-
ing Instrument. Then, the children were followed for a number of years to see
if depressive symptoms developed. In their review, Alloy and her colleagues
cited four prospective studies. Each provided some evidence that parenting
styles characterized by a lack of warmth and excessive control were followed
by an increase in the likelihood of depressive symptoms.22
So, it looks very much as if both lack of affection and over control can be
risk factors for depression and the combination of the two may be particularly
injurious. However, there is an important caveat here. While sub-optimal par-
enting can promote depression, it can also promote the development of other
types of emotional problems. In one of the prospective studies on parenting,
it was reported that the odds that affectionless control by the parents would be
followed by substance-abuse in the children were even higher than they were
for depression.23 Sub-optimal parenting is not specific to depression; it is a risk
factor for a number of unhappy developments in the children, one of which is
depression.
Going beyond these two patterns, we know that parents who are angry, or
worse, cruel and abusive, can leave emotional scars on children. The effects of
physical abuse of children are found in poor performance in school, conduct
problems, anxiety and social withdrawal, as well as depressed reactions.
In discussing their study of children who were inpatients in a psychiatric
facility, Alan Kazdin and his colleagues reported that children who had been
physically abused, “Evince higher levels of depression and hopelessness and

lower self-esteem than do nonabused patients ... and viewed themselves and
their futures more negatively than did children without physical abuse.”24 A
retrospective study using a nationally representative sample found that people
reporting sexual abuse as children also showed an increased risk of depression
as well as other emotional problems.25
In reviewing the studies carried out over the years linking abuse of chil-
dren with subsequent depression, Alloy and her colleagues concluded that emo-
tional abuse by the parents— even more than physical or sexual abuse was a
precursor of depression in the children. Humiliating and belittling statements
that tear down the child’s self esteem can have destructive effects on the child,
leading to depression and other emotional problems.26
Other sources of potential problems are homes in which there are high
levels of parental discord. Such homes are a fertile environment for children
to germinate the seeds of emotional difficulties. It can be a severe strain on chil-
dren to witness a declared or undeclared war between their parents. Children
who go through the divorce of their parents not only experience this tension,
but they experience the subsequent loss of separation. It is no wonder that
anger, depressed reactions and withdrawal are among the common reactions
observed in children to the divorce of their parents.27 There are parallels here
with the reactions described by Bowlby when attachments were severed in very
young children.
The Importance of Confidence-Building Activities

One of the important aspects of early attachment relationships is that they
give the child a secure base with which to explore his or her world and begin
to develop competence in mastering the environment. This builds feelings of
confidence. Competence and confidence are very important in becoming a fully
effective individual. The home atmosphere that promotes these tendencies will
help the child develop a sense of self-esteem. The home atmosphere that does
not may promote learned helplessness, which increases the risk of a depressive
reaction.
To grow in competence and gain the confidence that comes with it, chil-
dren need the opportunity to explore, to try and to succeed. Parents like Alexan-
dra’s mother and Aunt Josie, whose repetitive messages to the child are “no,”
“don’t,” and “you can’t,” are not providing her this opportunity. The parent
who is impatient with the child, who takes over and says, “Here, I’ll do it,” when
the task is within the child’s capabilities, prevents the child from developing a
sense of mastery in dealing with her or his environment.
Confidence-building activities are vital in the formative years. In addition
to the early home environment, school is an important setting for this kind of
learning. Some children prosper in school, but not all do. Think back to your
classrooms in elementary and junior high school. Do you remember some of
the very bright kids in the class? It seems like their hands were always flying
high to answer the teacher’s questions and the teacher called on them time and
again. The children were praised; their marks were glowing. Whatever else was
happening in their lives, these children knew they were good students. But what
about the children who were not as quick? Who praised them? Chances are
many such students faded into the woodwork and were ignored. And what
about the children who really had to struggle in school? Some of these children
took a psychological beating.
The message of years of being ignored or worse, put down, is cumulative
and clear: “You’re not competent — you don’t measure up.” If the child has
compensating talents like athletic ability or artistic or mechanical skills, these
can go a long way as a self-confidence booster. The important thing is that chil-
dren need to experience success as they grow up.
Self-confidence comes not only from academic success but from interper-
sonal success as well. Children who do not develop social skills tend to expe-
rience rejection and loneliness. Poorly developed social skills in children can
be a harbinger of possible future psychological and social difficulties.
Researchers have found that children who experience a “double whammy,” hav-
ing both poorer academic and social skills, are more likely to be depressed.28
We are sketching a picture of what is often a subclinical depression in
children. Picture a child who is neglected or rejected by his peers and not doing
well academically. Such a child is unlikely to feel very good about himself.
Teachers can often spot such a lonely, unhappy child. The child’s classmates
may be even better at it. The consensual opinion of children about their class-
mates is often revealing.
It is possible to obtain such opinions in research. To cite an example, using
a “peer nomination” technique, Monroe Lefkowitz and Edward Tesiny gath-
ered groups of children into a schoolroom and read aloud a series of descrip-
tive statements that included such items as, “Who often plays alone?” “Who
thinks they are bad?” “Who says they can’t do things?” “Who doesn’t have
much fun?” “Who thinks others don’t like them?” “Who often looks lonely?”29
The children’s tasks were to think about their classmates and check all the
names on their class roster that best fit the description.
What happened in Lefkowitz’s and Tesiny’s study was that most of the
children in the class received no votes at all. Most of the children were not
viewed by their peers as depressed. However, there were some children who
were clearly picked out by their peers as depressed.
When the researchers compared these “nominated” children with their
classmates, they uncovered some interesting findings. First, the nominated chil-
dren were rated by themselves as depressed. They recognized that they had a
problem. These children also had lower self-esteem on psychological testing.
Like adults who are depressed, they more often saw the sources of gratification
in life as under external control. They were more often absent from school and
performed less well on reading and math achievement tests.
Depressive symptoms in children are not only correlated with lowered
estimates of self-esteem and diminished perceptions of one’s competence,
they are correlated with the child’s perceptions of how other children view
them and like them. Depressive feelings in children can deflate their views of
how well other children accept them and as research has shown, this can be a
good deal worse than the reality. Researchers have found that children with
depressed tendencies are often both more competent and accepted than they
believe.30
Notwithstanding this, children with depressive tendencies often have
difficulties relating to other children. Part of the problem may be a self-fulfilling
prophecy, in which low self-esteem and questions about one’s acceptability
usher in a demeanor and behaviors that may be unattractive to others and lead
to rejection.
These tendencies may even influence the way the depressed children inter-
act with their best friends. In an experiment demonstrating this, children scor-
ing either high or low on the Children’s Depression Inventory were paired with
their best friends to play video games. The best friends of the children with
depressive tendencies showed more negative emotions during the games than
the best friends of the children who did not have depressive tendencies. Nei-
ther the children with depressive tendencies nor their best friends enjoyed the
games as much the children who had low scores on the Children’s Depressive
Inventory and their best friends.31
The psychology of these children, their lowered self-esteem and external
view of control of gratification, seems very similar to the patterns we saw ear-
lier in depressed adults. Do depressed children also show some of the other
thinking patterns typical of depressed adults, such as overgeneralization and a
tendency to blame oneself ?
Harold Leitenberg and his colleagues carried out an interesting study,
which addressed this question. They presented hypothetical situations to chil-
dren concerning three areas of their lives: social, academic and athletic. Fol-
lowing the hypothetical situations, they offered a negative thought pattern type
of reaction. For example: “You call one of the kids in your class to talk about
your math homework. He/she says, ‘I can’t talk to you now, my father needs
to use the phone.’ You think, ‘He/she didn’t want to talk to me.’” And, “Your
cousin calls you to ask if you would like to go on a long bike ride. You think,
‘I probably won’t be able to keep up and people will make fun of me.’” The
children were asked to respond to each situation using a scale ranging from “not
at all like I would think” to “almost exactly like I would think.”32 The results
were revealing. Similar to findings of the peer nomination study, the researchers
found that most of the children did not believe that they would usually react
to these situations with such negative interpretations. Negative thought pat-

terns were not typical for young children.
The researchers reported some interesting observations. First, when neg-
ative thought patterns arose, they were most likely to arise in the social area.
Young children were more likely to overgeneralize or catastrophize from inci-
dents in their peer relationships than from events in the classroom or athletic
field. Second, very young children were more prone to catastrophize and per-
sonalize mishappenings than older children. As the researchers suggest, very
young children lack the experience to understand that mistakes and failures do
not necessarily have dire consequences. Young children may blow the situation
out of proportion. Third, and most important for our inquiry, the children
who showed tendencies to overgeneralize, catastrophize and hold themselves
responsible for bad outcomes were more likely to report depressed feelings.
This is the same pattern we see in adults.
These findings for children then are in some respects a mirror for what we
observe in adults. Most children do not have negative thinking patterns; those
who do are more likely to be depressed. Most adults do not think that way
either. Those who do are more likely to feel depressed. These parallel findings
recall the idea of building blocks— the impact of one stage of development on
the next. The child is indeed the father of the man. The elements of adult depres-
sion are forming in the child. One sees loneliness, low self-esteem, perception
of external control, a tendency to overgeneralize and catastrophize failures and
blame oneself. All of these adult tendencies may be observed in vulnerable chil-
dren, presumably resulting from the interplay of genetics and psychologically
punishing environments. When environmental stressors become too difficult
to handle, a depressive reaction may develop — even in children.
In carrying out research on the way children evaluate good and bad events,
Martin Seligman and his colleagues arrived at a similar conclusion. They wrote,
“children with depressive symptoms share some characteristics of adults with
depressive symptoms. Both have an attributional style in which bad events are
seen as caused by internal, stable, and global factors. Both may be put at risk
for future depression by processing information about bad events through this
insidious attributional style.”33
The potential for depression that is developed in childhood is carried into
adolescence. Biological changes that take place at puberty create profound
changes in the child’s life. Rapid physical and sexual maturation accompanied
by increased independence from parents generate considerable uncertainty and
stress. Psychological vulnerabilities that may have been created in childhood
can lead to poorer skills for coping with these stresses, making adjustment more
difficult. Many adolescents experience periods of mild to moderate depression.
Difficulties in relationships within one’s own family are often the biggest
problem for adolescents and sometimes are related to depressive episodes. Ten-
sions in the relationship of the adolescent and parents can create problems for
both parties. Problems in social relationships are another prime source of emo-
tional discord for teenagers as acceptance by one’s peer group assumes a very
high place in the world of adolescence. The depressed symptoms of the ado-
lescent are in most respects similar to those of adults. In addition to the litany
of depressed symptoms we have outlined earlier, the depressed teenager is likely
to have trouble with school work and get poorer grades.
Researchers studying teenagers with depressive symptoms have reported
that there are some differences in the way boys and girls show their depressed
feelings. Adolescent boys who are depressed are more likely than girls to appear
antagonistic, unrestrained and discontented. They feel worried and alienated.
They often get into trouble in school and don’t do well in their school work.
Depressed adolescent girls also feel alienated and angry, but these feelings usu-
ally are less observable in the girls’ behavior. Depressed adolescent girls may
appear passive. They may become introspective and frequently have problems
with self-esteem.
Young adolescent boys are often concerned about their lack of ability in
sports and not measuring up, while adolescent girls tend to be particularly sen-
sitive to the possibility of rejection.34 Girls who have depressive tendencies
sometimes engage in excessive reassurance seeking to cope with these con-
cerns.35 But this behavior can be counter productive, sometimes bringing on
what these girls fear — rejection. Frequent family moves with resulting dislo-
cations and loss of friends can be challenging for both boys and girls.36
While problems within the family circle and difficulties relating to peers
are often sources of stress in adolescence, it is important to recognize that both
family and peers may also act as a buffer against stress for the teenager. The
teenager who feels he or she is part of a functioning family where people feel
connected and care about each other has a real advantage in coping with the
problems of adolescence. Having good friends is also a very important source
of support for the teenager.
There are a number of growth experiences—“developmental tasks” we
think of as important in adolescence — skills that we normally expect teenagers
to develop during this important phase of life. We think of such things as gain-
ing a substantial measure of independence from one’s parents, finishing high
school and beginning to date. Successful experiences in adolescence promote
successful experiences in adulthood to follow. Failure to develop these skills
may not only be associated with a troublesome adolescence but could lay the
groundwork for future difficulties.
6. Stress and Depression
It is very common for depressed moods to develop during periods of stress.

Though not always the case, when depressed people are questioned about what
was going on in their lives when they began to feel depressed, they often relate
stories of being under stress. Both clinical observation and research evidence
point to the conclusion that when people have a vulnerability toward depres-
sion, stressful events in life may trigger a depressed reaction
In describing their model of the depressive process, H. A. Meyersburg and
his colleagues presented some case material that illustrates the way mounting
stress can precipitate a depressive reaction. Consider Judith, a 40-year-old
woman who once had a depressive episode during college but had been rela-
tively free of problems since that time. One day her husband informed her that
there was another woman in his life. He then filed for divorce. When the divorce
was granted, Judith moved away, taking her three children. She felt over-
whelmed by the changes in her life, experienced intense anxiety, and was unable
to care for herself and her children. She was subsequently hospitalized for
depression. In the hospital, she spoke about a vague, diffuse anxiety, and feel-
ing helpless and needy.
Or take the case of Sally, a woman in her early twenties. Sally came from
a family in which both parents had depressive problems, suggesting that Sally
was at increased risk. The precipitating stressor in Sally’s case was a romantic
relationship. Sally became involved with a young man whom she found attrac-
tive, but at the same time she was frightened of sexual experience. As the rela-
tionship developed, her anxiety about physical intimacy mounted. She rebuffed
him and he broke off the relationship. Following the breakup, she became
severely depressed.1
Researchers have accumulated a large amount of data that suggests that
major changes in life act as stressors and may trigger depression in those who
are vulnerable. By major life changes, we mean such events as developing a
serious illness, changing jobs, moving to a different part of the country, get-
ting divorced, as was the case for Judith, having a child or losing a close friend.
Researchers have compiled lists of such events, put them in the form of a
questionnaire and found that people who have been going through major life
88
6. Stress and Depression 89
changes are more vulnerable to emotional problems including depression. A

review of studies linking major life changes to the onset of depression indi-
cated that the presence of such stressors was two to three times more common
among depressed people then among controls. Studies carried out in commu-
nity settings indicated that depression was preceded by major life events in
about 80 percent of the cases.2
One of the key elements in many of these changes is loss. When a young
man or woman goes away to college, for example, it is a challenging experi-
ence with great potential for personal growth, but it also means separation from
long-standing sources of security —from family, friends and the familiar envi-
rons of one’s formative years. Such separation can be very distressing.
Ellen’s experience is a good illustration of this. Ellen was a student in one
of our research projects who found the transition to a large urban university
very difficult and reported she was experiencing very high stress. She had pre-
viously boarded at a small all girls’ school where she had lots of friends and
close-knit relationships. The small classes had allowed an opportunity for stu-
dents to discuss issues with their instructors and Ellen had found the atmos-
phere academically stimulating. Now, her classes were held in large lecture halls,
sometimes with hundreds of students. She disliked the impersonal nature of
the university and missed her old friends badly.
Breakups in romantic relationships are one of the most painful of human
experiences. It is the stuff that novels are made of, the basis of folk ballads and
popular songs. Breaking up is also a source of countless depressive reactions.
Research has demonstrated that having a network of strong, supportive rela-
tionships seems to act as a barrier against depression. The loss of such ties is
difficult to cope with.3
The observation that the experience of loss is often implicated in depres-
sion is, of course, not a new idea. As we indicated, Freud recognized the impor-
tance of loss in triggering depression many years ago in his essay Mourning and
Melancholia . The theme has been amplified by Bowlby and others.4 However,
it should be pointed out that there is no inevitability that loss, or other types
of stressors, will bring on a depressive reaction. People differ greatly in their
resiliency when exposed to stressors. Some people who experience the loss of
a spouse or paralyzing injuries show little evidence of depressed reactions after
the event or experience noticeable depressive problems later on.5
It is not only the big changes in life that increase one’s risk of experienc-
ing a depressive reaction; it is also the seemingly unremitting pounding away
of everyday problems. Roland Tanck and I asked college students to look over
a checklist of problems that students might typically encounter (e.g., not doing
well at school, having conflicts with parents, being short of money) and to
check the problems that they were currently experiencing. We found that the
more problems the students checked, the higher they scored on the measure of
depression.6 One problem might not get you down, but three, or four or five?
These findings bring to mind the old adage about the straw that broke the
camel’s back. In a somewhat similar vein, A.D. Kanner and his colleagues devel-
oped a questionnaire that measures daily hassles, events like experiencing traffic
noise, preparing meals and having to wait. The more hassles people reported,
the greater the chance they felt depressed.7
These studies point to the role of the everyday stressors in our lives in trig-
gering depression. And where better to look for such stressors than in our places
of work, at school, in our marriages and families, and our relationships. These,
our primary sources of joy and fulfillment in life, can also be causes of stress,
playing a part in the development of depressed reactions.
The Link Between Stress and Depression: A Closer Look

As we explore the relation between stress and depression, we find that it
becomes more complex as we probe into it more deeply. First, as we indicated,
not all people react to major stressors by becoming depressed. There are bio-
logical, psychological, and social factors which we will discuss later that mod-
erate the effects of stressors, making depressive reactions more or less likely.
Second, not all stressors are alike. Some types of stress-provoking situations,
and some types of circumstances, may be more likely to bring on depression
than others. One aspect of a stress-provoking situation, that seems to have an
important bearing on whether a person will experience a depressive reaction is
the extent to which the person may have been involved in bringing on or exac-
erbating the stressful situation. Imagine, for example, a deteriorating roman-
tic relationship — one on the verge of a break up. This can be very stressful for
one or both parties involved. Imagine further that one of the persons experi-
encing this loss also feels that he or she has contributed to the problem, per-
haps with hasty, harsh words that were painful to the other party. The person
may feel guilt and self blame and these are depressive inducing emotions.
Researchers have tested the idea that self-generated stress tends to be more
often followed by depression than stress brought on by external agencies. In a
review of research on stress and depression, Constance Hammen noted that
researchers have found evidence supporting this idea in studies carried out
with both adults and children.8
A second factor is the degree to which the stress provoking situation
appears uncontrollable. It is my belief that when stress reaches uncomfortable
levels and no solution is in sight to change things, depression is more likely to
occur. When depression persists and becomes a lingering event, there may be
some change in focus— a shift from thinking about the external stressors to a
preoccupation with oneself. The focus may change from, “The situation is
awful” to “The situation is awful and I can’t function.” A kind of psychological
paralysis may set in. One of the effects of this immobilization is that the per-
son may begin to avoid the stress situation. He may take sick leave from work,
drop that difficult course in school or avoid social contacts. Depression in this
sense functions like a psychological defense, protecting the ego from further
stress. The price exacted is pain and suffering of another kind.
Interestingly, researchers have reported that stressors which are uncontrol-
lable tend to have a greater effect on raising cortisol levels and elevated corti-
sol levels have been related to depression.9
Here is an interesting study which seems consistent with the hypothesis
that the uncontrollability of stressors is a factor in promoting depression. A
group of researchers led by Carolyn Cutrona studied over 700 African-Amer-
ican women in selected areas of two states, Iowa and Georgia.10 Both poor and
more affluent neighborhoods were included in the study. In interviews, data
were collected about negative life events experienced during the past 12 months
(e.g., “Did you have a family member with a serious illness or injury?”) and
the symptoms of major depression. As one would expect from the findings of
previous research, the number of negative events was correlated with the onset
of depression. However, it made a big difference whether or not the woman was
living in a poor, economically depressed neighborhood. Experiencing negative
events in a poor neighborhood was much more likely to lead to depression.
While there are probably a number of reasons for this finding, the researchers
interpretation of their data parallels my own view of uncontrollability. They
wrote, “Women who experienced multiple negative life events were more likely
to report the onset of depression if they lived in neighborhoods high rather
than low in economic disadvantage/disorder.” And later, “Neighborhoods high
on economic disadvantage offer few economic opportunities and few role mod-
els for economic success, which undermines optimism and belief in personal
mastery among residents. Neighborhoods high on social disorder inhibit the
formation of supportive relationships with neighbors, prevent a sense of pre-
dictability, and offer threats to physical safety. When negative life events occur
in this context, their impact is intensified because the worldview of the victim
probably offers little hope for assistance from others and little experience with
personal efficacy.”11
The implication of the uncontrollability hypothesis is that if a person feels
he or she is able to cope with an ongoing stress situation and reduce its impact,
the situation is less likely to cause serious emotional problems.
Individual Differences in Response to Stressors

As we mentioned, not everybody who experiences a major stressful event
becomes depressed. This is a commonplace, everyday observation. Some peo-
ple experience the worst kind of traumas; combat, natural disasters, or severe
interpersonal loss. They may experience a profoundly upsetting experience,
but they weather the storms and do not develop a major depression. Why?
What accounts for their resiliency in the face of turmoil? And, conversely what
are the factors that make one more vulnerable to react to stressful experiences
of far less intensity with depression?
The findings from research suggest that there is no single answer to this
question. The answers probably lie in biological differences— some people have
a genetic makeup that makes them more vulnerable to depression, in child-
hood experience, in psychological differences in the way people evaluate stress-
arousing situations, in the way they cope with these situations, and in the level
of social support available.
In regard to genetic factors, recall the study of Caspi and his colleagues
that showed that people carrying the short variant of the promoter region of
the serotonin transporter gene were more likely to react to stressful life events
by becoming depressed.12 This study suggests that we begin the race of life
unevenly in our capacity to withstand the depressogenic effects of stressors.
As we have seen in the preceding chapter, childhood experiences and par-
ent-child relationships are important influences in molding vulnerability or
resiliency to depression. In her review article on stress and depression, Con-
stance Hammen noted that exposure to early stressors can have a significant
effect on the way adults react to stressors.13 In one of her own studies, she found
that exposure to earlier adversities in life appeared to predispose her sample of
adult women to react to stressors with depression. Their threshold for becom-
ing depressed when stressed appeared to be lowered.14
Troubled childhoods can lead to insecure attachment patterns as adults.
Such insecurities in adulthood can lead to both stresses in relationships and
lack of support from others when difficulties arise.15 Both developments favor
depression.
When we consider current, ongoing psychological factors that are likely
to make a difference in whether exposure to stressors will be followed by a
depressive reaction, we need to take account of the way people interpret and
evaluate the stress situations that they encounter. One person might see the sit-
uation as very serious, with potential dire consequences; he or she may feel pes-
simistic about the outcome and hold himself or herself to blame for the
situation. Another person might take a more benign view of the situation, try-
ing to look for the brighter aspects of the picture, holding out hope for better
things in the future and not blaming himself or herself for bringing on the
problem. Researchers interested in depressogenic cognitive styles have carried
out a number of studies in which measures of dysfunctional attitudes taken in
conjunction with reports of stressors experienced were related to the develop-
ment of depressive episodes. While the evidence from these studies is not alto-
gether clear, it looks as if the activation of depressive cognitive sets helps
promote depressive reactions to stressors.16
The individual’s self-esteem or lack thereof can also have a moderating
effect on reaction to stressors. A strong sense of one’s own strengths and capa-
bilities can help buffer the impact of stressors. In contrast, research suggests
that low self-esteem makes one more vulnerable to the effects of stressors and
can be a factor in promoting depression.17
As a way of illustrating the effects of psychological factors in moderating
the effects of stress on depression, consider the reactions of two employees
working for a consulting firm. There are half-finished reports lying on both of
their desks. One of the employees, Dave, thinks it’s extremely important to get
the job done. He thinks, “If I don’t work late tonight and finish it — no matter
how long it takes— the boss and my co-workers will think I’m not up to the
job.” In contrast, Bill’s attitude is, “The work will still be there tomorrow. The
world won’t come to an end if it takes an extra day. If I wait until tomorrow,
I’m not going to lose my job and the company isn’t going to go broke.”
The company may be much happier with Dave’s attitude than Bill’s, but if
that is Dave’s characteristic approach to life, he may be setting himself up for
trouble. He may be over evaluating or inflating the importance of what he is
doing — not distinguishing between what is important and what is not — and
not recognizing where a maximum effort is really needed. He may also be invest-
ing too much of his self-esteem in the activity. If things don’t work out, he’ll
take the setback harder.
Research has suggested that people who become depressed tend to inflate
the importance of the problems they face, feeling there is more at stake and
more to lose. Their self-esteem is more often on the line.18 When higher stakes
are placed on an outcome, insecurity and anxiety are likely to develop during
the process of resolving the problem. The person is more likely to experience
the symptoms of stress— edginess, irritability and physical complaints.
If the situation is confrontational, involving another person, there is a
higher chance of the stressed individual reacting emotionally. As the confronta-
tion mounts, anger mounts. He or she may explode in an emotional outburst
or the anger may be vented later at someone else who just happens to be around.
Or worse yet, for the prospect of becoming depressed, the anger may be directed
inwardly, against oneself. If the problem is not resolved in a satisfactory way,
which happens occasionally to everyone, more hurt and disappointment may
be experienced. High stakes can lead to a greater sense of loss and lowered self-
esteem. Depressed people often report that their feelings are easily hurt, that
they take things hard. Part of the reason for this reaction is that they have men-
tally turned hills into mountains. When the hill collapses, it seems like the
mountain has collapsed. Setbacks and failures have been catastrophized.
We have suggested in our discussion of the controllability of stressors that
the way an individual copes with stress can make a difference in the likelihood
that he or she will become depressed. When responding to stress, people who
become depressed are less likely to cope with the situation by taking the kinds
of concerted action needed to solve the problems. Instead of engaging in prob-
lem solving behavior or trying some coping strategies that might prove help-
ful in lessening stress, they often become bogged down in inaction, self analy-
sis and rumination. Wishful thinking and avoidance sometimes provide a
defense for the faltering ego, but obviously have only limited value for the long
term.
A study carried out by Roland Tanck and myself points to the depresso-
genic effects of ineffective coping.19 Using questionnaires we asked college stu-
dents, “Do you find that your own life as a college student is stressful?” We
followed this question with three alternatives, “Yes— it is very stressful,” “Yes—
it is somewhat stressful,” and “No.” Only three of our 84 subjects replied, “No.”
We assessed the students on two other measures, an inventory of coping behav-
iors that Tanck and I had developed using factor analysis and the Beck Depres-
sion Inventory. What we found was that the students who indicated that their
lives as students were very stressful were more likely to score higher on the
depression measure if they had a pattern of coping with stress which we called
dysfunctional behavior. This pattern included such items as daydreaming or
fantasiszing, spending endless hours thinking about things, becoming irrita-
ble and easily annoyed, eating constantly, and becoming ineffective. The stu-
dents who indicated that their lives as students were also very stressful, but did
not usually engage in this pattern of dealing with stress did not have high
depression scores on the Beck scale. There are many ways to cope with stress,
but lapsing into a passive, ruminating, irritable state seems like a way station
on the road to depression.
Finally, the availability of social support can be very important when an
individual is under stress. Having others to talk to, to share what he or she is
going through can make a big difference in weathering the difficulties that we
all will encounter at one time or another.
Can Depression Promote Stress?

The evidence is quite clear that exposure to significant stressors frequently
precedes the onset of an episode of depression. Some researchers have turned
the question around, asking whether depression might generate stress. David
Cole and his colleagues suggested that, “Depression compromises a person’s
ability to function effectively, thereby increasing the occurrence of negative or
stressful life events.”20 Consider, for a moment, a person disabled from depres-
sion who nonetheless has many responsibilities. He has a wife and several chil-
dren to provide for, a job with the work piling up every day, a mortgage to pay,
and bills coming in all the time. Being depressed offers a degree of escape from
this pressure; he has the protection of the “sick role,” a status we all find our-
selves in at one time or another when we are ill or injured; a status which
informs society that we have a legitimate reason not to carry out our usual
responsibilities. One can almost hear the reassuring words from one’s family
and friends, “Don’t worry about a thing. Just get well.”21 However, the protec-
tion offered by the sick role is probably not as good for depression as it is for
a physical illness such as a heart attack, for some people still look at mental and
emotional disorders as “suspect,” with the hard-to-dissuade belief that the per-
son could straighten himself out “if he really wanted to” or if he only had enough
“will power.” I remember a very unsympathetic wife who told me to straighten
out her depressed husband so he could get back to work and take care of her.
So, pressure can mount from both within the patient and without.
The possibility that depression might generate stress has not been nearly
as well studied as the more intuitive idea that stress can act as an agent to bring
on depression. A recent study carried out on children and adolescents found
that self reports of depressive symptoms were followed by increased stress
(report of negative life events).22 Even in this non-clinical sample of school-
age children, feelings of being depressed may have generated more problems.
Stress and the Recurrence of Depression

Researchers have observed that the tendency for stress-provoking situa-
tions to precede an episode of depression was more likely to occur for the first
episode of depression than for subsequent episodes. As depression reoccurred,
the role of stress as a precipitant becomes less clear. In time, episodes of depres-
sion appeared to occur without the stimulus of stress. It has been theorized
that the onset and then recurrences of depression creates changes in our biol-
ogy — possibly at the level of gene expression — which sets a person up for fur-
ther episodes of depression without obvious causes. The individual has
apparently become “sensitized” and may in time experience what appears to be
a spontaneous episode of depression.23
In an article in the Psychological Review, Scott Monroe and Kate Harkins
described two lines of explanation that would account for this observation.24
The first line of explanation is that the individual who is prone to depression
has become sensitized so that it takes lower and lower levels of stress to trig-
ger a depressive episode. When it once may have taken a major stressor to
induce depression, in time, minor stressors can bring on an episode. The other
line of explanation is that depression has become independent of stress. At this
point, stressors become almost irrelevant. Depression occurs with or without
the stressor trigger. In this view, stressors have lost a causal relation to depres-
sion.
While sophisticated longitudinal studies are probably needed to more fully
understand what is actually happening here, the data obtained so far carry an
important implication for the treatment of depression. If repeated episodes of
depression produce sensitization, the treatment for the first episode of depres-
sion becomes very important. Thorough treatment of the first episode of depres-
sion leading to a complete remission of symptoms may help protect against the
possibility of a spiraling sensitization and repeated recurrences. In subsequent
chapters, we will discuss the approaches to therapy for depression that might
be most likely to put a damper on the sensitization process.
Coping with Stress as a Means

of Depression-Prevention
Because stress plays a role in the development of depressive episodes, par-
ticularly the early episodes, it makes good sense for people who are prone to
depression to find effective ways to cope with stress. Coping skills can be taught
in therapy. They can also be learned through self study. My recent book, Cop-
ing with Stress: Commonsense Strategies is an example of a source for self study.
Stress management programs at one’s job or stress support groups in the com-
munity offer other possibilities for controlling stress.
Prompt intervention for people experiencing severe stress can be helpful
in controlling depressive reactions. In a recent study, women who were assaulted
and then diagnosed as suffering from posttraumatic stress disorder were given
supportive counseling or brief cognitive-behavioral therapy. Both treatments
helped reduce depressive symptoms.25
So, if there is one clear-cut message suggested by research on stress and
depression, it is to try not to let stress build up. Take what steps you can to
mitigate the stress you are experiencing. The old adage about a stitch in time
saves nine may well apply here.
7. Depression, Alcohol
and Drugs
Alcohol is a substance that has been used and abused since the develop-
ment of urban civilization in ancient Mesopotamia. Archaeologists have
unearthed metallic drinking straws dating back thousands of years, which may
have been used for imbibing beer.
Today, the use of alcohol permeates our society, as well as many others.
As Leif Crowe and William George put it, “Its consumption provides mystical
trance, holy communion, celebration and consolation, social acceptance and
condemnation, prowess and impotence, languor and lust. Indeed, there is
scarcely a human activity that has not been said to be both impoverished and
improved by the addition of alcohol.”1
As we all know, alcohol abuse is a widespread problem. So, too, is drug
abuse, which is now high on the agenda of social problems to address. Millions
of Americans are alcoholics and many more millions have serious drinking
problems. Moreover, millions of Americans use illegal drugs, some of which,
like heroin, are addictive.
If you talk with patients being treated for alcohol or drug addiction in
hospital wards or in clinics, you will often find that these patients are or have
been depressed. This is an important observation that has implications for the
treatment and rehabilitation of substance abusers. In this chapter we will
explore how depressed mood is linked to substance abuse.
Depression and Alcohol Abuse

Let us begin with alcoholism.There are a variety of terms that have been
used to describe alcoholism. Some examples are problem drinking, alcohol
addiction, alcohol abuse, and alcohol dependence. While there are shades of
differences in the meaning of these terms, they do share a core of meaning. They
all convey the idea that the individual’s need for alcohol has reached a funda-
mentally different level than that of the light or moderate drinker. The light or
97
moderate drinker can have a drink or two, enjoy the relaxing of effects of the
drink, and then put the bottle away for another day. The alcoholic typically
cannot.
I like the term alcohol dependence because it has been used in the Diag-
nostic and Statistical Manual (DSM IV) to describe one of the principal alco-
hol abuse disorders and has been anchored in empirical data as well. Alcohol
dependence denotes a loss of control over drinking. Indicators of alcohol
dependence include withdrawal symptoms such as anxiety, shaking, and sweat-
ing; an inability to stop or even cut down drinking when one tries; giving up
or curtailing social and recreational activities in favor of drinking; and con-
tinuing to drink in spite of problems brought on by the drinking.2
How many people are believed to have alcohol abuse disorders in the
United States? A national survey carried out on over 40,000 people suggested
that about 8 percent of the population had an alcohol use disorder during the
12 months preceding the survey. These alcohol disorders include both alcohol
dependence and hazardous acts committed under the influence of alcohol such
as reckless driving.3
Many years ago a noted authority on alcoholism wrote, “It is therefore a
matter of clinical observation that preceding the use of alcohol there is always
a depression.”4 While this assertion clearly overstates the case, there is little
doubt that in many people, depressed mood and the use of alcohol are linked.
The linkage, however, is complicated.
On the one hand people may drink or use drugs as a way of relieving anx-
ious and depressed moods. Alcohol and drugs are forms of self-medication: they
make one feel better, at least temporarily. On the other hand, protracted sub-
stance use can lead to changes in lifestyle that can bring on depression. In this
case the depression is considered secondary to the alcoholism.
To make the distinction between primary and secondary depression
clearer, compare Eileen and Dan, two patients being treated for alcohol abuse.
Eileen has had a plethora of emotional problems beginning in childhood. She
experienced a rocky adolescence in which she had difficulties in getting along
with her father, with her sexuality and in overcoming shyness. Both in her early
childhood and teenage years, there were times in which she was withdrawn and
very depressed.
Eileen’s father and her father’s family have a tradition of heavy drinking.
When family members get together to eat or talk, there always seems to be
an open bottle. Eileen joined in the family drinking in her teenage years and
found that it made her feel better. She felt more confident and less tense. By
the time she was out of college, she was a heavy, compulsive drinker who, in
her own words, was “no longer drinking for fun” but because “she needed it.”
Drinking had become the preferred method of relieving tension and depres-
sion.
While Eileen’s depressive problem preceded her alcoholism, Dan had no
7. Depression, Alcohol and Drugs 99
noticeable depressive problems until long after he began drinking. During high
school Dan used “to party” with his friends. In his circle it was a matter of pres-
tige to see how drunk you could get on weekends. The pattern of heavy drink-
ing stayed with him after graduation and continued into his adult years.
Drinking first cost him his job because of absenteeism and later his marriage.
By the time he joined Alcoholics Anonymous, he felt hopeless about his life,
was filled with remorse and guilt and was considering suicide. For Eileen,
depression was primary to alcoholism. For Dan, depression was secondary to
alcoholism. For some people depression precedes alcoholism and is intensified
by it. Self-medicating only exacerbates the original problem.
Many alcoholic patients will report the usual symptoms of depression,
ranging from poor sleep to feelings of hopelessness. A study carried out by
David Clark and his colleagues using the Beck Depression Inventory suggested
that the particular symptoms to look for in alcoholics, symptoms that point to
depression, are guilt, self-disgust, irritability, indecision, dissatisfaction, work
inhibition and loss of social interest.5
Just how strong is the tie-in between alcohol abuse and depression? If not
all alcoholics are depressed, how many are? A number of studies have been car-
ried out on patients hospitalized for alcoholism. Sometimes these patients have
been given psychiatric interviews using the Diagnostic and Statistical Manual’s
criteria for depressive disorders. Sometimes they have been given self-report
measures of depression. In reviewing these studies, David Lutz and Peggy Snow
found that the estimates for depression among alcoholic inpatients varied con-
siderably. Studies using the depression inventories suggested that a majority of
alcoholic patients were depressed. The figures from the psychiatric interviews
did not seem as high but there were still estimates that exceeded 50 percent.
Because of the different methods used to assess depression and the variable
results obtained, it is difficult to offer a precise figure of the rate of depression
among hospitalized alcoholic patients. However, the numbers appear to be sub-
stantial.6
With over eight percent of the adult population estimated to have an alco-
hol use disorder which would put the number into the many millions, it is clear
that only a small fraction of these people are hospitalized or even in some kind
of outpatient treatment program. What about these people with alcohol use
disorders who are not receiving treatment? Are they likely to be as depressed
as the people in treatment? One would argue that the answer is very likely no.
Everyday observation tells us that many of these people simply live with the
problems caused by alcohol, often to the detriment of those close to them.
Clinical experience suggests that many of them are using the defense mecha-
nism of denial. Others become aggressive while drinking, scaring off those who
might want to help them. In any event, the person’s pattern of life has not been
sufficiently degraded to do anything meaningful about the problem and their
emotional state may still be far from rock bottom.
Some empirical data obtained in the national survey of over 40,000 peo-
ple cited earlier in this chapter indicated that about 16 percent of the respon-
dents living in communities who were evaluated as having an alcohol use
disorder during the past 12 months also had a “mood disorder” of some kind.7
Mood disorders are typically some form of depression. While this was double
the figure reported by persons not reporting alcohol use disorders, it seems a
good deal less than the estimates researchers have made for people hospital-
ized for alcohol use problems.
It is difficult to tell in how many of these people depression preceded the
alcoholic problem and vice versa. To do so we usually have to depend on
patients’ memories about the past and we know that such memories can be
faulty. It is interesting that when such studies are undertaken, the figures for
depression preceding alcoholism run considerably higher for women than men.
In studies cited in Lutz’s and Snow’s review, the figures for a preexisting depres-
sion in women were in the 25 percent range, while they were less than 10 per-
cent for men.
A recent study which utilized a sample of 7,000 twins to obtain informa-
tion about genetic factors as well as the onset of alcohol use and major depres-
sive disorders found that the onset of alcohol use disorders tended to occur at
an earlier age than major depressive disorder. Alcohol use disorders occurred
in young adulthood while major depressive disorder had a more variable age
of onset. The study confirmed the conclusion from earlier studies that for
women major depressive disorder often preceded the development of alcohol
use disorders.8
The tendency for depression to precede alcoholism occurs often enough
in women to warrant consideration from a public health standpoint in terms
of the prevention of alcoholism. The statistics suggest that alcohol has been
adopted by a large number of women as a means of relieving depressed feel-
ings. Therefore, one approach to attacking the problem of alcoholism in women
is to attack the causes of depression in women. The suggestion would be for
society to deal more aggressively with the underlying problems that cause emo-
tional difficulties in women rather than simply treating the symptoms of alco-
holism.
When people are asked why they drink, or even more specifically, what
effect they expect from drinking, they typically give the following answers:
They expect to be more sociable, and to feel more relaxed and less inhibited.
They also believe it will increase their enjoyment of sex.9 They see some down-
side risks in drinking, such as acting foolishly or becoming aggressive, but in
general they have a pretty rosy view of how they are going to feel while drink-
ing. For people who are light to moderate drinkers, these expectations are often
confirmed and this will sustain future drinking.
The problem comes when one is tempted to push the idea a little too far.
If drinking can make one feel better and relieve the feelings of tension and
pressure that have built up during the day, why not drink a little more and
a little earlier? You’ll feel better faster. And maybe alcohol will relieve the
blue feelings we all experience at times when things go wrong and we are
disappointed. These plausible ideas, unfortunately, lead one down the garden
path.
There are several reasons for this. Heavy drinking throws one’s normal
intellectual and social abilities from order into chaos. One makes a mess out
of what one is doing and one often ruins social relationships. Instead of increas-
ing sexual enjoyment, heavy drinking often makes men impotent.10 Heavy
drinking is a path to alcohol dependence. And alcohol is not particularly use-
ful for relieving depression — other than blotting out reality entirely —for alco-
hol, itself, can have depressant effects.
People don’t drink to feel more depressed, but that can happen, particu-
larly for heavy drinkers. In a study carried out with alcoholics, the subjects were
given adjective checklists to assess their moods before and after drinking. The
scores for depressed mood were higher after drinking.11 As alcohol can have
depressant effects, it is of dubious value as an aid for coping with a depressed
mood. Chances are that if alcohol is consumed in large amounts, it will only
make matters worse. However, alcohol is inexpensive, available and people
usually don’t expect that to happen.
Secondary depression — the psychological effects of a deteriorating lifestyle
that follows from prolonged alcohol use — may be a slow and insidious devel-
opment, for the course of alcoholism itself is often protracted. Increasing
dependence on alcohol doesn’t happen overnight and one may exist with the
problem for years before the roof finally caves in. By the time the person fully
recognizes his or her alcoholic problems and enters a treatment program, a great
deal of personal damage may have accumulated. J. F. Nugent and I conducted
a study of alcoholic patients at a Veterans Administration Hospital, in which
we asked the patients whether their alcohol problem had caused any of a num-
ber of things to happen.12 We included the checklist of 17 items, which appears
below. The percentage of the patients who responded yes are given in the col-
umn on the right.
Percentage
Checklist Item Answering Yes
1. Found it difficult to do my job well 49
2. Made me lose a job 38
3. Found myself in serious financial difficulties 54
4. Strained my relationship with members of
my own family 73
5. Strained my relationship with my friends 43
6. Tried to conceal my using drugs from others 51
7. Got in trouble with the law 44
8. Spent time in jail 37
Percentage
Checklist Item Answering Yes
9. Stopped enjoying many of the things I used
to enjoy 72
10. Began to find myself isolated 55
11. Found it difficult to concentrate 69
12. Began to feel tense and anxious 85
13. Began to have periods of depression 85
14. Had thoughts of suicide 27
15. Developed strong feelings of guilt about
using drugs 78
16. Found I was living from day to day without
planning for the future 67
17. Felt my life was in a downhill slide 75
As you can see from the percentages of patients who responded, “yes, this
problem happened to me,” almost all of the patients had experienced tension
and depression that they attributed to their alcohol problem. Psychologically,
the patients felt that they were on a downhill slide. They felt guilty, aimless,
were not enjoying their usual activities and felt increasingly isolated. All of
these responses are consistent with a picture of depression. Typically, family
relationships had been strained. Many of the patients had tried to conceal their
problem from others. A sizeable number of the patients had experienced prob-
lems on their jobs, and over one-third of the patients had lost their jobs. Almost
half of the patients reported having problems with the law and over a third had
spent time in jail.
The negative, depressing consequences of alcoholism emerge from these
data. The real life stories that flesh out this skeleton of statistics may be heard
over and over again at treatment centers and AA meetings. We also encounter
such narratives in the psychology clinic. The following is an example showing
the destructive interplay of depression and alcohol in the life of a young woman,
Leila.
When Leila entered therapy at an outpatient clinic in San Francisco, she
was recovering from alcoholism. She had been in AA for several years and had
finally ceased drinking. As therapy began, Leila was tense. Her words were halt-
ing and measured and she was reticent in discussing many things that were still
painful for her.
Leila was born in North Carolina and was raised by her mother, who had
a chronic illness, and by her grandfather. Her father had been killed in an auto-
mobile accident when she was three years old. Her grandfather was a very strict
person who raised her by the book and would tolerate no nonsense. Leila grew
up to be a shy, passive person, used to being in the background. She did what
she was told, though inwardly she felt resentful and spent as much time as she
could away from her grandfather. In her school years she was something of a
loner, never quite comfortable with the other children. Sometimes she felt lonely
and rejected. The situation was only marginally improved when she went to
college. She began to feel depressed. She thought about seeking help at the Uni-
versity Counseling Center, wrestled with the idea, but never made an appoint-
ment.
In her final year of college, she met Frank. Frank was good looking, bright,
with an assertive, dominating personality. Frank was the sort of person who
would “take over.” He was attracted to her physically, swept her off her feet and
they were married shortly before graduation. Leila and Frank settled in a rather
isolated community in southwestern Texas. Frank was busy with his job and
Leila found herself alone a good deal of the time. This is when she began to
drink.
Frank and Leila never knew each other very well before they were mar-
ried, and early on Frank began to show evidence of boredom with the mar-
riage. Leila seemed dispirited by her surroundings and had little to say that was
new and interesting. When Frank began to drift away from her and show her
less attention, she became clinging, and this turned Frank off further. She
became increasingly tense about the relationship. She felt uncertain, tentative,
almost cowed; it seemed something like a replay of her childhood days with
her grandfather. The more tense she became, the more she drank.
When their daughter, Charlotte, was born, Leila and Frank began to get
along better, at least for a while. They moved first to Denver and then to San
Francisco, where Frank’s job put him into contact with many interesting peo-
ple. Leila remained at home with Charlotte. Frank grew in the job. Leila just
seemed to languish. Leila became unsettled emotionally. She felt trapped, tense
and depressed. She drank heavily.
Alcohol gave her courage. She got into bloody arguments with her hus-
band, often in front of her young daughter. However, alcohol only dulled her
wits. She became incoherent, angry and emotionally out of control. Frank
reacted by leaving home for days at a time and became involved with several
women. Finally, he left altogether and filed for divorce.
When the marriage was shattered, Leila found herself with few resources,
an alcohol problem and depression. She tried making it on her own, but lacked
confidence and was drinking too much. She couldn’t hold a job. She had
difficulty making new friends and felt isolated. She contemplated suicide and
for a while was hospitalized.
Alcoholics Anonymous helped her turn things around. In therapy she
began to explore her own needs and to develop a more positive sense of her
own identity. In therapy, the focus in her life changed for the first time to what
she could do for herself and what she could become. She was able to get a job
and to begin the slow process of building a life of her own.
Leila’s story brings to mind a recent study of alcohol use and marital rela-
tionships. The study found that it was not so much the quantity of alcohol con-
sumed by one of the spouses that led to the deterioration of the relationship,
as much as it was the difference in the amount they drank. When one spouse
was a heavy drinker and the other was not, look out!13
Depression and Illegal Drugs

Let’s talk about illegal drugs— the black market drugs that are sold on the
street. The most widely used illegal drug in the United States and world wide
is marijuana. World wide estimates provided by an agency of the United Nations
for the number of marijuana abusers during the 1990s exceeded 140 million peo-
ple. Studies suggest that marijuana use disorders in the United States have been
on the increase over the past decade.14
Marijuana has certain pharmacological depressant effects. Research has
been carried out on a variety of animals— squirrels, monkeys, cats and rats
looking at the effect of the drug on activity level. Interestingly, the effect of the
drug is often biphasic; i.e., there is an initial period of excitement and stimu-
lation, which is followed by quiet behavior in which the animals move about
less and do little.15 Similar effects have been reported with human subjects.
Many people become sleepy after using marijuana and report a decline in activ-
ity.
People use marijuana because of the anticipated effects of the drug. They
expect a “high” from the drug and to feel relaxed. They usually hope to attain
these pleasant moods in the company of friends. Smokers report such sensa-
tions as lightheadedness, giddiness, intensified perception such as seeing col-
ors more intensely, sexual arousal, dryness in the mouth, hunger and sleepiness.
Adverse effects from the drug are not usual, but happen often enough to be of
concern. Users of the drug at times experience feelings of anxiety and depres-
sion. In one study, 40 percent of the users questioned reported that they had
experienced such reactions.16
My own research on marijuana users suggested that people who used mar-
ijuana on an occasional, recreational basis were unlikely to have concomitant
emotional problems to a greater degree than nonusers. This research carried
out on university students who were for the most part recreational users indi-
cated that they did not differ very much on psychological tests from students
who did not use the substance. Nor did they view their behaviors on the days
they used the drug as being noticeably different from the days on which they
did not use the drug. Beyond the fact that they reported they more frequently
smoked cigarettes than the other students, statistically they were not particu-
larly distinguishable from the non-users.17
I suspect that where marijuana users begin to look differently on psycho-
logical measures is when they began to use more powerful drugs as well as mar-
ijuana and especially if they become dependent on the drug. When we think of
drug dependence, we think of a person who uses the drug frequently, for pro-
longed sessions, where drug use has become compulsive, and the problems
brought on by using the drugs are ignored. And for some drugs, where toler-
ance develops for the drug, the user must search for more potent doses of the
drug to produce the desired effects.
When marijuana use becomes marijuana dependence, unwelcome psy-
chological correlates are often observed. Preoccupation with the drug may
impair one’s ability to perform well in school and on the job. In a large-scale
study carried out under the auspices of the National Institutes of Alcohol Abuse
and Alcoholism, marijuana dependence was linked to personality disorders of
various kinds, anxiety disorders, and depressive disorders. Nearly half of the
people who were classified as having a marijuana dependence during the pre-
vious 12 months had some kind of depressive disorder. Very interestingly, this
depressive disorder was very frequently bipolar I. Nearly 23 percent of the
respondents identified in the survey as having a marijuana dependence were
also classified as having bipolar I disorder which is far above the rate in the
population.18 I have no ready explanation to offer for this provocative finding.
A lifestyle in which illegal drugs become a centerpiece carries with it
increased risk of psychological problems. People who are under treatment for
dependence on the more powerful illegal drugs currently in use in this coun-
try often report a variety of psychiatric problems including depression. As is
true for alcoholism, it can be difficult to distinguish between pre-existing per-
sonality tendencies that lead to the use of these drugs and the emotional difficul-
ties that often result from drug dependence.
Let’s consider psychiatric correlates of two of the more widely used ille-
gal drugs, methamphetamine and cocaine. Methamphetamine is a designer
drug manufactured in clandestine laboratories many of which are scattered
around the United States. Cocaine, derived from the cocoa plant that grows in
South America is smuggled into this country. In a study of over 1000 metham-
phetamine users receiving outpatient treatment in Oakland, California, many
of the patients reported depression, attempts at suicide, and serious problems
controlling angry feelings.19 In another study, employing a sample of Internet
users, methamphetamine users tended to be more depressed and apathetic than
nonusers.20 In a third study, which used a sample of people who had been
arrested and were in the criminal justice system, methamphetamine users were
more depressed and more likely to have suicidal thoughts than people not using
the drug.21
Cocaine dependence can also be accompanied by depression. In a study
carried out in Texas, cocaine dependent patients who were also depressed
reported more distress than the cocaine-dependent patients who were not
depressed.22 And, what has important implications for drug treatment, the
depressed patients’ craving for cocaine was higher and their confidence about
being able to refrain from using the drug was lower.
With depression as a complicating factor in the treatment of dependence

on these drugs, there have been attempts to augment treatment of both sub-
stances with antidepressant medicines. The results, to date, have not been prom-
ising.23
Perhaps, the most strategic place to view the psychological difficulties that
arise from a life style centered on illegal drugs are the experiences of heroin-
addicted patients. Their stories are both sad and instructive. Heroin is often
the end-of-the-line drug when everything else has been tried. Heroin was orig-
inally developed with the best of intentions, as a “nonaddictive substitute” for
morphine, which was in medical use as a painkiller. The problem was that
heroin turned out to be highly addictive, producing both tolerance (the user
doesn’t get as much effect from the drug upon continued use, so he or she has
to step up the dose to get the same effect) and physical dependence (the user
needs to keep using the drug to prevent the beginning of uncomfortable with-
drawal symptoms).
Heroin is a very potent pain reliever. Unlike marijuana, which may be
associated with increased sexual arousal, heroin use may decrease sexual inter-
est. The drug may have an uplifting effect on many people, can act as a tran-
quilizer for tension, and may detach the individual from the realities of the day.
Life may take on a rosy hue until the effect of the drug wears off. It is this
euphoric effect that draws many people to the drug.
When a person becomes physically addicted to heroin and stops using it,
withdrawal symptoms occur. Such symptoms may include nausea, diarrhea,
vomiting, abdominal cramps, profuse sweating, nervousness and insomnia.
Symptoms usually diminish within a few days, but a craving for heroin may
persist for years. This craving often leads to resumption of use.
Dependence on a drug such as heroin can become overwhelming. Some
people who are addicted to this drug may do almost anything to again expe-
rience the sensations that they remember from past use of the drug. They will
put aside all of the other memories— the misery that drug abuse has caused
them in their lives— to experience the drug sensation. Hard drugs can exert a
fatal attraction that reminds one of the story of the Sirens in the Odyssey, in
which the song of these nymphs lured sailors to their deaths as their ships
smashed on the rocks.
The psychological and social destruction of the heroin addict is similar in
many ways to that of the alcoholic. The main difference is that it is usually
quicker. There are reasons for this precipitous decline. Heroin use causes a
physical addiction that requires continued use of the drug to prevent with-
drawal symptoms. Unlike alcohol, which is also addictive, heroin is expensive
and to sustain this drug habit costs a bundle. The victim soon has an empty
pocketbook and often is induced into illegal activities, such as robbery or sell-
ing drugs, to buy more drugs. The chances of being arrested are pretty high.
Take a second look at the list of consequences we used in our research with
alcoholics. We gave the list with the same instructions to two samples of patients
under treatment for heroin addiction. One group of patients was hospitalized,
undergoing detoxification and therapy. The other group of patients was being
treated on an outpatient basis; most were on methadone maintenance. Some
statistics from our study showed that the inpatients in particular had encoun-
tered very serious financial and legal problems as a consequence of drug
dependency. Eighty-five percent of the hospitalized patients reported they had
experienced serious financial difficulties. Eighty-two percent had gotten into
trouble with the law. Sixty-seven percent had spent time in jail. The psycho-
logical consequences of addiction for these inpatients were also severe. Ninety-
seven percent of the patients reported they had periods of depression.
Ninety-four percent felt their lives were on a downhill slide. Eighty-eight per-
cent reported they were becoming isolated. Forty-two percent had thoughts of
suicide. At this point in time it is not possible to say with precision how many
of these patients would meet the criteria for major depressive disorder, but it
seems likely from these data that many of them would.24
As we can see from the responses to the questionnaires, almost all of the
inpatients in the study indicated that depression was one of the consequences
of heroin addiction. From interviews we conducted with other heroin-addicted
patients, however, I have the impression that for many people who use heroin,
depressive tendencies had set in earlier in life and were intensified by the lifestyle
of the heroin addict.
Many of the patients interviewed had experienced a childhood and ado-
lescence that nurtured a depressive outlook.25 A large number of the patients
had come from homes in which there was no father present, or, perhaps worse,
a father who was alcoholic, indifferent or abusive. We know from research on
child development that such circumstances increase the chances of depressive
problems. The experience of school for many was not helpful and the jobs that
were available tended to be boring and dead-end.
A growing sense of futility opened the way for drug experimentation. To
many, it seemed as if there was little going for them and little to hope for — so
why not go for some kicks in life? Most of the patients felt that they would not
become addicted; there was a sense of invulnerability: “It won’t happen to me.”
The consequences of addiction, however, often proved devastating, resulting
in severe depressive problems. Almost all the studies that I have seen found
elevated levels of depression among inpatients being treated for heroin addic-
tion.
Drug addiction often leads to a kind of twilight existence. Addicts move
surreptitiously in circles of other addicts and pushers. Many of them conceal
what they are doing from their families as long as they can but the unrelenting
need for the drug usually leads to family strains and financial disaster. The
resulting conflict and misery can be glimpsed in excerpts from statements of
the addicts themselves.
“I feel very depressed. I was unhappy with being out of work, out of money,
being drug addicted. Using drugs has hurt my self-confidence. I feel I have
messed up so many times in the past, I will do it again in the future.”
“My wife got ready to leave me. I attempted suicide.”
“I feel super depressed. Things piling up, bills, family things-makes me
worried and depressed. Life on drugs made me go through more hell and frus-
tration and more sickness than it’s [possible] to imagine.”
“I couldn’t trust myself when I was strung out.”
“The problem has been a constant struggle for my wife ... I get disgusted
at myself in preparation stage, but once I am high, I don’t give a damn.”
“I felt I was going down, down, down. I had to get off of it.”
“Living the life of an addict is really hell. After you’ve become hooked it’s
pure hell. An addict may be smiling on the outside-but inside he’s crying — it’s
a thing that bites and bites.”
8. Coping with
Depressed Feelings
Now that we have completed our inquiry into the nature of depressed
moods and states, it is time to ask what you can do about them. What steps
can you take to help reduce the risk of becoming depressed? And, how can you
cope with depressed feelings when they occur? In addressing these questions,
we are going to first look at what a person can do to deal with his or her own
depressed feelings. Next, we will look at the way family and friends can help.
Then, we will look at what mental health professionals may offer in the way of
medicine, psychotherapy and other treatments. Finally, we will examine some
alternative medicine approaches that appear promising.
When we discuss self-help in preventing depression, we are largely talk-
ing about gaining increased control over your life. To move in this direction
may require both changes in thought patterns or mind-sets and changes in
behavior. In this process you should begin to view life in more positive terms,
to recognize that you can bring changes into your life, and that your efforts can
make a difference in the way you feel.
If you have read my book Coping with Stress: Common-sense Strategies,
you will probably notice some overlap with the ideas and suggestions that will
be offered in this chapter. This is almost inevitable because stress and depres-
sion are closely linked. An action that may be helpful in the control of stress
may also be helpful in coping with depression.
Setting Rewarding and Reachable Goals

In looking at some of the ways you can gain more control over your life;
let’s begin with the question of setting rewarding, yet reachable goals. Consider
these questions: Do you have goals for the near future–for the next weeks or
months? Do you have longer range goals—for the years ahead? Take a few
moments and try spelling out what you would like to accomplish, both in the
near term and in the more distant future. Now consider, are these reasonable
109
goals, things that you have a decent chance of achieving? If they are, fine. But
if they seem unrealistic, where does that leave you? You may be setting your-
self up for more failure and disappointment, which may lead to the question,
“What’s wrong with me?” The result may be a further erosion of self-esteem.
A woman came to see me in therapy. She was 45 years old. She had aver-
age ability. Her college grades had been mostly Cs. She told me she was think-
ing about applying to law school. Realistically, the chances are that she would
have a hard time both getting into and through a law school and would be
pushing 50 if and when she got her degree. Further, it is questionable how com-
petitive she would be in the job market at that point. One doesn’t like to dis-
courage aspirations, but if she had chosen a more attainable goal, it would have
increased the chances of her experiencing success rather than disappointment.
There is a wonderful song in the musical The Man of La Mancha called
“The Impossible Dream.” You may remember both the song and the play, based
upon Cervantes’s story of Don Quixote. The lyrics of the song speak about
reaching unreachable goals. Now, there are people who are made of sturdy
enough stuff to try this, who can tolerate endless frustrations in the search of
deeply rooted ambitions. One thinks of artists like Van Gogh, who painted
masterpieces that no one would buy, actors who lived from hand-to-mouth
while trying to make it on the stage or the minor league baseball player who
couldn’t make it into the big leagues, but never quit trying.
I have always encouraged patients who believe that they have the talent to
do something to go ahead and give their dreams their best shot so they will not
spend life wondering what they might have been. But I also advise them to keep
a dash of realism — not to end up tilting at windmills like Don Quixote.
While unrealistic goals can lead to disappointment and depressed reac-
tions, the extreme alternative of setting goals that are very low, unchallenging
and raise little risk, can also lead to a life of frustration and unrealized poten-
tial. A life of self-selected mediocrity can be bitter and depressing.
There are, of course, many reasons that people aren’t able to do things that
challenge them and afford them the opportunity to develop their full poten-
tial. Job openings may not be available. The person may lack education or eco-
nomic resources, or be burdened by heavy responsibilities for the care of family
members. However, for many people, selecting a restrictive lifestyle is a result
of psychological factors. Fear of failure and taking risks has kept many people
locked into situations that offer little fulfillment. The result is often depend-
ency, frustration and depressed mood.
Goal setting that is unrealistic on the one side or unchallenging on the
other raises the potential for problems. Ideally, when we set goals, we would
like them to be desirable, challenging, yet attainable. It should be not only what
we want to achieve, but the sort of things that our talents, resources and per-
sonal characteristics give us a reasonable chance of bringing to fruition.
Clearly, some self-evaluation is required in goal setting. There are impor-
8. Coping with Depressed Feelings 111
tant questions to consider. What are the things you really want? What things
do you do best? What are your weaknesses? Do you have the patience and per-
sistence necessary to follow through to achieve what you want? Do you have
problems like fear of failure or difficulties in asserting yourself that might inter-
fere with reaching your goals? If such issues are troublesome for you, perhaps
you may want to discuss them with a counselor or therapist.
Analysis of the goals themselves and what is necessary to achieve them is
also important. Consider career decisions as an example. Do you know the
kinds of training that are necessary to get into the type of work that you would
like to do? Do you know what future job opportunities are likely to exist in this
line of work?
When you think about career goals, you might want to research such ques-
tions. It may be helpful to talk to people who are working in the field. Also,
look over the resources in the public library. Ask the librarian for The Occupa-
tional Outlook Handbook which is loaded with information. If you are unsure
about your aptitudes and interests, you may find it useful to call the counsel-
ing center at your local college or university. They may offer vocational coun-
seling and have interesting tests to help you more objectively evaluate yourself.
Taking a Look at Where You Are

If you have been feeling depressed, chances are that you could profit from
making a general reassessment of what’s going on in your life. I have to intro-
duce a word of caution, here, because people who are depressed tend to put a
negative spin on their situations, viewing their lives more pessimistically than
is often warranted. So, in making an assessment, it is prudent to talk things
over with people who you have confidence in — people who can react to your
ideas and offer another perspective. Consider a minister, a counselor, a thera-
pist, someone whom you trust and feel comfortable with. Listening to the reac-
tions of another person is helpful for most people and can be particularly
important if you are prone to depression.
The idea in this assessment is to identify what is going right in your life
and what is not. Ask yourself what are the things that bring satisfaction to your
life and what are the sources of stress and unhappiness. This task is something
like taking personal inventory, but it is also a beginning of diagnosis. Your
objective is to determine where it is desirable to make changes in what you are
doing.
Be specific in your thinking. If you say, “I don’t like my job,” it may be
that there are only some aspects of your job you don’t like. Perhaps it is a co-
worker who is giving you a problem or it may be one of your duties that you
particularly dislike. When you pinpoint things, it is easier to discuss making
possible changes. Remember, people who get depressed have a tendency to
overgeneralize. The fact that there are some problems does not mean every-
thing is bad.
Frequently the problem that is upsetting you will be in human relation-
ships. For example, you may find yourself in a situation where you care a great
deal about another person, but there are things about that person that you find
irritating. Ambivalence — having both positive and negative feelings toward
another person — is part of the human experience. Can you pinpoint the neg-
atives, the things that are bothering you? Ask yourself how significant these
negatives are in the total context of the person. If they appear to be minor blem-
ishes in a person who is otherwise more than okay, this realization can lead to
a change in your thinking. You may conclude that there really isn’t a problem,
that things are basically all right. Maybe what is needed is a little tolerance and
forbearance on your part and these apparently troubling issues will vanish like
a puff of smoke. After all, in seeking the company of others and especially a
romantic partner, you were not looking for someone who is a clone of your-
self. Why not accept and enjoy the differences between you? On the other hand,
if these issues that are troubling you are profound, perhaps it is time to begin
to think about taking steps to change things.
In pinpointing the things that are upsetting you — the situations that are
creating stress in your life — you may look at your environment (your home
life, your place of work, your relationships) and you may also look at yourself.
Are you doing things now that you would like to be doing differently? Ask your-
self, where would you like to see changes in yourself ?
Changing Patterns of Thinking

When we talk about changes, we include both changes in thought patterns
or mind-sets and changes in behavior. Sometimes just looking at situations dif-
ferently can make a difference in whether you are likely to feel depressed.
I have discussed research that indicates that the way a person evaluates a
situation makes a difference. If you tend to inflate the importance of events, to
magnify what is at stake, then you may be setting yourself up for an overreac-
tion. The trick is to be able to distinguish between what is really important and
what is not. If you act as if everything falls in the former category, then be pre-
pared to ride on an emotional roller coaster and have your self-esteem beaten
down like a rug at spring cleaning. When you sense you are about to get riled
up over something that is trivial, stop and ask yourself, “What am I doing?”
Surely there are enough important things in your life to be concerned about
without going bonkers over things that don’t really matter.
A woman with a teenage son developed an acrimonious relationship with
him, putting both of them under a lot of unnecessary stress by making repeated
issues out of such things as the way he decorated his room with rock star posters,
the way he dressed and the way he sometimes procrastinated in doing chores
like mowing the lawn. The relationship would have been a lot smoother had
she acknowledged that the important things in his life were going well-he got
good grades in school, stayed clear of drugs and had many friends. What the
mother needed was a larger measure of tolerance, an understanding that other
people can do things in a different manner from her and her world will not fall
apart.
I have also mentioned being hung up on comparisons with other people
as a thinking pattern that promotes depression. One of my favorite examples
of these comparison traps is a patient who came to see me who was the oper-
ator of a photocopy business. The man had practically no formal education.
He worked very hard in his business, putting in long hours, and made an excel-
lent income. I thought he had done very well, having started and successfully
run a small business. When I ventured this opinion to him, he shook his head
forlornly and replied that he was a failure. In explaining his feelings, he told
me about a man who had a similar business three blocks away. It was a larger,
more attractive shop that offered more services and had more machines. The
other shop was doing more business and making more money than my patient’s
shop and he felt demoralized by this.
We grow up in a world of comparisons. As children and adolescents we
are defined by others as being bigger or smaller or smarter or not so smart or
more attractive or less attractive, and so on. While such comparisons are
inevitable in the way we are raised, it does not mean that we have to bound by
such notions in our adult thinking and live this way. There is an alternative
approach. This approach is to carefully define your own goals— goals that are
desirable and attainable for yourself — and go after them. The measure of your
success is the extent to which you attain your goals. What other people decide
to seek in life is their concern, and need not be a gauge for your own evalua-
tion of success.
If you measure yourself against what everyone else is doing, it’s almost
impossible to win. If you have your own goals in life and meet them, you can
feel you are doing what you want and can experience a sense of satisfaction.
It’s all in the way you define success. My patient’s attitude was self-defeating.
Even if he had owned the larger of the two photocopy shops, there would always
be someone else who had a larger one.
In discussing thinking patterns that need changing, let’s recall another
source of difficulty: perfectionist thinking. Do you have this tendency? Here
are a few signs:
You are chronically dissatisfied.

Nothing is ever good enough to please you.
Things have to be ordered just so-nothing can be out of place.
Everything has to be done on time.
Your house and yard must look like a museum.

You find faults with everybody.
You obsess about the quality of your work.
You seldom finish anything because “it isn’t good enough.” Your motto is,
“Don’t do anything unless you can do it right.”
People tell you that you are a nitpicker.
If you find yourself nodding your head and saying, “That’s me, all right,”
you have a problem.1 What can you do about it? As a beginning, try to recog-
nize these patterns in your thoughts and behavior when they occur. Recogni-
tion of a tendency toward perfectionism is an important step in doing something
about it. Then take a good look at your behavior, or better yet, what such behav-
ior is doing to you and the other people in your life. As you reflect on this, you
will probably find that your perfectionistic standards are interfering with your
ability to get things done and with your feelings of satisfaction from what you
are doing. It is also turning off other people and causing them problems.
This may be a hard idea to accept and you could be inclined to argue,
“Well, isn’t it important to do things well?” The answer is sure. Making a solid
effort and turning out high-quality work are very important values. To be hung
up on an error-free existence, however, is something else, a burden one would
not wish on anyone. If you are a perfectionist, loosen the screws on yourself
and others. Try being more tolerant and less critical. See if you and everyone
else are not a little more relaxed and a lot happier as a result.
Reinforce Yourself Instead of Kicking Yourself

We could title this section, “give yourself a break.” Many people who
become depressed are much more inclined to get down on themselves for mak-
ing mistakes than to pat themselves on the back for doing something well. It is
something like a football game where the fans boo when you fumble the ball
but don’t cheer when you score a touchdown. Consider this: positive reinforce-
ment builds up self-esteem, nonconstructive criticism tears it down.
When you do something well, tell yourself that you “did OK.” When you
accomplish something that you’ve wanted to do, smile and give yourself some
credit. When you’ve done something especially satisfying, how about going out
and celebrating? Do something you really like or buy something you’ve always
wanted. How about that new sweater or jacket? It will help you move away
from the idea that life is nothing but a series of negatives.
A psychologist, E. M. Heiby2 developed a measure that assesses the fre-
quency of self reinforcement. Not surprisingly, researchers have found an asso-
ciation between low scores on this measure and symptoms of depression.3
Reinforcing yourself is one of the ways of moving toward a more optimistic
perspective about your life. Another mind-set that will help nudge you in this
direction is to give yourself the benefit of the doubt when something goes wrong.
When things go awry, too often depression prone people look inwardly and stop
there. The conclusion may be almost automatic, “It’s my fault.”
The conclusion may be true, it may be partly true or it may not be true at
all. We live in a complex world where cause and effect is seldom very clear. How
many things are totally under your control? Not many, if you think about it.
You depend on other people to do things in a very interrelated society. When
someone else fails to come through, it may affect your ability to do what you’re
trying to do. What do you do when someone else screws up? Or consider all
the uncontrollables in life. Can you control traffic, the weather, catching a
virus, your boss’s temperament, the state of the job market? If something goes
wrong, there may be some very good reasons for what happened other then
something you did. Let’s suppose you did make a mistake on something. Before
overreacting and lapsing into a sea of gloom, ask yourself these questions: Do
you know anyone who doesn’t make mistakes? Is the mistake you made cata-
strophic? The answer is likely to be no to both questions. So, pick up the pieces
and move on.
When you do have negative experiences, it is vital that you do not over-
generalize. As we have indicated, many people who become depressed have a
tendency to turn negative experiences into calamities. In contrast, the person
who remains emotionally intact often finds a way to shrug it off. Her reaction
may be, “C’est la vie,” or “So what?” She limits the impact. She does not get
down on herself; rather, she searches for the next opportunity, recognizing that
success is likely to come only if she keeps trying. The person who resists depres-
sion may not only brush aside the negative experience but downgrade its impor-
tance. Defense mechanisms rationalize failures away. This may seem unrealistic,
but it offers protection. While you may not always be able to put the best face
on a negative experience, to avoid becoming depressed try not to put the worst
face on it. It helps if you keep your sense of perspective and don’t overgener-
alize.
Changes in Behavior
Changing attitudes and thought patterns are important steps in protect-
ing oneself against the onset of depressive episodes. Equally important are
changes in behavior. In your assessment of things that you would like to do
differently, you probably spelled out some specific changes you would like to
make. Let’s talk about getting started.
One way of approaching change is to adopt a strategy of small wins.4 This
strategy recognizes that you can’t do everything at once, and to try too much
too soon can set you up for more experience of failure. If you’ve been depressed,
you don’t need any more of that. In a strategy of small wins, you begin with a
defined goal and start taking steps toward realizing it. When you’ve taken a step
in the right direction and experienced some success—“a small win”— reinforce
yourself.
A woman who was feeling depressed came to see me. She reported that
one of her biggest problems was feeling lonely. Too many nights she had noth-
ing to do and no one to see. The weekends were particularly depressing. After
a few therapy sessions, she agreed to join a club where she would have an oppor-
tunity to meet people. Finding out about clubs and organizations that might
interest her was an important first step. She did this by looking through the
notices posted at her public library. As she was an outdoors-type person, she
chose a local hiking club that went on outings on the weekends. She called the
number listed on the notice and with some anxiety attended her first meeting.
She found that the people were nice and she enjoyed the walks. On her third
outing, she met an interesting man and began dating him. She wasn’t sure
whether the relationship would pan out, but she is making friends and her
loneliness is fading. My patient told me that at each step toward becoming more
involved in the club, she felt a little anxious. There is a certain amount of risk
involved in starting new undertakings. But risk taking is necessary if you are
going to make changes. And if you are depressed, changes are usually neces-
sary.
A careful, step-by-step approach minimizes risks and anxiety that might
be aroused. A strategy of small wins builds confidence and provides the oppor-
tunity for larger successes. My patient who joined the hiking club experienced
some stress in the process of becoming a member and making friends. Going
through this discomfort was necessary to attain an important objective-deal-
ing with her loneliness. Many people who are prone to depression already have
too many stressors in their lives, stressors they can’t handle, so care and tim-
ing are important when a person who is depressed contemplates adding new
activities. But these steps are important as they can rebuild confidence and
rekindle hope, both of which are important psychological bulworks against
depression. A poet once put it well, “Each forward step we take we leave some
phantom of ourselves behind.”5
Overcoming Resistance to Change

Change is sometimes a difficult thing to bring about. You’ll often find
resistance to making needed changes both in yourself and in others. I men-
tioned that change involves taking risks. The anticipation of risks elicits anxi-
ety, and anxiety can be very uncomfortable. An all-too-easy way to terminate
anxiety is to call a halt to what you are planning to do. Of course, that leaves
you right where you started from, in a malaise.
You might use rationalizations to prop up a decision not to carry your plan
through. Can you hear the inner voice, “I didn’t really want to do that anyway.
Besides, it wouldn’t have worked.” People who are depressed often have a neg-
ative perspective and it is very easy to convince themselves that anything they
try won’t work. After all, hasn’t their history been one of failure? Why should
they expect anything different?
It can be very hard to break through a demoralized attitude. Encourage-
ment from family and friends can be helpful and so can the actions of an ener-
gizing therapist. Still, the bottom line comes down to the person who is feeling
depressed. If you want to feel better, you have to start doing things. Reading
books such as this is an indication that you want to make changes and is a pos-
itive sign that you can. Beginning steps, small wins and confidence building
are the orders of the day.
Many of the sources of stress that make life difficult involve our relation-
ships with other people. Stress on the job often involves your relationship with
your boss or conflicts with other employees. Stress in the home life usually
involves other people. And stress in romantic relationships can be an impor-
tant, and at times, overwhelming concern.
To make changes in the way people interact can be a difficult undertak-
ing. When you express the wish to introduce changes in a relationship, the idea
that is generated is, “something is wrong.” And if you do not handle the situ-
ation adroitly, the other person may then think, “You’re accusing me of doing
something wrong.” This notion can trigger an emotional reaction of defensive-
ness. You may encounter hurt feelings, avoidance, the silent treatment or indig-
nation. One can almost hear the denials. “I did not! I am not!” The anger that
is provoked may lead to retaliation. “You’re the one who is at fault.” The attempt
to reduce stress has only resulted in increased levels of stress.
The possibility of this all-too-familiar scenario is enough to discourage
many people from even trying to suggest changes. However, if the current sit-
uation is making life unlivable, you have little choice but to try. Diplomacy is
often the best bet. One approach is to say something like this: “You know, I’ve
been under a lot of stress. I’ve been feeling bad and I’m trying to make a few
changes to see if it can help. Can you help me in this?” In this context, it makes
it a little harder to refuse.
One of the ways to lower resistance in others is to ask for their input, their
ideas. If some of the things they suggest make sense to you, incorporate these
ideas into an overall package that includes your own ideas. Propose the over-
all package as a joint plan and see if you and the other party or parties can agree
to the plan. A process like this where everyone’s ideas are considered seriously,
and where an agreement can be reached, has added force and staying power.
Many people who become depressed have problems in asserting them-
selves, in making known what they want to do and what they don’t want to do.
Such people often have a hard time in saying no. This reluctance to commu-
nicate one’s true wishes adds to the difficulty of making needed changes. The
alternative of not speaking up, of accepting a bad situation, of course, merely
prolongs the situation that help bring on the depressed reaction.
There are books, even courses, on assertiveness training. The goal of
assertiveness training is usually to learn how to state your wishes in a clear,
convincing manner without being argumentative, and if you don’t want to do
something, you practice saying no. You learn how to give a simple reason for
your decision without becoming bogged down in lengthy explanations, which
may only weaken your case. Being able to be assertive when you need to be is
an important tool is making the kind of changes you wish to make. If you have
a problem being assertive, it is a skill you can learn.
Start with Exercise

When people come to see me and tell me that they are feeling depressed,
one of the first things I often recommend is that they start an exercise program.
I always ask them to check with their doctors first to be clear about their phys-
ical condition and to find out what level of exercise is safe and appropriate —
what is well within their capabilities.
Within these guidelines, I don’t think it really matters very much what type
of exercise you choose, whether it’s tennis, riding an indoor bicycle or walk-
ing. The latter is usually a safe and satisfying way to begin. Imagine a daily rou-
tine that includes a pleasant walk in the park, or along city streets with
interesting shops and lots of people, or perhaps a tree lined suburban road.
Some people find that just being in a pleasant setting, enjoying the beauties of
the natural world is therapeutic. The poet John Keats wrote about immersing
oneself in nature when downcast. In his poem, Ode on Melancholy, he wrote,
But when the melancholy fit shall fall
Sudden from heaven like a weeping cloud,
That fosters the droop-headed flowers all,
And hides the green hills in an April shroud;
Then glut thy sorrow on a morning rose,
Or on the rainbow of the salt sand-wave,
Or on the wealth of globed peonies ...
Whether it is a park, a suburban road, or a modern health spa — whatever you
prefer as a setting —find a place that’s safe and pleasant, then move. In a word,
exercise is the thing!
The reason I suggest starting an exercise program as a first step in com-
bating depressed feelings is that there is considerable research evidence that
indicates that exercise has an antidepressive effect. Three different types of
studies have been carried out, all with positive results. The first type of study
is a randomized controlled trial in which subjects are assessed for levels of
depression, then given various intensities of exercise levels in laboratory set-
tings and assessed for changes in depression. The second type of study is epi-
demiological in design, in that samples of people in the community are assessed
in surveys for self reported exercise levels and levels of depression. The third
type of study uses people who are being treated for clinical depression. Once
again their self reports of exercise and their levels of depression are assessed,
sometimes in longitudinal designs over a period of years.
A recent report of a randomized controlled trial carried out in a labora-
tory setting found that exercise appeared beneficial in reducing symptoms of
depression and that higher levels of exercise were the most beneficial.6 Com-
munity studies generally found a correlation between self reports of exercise
and lower levels of reported depression.7 The same is true for correlational stud-
ies of depressed patients.8 While none of these studies would indicate that exer-
cise is a cure for depression, all of these studies suggest that exercise can be
helpful.
Some of the reasons for the beneficial effects of exercise may be physio-
logical, but there are important psychological benefits as well. Among the psy-
chological effects is the fact that you can see that you are accomplishing
something and you will make measurable progress in accomplishing more. For
example, if you are riding an indoor bicycle, you can ride increasingly longer
distances. This can give you a psychological lift. Exercise is a good way to reduce
tension. Moreover, exercise tones you up. You feel better, you look better, your
wind and stamina are better. You feel more alive.
When you select an exercise program, it is important to choose something
you really like to do. Don’t start a regimen of doing sit-ups if you hate sit-ups.
A pleasant routine of exercise is most likely to be antidepressant.
Look Better, Feel Better

Exercise may help you look better, and for many people, that in itself may
make them feel better. Studies have shown that people who feel better about
their appearance tend to have brighter psychological outlooks.9 This is partic-
ularly true for adolescents and young adults where appearance is usually highly
valued. Body dissatisfaction in young adolescent girls can be predictive of sub-
sequent depressed mood as they transition through adolescence.10 It’s not so
much the way a person looks in the eyes of other people that tends to be depres-
sogenic, it’s the way one feels about one’s self. Looking better in your own eyes
is the objective and that is something almost everyone can try to do.
If one is pleased about the way one looks, it can help boost one’s confidence
and self-esteem. For many people, shaping up to look better can be part of an
overall therapeutic plan of behavioral change to cope with depressed feelings.
Shaping up may include weight loss, if weight is a problem, and toning up one’s
body.
Some therapists have suggested to their depressed patients to consider

buying new clothes. For many people, an attractive wardrobe has a place in
looking better and feeling better about oneself.
Mirror, mirror on the wall.
Who is looking better these days? C’est moi!
Introduction of Pleasant Activities

Could you list five or six activities you really enjoy? Taking walks, going
to the movies, swimming, going to a party, listening to music, whatever. Take
a few minutes and come up with your own list. All right, how many of these
things are you doing now? If you’re not doing some of these things, wouldn’t
it make sense to start? A life with no fun is depressing.
In planning changes in your life, see if it is possible to give a higher pri-
ority to these activities. If you can, you will probably find that this will cause
a shift in the negative-positive balance in your daily life. You will have more
things to look forward to and this is likely to elevate your mood.11
In thinking about this idea, try not to put it into a “must-do” framework.
These activities should be things you want to do, not things you feel you have
to do. Viewing such activities as ordered or imposed will only take the joy out
of them. Just start doing some of the things you’ve always liked doing and do
them at a pace you find right for you.
Developing Meaningful Social Relationships

Much of what is meaningful and important in life is having friends and
loved ones, feeling a sense of connectedness with other people. Many people
who report depressed feelings feel lonely. They don’t have many friends; they
often feel isolated. When things go well, they may not have people with whom
to share their good tidings. When things go badly, they may have no one to
reach out to.
Social support — the caring and responsiveness of others when one is expe-
riencing difficulties—can be a significant buffer against stress. The support of
others can help deflect and mitigate the deleterious effects of stress which for
many people may help ward off or at least tone down depressive reactions. Peo-
ple who can count on the support of others during difficult times have an advan-
tage. Indeed, a study carried out on patients being treated for depression in
Australia found that more than half of the people studied believed that a lack
of social support was instrumental in maintaining their depressive state.12
While the perceptions of these patients probably overstates the case, as
depression is a complex, multilayered phenomenon, there is little doubt that
being able to talk to people whom you feel are accepting and understanding is
an asset in dealing with a range of mental and emotional difficulties, and this
certainly includes both anxiety and depressive disorders. Studies carried out
in such disparate countries as the United Kingdom, Sweden, and Japan suggest
that the association between social support and better mental health holds across
cultures and may be universal.13
Most of us recognize the importance that friends play in our lives and
people who are lonely and depressed perhaps appreciate this truth even more
keenly. However, many depressed people have had difficulties in building
friendships in their lives. They may feel qualms and uncertainties about how
to meet new people and make friends however, many of these people have
difficulties in building such relationships in their lives.
Making friends is not always easy to do, even when you’re young and in
school and it probably doesn’t get any easier as you find yourself separated
from the people you grew up with in an ever-larger and often fragmented soci-
ety. You might recall the example of my patient who rather systematically exam-
ined the notices of community organizations and joined a hiking club. This is
certainly a reasonable approach. In metropolitan areas, there are usually plenty
of groups like this to choose from. The recreation department in the suburban
community in which I live offers classes in activities ranging from archery to
yoga. Churches offer social activities. Some community colleges are becoming
Mecca’s for adults seeking to upgrade their skills and pursue their interests.
When you get involved in such activities, you increase the opportunities for
making new friends. And, of course making friends through sites provided on
the Internet is now an everyday occurrence.
Research indicates that many people who become depressed do not have
fluent social skills. They may not present themselves well or feel at ease with
other people.14 This can increase the difficulties of developing satisfying friend-
ships. The point has to be made, however, that social skills, like most other
skills, may improve considerably with practice. Isolating oneself to avoid dis-
comfort and discouragement will not afford the opportunity to make this
improvement and establish these vital connections.
Some thoughts about making new friends for people who are feeling
depressed. When you meet new people, projecting gloom and low self-esteem
will probably turn them off. You will probably have more success if you can
get out of yourself and the problems that have been consuming you and focus
your attention on what other people are saying. There is an added benefit to
this. One of the surest ways to make new friends is to be a good listener.
If you project the feeling that you are really interested in what the other
person is saying, you will find yourself in increasing demand. Think of each
person that you meet as a special individual who has a unique story to tell, with
experiences and ideas that might be interesting to learn about. If you follow
this advice, you might be tempted to ask people a ton of questions. This really
isn’t necessary. A few general questions are usually enough. And one thing to
avoid are pointed questions. Such questions can make people defensive.
At a party, a man asked a woman who taught at a high school experienc-
ing some bad problems, “Isn’t it awful working there?” The woman became
uncomfortable and soon broke off the conversation. The man might have
phrased the question, “How do you like working there?” Chances are the con-
versation would have continued.
In projecting an attitude that you are interested in what the other person
is saying, you will probably find it helpful to maintain some eye contact, to
nod your head occasionally to indicate that you are paying attention, and —
perhaps most importantly — to remember what the other person is saying so
that your comments and reactions reflect this. Referring to names, places and
ideas that a person has brought up tells the person that you are really tuned in.
It’s easier to make and keep friends if one maintains a latitude of toler-
ance both towards others and oneself. If you look at almost any individual
through a microscope, you can usually find something that is “wrong.” As we
indicated earlier, perfectionism in the choice of friends is about as useful as
perfectionist demands on oneself. One may end up without friends.
The starting point in making friends is the attitude that people are differ-
ent, most people are interesting and good social relationships can enrich your
life. Can some people be irritating and a pain in the neck? You bet! But the alter-
native to trying to develop lasting friendships is isolation, loneliness and
increased risk of depression.
Finding a Support Group for Depression

Social support is not only useful in buffering the effects of stress, it can
play a significant role in helping a person move through the recovery process
for both physical and emotional illnesses. This idea has been institutionalized
into networks of support groups scattered around the country to help people
cope with various kinds of disorders. For people experiencing depression and
bipolar disorder, the Depression and Bipolar Support Alliance (DBSA) coordi-
nates a grassroots network of more than 1000 support groups. Each group is
peer-led, has a professional advisor, and welcomes both people who experience
depression and bipolar disorder and their loved ones. DBSA support group
meetings provide an opportunity for participants to share their experiences and
learn from each other in an atmosphere of mutual acceptance. Contact infor-
mation for local support groups can be obtained from the Alliance by telephone
or from the organization’s web site, www.DBSAlliance.org.
Many people who join support groups find that being in the group helps
them cope with their depression. Participation in group meetings can play a
significant role in helping people with depressive disorders through the illness.
One participant in a support group for depression sponsored by the Depres-

sion and Bipolar Support Alliance put the matter succinctly, “These meetings
work miracles. They save lives and they give people hope. It’s like watching a
flower bloom sometimes.”15
Bibliotherapy: Some Useful Homework

Bibliotherapy is a common-sense idea. If you have some understanding
of a problem, you can deal with it more effectively, and what better way to learn
about a problem in depth than reading about it. The idea has lead to books and
pamphlets about a whole range of physical and emotional disorders, including
depression. This book is an example.
Now, a book about a disorder such as depression can range from simply
providing information to attempting to directly assist the reader in treating the
problem. The present book takes a position somewhere between these points
of view; we try to provide both information about depression and ideas that
may help in the management of the problem. In no way, however, is this work
conceived as a substitute for the professional treatment of depression.
The idea that books and their successors (computer programs) may func-
tion as a partial or even complete substitute for face to face professional treat-
ment dates back into the 1980s and probably before. An issue of the Psychological
Bulletin in 1978 provided a review of self-help behavior therapy manuals.16
Two of the earlier books that were written for general readers with the
intent of being helpful in a therapeutic context, Feeling Good by David Burns
and Control Your Depression written by Peter Lewinshon and his colleagues
have been studied for their possible effectiveness in helping people with depres-
sion. The first book presents a cognitive approach to dealing with depression
while the later book presents a behavioral approach. We shall discuss these
therapeutic approaches to treating depression singly and in combination in a
later chapter. Suffice it to say for the moment, that a study carried out by Fred
Scogin and his colleagues on a sample of older depressed people showed that
reading either of these books over a period of a month was related to decreases
in depression measures.17
Most of the participants in the study seemed motivated by the task; they
reported that they read nearly the entire book assigned to them. While noting
the possible benefits of bibliotherapy for depression, the researchers commented
that asking people to engage in bibliotherapy on their own (without the backup
of trained people) could present both ethical and practical problems.
The potential problems that might ensue by leaving people on their own
without the backup of a trained professional has not deterred researchers from
developing programmed instruction to help people cope with their depres-
sions. These programs offer computerized versions of cognitive-behavioral
therapy. An example of these programs is mood GYM, developed by Australian

researchers Kathleen Griffiths and Helen Christensen.18 The program has been
well studied and evaluated and is currently available on the Internet
(http://moodgym.anu.edu.au) without cost or restriction. Providing an auto-
mated form of cognitive-behavioral therapy, the program has been used both
by interested individuals and in Australian schools under the supervision of a
teacher. Mood GYM uses five modules and a workbook that contains a series
of exercises. The program teaches such skills as cognitive restructuring and
assertiveness and self-esteem training. The authors point out the program could
be particularly useful in rural areas where there is a scarcity of trained psy-
chotherapists.
What can one expect from bibliotherapy? If you read pamphlets or books
which emphasize information, you will probably become a lot more knowledge-
able about depression, although this may not translate directly into your feel-
ing less depressed.19 A recent study carried out in Germany, however, did suggest
that knowledge about depression might help lessen the chances of recurrence
of the disorder, so this is still an open question.20 The computer programs which
try to influence perceptions and behaviors which promote depression seem
more likely to have a direct impact on depressive symptoms. A review of eval-
uation studies conducted on several of these programs concluded that they were
helpful.21 There is a caveat, however. The user must take the task seriously, fol-
lowing through on the tasks presented. A dilettante approach to using these
programs is likely to yield little or nothing in the way of benefits. Also, one
must keep in mind the possibility of problems arising, if one proceeds on this
task, alone, and without any knowledgeable backup.
Maintaining a Good Balance in Your Life

We have discussed adding more pleasant experiences in your life and
increasing your social activities. These steps are likely to have an antidepres-
sant effect. Implicit in this advice is the notion that all of us have a kind of opti-
mal balance point in our lives— a balance between our various needs— whether
the needs be for love and affection, for being with friends, for creative activi-
ties, to work on a job, to spend time with children, to exercise, or to spend quiet
time alone or in religious observances. Each person’s balance of activities is dif-
ferent, depending on how strong one’s needs are in different areas. Regardless
of the nature of our activities, it is important to try to maintain our different
activities at levels that keep us reasonably close to our optimal balance.
Putting all one’s eggs into a single basket and letting everything else go is
a recipe for emotional distress for many people. If you live for your work or
for that passionate love affair, you are putting yourself at risk if something goes
wrong. Ask yourself, “If things go badly, what will you have left?” If you take
some pains to keep a balance of meaningful activities in your life, you should
have a cushion if disappointments happen in one area of your life, a cushion
that will help sustain you while you try to fix the things that have gone wrong.
Maintaining a balance in activities helps keep good things happening in
life and guards against developing a victim or martyr mentality, which may hap-
pen when one is consumed by a single, overriding role in life. When there is
more in your life that is gratifying, the chances of experiencing overwhelming
disappointment and depression are less. So, set a proper balance for your activ-
ities and try not to get too far away from it. If you find yourself becoming too
one-sided in your behavior, take steps to bring yourself back to the balance of
activities that works best for you.
To briefly recapitulate, the self-help plan I have outlined consists of a
number of interrelated ideas. These ideas include (1) setting reasonable but
satisfying goals, (2) examining the pattern of your daily activities to identify
sources of satisfaction and stress-provoking situations, (3) recognizing mal-
adaptive thought patterns which promote problems, and changing these to pat-
terns that promote more positive emotional health, (4) making changes in your
life to increase your level of satisfaction, and (5) creating a more optimal bal-
ance among your daily activities.
The types of actions I propose are drawn from research and clinical expe-
rience and are not unique to this writer. Similar ideas for ways of better han-
dling the pressures of daily life have been advanced by other writers. For
example, an article by Donald Jewell and Maureen Mylander is very much along
these lines.22
What I am suggesting represents movement toward a more problem solv-
ing approach to life. Remember that people who become depressed often react
in dysfunctional ways, such as catastrophizing situations. These dysfunctional
responses can be steps on the path to depression. A path away from depression
requires a different approach, beginning with a careful examination of what
has gotten you into trouble and then taking steps to move in new and more
constructive directions.
Dr. Arthur Nezu and his colleagues used a problem solving approach in
successfully treating depressed patients. They believed, as I do, that it is impor-
tant to help depressed individuals identify the situations that are causing, or
have caused, stress in their lives and to increase the patient’s effectiveness in
coping with these situations. They developed an interesting program that
teaches problem solving skills to patients to help them deal more effectively with
future problems. 23
James Mahalik and Dennis Kivlighan raised the interesting question of
what sorts of persons are likely to profit from using self-help manuals for
depression. They carried out a study on mildly depressed students using a self-
help manual that laid out a seven-week therapeutic program. The researchers
also gave the students personality tests. The investigators found that persons
who were “realistic types” seemed to benefit more from the program. The
researchers also suggested that persons, “who persevere in situations that are
challenging and require effort succeed in self-help programs that ask its user
to go it alone.”24
Having said this, there is generally little reason for people to try to work
their way through a depression on their own. Support groups for people with
depression are widely available as well as professional help. The self help strate-
gies that we have described here may well work better in the context of this
support.
9. Some Counsel for the
Family and Friends of
a Depressed Person
In earlier chapters, I discussed how family and friends can be the sources
of stress that trigger a depressive reaction. Paradoxically, we also saw how fam-
ily and friends can be a buffer, helping to shield a vulnerable person from expe-
riencing a depressive reaction. Let’s see if we can unravel this seeming
contradiction.
Difficulties in interpersonal relationships are among the more significant
stressors that we encounter. These stressors may arise in a parent-child rela-
tionship where the child suffers at the hands of an unaffectionate, neglectful or
abusive parent. Sometimes, the shoe may be on the other foot. Consider the
stresses generated in parents whose teenage children become involved in drugs
or delinquency. The stresses of romantic love with its passions, disappoint-
ments and breakups sometimes are overwhelming. The stresses of a bad mar-
riage can lead to an emotional debacle for both parties.
When relationships are destructive, they are part of the problem in depres-
sion. When they are not, they are part of the solution. Fortunately, most of us
have relationships that have a lot of good in them. We are not talking about
perfect relationships; we are talking about relationships where there are posi-
tive bonds, and whatever difficulties exist are manageable. Perhaps the critical
factors are a feeling of belongingness —a feeling that these are my people — and
a sense of support —a sense of assurance that they are here for me in times of
trouble.
The concept of bonds is basic to human security. Remember the attach-
ment that infants develop as a basis for beginning their explorations of the
unknown environments about them. The need to be related to others remains
with us in varying degrees for the rest of our days. People who have close, pos-
itive relationships tend to be happier and healthier. Married people are more
likely to live longer than single people. If good relationships are a prophylaxis
127
for depression, the question becomes, “How can we best utilize such relation-
ships to assist those who are vulnerable to depressive problems?” Or put very
simply, “How can family members or good friends help?”
The first key to being helpful is to understand. Understanding begins with
being knowledgeable about depression. Here is a brief checklist of some impor-
tant things to keep in mind about depression.
1. Remember the symptoms of depression. Understand the difference
between transitory depressed mood and depressive disorder. If depressed
symptoms persist, there is a problem that needs attention.
2. Remember that there are different types of depression. While most
depressions are unipolar, some people have bipolar disorder. The
symptoms of bipolar disorder are different and the treatment is different.
3. Keep in mind that depression often has a genetic basis. Some people
have inherited vulnerabilities and are more likely to react with
depression than others. Remember that the mechanisms for depression
are in part biological, including disturbances in the action of the
neurotransmitters in the brain.
4. Remember that stressors often trigger depression.
5. Keep in mind that support from friends and loved ones is very good
medicine for depression.
Knowledge about depression is most useful when it is translated into alert-
ness that there is a problem in your family or with your friends and that some-
thing needs to be done. When you recognize very clear signs of depression in
persons close to you, it may prove helpful if you can find out what mental
health resources are available in your community so you can offer reasoned
advice when the opportunity seems appropriate. Find out about the availabil-
ity of psychiatrists, psychologists, clinical social workers, mental health clinics
and depression support groups.
When things are clearly going wrong, you can suggest going for a profes-
sional consultation, perhaps starting with the family doctor. If the troubled
person feels unsure, consider volunteering to go along with the person. The
important thing is that you do whatever you can reasonably do to ensure that
the person who needs help gets it. If you make a suggestion that someone should
consult a professional for a depressive problem, you may well run into resist-
ance. You may hear responses like, “I don’t need help,” or “Nobody can help
me, there’s nothing anyone can do.” These statements may reflect the confu-
sion, hopelessness and inertia that are part of the depressive problem.
One approach to dealing with such resistance is to first make it clear that
you recognize the pain and suffering that the person is going through and what
a difficult problem it is. Try to communicate the idea that, “I understand that
you’re going through a lot of distress and I want to help.” Then, you might state
that there are a variety of treatments available that are effective for most peo-
9. Some Counsel for the Family and Friends of a Depressed Person 129
ple who have depressive problems. Explain that there are different kinds of
medicines and short-term psychotherapies that have proven useful. One of
these treatments may help him or her feel better.
Alertness on your part as a member of the family or close friend should
extend beyond recognizing the need for outside help and suggesting that the
person seek it. When a person is severely depressed, alertness also means keep-
ing an eye open for potential signs of self-inflicted harm. The possibility of sui-
cide is a very troubling idea, but you must be aware of it. While no one can
predict with any certainty when a seriously depressed person might make a sui-
cidal attempt, there are a number of signs that suggest the possibility of one.
Here are three signs that are particularly worrisome.
1. The person expresses feelings of hopelessness. He or she sees the future
as bleak and sees, “no way out.”
2. The person talks openly about suicide. There may be statements like “I
can’t stand this pain anymore” or “I won’t be around.”
3. The person has made a previous suicide attempt.
The first sign suggests a state of thorough demoralization. Charles
Neuringer painted a portrait of such demoralization in describing a group of
women who threatened suicide after experiencing a personal crisis.
They felt life to be duller, emptier, and more boring than the other women did.
They also seemed less interested and responsive to people and to events than did
the other groups. They felt angrier than the other participants; they had less inter-
est in their work and were more dissatisfied with it than were the other women.
Their thought processes were experienced as slow and sluggish, which was not
true for the other participants. They felt that thinking was a great effort and that
their ideas were valueless .... The high-lethality women felt more anxious than
the others. They also felt more guilt-ridden and were less self-approving than the
other women. Their feelings of inadequacy and helplessness were greater than
those of the other participants. They also felt more depressed and weary than the
other women.1
No matter how careful family and friends try to be, there is always a chance
of self-inflicted tragedy. A survey of psychologists revealed that about one-
quarter of them had a patient who committed suicide while under their care.
The emotional effects of this tragedy on the psychologists were severe. The
effects on members of the family can be devastating.
As a general rule, it seems unfair to hold anyone responsible for another
person’s suicide. A therapist may see a patient for an hour or two a week. Mem-
bers of the family have a multitude of other responsibilities. It is virtually impos-
sible to prevent a suicide by someone who is determined to carry out the act,
unless the person is hospitalized and kept under 24-hour surveillance. The cru-
cial thing would be to know when to hospitalize, and we simply do not have
the scientific basis to allow us to know this with certainty.
If a patient exhibits signs of suicide, then family consultation with the
attending physician and/or therapist seems warranted. A decision by the patient

and the therapist for voluntary hospitalization may be in order. Hospitalization
would last until the crisis is over and the high risk of suicide has abated.
If there is a high risk of suicide and the patient is unwilling to be hospi-
talized, a very difficult situation emerges. The options are to live with a high
risk or to set into motion the coercive power of the state to hospitalize the
patient against his or her will. This can be a very unpleasant dilemma; it is not
only a wrenching emotional experience but places one in a briar patch of eth-
ical and legal thorns.
Maverick psychiatrist Thomas Szasz once suggested that it is questionable
for mental health professionals to get into the business of suicide prevention,
suggesting that, “Forcibly imposed interventions to prevent suicide deprive the
patient of liberty and dignity” and “the use of psychiatric coercion to prevent
suicide is at once impractical and immoral.”2
I think one has to recognize that the thought of suicide in depressed peo-
ple comes near the bottom of a psychological well, probably exacerbated by bio-
logical dysregulation. It is not a condition in which one expects to find rational
decision making. A few weeks of time and treatment may make the world look
very different to the patient. The argument for intervention is to allow this
change of attitude to happen.
Learning about depression and community mental health resources, and
becoming alert to signs of depression in those who are close to you are con-
structive steps to take in being of help to loved ones or friends who are expe-
riencing a depressive problem. Recognition of strains and stressors in the home
environment is another important area where family members may be partic-
ularly helpful. Try to become aware of any environmental problems and inter-
personal strains that are exacerbating the stress levels of the patient. If there
are chronic hassles in the home situation that are irritating the patient, can
something be done to defuse them? Stress-free environments are not reason-
able goals, but lowering levels of stress certainly are. If a member of the fam-
ily is doing something roughly equivalent to beating on a drum all day long,
maybe you can do something to stop it. A more peaceful environment may be
a good idea for everyone.
It may be a time to look inward, too. Is there anything you might be doing
that is exacerbating the problem, something that is causing stress for the patient.
Give it some thought. If there is, would it be possible to make some changes?
As a person who is concerned about depression in a friend or loved one,
you might have as one of your objectives to increase your sensitivity to the con-
cerns, thinking processes and feelings of the person. What this comes down to
in large part is better listening, paying attention to what is said and trying to
put yourself into the shoes of the other person so you can better understand
what is happening. When you do this, the other person will sense that you care
and you will have increased understanding of the problem.
In interactions with a depressed family member, The Depression and Bipo-

lar Support Alliance (DBSA) suggests that in times of crisis, not to take a loved
one’s actions or hurtful words personally or to use phrases like, “snap out of
it.” As a general guide, DBSA urges patience and respect for the patient’s bound-
aries.3
The emphasis on respecting the patient’s boundaries strikes me as partic-
ularly important because some studies have reported the counterintuitive
finding that a family’s social support can sometimes have a detrimental impact
on people recovering from depression.4 It is not clear why this is so. It may be
that an excess of interactions may lead the depressed person to feel he or she
is being forced back into situations and roles that in the past were difficult or
confining. I hesitate to use the term “smothering” because I have not seen the
evidence to support this idea, but I can well imagine that for some people recov-
ering from depression, too much attention might be as big a problem as too
little. In some situations, it can be a difficult judgment call for the patient’s
family, a delicate balancing act.
If the depressed person is undergoing psychotherapy, the spouse may be
asked to come in for one or more sessions. Many therapists like to do this, as
it enables them to see the patient’s behavior from another perspective. As fam-
ily problems and particularly marital conflicts can play a role in triggering
depressive episodes, it often makes good sense to try to deal with these prob-
lems as part of therapy. If these difficulties cannot be resolved to a reasonable
degree, the chances are high that there will be further episodes of depression
in the future. Interestingly, marital therapy itself, in which the focus is on both
parties, can sometimes be as effective in treating depression as therapy focused
on the depressed person.5
If it becomes clear in therapy that changes are needed in the patient’s
lifestyle, there may be an opportunity for you to participate in making these
changes. For example, exercise usually has antidepressive effects. How about
starting a walking or jogging program or some other exercise program on a reg-
ular basis with the patient? As we have emphasized, it should be exercise that
is approved by the family physician and something you both enjoy.
There may be a need to introduce more pleasant activities into the patient’s
life. When the time seems right, you can help in arranging that dinner out, that
ride in the countryside, that visit with friends or whatever the two of you feel
is fun and not too stressful. These activities should be paced into the recovery
process as part of a plan to establish a more balanced lifestyle.
As you do these things, it is important to recognize signs of resistance and
not to push too hard when you detect them. Go with what works and build on
successes. A little praise on your part when there has been progress may help
keep things moving along.
The behavior of depressed persons turns off many people; the sad expres-
sion, the tears, the stream of self-deprecatory comment, the pessimism and
hopelessness can be difficult to take. There will be times when you may be
tempted to throw in the towel and give up trying to help. Try not to do that.
Remember, most people who are depressed usually get better. Some people get
better even without medication or therapy. Moreover, drugs and psychother-
apy are both proven means of helping patients overcome episodes of depres-
sion. It is important to keep in mind that even when things look bleakest, the
odds for most people are that the symptoms will abate and the afflicted indi-
vidual will become a good deal better.
While not giving up is the marching order of the day, the spouse and chil-
dren of a depressed person may have to take steps to protect their own men-
tal health during the depressive episode. Living with a person who is depressed
can be very difficult. Studies of the families of depressed patients have found
that family members are likely to encounter a variety of difficulties stemming
from the depressive illness. Family members may experience restrictions in social
and recreational activities, a tightening of the family budget and interpersonal
strains.6 The patient’s spouse may not know how to cope with a husband or
wife who may be withdrawn and sad and sometimes says things which are
unkind. Many spouses worry about their husbands’ and wives’ conditions. Will
they get better? What will the future be like? Spouses may find their lives bur-
dened by having to take on extra responsibilities in the home and in child care.
And the children, themselves may shows signs of stress. They may become more
difficult, do less well in school or have problems sleeping. It can be a big load
for the spouse, and if the depressive episode is protracted, it is little wonder
that the spouses of depressed patients often develop emotional problems and
frequently show signs of depression, themselves. In carrying out research on
persons living with depressed individuals, James Coyne and his colleagues
observed, “Overall, 40 percent of the respondents living with a depressed per-
son in the midst of an episode were sufficiently distressed themselves to meet
the criterion for needing psychological intervention.”7 Subsequent studies have
confirmed the tendency for the spouse of depressed patients to develop depres-
sive symptoms.8 With this kind of risk, it is prudent for the spouse and chil-
dren to do things to protect themselves from being overwhelmed by the problem.
Some obvious suggestions are getting away from the house at times, and
doing things that the individuals enjoy. Perhaps it is spending time with friends,
going for a walk, or taking in a movie. The objectives are to keep one’s own
routines as normal as possible during the illness and to divert oneself from the
problem to keep it from reaching overwhelming proportions. You can’t help
the distressed member of the family if you are going under yourself. Caretak-
ers need a safety valve too: few people are emotionally indestructible.
If there are young children in the family, the intact spouse has the respon-
sibility of insulating them from the more emotionally destructive effects of the
illness. It is not going to do the children any good to spend a lot of time with
a parent in the depths of a depressive episode. Try to find things for the chil-
dren to do when things are bad. Look for means of getting them out of harm’s
way. When the situation improves, the children can be helpful in the recovery.
Perfectionism and guilt are psychological factors that probably contributed
to the depression of the patient. Perfectionism and guilt are equally unlikely to
benefit the people caring for the patient. It may be helpful to know that at times,
the best of therapists make mistakes in their conversations with their patients.
They may wish that they had picked up on something the patient had said or
responded to the patient somewhat differently. The patient’s spouse or care-
giver is facing a difficult situation. Trying to be sensitive and patient are impor-
tant virtues here. But having unrealistic expectations about one’s own behavior
and feeling guilty about coming up short is not going to help one’s self or the
depressed patient. It is a case where the old cliché of trying to do the best one
can fits very well.
10. Seeking Professional Help:
Changing Patterns
I would like to begin this chapter by telling again a story I related in the
first edition of this book. The story was a brief account of how a man, Jack,
experiencing what was eventually diagnosed as major depressive disorder, found
his way into treatment for the disorder.
When Jack’s wife, Erica began to notice his symptoms, she didn’t know
what to make of them. Jack had trouble falling asleep at night. When Erica
awoke at night, she saw him lying there wide awake. Sometimes he would get
up and pace the floor. In the morning there were circles under his eyes; he
looked exhausted. Jack used to be a big eater, but now his appetite had dwin-
dled. Breakfast was no more than coffee and it seemed that he hardly touched
his dinner. Jack looked sad and at times he brooded. He complained of
headaches and stomach cramps. He said he had no energy to do anything and
worse, he didn’t seem interested in doing anything. They used to go bowling
every Friday night and visit her mother on Sunday. Now he didn’t want to do
either. And his interest in her sexually had almost disappeared.
Erica knew something was wrong, but didn’t know what it was or what to
do about it. She confided in her sister Robin, who suggested that Jack see a doc-
tor. When Erica broached the idea to Jack, he resisted it, but she kept at it and
finally Jack consulted his physician, Dr. Sutherland. Dr. Sutherland was in the
midst of a very busy day. He listened to Jack for a few minutes and thought
Jack sounded like a “croc,” a patient with lots of complaints without any phys-
ical basis for them. Dr. Sutherland ordered some routine lab tests. When all
tests proved negative, he suggested that Jack take a few days off from work and
see if he felt better. In his brief examination, Dr. Sutherland did not identify
the problem for what it was: depression.
Jack’s short vacation helped only a little. When he began to have difficul-
ties on his job and wanted more time off, Jack spoke to the counselor in the
personnel office at work. She talked with Jack several times, and then recom-
mended that he consult a therapist. She gave him the names of a psychiatrist
and a psychologist who had worked with other employees in the company who
134
¡0. Seeking Professional Help 135
had emotional problems. Jack was able to get an early appointment with the
psychologist. When Jack began therapy he became one of some ten million peo-
ple who made a visit that year for professional mental health care.
Jack’s story took place some time ago. Things have changed since then, and
continue to change. Let’s pose some questions about the changing patterns of
professional care for mental and emotional disorders.
1. You can see that there was a delay between the time Jack first developed
symptoms and the time he began to receive treatment for his depressive
disorder. Are such delays still common today?
In a recent large-scale interview study, it was found that most people with
psychiatric disorders will eventually receive treatment, but delays, sometimes
very long delays are not uncommon.1 People with depressive disorders are more
likely to enter treatment sooner than people with anxiety disorders, impulse-
control disorders, or substance abuse disorders, but delays in receiving treat-
ment for depression sometimes extend into years rather than weeks or months.
2. Are physicians still the gatekeepers for treatment of depressive disorders?
Yes. While Jack saw his family doctor first, and without success, for many
people, perhaps a majority, their primary care physicians facilitates the begin-
ning of treatment for mental and emotional disorders. Not only is the physi-
cian’s office frequently the entry point for beginning treatment for mood
disorders such as depression, the family doctor is frequently the sole provider
of treatment. With the rising acceptance of antidepressant drugs, there has been
an increasing likelihood that the primary care physician will be the only pro-
fessional to work with the patient. Recent data suggest that the practice of pri-
mary-care physicians treating depression on their own using antidepressant
medicines— without referring the patient to a mental health specialist is the
most frequent way that depression is treated in America today.2 It should be
stated that such physicians are more likely to treat cases of depression on their
own which are less severe.
3. Are primary-care physicians more likely today to recognize and identify
depression than they were in Dr. Sutherland’s day?
Very likely. There has been considerable education about mental health
issues for physicians. One study suggested that primary care physicians iden-
tify about two out of three cases of major depression which isn’t bad, although
this leaves a very large number of people who are missed and may go untreated.3
The primary care physician is probably more likely to miss the case that is less
overtly symptomatic. It is obviously important for the primary care physician
to take the time to engage the patient about what is happening in his or her
life, if the physician is going to go be able to pick up on less severe depressive
symptoms.
4. Do primary care physicians experience roadblocks when they want to refer

patients to mental-health specialists?
A recent study reported that this is often the case.4 Interestingly, pediatri-
cians seem more likely to experience problems in making referrals for their
young patients to mental health specialists than primary care physicians who
work with older patients.
5. How do primary care physicians and mental health specialists differ in terms
of their treatment of depression?
When compared to the time spent with a mental health specialist, the time
spent in visits to a primary-care physician for depression is likely to be brief.
This difference reflects the fact that mental health specialists schedule extended
times (typically, fifty minutes) for their patients while visits to primary care
physicians are often considerably shorter. In addition, the primary care physi-
cian relies primarily on medications, and is usually not trained to do psy-
chotherapy.
6. As Jack eventually did, can a person who is feeling depressed go to a mental
health specialist without referral from a primary care physician?
Usually yes, unless the patient has a medical insurance plan that disallows
this. If the individual is in an HMO, he or she may experience difficulties in
going to a therapist who is not affiliated with the HMO. Interestingly, the use
of psychotherapy alone, without medication has been in decline since the 1990s.5
In contrast, the use of psychotherapy in conjunction with antidepressant drugs
has been on the rise. This is true whether the therapist is a psychiatrist who
prescribes the drug or a psychologist or clinical social worker who provides ther-
apy while the family physician typically writes a prescription for antidepres-
sant drugs.
Research suggests that, overall, most people in the United States today
who have a mental or emotional disorder are not receiving treatment for the
disorder.6 The situation is probably better for depression because antidepres-
sant medicines have won wide public acceptance and are now routinely dis-
pensed by primary care physicians. Researchers, however, have questioned the
adequacy of treatment of depression solely by the primary care physician sug-
gesting that it falls short of what is needed.7 In particular, for people who are
seriously depressed, antidepressant drugs may not be enough. In this context,
it is useful to recall the studies linking stress to depression which found that
this link weakens over time as the depression reoccurs and the depression tends
to occur without stressor-triggers.8 The inference from these data is that it is
important to treat depression thoroughly the first time its surfaces in the hope
that this may help prevent recurrences. For many depressed patients, thorough
treatment of depression may require more than antidepressant medicines. It
may require the insights provided by psychotherapy.
¡0. Seeking Professional Help 137
Let’s consider some of the typical barriers that people may encounter
which can reduce the chances of their receiving fully effective treatment for
depression. First and often foremost is the cost of treatment. Psychotherapy is
expensive. Insurance plans may limit the number of treatment sessions that the
patient may receive and many patients may need more than the stipulated num-
ber of visits to adequately address their problems. In addition, a very large
number of Americans, perhaps 45 million have no health insurance at all. Peo-
ple who cannot afford to pay for psychotherapy or for that matter repeated vis-
its to a primary care physician may not receive anything close to adequate
treatment for their depressive disorder.
The belief that mental and emotional disorders carry with them a stigma
has not disappeared from American culture. While this perception is not as
strong and widespread as it was years ago, even today many people would not
want it known that they are seeing a psychiatrist or a psychologist. In a recent
study, a majority of the people surveyed reported that they would still feel at
least somewhat embarrassed if other people found out that they were seeking
help from a mental health professional.9 Holding a stigma-related view of men-
tal illness or feeling that others may hold this view would engender reluctance
to seek help.
The availability of a competent mental health professional varies from
place to place. People who live in urban areas often have a substantial number
of mental health professionals to choose from. However, those who live in small
towns or rural areas may not have anyone available who could offer such serv-
ices. Interestingly, research suggests that people experiencing depression who
live in rural areas are more likely to find themselves hospitalized for the dis-
order.10
Finally there are cultural factors. The acceptability of seeking professional
help for mental and emotional illnesses varies somewhat within the many eth-
nic strands that make up American society. The studies of David and Stanley
Sue, for example, suggested that the stigma associated with mental illness may
run higher among Asian Americans then among their Anglo counterparts.11 Be
it cultural factors or economic factors, or both, professional mental health serv-
ices are underutilized by both African-Americans and Hispanic Americans.
Among African-Americans, this is particularly true for the very young and eld-
erly.12
The good news is that despite such barriers, increasing numbers of Amer-
icans are receiving treatment for mental and emotional disorders and this
includes depression.13 While many people who need treatment for depression
still find themselves outside the system of professional care, the trend is in the
right direction.
It is now time to turn to a detailed examination of the treatments now
being offered by primary care physicians and mental health professionals for
depression. We will begin with antidepressant medications.
11. Antidepressant Drugs
Antidepressant medicines are the most widely used treatment, today, for
depression. Many millions of prescriptions are written for these drugs each
year both in the United States and abroad. For many people antidepressant
medicines are the only treatment they will receive for their depressive disor-
der. Other people will use these drugs in combination with psychotherapy.
Antidepressants work well for many depressed people but not for many oth-
ers. Important as these drugs are for the treatment of depression, they are not
a cure for the disorder and at present are far from an invariantly successful
treatment for controlling depressive symptoms.
A few preliminary words about our discussion of antidepressant drugs.
We will not attempt to offer an exhaustive review of all antidepressant drugs
currently on the market, complete with details of the chemistry involved, warn-
ings about all known drug interactions and a complete list of possible side
effects. There are a number of excellent references, such as the Physician’s Desk
Reference available in many public libraries which can provide detailed infor-
mation about individual antidepressant drugs for those who are currently using
them or are considering using them. In addition the National Library of Med-
icine’s Medline Plus available on the Internet presents very readable concise
information for users of specific drugs.
What we shall try to do here is to provide an overview of what antidepres-
sant drugs are all about. We will describe something of the history of how anti-
depressant drugs were discovered, their presumed mechanisms of action, their
efficacy in the treatment of depression, and some cautions about their use.
The discovery that certain drugs may have antidepressant effects has a his-
tory of about 50 years. If there is a bottom-line to the story of these drugs, it
is that they are not magic bullets. They do not work with the effectiveness of
an antibiotic clearing up a bacterial infection. Antidepressant drugs do not
cure depression. For many, if not most users, they will probably not eliminate
all of the symptoms of depression, and if they do, the effects may not be per-
manent. Having said this, they can alleviate the symptoms of depression for
perhaps half, or somewhat more than that of the people taking them (depend-
ing on the studies you look at) and can bring about a remission of symptoms
138
¡¡. Antidepressant Drugs 139
in perhaps a quarter of the users.1 So, while antidepressant drugs can make an
important difference for many depressed patients, they may be of little help for
many others.
As a generalization, antidepressant drugs do not vary that much from one
to the other in terms of their efficacy in treating depression. In clinical trials
comparing antidepressant drugs, one drug is likely to be about as effective as
another in relieving depressive symptoms and all of these drugs are likely to
show some advantage when compared with a placebo— pills that look like real
medicine but contain no active antidepressant ingredients. Interestingly, there
have been studies in which antidepressant drugs have not performed better
than placebos, but these trials are unlikely to be reported.2
While antidepressant medicines do not differ appreciably in their efficacy
when compared in sizeable groups of research subjects, some antidepressant
medicines are better tolerated than others. They have fewer side effects and
hence are easier to live with over extended periods of time. In addition, it is
always possible that one type of antidepressant drug might work better for a
given individual than another. Switching antidepressants in the hope of achiev-
ing better results is not uncommon and research suggests that this can be an
effective strategy for many patients.3 Increasing the dose is another common
strategy when no results are obtained. Combining certain antidepressant has
also been tried. If none of the above strategies appear promising, then psy-
chotherapy is the best alternative for mild to moderately depressed people. For
severely depressed people, hospitalization may be required, and if both med-
ication and psychotherapy fail, electroconvulsive therapy remains a viable
option.
The Tricyclics
My description of the discovery of antidepressant drugs is based largely
on David Healy’s excellent book The Antidepressant Era. Judging from Healy’s
account, the discovery of the first class of antidepressant drugs that entered
widespread public use, the tricyclics, was something of a helter-skelter process.
After the discovery of the antipsychotic drug, chlorpromazine in 1952, there
was renewed interest in looking at the possible uses for other chemically sim-
ilar compounds. One of these compounds, iminodibenzye, synthesized way
back in 1898 and subsequently discarded because there were no apparent uses
for it was, so to speak, gathering dust in the basement of the pharmaceutical
company, Geigy. In the 1950s it was resurrected for study, but once again no
immediate uses were uncovered. The drug was tried on schizophrenic patients.
However the effects, if anything, seemed to be adverse. Interestingly, some of
the patients given the drug appeared to develop a form of mania. Healy describes
how when one of the patients given the drug escaped from a hospital and rode
into town on a bicycle in his nightshirt, singing loudly, trial of the drug on schiz-
ophrenics was discontinued.
This experience, however, led to the idea that the drug could have an ele-
vating effect on mood. Accordingly, the drug was tried out on 40 depressed
patients. For some of the patients the positive effects on mood were dramatic.
One of the central figures in the discovery of the antidepressant effects of
the drug which was given the name imipramine was a Swiss born psychiatrist
named Roland Kuhn. Kuhn gave the drug to several hundred patients and
found that for many patients imipramine not only elevated the patients’ moods,
it had positive effects on their activities and social interactions. The drug also
had positive effects on the patients’ sleep and appetite. Kuhn described his
findings at a meeting in 1958 and his work was reported in an issue of the Amer-
ican Journal of Psychiatry. The drug was marketed under the brand name
Tofranil.
Imipramine is a tricyclic, so named because of its molecular structure
which includes three rings of atoms. Tricyclics are believed to be effective in
relieving depressive symptoms because they inhibit the reuptake of the neuro-
transmitters, norephinepherine and serotonin.4 Following the release of
imipramine, a number of different tricyclics were offered by the pharmaceuti-
cal industry to the public. Some examples are amitriptyline, desipramine, nor-
triptyline, doxepin, protriptyline, and dothiepin. These drugs were effective
in relieving depressive symptoms in many depressed patients.
Here is an example of an early study that investigated the efficacy of the
initial antidepressant marketed, imipramine.5 A research team led by James
Kocsis wanted to evaluate the effectiveness of this drug in treating depression.
For their study they recruited subjects from among adults who sought outpa-
tient treatment for depression at two medical centers, one in New York, the
other in Maine. The subjects were screened by psychiatrists to make sure they
met the currently established criteria for chronic unipolar depression and had
not been on antidepressant medications during the preceding six months.
All patients who were accepted into the study were given placebo tablets
for two weeks. These tablets had the same appearance as the imipramine tablets
but had no therapeutic action. At the end of two weeks, the patients were ran-
domly assigned either to continue with the placebo or to receive imipramine.
In a “double blind” design, neither the patients nor the evaluating psychiatrists
knew who had been given the medication and who had been given the placebo.
After six weeks, the patients were reevaluated. The patients who showed
a substantial improvement in their depressive symptoms were called “respon-
ders.” The patients who did not were called “nonresponders.” The results: 59
percent of the patients given imipramine and 13 percent of the patients given
the placebo were characterized as responders. The study indicated that
imipramine can be an effective antidepressant with many patients, though
clearly not with all.
The tricyclics have now been well researched. The statistics for efficacy of
the tricyclics vary somewhat according to the criteria used in the clinical tri-
als. Some researchers looked at stipulated decreases in scores on the Hamilton
rating scale, an observer-based assessment of depression while other researchers
used the more stringent criteria, the absence of depressive symptoms— true
remission. One would not expect the drugs to show as well using the latter cri-
terion. A review of studies conducted on tricyclics and other antidepressant
drugs published in 1999 indicated that about 58 percent of the patients were
improved, which is similar to the figure reported by Kocsis and his collegues.6
The Trouble with Tricyclics

Tricyclics helped many people who were experiencing depression, but the
medications were far from being a magic bullet for the disorder. First, tricyclics
did not work for large numbers of people. Second, there is a time lag between
first use of the medicine and benefits from taking the drug. It might be a week
or as much as a month or even more before the medicine becomes fully effec-
tive. For people with mild to moderate depression, this time lag might present
little problem. However, for people who are severely depressed, particularly
those who are suicidal, weeks of waiting for effective treatment could entail real
risks.
The third issue was adverse effects (side effects) from taking the drugs.
Most drugs have adverse effects, some occurring infrequently, even rarely, oth-
ers occurring all too often.
Here are some of the more common side effects of tricycles; dry mouth;
blurred vision; constipation; and difficulties with urination.
And there is a long list of less frequent side effects. These include drowsi-
ness, confusion, dizziness, increased heart rate, sexual dysfunction, increased
appetite with weight gain, sweating, weakness, nausea, and muscle twitches.
For some people, these uncomfortable side effects proved too much of a bur-
den and they simply discontinued the medicine.
Tricyclics have the potential for overdose. The dose needed to obtain a
therapeutic effect is fairly close to what can be a toxic dose. Overdosing on
these antidepressant drugs was not uncommon. A report in the Emergency Med-
icine Journal noted that overdoses of tricyclic antidepressants are among the
most frequent causes of drug poisoning observed in emergency rooms.7
Monoamine Oxidase Ihibitors

The second class of antidepressant drugs, monoamine oxidase inhibitors
(MAOIs) were developed and marketed in the same general time frame as the
tricyclics. As was the case for the tricyclics, the researchers investigating the use
of these drugs were not initially looking for an antidepressant. The discovery
of the antidepressant effects of these drugs was largely serendipitous.
In his book, Healy traces the discovery of the MAOIs to basic research car-
ried out in England in the late 1920s and early 1930s. Researchers at Cambridge
University and other sites discovered an enzyme that was named monoamine
oxidase (MAO) that could break down chemicals used in the body now recog-
nized as neurotransmitters. These chemicals included epinephrine, norepi-
nephrine, dopamine and serotonin
This basic research was followed years later by discoveries made by
researchers working in the Hoffman-la-Roche laboratories in New Jersey. These
researchers synthesized a chemical called iproniazid which had the very inter-
esting property of inhibiting the breakdown of these neurotransmitters.
Based on previous research with tuberculosis drugs, this new drug looked
as if it might be useful in the treatment of tuberculosis. Accordingly, the drug
was given to TB patients to see if it might be useful in healing tuberculosis
lesions. What the researchers found that while the drug did have possible use-
fulness in treating tuberculosis, it also had the effect of elevating the patient’s
mood and behavior. It looked as if the drug might be an antidepressant.
Studies of the drug were carried out in France and in America. The research
of Nate Kline, a professor of psychiatry at Columbia University who also
directed the research facility at Rockland State Hospital led him to conclude
that use of the drug was associated with remarkable improvements in psychi-
atric patients. Kline played a pivotal role in bringing the antidepressant effects
of MAOIs to public awareness.
MAOIs are believed to impact depression by inhibiting the activity of
monoamine oxidase, thus preventing the breakdown of neurotransmitters such
as serotonin and norepinephrine. The use of MAOIs would leave more of these
neurotransmitters available in the synapses between neurons.
A number of MAOIs have now been developed. These drugs differ in their
selectivity of action. For example, one of the newer drugs, moclobemide is more
likely to target the form of monoamine oxidase that depletes serotonin.
MAOIs currently approved for the treatment of depression are isocarbox-
azid, phenelzine, selegiline, and tranylcypromine.
The Trouble with MAOIs

If there are problems with tricyclics, there are still bigger problems with
the MAOIs. As a starting point, there is a long list of possible side effects that
might occur from the use of these drugs. A Mayo Clinic Internet posting on
MAOIs listed a total of 23 possible side effects. However, side effects are just
the beginning of the story. The biggest concern for many people using MAOIs
are possible drug interactions, not only with other medicines but with certain
foods that they might be accustomed to eating. The users of MAOIs should be
very careful what they eat. Eating restricted foods while using MAOIs can pre-
cipitate a sharp rise in blood pressure (a hypertensive crisis) that could lead to
a stroke.
Here is a partial list of foods that should be avoided entirely or restricted
in amounts when using MAOIs: Aged cheeses, beer, caffeine in excessive quan-
tities, certain kinds of beans, liver, pickled foods, yeast extracts, and wines.
People using MAOIs should consult with their physicians to be certain that they
are fully aware of what foods and drinks they should avoid completely and
what foods and drinks they should restrict in quantity. Accurate information
is the first line of defense.
Among the medications one should avoid while using MAOIs are over-
the-counter decongestants, other antidepressants, and the herbal, St. John’s
wort. It is always a good idea for MAOIs users to check with their physician or
pharmacist before using any new prescribed or over-the-counter medicine.
Here is some good news for people using MAOIs. The Food and Drug
Administration has approved a new means of administering the MAOI, Selegi-
line (trade name Emsam).8 Instead of using a pill, the drug is absorbed through
the skin into the bloodstream by means of a three layered transdermal patch.
Using the patch rather than the pill reduces the risks of the drug interacting
with food. The FDA notes that for the lowest dose of the drug (6 mg for 24
hours), the drug can be used without the usual dietary restrictions for MAOIs.
Currently, the FDA advises patients who require higher doses of the drug to
continue to observe the usual dietary restraints. The cautions for interactions
with other drugs were not altered in the FDA release. The FDA noted that using
the patch may produce some redness on the skin.
Studies suggest that the MAOIs, phenelzine and tranylcypromine are par-
ticularly effective in the treatment of atypical depression — depression that is
characterized by such behaviors as oversleeping and overeating.9
Selective Serotonin Reuptake Inhibitors

When the antidepressant properties of the tricyclics and MAOIs were first
uncovered, there was some skepticism expressed in the pharmaceutical com-
panies developing these drugs that there really was a sizeable market for anti-
depressant drugs. Whatever remained of such skepticism must have vanished
like a puff of smoke into a bright blue sky when the selective serotonin uptake
inhibitor fluoxetine was released. Marketed under the brand name Prozac, the
drug skyrocketed into public awareness. The name Prozac became part of every-
day language.
Prozac was licensed in the United States in 1987. However, it was not the
first of the SSSRIs to be marketed. I believe that the honor belongs to Fluvox-
amine (trade name Luvox), marketed by Luvox-Faverin in Europe in 1983. Still,
it was Prozac developed by David Wong and his colleagues at Eli Lily that got
the ink. Peter Kramer’s best-selling book Listening to Prozac and an appearance
of the drug on the cover of Newsweek help make Prozac part of the popular
culture.
After the success of Prozac, a number of other SSRIs were developed and
approved by the Food and Drug Administration. The list includes citalopram
(e.g., trade name Celexa), escitalopram (e.g., trade name Lexapro), paroxetine
(e.g., trade name, Paxil) and sertraline (e.g., trade name, Zoloft). Why the pop-
ularity of the SSRIs? Was it simply a matter of media hype or were these drugs
actually more efficacious and better tolerated than the tricyclics?
A meta-analysis of randomized controlled trials involving over 10,000
patients found no overall difference in the effectiveness of the two classes of
drugs. And if anything, the studies suggested that the tricycles were more effec-
tive for hospitalized, presumably more seriously depressed patients.10
For an illustrative study investigating the efficacy of SSRIs, consider this
study of the SSRI, citalopram. Over two thousand outpatients in both psychi-
atric and primary care settings were given the drug. After using the drug for
approximately eight weeks, the researchers reported a response rate of 49 per-
cent, with remission rates of about half that.11
Based on such reports, the edge for the SSRIs over the tricyclics is not
efficacy. Rather, it is that for many people, they are better tolerated than
the tricyclics. The reports of adverse affects in the randomized controlled
trials are not as high as for the tricyclics, and people using these drugs are
less likely to discontinue use of the drug than is the case for the tricyclics.12
The same patterns have been reported for patients seen by primary care physi-
cians.13
Does this mean that SSRIs are free from side effects? No. Far from it. The
use of SSRIs are linked to a number of complaints such as nausea, drowsiness,
insomnia and anxiety.
Many of the antidepressant drugs can have adverse effects on sexual desire,
performance, and satisfaction. Among the antidepressant drugs, the SSRIs prob-
ably have the most notorious reputation for engendering these effects. While
the statistics vary somewhat from study to study, the frequency with which
these effects are reported tend to be uncomfortably high. A study carried out
in the United States on men and women questioned in primary care clinics
found that adverse effects for sexual behavior were reported by about 40 per-
cent of those using SSRIs. The figures for a similar study carried out in Spain
were even higher, in the 60 percent range.14 For a great many people sex is a
very big part of life, so these side effects can be a big problem. Many of the peo-
ple questioned in the study carried out in Spain said as much.
Some cautionary notes about the use of SSRIs.
1. SSRIs have been linked to reports of suicidal thinking in children and

adolescents. Although it is not yet clear that SSRIs actually cause suicidal
thinking in children, as a precautionary note the Food and Drug
Administration has ordered warning boxes on SSRIs informing people
about this possibility.15
2. The use of SSRIs during pregnancy remains somewhat controversial.
These drugs can cross the placenta and have the potential to affect the
developing child. Some recent studies, however, have reported that using
SSRIs during pregnancy did not lead to an increase in major deformities
in the baby.16
3. One of the rare effects of SSRIs is to cause bleeding. People who have a
bleeding disorder should notify their physicians before taking these
antidepressant medications.17
4. When discontinuing an SSRI, it is important to check with your
prescribing physician. Abrupt discontinuation of an SSRI can precipitate
a variety of unpleasant symptoms such as agitation and insomnia which
may persist for a few weeks or even longer.
Perhaps a summary statement for the SSRIs would be that they are effec-
tive in reducing depressive symptoms for many (roughly half, perhaps more,
once again depending on the studies one looks at) of the people who use them,
are better tolerated than the first generation of anti-depressants, the tricyclics,
have some adverse effects, particularly on sexual behaviors which for many
people can be a particularly significant problem.
The Newer Antidepressants

While serotonin has been the major target for antidepressant drug research,
the neurotransmitters norepinephrine and dopamine have always been good
secondary targets. And, indeed drugs which inhibit the reuptake of these neu-
rotraansmitters have been shown to be effective in treating depression. Bupro-
pion (trade name, e.g., Wellbutrin) which inhibits the reuptake of both
norepinephrine and dopamine is now in very wide use, with prescriptions num-
bering in the many millions. One of the biggest advantages of bupropion is that
it is far less likely to cause sexual dysfunction than the SSRIs. To treat sexual
dysfunction caused by other antidepressants, some physicians will substitute
bupropion for these drugs or simply add bupropion to the current antidepres-
sant.18
Serotonin, Norepinephrine Reuptake Inhibitors

Venlafaxine (brand name Effexor) and duloxetine (brand name Cymbalta)
are two of the drugs called SNRIs which act to inhibit the reptake of both nor-
epinephrine and serotonin. Duloxetine has only recently been approved by the
Food and Drug Administration (2004) so there is less experience for the use of
the drug in everyday clinical practice than for the SSRIs. In our comments
about the SNRIs, it should be understood that these promising drugs are not
that far off the shelf, so our remarks will be tentative.
It is not yet clear how the SNRIs compare with the older SSRIs in terms
of efficacy. A meta-analysis suggested that the newer SNRIs may have an advan-
tage over both the SSRIs and the tricyclics.19 However, I have seen studies in
which venlafaxine was compared with an SSRI and the two drugs had about
the same effect on depression.20 A recent study found no difference in the efficacy
of Duloxetine and the SSRI escitalopram.21 Clearly, more research is needed to
establish whether these newer drugs are more efficacious than the earlier drugs.
Still, these drugs look interesting and could provide possible alternatives for
people not responding to SSRIs
Both drugs have a range of side effects. Duloxetine, for example, may cause
nausea, dizziness and tiredness. The discontinuation of either medicine pre-
cipitously could engender problems. Once again, consultation with one’s pre-
scribing physician is important.
Medicines for the Treatment of Bipolar Disorder

The pharmacological treatment for bipolar disorder is different from that
of unipolar depression. It is not a good idea to treat bipolar disorder with an
antidepressant alone, because the antidepressant when used alone may precip-
itate an episode of mania or hypomania (a less intense form of mania).
Mood stabilizers are used both to control acute episodes of mania and to
try to maintain more even mood over the long haul. Of the drugs used to sta-
bilize mood in bipolar illness, the first one that comes to mind is lithium.
Lithium is a popular name for the chemicals lithium carbonate and lithium cit-
rate. Lithium compounds are found in some rocks, in the sea and in sparse
quantities in the tissues of plants and animals. As a drug, lithium carbonate is
taken orally in the form of a capsule or tablet. Some trade names for lithium
carbonate are Eskalith, Lithane and Lithobid.
An Australian physician, John Cade, used lithium successfully as a treat-
ment for mania in the late 1940s, but his work was not fully exploited until many
years later. A major problem with lithium was that if the drug were used at too
high a dose, it could have very dangerous effects. When the problems relating
to drug safety were resolved, the drug was approved by the FDA for psychi-
atric use and is now in widespread use.
Lithium has been the most commonly used medicine for bipolar disorder.
The chemical can be effective in reducing manic episodes. The National Insti-
tute of Mental Health’s publication Medications for Mental Illness notes that
while lithium should have some effect within five to fourteen days, it may take
considerably longer than that, weeks or even months to fully control the symp-
toms.22
The response of people with bipolar disorder to lithium is variable. For
many people with bipolar disorder, lithium works very well in maintaining
stable mood; for many others, lithium is helpful but not fully effective in con-
trolling mood swings, and for still others, it may not be helpful at all.
Because the difference between an effective dose of lithium and one which
is toxic is not all that large, care must be taken that the patient remains on the
proper dose. Periodic blood tests are required to monitor the amount of lithium
in the blood. In addition to monitoring lithium levels in the blood, thyroid
functioning should be monitored as well.23
Lithium has its share of side effects. These include drowsiness, fatigue,
weakness, increased thirst, frequent urination, weight gain, and hand tremors.
Some of these symptoms may subside with continued use of the drug.
There are additional cautions the lithium user should be aware of. It is
important for lithium users to maintain an adequate level of sodium in their
blood. Reduced sodium levels can lead to a buildup of lithium in the blood
which can lead to toxicity. While most people get plenty of sodium in their
normal diets, this could be a concern for people who are using lithium and are
also using diuretics or are on restricted sodium diets as part of their treatment
for high blood pressure. Situations which could reduce sodium levels such as
engaging in vigorous exercise on a hot day, simply living in a hot climate, or
experiencing a bout of diarrhea which can be dehydrating pose potential risks
for lithium users. These contingencies should be discussed fully with the pre-
scribing physician.
In Medicines for Mental Illness, The National Institute of Mental Health
noted that, “Doctors either may not recommend lithium or may prescribe it
with caution when a person has thyroid, kidney, or heart disorders, epilepsy or
brain damage....”24 Lithium use by pregnant women could increase the risk of
congenital malformations in their babies.25
So, it should be clear that lithium is not one of those pills that one can
take casually and put out of mind. While lithium can help stabilize mood swings
and in so doing help people with bipolar disorder experience more normal
lives, it is a drug that requires both monitoring by the prescribing physician
and knowledge on the part of the user about possible problems.
Because of its unpleasant side effects or because of reasons such as the
patients’ feeling they don’t need the drug anymore, a large number of patients
stop using the drug. This could leave many bipolar disorder patients vulnera-
ble to the onset of mood swings. Fortunately, there are other useful drugs to
try.
The main alternatives to lithium for stabilizing mood are certain anticon-
vulsive drugs used to control seizures. Valproic acid (trade name, e.g.,
Depakote) is an anticonvulsant that has been widely used to control bipolar

disorder. In Medications for Mental Illness, the National Institute of Mental
Health noted that valproic acid is as effective as lithium in controlling the dis-
order and may be superior to lithium in controlling rapid cycling bipolar dis-
order.26 Adverse effects that sometimes happen from using the drug include
gastrointestinal symptoms, headache, double vision, dizziness, anxiety, and
confusion. As there is a possibility that the drug may cause liver dysfunction,
liver function tests should be carried out periodically to insure that this prob-
lem is not developing. The use of this drug by teenage girls and young women
could raise their testosterone levels which could lead to a variety of unpleas-
ant consequences including obesity and amenorrhea.27
A second anticonvulsive drug that appears to be effective in controlling
episodes of acute mania is lamotrigine (trade name, Lamictal). A third drug in
this class recently approved by the Food and Drug Administration for use with
bipolar patients is carbamazepine extended-release (trade name, Equerro).
If the use of a mood stabilizer, either lithium or an anticonvulsive proves
ineffective in controlling an episode of mania, there is another pharmacologi-
cal option to try: atypical antipsychotics. Several of these drugs have been
approved by the Food and Drug Administration for the treatment of bipolar
illness. These include olanzapine (trade name, Zyprexa) quetiapine (trade name
Seroquel), risperidone (trade name, Risperdal), aripiprazole (trade name, Abil-
ify), and ziprasidone (trade name, Geodon). Studies of the efficacy of atypical
antipsychotics (e.g., olanzapine, quetiapine) indicate that they are effective in
reducing manic symptoms.28
Possible side effects associated with the use of atypical antipsychotics
include weight gain, drowsiness, constipation, dry mouth, blurred vision, and
sexual dysfunction. And importantly, the Food and Drug Administration
requires all of these drugs to carry a warning label about possible risks for
hyperglycemia and diabetes.
So, the prescribing physician has a variety of drugs to select from that can
be effective in controlling manic episodes and or maintaining stable moods
over time. Finding the best combination of medications to control bipolar dis-
order is important and requires judicious selection, careful monitoring of the
patient, and sometimes switching medications.
As an illustration of the sometimes uncertain road one travels in finding
the right medicines, consider the case of Ben, a man in his mid–20s, living in
a large Midwestern city. Ben was diagnosed with Type I bipolar disorder. Ben
was 15 years old when he had his first episode of manic behavior. His manic
symptoms were so florid, bordering on psychotic that his parents decided to
hospitalize him. At the hospital he was put on three drugs, a mood stabilizer
(valproic acid), an atypical antipsychotic (risperidone), and an antidepressant
(fluoxetine). It took about 10 days for the symptoms to begin to abate. When
he was discharged from the hospital and returned home, he felt over-med-
icated, sluggish and occasionally showed symptoms of his disorder. In view of

his condition, his parents decided not to send him back to school; instead, they
arranged home schooling for him. During this time, he continued using the
three medications. His physician decided to switch him from the mood stabi-
lizer, valproic acid to lithium. Ben did not like being on lithium because of its
side effects and in time he discontinued all of his medications.
Ben was fortunate in that for a period of several years his bipolar symp-
toms went into remission and he was able to finish school. Later on, however,
he had renewed outbreaks of mania, and he was again put on medications. In
time, he tried the mood stabilizer, lamotrigine and the atypical antipsychotic
Aripiprazole. Ben found that he tolerated these medicines quite well and was
able to live a more normal life. He went to college and now holds a full-time
job.
Recent reviews of studies comparing the efficacy of some of the drugs used
to treat bipolar disorder (lithium, lamotrigine, valproate semisodium, olanza-
pine, quetiapine) in preventing relapse of symptoms, concluded that all of these
drugs were more effective in preventing relapse than a placebo.29 However, the
use of lithium was more likely to be followed by the patient discontinuing use
of the drug because of adverse effects.
As we end this chapter, I think it is fair to conclude that while antidepres-
sant drugs are not a panacea for the treatment of depression, they do represent
an important advance in the treatment of the disorder. This conclusion is sup-
ported not only by research, but by a vast amount of clinical experience in the
use of these drugs in everyday clinical practice. We should close, however, by
temporing this conclusion with a few additional words about the use of anti-
depressant drugs with two special populations— young children and adolescents
and pregnant women.
In regard to children and adolescents, there is evidence that the use of
antidepressant medications is associated with increased risk of suicidal think-
ing. The Food and Drug and Administration has issued a black box warning
that if young people are given antidepressants, they should be carefully moni-
tored for signs of worsening depression and possible suicide. This is an excel-
lent admonition, but at times it may be unrealistic. The burden of monitoring
the child or adolescent will usually fall largely on the parents. Circumstances
may render effective monitoring of their child very difficult, if not impossible.
The child may live in a single-parent home in which the resident parent has a
full time job. In many homes where there is a two parent family, both mother
and father may be working. And in the best case, monitoring the thoughts and
behavior of an adolescent can be difficult. Because of these difficulties and the
attendant risks that antidepressants pose for suicidal thinking, if there are alter-
native treatments for depression available such as psychotherapy, it makes sense
to consider these first.
What happens when a child or adolescent is taken to the family doctor is
judged to be depressed and there is no child psychologist available? A pedia-

trician related a story to me of such a case. He was faced with the dilemma of
accepting the risks of increasing the possibility of suicidal ideation by prescrib-
ing an antidepressant, or doing nothing which could also result in very seri-
ous consequences for the child. It was not a happy choice.
In regard to the use of antidepressant drugs during pregnancy, I would like
to pass on some advice offered by the National Institute of Mental Health in
the pamphlet Medicines for Mental Illness.“Because there is a risk of birth defects
with some psychotropic medications during early pregnancy, a woman who is
taking such medication and wishes to become pregnant should discuss her plans
with her doctor. In general, it is desirable to minimize or avoid the use of med-
ication during early pregnancy. If a woman on medication discovers that she is
pregnant, she should contact her doctor immediately. She and her doctor can
decide how best to handle her therapy during and following the pregnancy.”30
12. Psychotherapy
Antidepressant drugs have proved helpful for many people in dealing with
depressive problems. However, for some of these people, the side effects of the
drugs are quite uncomfortable. Moreover, there are many people who are not
helped appreciably by these drugs. Fortunately, there is an alternative approach
to the treatment of depression, which is drug free. This approach is psychother-
apy.
The evidence to date indicates that psychotherapy can be an effective treat-
ment for mild to moderate unipolar depression. There is, however, still some
controversy in regard to the effectiveness of psychotherapy for cases of severe
depression.
Drugs act to inhibit the reuptake of neurotransmitters to achieve their
effects. Psychotherapy has its impact on thoughts, feelings and behavior. Psy-
chotherapy can have significant effects on a person’s attitudes and lifestyle,
helping him or her better cope with the interpersonal and environmental stres-
sors that tend to trigger depression. The singular advantage of psychotherapy
is that it can teach the patient important things about himself or herself that
can be useful in making adaptive changes in perceptions and behaviors.
While almost all of us are familiar with medicines, many people have only
a vague idea of what psychotherapy is. One’s image of therapy may be some-
thing like the cartoon character of a bearded analyst holding a small notebook,
sitting behind a patient who is reclining on a couch, listening to the patient
talk at length about what is on his or her mind. While this picture may once
have been close to the mark, it is not typical today.
The poet Elizabeth Barrett Browning wrote a memorable sonnet that
began, “How do I love thee? Let me count the ways.” If she had counted as many
ways as there are ways of doing psychotherapy today, her brief sonnet would
have turned into a multipaged epic.
A few decades ago the choices in psychotherapy consisted of not much
more than several varieties of psychoanalysis and client-centered therapy devel-
oped by Carl Rogers. How the situation has changed! Let me quote from an
article by Alan Kazdin: “Although at any given time it is difficult to pinpoint
the precise number of techniques in use, surveys have revealed tremendous
151
growth. In the early 1960s, approximately 60 different types of psychotherapy

were identified. By the mid–1970s, more than 130 techniques were delineated....
By the late 1970s, growth continued to encompass more than 250 techniques
.... A more recent count has placed the number of existing techniques well over
400.1 While it has not yet reached the point where there are as many brands of
therapy as there are therapists, there is certainly a variety of approaches for a
therapist to use. Such diversity creates choices for people who are seeking help.
The situation, however, may be confusing.
Let me try to clarify this situation. First, it is important to recognize that
most therapies have significant elements in common. For example, most ther-
apists provide a supportive atmosphere for the patient: They are interested in
the patient and his or her well being. Also, the relationship that develops
between therapist and patient is important in almost all therapies. Moreover,
almost all therapies have an effect on the restoration of morale. The patients
usually experience a regeneration of hope. They become more enabled and
energized and can begin to do things for themselves, which has the effect of
rebuilding confidence.
Second, you will find that many therapists are not doctrinaire. They take
an eclectic position, picking out what seems to work best for their patients from
what is available in the different therapeutic techniques. Moreover, many ther-
apists continue their education after graduate or professional school, learning
new, innovative techniques. It may be helpful to briefly describe some of the
major approaches to therapy that are being used today to treat depression.
Three of the better known and most influential approaches are (1) psychody-
namic therapy, in which the focus is on intrapsychic conflicts, (2) cognitive-
behavioral therapy, which focuses on thought processes and behavior and (3)
interpersonal therapy, which focuses on human relationships.
Psychodynamic Therapy
Psychotherapy as we know it began with Freud and his invention of psy-
choanalysis. Psychoanalysis is both a complex theory about human personal-
ity and a technique for treating emotional disorders, particularly those disorders
that have been labeled as neuroses or neurotic behavior. Therapies that draw
heavily on Freud’s psychoanalytic theories are usually referred to as psychody-
namic therapies.
Psychodynamic therapies focus on conflicts within the person. Typically
these conflicts have their roots in childhood experiences, and often in parent-
child relationships. The roots of these conflicts are not usually accessible to the
patient. Much of the troubling material is believed to be out of the patient’s
awareness, or in Freud’s term, unconscious. In order to resolve the conflicts that
underlie the patient’s current symptoms, it is important in psychoanalytic ther-
¡2. Psychotherapy 153
apies to bring this material into the open. The analyst works with the patient
to bring these ideas to light and shows the patient how they relate to her or his
current problems.
In classical psychoanalysis, making what is unconscious known is accom-
plished by such techniques as free association and dream analysis. In free asso-
ciation, the patient speaks about whatever is on her or his mind, trying not to
hold back anything or to suppress any idea. The patient’s flow of ideas tends
to form links with unconscious materials. In dream analysis, free association
is used to work back from the dream content to the unconscious materials that
are believed to have given shape to the dream. In the procedure, the patient is
asked to freely associate to different parts of the dream.
During therapy, the analyst will try to stay in the background and allow
the patient to talk freely. She or he listens attentively, trying to pick up clues
about the conflicts that are causing distress in the patient. From time to time
the analyst will interpret the patient’s narrative, linking current materials to
events of the past and offering some explanation of what has happened in the
patient’s life.
One of the important ideas in psychodynamic therapies is the concept of
transference. Transference is a replay or revival, in a current relationship, of
conflicts that remain unresolved from earlier experiences, particularly those
involving parent-child relationships. A basic tenet of psychodynamic therapy
is that the feelings and thoughts of these prior relationships arise again in ther-
apy, with the therapist finding himself or herself in a position very much like
the parent. Feelings of love, anger or dependency that develop toward
the therapist are part of this transference. Transference is felt to be an essen-
tial part of therapy, but the process should be resolved by the time therapy is
terminated.
Freud’s approach to therapy was originally developed to deal with such
emotional disorders as hysteria and obsessive-compulsive behaviors. He later
turned his attention to depression in Mourning and Melancholia, pointing to
the experience of loss and internalized anger as important aspects of the prob-
lem.2 Over the years a number of writers in the psychoanalytic movement have
expanded on Freud’s thinking about depression. These writers include Karl
Abraham, Otto Fenichel, Edith Jacobson and Leopold Bellak.3 Bellak presented
a rather comprehensive list of the issues he believed psychoanalytic therapists
should pay particular attention to in treating depression. The list includes prob-
lems relating to self-esteem, a severe super-ego, aggression turned against the
self, feelings of loss, feelings of disappointment, feelings of having been deceived
by others, dependence on positive input from other people, an excessive need
to be loved and the use of denial as a defense mechamsm.
Bellak’s list suggests the kinds of issues one might anticipate being
addressed in a contemporary psychoanalytic approach to depression. These
problems are clearly important, but could take considerable time to cover in
therapy, particularly in psychoanalytic therapy, which traditionally proceeds at

a slow pace. However, Bellak believes that if the therapist is sensitized to these
issues, effective therapy for depression can be carried out in a relatively short
period of time. Typically, the therapist will approach these issues by exploring
the life history of the patient, considering recent incidents that triggered the
depression, and pointing out common denominators between the past and pres-
ent to improve the patient’s understanding and insight.
Some psychodynamically oriented therapists interested in the possibility
of radically shortening the course of treatment but still drawing on the legacy
of Freud’s ideas have developed various forms of brief dynamic therapies. In
these therapies, the therapist does not try to deal with all of the patient’s per-
sonality problems; rather, the therapist and patient focus on an important prob-
lem area. They attempt to deal with this problem in a limited number of
sessions, usually less than 20. Within these restrictions, the therapist will view
symptoms from a psychoanalytic or modified psychoanalytic framework and
use some of the techniques of psychoanalysis. The therapist may analyze defense
mechanisms, show how current symptoms have their roots in early childhood
experiences, and interpret relationships in terms of transference.
A Case Study of Psychodynamically

Oriented Therapy
We are going to present a case study of psychodynamically oriented ther-
apy of a severely depressed patient. Although treatment by antidepressant drugs
or brief psychotherapy are the norms today for most depressed patients, there
are times when a clinical judgment is made that long term, intensive therapy
offers the best chance for a successful outcome. This is such a case.
The case was provided by clinical psychologist Donald S. Jewell. Jewell
offers an interesting, somewhat different perspective on the long-term treat-
ment for depression. While generally speaking, people entering short-term
therapy who are less depressed seem to benefit more from therapy than people
who are more depressed, Jewell believes this may not necessarily be the case
for people who enter long term treatment. Motivation to persist in treatment
becomes an important factor in whether such treatment will be effective. Jew-
ell hypothesizes that people who have been experiencing the acute stress of
depression will be more inclined to stay with the treatment and deal with the
difficult emotional issues that are likely to arise. The idea that the time of acute
pain in depression is a strategic point to begin intensive therapy is an intrigu-
ing hypothesis that merits testing in research.
The patient treated was extremely depressed and overtly suicidal. Often,
the choice that is made for such patients is to hospitalize them and try a course
of electroconvulsive therapy. In this case the decision was made to try inten-
sive psychoanalytically oriented therapy. As we shall see, the decision proved

to be a good one. Here, then, is the case as presented by Jewell.
Jay is a 39 year old professional referred to me because of increasing suicidal

ideation. He is extremely bright, did well in academics, but is an underachiever
in his professional life. He has attempted suicide three times in his life. Each
episode occurred during a period of transition, graduation from college, moving
from home, and passing his professional board exam. The last attempt would
have been successful had he not been discovered by chance by a friend. His every-
day childhood consisted of endless terrorizing by a paranoid schizophrenic father
and lack of protection from a passive and frightened mother. The house was a
pathway of flea market debris with barely room to turn around in and guns which
were held to Jay’s head with threats of what would happen to him if anyone found
out the nature of things.
When Jay related this tale of horror it was with composed, modulated, feelin-
gless tones. It was as if he were reading someone else’s case history, suicides, death
threats and all. He told me that he was on three different medications and com-
plained that he woke up every morning wanting to kill himself and it was get-
ting worse. It was clear that Jay was very depressed.
I told him that it was “great” that he was able to tell me these things, an indi-
cation of increasing personal strength. He was trying to overcome his depression
and becoming more in touch with himself and that it was time to get off the med-
ication which had not been effective in resolving his depression. I said I would
arrange to meet with the psychiatrist I worked with to begin weaning him off the
medication and that I wanted to hear all he had to say about the suicidal thoughts.
I suggested the more he cut back on the medication, the more we might learn
about his feelings. When I said this to him, be looked at me as though the ther-
apist was crazier than the patient, so I spent some time talking with him about
the nature of depression.
Jay was immediately seen in individual therapy with a view to discovery in
terms of the impact of his nightmare childhood and the impact of this on his pres-
ent day living. After some time in therapy, he moved into a men’s group in con-
junction with the individual therapy. This gave him a place to experiment with
new ways of both understanding and dealing with some of the misconceptions
of his old life.
The path we embarked on was not an easy one for either therapist or patient.
There were times when I lost sleep about how close to the edge we came. This
was especially true when we hit periods of transition in the therapy, i.e., a new
discovery in historical development or a current failed romantic relationship. On
the other hand, transitions were interspersed with comments like, “I woke this
morning and for the first time that I can remember I didn’t want to kill myself ”
or “every time I go through one of these changes, I feel like someone has a gun
to my head.” This was followed by an amazed stunned look and, “Oh my God
what did I say!”
Today, Jay still has occasional suicidal thoughts. He has added another gradu-
ate degree. He no longer lives with his mother. He is looking for a position com-
mensurate with his abilities and is now seeing a girlfriend. This, after two years
of hard work. In my experience, if you have been depressed for 35 years, you are
unlikely to turn around in 12 visits to a therapist or even with a pill, or two, or
three.
Cognitive Therapy
In contrast to traditional psychodynamic therapy, which delves deep into
the personality and may take years to complete, cognitive therapy is usually
carried out in a matter of weeks or months. The basic premise underlying cog-
nitive therapy is that depressed emotion is triggered in large part by maladap-
tive thought patterns. The objectives of cognitive therapy are to work with the
patient to identify maladaptive thought patterns and then to help the patient
change these patterns— to begin to think in ways that are adaptive rather than
disabling. In his book Cognitive Therapy and the Emotional Disorders, Aaron
Beck spoke of the challenge to psychotherapy as one of giving the patient effec-
tive techniques to overcome his or her faulty perceptions. The therapist reaches
the patient’s emotions through the patient’s cognitions. Beck proposed that by
correcting faulty beliefs, the excessive, emotional reactions will be diminished.4
We have previously discussed some of the typical maladaptive thought
patterns found in patients experiencing depression, including over generaliz-
ing, perfectionistic and black-and-white thinking. The patient may not be aware
of these tendencies, and if he is, may not see anything wrong in thinking this
way. He may not see that these patterns are causing trouble. The therapist
attempts to discover these thoughts and help the patient understand his or her
role in the depressive problem.
In the early stages of cognitive therapy, the therapist tries to elicit from
the patient any automatic thoughts that the patient has been experiencing.
Later, the therapist will attempt to weave these fragmented thoughts into more
general patterns— the views that the person has about him or herself, his or her
life and the outside world. As an aid in therapy, the therapist may ask the patient
to keep a diary to record thoughts that occur during feelings of depression. The
therapist will discuss the material in the diary during the therapy hour.
In cognitive therapy, the therapist might ask questions like “Before you
started feeling sad this morning, what were you thinking about? What was on
your mind?” Or, “When you were lying awake last night and couldn’t get to
sleep, imagine you had a tape recorder, recording your thoughts. Try playing
some of that tape back for me. What would it sound like?” The questions may
vary, but the objective is to bring out the patient’s thoughts, particularly those
automatic thoughts that are believed to trigger and sustain depressed mood.
To illustrate a cognitive therapy approach, here are some excerpts from a case
reported by Jeremy Safran and his colleagues. The client, a 25-year-old male,
was being treated for depression, apathy and procrastination. At the time of
entering therapy he had been thinking about applying for admission to a uni-
versity, but found himself unable to get moving. During the stage of therapy
illustrated here, the therapist was concerned with uncovering the thought
processes that were supporting this pattern of immobilization.
The client told the therapist that he planned to have his transcripts sent
to the university; instead, he found himself lying in bed, thinking of telephon-

ing the transcript office but not doing so. The therapist asked the client to recall
how he was feeling at the time and to relate any images or thoughts that seemed
relevant. The young man described how he imagined the people in the tran-
script office would react to his call. “I see a picture of some of the people that
I have to contact to try to get something moving on this and I see them hating
me. They see me as a nuisance.” He imagined that he would receive a curt,
unpleasant response, something like, “Sorry you’ve got your answer and that’s
all there is to it.” On afterthought, he added that this fear was probably ridicu-
lous.
The therapist commented that the fear was real for the client. The client
agreed that it was indeed very real. As the session continued, the therapist asked
him to elaborate on his imagery. “Like I’m lying here in bed and the thought
occurs to me ‘this is what I’ve got to do. I’ve got to phone this woman.’ Ah ...
it’s funny, after describing all this, suddenly it doesn’t seem as surprising to
me, that what happens is that I stay in bed for another hour.”
The client later observed, “Yeah. I can see when I was lying there in bed
thinking ... ‘I should call the transcript office,’ the other part of me was saying
‘No way ... I’m not going to call that woman.’’‘ The therapist asked whether
he could make a case for not calling the woman. The client replied, “You bet
I can!” He then related automatic thoughts, catastrophizing the scenario. He
saw the woman as threatening and himself as powerless and helpless. “And
suddenly, it’s like I’m wrong and she’s in the right. I can imagine her saying
‘I’m going to call the principal,’ and it’s like I’ve got to hang up and run and
hide.”
The therapist observed that it was like he was a powerless child who had
done something wrong. The client agreed, “Yeah, I’m in the wrong. And I’m
gonna get squashed like a bug. And 1 have no defense, no defense at all.”5
The interchange had elicited a group of automatic thoughts suggesting a
self-image of a powerless child victimized by powerful and threatening adults.
As therapy continued, other tendencies of the client — to seek the approval of
others and not to express his own anger became clearer in light of this funda-
mental perception of powerlessness and his exaggerated fear of retaliation. In
later sessions, the therapist was able to work along with the young man to take
a more critical look at these debilitating ideas and successfully challenge them.
One of the techniques of cognitive therapy is to challenge the maladaptive
beliefs— the basic assumptions of the patient that are believed to underlie the
depression. An effort is made to break through the patient’s closed systems of
thought, to open up the patient’s thinking so that he or she can entertain new
information and alternative ways of looking at problems. The process of chal-
lenging the patient’s beliefs is not unlike a Socratic dialogue and sometimes can
have the flavor of a debate. The therapist may bring up facts and counter exam-
ples that tend to question and contradict the negative mind sets of the patient.
At times, the actions of a cognitive therapist resemble those of a lawyer for the
defense of the patient, and particularly his or her self-esteem.
Cognitive therapy is compatible with a number of elements of behavior
therapy such as teaching patients relaxation techniques and activity schedul-
ing to increase the frequency of pleasant activities. A hybrid form of therapy
(cognitive-behavioral therapy) emphasizing both cognitive and behavioral
change is now widely practiced and has been widely used both in the treatment
of depression and anxiety disorders.6
Interpersonal Therapy
Like brief dynamic and cognitive therapies, interpersonal psychotherapy
(IPT) is designed to be time limited and can be carried out in a few months.
IPT provides an alternative focus to the treatment of depression, moving away
from the patient’s psyche and belief systems to his or her interpersonal rela-
tionships. Since we know that interpersonal stresses often trigger the onset of
a depressive episode, it makes sense to consider these problems in treating
depression. IPT endeavors to help the patient develop more effective ways of
coping with the interpersonal problems that appear to have played a role in
bringing on the depression.
The therapist tries to identify the interpersonal problems that are of cen-
tral importance to the patient; then the therapist helps the patient deal more
effectively with the problems. The IPT therapist is particularly sensitized to
look for problems in the following areas: grief, interpersonal disputes, changes
in roles and interpersonal deficits such as loneliness.
With regard to grief, the therapist looks for indications of abnormal grief —
reactions to loss that have not been resolved in a reasonable period of time.
The therapist tries to help the patient facilitate the mourning process and free
himself or herself from a crippling attachment to someone who has gone.
With regard to interpersonal disputes, the therapist looks for possible
problems with the patient’s spouse, children, other family members, cowork-
ers and friends. If significant disputes are uncovered, the therapist and the
patient will try to work out plans to better resolve the disputes. The plans might
involve changing the patient’s expectations about the people involved or try-
ing to improve communication with the other people.
There are many role changes or transitions that may be associated with
the onset of depression. Think of such changes as leaving for college, getting
married, becoming a parent and changing jobs. As indicated earlier, such
changes often generate stress, and high levels of stress can trigger depression.
The therapist looks for difficulties that have occurred during these role transi-
tions. As the therapist explores these changes, he or she looks for losses of famil-
iar support in the patient’s life, how the patient has managed emotions such as
anxiety or anger that have been aroused by the transition and whether the
patient has experienced loss of self-esteem. The therapist also assesses the types
of new social skills that may be required to cope effectively with the changed
situation. The therapist tries to help the patient put the old role in perspective,
as well as to acquire the skills needed in the new role.
With regard to loneliness and social isolation, we know that loneliness
and depression are highly related. In helping the patient cope with this prob-
lem, the therapist explores the patient’s past and present relationships and
employs techniques such as role playing to diagnose specific difficulties the
patient may have in communicating and relating to others.
Role playing is a technique in which the therapist and patient engage in
a spontaneous drama. The therapist and patient each take a part (role) in a
situation in which they make up their lines as they go along. For example, let’s
say that therapist Debra Carter is working with a patient, Don, who has
great difficulty asking a woman for a date. Dr. Carter may play the part of the
woman Don is interested in. She and Don will engage in a dialogue in which
he asks her out. Dr. Carter may critique Don’s performance, helping him to
sharpen his approach. Practice in role playing may improve Don’s skill and
confidence.
In the book Interpersonal Psychotherapy of Depression, the developers of
this technique provided case examples illustrating the way IPT is carried out.
One example, the case of Ellen F. described a woman whose central problem
involved role transition.7 Ellen had been in an unhappy marriage for about ten
years. She had married at age 17, in part as a way of escaping an over intrusive
mother. Her husband turned out to be an alcoholic who when intoxicated could
be both verbally and physically abusive. Ellen had an abortive affair, which
proved disastrous, precipitating her suicide attempt. Ellen wanted to end the
marriage but found herself incapable of doing so. She hoped therapy would help
her take this step.
After beginning therapy she asked her husband to leave the house; he
proved more than willing to do so, having complaints of his own. Therapy then
focused on helping Ellen manage the transition out of marriage. The therapist
helped her identify new social relationships to fill the vacuum left by the shat-
tered marriage, helped her deal with her fears of being alone, and helped her
understand that her own self-worth should not depend on having a man to call
her own.
Therapy also strengthened her resolve not to reconcile with her husband
when he came back and asked her to try again. She realized that being lonely
for a period of time was better than the misery that she had been through.
During therapy, Ellen widened her circle of friends and began dating again.
When therapy ended she had not reached the point where she had achieved a
comfortable life, but she had made a difficult transition away from a destruc-
tive situation.
Effectiveness of Therapy
How effective is psychotherapy in the treatment of depression? Are some
approaches to therapy more effective than others in treating depression? Does
the competence of the therapist make a difference in the outcome of therapy?
Are there characteristics of the patient that make a difference in whether ther-
apy will be effective? These are some of the questions that researchers have
posed and are seeking to answer in clinical studies. These questions are impor-
tant both to the practitioner of therapy and to the person in need of therapy.
In conducting research to answer these questions, investigators must exer-
cise considerable care in the way they design and carry out their studies to
ensure that their results are as clear-cut as possible. For example, in studying
the effectiveness of therapy, researchers are careful to ensure the following:
1. All patients included in the study are clearly diagnosed as depressed.
The selection of patients is usually based upon a clinical assessment such
as is provided by the Hamilton rating scales.
2. The patients selected for inclusion in the study are randomly divided
into two groups: One group receives therapy; the other group is usually
put on a waiting list for treatment and serves as a control group.
3. Measures of depression are taken before therapy begins, at the end of
therapy and at a subsequent follow-up time.
The gold standard for these evaluation studies is a randomized, controlled
clinical trial.
Many studies have now been carried out comparing patients given psy-
chotherapy with patients serving as controls. Inasmuch as idiosyncratic factors
and research allegiances to a particular form of therapy can affect the results
of any given study, meta-analyses examining the overall trends from a variety
of studies provide the most reliable evidence for the efficacy of a treatment that
we have available today.
Because of the energy the proponents of cognitive-behavioral therapy have
put into evaluating this technique, we have more evidence for the efficacy of
cognitive-behavioral therapy in treating depression than we have for any other
therapeutic approach. In brief, meta-analyses have found that cognitive-behav-
ioral therapy is an effective treatment for adult depressed patients and for chil-
dren who are depressed as well. Using the conventions established in
meta-analysis research for assessing the size of an effect, the effect of cognitive-
behavioral therapy on depression has been described as large.8
A recent meta-analysis of 13 studies looking at the efficacy of interpersonal
therapy in treating depression also found positive results. As is true for cogni-
tive-behavioral therapy, interpersonal therapy appears to be an effective treat-
ment for depressive disorders.9 Interpersonal therapy appears to be effective
for both adults and adolescents.10
The efficacy of brief psychodynamic therapy for treating depression is more

problematic. I have criticized the research efforts of proponents of psychody-
namic therapies for not carrying out the research necessary to objectively eval-
uate the effectiveness of their therapeutic procedures. I am pleased to
acknowledge that for the proponents of brief psychodynamic therapy, the sit-
uation is changing. There is now some evidence available to evaluate the efficacy
of brief psychodynamic therapy for depression. Having said this, there remains
much work to do. Carefully conducted randomized clinical trials for psycho-
dynamic therapy are still relatively hard to come by. While early meta-analy-
ses produced inconsistent results, recent analyses of data suggest that brief
psychodynamics therapy can be an effective treatment for depression. Psycho-
dynamic therapy has been used to successfully treat depression in both chil-
dren and adolescents.11
So, the evidence is strong that both cognitive-behavioral therapy and inter-
personal therapy are effective treatments for depression and there is develop-
ing evidence that this may be also true for brief psychodynamic therapy.
In addition there is now evidence that cognitive-behavioral therapy can be
an effective alternative therapy when an antidepressant medicine proves want-
ing.12
Although a great many depressed people have been helped by psychother-
apy, as is the case for antidepressant medications, not everyone responds to
psychotherapy. And, while there is ample evidence that psychotherapy is effec-
tive in the treatment of depression, there still remains some question as to how
effective. When a person is improved, what precisely do we mean? Do people
who are treated by psychotherapy achieve the same level of well being as peo-
ple who were not depressed to begin with? The answer is probably no. While
improved, people who are treated for depression are still likely to experience
higher levels of depressive symptoms than “normal” people.13
To use a very rough analogy, therapy for depression in some respects is
like treatment for chronic diseases such as heart disease or arthritis. Treatment
for such conditions helps control symptoms and prevent flare-ups of the prob-
lems. Likewise, in psychotherapy for these diseases, one may not find a magic
bullet that cures the problem of depression in the same way an antibiotic wipes
out a bacterial infection. After psychotherapy, the person prone to depression
usually feels a lot better and should be in a better position to effectively man-
age himself or herself, which will reduce the chances of further symptoms. But
underlying genetic vulnerabilities remain and the problems in the environ-
ment that triggered the depression may also remain. There is a clear potential
for further problems.
Having shown that the major types of psychotherapy offered today appear
to be effective treatments for depression, researchers turned to the question of
directly comparing different types of therapies. Is one approach to therapy for
depression more effective than another? This is a very practical question for any-
one considering therapy; one would like to know which approach is most likely
to be beneficial.
In “comparative outcome” studies, patients are randomly assigned to one
of the several types of treatments under investigation. Particular care has to be
given so that all types of therapy are carried out in the clinical trials in the man-
ner in which they are designed to be carried out. Evaluation measures may
include psychological testing and clinical assessments such as the Hamilton
rating scale.
To date, the tentative conclusion from comparative outcome studies is
that there is not much difference between the therapeutic approaches that have
been tested in terms of their effectiveness in treating depression. In an impor-
tant paper, B. E. Wampold pointed out that the important thing is not what
kind of therapy is offered, but whether the therapy has a rational basis for
addressing depression. Therapies that target depressions are likely to work
roughly equally well.14
There are some practical consequences to the observation that different
forms of psychotherapy do not differ appreciably in their efficacy of treating
depression. People looking for help can pay attention to the qualities of the indi-
vidual therapist and how they relate to the person without worrying too much
about the technical aspects of therapy. Also, prospective patients can select
an approach that is short term and feel some confidence that they will be helped.
There is little evidence at this point to indicate that a person is likely to profit
more by undergoing long-term, deep therapy to deal with an ongoing depres-
sive problem. A person may want to choose long-term, intensive therapy
for other, more fundamental reasons, but it is not usually necessary for the
alleviation of depressive episodes. If proponents of long term, intensive ther-
apy could demonstrate in controlled research that the effects of such therapy
are more robust — that there is less chance of a recurrence of depressive symp-
toms— a stronger case could be made that it is the treatment of choice.
Let’s talk about the individual therapist. Doctors, lawyers and teachers
differ in how competent they are and this can make a difference in what you
get from them. A good lawyer may win your case for you; a bad one may lose
it. In much the same way, a skilled therapist is more likely to do more useful
things in therapy than a less skilled therapist. Observations of ongoing ther-
apy indicate that a skilled therapist is more likely to help patients explore issues
and problems and to do so without arousing the patient’s hostility or causing
unnecessary distress. Researchers have reported a relation between the compe-
tence of the therapist and the extent to which a patient improves during treat-
ment for depression.
As the skill of a therapist can make a difference in the outcome of ther-
apy, the question that must inevitably arise is how does one find a good ther-
apist? This is not an easy question to answer, but here are some ideas. Probably
the most useful benchmark in choosing a therapist is how effective he or she
has been with previous patients. Unfortunately, this kind of information is

unlikely to be available in a systematic way. No one takes polls of this situa-
tion. However, it is possible to ask around. If someone has been to a therapist,
you should be able to find out whether the person felt the therapist was help-
ful and what the therapist was like as a person.
If you cannot get a likely name from a friend, then your next best bet may
be the referral services of the local professional associations for psychiatrists,
psychologists and clinical social workers. The referral services will usually give
you several names of people who are licensed practitioners. They may also have
background information about each person, which will allow you to make some
inquiries. If you decide to call one of the names, see if you can talk briefly with
the therapist on the phone to gain a sense of what he or she is like and whether
you feel comfortable talking with the person. You should also ask about fees.
If they are way out of line, you might want to try someone else. A sky-high fee
does not guarantee a better therapist.
Some other possible sources of referral are community mental health asso-
ciations and the psychology, psychiatry and social work departments of local
universities. You will also find listings in the Yellow Pages of your phone book.
Let’s now turn our spotlight away from the therapist and onto the patient.
Are there characteristics of patients that may make a difference in whether ther-
apy is likely to prove helpful? Certainly one of the most important factors is
how depressed the patient is when he or she enters therapy. People who begin
therapy feeling mildly or moderately depressed are more likely to emerge from
therapy in decent shape than people who are severely depressed.15 Individuals
whose personal and social resources are in better condition to begin with are
likely to do well.16
Personality factors and the ease with which one can attach oneself to other
people can affect the way one will respond to different types of therapies. Peo-
ple with serious problems in forming attachments (attachment avoiders) may
find interpersonal therapy too threatening and may do better with cognitive-
behavioral therapy.17
Finally, the patient’s attitude can make a difference. If the patient has a
positive attitude about psychotherapy — a willingness to believe that it can
help — the chances are better that it will help. This “expectation factor” is not
only important in psychotherapy, it plays a role in almost all kinds of human
healing processes. Hope and belief are important in the treatment of physical
problems as well as emotional problems.
Comparisons of Psychotherapy and Drugs

Studies comparing antidepressant drugs with psychotherapy began in the
late 1970’s. Patients given cognitive therapy were compared with patients given
the first generation of antidepressants. The results of these initial studies sug-
gested that cognitive therapy was at least as effective as antidepressants in treat-
ing depression, perhaps even better.18
After these initial studies were reported, it was felt that a larger scale study
was needed to provide a more definitive answer to the question of drugs ver-
sus therapy for the treatment of depression. Under the aegis of the National
Institute of Mental Health, a collaborative study was undertaken at three dif-
ferent sites: the University of Pittsburgh, the University of Oklahoma, and
George Washington University. Two hundred fifty unipolar depressed outpa-
tients were randomly assigned to one of four treatment conditions: cognitive-
behavioral therapy, interpersonal therapy, an antidepressant drug, imipramine
plus clinical management, and a pill-placebo control plus clinical management.
Clinical management provided patients with support, encouragement, and
advice and as such constituted supportive therapy. Post treatment evaluation
of the patients revealed little difference among the three groups of treated
patients which seems more or less in line with the findings of previous stud-
ies. However, an analysis conducted on the patients who had been most severely
depressed at the onset of the study, found that those treated with the antide-
pressant drug seemed better off than those receiving psychotherapy.19
The results relating to severe depression were received as gospel by some
in the mental health community who proceeded to downplay, if not dismiss
the usefulness of psychotherapy for the treatment of severe depression. For
example, the United States Government’s Agency for Health Care Policy and
Research stated, “For severe and psychotic depressions, there is strong evidence
for the efficacy of medication and little or none for the efficacy of psychother-
apy alone.”20
“Not so,” replied the proponents of psychotherapy. They argued, justifiably
that one study is hardly definitive. They pointed to inconsistencies in the results
of the collaborative study and cited other studies which found no advantage
for drugs over psychotherapy or an advantage for psychotherapy. An exami-
nation of the raw data from four separate studies, including the collaborative
study, was carried out by Robert DeRubeis and his colleagues at the University
of Pennsylvania. The researchers concluded that cognitive-behavioral therapy
faired as well as antidepressant medication in the treatment of severely
depressed outpatients.21
So where does this leave us? Unfortunately, with an unresolved, and at
times heated debate. Partisans espousing one position or the other published
articles in the scientific journals which were followed by rejoinders attacking
the technical merits of these articles. Moreover, it has been observed that the
findings of a particular study seemed to bear a relation to the allegiance of the
researcher. While ideally, science is supposed to be neutral and dispassionate,
it is possible that a proponent of one type of treatment of depression may do
things which unconsciously bias the results of the study. What seems needed
are more large scale collaborative studies involving many researchers to nail
down convincing answers. Replication is one of the hallmarks of good science.
And, clearly replication is needed here, because these findings have affected
practice guidelines for patient care. Without such replication, it seems prema-
ture to draw firm conclusions about the relative efficacy of drugs versus ther-
apy in the treatment of severe depression.
How should these mixed results affect a patient’s choice of available ther-
apies? Here is my take on this question. For patients suffering from mild and
moderate levels of depression, it seems clear that either antidepressant drugs
or psychotherapy are potentially useful treatments, at least in the near term.
For people suffering from severe depression, it makes sense that the patient be
put on an antidepressant as soon as possible. Because antidepressant medicines
sometimes take weeks to be effective, it makes equally good sense that if the
patient is not hospitalized, he or she should have a consultation with a psy-
chotherapist at the earliest opportunity. Severely depressed patients need all the
help they can get and as soon as they can get it.
Combining Psychotherapy and Antidepressant Drugs

The foregoing studies placed the psychotherapeutic community and the
advocates of antidepressant drugs in what appeared to be an adversarial rela-
tionship. However, a cooperative relationship makes more sense for both groups
of mental health professionals and their patients. One area where such coop-
eration has been manifest is the study of the efficacy of combining psychother-
apy and medicine in the treatment of depression. Since antidepressant drugs
and psychotherapy appear to act in different ways to lessen depressive symp-
toms, one might reasonably expect that a combination of treatments would be
more effective than either used alone.
A number of studies have been undertaken to evaluate combination treat-
ment for depression, dating back to at least the 1980s.22 The conclusion of the
early studies was that while the use of combined treatment may have some
benefits, it did not produce the substantial improvement that one might have
hoped for. I have recently looked at half a dozen recent reports evaluating the
effectiveness of combined treatment and the conclusions of the earlier studies
seems to generally hold. Improvements in depression symptoms can be detected
from the use of both medicine and psychotherapy, but the improvements noted
are not typically robust and dramatic.23 Even with these less than stellar results,
for people who are not responding well to a single modality of treatment for
depression, I would recommend a trial of combined treatments, as in many
cases, it could be beneficial.
As a final word, I should note that patient noncompliance with treatment
is a problem for both pharmacological and psychotherapeutic approaches. Many
patients will stop taking their antidepressant drugs either because the medica-
tion isn’t working, they experience side effects, or just simply decide to stop.
At the same time, a significant number of patients referred to psychotherapy
may not follow through with seeking care or will stop coming to the therapist
before maximum benefits are obtained.
Cost factors may be involved in the patient’s willingness to adhere to a
treatment program. Even short-term psychotherapy (say, a course of a dozen
visits) can be expensive. Use of prescription drugs for an extended period may
not prove to be that inexpensive of an alternative. For patients with liberal
health insurance benefits, such costs may be a minor factor, but for many peo-
ple, it is not.
Successful completion of initial treatment seems to have value in prevent-
ing a recurrence. An incomplete recovery from a major depression episode is
a predictor of future depressive problems. Patients who show signs of depres-
sion after treatment are more likely to experience subsequent depressive symp-
toms than patients who are symptom free after treatment.
13. Hospitalization for
Depression and the Use of
Electroconvulsive Therapy
When should a person be hospitalized for the treatment of depression? As

a general rule, hospitalization should be considered when the patient’s symp-
toms are unmanageable through outpatient care. Two clear-cut cases of this
are when the depression includes psychotic features such as delusions and when
the patient is overtly suicidal.
Many depressed people think about suicide; some talk about it. When a
person is openly suicidal, there may be little choice but to consider hospital-
ization. It may be impossible to adequately monitor the person’s behavior and
protect her or him against self-harm outside of a hospital setting.
The decision to hospitalize may be made in the psychiatric emergency
service in the hospital or by the patient’s psychiatrist (if he or she has one) in
consultation with the patient and/or the patient’s family. In making the deci-
sion, the attending psychiatrist will likely consider a number of factors such as
the likelihood of self-harm, the severity of psychotic symptoms if present, the
capability of the patient for self-care, the degree of impulse control, and the
severity of the depression.1
Psychiatric hospitals can provide care and safety for the severely depressed
patient. Throughout the United States there are both public and private psy-
chiatric hospitals. The National Mental Health Information Center in Rockville,
Maryland, has compiled lists of these hospitals.2 In addition, you can probably
obtain information about hospitals in your area by calling your state’s mental
health agency. Judging from the brochures that inundate private practitioners,
some of the private psychiatric hospitals look very attractive, resembling resorts
more than the infamous asylums of the not-too-distant past.
Psychiatric hospitals may offer several modalities of treatment for
depressed patients. These include medication, individual and group therapy and
electroconvulsive therapy. With regard to psychotherapy, you may find in-
167
creased emphasis on group therapy in hospitals. The patients are all gathered
together under one roof, which can reduce or eliminate scheduling problems.
In addition, group therapy is cost effective for a hospital; one therapist can
work with a number of patients simultaneously. Group therapy can be of par-
ticular benefit to patients whose problems have to do with difficulties in inter-
personal relations. One learns to relate by relating and group therapy provides
a relatively safe training forum in which to learn.
Electroconvulsive therapy, more popularly known as “shock treatment” or
“shock therapy,” is a procedure used to treat severe depression, as well as other
mental illnesses such as schizophrenia, that involves the use of an electric cur-
rent to induce a seizure similar to what one sees in epilepsy. The procedure,
which has generated a lot of controversy over the years, can have a significant
therapeutic effect on depression.
Electroconvulsive therapy has it roots in experiments conducted in Europe
in the earlier part of the twentieth century in which insulin and metrazol were
used to induce seizures in schizophrenic patients. These seizures led to at least
temporary improvements in many of the patients. The procedure in which
electric current is used for a few seconds to induce such seizures was devel-
oped in the 1930s by the Italian researchers Ugo Cerletti and Lucio Bini. Because
electroconvulsive therapy was about all that was available at the time to treat
severe mental illness, the procedure was widely used. In time it was recognized
that electroconvulsive therapy seemed to be particularly beneficial for patients
suffering from depressive disorders.3
In these early days when electroconvulsive therapy was coming on board
as a treatment for psychiatric disorders, the procedure had a very bad reputa-
tion. And this reputation was fully deserved. The procedure might be carried
out without anesthesia, and this may still be the case in some countries. More-
over, there was no way to stop the often violent, jerky muscular reactions that
ensued. Broken bones were commonplace. And there was memory loss, par-
ticularly of the recent past. Sometimes one’s memory returned, but sometimes
it did not. And perhaps most damning to the procedure’s image were accounts
of hospitalized patients being given the treatment without their consent as a
means of controlling their behavior.
While the reputation of electroconvulsive therapy in its early days of use
was probably better than that of an alternative procedure, frontal lobotomy,
which was an even more desperate venture to deal with what seemed to be an
intractable psychiatric disorder, electroconvulsive therapy was still thought of
as a last resort, and subsequent depictions on television and in films such as
One Flew Over the Cuckoo’s Nest just added to its unsavory image. To add to
the unsettling view of the procedure, no one really knew why it worked when
it did. A sociologist who had been working in that period on a study of the reac-
tions of the family to mental illness in one of its member suggested wryly to
me that it worked “because it scared the hell out of the patient.”4 The impli-
¡3. Hospitalizaion for Depression and the Use of Electroconvulsive Therapy 169
cation was that anything was better than going through electroconvulsive ther-
apy and the patient would do whatever it took to avoid it.
Happily, the administration of electroconvulsive therapy has improved
dramatically over the years. Short acting anesthesia is now routinely given to
the patients so that they can sleep through the procedure. A muscle blocker such
as succinylcholine is used to immobilize the muscles and prevent the once
feared fractures. Oxygen may be administered to the patient. And there have
been refinements in the ability of the medical team to monitor what is happen-
ing to the patient’s brain.5 Still, with all of these improvements in technique,
as late as 1985, a consensus statement issued by a group of experts convened
by the National Institute of Mental Health called the procedure the most con-
troversial in psychiatry.6
Here, briefly, are some of the pros and cons for the use of electroconvul-
sive therapy for depression. On the positive side, favorable response rates are
at least as good as antidepressant medicines, and probably better. The proce-
dure has helped many patients who were unresponsive to medications.7 When
nothing else seems to work for a big-time depression, electroconvulsive ther-
apy has a good chance of being effective. Proponents of electroconvulsive ther-
apy see it not only as a last resort treatment, they recommend its use at an
earlier stage in the treatment for severe depression. The argument is that if it
works well later why not try it sooner?
Let’s consider some of the negatives. There are a number.
Sending electric shocks in the brain and producing an artificial seizure
such as one sees in epilepsy is a scary idea, no matter how much it is soft ped-
dled. The patient may be reassured that the death rate for the procedure has
dropped precipitously to now where it is roughly similar to childbirth and that
the confusion he or she will most likely feel after awakening will go away along
with the headache and nausea, that memory loss will most likely be transitory,
and that there is no compelling data that indicates the procedure may cause
damage to the brain. Such reassurances may help calm the fears of the patient
and then again they may not.
We still don’t know why electroconvulsive therapy works.
The patient may lose some memories. Such lost memories will most likely
be about the recent past, but memory losses that plunge deeper into time are
possible. Research suggests that lost memories are more likely to concern imper-
sonal events such as the events one might hear about on the nightly television
news rather than the events that are part of one’s personal life.8
Currently, electroconvulsive therapy is usually administered in the hospi-
tal, sometimes on an inpatient basis, sometimes on an outpatient basis. It takes
a team of skilled professionals which includes a psychiatrist and an anesthesi-
ologist to carry out the procedure. Compared to other ways of treating depres-
sion, electroconvulsive therapy is difficult to carry out and expensive.
Electroconvulsive therapy affects the cardiovascular system. For example,
it may cause significant decreases in pulse and blood pressure. While these
effects are usually transitory, and can be counteracted by drugs, the cardiovas-
cular system needs to be constantly monitored during the procedure. If the
patient has a heart problem, it is prudent that his or her cardiologists be brought
into the decision making process.9
As is true for other types of treatment for depression, electroconvulsive
therapy is not a magic bullet. A single treatment may do little. Typically elec-
troconvulsive therapy is given three times a week for a series of six to twelve
treatments. For many if not most patients the beneficial effects of electrocon-
vulsive therapy are likely to dissipate over time. It has been recommended that
following a course of electroconvulsive therapy the patient should be put on a
regimen of antidepressant drugs. Another possibility that has been suggested
is to continue electroconvulsive therapy treatments periodically.
With these pros and cons, the bottom line still seems to be that if a patient
has a severe and seemingly intractable depression, and particularly if he or she
is suicidal, electroconvulsive therapy is probably the best option now available.
Chances are that the treatment will help the patient considerably. To use elec-
troconvulsive therapy under less compelling circumstances seems to me ques-
tionable if other possible treatments have not been exhausted.
A few notes about electroconvulsive therapy
1. Because anesthesia is involved, the patient will be asked to fast before
beginning the procedure
2. The patient may be asked to temporarily discontinue the use of lithium
as lithium could affect the seizures.10
3. The medical team will have to decide whether to place the electrodes
delivering the shock in a bilateral position (on either side of the head, at
the temples) or position both electrodes on the same side of the head.
The bilateral position is the usual choice because it seems to work better,
although there may be more impairment of memory.
4. The medical team will also have to determine the dose of electricity
administered. In making this decision, they may use the age of the
patient as a guideline, utilize previous experience with the patient, or
attempt to titrate the dose in a kind of trial and error procedure. The
goal is to induce a seizure that lasts at least 30 seconds. This is
considered the minimum time for the procedure to be therapeutic.
As is true for other approaches to treating depression, researchers have
tried to tweak the procedures involved in electroconvulsive therapy to improve
its efficacy. Recently, for example, researchers working out of Duke University
Medical Center added a different anesthesia to the preoperative regimen for
electroconvulsive therapy called ketamine for which there was suggestive evi-
dence that it may have antidepressant properties on its own.11 The researchers
added ketamine to the mix of preoperative meditations and then carried out
¡3. Hospitalizaion for Depression and the Use of Electroconvulsive Therapy 171
electroconvulsive therapy with rather dramatic results which they reported in

the following case study.
The patient was a 54-year-old man who had been severely depressed for
several months. His appetite was very poor; he lost 35 pounds. He had difficulty
sleeping at night, took little personal care of himself, and thought about sui-
cide. The patient was described as profoundly withdrawn. On occasion, he
became physically aggressive. His depression was complicated by psychotic fea-
tures. The man had been using lithium and an antidepressant. But these did
not seem to help him. As the patient had been given electroconvulsive therapy
in the past, this seemed like the best bet to deal with his very severe symptoms.
Following a single treatment of electroconvulsive therapy augmented with
ketamine, the researchers reported that the patient responded in a very dra-
matic and unexpected way. Eight hours after the treatment was completed the
patient began to show major signs of improvement. He began to interact with
other people, had an increased appetitive and slept much better. The improve-
ment continued without further treatment over the next days. The researchers
observed the case was notable in that it showed that an episode of severe major
depression accompanied by psychotic features responded immediately to one
treatment of bilateral electroconvulsive therapy that included the use of this
different type of anesthesia. One case of successful treatment, of course, proves
very little, but it does suggest an avenue of research that needs to be further
explored.
14. Alternative Treatments
for Depression
People sometimes treat their depression using methods which are not
under the control or supervision of their physician or psychotherapist. These
methods go beyond some of the self-help strategies we have previously talked
about such as talking with friends or exercise which many people would view
as not really under the rubric of medicine, alternative or otherwise. These
“alternative methods” may be sought out by an individual as specific treat-
ments for depression which he or she can use with or without a physician’s or
therapist’s authorization or blessing.
Surveys indicate that millions of people in the United States— and I sus-
pect many more millions around the world use one or another form of alter-
native medicine in dealing with physical and emotional problems.1 Sometimes
techniques of alternative medicine are used to complement conventional, tra-
ditional medicine and sometimes they are used in place of conventional med-
icine.
The National Center for Complementary and Alternative medicine was
founded to study the safety and effectiveness of alternative medicines. There
was a clear need for such an institute because many claims have been made for
alternative medicines, especially dietary substances which have not been rig-
orously evaluated. It is important for consumers to know whether alternative
medicines offered in the marketplace are safe and effective. One of the ways
that the Center for Complementary and Alternative Medicine evaluates alter-
native medicine is to convene a panel of experts drawn from universities and
medical schools, asking the panel to review existing research and present its
conclusions. My reading of several of these reviews is that these expert panels
tend to be guarded in drawing conclusions and may not offer clear-cut guid-
ance about whether to use an alternative medicine approach.
My own view is that the standards for evaluating the safety and efficacy of
alternative treatments for depression should be equivalent to the standards for
evaluating the products of the pharmaceutical industry and the work of psy-
chotherapists. The standards should be equivalent, but not arbitrarily higher
172
¡4. Alternative Treatments for Depression 173
on the belief that alternative approaches are not really medicine. We have dis-
cussed allegiance biases in carrying out and interpreting scientific research.
These are very real and hard to overcome because scientists are human beings
with their own hopes, needs, and disciplinary biases. In evaluating what has
been written about alternative medicine, we must watch out carefully for both
pro and con biases towards alternative medicine. In my view an ideal panel of
reviewers might be one which includes both those who swear by alternative
medicines and those who swear at them.
This admonition about the need to be open-minded does not in any way
diminish the need for rigorous research on alternative medicines. In a 1998
review of complementary therapies for depression E. Ernst and his colleagues
at the University of Exeter noted that the quantity of rigorous scientific data
supporting the efficacy of complementary therapies for depression was
extremely limited.2 The situation has clearly improved but we still have a long
way to go.
The list of what constitutes alternative medical treatments is not constant
and unchanging. New possibilities for treatment arise from time to time and
as the National Center for Complementary and Alternative Medicine points out
some alternative treatments become widely accepted and enter the domain of
traditional therapies. The National Center for Complementary and Alternative
Medicine classifies current alternative treatments into five : (1) alternative med-
ical systems such as traditional Chinese medicine, (2) mind-body interven-
tions techniques such as meditation which are believed to enhance the mind’s
capacity to affect bodily function and symptoms, (3) biologically based thera-
pies which utilizes substances found in nature such as vitamins and herbs), (4)
manipulative methods which include chiropractic manipulation and massage,
(5) energy therapies such as the use of electromagnetic fields.
In our discussion of alternative treatments for depression we will consider
five possible treatments, most of which fit into the Center’s system of categories.
The alternative treatments for depression we will consider are meditation, mas-
sage therapy, the herb St. John’s wort, the use of omega-3 fatty acids, and bright
light therapy. Most of these approaches have shown some promise in research
as possible treatments or adjunct treatments for depressive symptoms.
Meditation
Meditation has a number of different meanings. One might think, for
example, of a young man reflecting on the events of his life. But what we are
thinking about here is a deliberate mental process, arising in the main out of
Eastern religions and spiritual traditions in which a studied effort is made to
focus one’s attention. Probably, the most well-known form of meditation is
focusing on an image in the mind’s eye, or on a repetitive sound or phrase
sometimes called a mantra, or on one’s breathing. One popular form of med-

itation used in America today is Transcendental Meditation. In its publica-
tions, The National Center for Complementary and Alternative Medicine notes
that Transcendental Meditation (TM) “originated in the Vedic tradition in
India. It is a type of meditation that uses a mantra, a word, sound, or phrase
repeated silently to prevent distracting thoughts from entering the mind. The
intent of TM might be described as allowing the mind to settle into a quieter
state and the body into a state of deep rest.”3
Another type of meditation that has attracted much attention is mindful-
ness meditation. This type of meditation originated in Buddhism. The National
Center for Complementary and Alternative Medicine notes that mindfulness
meditation, “Is based on the concept of being mindful, or having an increased
awareness and total acceptance of the present. While meditating, the medita-
tor is taught to bring all her attention to the sensation of the flow of the breath
in and out of the body. The intent might be described as focusing attention on
what is being experienced, without reacting to or judging that experience.”
Mindfulness mediation is thought to help the individual learn to experience
the thoughts and emotions of daily life with greater balance and acceptance.4
In a review article of electrical and neuroimaging studies of meditation,
B. Rael Cahn and John Polich describe meditation as practices which, “Self-
regulate the body and mind, thereby affecting mental events by engaging a
specific attentional set.”5 They view meditation as a subset of the techniques
used to induce relaxation or altered states such as hypnosis. In their view the
key to all of these practices is the, “Regulation of attention.”6
To help in the focusing of attention, The National Center for Complemen-
tary and Alternative Medicine notes that most types of meditation encourage
the individual to find a quiet location with as few distractions as possible, to
adopt a specific comfortable position whether it is sitting down, standing, or
even walking and to maintain an open attitude, “Which means letting distrac-
tions come and go naturally without stopping to think about them. When dis-
tracting or wandering thoughts occur, they are not suppressed; instead, the
meditator gently brings attention back to the focus. In some types of medita-
tion, the meditator learns to observe the rising and falling of thoughts and
emotions as they spontaneously occur.”7
Meditation has a quieting effect on the body. Meditation can reduce heart
rate and blood pressure and cortisol levels, the so-called “stress hormone.” As
Cahn and Polich note, “A considerable body of research supports the idea that
meditation training can mitigate the effects of anxiety and stress on psycho-
logical and physiological functioning.”8 Studies of the brain using the elec-
troencephalograph show that meditation also affects the electrical activity of
the brain; among the changes observed are increases in theta and alpha band
power and decreases in overall frequency.9
These changes in the body and brain are accompanied by short term psy-
chological effects which have been described as a, “Deep sense of calm peace-
fulness, a cessation or slowing of the mind’s internal dialogue, and experiences
of perceptual clarity....”10
Although it is clear that meditation can be an effective stress reducer, it is
not as clear that by itself, meditation is an effective treatment for depression.
We do not have enough evidence yet to be certain on this point, one way or
the other. Almost all of the research I have seen using meditation as a treat-
ment for depression uses mindfulness meditation. At first look, the case for
using meditation as a potential alternative medicine treatment for depression
would not appear as promising as it is for anxiety and stress related disorders.
Many depressed people appear lethargic and dispirited and one might wonder
how meditation would help them. One could certainly make the case that when
the depressive picture includes agitation or is accompanied by a comorbid anx-
iety disorder which happens frequently, meditation might prove beneficial. One
could also hypothesize that controlling stress could be helpful in treating the
depressive problem. Indeed, a study reported by Kabat-Zinn and his colleagues
showed that a stress reduction program emphasizing mindfulness meditation
had a long lasting impact in reducing both stress and depression levels of anx-
iety disorder patients, a number of whom were also diagnosed as having major
depressive disorder.11 It would be interesting to see whether meditation, by
itself, might be useful in patients whose depression is in remission to see
whether it might be helpful in preventing recurrences.
In the treatment of depression, mindfulness meditation has sometimes
been used as part of a therapeutic package along with other more traditional
therapies such as cognitive therapy. At first blush, the combination of mind-
fulness meditation and cognitive therapy may raise some eyebrows for as Mark
Lau and Shelley McMain pointed out in a review article there are some seem-
ing contradictions in the approach of these two techniques.12 If you are living
with a dysfunctional belief such as, “Nobody really likes me,” a cognitive ther-
apist might try to alter this belief to one that is not disabling such as, “some
people may not like me, but that’s true for almost everyone. It’s unrealistic to
expect everyone to like you.” Rather than attempt to challenge the idea in the
dialogue of therapy, mindfulness meditation would ask you to experience this
dysfunctional belief as part of your stream of consciousness, and in a non-judg-
mental way, accept the thought — but recognize that that’s all it is, a thought —
not a reality. Mindfulness meditation allows one to decouple the thought from
other aspects of your experience and not allow it to become a central part of
your beliefs.
While these techniques may seem somewhat at odds, researchers have
combined the two approaches into a form of therapy called mindfulness based
cognitive therapy (MBCT).13 MBCT has been developed into an eight week
course integrating mindfulness meditation and cognitive therapy. A recent
exploratory study of the efficacy of this combined treatment carried out on
patients in primary care settings who were experiencing symptoms of depres-

sion and anxiety yielded positive results. Depression scores declined following
treatment.14 However, it is not possible to say at this point, how much mind-
fulness meditation contributed to the results as the therapeutic package included
a number of different elements.
How efficacious is mindfulness meditation by itself as a treatment for
depression? The amount of research that has been carried out on this problem
is currently insufficient to render anything like a definitive conclusion. A recent
meta-analysis carried out on the available research that used measures of anx-
iety and depression yielded equivocal results. The researchers concluded that
mindfulness based stress reduction did not have a reliable effect on depres-
sion.15
Because of the paucity of research on this question, I would suggest a
Scotch verdict: the efficacy of this treatment for depression is as yet unproven.
Massage Therapy
As was true for meditation, massage therapy has a long lineage. In a review
article evaluating the effects of massage therapy, Christopher Moyer and his
colleagues noted that the practice of massage therapy was recorded as far
back as 2000 B.C. Physicians in ancient Greece such as Hippocrates, Celsus, and
Galen discussed massage as a therapeutic treatment.16 Interest in massage as a
form of therapy was rekindled in the 19th century and has flourished in recent
years.
In practice, the client receiving massage therapy usually disrobes, and then
loosely covered by a sheet or a towel lies down on the massage table. Some-
times, massage is given to a fully clothed individual seated in a chair. The mas-
sage-therapist will then apply pressure, strokes or perhaps vibrations to the
various parts of the client’s body. Many varieties of applying massage to the
body have been developed over the years and these have been given different
names, such as Swedish massage, deep tissue massage, and trigger or pressure
point techniques. The time given to massage treatment may vary from a few
minutes to over an hour.
Surveys carried out in the states of Connecticut and Washington have
found that the great majority (85 percent) of today’s practitioners of massage
therapy are women.17 Most of the clients are self-referred rather than referred
by a physician. Most of the clients who come to see massage therapists for help
in dealing with muscle-skeletal problems, particularly problems with their
backs, shoulders, and necks. While far fewer people seek massage therapists for
relief from psychological distress than for physical complaints, the benefits of
using massage therapy for psychological distress are clear. As massage therapy
can be quite relaxing, it is a natural fit for reducing stress and stress-related
disorders. In carrying out a meta-analysis of studies looking at the effects of

massage therapy on a variety of stress-related indicators, Moyer and his col-
leagues concluded that massage therapy tended to reduce heart rate, blood pres-
sure, and self reported levels of anxiety.18
As was true for meditation, the rationale for using massage therapy as a
treatment for depression is not as clear cut as it is for treating stress and stress
related disorders. However, there are circumstances where stress reduction in
the treatment of depression makes intuitive sense. As was the case for medita-
tion, the rationale for using massage therapy for depression seems reasonable
when the depressive picture includes agitation or is accompanied by a comor-
bid anxiety disorder or where current levels of stress have brought on or are
exacerbating the depression.
What if we are dealing with a relatively uncomplicated case of major
depression disorder or dysthymic disorder? Is there clear-cut evidence to indi-
cate that massage therapy would be useful in these cases? I have not yet seen a
definitive study in this regard, but there is some research evidence which sug-
gests that massage therapy could indeed be useful in helping people who feel
depressed.
Most of the research studying the effects of massage therapy on depres-
sion has been carried out by the Touch Research Institute of the University of
Miami School of Medicine. In some very intriguing studies in which serotonin
levels were assessed in urine samples, the researchers noted an average 28 per-
cent increase in serotonin following massage therapy.19 If massage therapy does
in fact increase serotonin levels, there would be a rational basis for believing
massage therapy might be beneficial for depressed mood. And the studies car-
ried out by the Institute suggest that this is the case.
Moyer and his colleagues carried out a meta-analysis of 10 studies carried
out by the Institute in which a measure of depression was included in a bat-
tery of tests to study the effects of massage therapy. It is important to note that
in none of the studies were the subjects selected as a group of clinically depressed
patients. Rather, the subjects included groups of headache patients, adults with
hypertension, and patients with Alzheimer’s disease. With these samples of
patients massage therapy proved very effective in lessening depressed mood.
As Moyer and his colleagues noted, the average patient who had undergone
multiple sessions of massage therapy experienced, “A reduction of depression
that was greater than 73 percent of comparison group participants.”20 This
effect would be similar to what one might expect using psychotherapy. While
these effects are impressive, it should be recognized that the subjects were not
selected as clinically depressed patients.
One of the more direct tests of the effectiveness of massage therapy on
depression was reported in a study carried out by researchers at the Touch
Research Institute using 84 depressed pregnant women as subjects. One group
of the women received massage therapy in 20 minute sessions administered by
a “significant other” each week for 16 weeks of pregnancy, starting during the
second trimester. Another group of women received training in progressive
muscle relaxation. Not only did the massage therapy have an immediate effect
on the women’s reports of both anxiety and depressed mood, by the end of the
study these women had higher serotonin levels. Interestingly, the women given
massage therapy experienced lower incidences of prematurity and lower birth
weights.21
One of the problems in evaluating the effectiveness of massage therapy —
and this difficulty is shared by almost any intervention technique — is ruling
out the effects of the extra attention the subject is receiving simply by under-
going the treatment. In the study of pregnant women just cited, it is difficult
to say how much of the benefit resulted from the specific effects of massage —
and how much from the attention — in this case intimate attention of a loving
partner.
The same point might be made with an interesting study carried out in
Korea. Women, recruited from a community health center were tested on a vari-
ety of measures including depression, and then taught a self administered form
of foot massage.22 The women practiced this massage technique both at home
and in the clinic. After six weeks, the women’s depression scores were clearly
improved. Was it the specific form of massage that produced the effect (which
would be very intriguing as this is a self-administered technique) or was it the
added attention the patients got from the nursing staff during training and
practice?
One way of teasing out the effects of extra attention is to compare mas-
sage therapy with another treatment and better yet a sham treatment that func-
tions as a placebo. In a recent study carried out at Stanford University, massage
therapy was compared with another treatment, active acupuncture and a “con-
trol” version of acupuncture. The patients, 61 pregnant women with major
depressive disorder were initially assessed for depression, then randomly
assigned into one of these three treatment groups (massage therapy, active
acupuncture, active control acupuncture), then assessed again after eight weeks.
The women who received active acupuncture had the best response (69 percent
were judged to be improved) while only 32 percent of the women given mas-
sage therapy were judged so. The women given massage therapy did not do any
better than the women given the sham acupuncture treatment.23
Where does this leave us? Clearly, there is a need for additional carefully
controlled studies using clinically depressed subjects in which massage ther-
apy is compared with both potentially useful treatments and sham treatments.
Until we have such data, it is difficult to fully assess the potential usefulness of
massage therapy as a treatment for major depression. Because massage ther-
apy is a well tolerated, usually benign technique it may be worth trying to see
if it is helpful, particularly where the depression is linked to ongoing stress.
Actions which help keep stress under control could be beneficial in the long
range treatment of depression and there is enough evidence from the studies
carried out at the Touch Research Institute to believe that massage therapy
could have a positive impact on depressed mood. Above all, massage therapy
is a low risk treatment that can have widespread positive effects.
St John’s Wort
St. John’s wort (Hypericum perforatum) is a yellow-flowered plant that is
native to Europe and was subsequently transported to America. The plant is a
perennial that grows wild in both continents. It is considered noxious when
eaten by livestock and its growth has been controlled by both the use of her-
bicides and the introduction of beetles that feast on it. The name St. John’s
Wort stems from a tradition of harvesting the flowers on or by St. John’s Day
which is June 24th. The flowers were hung in the house in the belief that they
would ward off evil.
The medicinal use of the herb has a long history. In its publication, St.
John’s Wort and the Treatment of Depression the National Center for Comple-
mentary and Alternative Medicine notes that in ancient times physicians wrote
that the plant could be used as a sedative, and to treat burns, insect bites and
wounds.24 Currently the major medicinal use of the plant as a medicine is in
the treatment of depression. To use St. John’s wort for this purpose, extracts
from the plant can be purchased in the form of capsules or may also be brewed
into an herbal tea.
How effective is St. John’s wort in treating depression? The answer to this
question is not altogether clear. Some studies have found the herbal to be effec-
tive. Others have not. At one end of the spectrum of these variable results is a
recent study carried out in Brazil in which 72 patients suffering from mild to
moderate depression were randomly assigned to receive either St.John’s wort
(900 mg per day), an antidepressant, fluoxetine (20 mg per day) or a placebo.
Only 12 percent of the patients receiving St. John’s wort achieved remission sta-
tus. The patients receiving the antidepressant did better, 35 percent achieving
remission. But hold on! The patients receiving the placebo did better than either.
Forty-five percent were classified as being in remission.25
While the study did not shower kudos on the two would-be treatments
for depression, there are positive findings from enough other studies to cau-
tion us not to throw out either the plant or the pharmaceutical as ineffective.
However, such negative results should make one skeptical of extravagant
claims that either of these substances is the end-all and be-all treatment for
depression. As we have said, no one has yet found a magic bullet to treat
depression.
A meta-analysis of clinical trials of St. John’s wort as a treatment for
depression published in the British Medical Journal in 1996 found that the herb
was indeed more effective than the placebos. As over 1700 patients were included
in these clinical studies, one would have to give this meta-analysis credence. It
would appear that St. John’s wort is an effective treatment for depression. Two
subsequent meta-analyses have confirmed this conclusion. However, a collab-
orative study funded through the National Institutes of Health found that the
herb was ineffective in treating people with major depressive disorder.26
So, where does this leave us? How about perplexed? Relying principally
on the results of the collaborative study, The National Institutes of Health
voiced the position in the publication St. John’s Wort and the Treatment of
Depression that the herb, “Is not a proven therapy for depression.”27 It was
further stated that, “Recent studies suggest that St John’s wort is of no benefit
in treating major depression of moderate severity.”28 These statements seem
rather dismissive of the herb as a therapy for depression. The implicit recom-
mendation is that people who are depressed should try something else, pre-
sumably a pharmaceutical antidepressant. What the publication failed to
mention, however, is that in the collaborative study cited as a basis for dismiss-
ing St John’s wort, an antidepressant, seratline, was also used as a comparative
treatment, and on the principal outcome measures used, it, too, fared no bet-
ter than the placebo in treating depression. The publication, however, did not
conclude that antidepressant medications are unproven therapies for depres-
sion.
And most interestingly, in a recent study carried out in Germany, 251 out-
patients diagnosed with acute major depression were randomly assigned to
receive either St. John’s wort or the antidepressant, paroxetine. The patients
given St. John’s wort evidenced over a 50 percent decrease in their depression
scores which was somewhat more than that achieved by the patients given
paroxetine. So, the herbal treatment was at least as effective as the antidepres-
sant and better tolerated.29
Clearly, St. John’s wort does not have a track record of proving effective
in every study testing its efficacy. But, the same could be said about antidepres-
sant medicines and psychotherapy. That is one of the reasons we use meta-
analyses, to look through a series of studies for overall trends. So far, the
meta-analyses for St. John’s wort have looked good.
Because there seems to be enough evidence accumulated to indicate that
St. John’s wort could well be effective in ameliorating depression, many peo-
ple who are experiencing depression may want to try it. This might be partic-
ularly true for people who have a preference for “natural medicines” over
pharmaceuticals or like the fact that it is an over-the-counter substance not
requiring a prescription, or that the herbal may be less expensive than the phar-
maceutical. If one decides to make a trial of the herbal, what things should one
look out for?
We must preface any cautionary statements with the overall conclusion
that St. John’s wort seems to be generally well tolerated. Postmarketing sur-
veillance studies of thousands of users find the incidence of side effects not only
appears to be quite low, but seems to be considerably lower than for pharma-
ceutical antidepressants.30 St. John’s wort, of course, can have side effects. These
include fatigue, dry mouth, dizziness, diarrhea, nausea, and increased sensi-
tivity to sunlight. It is important to recognize that the herb also interacts with
some pharmaceuticals, including antidepressant medicines and some anti-can-
cer drugs. If you are currently using any medicine, it is a very good idea to check
with your physician and pharmacist before trying St. John’s wort to make sure
that using the herbal will not interact with your current medicines.
Because St. John’s wort is an herbal and therefore not regulated by the
Food and Drug Administration in the same way as pharmaceuticals, it is pru-
dent to buy only products from a trusted and recognized manufacturer of herbal
products.
There is also another less constraining caveat. At this point, we simply
don’t know what it is in the plant that does what it does. Scientists have amassed
a list of suspects, constituents of the plant (e.g., hyperforin) which might pro-
duce the antidepressant effects, but the conclusions of two recent papers are
that we don’t really have enough information yet to be sure of what is produc-
ing the antidepressant effects.31
Omega-3 Polyunsaturated Fatty Acids

Omega-3 polyunsaturated fatty acids (PUFAs) are long chain acids found
in the oils of some saltwater fish, especially salmon, tuna, and herring. Some
other sources for these acids are flaxseed and canola oil and walnuts. The two
omega-3 fatty acids which have particularly stirred the interest of researchers
for their potential therapeutic value are eicosapentaenoic acid (EPA) and
docosahexaenoic acid (DHA). It is important to recognize that our bodies can-
not synthesize these acids. They must be consumed as part of our diet or by the
use of supplements.
Omega-3 polyunsaturated fatty acids are one of the current hot items in
a fad-prone culture attracting both researchers and the health-conscious pub-
lic. Particularly exciting findings have been reported about coronary heart dis-
ease. Patients with coronary heart disease given omega-3 fatty acids were
substantially less likely to suddenly die from sustained ventricular arrhythmias
than patients not given these supplements.32 Researchers have turned their
attention to look for possible links of the omega-3 fatty acids to other diseases
such as rheumatoid arthritis and quite interestingly, depression. Although large
scale definitive studies proving beyond a reasonable doubt that increasing the
amount of PUFAs in the body either by dietary supplements or by increasing
the amount of fish in the diet will reduce the chances of becoming depressed
or be a useful treatment for ongoing depression are still lacking, there are
enough straws in the wind to make this a very attractive area for researchers
to investigate.
Here are some of the straws in the wind. Studies have found statistical
links between seafood consumption and prevalence rates for major depression.
For example, in a note published in the British medical journal Lancet, Joseph
Hibbeln looked at nine different countries and found that the countries in
which seafood intake was highest had the lowest rates of depression.33
Researchers have reported that patients who are depressed had lower con-
centrations of PUFA’s in their blood than controls. This finding has been repli-
cated in several studies.34
In an interesting clinical report, physicians in Taiwan treating a pregnant
woman who was suffering from recurrent major depressions but would not
take antidepressant medicines for fear of hurting her unborn child was given
omega-3 supplements. Within a month, her depression began to lift.35
In a study carried out in New York City 33 medication free depressed
patients were assessed for levels of omega-3 fatty acid and then monitored over
a two-year period for suicidal behavior. During the two years seven of the
patients attempted suicide. These patients had lower levels of DHA in their ini-
tial assessments.36
Researchers in Israel carried out a study on 26 children with childhood
depression. Half of the children were randomly selected to receive omega-3
fatty acids, half were given a placebo. Using a variety of measurements for
depression, the children given the omega-3 fatty acids supplements were less
depressed than the children given the placebo.37
In a study carried out in London, England, patients diagnosed with bipo-
lar depression were randomly assigned to receive EPA or a placebo. After 12
weeks, the patients who had received EPA were less depressed than those receiv-
ing the placebo.38
Results such as these are certainly interesting!
A number of possible mechanisms have been proposed to explain why
omega-3 fatty acids could have beneficial effects on depression. One of the more
intriguing of these explanations is that omega-3 fatty acids affect the serotonin-
ergic neurotransmitter system. Researchers have found evidence that levels of
plasma DHA are related to levels of a serotonin metabolite, and we know that
low levels of serotonin are a factor in depression.39 It may be that adding omega-
3 acids to the diet would affect serotonin activity in a somewhat similar way to
taking SSRI antidepressant medications. This possibility needs further study.
Reports suggest that omega-3 fatty acids are generally well tolerated,
although supplements may cause gastrointestinal distress and nausea in some
people. It is an unsettled question of what might constitute an effective dose
for treating depressive disorder. In some of the small clinical studies conducted
to date, (e.g. the study carried out in London) a dose of 1 gram per day of EPA
seemed to be effective. A helping of salmon or a tuna sandwich might well pro-
vide what is needed. Piling on supplements on the theory that if a small amount
is helpful, more might be better could present problems, because high doses
might pose a risk of bleeding and if one has a bleeding disorder, one should
certainly exercise caution. But, substituting fish frequently for meat is not only
good for your heart, it may be of value in ameliorating depression. Are we cer-
tain of this yet? By no means. The idea may yet fizzle when large scale random-
ized controlled studies are undertaken, but adding some fish to the diet is
certainly about as low risk a strategy for possibly affecting depression that any-
one has yet come up with.
Bright Light Therapy

Bright light therapy is an intuitive treatment for seasonal affective disor-
der. If the dark makes you depressed, turn on the lights! When the disorder was
first elucidated in a 1984 paper in the Archives of General Psychiatry the authors
also presented a study of the effectiveness of bright light therapy. They found
that bright light therapy was an effective treatment for SAD and this finding
has been replicated over the years.40 Two of the questions that subsequently
engaged researchers were (1) How could one use bright light therapy in the
most effective way to treat SAD and, (2) Would this therapy have any value in
treating depressive disorders besides SAD?
Among the issues relating to the first question was should the bright lights
be used in the morning or evening? Or perhaps at both times? How long should
the exposure to the bright light be? What kind of light and what intensity would
work best? In a comprehensive review of bright light therapy Michael and Juian
Su Terman examined the results of many studies and concluded that morning
treatments were effective for more people than either evening or midday treat-
ments. Adding a second session of exposure to the morning sessions was
unlikely to improve the results. Brighter lights worked better than dimmer
lights. Based on existing research the Termans recommended that SAD patients
should initially try morning light shortly after awakening. They further rec-
ommended a light providing 10,000 lux be used for 30 minutes.41
As it is true that some people respond to bright light therapy better in the
evening than they do in the morning, if morning light therapy doesn’t work it
makes sense for the individual to try it in the evening.
The answer to the second question, does bright light therapy work for
depressive problems other than SAD appears to be a qualified “yes.” The
qualification is that the research basis is not yet that extensive to draw firm con-
clusions. However, some studies using patients diagnosed with major depres-
sive disorders have reported significant beneficial effects. For example, a study
published in Psychological Medicine reported a 50 percent remission rate in one
measure of depression for patients treated with bright light therapy.42 Given
the relatively low risk in using bright lights, it seems worth a try for people suf-
fering from major depressive disorder.
While bright light therapy appears to be a relatively benign treatment for
depression, there are some potential side effects from its use. The principal side
effects so far reported for bright light therapy are about what one might expect
from being close to very bright lights for prolonged periods: headaches, nau-
sea, and eye-irritation, and perhaps less predictable, jitteriness. Interestingly,
there have been some cases of reported manic reactions to bright light therapy
and several people using this therapy have committed suicide.43 Whether the
bright lights had anything to do with provoking these suicides is unknown.
To obtain the full benefits from bright light therapy, a special apparatus is
required. Some people have constructed an apparatus, themselves, but the Ter-
mans do not recommend this, pointing out that some do-it-yourselfers have
experienced corneal and eyelid burns. Commercial products come in different
sizes and shapes. It is essential that the apparatus filter out ultraviolet light
which is harmful. The apparatus should also be comfortable to sit near and
be used for reading. The Termans describe a clinically tested model which
uses high output white fluorescent lights which are elevated and tilted slightly
downward. The device uses a polycarbonate diffusion screen for filtering out
ultraviolet waves and yields an illumination of 10,000 lux.44 In choosing an
apparatus, it is clearly important to find manufacturers who are knowledge-
able and experienced in designing and constructing these devices. Eye protec-
tion is of paramount importance in using bright light therapy.
15. The Problem
of Recurrence
A patient diagnosed with major depressive disorder is being treated with

an antidepressant. For awhile, the signs are encouraging. He is sleeping better,
eating better, he has returned to work after a brief period of sick leave, and
seems much more upbeat. Then, after a few weeks he seems to be going down-
hill again. This all too frequent situation is usually referred to as a relapse.
While the depression had substantially improved, even appearing to be in remis-
sion, the patient has not yet reached the point where one could confidently
assert that he was now experiencing a sustained recovery. And now, the attend-
ing physician has to once again make decisions about his medication.
If the patient has discontinued the antidepressant, should he be started on
it again? If he is still using the medication, should the dose be increased or
should another antidepressant be tried? Or should drug treatment be aug-
mented by psychotherapy?
If the patient had discontinued the medicine when he felt better, chances
are the prescribing physician will put him back on the medicine. There is a com-
pelling logic in the argument that if the drug worked well before, why not try
it again. Only this time, stay with it longer.
If the patient is still using the medicine, the usual thing to try is to raise
the dose. There is empirical evidence that demonstrates that this strategy is
often effective and a survey of over 400 clinicians indicated that increasing the
dose is the most frequently reported “next step” in treatment.1
A relapse in depression and a recurrence of the disorder are very similar
ideas. In both cases it appears that the depression has cleared up and seems to
be in remission. The patient feels better and is doing better. However, in time
the symptoms of depression flare-up again. The distinction between relapse
and recovery has mostly to do with the length of the time the depression is in
remission before symptoms of depression return. We call it a relapse when the
remission of symptoms is a relatively short period and a recurrence when the
period of remission is relatively long. One of the conventions proposed is that
it is a relapse if the period of recovery is less than two months and a recurrence
185
if the period is more than two months.2 The distinction is, of course, arbitrary
but the point is clear. After a decent interval of time the operative word is
recurrence.
The recurrence of depression is one of the most nagging, troublesome
problems facing mental health researchers and clinicians in their efforts to try
to treat depression effectively. It must also be very discouraging to the patient
and his or her family to have appeared to have shaken off the disorder only after
a period of months or years to be faced with the problem all over again.
Now for many people who have experienced depression and have recov-
ered, recurrence is not inevitable. A study carried out in California by Andrew
Billings and Rudolph Moos demonstrated that many ex-patients do very well.
In the study which followed up patients who had been treated in hospitals and
community mental health centers, the researchers found that many patients
were not only experiencing few depressive symptoms, but had improved self
esteem and were coping better with stressful events. And although they
still had relatively few friends and the interactions within their families were
not as supportive as they could be, their social lives were getting better.3
In contrast to these ex-patients who were doing quite well, we know that
many other patients experience a recurrence of depressive symptoms. The bad
news is that neither treatment by medication nor psychotherapy is a guaran-
tee that a person who has recovered substantially from an episode of depres-
sion will remain symptom free. And the same holds true for persons who have
received electroconvulsive therapy. According to published reports, the chances
are approximately one in two that people treated for unipolar depression will
experience a recurrence of depression at some point during their lives and the
odds rise precipitously that if there is a second episode, it will be followed by
more.4
Some of the factors that promote the recurrence of depression are the same
as the ones that promoted the risk of developing depression in the first place.
Some are different. The patient’s gender, for example, seems less predictive of
recurrence than of experiencing the initial episode.5
Here, briefly are some of the factors that research has linked to increased
risk for recurrence of depression.6
1. A family history of depression. Both genetic and experiential factors are
probably involved here.
2. The initial episode of depression is severe.
3. The presence of comorbid disorders such as anxiety disorders and
substance abuse.
4. Dysfunctional mind-sets and beliefs.
5. Continued high stress levels after recovery from the first episode.
6. Inadequate levels of social support.
If as research suggests, these are factors that promote the recurrence of
¡5. The Problem of Recurrence 187
depression, then we have an obvious starting place to offer suggestions about

things to do to try to prevent such recurrences. The goal would be, wherever
feasible, to mitigate the effects of these factors, to dampen them down.
A family history of depression is one of those roles of the dice that the new-
born child has nothing to say about. A child comes into the world and has to
take what he or she finds. We are beginning to make inroads into discovering
the genes that contribute to depression and when the genetic influences are
more fully understood, we may be able to find ways to counteract the effects
of unhelpful genetic variations or perhaps even attempt to alter the genes them-
selves. This may well come, but we are not there yet.
At the present time, the environmental component of family influence
may offer a more achievable target, particularly if we are dealing with a
depressed child or adolescent. Family therapy offers a potential pathway to
making changes in the child’s environment to make it less depressogenic.
What about someone who has grown up in a dysfunctional family and is
now a depressed adult? Would exploring these family dynamics in psychother-
apy and hopefully coming to terms with what happened help prevent a recur-
rence of depression? I am not sure that there is research evidence which bears
directly on this question, but it seems like a reasonable thing to try and I hope
that in time research will address this issue move fully.
There is intuitive sense to the idea that a severe depression is more likely
to persist in the face of treatment and more likely to recur than depression
which is mild to moderate in severity. There is also empirical research which
supports this view.7 The severely depressed person may require a full range of
antidepressant treatments— medication, psychotherapy, and possibly electro-
convulsive therapy. At the present time the best hope for preventing recurrence
of severe depression is through thorough treatment when it first occurs followed
by some form of continuation or maintenance therapy which we shall discuss
shortly.
In considering the impact of comorbid conditions on recurrence, I would
like to use a metaphor. I would like to liken being depressed to being weighed
down by a heavy load. For a moment, picture in your mind’s eye a man or
woman walking almost stooped shouldered by the weight they are carrying, per-
haps a bundle of wood, or a sack of stones. The metaphor is not that far-fetched,
for I have sat across from patients, their shoulders hunched, their eyes down-
cast looking very much as if they had been carrying a great load. Treatment for
depression is something like taking this weight away.
But suppose that the individual has not only been carrying on one side of
his shoulder that sack of stones but on the other side has been carrying and will
continue to carry additional stones. With these additional burdens, it would
not take a great deal of new stress on the other shoulder to weigh him or her
down again.
The image of a man or woman caring a sack of stones or a pile of wood
is, of course, only a metaphor but think for a moment of a person who is not
only depressed, but is troubled by other problems such as anxiety disorders
(e.g., phobias, panic attacks) or has a lingering problem of drug or alcohol
abuse. Treating depression and not addressing these other problems leaves the
individual with a perpetual drain on his or her psychological resources. With
these ever-present vulnerabilities, it would not take a lot of stress to reactivate
the depression.
As a preventive for the recurrence of depression, it makes sense to treat
these comorbid conditions and get them under better control. For anxiety dis-
orders there are anti-anxiety drugs (e.g., benzodiazepines) which can help at
least in the short term for controlling anxiety disorders. Therapists trained in
cognitive and behavioral techniques have effective procedures to deal with pho-
bias and panic disorders. Twelve step programs are often the most effective
ways of dealing with alcohol or drug abuse. The bottom-line is to treat, not
ignore comorbid conditions as this may help prevent a recurrence of depres-
sion.
How does one change dysfunctional mind-sets such as a tendency towards
overgeneralization or perfectionist thinking? Reading books like this which
point out the links between such mind-sets and depression may help. Com-
puterized programs of cognitive-behavior therapy such as Moodgym may be
better. Working with a psychotherapist who is familiar with the techniques of
cognitive therapy is probably the best bet. This approach to therapy has demon-
strated effectiveness in treating depression, but like other forms of psychother-
apy, it is no guarantor of recurrence of depression.8
Reducing stress in one’s life is important for a great many people and par-
ticularly for people who are vulnerable to depression. While the most strate-
gic time to do this is before there is an episode of depression — in the hope of
preventing depression from ever occurring, the next best opportunity is dur-
ing treatment for the initial episode and shortly thereafter, before depression
becomes a recurrent problem. There are changes that one can make in one’s
life style that can reduce stress, such as increasing exercise and developing net-
works of supportive friends.
In addition to pursuing a range of self-help strategies, many people find
that talking about their problems with a therapist is useful in controlling stress.
Indeed, there is research evidence which supports the usefulness of psychother-
apy in improving one’s capability of dealing with stress. A recent study com-
pared patients treated with either cognitive-behavioral or interpersonal therapy
with patients treated with an antidepressant in terms of their post treatment
resiliency to stressors. Compared to the patients receiving medication, the
patients receiving therapy showed increased resiliency to stressors in the months
following treatment.9
We have discussed the importance of social support in some detail earlier
in the book. When things go bad, when problems arise, and stresses mount,
there is nothing like having a sympathetic soul to talk to. A person with an
understanding heart, an ability to listen, and empathize with what you’re going
through is a priceless commodity. Lucky the person who has such a friend! But
lacking this, just to have somebody with whom you can sit down and talk over
what is happening in your life can bring a sense of objectivity and perspective
to your mounting concerns. Indeed, it may help prevent the escalation of neg-
ative thoughts and feelings into a depressive cycle.
Two practical suggestions. When you are depressed, utilize the help offered
by the network of support groups for depression in this country. The Depres-
sion and Bipolar Support Alliance is a very good source for locating such sup-
port groups. When you are feeling well, try to increase your social contacts and
when you can, make and nurture your friendships.
Continuation and Maintenance Therapies

The proponents of cognitive therapy are very good at carrying out research
to demonstrate what they are doing. They report the good news that cognitive
therapy or cognitive-behavioral therapy, as the case may be, is effective in treat-
ing depression. They present statistics on the percentage of cases that improve
using standardized measures of depression and/or go into remission. To their
credit, they also report the bad news— that significant numbers of patients who
have successfully completed therapy began to develop depressive symptoms
and not all that long after treatment is over. These flare-ups of depressive symp-
toms have been called discontinuation-risks or temporary spikes in symptoms.
In other words the patient is showing signs of relapse to a greater or lesser
extent. No one is sure what causes these flare-ups of symptoms. In a research
paper, a research team led by T. M. Kashner suggested that these symptoms may
have been temporarily suppressed by therapy only to emerge later when ther-
apy had been completed. Or, alternatively that the discontinuation of therapy,
itself, created sufficient stress to reignite the symptoms.10 Critics of cognitive-
behavioral therapy might argue that such therapy is too short-term and
superficial to really dig down deep and root out the problem. For those who
espouse this position, it seems to me that proponents of long term therapy
should try to demonstrate in research that such therapy is followed by lower
recurrence rates. I would be very interested in seeing such data.
How about medication and recurrence? When medication is stopped and
the patient is on his or her own, recurrence statistics are likely to be no better
than for cognitive-behavioral therapy. In fact, some data suggest that the recur-
rence rates may be worse.11 All of which reinforces my own conclusion that
whatever the initial treatment for depression — no matter what is done — it is
a throw of the dice whether a single course of therapy will fix things up. Admit-
tedly, a single course of therapy will work for many people. But for perhaps
half of the people who are treated initially by psychotherapy or medication will
sooner or later find that their improvement is only a temporary respite. In view
of these hard facts, we need to rethink the model of treatment.
I have long held this view. In the first edition of Understanding Depression,
I voiced the following opinion.
With regard to the use of psychotherapy as a preventive measure, it would
take some rethinking of the traditional model of psychotherapy to utilize ther-
apy as a preventive technique. In the traditional mode of therapy, a patient
comes to the therapist with problems, has these problems thoroughly aired and
hopefully resolved, and is then discharged. This traditional approach is based
on an implicit assumption that bringing up and working through unresolved
conflicts will result in a “cure” for the patient. While this may or may not be
so for most emotional problems, we know that depression has a high rate of
recurrence, so a different type of model may be more appropriate in treating
depression. This model postulates that for many patients, there is a need for
continuing contact on a much-reduced level between therapist and patient after
initial discharge. It may be something like coming in for a visit once or twice
a year-or, more importantly, when things begin to get rough.
My view is that for people who have suffered from recurrent depression,
the time to see your psychotherapist is when stress is building up. Why wait
until the stress level passes your tolerance level and the chances of a severe
depressive reaction loom large? Wouldn’t it be better to consult the therapist
with whom you previously worked to help you over the difficulties before things
get out of hand? This is the view that I left with my patients when they have
finished the primary course of therapy.
Now, the view I expressed here — that for many patients it may be unre-
alistic to look at psychotherapy for depression as a single course of treatment
with a fixed termination point — has been voiced by others as well. As far back
as 1985, for example, researchers working at the University of Oregon expressed
a similar position. Having completed a follow-up study of people with unipo-
lar depression who were treated by cognitive-behavioral approaches, Linda
Gonzales and her colleagues wrote, “The results suggest that although most
patients are improved at the end of treatment, for some this improvement is
relatively transient and by the LIFE criteria does not constitute recovery from
the episode that led them to seek treatment. A potential implication of these
results for cognitive behavioral treatments is that they are either too short to
produce more enduring improvement in a greater proportion of patients and/or
that they need to be supplemented with posttreatment maintenance and booster
sessions to assist patients in maintaining the improvements they make in treat-
ment.”12
Procedures for continuation or maintenance therapy (e.g., seeing the
patient on a reduced basis) have been developed by both practitioners of inter-
personal therapy and cognitive-behavioral therapy. Researchers using inter-
personal therapy have reported that seeing remitted patients as infrequently as

once a month reduced the risk of recurrence.13 Continuation-based cognitive
therapy has also been found to lower the risk of recurrence.14
The need for continuation treatment with the use of antidepressant drugs
has been widely recognized for some time. It has been recommended that fol-
lowing remission, patients should remain on antidepressant drugs for a period
of up to nine months or perhaps a year, with people who have experienced
recurrent episodes staying on the drug even longer.15 The value of continua-
tion therapy with antidepressant drugs has been demonstrated in a number of
studies. Rates of recurrence diminish significantly with the continued use of
the drugs. It has been suggested that the full dose of medicine used during
treatment be maintained during the continuation period.16
With the high risk of recurrence of depression, I think it is altogether pru-
dent for patients using antidepressant medicines which have proven effective
for them to stay on the medicine for an extended period of time following
remission of symptoms. For patients who have been through psychotherapy, it
makes sense to maintain contact with the therapist and schedule occasional
visitors to see the therapist, particularly when there are signs of trouble devel-
oping. There are no guarantees that these two steps or the self-help steps I out-
lined earlier will prevent the recurrence of depression, but it seems likely that
a combination of such actions may have value as preventive measures.
16. Concluding Remarks
Depression, like other mental and emotional disorders, is a worldwide

problem. One is likely to find the disorder in every corner of the globe. Joseph
Westermeyer put it this way: “Psychiatric signs and symptoms are remarkably
consistent from culture to culture. Patients everywhere complain of insomnia,
worry, crying spells, weakness, suicidal ideation.”1
Depression is not a new problem that has arisen in the wake of our mod-
ern technologically advanced society, although we may well be witnessing
an increase in its prevalence. While depression has probably adversely affected
people since the early days of recorded history, until recently we have not
had much understanding of it or known how to treat it effectively. There
were a few spots of light in this void. Freud, for example, offered some theo-
retical contributions highlighting the role of loss in depression and suggesting
that self-directed anger plays a role in the disorder. Descriptive psychiatry
produced some categories for classifying types of depression, but the distinc-
tions were not all that clear and the terms were not universally accepted.
In their early investigations, the biologically oriented researchers, lacking
sophisticated techniques found little to write home about and the attention of
research psychologists was turned elsewhere to problems that were more
amenable to study. Over the past few decades the situation has changed dra-
matically.
Psychological and psychiatric journals have become inundated with
research on depression. Researchers have been hard at work both improving
the techniques needed to better study depression and producing substantive
knowledge about the causes of depression and its treatment.
In listing the advances in knowledge brought about by this flurry of activ-
ity, one could begin by pointing to better methods of diagnosing depression.
This has resulted in part from more clarity about the symptoms of depression.
The Diagnostic and Statistical Manual, for example, lays out specific criteria to
help the researcher and practitioner in making diagnoses of both depression
and bipolar disorder. In addition, we now have both self-report and observa-
tionally-based psychological measures that can indicate with reasonable accu-
racy the presence of depression in adults. These measures are not only useful
192
¡6. Concluding Remarks 193
in clinical settings; they can also be used for large-scale studies in the commu-
nity.
Community surveys have revealed that all groups in our society are sus-
ceptible to depression. Racial and ethnic backgrounds seem to make some dif-
ference in whether a person is at risk for depression. African Americans and
Hispanic Americans tend to report symptoms of depression less frequently than
non–Hispanic whites. Gender is probably a better indicator of risk. For rea-
sons that we can only speculate about, women seem to be more vulnerable than
men. While depression can occur at almost anytime during the life span, peo-
ple in the prime time of life, those who have major responsibility for carrying
out the workload of the society, seem to be particularly vulnerable. The latter
finding points to stress as one of the factors that trigger depression. And, indeed,
many psychological studies support this idea. Changes in life, particularly those
involving personal loss, are related to depression. Cumulative stresses whether
major or minor may also bring on depression.
Still, we know that not everyone subjected to stress becomes depressed.
Studies have shown that the way we appraise stressful situations makes a dif-
ference. If we don’t exaggerate the importance of what is happening, we are less
likely to overact and less likely to experience an emotional downswing. The way
we think about things makes a difference. Both theory and research indicate
that thought patterns such as overgeneralization, perfectionistic and absolutist
thinking and a predilection for fixing blame on oneself can interfere with mak-
ing a rational appraisal of a stress provoking situation. Instead of reacting in a
measured, problem-solving way, the tendency is to overreact, catastrophizing
the situation, opening up the floodgates to depression.
While psychological researchers have been unraveling the thought pro-
cesses that trigger and sustain depressed mood, researchers trained in the bio-
logical sciences have been exploiting new technologies to study the relation of
depressed mood and the functioning of the body. Significant discoveries have
been made linking depressed states to aberrations in the neurotransmitters in
the brain. Genetic links to depression are being explored with interesting and
provocative results. The day may not be far off when biological tests will be
used in the diagnosis and treatment of depression.
I think it is fair to say that our understanding of depression is something
that has gradually evolved over the past decades. While there have been occa-
sional leaps forward in both our understanding of the disorder and how to
treat it, such as the recognition of the role of the neurotransmitters in depres-
sion and the development of antidepressant drugs and forms of psychotherapy
which are more targeted to deal with depression, with only a few exceptions
(e.g., research on the serotonin transporter gene which may prove to be truly
groundbreaking), a comparison between the first and second editions of Under-
standing Depression will show more of a tendency towards continuity and filling
in the gaps in our knowledge than radical shifts in thinking about depression.
This suggests the study of depression is reaching a level of maturity in both the
science base and in the treatment of depression. Obviously, there is a great deal
more to learn and I feel confident that research over the next decades will add
greatly to our understanding of the disorder.
Depression is a multilayered phenomenon. Even from fragmentary data
we can see that there are social, cultural and environmental aspects of the dis-
order, as well as the more obvious psychological manifestations such as deep
sadness which help define the disorder, and, of course, the underlying biolog-
ical mechanisms. The lack of connectedness among many people in contem-
porary society and the high levels of stress generated in the society may be
latent causes contributing to the increase in depression observed in our house-
hold surveys. While such social structures and institutions are difficult to
change, one can envision potentially useful remedies such as support groups
for people who experience stress and depression, as well as an expanded need
to establish mechanisms in the workplace to reduce levels of stress. The treat-
ment of depression, however, must almost inevitably focus on the psycholog-
ical and biological levels. For here it is where the disorder is manifest, and here
lie the treatments that are known to be efficacious.
Today the mental health profession can offer antidepressant medicines
and psychotherapy. Both treatments are often effective. There is now a variety
of antidepressant drugs which inhibit the reuptake of several important neu-
rotransmitters, either singly or in combination, giving the prescribing physi-
cian more options in choosing medicines. These antidepressant medicines may
improve mood and help get a person functioning. There is also a wider assort-
ment of drugs with which to treat bipolar disorder. Psychotherapy can help
change maladaptive thought patterns and destructive patterns of living which
are contributing to the depressed state. While both types of treatment are help-
ful, neither is a panacea. Medicines have side effects that may not be tolerated
by some patients. Therapy takes time and is expensive, and the patient has to
be willing to put in the required time and effort. And there are a large number
of people who are not helped by either medication or therapy.
Perhaps the biggest problem with current treatments for depression is that
once the course of treatment is completed, there is a sizeable risk that in time —
perhaps even in a matter of months— the symptoms may reappear. Not every-
one experiences recurrence of symptoms, but enough people do to make it a
worrisome possibility. At this point in time we are not certain of the best ways
to prevent recurrence of depressive episodes. Continued use of antidepressant
medicines well beyond the point of remission of symptoms can be helpful in
preventing recurrence. I have recommended that when patients who have gone
through psychotherapy begin to experience uncomfortable levels of stress in
their lives, this is the time to consult their therapists, not wait until everything
falls apart. A stitch in time may well save nine.
I believe that there is a good deal patients can do for themselves to help
¡6. Concluding Remarks 195
prevent further episodes of depression. A lifestyle that reduces the risk of depres-
sion is within the power of many people, just as a lifestyle that reduces the risk
of a heart attack. In the latter case, if you stop smoking, keep your weight
down, avoid dietary fats and unneeded salt and engage in a prudent program
of exercise, the chances of developing coronary heart disease drop consider-
ably. To reduce the risk of depression, you have to pay attention to the build-
up of stress in order to take actions that keep it within acceptable limits. You
should aim for a balanced lifestyle that includes activities that are personally
gratifying.
It is also important to look at what is happening in life from a perspective
that does not turn everyday problems into overwhelming ones. Give yourself
a break when things go wrong. Don’t get down on yourself to the point you
can’t make a comeback tomorrow. Remember that everyone has bad days. The
trick is to learn to take them in stride. Research tells us that people who don’t
catastrophize events are less likely to become depressed.
In this book I have tried to present information and ideas that may be help-
ful to people who have experienced the symptoms of depression or have seen
such symptoms in others who are close to them. I hope that this information
will be useful in increasing your understanding of the nature of depressed mood
and depression and the options that are available to treat depression.
I have tried to emphasize prevention and the importance of healthy atti-
tudes and a balanced lifestyle. But when depressed feelings are severe or one
has been in the throes of a protracted malaise that has eroded the joy of life,
one would do well to consider consultation both with their physician and with
a mental health professional. This book was not intended as a substitute for
such consultation. I hope, however, that it will assist you in making an informed
decision about what to do if such a time should come to pass.
Notes
Chapter 1 16. For examples of experimental dem-
onstrations of the effects of depression on
1. The technique was developed by E. the processing of emotional materials, see
Velten (1986). Rinck & Becker (2005) and Weniger, et al.
2. See Forgas, et al. (1984). (2006).
3. Beck has written extensively about 17. Gallagher (1986), page 4.
the cognitive approach to understanding 18. Our sources for the risk factors for
and treating depression. See, for example, suicide in people with major depressive dis-
Beck, et al. (1979). order studies are studies by Dumais et al.
4. Four fluids (cardinal humors) were (2005), Oquendo, et al. (2004), McGirr, et
thought to influence one’s health: blood, al. (2006) and Solkero, et al. (2005).
phlegm, choler, and melancholy (black 19. Johnson & Magaro (1987), page 29.
bile). 20. The study in Norway was reported by
5. See Goethe (1774), page 1. Wang, et al. (2006)
6. See Folkenberg (1983), page 1. 21. See Robbins & Tanck (1982).
7. See Jaminson (1993), pages 267–270. 22. See Zimmerman, et al. (2006).
8. See Kraepelin (1913). 23. For a statistical study indicating that
9. This important reference has gone the dimensional model may be a better fit
through several revisions. The current edi- for depression than the category model, see
tion published in 1994 is known as DSM IV. Prisciandaro & Roberts (2005).
10. For studies of the facial muscle pat- 24. See Hamilton (1960).
terns of depressed people see Schwartz, et al. 25. For the first version of the BDI, see
(1976) and Sirota & Schwartz (1982). Beck, et al. (1961). For the most recent, see
11. See, for example, Cornell, et al. (1984). Beck et al. (1996).
12. The study of driving skill was carried 26. See Radloff (1977).
out by Bulmash, et al. (2006). 27. See Robbins & Tanck (1994).
13. Freud (1959), page 155. 28. See McMillan & Pihl (1987).
14. The empirical studies that have ex- 29. See Robbins & Tanck (1987).
amined guilt in depressed patients seem to 30. Cook’s narrative first appeared in
confirm the clinical picture. Robin Jarrett & 1909, was reprinted in 1998 (see Cook, 1998)
Jan Weissenburger, for example, found that and was excerpted in Palinkas (2003). The
depressed patients reported higher levels of passage quoted here was taken from Pa-
guilt than control subjects in a variety of sit- linkas, page 353.
uations: doing unintentional harm, failure 31. See Palinkas, pages 353–354.
of self-control, disregard for relationships, 32. Ibid., page 356.
expression of anger, the failure to meet need 33. Shakespeare, The Tragedy of Richard
and violation of principles. Jarrett & Weis- the Third, Act I, scene I. In Parrott, page
senburger (1990). 252.
15. See Dauber (1984) and the doctoral 34. See Rosenthal, et al. (1984).
thesis of Schmidt (1981). 35. The telephone survey of seasonal
197
198 Notes. Chapter 2
mood changes was reported by Kasper, et al. 15. Ibid., page 785.
(1989). 16. Ibid., page 786.
36. See Potkin, et al. (1986). 17. Hammen and Peters (1977). See in
37. Wehr, et al. (1987), page 1603. particular pages 995–996.
38. Falret’s work is described in a paper 18. The observations in New Guinea on
by Sedler (1983). the Kaluli tribe were made by Edward Schi-
39. See Spearing (2002). effelin. The study of the Amish was carried
40. Depue et al. (1981), pages 436–437. out by Egeland and Hostetler (1983).
41. These characteristics of rapid cyclers 19. Blazer, et al. (1985). The statistically
were reported by Kupka et al. (2005). controlled analysis suggested that the rate
42. The study showing the stability of of depression in urban areas was twice as
rapid cycling over time was carried out by high as in rural areas.
Koukopoulos et al. (2003). 20. Rural-urban comparisons in other
43. For reports of very rapid cycling, see countries include studies by Weich, et al.
Kramlinger and Post (1996). (2006), St. John, et al. (2006), Kovess, et al.
44. The study comparing the personality (1987), and Colla, et al. (2006).
patterns of type I bipolar patients, Type II 21. The comparison of immigrants with
bipolar patients and unipolar patients was native born Americans was reported by
reported by Akiskal, et al. (2006). Grant, et al. (2004). See also the study by
45. Studies with apparent conflicting Ortega, et al. (2000).
findings were reported by Summers, et al. 22. See, for example, McGuire (1999).
(2006) and Torrent, et al. (2006). 23. See Breslau, et al. (2005).
46. See Valtonen, et al. (2006) and Valto- 24. Ibid.
nen et al. (2005) for studies of suicide at- 25. See Grant, et al. (2004) and Ortega,
tempts in bipolar patients. et al. (2000).
26. Karno, et al. (1987). For a discussion
of ethnic comparisons, see page 700.
27. The study of the use of health facili-
Chapter 2 ties by Asian Americans was reported by
1. Details on the development of the Bareto and Segal (2005).
NIMH Interview Guide are given in Robins, 28. The incident was described in Mar-
et al. (1981). cos, et al. (1979), page 173.
2. Statistics for the lifetime prevalence 29. Sue and Sue (1987), page 480.
of depressive disorder are presented in 30. The Internet sample study was re-
Robins, et al. (1984). ported by Fogel and Ford (2005).
3. See Kessler, et al. (2005). 31. See Zhang and Snowden (1999).
4. See Hasin, et al. (2005). 32. See Takeuchi, et al. (1998).
5. See Durkheim (1966). 33. The Oregon study was reported in an
6. This estimate was based on the re- article by Lewinsohn, et al. (1986).
search review by Goldbart (2006). 34. Kashani, et al. (1986), page 1141.
7. See McLearn, et al. (2006a). 35. Lefkowitz and Tesiny (1980), page 43.
8. See Goldbart (2006). 36. See Mcfarlane, et al. (1954).
9. The meta analysis was reported by 37. See Hankin and Abramson (2001),
Carter, et al. (2006). page 774.
10. For a review of risk factors for post- 38. See Kovacs (1985) and Kovacs (1992).
partum depression see McCoy et al. (2006). 39. The study of the Children’s Depres-
11. For an example of a study showing sion Inventory carried out in Belgium was
the relation of postpartum depressive levels reported by Timbremont, et al. (2004).
and maternal-child behaviors see McLearn, 40. Carey, et al. (1987), page 761.
et al. (2006b). 41. See Doerfler, et al. (1988).
12. See Angold, et al. (1998). 42. See Larson, et al. (1990).
13. See Brooks-Gunn and Warren (1989). 43. See Kerr, et al. (1987).
14. These data are reviewed in Hankin 44. For a discussion of adolescent suicide
and Abramson (2001). See page 784. and suicidal ideation, see Robbins (1998).
Notes. Chapter 3 199
45. See Reynolds and Coats (1982). and non-depressed subjects was reported by
46. The study of French high school stu- Campbell, et al. (2004).
dents was reported by Chabrol, et al. (2002). 8. For a discussion of hippocampal nerve
47. A Graph showing the age distribution cell genesis see Dranovsky and Hen (2006).
for the onset of bipolar illness was presented 9. Research on the amygdala in de-
in Grant, et al. (2005), page 1210. pressed patients is reviewed by Weniger, et
48. See, for example, the study by Sou- al. (2006) and Campbell, et al. (2004).
rander et al. (1999). 10. See Weniger, et al. (2006).
49. For data showing the risk of onset of 11. For a review of MRI studies on early-
depression during adolescence and young onset bipolar patients, see Frazier, et al.
adulthood, see Burke, et al. (1990). See Hasin (2005).
et al. (2005) for more recent data indicating 12. See Wurtman, et al. (1982).
a shift in maximum risk toward middle age. 13. See Neumeister, et al. (2004) and
50. The study in Canada of rural and Neumeister et al. (2006).
urban elderly people was reported by J. L. 14. See, for example, Owens and Nemer-
Wang (2004). off (1994) and Mann, et al. (1986). There are
51. See Kessler, et al. (2005). research findings indicating an increase in
52. The data showing the often pro- the number of serotonin binding sites in the
longed nature of depression in the elderly frontal cortices of violent suicide victims.
was reported by Beekman, et al. (2002). For a further discussion of this issue, see
53. The study of physical decline in the Pandy (1997).
depressed elderly was reported by Penninx, 15. See Gorman, et al. (2000).
et al. (1998). Similar results were reported by 16. See Siever and Davis (1985).
Lenze, et al. ( 2005). 17. See Dickerson and Kemeny (2004).
54. See Rapp, et al. (1988). 18. For a discussion of the DST as a tool
in the diagnosis of depression, see the re-
port of the APA Task Force on Laboratory
Tests in Psychiatry (1987).
Chapter 3 19. Ibid. See, also Meller, et al. (1988).
20. The improvements using the DEX/
1. Positron emission tomography (PET) CRH test in identifying depressed patients
and functional MRI (fMRI) are two of the was reported by Heuser, et al. (1994). The
more widely used techniques to measure ac- findings for chronic depressed patients were
tivity levels in a given area of the brain. For reported by Watson, et al. (2002).
a more extended description of PET see 21. The study in Japan was reported by
Robbins (2007). Kunugi, et al. (2006).
2. For a review of family studies and de- 22. The study of bipolar patients was re-
pression, see Weissman (2006). The finding ported by Watson, et al. (2004).
that people with a family history of depres- 23. For a discussions of REM studies in
sion often had early onset anxiety symptoms depressed patients see Kupfer (2006) and
was reported by Weissman. Shaffery, et al. (2003).
3. Data for second degree relatives of 24. See Ehlers, et al. (1988). More recent
depressed people were cited in Sargent estimates put the figures for 70 percent for
(1986). outpatients and 80 percent for inpatients.
4. See Kendler (1986). See Lam (2006).
5. The two twin studies were reported 25. For a discussion of circadian rhythms
by Bierut, et al. (1999) and Kendler and and SAD, see Lewy, et al. (2006).
Prescott (1999). 26. For a review of antidepressant med-
6. The studies reporting heritability es- ications and sleep, see Wilson and Argyra-
timates for bipolar disorder were reported poulos (2005) and Lam (2006).
by Kieseppa, et al. (2004) and McGuffin, et 27. See Kufper (2006).
al. (2003). 28. The dreams of depressed people are
7. The meta-analysis of studies compar- discussed in Robbins (1988), Chapter 7. See
ing the size of the hippocampus in depressed also Robbins and Tanck (1988).
29. The study of the dreams of bipolar 7. The scale which has been widely used
patients was reported by Beauchemin and to measure the perceptions of the control of
Hays (1966). reinforcement was developed by Julian Rot-
30. See Blaise, et al. (1986). ter. See Rotter (1960).
31. See, for example, Denney, et al. (1988). 8. See Benassi, et al. (1988), page 362.
32. See Weisse (1992). 9. For a review of research on learned
33. Ibid., page 481. helplessness, see the special February 1978
34. For a non-technical discussion of the issue of the Journal of Abnormal Psychology,
use of endophenotypes, see Dingfelder entitled “Learned Helplessness as a Model
(2006). For an application of the concept to of Depression.” See, in particular, the arti-
research on depression, see Hassler, et al. cle by Seligman.
(2004). 10. This experiment was carried out by
35. Recently, the picture has become Hiroto (1974).
more complex, as functional variants have 11. See Altman and Winterborn (1980).
been identified in the long (L) form. 12. Anouilh (1959), Act 3, p. 64.
36. For a discussion of the serotonin 13. See Hawkins, et at. (1988).
transporter and the long and short variants, 14. See Wenzloff and Grozier (1988),
see Hariri and Holmes (2006). page 93.
37. See, for example, a meta-analysis re- 15. See Carver and Ganellen (1983), page
ported by Sen, et al. (2004). 333.
38. See Hariri (2002). See also Bertolino, 16. The study identifying the aspects of
et al. (2005). perfectionism that had particular relevance
39. See Caspi, et al. (2003). to depression was carried out by Enns and
40. See Zalsman, et al. (2006). Cox (1999). See also Packard (2006).
41. These data were presented as a fol- 17. The study of people suffering from
low-up report to the NIMH study of 2004. insomnia was reported by Vincent and
See Neumeister, et al. (2006). Walker (2000).
18. See, for example, Blatt, et al. (1988),
Zuroff, et al. (2000), and Hawley, et al.
(2006).
Chapter 4 19. See Ellis (1962).
1. While Beck viewed, “the negative 20. See Beck (1976), page 255.
processing of information” as primary, in 21. For a study of social comparisons and
that it leads to the other symptoms of de- depression, see Bazner, et al. (2006). A
pression, he did not view negative thoughts meta-analysis of the results of many studies
as the cause of depression. In reviewing the found that self-focusing was related to neg-
status of cognitive therapy, he wrote, “It ative mood, anxiety and depression. See
seems farfetched to assign a causal role to Mor and Winquest (2002).
cognitions because the negative automatic 22. See Freud (1959).
thoughts constitute an integral part of de- 23. See Robbins and Tanck (1997).
pression, just like the motivational, affec- 24. The items for the automatic thoughts
tive, and behavioral symptoms. To conclude questionnaire are listed in Table I of the
that cognitions cause depression is analo- paper of Hollon and Kendall (1980). See
gous to asserting that delusions cause schiz- page 389.
ophrenia.” See Beck (1991), 373, 369. 25. The Dysfunctional Attitudes Scale is
2. See, for example, Incoviello, et al. described in Weissman and Beck (1978).
(2006). 26. The study of dysfunctional attitudes
3. For research on the recognition of fa- and postpartum depression was reported by
cial expressions, see Joorman and Gotlib Church, et al. (2005).
(2006) and Surguiazde et al. (2004). 27. See, for example, Seligman, et al.
4. See Beck (1976), page 33. (1979).
5. See Buchwald (1977). 28. For a discussion of the Attribution
6. See, for example, Lewinsohn, et al. Style Questionnaire, see Peterson and Vil-
(1980). lanova (1988). The meta-analyses involved
thousands of subjects. A meta-analysis for 18. See Alloy et al. (2006).

adults was reported by Sweeney, et al. (1986). 19. See McCraine and Bass (1984), page
A meta-analysis for children was reported 7.
by Gladstone and Kaslow (1995). 20. These statements were excerpted
29. See Meyersburg, et al. (1974), page from Cofer and Winterborn (1980), page
376. 313. See in particular Table 5.
30. See Lewinsohn, et al. (1980), page 21. These data were obtained in a study
205. relating Beck Depression Inventory scores
31. Ibid., page 212. to reports of early memories. See Robbins
32. Ibid., page 211. and Tanck (1994).
33. See Snyder (1984). 22. The prospective studies varied in
terms of the length of follow up. See Alloy
et al. (2006). The follow-up period in one of
the studies, Pilowsky et al. (2006) has now
Chapter 5 exceeded two decades.
23. These data were reported by Pilowsky
1. See Bowlby (1982), page 668. et al. (2006).
2. See, for example, Harlow (1958). 24. See Kazdin et al. (1985), page 304.
3. The study comparing attachment 25. Data linking childhood sexual abuse
patterns of children from divorced families and psychiatric disturbances including de-
with those from intact families was reported pression was reported by Molnar et al.
by Nair and Murray (2005). (2001).
4. For a discussion of the early research 26. See Alloy et al. (2006).
relating to attachment, see articles by Gold- 27. For a discussion of the psychological
smith and Alansky (1987) and Cicchetti affects of divorce on children, see Hether-
(1987). ington (1989). For a recent report of a lon-
5. See Ainsworth (1989), page 710. gitudinal study linking measures of parental
6. The study of reactions to the play of discord to subsequent depression in the off-
toddlers was reported by Fagot (1997). spring, see Pilowsky et al. (2006).
7. For reports of the longitudinal study 28. See, for example, Coleg (1990).
of children evaluated in the strange situa- 29. See Lef kowitz and Tesiny (1980),
tion, see Stroufe et al. (2005). page 44.
8. The study of attachment in nine- to 30. McGrath and Repetti (2002) found
eleven-year-old children was reported by that children with more symptoms of de-
Kearns et al. (2007). pression underestimated their actual com-
9. The study of adult attachment and petence. See, also, related studies by Hoff-
depression was carried out by Bifulco, et al. man et al. (2000) and Kistner et al. (2006).
(2002a) and Bifulco, et al. (2000b). For a more general look at the relation of
10. The studies of fear of rejection and childhood competence and depression, see
depression were conducted by Reis and Blechman et al. (1986).
Grenyer (2004). 31. This study was carried out by Rock-
11. See Blatt (1974). hill et al. (2007).
12. This analysis was reported by Nelson 32. See Leitenberg et al. (1986), pages
(1982). See, also, Barnes and Prosen (1985). 529–530.
13. See Agid, et al. (1999). 33. See Seligman et al. (1984), page 238.
14. The study relating rejecting parents 34. For illustrative studies pointing out
to self-hatred self-criticism was reported by these gender differences in adolescence, see
Irons et al. (2006). See also Robbins and Gjerde et al. (1988) and Oldenhinkel et al.
Tanck (1997). (2007).
15. See Parker (1979) and Parker, et al. 35. See Prinstein et al. (2005).
(1979). 36. See, for example, Sund, et al. (2003).
16. For a description of some of this re-
search see Alloy, et al. (2006).
17. See Parker (1983).
202 Notes. Chapters 6 and 7
Chapter 6 particular Table 1, page 150. There have been

a number of studies that related techniques
1. See Meyersburg et al. (1974), page people used to cope with stress to feelings of
384. depression. An example would be the stud-
2. The review was carried out by C. M. ies carried out by Charles Holahan and
Mazure (1998). The statistics were cited in Rudolph Moos. They assessed their subjects
Hammen (2005). on a number of measures including coping
3. There are a large number of studies techniques, then followed the subject for
which show the buffering effect of social several years. They reported, “We have
support. For an example of a recent study, found that personality characteristics that
see Krohne and Slangen (2005). They found involve more self-confidence and more
that social support reduced anxiety levels in easy-going disposition, more family sup-
patents undergoing surgery. port, and fewer avoidant coping strategies
4. See Freud (1959) and Bowlby (1980). predict lower levels of depression.” See, Ho-
5. While the evidence indicates that lahan and Moos (1991).
many people are able to cope with serious 20. See Cole et al. (2006), page 40.
losses without experiencing depression, the 21. The concept of the sick role was elu-
chances of becoming depressed nonetheless cidated by sociologist Talcott Parsons. See,
are increased. A study by Patrick Shrout and for example, Parsons (1975).
his colleagues (1989) suggested that experi- 22. See Cole et al. (2006).
encing fateful losses such as the death of a 23. The hypothesis of biological changes
spouse or child, the loss of a home or job following repeated episodes of depression
or being unable to find treatment for a seri- was developed in a seminal article by Post
ous illness raises the odds of becoming de- (1992).
pressed. A study by Stanley Murrell and 24. See Monroe and Harkness (2005).
Samuel Himmelfarb (1989) indicated that 25. The study of assault victims was re-
the depressive effects of bereavement in ported by Foa et al. (2006).
older adults began to dissipate within a year.
6. See Robbins and Tanck (1984).
7. See Kanner et al. (1981). Chapter 7
8. See Hammen (2005). The citation is
on page 303. 1. See Crowe and George (1989), page
9. The tendency for cortisol levels to be 374.
particularly elevated during stress arousing 2. A factor analytic study showing how
situations which are uncontrollable was re- items assessing these indicators form a fac-
ported in a review of research carried out tor of alcohol dependence was reported by
by Dickerson and Kemeny (2004). Grant et al. (2006).
10. See Catrona et al. (2005). 3. The 12 month prevalence for alcohol
11. Ibid., page 12. disorders was reported in a study by Stinson
12. See Caspi et al. (2003). et al. (2005). See, in particular, page 109.
13. See Hammen (2005), page 310. 4. This assertion made by Benjamin
14. See Hammen et al. (2000). Karpman was cited by Wall (1937).
15. For an illustrative study of the rela- 5. See Clark et al. 1985, pages 483–485.
tion of adult attachment style to childhood 6. See Lutz’s and Snow’s (1985) review.
adverse events and current social relation- These studies should be interpreted cau-
ships, see Bifulco et al. (2002). tiously as the data are retrospective.
16. For a review of the studies, see Ham- 7. See Stinson et al. (2005). See, in par-
men (2005). The importance of activating ticular, Table 2.
depressive cognitions was indicated in a 8. See Kuo et al. (2006).
study carried out by Abela et al. (2004). 9. For discussions of expectations from
17. See Hammen (2005), page 311. drinking see Brown et al. (1980) and Smith
18. See Folkman and Lazarus (1986), (1994).
page 110, Table 2. 10. See Crowe and George (1989), page
19. See Robbins and Tanck (1992), in 375.
11. See Nathan et al. (1970). and McCabe and Marwit (1993) for a study
12. See Robbins and Nugent (1975). of this relation in children.
13. The study carried out by Homish et 10. See the work of Betty Allgood-Merten
al. was cited by Munsey in the Monitor on et al. (1990). In discussing their research on
Psychology (2007). adolescence, Allgood-Merten and her col-
14. These statistics on marijuana use leagues state, “The results also corroborate
were taken from Stinson et al. (2006). the finding that body image is an important
15. See Robbins (1983), page 27. correlate of depression in adolescence.
16. See Keeler et al. (1971). (Body image) is a critically important aspect
17. See Robbins and Tanck (1973). of self-esteem in this age group that func-
18. These interesting findings relating to tions as an antecedent as well as a strong
bipolar disorder were reported in Stinson, et correlate of depressive symptoms in adoles-
al. (2006). cents.” Allgood-Merten et al. (1990), page
19. The study in Oakland was reported 61. See, also, Paxton et al. (2006).
by Zweben et al. (2004). 11. A study reported by Douglas Needles
20. The Internet study was reported by and Lynn Abramson suggested that the in-
Looby and Earleywine (2007). troduction of pleasant activities into one’s
21. The study of arrestees was reported daily life would be most beneficial when ac-
by Kalechstein et al. (2000). companied by changes in the person’s out-
22. The study on cocaine users was re- look and attitudes that enable him or her to
ported by Schmitz et al. (2000). more fully enjoy the activities. See Needles
23. See, for example, Schmitz et al. (2001) and Abramson (1990).
and Galloway et al. (1994). 12. See Gladstone et al. (2007).
24. See Robbins and Nugent (1975). A re- 13. For examples of studies carried out
cent study drawing from a very different abroad, see Stansfeld, et al. (1998), Ostberg
population, heroin patients entering treat- and Lennartsson (2007), Aro, et al. (2001),
ment centers in Australia reported major and Koizumi, et al. (2005).
depressive disorder in about one-fourth of 14. For illustrative studies, see Libet and
the subjects with higher rates among females Lewinsohn (1973) and Petty et al. (1994).
than males. See Teesson et al. (2005). 15. The comment was provided by
25. For further discussion of these data, DBSA.
see Robbins (1974). 16. This early review on self help manuals
was written by Glasgow and Rosen (1978).
17. See Scogin et al. (1989) and Floyd et
al. (2004).
Chapter 8 18. See Griffiths and Christensen (2007)
1. Paul Hewitt and Gordon Flett devel- for a review of research using moodGYM.
oped a reliable scale to measure perfection- 19. For a study suggesting that while self-
ist tendencies. See Hewitt and Flett (1991). help information may increase knowledge
2. See Heiby (1982). about depression it may not translate into
3. The study linking a lack of self rein- reduction of depressive symptoms. See Sal-
forcement to depression was reported by kovskis, et al. (2006).
Wilkinson (1997). 20. The study carried out in Germany
4. The strategy of small wins was dis- was reported by Kronmuller (2007).
cussed in Weick (1984). 21. The review of evaluation studies for
5. This line was attributed to J. L. computerized cognitive-behavioral therapy
Spaulding. was written by Kaltenthaler (2006). It
6. The randomized controlled trial should be stated that there are studies which
studying the effects of exercise on depres- report little effect from using these types of
sion was reported by Dunn et al. (2005). programs.
7. For a discussion of community stud- 22. See Jewell and Mylander (1988).
ies, see Harris et al. (2006). 23. See Nezu et al. (1989) and Nezu et al.
8. Ibid. (1990).
9. See, for example, Noles et al. (1985) 24. See Mahalik et al. (1988), page 241.
204 Notes. Chapters 9–11
Chapter 9 12. For studies of underutilization of

mental health services among minorities,
1. See Neuringer (1982), page 185. see Alegria et al. (2002) and Neighbors et
2. See Szasz (1986), page 809. al. (2007).
3. DBSA provides a number of helpful 13. See, for example, Kessler et al.
suggestions. See, for example, “Helping (2005), and Olfson et al. (2002).
Someone with a Mood Disorder” posted on
its website.
4. Papers by Veil and Kuhner (1990) and
Veil (1993) describe these counterintuitive Chapter 11
findings.
5. See, for example, Beach (1987). 1. These estimates for the effectiveness
6. For research of the social and psycho- of antidepressant drugs are based on reviews
logical impact on the family, see Benazon and meta-analyses of many studies. See, for
and Coyne (2000), van Wijngaarden, et al. example Bollini, et al. (1999).
(2004), and Fadden, et al. (1987). 2. For an example of a study in which an
7. See Coyne, et al. (1987), page 350. antidepressant did not perform better than
8. See, for example, Benazon and Coyne a placebo, see Moreno, et al. (2006).
(2000). 3. The study showing the possible
benefits of trying several antidepressants
was reported by Quitkin, et al. (2005).
4. See Medications for Mental Illness,
Chapter 10 page 16.
5. See Kocsis et al. (1988).
1. The often long delay between the 6. The review of the efficacy of tricyclics
onset of mental and emotional disorders and and other antidepressants was reported by
treatment for these disorders was reported Einarson, et al. (1999).
by Wang at al. (2005). 7. The article in the Emergency Medi-
2. See Wang et al. (2006). cine Journal was written by Kerr, et al.
3. These statistics for physician recogni- (2001).
tion of depression were reported by Simon 8. See FDA approves Emsam (selegiline)
and VonKorff (1995). as first drug patch for depression (2006). See
4. The study looking at difficulties in re- also Frampton and Plosker (2007) for stud-
ferral was reported by Trude and Stoddard ies of the use of this drug patch.
(2003). 9. For a discussion of the treatment of
5. The decline in use of psychotherapy atypical depression see Rapaport (2007).
without medication was reported by Wang 10. The comparison between SSRIs and
et al. (2006). tricyclics was reported by Anderson (2000).
6. This conclusion was reached by Kess- 11. The study of the efficacy of the SSRI,
ler et al. (2005). citlapram was carried out by Trivedi et al.
7. Questions of the adequacy of treat- (2006).
ment for depression by primary care physi- 12. See, for example, Anderson (2000).
cians have been raised in a number of stud- 13. The review of the efficacy of SSRIs in
ies. See, for example, Young et al. (2001). comparison with tricyclics when used in
8. For a discussion of the changing re- primary-care settings was reported by Mac-
lation between stress and depression, see Gillivray, et al. (2003). See, also, Arroll, et al.
Monroe and Harkness (2005). (2005).
9. For a look at the stigma associated 14. The study carried out in United
with mental illness in past years, see Yarrow States primary-care clinics was reported by
et al. (1955). The recent survey of attitudes Clayton et al. (2002). The study in Spain was
about mental-health treatment was reported reported by Montejo et al. (2001).
by Mojtabi (2007). 15. For a discussion of the possible links
10. See Rost et al. (2007). between SSRIs and suicidal thinking, see
11. See Sue and Sue (1987). Whittington (2005).
Notes. Chapters 12 and 13 205
16. For studies evaluating the effects of itive activities, as a treatment for depression
using SSRIs during pregnancy on the new- revealed positive findings. The meta-analy-
born child, see Malm et al. (2005) and the sis was carried out by Cuijpers et al. (2007).
article in the Health Section of the Wash- 7. See Klerman et al. (1984) for a discus-
ington Post, “Birth defects: Risks appear low sion of interpersonal therapy including the
when mother uses SSRI antidepressants.” case of Ellen F.
17. See Serebruany (2006). 8. For a review of meta-analyses carried
18. For a study comparing bupropion out for cognitive-behavioral therapy, see
with SSRIs in terms of reported sexual dys- Butler et al. (2006).
function, see Clayton et al. (2002). 9. The meta-analysis for interpersonal
19. For a meta-analysis comparing the therapy was carried out by de Mello et al.
efficacy of the SNRI venlafaxine with that of (2005).
SSRIs, see Einarson et al. (1999). 10. The review of studies which used in-
20. See, for example Sir, et al. (2005). terpersonal therapy with adolescents was re-
21. The comparison between duloxetine ported by Brunstein-Klomek et al. (2007).
and escitalopram was reported by Nieren- 11. For recent papers looking at the
berg, et al. (2007). efficacy of psychodynamic therapy for de-
22. See Medicines for Mental Illness, page pression see Bond (2006) and Trowell et al.
10. (2007).
23. Ibid., page 11. 12. This research is described by Weiss-
24. Ibid., page 11. man (2007).
25. Ibid., page 11. 13. See, for example, Nietzel et al. (1987).
26. Ibid., page 12. 14. See Wampold et al. (2002).
27. Ibid., page 13. 15. For examples of studies that show
28. See, for example, Bridle, et al. (2004). that people with more severe depression do
29. See Bridle et al. (2004) and Smith et less well in therapy, see Gonzales et al.
al. (2007). (1985) and Hoberman et al. (1988). A recent
30. See Medications for Mental Illness, meta-analysis showed that the severity of the
page 27. disorder affects the outcome not only for de-
pression but for anxiety disorders as well.
See Haby et al. (2006).
16. See, for example, Hoberman et al.
Chapter 12 (1988).
17. See McBride et al. (2006).
1. See Kazdin (1986), page 96. 18. See, for example, the review of re-
2. See Freud’s essay Mourning and search carried out by Steinbrueck et al.
Melancholia, republished (1959). (1983) which concluded that, “Psychother-
3. For a discussion of psychoanalytic apy appears to be somewhat more effective
thinking about depression see Bellak (1981). than drug therapy.”
4. Beck (1976), pages 213–14. Robert De- 19. The collaborative study is described
Rubeis and his colleagues (1990) suggest that in Elkin et al. (1989).
the basis for the effectiveness of cognitive 20. See Agency for Health Care Policy
therapy lies not only in the changes in think- and Research (1993).
ing that take place in therapy, but in the ac- 21. See DeRubeis et al. (1999).
tive application of their principles in the pa- 22. See Conte et al. (1986).
tient’s everyday life. The same maxim would 23. For an illustrative study, see de Maat
seem to hold for most forms of therapy; ther- et al. (2007).
apy does not stop in the therapist’s office.
One must practice what one has learned.
5. The case was excerpted from Safran
et al. (1986). See pages 516–518. Chapter 13
6. A recent meta-analysis looking at the
efficacy of the behavioral therapy technique, 1. See Way and Banks (2001).
teaching activity scheduling to increase pos- 2. The current telephone number for
the National Mental Health Information 14. The study exploring the efficacy of
Center is 1-800-789-2647. Their web site is MBCT was reported by Finucane and Mer-
www.mentalhealth.samhsa.gov. cer (2006).
3. For a very readable account of the de- 15. The meta-analysis was reported by
velopment of electroconvulsive therapy see Toneatto and Nguyen (2007).
Sabbatini (2007). For a general overview 16. See Moyer et al. (2004), page 3.
of electroconvulsive therapy, see Taylor 17. The survey of massage therapists was
(2007). reported by Sherman et al. (2005).
4. Personal communication 18. See Moyer et al. (2004), page 12.
5. For a description of electroconvulsive 19. The studies showing increased sero-
therapy in modern dress, see S. Wang tonin levels following massage therapy are
(2007). described in Field et al. (2005).
6. See Consensus Development Confer- 20. See Moyer et al., page 14.
ence Statement (1985). 21. See Field et al. (2005), pages 1399–
7. See Taylor (2007). Taylor cites data 1400.
which indicates that as many as 55 percent 22. See Lee (2006). The article is in Ko-
of depressed patients not helped by other rean. I have relied on the translated abstract.
treatments have responded well to electro- 23. The study comparing the effects of
convulsive therapy. acupuncture and massage on depression
8. The study of differential memory loss measures was reported by Manber et al.
was reported by Lisandby et al. (2000). (2004).
9. See Taylor (2007). 24. See St. John’s Wort and the Treatment
10. Ibid. of Depression (2004), page 2.
11. The case study was reported by Go- 25. The study in Brazil was carried out
forth and Holsinger (2007). by Moreno et al. (2006).
26. The 1996 meta-analysis on the
efficacy of St. John’s wort was reported by
Linde et al. (1996). The two subsequent
Chapter 14 meta-analyses were reported by Kim et al.
(1999) and Whisky et al. (2001). The collab-
1. See Kessler et al. (2001) or Barnes et orative study carried out by the National In-
al. (2004). stitutes of Health was cited in St. John’s Wort
2. See Ernst et al. (1999). and the Treatment of Depression, page 4. See
3. See Meditation for Health Purposes the Journal of the American Medical Associ-
(2006), page 3. ation, 2002, volume 287, page 1907 for more
4. Ibid. details.
5. See Cahn and Polich (2006), page 27. See St. John’s Wort and the Treatment
180. of Depression, page 4.
6. Ibid. 28. Ibid., page 1.
7. See Meditation for Health Purposes 29. The study of St. John’s wort carried
(2006), page 2. out in Germany was reported by Szegedi, et
8. See Cahn and Polich, (2006), page al. (2005).
201. 30. For a discussion of the incidence of
9. Ibid., page 182 adverse affects reported by users of St. John’s
10. Ibid., page 181. wort, see Schultz (2006).
11. Most of these subjects in this study 31. The two papers were authored by
were retested in a three year follow-up. The Caccia (2005) and by Wurglics and Schu-
improvements in depression and anxiety bert-Zsilavecz (2006).
scores were maintained. See Kabat-Zinn et 32. These data were cited in Covington
al. (1992). (2004).
12. See Lau and McMain (2005), page 33. See Hibbeln (1998).
864. 34. See Sontrop and Campbell (2006) for
13. For Information on the development a review of the studies.
of MBCT, see Teasdale et al. (1995). 35. The case was reported by Chiu et al.
Notes. Chapter 15 and 16 207
(2003) in a letter to the American Journal of 3. See Billings and Moos (1984) and
Psychiatry. Billings and Moos (1985).
36. The study of suicide attempts was re- 4. See Burcusa and Iacono (2007).
ported by Sublette et al. (2006). 5. Ibid.
37. The study of children in Israel was 6. These factors, similar to ones listed
carried out by Nemets et al. (2006). in the 1993 edition of Understanding Depres-
38. The study of bipolar patients was re- sion were taken from Burcusa and Iacono
ported by Frangou et al. (2006). (2007).
39. See Hibbeln et al. (1998). 7. A study by Melartin et al. (2004)
40. SAD and bright light therapy were showed that the severity of depression was
described in Rosenthal, et al. (1984). For an related to both the length of the episode and
example of a subsequent study, See, Lam et recurrence.
al. (2006). 8. See Vittengl et al. (2007).
41. The excellent review by the Termans 9. The study comparing psychotherapy
covers many issues relating to the use of and antidepressant medicine in terms of
bright light therapy. See Terman and Ter- post treatment resiliency to stressors was
man (2005). carried out by Hawley et al. (2007).
42. See Goel et al. (2005). 10. See Kashner et al. (2007).
43. These reports were mentioned in the 11. See Vittengl et al. (2007).
review of bright light therapy by Terman 12. See Gonzales et al. (1985).
and Terman (2005). 13. The study was reported by Frank et
44. Ibid. al. (2007).
14. See Vittengl et al. (2007), Kashner et
al. (2007), and Bockting, et al. (2005).
15. See, for example, Thase (2006) and
Chapter 15 Fava et al. ( 2006).
1. The survey of clinicians was reported 16. See Thase (2006).
by Friedman, et al. (2000). For a study
showing the value of raising the dose of an-
tidepressants to deal with relapse, see Fava
et al. (2006). Chapter 16
2. For a discussion of the terms relapse
and recurrence see the review of Burcusa 1. See Westermeyer (1987), page 475.
and Iacono (2007).
Bibliography
Abela, J. R., Browa, K., & Seligman, M. E. (2004). A test of integration of the activation
hypothesis and the diathesis-stress component of the hopelessness theory of depression.
British Journal of Clinical Psychology, 43, 111–128.
Agency for Health Care Policy and Research (1993). Clinical practice guidelines: Depression
in primary care, Volume 2: Treatment of major depression. Washington, D.C., U.S. Govern-
ment Printing Office, AHCPR Publication 93-0551.
Agid, O., Shapira, B., Zislin, J., Ritsner, M., Hanin, B., Murad, H., Troudart, T., Bloch, M.,
Heresco-Levy, U., & Lerer, B. (1999). Environment and vulnerability to major psychi-
atric illness: A case control study of early parental loss in major depression, bipolar dis-
order, and schizophrenia. Molecular Psychiatry, 4, 163–172.
Ainsworth, M. D. S. (1989). Attachments beyond infancy. American Psychologist, 44, 709–716.
Akiskal, H. S., Kilzieh, N., Maser, J. D., Clayton, P. J., Schettler, P. J., Shea, M. T., Endicott,
J., Scheftner, W., Hirschfeld, R. M. A., & Keller, M. B. (2006). The distinct tempera-
ment profiles of bipolar I, bipolar II and unipolar patients. Journal of Affective Disor-
ders, 92, 19–33.
Alegria, M., Canino, G., Rios, R., Vera, M., Calderon, J., Rusch, D., & Ortega, A. N. (2002).
Inequalities in use of specialty health services among Latinos, African-Americans, and
non–Latino Whites Psychiatric Services, 53, 1547–1555.
Allgood-Merten, B., Lewinshon, P. M., & Hops, H. (1990). Sex differences and adolescent
depression. Journal of Abnormal Psychology, 99, 55-63.
Alloy, L. B., Abramson, L. Y., Smith, J. M., Gibb, B. E., & Neeren, A. M. (2006). Role of par-
enting and maltreatment histories in unipolar and bipolar mood disorders: Mediation
by cognitive vulnerability to depression. Clinical Child and Family Psychology Review.
Altman, J. H., & Winterborn, J. R. (1980). Depression-prone personality in women. Journal
of Abnormal Psychology, 89, 303-308.
American Psychiatric Association (1994). Diagnostic and statistical manual of mental disor-
ders (fourth edition). Washington, D.C.
Anderson, I. M. (2000). Selective serotonin reuptake inhibitors verses tricyclic antidepres-
sants: A meta-analysis of efficacy and tolerability. Journal of Affective Disorders, 58, 19–
36.
Angold, A., Costello, E. J., & Worthman, C. M. (1998). Puberty and depression: The roles of
age, pubertal status and pubertal timing. Psychological Medicine, 28, 51–61.
Anouilh, J. (1959). Restless Heart. In Five Plays, Volume II. New York: Hill and Wang.
The APA Task Force on Laboratory Tests in Psychiatry (1987). The Dexamethasone Suppres-
sion Test: An overview of its current status in psychiatry. American Journal of Psychia-
try, 144, 1253–1262.
Aro, A. R., Nyberg, N., Absetz, P., Henriksson, M., & Lonnqvist, J. (2001). Depressive symp-
toms in middle-aged women are more strongly associated with physical health and social
support than with socioeconomic factors. Nordic Journal of Psychiatry, 55, 191–198.
Arroll, B. MacGillivray, S., Ogston, S., Reid, I., Sullivan, F., Williams, B., & Crombie, I. (2005).
209
210 Bibliography
Efficacy and tolerability of tricyclic antidepressants and SSRIs compared with placebo
treatment for depression in primary care: A meta-analysis. American Family Medicine,
3, 449–456.
Barcusa, S. L., & Iacono, W. G. (2007). Risk for recurrence of depression. Clinical Psychology
Review (in press).
Barnes, G. E., & Prosen, H. (1985). Parental death and depression. Journal of Abnormal Psy-
chology, 94, 64–69.
Barnes, P., Powell-Griner, E., McFann, K., & Nahin, R. (2004). Complementary and alter-
native medicine use among adults: United States, 2002. CDC Advance Data Report #343.
nccam.nih.gov/news/camsurvey.
Barreto R. M., & Segal, S. P. (2005). Use of mental health services by Asian Americans. Psy-
chiatric Services, 56, 746–748.
Bazner, E., Bromer, P., Hamelstern, P., & Meyer, T. D. (2006). Current and former depres-
sion and their relationship to the effects of social comparison processes. Results of an
internet study. Journal of Affective Disorders, 93, 97–103.
Beach, S. R. H., Sandeen, E. E., & O’Leary, K. D. (1987, November). Treatment for the
depressed maritally discordant client: A comparison of behavioral marital therapy, indi-
vidual cognitive therapy, and wait list. Paper presented at the annual meeting of the Asso-
ciation for the Advancement of Behavior Therapy, Boston, Massachusetts.
Beauchemin, K. M., & Hays, P. (1996). Dreaming away depression: The role of REM sleep
and dreaming in affective disorders. Journal of Affective Disorders, 25, 125–133.
Beck, A. T. (1976). Cognitive therapy and the emotional disorders. New York: International
University Press.
_____ (1991). Cognitive therapy: A 30-year retrospective. American Psychologist, 46, 368–375.
Beck, A. T., Rush, A. J., Shaw, B. F., & Emery, G. (1979). Cognitive therapy for depression. N.Y.:
Gilford Press.
Beck, A. T., Steer, R. A., & Brown, G. K. (1996). Manual for the Beck Depression Inventory-
II. San Antonio, Texas: Psychological Corporation.
Beck, A. T., Ward, C. H., Mendelson, M., Mock, J., & Erbaugh, J. (1961). An inventory for
measuring depression. Archives of General Psychiatry, 4, 561–57l.
Beekman A. T., Geerlings, S. W., Deeg, D. J., Smit, J. H., Schoevers, R. S., deBeurs, E., Braam,
A. W., Penninx, B. W., & van Tilburg, W. (2002). The natural history of late-life depres-
sion: A 6-year prospective study in the community. Archives of General Psychiatry, 59,
605–611.
Bellak, L. (1981). Brief psychodynamic psychotherapy of nonpsychotic depression. American
Journal of Psychotherapy, 35, 160–172.
Benassi, V. A., Sweeney, P. D., & Dufour, C. L. (1988). Is there a relation between locus of
control orientation and depression? Journal of Abnormal Psychology, 97, 357–367.
Benazon, N. R., & Coyne, J. C. (2000). Living with a depressed spouse. Journal of Family Psy-
chology, 14, 71–79.
Bertolino, A., Arciero, G. Rubino, V., Latorre, V., DeCandia, M., Mazzola, V., Blasi, G.,
Caforio, G., Hariri, A., Kalachana, B., Nardini, M., Weinberger, D. R., & Scarabino, T.
(2005). Variation of human amygdala response during threatening stimuli as a function
of 5- HTTLPR genotype and personality style. Biological Psychiatry, 57, 1517–1525.
Bierut, L. J., Heath, A. C., Bucholz, K. K., Dinwiddie, S. H., Madden, P. A., Statham, D. J.,
Dunne, M. P., & Martin, N. G. (1999). Major depressive disorder in a community-based
twin sample: Are there different genetic and environmental contributions for men and
women? Archives of General Psychiatry, 56, 557–563.
Bifulco, A., Moran, P. M., Ball, C., & Bernazzani, O. (2002). Adult attachment style: I. Its
relationship to clinical depression. Social Psychiatry and Psychiatric Epidemiology, 37,
50–59.
Bifulco, A., Moran, P. M., Ball, C., & Lillie, A. (2002). Adult attachment style. II. Its rela-
tionship to psychosocial depressive-vulnerability. Social Psychiatry and Psychiatric Epi-
demiology, 37, 60–67.
Bibliography 211
Billings, A. G., & Moos, R. H. (1984). Treatment experiences of adults with unipolar depres-
sion: The influence of patient and life context factors. Journal of Consulting and Clini-
cal Psychology, 52, 119–13l.
_____ and _____ (1985). Psychosocial processes of remission in unipolar depression: Com-
paring depressed patients with matched community controls. Journal of Consulting and
Clinical Psychology, 53, 314–25.
“Birth defects: Risk Appears Low when Mother Uses SSRI antidepressants.” (2007). Wash-
ington Post Health Section, Quick Study. July 3, page F-2.
Blatt, S. J. (1974). Levels of object representation in anaclitic and introjective depression. Psy-
choanalytic Study of the Child, 29, 107–157.
_____, Zuroff, D. C., Bondi, C. M., Sanislow, C. A., III, & Pilkonis, P. A. (1998). When and
how perfectionism impedes the brief treatment of depression: Further analysis of the
National Institute of Mental Health treatment of depression collaborative research pro-
gram.” Journal of Consulting and Clinical Psychology, 66, 423–428.
Blazer, D., George, L. K., Landerman, R., Pennybacker, M., Melville, M. L., Woodbury, M.,
Manton, K. G., Jordan, K., & Locke, B. (1985). Psychiatric disorders: A rural/urban com-
parison.. Archives of General Psychiatry, 42, 651–656.
Blechman, E. A., McEnroe, M. J., Carella, E. T., & Audette, D. P. (1986). Childhood compe-
tence and depression. Journal of Abnormal Psychology, 95, 223–227.
Bliwise, D. L., Yesavage, J. A., Sink, J., Windrow, L., & Dement, W. C. (1986). Depressive
symptoms and impaired respiration in sleep. Journal of Consulting and Clinical Psychol-
ogy, 54, 734–35.
Bockting, C. L., Schene, A. H., Spinhoven, P., Koeter, M. W., Wooters, L. F., Huyser, J., &
Kamphuis, J. H. (2005). Preventing relapse/reoccurrence in recurrent depression with
cognitive therapy: A randomized controlled trial. Journal of Consulting and Clinical Psy-
chology, 73, 647–657.
Bollini, P., Pampallona, S., Tibaldi, G., Kupelnick, B., & Munizza, C. (1999). Effectiveness of
antidepressants: Meta-analysis of dose-effect relationships in randomized clinical tri-
als. British Journal of Psychiatry, 174, 297–303.
Bond, M. (2006). Psychodynamic psychotherapy in the treatment of mood disorders. Cur-
rent Opinion in Psychiaty, 19, 40–43.
Bowlby, J. (1980). Loss: Sadness and depression (Attachment and loss, Volume 3). New York:
Basic Books.
_____ (1982). Attachment and loss: Retrospect and prospect. American Journal of Orthopsy-
chiatry, 52, 664–678.
Breslau, J., Gaxiola, S. A., Kendler, K. S., Su, M., Williams, D., & Kessler, R. C. (2005). Spec-
ifying race-ethnic differences in risk for psychiatric disorder in a USA national sample.
Psychological Medicine, 35, 1–12.
Bridle, C., Palmer, S., Bagnall. A. M, Darba, J., Duffy, S., Sculpher, M., & Riemsma, R. (2004).
A rapid and systematic review and economic evaluation of the clinical and cost-effec-
tiveness of newer drugs for treatment of mania associated with bipolar affective disor-
der. Health Technology Assessment, 8, 1–187.
Brooks-Gunn, J., & Warren, M. P. (1989). Biological and social contributions to negative affect
expression in young adolescent girls. Child Development, 60, 40–55.
Brown, S. A., Goldman, M. S., Inn, A., & Anderson, L. R. (1980). Expectations of reinforce-
ment from alcohol: Their domain and relation to drinking patterns. Journal of Consult-
ing and Clinical Psychology, 48, 419–426.
Brunstein-Klomek, A., Zalsman, G., & Mufson, L. ( 2007). Interpersonal psychotherapy for
depressed adolescents (IPT-A.). Journal of Psychiatry and Related Sciences, 44, 40–46.
Buchwald, A. M. (1977). Depressive mood and estimates of reinforcement frequency. Jour-
nal of Abnormal Psychology, 86, 443–446.
Bulmash, E. L., Moller, H. J., Kayumov, L., Shen, J., Wang, X., & Shapiro, C. M. (2006). Psy-
chomotor disturbance in depression: Assessment using a driving simulator paradigm.
Journal of Affective Disorders, 93, 213–218.
212 Bibliography
Burke, K. C., Burke, J. D., Jr., Regier, D. A., & Rae, D. S. (1990). Age at onset of selected men-
tal disorders in five community populations. Archives of General Psychiatry, 47, 511–518.
Burns, D. D. (1980). Feeling good: The new mood therapy. N.Y: Morrow.
Butler, A. C., Chapman, J. E., Forman, E. M., & Beck, A. T. (2006). The empirical status of
cognitive-behavioral therapy: A review of meta-analyses. Clinical Psychology Review, 26,
17–31.
Caccia, S. (2005). Antidepressant like components of hypericum perforatum extracts: An
overview of their pharmacokinetics and metabolism. Current Drug Metabolism, 6,
531–543.
Cahn, B. R., & Polich, J. (2006). Meditation states and traits: EEG, ERP, and neuroimaging
studies. Psychological Bulletin, 132, 180–211.
Campbell, S., Marriott, M., Nahmias, C., & MacQueen, G. M. (2004). Lower hippocampal
volume in patients suffering from depression: A meta-analysis. American Journal of Psy-
chiatry, 161, 598–607.
Carey, M. P., Faulstich, M. E., Gresham, F. M., Ruggiero, L., & Enyart, P. (1987). Children’s
Depression Inventory: Construct validity across clinical and nonreferred (control) pop-
ulations. Journal of Consulting and Clinical Psychology, 55, 755–761.
Carter, F. A., Frampton, C. M., & Mulder, R. T. (2006). Caesarean section and postpartum
depression: A review of the evidence examining the link. Psychosomatic Medicine, 68,
321–330.
Carver, C. S., & Ganellen, R. J. (1983). Depression and components of selfpunitiveness: High
standards, self criticism, and overgeneralization. Journal of Abnormal Psychology, 92,
330–337.
Caspi A., Sugden, K., Moffitt, T. E., Taylor, A., Craig, I. W., Harrington, H., McCloy, J., Nill,
J., Martin, J., Braithwaite, A., & Poulton, R. (2003). Influence of life stress on depres-
sion: Moderation by a polymorphism on the 5-HTT gene. Science, 301, 386–389.
Chabrol, H., Montovany, A., Chouicha, K., & Duconge, E. (2002). Study of the CES-D on a
sample of 1953 adolescent students. Encephale, 28, 429–432.
Chiu, C-C., Huang, S-Y., Shen, W. W., & Su, K-P. (2003). Omega-3 fatty acids for depres-
sion in pregnancy. American Journal of Psychiatry, 160, 385.
Church, N. F., Brechman-Toussaint, M. L., & Hine, D. W. (2005). Do dysfunctional cogni-
tions mediate the relationship between risk factors and postnatal depression sympto-
matology? Journal of Affective Disorders, 87, 65–72.
Cicchetti, D. (1987). Developmental psychopathology in infancy: Illustration from the study
of maltreated youngsters. Journal of Consulting and Clinical Psychology, 55, 837–845.
Clark, D. C., Gibbons, R. D., Fawcet, J., Aagesen, C. A., & Sellers, D. (1985). Unbiased cri-
teria for severity of depression in alcoholic inpatients. Journal of Nervous and Mental
Disease, 173, 482–487.
Clayton, A. H., Pradko, J. F., Croft, H. A., Montano, C. B., Leadbetter, R. A., Bolden-Watson,
C., Bass, K. I., Donahue, R. M., Jamerson, B. D., & Metz, A. (2002). Prevalence of sex-
ual dysfunction among newer antidepressants. Journal of Clinical Psychiatry, 63, 357–366.
Cofer, D., & Winterborn, J. R. (1980). Personality characteristics of formally depressed
women. Journal of Abnormal Psychology, 89, 309–314.
Cole, D. A., Nolen-Hoeksema, S., Girgus, J., & Gilda, P. (2006). Stress exposure and stress
generation in child and adolescent depression: A latent trait-state-error approach to
longitudinal analyses. Journal of Abnormal Psychology 115, 40–51.
Coleg, E. A. (1990). Relation of social and academic competence to depressive symptoms in
childhood. Journal of Abnormal Psychology, 99, 422–429.
Colla, J., Buka, S., Harrington, D., & Murphy, J. M. (2006). Repression and modernization: A
cross-cultural study of women. Social Psychiatry and Psychiatric Epidemiology, 41, 271–279.
Consensus Development Conference Statement (1985). Electroconvulsive Therapy. 5, no. 11,
National Institutes of Health.
Conte, H. R., Plutchik, R., Wild, K. V., & Karasu, T. B. (1986). Combined psychotherapy and
pharmacotherapy for depression. Archives of General Psychiatry, 43, 471–479.
Bibliography 213
Cook, F. A. (1998). Through the first anarctic night 1898–1899. Pittsburgh, PA.: Polar. First
published 1909.
Cornell, D. G., Suarez, R., & Berent, S. (1984). Psychomotor retardation in melancholic and
nonmelancholic depression: Cognitive and motor components. Journal of Abnormal Psy-
chology, 93, 150–157.
Covington, M. B. (2004). Omega-3 fatty acids. American Family Physician, 70.
Coyne, J. C., Kessler, R. C., Tal, M., Turnbull, J., Wortman, C. B., & Greden, J. F. (1987). Liv-
ing with a depressed person. Journal of Consulting and Clinical Psychology, 55, 347–352.
Crowe, L. C., & George, W. H. (1989). Alcohol and human sexuality: Review and integra-
tion. Psychological Bulletin, 105, 374–386.
Cuijpers, P., Van Stratten, A., & Warmerdam, L. (2007). Behavioral activation treatments of
depression: A meta-analysis. Clinical Psychology Review, 27, 318–326.
Cutrona, C. E., Russell, D. W., Brown, P. A., Clark, L. A., Hessling, R. M., & Gardner, K. A.
(2005). Neighborhood context, personality, and stressful life events as predictors of depres-
sion among African American women. Journal of Abnormal Psychology, 2005, 114, 3–15.
Dauber, R. B. (1984). Subliminal psychodynamic activation in depression: On the role of
autonomy issues in depressed college women. Journal of Abnormal Psychology, 93, 9–18.
De Maat, S. M., Dekker, J., Schoevers, R. A., & de Jonghe, F. (2007). Relative efficacy of psy-
chotherapy and combined therapy in the treatment of depression: A meta-analysis. Euro-
pean Psychiatry, 22, 1–8.
de Mello, M. F., de Jesus, Mari, J., Bacaltchuk, J., Verdeli, H., & Neugebauer, R. (2005). A
systematic review of research findings on the efficacy of interpersonal therapy for depres-
sive disorders. European Archives of Psychiatry and Clinical Neuroscience, 255, 75–82.
Denney, D. R., Stephenson, L. A., Penick, E. C., & Weller, R. A. (1988). Lymphocyte subclass
and depression. Journal of Abnormal Psychology, 97, 499–502.
Depue, R. A., Slater, J. F, Wolfsetter-Kausch, H., Klein, D., Goplerud, E., & Farr, D. (1981).
A behavioral paradigm for identifying persons at risk for bipolar depressive disorder: A
conceptual framework and five validation studies. Journal of Abnormal Psychology, 90,
381–438.
DeRubeis, R. J., Evans, M. D., Hollon, S. D., Garvey, M. J., Grove, W. M., & Tuason, V. B.
(1990). How does cognitive therapy work? Cognitive change and symptom change in
cognitive therapy and pharmacotherapy for depression. Journal of Consulting and Clin-
ical Psychology, 58, 862–869.
DeRubeis, R. J., Gelfand, C. A., Tang, T. Z., Simons, A. D. (1999). Medications versus cog-
nitive behavior therapy for severely depressed outpatients: Mega-analysis of four ran-
domized comparisons. American Journal of Psychiatry, 156, 1007–1013.
Deutsch, A. (1948). The shame of the states. New York: Harcourt, Brace. Development con-
ference statement (1985). Electroconvulsive therapy. 5, No.11. National Institutes of
Health.
Dickens, C. (1981). David Copperfield. Oxford: Oxford University Press.
Dickerson, S. S., & Kemeny, M. E. (2004). Acute stressors and cortisol responses: A theoret-
ical integration and synthesis of laboratory research. Psychological Bulletin, 130, 355–391.
Dingfelder, S. F. (2006). The hunt for endophenotypes: Psychologists are leading the charge
to uncover the steps from genes to mental illness. Monitor on Psychology, 37, 20–21.
Doerfler, L. A., Felner, R. D., Rowlison,, R. T., Raley, P. A., & Evans, E. (1988). Depression
in children and adolescence: A comparative analysis of the utility and the construct
validity of two assessment measures. Journal of Consulting and Clinical Psychology, 56,
769–772.
Dranovsky, A., & Hen, R. (2006) Hippocampus neurogenesis: Regulation by stress and anti-
depressants. Biological Psychiatry, 59, 1136–1143.
Dumais, A., Lesage, A. D., Alda, M., Rouleau, G., Dumont, M., Chawky, N., Roy, M., Mann,
J. J., Benkelfat, C., & Turecki, G. (2005). Risk factors for suicide completion in major
depression: A case-controlled study of impulsive and aggressive behaviors in men. Amer-
ican Journal of Psychiatry, 162, 2114–2116.
214 Bibliography
Dunn, A. L., Trivedi, M. H., Kampert, J. B., Clark, C. G., & Chambliss, H. O. (2005). Exer-
cise treatment for depression: Efficacy and dose response. American Journal of Preven-
tive Medicine, 28, 1–8.
Durkheim, E. (1966). Suicide. New York: Free Press.
Egeland, J. A & Hostetter, A. M. (1983). Amish study: I. Affective disorders among the Amish,
1976–1980. American Journal of Psychiatry, 140, 56–61.
Ehlers, C. L., Frank, E., & Kupfer, D. J. (1988). Social zeitgebers and biological rhythms.
Archives of General Psychiatry, 45, 948–952.
Einarson, T. R., Arikian, S. R., Casciano, J., & Doyle, J. J. (1999). Comparison of extended-
release veniafaxine, selective serotonin reuptake inhibitors, and tricyclic antidepres-
sants in the treatment of depression: A meta-analysis of randomized controlled trials.
Clinical therapy, 21, 296–308.
Elkin, L., Shea, T., Watkins, J. T., Imber, S. D., Sotsky, S. M., Collins, J. F., Glass, D. R., Pilko-
nia, P. A., Leber, W. R., Docherty, J. P., Fiester, S. J., & Parloff, M. B. (1989). National
Institute of Mental Health Treatment of Depression Collaborative Research program:
General effectiveness of treatments. Archives of General Psychiatry, 46, 971–982.
Ellis, A. (1962). Reason and emotion in psychotherapy. New York: Lyle Stuart.
Enns, H. W., & Cox, B. J. (1999). Perfectionism and depressive symptom severity in major
depressive disorder. Behavior Research and Therapy, 37, 783–794.
Ernst, E., Rand, J. I., & Stevinson, C. (1998). Complementary therapies for depression: An
overview. Archives of General Psychiatry, 55, 1026–1032.
Fadden, G., Bebbington, P., Kuipers, L. (1987). Caring and its burdens. A study of the spouses
of depressed patients. British Journal of Psychiatry, 151, 660–667.
Fagot, B. I. (1997) Attachment, parenting, and peer interactions of toddler children. Devel-
opmental Psychology, 33, 489–499.
Fava, M., Detke, M. J., Balestrieri, M., Wang, F., Raskin, J., & Perahia, D. (2006). Manage-
ment of depression relapse: Re-initiation of duloxetine treatment or dose increase. Jour-
nal of Psychiatric Research, 40, 328–336.
FDA approves Emsam (selegiline) as first drug patch for depression. (2006). FDA News (Feb-
ruary 28th, 2006). Http://www.fda.gov/bbs/topics/news/2006New01326.html.
Field, T., Hernandez-Reif, M., Diego, M., Schanberg, S., & Kuhn, C. (2005). Cortisol decreases
and serotonin and dopamine increase following massage therapy. International Journal
of Neuroscience, 115, 1397–1413.
Finucane, A., & Mercer, S. W. (2006). An exploratory mixed methods study of the accept-
ability and effectiveness of mindfulness-based cognitive therapy for patients with active
depression and anxiety in primary care. BMC Psychiatry, 6, 14.
Floyd, M., Rohen, N., Shakelford, J. A., Huibbard, K. L., Parnell, M. B., Scogin, F., & Coates,
A. (2006). Two-year follow-up of bibliotherapy and individual cognitive therapy for
depressed older adults. Behavior Modification, 30, 281–294.
Foa, E. B., Zoellner, L. A., & Feeny, N. C. (2006). An evaluation of three brief programs for
facilitating recovery after assault. Journal of Traumatic Stress, 19, 29–43.
Fogel, J., & Ford, D. E. (2005). Stigma beliefs of Asian Americans with depression in an inter-
net sample. Canadian Journal of Psychiatry, 50, 470–478.
Folkenberg, J. (1983, October). Using drugs to lift that dark veil of depression. FDA Con-
sumer, 16–19.
Folkman, S., & Lazarus, R. S. (1986). Stress processes and depressive symptomatology. Jour-
Forgas, J. P., Bower, G. H., & Krantz, S. E. (1984). The influence of mood on perceptions of
social interactions. Journal of Experimental Social Psychology, 20, 497–513.
Frampton, J. E. & Plosker, G. L. (2007). Selegiline transdermal system in the treatment of
major depressive disorder. Drugs, 67, 257–265.
Frangou, S., Lewis, M., & McCrone, P. (2006). Efficacy of ethyl-eicosapentaenoic acid in
bipolar depression: Randomized double-blind placebo-controlled study. British Journal
of Psychiatry, 188, 46–50.
Bibliography 215
Frank, E., Kupfer, D. J., Buysse, D. J., Swartz, H. A., Pilkonis, P. A., Houck, P. R., Rucci, P.,
Novick, D. M., Grochocinski, V. J., & Stapf, D. M. (2007). Randomized trial of weekly,
twice-monthly, and monthly interpersonal psychotherapy as maintenance treatment for
women with recurrent depression. American Journal of Psychiatry, 164, 7, 761–767.
Frazier, J. A., Ahn, M. S., Dejong, S., Bent, K. E.. (2005). Magnetic resonance imaging studies
in early-onset bipolar disorder: A Critical Review. Harvard Review of Psychiatry, 13, 125–140.
Freedman, S. J., Fava, M., Kienke, A. S., White, C. H., Nierenberg, A. A., & Rosenbaum, J.
F. (2000). Partial response, nonresponse, and relapse with selective serotonin reuptake
inhibitors in major depression: A survey of current “next-step” practices. Journal of
Clinical Psychiatry, 61, 403–418.
Freud, S. (1959). Mourning and melancholia. In Collected Papers, Volume 4, 152–170. New
York: Basic Books.
Friedman, R. A., Mitchel, J., & Kocsis, J. H. (1995). Retreatment for relapse following
desipramine discontinuation in dysthymia. American Journal of Psychiatry, 152, 921.
Gallagher, W. (1986, May). The dark affliction of mind and body. Discover, 7, no. 5, 6.
Galloway, G. P., Newmeyer, J., Knapp, T., Stalcup, S. A., & Smith D. (1994). Imipramine for
the treatment of cocaine and methamphetamine dependence. Journal of Addictive Dis-
orders, 13, 201–216.
Gjerde, P. F., Block, J., & Block, J. (1988) Depressive symptoms and personality during late
adolescence: Gender differences in externalization of symptom expression. Journal of
Abnormal Psychology, 97, 475–486.
Gladstone, T. R., & Kaslow, N. J. (1995). Depression and attributions in children and ado-
lescents: A meta-analytic review. Journal of Abnormal Child Psychology, 23, 597–606.
Glascoe, R. E., & Rosen, G. M. (1978). Behavioral bibliotherapy: A review of self-help behav-
ior therapy manuals. Psychological Bulletin, 85, 1–23.
Goel, N., Terman, M., Terman, J. S., Macchi, M. M., & Stewart, J. W. (2005). Controlled trial
of bright light and negative air ions for chronic depression. Psychological Medicine, 35,
945–955.
Goethe, J. W. von (1774). The Sorrows of Young Werther. New York: Random House. (1971).
Goforth, H. W., & Holsinger, T. (2007). Rapid relief of severe major depressive disorder by
use of preoperative ketamine and electroconvulsive therapy. Journal: ECT, 23, 23–25.
Goldbort, J. (2006). Transcultural analysis of postpartum depression. MCN American Jour-
nal of Maternal Child Nursing, 31, 121–126.
Goldsmith, H. H., & Alansky, J. A. (1987). Attachment: A meta-analytic review. Journal of
Consulting and Clinical Psychology, 55, 805–816.
Gonzales, L. R., Lewinsohn, P. M., & Clarke, G. N. (1985). Longitudinal follow-up of unipo-
lar depressives: An investigation of predictors of relapse. Journal of Consulting and Clin-
Gorman, J., & Sullivan, G. (2000). Noradrenergic approaches to antidepressant therapy. Jour-
nal of Clinical Psychiatry, 61, Supplement 1: 13–6.
Grant, B. F., Harford, T. C., Muthen, B. O., Yi, H. Y., Hasin, D. S., & Stinson, F. S. (2006).
DSM-IV alcohol dependence and abuse: Further evidence of validity in the general pop-
ulation. Drug and Alcohol Dependence.
Grant, B. F., Stinson, F. S., Hasin, D. S., Dawson, D. A., Chou, S. P., Anderson, K. (2004).
Immigration and lifetime prevalence of DSM-IV psychiatric disorders among Mexican
Americans and non–Hispanic Whites in the United States: Results from the National
Epidemiological Survey on Alcohol and Related Conditions. Archives of General Psychi-
atry, 61, 1226–1233.
Grant, B. F., Stinson, F. S., Hasin, D. S., Dawson, D. A., Chou, S. P., Ruan, W. J., & Huang,
B..(2005). Prevalence, correlates, and comorbidity of bipolar I disorder and axis I and
axis II disorders: Results from the National Epidemiologic Survey on Alcohol and Related
Conditions. Journal of Clinical Psychiatry, 66, 1205–1215.
Griffiths, K. M., & Christensen, H. (2007). Internet-based mental health programs: A pow-
erful tool in the rural health kit. Australian Journal of Rural Health, 15, 81–88.
216 Bibliography
Haby, M. M., Donnelly, M., Corry, J., & Vos, T. (2006). Cognitive behavioural therapy for
depression, panic disorder and generalized anxiety disorder: A mega regression of fac-
tors that may predict outcome. Australian and New Zealand Journal of Psychiatry, 40,
9–19.
Hamilton, M. A. (1960). A rating scale for depression. Journal of Neurology, Neurosurgery,
and Psychiatry, 23, 56–62.
Hammen, C. (2005). Stress and depression. Annual Review of Clinical Psychology, 1, 293–319.
_____, Henry, R., & Daley, S. E. (2000). Depression and sensitization to stressors among
young women as a function of childhood adversity. Journal of Consulting and Clinical
Psychology, 68, 782–787.
Hammen, C. L., & Peters, S. D. (1977). Differential responses to male and female depressive
reactions. Journal of Consulting and Clinical Psychology, 45, 994–1001.
Hankin, B. L., & Abramson, L. Y. (2001). Development of gender differences in depression:
An elaborated cognitive vulnerability-transactional stress theory. Psychological Bulletin,
127, 773–796.
Hariri, A. R., & Holmes, A. (2006). Genetics of emotional regulation: The role of the sero-
tonin transporter in neural function. Trends in Cognitive Science, 10, 182–191.
Hariri, A. R., Murray, V. S., Tessitore, A., Kolachana, B., Fera, F., & Goldman, D. (2002).
Serotonin transporter genetic variation and the response of the human amygdala. Sci-
ence, 297, 400–403.
Harlow, H. F. (1958). The nature of love. American Psychologist, 13, 673–685.
Harris, A. H. S., Cronkite, R., & Moos, R. (2006). Physical activity, exercise coping, and
depression in a 10-year cohort study of depressed patients. Journal of Affective Disorders,
93, 79–85.
Hasin, D. S., Goodwin, R. D., Stinson, F. S., & Grant, B. F. (2005). Epidemiology of major
depressive disorder: Results from the National Epidemiological Survey on Alcoholism
and Related Conditions. Archives of General Psychiatry, 62, 1097–1106.
Hasler, G., Drevets, W. C., Manji, H. K., & Charney, D. S. (2004). Discovering endopheno-
types for major depression. Neuropsychopharmacology, 10, 1765–1781.
Hawkins, W. L., French, L. C., Crawford, B. D., & Enzle, M. E. (1988). Depressed affect and
time perspective. Journal of Abnormal Psychology, 97, 275–280.
Hawley, L. L, Zuroff, D. C., Ho, M-HR, & Blatt, S. J. (2007). Stress reactivity following brief
treatment for depression: Differential effects of psychotherapy and medication. Journal
of Consulting and Clinical Psychology, 75, 244–256.
Healy, D. (1997). The Antidepressant Era. Cambridge, MA: Harvard University Press.
Heiby, E. M. (1982). A self-reinforcement questionnaire. Behavior Research and Therapy, 20,
391–401.
Hetherington, E. M., Hagan, M. S., Anderson, E. T. (1989). Marital transitions: A child’s per-
spective. American Psychologist, 44, 303–312.
Heuser, I., Yassouridis, A., & Holsboer, F. (1994). The combined dexamethasone/CRH test:
A refined laboratory test for psychiatric disorders. Journal of Psychiatric Research, 28,
341–356.
Hewitt, P. L., & Flett, G. L. (1991). Dimensions of perfectionism in unipolar depression. Jour-
Hibbeln, J. R. (1998). Fish consumption and major depression. Lancet, 351, 1213.
_____, Umhau, J. C., Linnoila, M., George, D. T., Ragan, P. W., Shoaf, S. E., Vaughan, M. R.,
Rawlings, R., & Salem, Jr., N. (1998 b). A replication study of violent and non-violent
subjects: Cerebrospinal fluid metabolites of serotonin and dopamine are predicted by
plasma essential fatty acids. Biological Psychiatry, 44, 235–249.
Hiroto, D. S. (1974). Locus of control and learned helplessness. Journal of Experimental Psy-
chology, 102, 187–193.
Hoberman, H. M., Lewinshon, P. M., & Tilson, M. (1988). Group treatment of depression:
Individual predictors of outcome. Journal of Consulting and Clinical Psychology, 56,
393–398.
Bibliography 217
Hoffman, K. B., Cole, D. A., Martin, J. M., Tram, J., & Seroczynski, A. D. (2000). Are the
discrepancies between self and others’ appraisals of confidence predictive or reflective
of depressive symptoms in children and adolescents: A longitudinal study, Part II. Jour-
Holahan, C. J., & Moos, R. H. (1991). Life stressors, personal and social resources, and depres-
sion: A four-year structural model. Journal of Abnormal Psychology, 100, 31–38.
Hollon, S. D., & Kendall, P. C. (1980). Cognitive self-statements in depression: Development
of an automatic thoughts questionnaire. Cognitive Therapy and Research, 4, 383–395.
Incoviello, B. M., Alloy, B., Abramson, L. Y., Whitehouse, W. G., & Hogan, E. (2006). The
course of depression in individuals with high and low cognitive risk for depression: A
prospective study. Journal of Affective Disorders, 93, 61–69.
Irons, C., Gilbert, P., Baldwin, M. W., Baccus, J. R., & Palmer, M.. (2006). Parental recall,
attachment relating and self-attacking/self-reassurance: Their relationship with depres-
sion. British Journal of Clinical Psychology, 45, 297–308.
Jamison, K. R. (1993). Touched with fire: Manic-depressive illness and the artistic temperament.
New York: Free Press.
Jarrett, R. B., & Weissenburger, D. E. (1990). Guilt in depressed outpatients. Journal of Con-
sulting and Clinical Psychology, 58, 495–498.
Jewell, D. S., & Mylander, M. (1988). The psychology of stress: Run silent, run deep. In G.
P. Chorousos, D. L. Loriaux, & P. W. Gold (Eds.), Mechanisms of physical and emotional
stress. New York: Plenum.
Johnson, M. H., & Magaro, P. A. (1987). Effects of mood and severity on memory processes
in depression and mania. Psychological Bulletin, 101, 28–40.
Joormann, J., & Gotlib, I. H. (2006). Is this happiness I see? Biases in the identification of
emotional facial expression in depression and social phobia. Journal of Abnormal Psy-
chology, 115, 705–714.
Kabat-Zinn, J., Massion, A. O., Kristeller, J., Peterson, L. G., Fletcher, K. E., Pbert, L.,
Lenderking, W. R., & Santorelli, S. F. (1992). Effectiveness of a meditation-based stress
reduction program in the treatment of anxiety disorders. American Journal of Psychia-
try, 149, 936–943.
Kalechstein, A. D., Newton, T. F., Longshore, D., Anglin, M. D., van Gorp, W. G., & Gawin,
F. H. (2000). Psychiatric comorbidity of methamphetamine dependence in a forensic
sample. Journal of Neuropsychiatry and Clinical Neuroscience, 12, 480–484.
Kaltenthaler, E., Brazier, J., Denigris, E., Tumur, I., Ferriter, M., Beverley, C., Parry, G.,
Rooney, G., & Sutcliffe, P. (2006). Computerized cognitive behaviour therapy for depres-
sion and anxiety update: A systematic review and economic evaluation. Health Tech-
nology Assessment, 10, 1–168.
Kanner, A. D., Coyne, J. C., Schaefer, C., & Lazarus, R. S. (1981). Two modes of stress meas-
urement: Daily hassles and uplifts verses major life events. Journal of Behavioral Medi-
cine, 4, 1–39.
Karno, M., Hough, R. L., Burnam, A., Escobar, J. L., Timbers, D. M. (1987). Lifetime preva-
lence of specific psychiatric disorders among Mexican Americans and non–Hispanic
whites in Los Angeles. Archives of General Psychiatry, 44, 695–701. Archives of General
Psychiatry, 44, 695–701.
Kashani, J. H., Holcomb, W. R., & Orvaschel, H. (1986). Depression and depressive symp-
toms in preschool children from the general population. American Journal of Psychia-
try, 143, 1138–1143.
Kashner, T. M., Henley, S. S., Golden, R. M., Rush, A. J., & Jarrett, R. B. (2007). Assessing
the preventive effects of cognitive therapy following relief of depression: A methodolog-
ical innovation. Journal of Affective Disorders (in press).
Kasper, S., Anghelescu, I. G., Szegedi, A., Dienel, A., & Kieser, M. (2006). Superior efficacy
of St. John’s wort extract WS5570 compared to placebo in patients with major depres-
sion: A randomized double-blind, placebo-controlled, multi-center trial. BMC Medi-
cine, 4, 14.
218 Bibliography
Kasper, S., Wehr, T. A., Bartko, J. J., Gaist, P. A., & Rosenthal, N. E. (1989). Epidemiological
findings of seasonal changes in mood and behavior. A telephone survey of Montgomery
County, Maryland. Archives of General Psychiatry, 46, 823–833.
Kazdin, A. E. (1986). Comparative outcome studies of psychotherapy: Methodological issues
and strategies. Journal of Consulting and Clinical Psychology, 54, 95–105.
Keats, J. (1958). The poetical works of John Keats. Oxford: Oxford University Press.
Keeler, M. H., Ewing, J. A., & Rouse, B. A. (1971). Hallucinogenic effects of marijuana as cur-
rently used. American Journal of Psychiatry, 128, 213–216.
Kendler, K. S., Heath, A., Martin, N. G., & Eaves, L. J. (1986). Symptoms of anxiety and
depression in a volunteer twin population. Archives of General Psychiatry, 43, 213–221.
Kendler, K. S., Prescott, C. A. (1999). A population-based twin study of lifetime major depres-
sion in men and women. Archives of General Psychiatry, 56, 39–44.
Kerns, K. A., Abramham, M. M., Schlegelmilch, A., & Morgan, T. A. (2007). Mother-child
attachment in later middle childhood: Assessment approaches and associations with
mood and emotion regulation. Attachment and Human Development, 9, 33–53.
Kerr, G. W., McGuffie, A. C., & Wilkie, S. (2001). Tricyclic antidepressant overdose: A review.
Emergency Medicine Journal, 18, 236–241.
Kerr, M. M., Hoier, T. S., & Versi, M. (1987). Methodological issues in childhood depres-
sion: A review of the literature. American Journal of Orthopsychiatry, 57, 193–198.
Kessler, R. C., Bergland, P., Demier, O., Jin, R., & Walters, E. E. (2005). Lifetime prevalence
and age-of-onset distribution of DSM-IV disorders in the National Comorbidity Sur-
vey Replication. Archives of General Psychiatry, 62, 593–602.
Kessler. R. C., Demier, O., Frank, R. G., Olfson, M., Pincus, H. A., Walters, E. E., Wang, P.,
Wells, K. B., & Zaslavsky, A. M. (2005). Prevalence and treatment of mental disorders,
1990 to 2003. New England Journal of Medicine, 352, 2515–2523.
Kessler, R. C., Soukup, J., Davis, R. B., Foster, D. F., Wilkey, S. A., van Rompay, M. I., &
Eisenberg, D. M. (2001). The use of complementary and alternative therapies to treat
anxiety and depression in the United States. American Journal of Psychiatry, 158,
289–294.
Kieseppa, T., Partonen, T., Haiskka, J., Kaprio, J., & Lonnqvist, J. (2004). High concordance
of bipolar I disorder in a nationwide sample of twins. American Journal of Psychiatry,
161, 1814–1821.
Kim, H. L., Streltzer, J,, & Goebert, D. (1999). St. John’s wort for depression: A meta-analy-
sis of well-defined clinical trials. Journal of Nervous and Mental Disease, 187, 532–538.
Kistner, J. A., David-Ferdan, C. F., Repper, K. K., & Joiner, T. E., Jr. (2006). Bias and accu-
racy of children’s perceptions of peer acceptance: Prospective associations with depres-
sive symptoms. Journal of Abnormal Child Psychology, 34, 349–361.
Klerman, G. L., Weissman, M. M., Rounsvaile, B. J., & Chevron, E. (1984). Interpersonal psy-
chotherapy of depression. New York: Basic Books.
Kocsis, J. H., Frances, A. J., Voss, C., Mann, J. J., Mason, B. J., & Sweeney, J. (1988). Imipramine
treatment for chronic depression. Archives of General Psychiatry, 45, 253–257.
Koizumi, Y., Awata, S., Kuriyama, S., Ohmori, K., Hozawa, A., Seki, T., Matsuoka, H., &
Tsuji, I. (2005). Association between social support and depression status in the elderly:
Results of a 1-year community-based prospective cohort study in Japan. Psychiatric Clin-
ical Neuroscience, 2005, 5, 563–569.
Koukopoulos, A., Sani, G., Koukopoulos, A. E., Minnai, G. P., Giardi, P., Pani, L., Albert, M.
J., & Reginaldi, D. (2003). Duration and stability of the rapid-cycling course: A long-
term personal follow-up of 109 patients. Journal of Affective Disorders, 73, 75–85.
Kovacs, M. (1985). The Childrens Depression Inventory (CDI). Psychopharmacology Bulletin,
21, 995–998.
_____ (1992). Children Depression Inventory Manual. Los Angeles: Western Psychological
Services.
Kovess, V., Murphy, H. B., & Tousignant, M. (1987). Urban-rural comparisons of depressive
disorders in French Canada. Journal of Mental and Nervous Disease, 175, 457–466.
Bibliography 219
Kraeplin, E. (1913). Textbook of Psychiatry. (R. M. Barclay, trans.). Edinburgh: Livingston.

Kramlinger, K. G., & Post, R. M. (1996). Ultra-rapid and ultradian cycling in bipolar affec-
tive illness. British Journal of Psychiatry, 168, 314–323.
Krohne, H. W., & Slangen, K. E. (2005). Influence of social support on adaptation to sur-
gery. Health Psychology, 24, 101–105.
Kronmueller, K. T., Victor, D., Schenkenbach, C., Postelnicu, I., Bachenstrass, M., Schroder,
J., & Mundt, C. (2007). Knowledge about affective disorders and outcome of depres-
sion. Journal of Affective Disorders (in press).
Kunugi, H., Ida, I., Owashi, T., Kimura, M., Inoue, Y., Nakagawa, S., Yabana, T., Urushibara,
T., Kanal, R., Alhara, M., Yuuki, N., Otsubo, T., Oshima, A., Kuda, A., Inoue, T., Kitaichi,
Y., Shirakawa, O., Isogawa, K., Nagayama, H., Kamijima, K., Nanko, S., Kanba, S.,
Higuchi, T., & Mikuni, M. (2006). Assessment of the dexamethasone/CRH as a state-
dependent marker for hypothalamic-pituitary-adrenal (HPA) axis abnormalities in
major depressive disorders: A multicenter study. Neuropsychopharmacology, 31, 212–220.
Kuo, P. H., Gardner, C. O., Kendler, K. S., & Prescott, C. A. (2006). The temporal relation-
ship of the onsets of alcohol dependence and major depression: Using a genetically
informative study design. Psychological Medicine, 36, 1153–1162.
Kupfer, D. J. (2006). Depression and associated sleep disturbances: Patient benefits with
agomelatine. European Neuropsychopharmacology, 16, supplement 5, S639–643.
Kupka, R. W., Luckenbaugh, D. A., Post, R. M., Suppes, T., Altshuler, L. L., Keck, P. E., Jr.,
Frye, M. A., Denicoff, K. D., Grunze, H., Leverich, G. S., McElroy, S. L., Walden, J., &
Nolen, W. A. (2005). Comparison of rapid-cycling and non–rapid-cycling bipolar dis-
order based on prospective mood ratings in 539 outpatients. American Journal of Psy-
chiatry, 162, 1273–1280.
Lam, R. W. (2006). Sleep disturbances and depression: A challenge for antidepressants. Inter-
national Clinical Psychopharmacology, 21, Supplement 1, S25–29.
_____, Levitt, A. J., Levitan, R. D., Enns, M. W., Morehouse, R., Michalak, E. E., & Tam, E.
M. (2006). The Can-SAD study: A randomized controlled trial of the effectiveness of
light therapy and fluoxetine in patients with winter seasonal affective disorder. Ameri-
can Journal of Psychiatry, 163, 805–812.
Larson, R. W., Rafaelli, M., Richards, M. H., Ham, M., & Jewell, L (1990). Ecology of depres-
sion in late childhood and early adolescence: A profile of daily states and activities. Jour-
Lau, M. A., & McMain, S. F. (2005). Integrating mindfulness meditation with cognitive and
behavioral therapies: The challenge of combining acceptance and change-based strate-
gies. Canadian Journal of Psychiatry, 50, 863–869.
Lee, Y. M. (2006). Effect of self-foot reflexology massage on depression, stress responses and
immune functions of middle aged women. Taehan Kanho Hakhoe Chi., 36, 179–188
(translation of abstract).
Lefkowitz, M. M., & Tesiny, E. (1980). Assessment of childhood depression. Journal of Con-
Leitenberg, H., Yost, L. W., & Carroll-Wilson, M. (1986). Negative cognitive errors in chil-
dren: Questionnaire development, normative data, and comparisons between children
with and without self-reported symptoms of depression, low self-esteem, and evalua-
tion anxiety. Journal of Consulting and Clinical Psychology, 54, 528–536.
Lenze, E. J., Schulz, R., Martire, L. M., Zdaniuk, B., Glass, T., Kop, W. J., Jackson, S. A., &
Reynolds, C. F., III. (2005). The course of functional decline in older people with per-
sistently elevated depressive symptoms: Longitudinal findings from the Cardiovascular
Health Study. Journal of the American Geriatrics Society, 53, 569–575.
Lewinsohn, P. M., Duncan E. M., Stanton, A. K., & Hautzinger, M. (1986). Age at first onset
for nonbipolar depression. Journal of Abnormal Psychology, 95, 378–383.
Lewinsohn, P. M., Mischel, W., Chaplin, W., & Barton, R. (1980). Social competency and
depression: The role of illusory self-perceptions. Journal of Abnormal Psychology, 89,
203–212.
220 Bibliography
Lewinsohn, P. M., Munoz, R. F., Youngren, M. A., & Zeiss, A. M. 1986. Control your depres-
sion. Englewood Cliffs, N. J.: Prentice-Hall.
Lewy, A. J., Lefler, B. J., Emens, J. S., & Bauer, V. K. (2006). The circadian basis of winter
depression. Proceedings of the National Academy of Sciences, 103, 7414–7419.
Libet, J. M., & Lewinsohn, P. M. (1973). The concept of social skills with special reference to
the behavior of depressed persons. Journal of Consulting and Clinical Psychology, 40,
304–312.
Lindy, K., Ramirez, G., Mulrow, C. D., Pauls, A., Weidenhammer, W., & Melchart, D. (1996).
St. John’s wort for depression-an overview and meta-analysis of randomized clinical
trials. British Medical Journal, 313, 253–258.
Lisanby, S. H., Maddox, J. H., Prudic, J., Devanand, D. P., & Sackeim, H. A. (2000). The effects
of electroconvulsive therapy on memory of autobiographical and public events. Archives
of General Psychiatry, 57, 581–590.
Looby, A., & Earleywine, M. (2007). The impact of methamphetamine use on subjective well-
being in an internet survey: Preliminary finding. Human Psychopharmacology, 22,
167–172.
Lutz, D. L., & Snow, P. A. (1985). Understanding the role of depression in the alcoholic. Clin-
ical Psychology Review, 5, 535–551.
Macfarlane, J. W., Allen, L., & Honzik, M. P. (1954). Developmental study of the behavior
problems of normal children between twenty-one months and fourteen years. Berkeley:
University of California Press.
MacGillivray, S., Arroll, B., Hatcher, S., Ogston, S., Reid, I., Sullivan, F., Williams, B., &
Crombie, I. (2003). Efficacy and tolerability of selective serotonin reuptake inhibitors
compared with tricyclic antidepressants in depression treated in primary care. System-
atic review and meta-analysis. British Medical Journal, 326, 1014.
Mahalik, J. R., & Kivlighan, D. M., Jr. (1988). Self-help treatment for depression: Who suc-
ceeds? Journal of Counseling Psychology, 35, 237–242.
Malm, H., Klavkka, T., & Neuvonen, P. J. (2005). Risks associated with selective serotonin
reuptake inhibitors in pregnancy. Obstetrics and Gynecology, 106, 1289–1296.
Manber, R, Schnyer, R. N., Allen, J. J., Rush, A. J., & Blasey, C. M. (2004). Accupuncture: A
promising treatment for depression during pregnancy. Journal of Affective Disorders, 15,
89–95.
Mann, J. J., Stanley, M., McBride, P. A., & McEwen, B. S. (1986). Increase serotonin and B-
adrenergic receptor binding and the frontal cortices of suicide victims. Archives of Gen-
eral Psychiatry, 43, 954–959.
Marcos, L. R. (1979). Effects of interpreters on the evaluation of psychopathology in
non–English speaking patients. American Journal of Psychiatry, 136, 171–174.
Mazure, C. M. (1998). Life stressors as risk factors in depression. Clinical Psychology Science
and Practice, 5, 291–313.
McBride, C., Atkinson, L., Quilty, L. C., & Bagby, R. M. (2006). Attachment as moderator
of treatment outcome in major depression: A randomized controlled trial of interper-
sonal psychotherapy verses cognitive behavior therapy. Journal of Consulting and Clin-
McCabe, M., & Marwit, S. J. (1993). Depressive symptomatology, perceptions of attractive-
ness, and body image in children. Journal of Child Psychology and Psychiatry, 34, 1117–
1124.
McCoy, S. J., Beal, J. M., Shipman, S. B., Payton, M. E., & Watson, G. H. (2006). Risk factors
for postpartum depression: A retrospective investigation at four-weeks postnatal and a
review of the literature. Journal of the American Osteopathic Association, 106, 181–182.
McCranie, E. W., & Bass, J. D. (1984). Childhood family antecedents of dependency and self-
criticism: Implications for depression. Journal of Abnormal Psychology, 93, 3–8.
McGirr, A., Renaud, J., Segin, M., Alda, M., Benkelfat, C., Lesage, A., & Turecki, G. (2006).
An examination of DSM-IV depressive symptoms and risk for suicide completion: A
psychological autopsy study. Journal of Affective Disorders (in press).
Bibliography 221
McGrath, E. P., & Repetti, R. L. (2002). A longitudinal study of children’s depressive symp-
toms, self-perceptions, and cognitive distortions about the self. Journal of Abnormal Psy-
chology, 111, 77–87.
McGuffin, P., Rijsdijk, F., Andrew, M., Sham, P., Katz, R., & Cardino, A. (2003). The heri-
tability of bipolar affective disorder and the genetic relationship to unipolar depression.
McGuire, P. A. (1999). Worker stress reaching critical point. APA Monitor, 30, 1.
McLearn, K. T., Minkovitz, C. S., Strobino, D. M., Marks, E., & Hou, W. (2006a). Maternal
depressive symptoms at 2 to 4 months post partum and early parenting practices. Archives
of Pediatric and Adolescent Medicine, 160, 279–284.
_____ (2006b). The timing of maternal depressive symptoms and mother’s parenting prac-
tices with young children: Implication for pediatric practice. Pediatrics, 118, 174–182.
McMillan, M. J., & Pihl, R. O. (1987). Premenstrual depression: A distinct entity. Journal of
Abnormal Psychology, 96, 149–154.
Medications for mental illness. Fifth edition. (2005). Bethesda, MD: National Institute of
Mental Health, NIH publication number 05–3929.
Meditation for health purposes. (2006). Backgrounder. National Center for Complementary
and Alternative Medicine. Bethesda, MD: National Institutes of Health.
Melartin, T. K., Rytsala, H. J., Leskela, U. S., Lesstella-Mielonen, P. S., Sokero, T. P., &
Isometsa, E. T. (2004). Severity and comorbidity predict duration and recurrence of
DSM-IV major depressive disorder. Journal of Clinical Psychiatry, 65, 810–819.
Meller, W., Kathol, R. G., Jaeckle, R. S., Grambsch, P., & Lopez, J. F. (1988). HPA axis abnor-
malities in depressed patients with normal response to the DST. American Journal of Psy-
chiatry, 145, 318–324.
Meyersburg, H. A., Ablon, S. L., & Kotin, J. (1974). A reverberating psychic mechanism in
the depressive processes. Psychiatry, 37, 372–386.
Mezulis, A. H., Abramson, L. Y., Hyde, J. S., & Hankin, B. L. (2004). Is there a universal
positivity bias in attribution? A meta-analytic review of individual, developmental, and
cultural differences in the self-serving attribution bias. Psychological Bulletin, 130,
711–747.
Miller, T. Q., Smith, T. W., Turner, C. W., Guijario, M. L., & Hullet, A. J. (1996). A meta-
analytic review of research on hostility and physical health. Psychological Bulletin, 119,
322–348.
Mojtabai, R. (2007). Americans’ attitudes towards mental-health treatment seeking: 1990–
2003. Psychiatric Services, 58, 642–651.
Molnar, B. E., Buka, S. L., & Kessler, R. C. (2001). Child sexual abuse and subsequent psy-
chopathology: Results from the National Comorbidity Survey. American Journal of Pub-
lic Health, 91, 753–760.
Monroe, S. M., & Harkness, K. L. (2005). Life stress, the “kindling” hypothesis, and the
recurrence of depression: Considerations from a life stress perspective. Psychological
Review, 112, 417–445.
Monroe, S. M., Torres, L. D., Guillaumot, J., Harkness, K. L., Roberts, J. E., Frank, E., &
Kupfer, D. (2006). Life stress and the long-term treatment course of recurrent depres-
sion: III. Nonsevere life events predict recurrence for medicated patients over 3 years.
Journal of Consulting and Clinical Psychology, 74, 112–120.
Montejo, A L., Llorca, G., Izquierdo, J. A., & Rico-Villademoros, F. (2001). Incidence of sex-
ual dysfunction associated with antidepressant agents: A prospective study of 1022 out-
patients. Spanish Working Group for the Study of Psychotropic-Related Sexual
Dysfunction. Journal of Clinical Psychiatry, 62, Supplement 3, 10–21.
Mor, N., & Winquist, J. (2002). Self-focused attention and negative affect: A meta-analysis.
Psychological Bulletin, 128, 638–662.
Moreno, R. A., Teng, C. T., Almeida, K. M., & Tarares, H., Jr. (2006). Hypericum perfora-
tum versus fluoxetine in the treatment of mild to moderate depression: A randomized
double-blind trial in a Brazilian sample. Revista Brasileira Psiquiatria de, 28, 29–32.
222 Bibliography
Moyer, C. A., Rounds, J., & Hannum, J. W. (2004). A meta-analysis of massage therapy
research. Psychological Bulletin, 130, 3–18.
Munsey, C. (2007, April). Differences in heavy alcohol use can jeopardize marriages. Moni-
tor on Psychology, 38, 11.
Murrell, S. A., & Himmelfarb, S. (1989). Effects of attachment bereavement and pre-event
conditions on subsequent depressive symptoms in older adults. Psychology and Aging,
4, 166–172.
Nair, H., & Murray, A. D. (2005). Predictors of attachment security in preschool children
from intact and divorced families. Journal of Genetic Psychology 166, 245–263.
Nathan, P. E., Titler, N. A., Lowenstein, L. M., Solomon, P., & Rossie, A. M. (1970). Behav-
ioral analysis of chronic alcoholism. Archives of General Psychiatry, 22, 419–430.
Needles, D. J., & Abramson, L. Y. (1990). Positive life events, attributional style, and hope-
fulness: Testing a model of recovery from depression. Journal of Abnormal Psychology,
99, 156–165.
Neighbors. H. W., Caldwell, C., Williams, D. R., Nesse, R., Taylor, R. J., Bullard, K. M., Tor-
res, M., & Jackson, J. S. (2007). Race, ethnicity, and the use of services for mental dis-
orders: Results from the national survey of American life. Archives of General Psychiatry,
64, 485–494.
Nelson, G. (1982). Parental death during childhood and adult depression: Some additional
data. Social Psychiatry, 17, 37–42.
Nemets, H. Nemets, B., Apter, A., Bracha, Z., Belmaker, R. H. (2006). Omega-3 treatment
of childhood depression: A controlled double-blind pilot study. American Journal of
Psychiatry, 163, 1098–1100.
Neumeister, A., Nugent, A. C., Waldeck, T., Geraci, M., Schwartz, M., Bonne, O., Bain, E. E.,
Luckenbaugh, D. A., Herscovitch, P., Charney, D. S., & Drevets, W. C. (2004). Neural
and behavioral responses to tryptophan depletion in unmedicated patients with remit-
ted by major depressive disorder and controls. Archives of General Psychiatry, 61, 765–773.
Neumeister, A., Xian-Zhang, H., Luckenbaugh, D. A., Schwartz, M., Nugent, A. C., Bonne,
O., Herscovitch, P., Goldman, D., Drevets, W. C., & Charney, D. S. (2006). Differential
effects of 5-HTTLPR genotypes in the behavioral and neural responses to tryptophan
depletion in patients with major depressive disorder and controls. Archives of General
Neuringer, C. (1982). Affect configurations and changes in women who threaten suicide fol-
lowing a crisis. Journal of Consulting and Clinical Psychology, 50, 182–186.
Nezu, A. M., & Nezu, C. M. (1990). Psychotherapy for adults within a problem-solving frame-
work: Focus on depression. Journal of Cognitive Psychotherapy, 4, 247–256.
Nezu, A. M., Nezu, C. M., & Perri, M. G. (1989). Problem-solving therapy for depression: The-
ory, research and clinical guidelines. New York: Wiley.
Nierenberg, A. A., Greist, J. H., Mallinckrodt, C. H., Prakash, A., Sambunaris, A., Tollefson,
G. D., & Wohlreich, M. M. (2007). Duloxetine versus escitalopram and placebo in the
treatment of patients with major depressive disorder: Onset of antidepressant action, a
non-inferiority study. Current Medical Research and Opinion, 23, 401–416.
Nierenberg, A. A., Trivedi, M. H., Fava, M., Biggs, M. M., Shores-Wilson, K., Wisniewski,
S. R., Blasubramani, G. K., & Rush, A. J. (2006). Family history of mood disorder and
characteristics of major depressive disorder: A Star* D (sequenced treatment alterna-
tives to relieve depression) study. Journal of Psychiatric Research (in press).
Nietzel, M. T., Russell, R. L., Hemmings, K. A., & Gretter, M. L. (1987). Clinical significance
of psychotherapy for unipolar depression: A meta-analytic approach to social compar-
ison. Journal of Consulting and Clinical Psychology, 55, 156–161.
Noles, S. W., Cash, T. F., & Winstead, B. A. (1985). Body image, physical attractiveness, and
depression. Journal of Consulting and Clinical Psychology, 53, 88–94.
Oldenhinkel, A. J., Rosmalen, J. G., Veenstra, R., Dijkstra, J. K., & Ormel, J. (2007). Being
admired or being liked: Classroom social status and depressive problems in early ado-
lescent girls and boys. Journal of Abnormal Child Psychology (in press).
Bibliography 223
Olfson, M., Marcus, S. C., Druss, B., Elinson, L., Tanielian, T., & Pincus, H. A. (2002).
National trends in the outpatient treatment of depression. Journal of the American Med-
ical Association, 287, 203–209.
O’Malley, S. S., Foley, S. H., Rounsaville, B. J., Watkins, J. T., Sotsky, S., Imber, S. D., & Elkin,
I. (1988). Therapist competence and patient outcome in interpersonal psychotherapy of
depression. Journal of Consulting and Clinical Psychology, 56, 496–501.
Oquendo, M. A., Galfalvy, H., Russo, S., Ellis, S. P., Grunebaum, M. F., Burke, A., & Mann,
J. J. (2004). Prospective study of clinical predictors of suicidal acts after a major depres-
sive disorder or bipolar disorder. American Journal of Psychiatry, 161, 1433–1441.
Ortega, A. N., Rosenheck, R., Alegria, M., & Desai, R. A. (2000). Acculturation and the life-
time risk of psychiatric and substance abuse disorders among Hispanics. Journal of Ner-
vous and Mental Disease, 188, 728-735.
Ostberg, V., & Lennartsson, C. (2007). Getting by with a little help: The importance of var-
ious types of social support for health problems. Scandinavian Journal of Public Health,
35, 197–204.
Owens, M. J & Nemeroff, C. B. (1994). Role of serotonin in the psychophysiology of depres-
sion: Focus on the serotonin transporter. Clinical Chemistry, 40, 288–295.
Packard, E. (2006). Perfectionists more vulnerable to depression, study finds. Monitor on Psy-
chology, 37, 14.
Palinkas, L. A. (2003). The psychology of isolated and confined environments: Understand-
ing human behavior in Antarctica. American Psychologist, 58, 353–363.
Pandey, G. A. (1997). Altered serotonin function in suicide: Evidence from platelet and neu-
roendrocine studies. Annals of the New York Academy of Science, 836, 182–200.
Parker, G. (1979). Parental characteristics in relation to depressive disorders. British Journal
_____ (1983). Parental “affectionless control” as an antecedent to adult depression: A risk
factor delineated. Archives of General Psychiatry, 40, 956–960.
_____, Tupling, H., & Brown, L. B. (1979). A parental bonding instrument. British Journal
Parsons, T. (1975). The sick role and the role of the physician reconsidered. Milbank Memo-
rial Fund Quarterly, 53, 257–278.
Paxton, S. J., Neumark-Sztainer, D., Hannan, P. J., & Eisenberg, M. E. (2006). Body dissat-
isfaction prospectively predicts depressive mood and low self-esteem in adolescent girls
and boys. Journal of Clinical Child and Adolescent Psychology, 35, 539–549.
Penninx, B. W., Guralinik, J. M., Ferrucci, L., Simonsick, E. M., Deeg, D. J., & Wallace, R.
B. (1998). Depressive symptoms and physical decline in community-dwelling-older per-
sons. Journal of the American Medical Association, 279, 1720–1726.
Peterson, C., & Villanova, P. (1988). An expanded attributional style questionnaire. Journal
of Abnormal Psychology, 97, 87–89.
Petty, S. C., Sachs-Ericsson, N., & Joiner, T. E., Jr. (2004). Interpersonal functioning deficits:
Temporary or stable characteristics of depressed individuals? Journal of Affective Disor-
ders 81, 115–122.
Pilowsky, D. J., Wickramaratne, P., Nomura, Y., & Weissman, M. M. (2006). Family discord,
parental depression, and psychopathology in offspring: 20-year follow-up. Journal of
the American Academy of Child and Adolescent Psychiatry, 45, 452–460.
Post, R. M. (1992). Transduction of psychosocial stress into the neurobiology of recurrent
affective disorder. American Journal of Psychiatry, 149, 999–1010.
Potkin, S. G., Zetin, M., Stamnekovic, V., Kripke, D., & Bunney, W. E., Jr. (1986). Seasonal
affective disorder: Prevalence varies with latitude and climate. Clinical Neuropharma-
cology, 9, 181–183.
Prinstein, M. J., Borelli, J. L., Cheah, C. S., Simon, V. A., & Aikins, J. W. (2005). Adolescent
girls’ interpersonal vulnerability to depressive emotions: A longitudinal examination of
reassurance-seeking and peer relationships. Journal of Abnormal Psychology, 114, 676–
688.
224 Bibliography
Prisciandaro, J. J., & Roberts, J. E. (2005). A taxometric investigation of unipolar depression

in the National Comorbidity Survey. Journal of Abnormal Psychology, 114, 718–728.
Quitkin, F. M., McGrath, P. J., Stewart, J. W., Deliyannides, D., Taylor, B. P., Davies, C. A.,
& Klein, D. F. (2005). Remission rates with 3 consecutive antidepressant trials: Effec-
tiveness for depressed outpatients. Journal of Clinical Psychiatry, 66, 670–676.
Radloff, L. S. (1977). The CES-D Scale: A self-report depression scale for research in the gen-
eral population. Applied Psychological Measurement. 1, 385–401.
Rapaport, M. H. (2007). Translating the evidence on atypical depression into clinical prac-
tice. Journal of Clinical Psychiatry, 68, Supplement 3, 31–36.
Rapp, S. R., Parisi, S. A., Walsh, D. A., & Wallace, C. E. (1988). Detecting depression in eld-
erly medical inpatients. Journal of Consulting and Clinical Psychology, 56, 509–513.
Reis, S., & Grenyer, B. F. (2004). Fear of intimacy in women: Relationship between attach-
ment styles and depressive symptoms. Psychopathology, 37, 299–303.
Reynolds, W. M., & Coats, K. I. (1982). Depression in adolescents: Incidents, depth, and cor-
relates. Paper presented at the 10th International Congress, International Association of
Child and Adolescent Psychiatry and Allied Professions, Dublin, Ireland.
Rinck, M., & Becker, E. S. (2005). A comparison of attentional biases and memory biases in
women with social phobia and major depression. Journal of Abnormal Psychology, 114,
62–74.
Robbins, P. R. (1974). Depression and drug addiction. Psychiatric Quarterly, 48, 374–386.
_____ (1983). Marijuana: A short course. Update for the eighties. Brookline Village, MA: Bran-
den.
_____ (1988). The psychology of dreams. Jefferson, NC: McFarland.
_____ (1998). Adolescent Suicide. Jefferson, NC: McFarland.
_____ (2007). Coping with stress: Commonsense strategies. Jefferson, NC: McFarland.
Robbins, P. R., & Nugent, J. F., III (1975). Perceived consequences of addiction: A compar-
ison between alcoholics and heroin-addicted patients. Journal of Clinical Psychology, 31,
367–369.
Robbins, P. R., & Tanck, R. H. (1973). Psychological correlates of marijuana use : An
exploratory study. Psychological Reports, 33, 703–706.
_____ and _____ (1982). Further research using a psychological diary technique to investi-
gate psychosomatic relationships. Journal of Clinical Psychology, 38, 356–359.
_____ and _____ (1984). Sex differences in problems related to depression. Sex Roles, 11,
703–707.
_____ and _____ (1985, October 23). There are ways to fight college anxiety and stress. Wash-
ington Post, Health Section.
_____ and _____ (1987). A study of diurnal patterns of depressed mood. Motivation and Emo-
tion, 11, 37–49.
_____ and _____ (1988). Depressed mood, dream recall and contentless dreams. Imagina-
tion, Cognition and Personality, 8, 165–174.
_____ and _____ (1992). Stress, coping techniques, and depressed affect: Explorations within
a normal sample. Psychological Reports, 70, 147–152.
_____ and _____ (1994). Depressed mood and early memories: Some negative findings. Psy-
chological Reports, 75, 465–466.
_____ and _____ (1997). Anger and depressed affect: Interindividual and intraindividual
perspectives. Journal of Psychology, 131, 489–500.
Robins, L. N., Helzer, J. E., Croughan, J., & Ratcliff, K. S. (1981). National Institute of Men-
tal Health Diagnostic Interview Schedule: Its history, characteristics and validity. Archives
of General Psychiatry, 38, 381–389.
Robins, L. N., Helzer, J. E., Wiessman, M. M., Orvaschel, H., Gruenberg, E., Burke, J. D.,
Regier, D. A. (1984). Lifetime prevalence of specific psychiatric disorders in three sites.
Rockhill, C. M., Fan, M. Y., Katon, W. J., McCauley, E., Crick, N. R., & Pleck, J. H. (2007).
Friendship interactions in children with and without depressive symptoms: Observa-
Bibliography 225
tion of emotion during game-playing interactions and post-game evaluations. Journal

of Abnormal Child Psychology (in press).
Rosenthal, N. E., Sack, D. A., Gillin, J. C., Lewy, A. J., Goodwin, F. K., Davenport, Y., Mueller,
P. S., Newsome, D. A., & Wehr, T. A. (1984). Seasonal affective disorder: A description
of the syndrome and preliminary findings with light therapy. Archives of General Psy-
chiatry, 41, 72–80.
Rost, K., Adams, S., Xu, S., & Dong, F. (2007). Rural-urban differences in hospitalization
rates of primary care patients with depression. Psychiatric Services, 58, 503–508.
Rotter, J. B. (1960). Generalized expectancies for internal verses external control of rein-
forcement. Psychological Monographs, 80, 609.
Sabbatini, R. (2007). The history of shock therapy in psychiatry. http://www.cerebromente.
org.br/n04/historia/shock:i.htm.
Safran, J. D., Vallis, T. M., Segal, Z. V., & Shaw, B. F. (1986). Assessment of core cognitive
processes in cognitive therapy. Cognitive Therapy and Research, 10, 509–526.
St. John, P. D., Blanford, A. A., & Strain, L. A. (2006). Depressive symptoms among older
adults in urban and rural areas. International Journal of Geriatric Psychiatry (in press).
St. John’s wort and the treatment of depression. (2004). Bethesda, MD.: National Center for
Complementary and Alternative Medicine.
Salkovskis, P., Rimes, K., Stephenson, D., Sacks, G., & Scott, J. (2006). A randomized con-
trolled trial of the use of self-help materials in addition to standard general practice treat-
ment of depression compared to standard treatment alone. Psychological Medicine, 36,
325–333.
Sargent, M. (1986). Depressive disorders: Treatments brings new hope. Publication no. ADM
86-1491.
Schmidt, J. M. (1981). The effects of subliminally presented anaclitic and introjective stim-
uli on normal young adults. Unpublished doctoral dissertation, University of Southern
Mississippi.
Schmitz, J. M., Averill, P., Stotts, A. L., Moeller, F. G., Rhoades, H. M., & Grabowski, J. (2001).
Fluoxetine treatment of cocaine-dependent patients with major depressive disorder.
Drug and Alcohol Dependence, 63, 207–214.
Schmitz, J. M., Stotts, A. L., Averill, P. M., Rothfleisch, J. M., Bailley, S. E., Sayre, S. L., &
Grabowski, J. (2000). Cocaine dependence with and without comorbid depression: A
comparison of patient characteristics. Drug and Alcohol Dependence, 60, 189–198.
Schulz, V. (2006). Safety of St. John’s wort extract compared to synthetic antidepressants.
Phytomedicine, 3, 199–204.
Schwartz, G. E., Fair, P. L., Salt, P., Mandel, M. R., &, Klerman, G. L. (1976). Facial muscles
patterning to affective imagery in depressed and nondepressed subjects. Science, 192,
489–491.
Scogin, F., Jamison, C., & Gochneaur, K. (1989). Comparative efficacy of cognitive and behav-
ioral bibliotherapy for mildly and moderately depressed older adults. Journal of Con-
Sedler, M. J. (1983). Falret’s Discovery: The origin of the concept of bipolar affective illness.
American Journal of Psychiatry, 140, 1127–1133.
Seligman, M. E. P., Abramson, L. Y., Semmel, A., & von Baeyer, C. (1979). Depressive attri-
butional style. Journal of Abnormal Psychology, 88, 242–248.
Seligman, M. E. P., Peterson, C., Kaslow, N. J., Tasnenbaum, R. L., Alloy, L. B., & Abram-
son, L. Y. (1984). Attributional styles and depressive symptoms among children. Jour-
Sen, S., Burmeister, M., & Ghosh, D. (2004). Meta-analysis of the association between a
serotonin transporter promoter polymorphism (5HTTLPR) and anxiety-related per-
sonality traits. American Journal of Medical Genetics. B. Neuropsychiatric Genetics, 127,
85–89.
Serebruany, V. L. (2006). Selective serotonin reuptake inhibitors and increased bleeding risk:
Are we missing something? American Journal of Medicine, 119, 113–116.
226 Bibliography
Shaffery, J., Hoffmann, R., & Armitage, R. (2003). The neurobiology of depression: Perspec-
tives from animal and human sleep studies. Neuroscientist, 9, 82–98.
Shakespeare, W. (1938). The tragedy of Richard the Third. In Shakespeare: Twenty-three plays
and the sonnets. New York: Scribners.
Sherman, K. J., Cherkin, D. C., Kahn, J., Erro, J., Herbec, A., Deyo, R. A., & Eisenberg, D.
M. (2005). A survey of training and practice patterns of massage therapists in two U.S.
States. BMC Complimentary and Alternative Medicine, 14, 13.
Shrout, P. E., Link, B. G., Dohrenwend, B. P., Skodol, A. E., Stueve, A., & Mirotznik, J. (1989).
Characterizing life events as risk factors for depression: The role of fateful loss events.
Journal of Abnormal Psychology, 98, 460–467.
Siever, L. J., & Davis, K. L. (1985). Overview: Toward a dysregulation hypothesis of depres-
sion. American Journal of Psychiatry, 142, 1017–1031.
Simon, G. E., & Von Korff, M. (1995). Recognition, management, and outcome of depres-
sion in primary care. Archives of Family Medicine, 4, 99–105.
Sir, A., D’Souza, R. F., Uguz, S., George, T., Vahip, S., Hopwood, M., Martin, A. J., Lam, W.,
& Burt, T. (2005). Randomized trial of sertraline versus venlafaxine XR in major depres-
sion: Efficacy and discontinuation symptoms. Journal of Clinical Psychiatry, 66, 1312–
1320.
Sirota, A. D., & Schwartz, G. E. (1982). Facial muscle patterning and lateralization during
elation and depression imagery. Journal of Abnormal Psychology, 91, 25–34.
Smith, G. T. (1994). Psychological expectancy as mediator of vulnerability to alcoholism.
Annals of the New York Academy of Sciences, 708, 165–171.
Smith, J. A., Cornelius, V., Warnock, A., Bell, A., & Young, A. H. (2007). Effectiveness of mood
stabilizers and antipsychotics in the maintenance phase of bipolar disorder: A system-
atic review of randomized controlled trials. Bipolar Disorder, 9, 394–412.
Snyder, C. R. (1984, September). Excuses, excuses. Psychology Today, 18, 50–55.
Solkero, T. P., Melartin, T. K., Rytsala, H. J., Leskela, U. S., Lestela-Mielonen, P. S., & Isometsa,
E. T. (2005). Prospective study of risk factors for attempted suicide among patients with
DSM-IV major depressive disorder. British Journal of Psychiatry, 186, 314–318.
Sontrop, J., & Campbell, M. K. (2006). W-3 polysaturated fatty acids and depression: A
review of the evidence and a methodological critique. Preventive Medicine, 42, 4–13.
Sourander, A., Koskelainen, M., & Helenius, H. (1999). Mood, latitude, and seasonality among
adolescents. Journal of the American Academy of Child and Adolescent Psychiatry, 38,
1271–1276.
Spearing, M. (2002). A story of bipolar disorder (manic depressive illness). Bethesda, Md.:
NIH Publication No. 06–5085.
Spitz, R. A. (1946). Anaclitic Depression. Psychoanalytic Study of the Child, 2, 313–342.
Stansfeld, S. A., Fuhrer, R., & Shipley, M. J. (1998). Types of social support as predictors of
psychiatric morbidity in a cohort of British civil servants (Whitehall II study). Psycho-
logical Medicine, 28, 881–892.
Steinbrueck, S. M., Maxwell, S. E. and Howard, G. S. (1983). A meta-analysis of psychother-
apy and drug therapy in the treatment of unipolar depression with adults. Journal of
Consulting and Clinical Psychology, 51, 856–863.
Stinson, F. S., Grant, B. F., Dawson, D. A., Huang, B., & Saha, T. (2005). Comorbidity between
DSM-IV alcohol and specific drug use disorders in the United States: Results from the
National Epidemologic Survey on Alcohol and Related Conditions. Drug and Alcohol
Dependence, 80, 105–116.
Stinson, F. S., Ruan, W. J., Pickering, R., & Grant, B. F. (2006). Cannabis use disorders in
the U.S.A.: Prevalence, correlates and co-morbidity. Psychological Medicine (in press).
Stroufe, L. A. (2005). Attachment and development: A prospective, longitudinal study from
birth to adulthood. Attachment and Human Development, 7, 349–367.
Sublette, M. E., Hibbeln, J. R., Galfalvy, H., Oquendo, M. A., & Mann, J. J. (2006). Omega-
3 polyunsaturated essential fatty acid status as a predictor of future suicide risk. Amer-
ican Journal of Psychiatry, 163, 1100–1102.
Bibliography 227
Sue, D., & Sue, S. (1987). Cultural factors and the clinical assessment of Asian Americans.
Journal of Consulting and Clinical Psychology, 55, 479–487.
Summers, M., Papadopoulou, K., Bruno, S., Cipolotti, L., & Rou, M. A. (2006). Bipolar I and
bipolar II disorder: Cognition and emotion processing. Psychological Medicine (in press).
Sund, A. M., Larsson, B., & Wichstrom, L. (2003). Psychosocial correlates of depressive symp-
toms among 12 to 14-year-old Norwegian adolescents. Journal of Child Psychology and
Surguiadze, S. A., Young, A. W., Senior, C., Brebion, G., Travis, M. J., & Phillips, M. L. (2004).
Recognition accuracy and response bias to happy and sad facial expressions in patients
with major depression. Neuropsychology, 18, 212–218.
Sweeney, P. D., Anderson, K., & Bailey, S. (1986). Attributional style in depression: A meta-
analytic review. Journal of Personality and Social Psychology, 50, 974–991.
Szasz, T. (1986). The case against suicide prevention. American Psychologist, 41, 806–812.
Szegedi, A., Kohnen, R., Dienel, A., & Kieser, M. (2005). Acute treatment of moderate to
severe depression with hypericum extract WS5570 (St. John’s wort): Randomized con-
trolled double blind non-inferiority trial versus paroxetine. http://bmjournals.com/cgi
Takeuchi, D. T., Chung, R. C. Lin, K. M., Shen, H., Kurasaki, K., Chun, C. A., & Sue, S. (1998).
Lifetime and twelve-month prevalence rates of major depressive episodes and dysthymia
among Chinese Americans in Los Angeles. American Journal of Psychiatry, 155, 1407–1414.
Taylor, S. (2007). Electroconvulsive therapy: A review of history, patient selection, tech-
nique, and medication management. Southern Medical Journal, 100, 494–498.
Teasdale, J. D., Segal, Z. V., & Williams, J. M. G. (1995). How does cognitive therapy pre-
vent depressive relapse and why should attentional control (mindfulness) training help?
Behavior Research and Therapy, 33, 25–39.
Teesson, M., Harvard, A., Fairbairn, S., Ross, J., Lynskey, M., & Darke, S. (2005). Depres-
sion among entrants to treatment for heroin dependence in the Australian Treatment
Outcomes Study (ATOS): Prevalence, correlates and treatment seeking. Drug and Alco-
hol Dependence, 78, 309–315.
Terman, M., & Terman, J. S. (2005). Light therapy for seasonal and nonseasonal depression:
Efficacy, protocol, safety, and side effects. CNS Spectrum, 10, 647–663.
Thase, M. E. (2006). Preventing relapse and recurrence of depression: A brief review of ther-
apeutic options. CNS Spectrum, 11, 12–21, Supplement 15.
Timbremont, B., Braet, C., & Dreessen, L. (2004). Assessing depression in youth: Relation
between the Children’s Depression Inventory and a structured interview. Journal of Clin-
ical Child and Adolescent Psychiatry, 33, 149–157.
Toneatto, T., & Nguyen, L. (2007). Does mindfulness meditation improve anxiety and mood
symptoms? A review of the controlled research. Canadian Journal of Psychiatry, 52,
260–266.
Torrent, C., Martinez-Aran, A., Daban, C., Sanchez-Moreno, J., Comes, M., Goikolea, J. U.,
Salamero, M., & Vieta, E. (2006). Cognitive impairment in bipolar II disorder. British
Journal of Psychiatry, 189, 254–259.
Trivedi, M. H., Rush, A. J., Wisniewski, S. R., Nierenberg, A. A., Warden, D., Ritz, L.,
Norquist, G., Lebowitz, B., McGrath, P. J., Shores-Wilson, K., Biggs, M. M., Balasubra-
mani, G. K., & Fava, M. (2006). Evaluation of outcomes with citalopram for depression
using measurement-based care in STAR*-D: Implications for clinical practice. Ameri-
can Journal of Psychiatry, 163, 28–40.
Trowell, J., Joffe, I., Campbell, J., Clemente, C., Almqvist, F., Soininen, M., Koskenranta-
Aalto, U., Weintraub, S., Kolaitis, G., Tomaras, V., Anastasopoulos, D., Grayson, K.,
Barnes, J., & Tsiantis, J. (2007). Childhood depression: A place for psychotherapy. An
outcome study comparing individual psychodynamic psychotherapy and family ther-
apy. European Child and Adolescent Psychiatry, 16, 157–167.
Trude, S., & Stoddard, J. J. (2003). Referral gridlock: Primary care physicians and mental
health services. Journal of General Internal Medicine, 18, 442–449.
Valtonen, H., Suominen, K., Mantere, O., Leppamaki, S., Arvilommi, P., & Isometsa, E. T.
228 Bibliography
(2005). Suicidal ideation and attempts in bipolar I and II disorders. Journal of Clinical
Psychiatry, 66, 1456–1462.
Valtonen, H. M., Suominen, K., Mantere, O., Leppamaki, S., Arvilommi, P., & Isometsa, E.
(2006). Suicidal behavior during different phases of bipolar disorder. Journal of Affec-
tive Disorders (in press).
Van Wijngaarden, B., Schene, A. H., & Koeter, M. W. (2004). Family caregiving in depres-
sion: Impact on caregivers’ daily life, distress, and help seeking. Journal of Affective Dis-
orders, 81, 211–222.
Veiel, H. O. (1993). Detrimental effects of kin support networks on the course of depression.
Journal of Abnormal Psychology, 102, 419–429.
_____, & Kuhner, C. (1990) Relatives and depressive relapse: The critical period after dis-
charge from in-patient treatment. Psychological Medicine, 20, 977–984.
Velten, E. (1986). A laboratory test for induction of mood states. Behaviour Research and
Therapy, 6, 473–482.
Vincent, N. K., & Walker, J. R. (2000). Perfectionism and chronic insomnia. Journal of Psy-
chosomatic Research, 49, 349–354.
Vittengl, J. R., Clark, L. A., Dunn, T. W., & Jarrett, R. B. (2007). Reducing relapse and recur-
rence in unipolar depression: A comparative meta-analysis of cognitive-behavioral ther-
apy’s effects. Journal of Consulting and Clinical Psychology, 75, 475–488.
Wall, J. H. (1937). A study of alcoholism in women. American Journal of Psychiatry, 93, 942–955.
Wampold, B. E., Minami, T., Baskin, T. W., & Callen, T. S. (2002). A meta-(re)analysis of the
effects of cognitive therapy versus other therapies for depression. Journal of Affective
Disorders, 68, 159–165.
Wang, C. E., Halvorsen, M., Sundet, K., Steffensen, A. L., Holte, A., & Waterloo, K. (2006).
Verbal memory performance of mildly to moderately depressed outpatient younger
adults. Journal of Affective Disorders, 92, 283–286.
Wang, J. L. (2004). Rural-urban differences in the prevalence of major depression and asso-
ciated impairment. Social Psychiatry Psychiatric Epidemiology, 39, 19–25.
Wang, P. S., Berglund, P., Olfson, M., Pincus, H. A., Wells, K. B., & Kessler, R. C. (2005).
Failure and delay in initial treatment contact after first onset of mental disorders in the
National Comorbidity Survey Replication. Archives of General Psychiatry, 62, 590–592.
Wang, P. S., Demier, O., Olfson, M., Pincus, H. A., Wells, K. B., & Kessler, R. C. (2006).
Changing profiles of service sectors used for mental health care in the United States.
American Journal of Psychiatry, 163, 1187–1198.
Wang, S. (2007). Shock value: Electroconvulsive therapy saves lives. But 70 years after it first
gained currency as a treatment for major depression, ECT continues to court contro-
versy. Washington Post. Health Section, July 24. Page F-1.
Watson, S., Gallagher, P., Del-Estal, D., Hearn, A., Ferrier, I. N., & Young, A. H. (2002).
Hypothalamic-pituitary-adrenal axis function in patients with chronic depression. Psy-
chosomatic Medicine, 32, 1021–1028.
Watson, S., Gallagher, P., Ritchie, J. C., Ferrier, I. N., & Young, A. H. (2004). Hypothalamic-
pituitary-adrenal axis function in patients with bipolar disorder. British Journal of Psy-
chiatry, 184, 496–502.
Way, B. B., & Banks, S. (2001). Clinical factors related to admission and release decisions in
psychiatric emergency services. Psychiatric Services, 52, 214–218.
Wehr, T. A., Sack, D. A., & Rosenthal, N. E. (1987). Seasonal affective disorder with summer
depression and winter hypomania. American Journal of Psychiatry, 144, 1602–1603.
Weich, S., Twigg, L., & Lewis, G. (2006). Rural/non-rural differences in rates of common
mental disorders in Britain: Prospective multicultural cohort study. British Journal of
Weick, K. E. (1984). Small wins: Redefining the scale of social problems. American Psychol-
ogist, 39, 40–49.
Weisman, R. (1984, March). Nutrition and neurotransmitters: The research of Richard Wurt-
man. NIMH Science Reporter, 1–8.
Bibliography 229
Weisse, C. S. (1992). Depression and immunocompetence: A review of the literature. Psy-

chological Bulletin, 111, 475–489.
Weissman, A. N., & Beck, A. T. (1978). Development and validation of the Dysfunctional Atti-
tudes Scale: A preliminary investigation. Paper presented at the 12th Annual American
Educational Research Association meeting. Toronto, Ontario, Canada.
Weissman, M. M. (2006). Recent advances in depression across the generations. Epidemiolo-
gia e Psichiatria Sociale, 15, 16–19.
Weissman, M. M. (2007). Cognitive therapy and interpersonal psychotherapy summit: 30
years later. American Journal of Psychiatry, 164, 693–696.
Weniger, G., Lange, C., & Irle, E. (2006). Abnormal size of the amygdala predicts impaired
emotional memory in major depressive disorder. Journal of Affective Disorders, 94,
219–229.
Wenzlaff, R. M., & Grozier, S. A. (1988). Depression and the magnification of failure. Jour-
Westermeyer, J. (1987). Cultural factors and clinical assessment. Journal of Consulting and
Clinical Psychology, 55, 471–478.
Whiskey, E., Werneke, U., & Taylor, D. (2001). A systematic review and meta-analysis of
Hypericum perforatum in depression: A comprehensive clinical review. International
Clinical Psychopharmacology, 16, 239–252.
Whittington, C. J., Kendall, T., & Pilling, S. (2005). Are the SSRIs and atypical antidepres-
sants safe and effective for children and adolescents? Current Opinion in Psychiatry, 18,
21–25.
Wilkinson, R. B. (1997). Interactions between self and external reinforcement in predicting
depressive symptoms. Behavior Research and Therapy, 35, 281–289.
Wilson, S., & Argyropoulos, S. (2005). Antidepressants and sleep: A qualitative review of the
literature. Drugs, 65, 927–947.
Wurglics, M., & Schubert-Zsilavecz, M. (2006). Hypericum perforatum: A ‘Modern’ herbal
antidepressant: Pharmacokinetics of acute ingrediieints. Clinical Pharmacokinetics, 45,
449–468.
Wurtman, R. J. (1982). Nutrients that modify brain function. Scientific American, 246, 50–59.
Yarrow, M. R., Clausen, J. A., & Robbins, P. R. (1955). The social meaning of mental illness.
Journal of Social Issues, 11, 33–48.
Young, A. S., Klap, R., Sherbourne, C. D., & Wells, K. B. (2001). The quality of care for
depressive and anxiety disorders in the United States. Archives of General Psychiatry, 58,
55–61.
Zalsman, G., Huang, Y. Y., Oquendo, M. A., Burke, A. K., Hu, X. Z., Brent, D. A., Ellis, S.
P., Goldman, D., & Mann, J. J. (2006). Association of a triallelic serotonin transporter
gene promoter region (5-HITTLPR) polymorphism with stressful life events and sever-
ity of depression. American Journal of Psychiatry, 163, 1588–1593.
Zhang, A. Y., & Snowden, L. R. (1999). Ethnic characteristics of mental disorders in five U.S.
communities. Cultural Diversity and Ethnic and Minority Psychology, 5, 134–146.
Zimmerman, M., McGlinchey, J. B., Young, D., Chelminski, I. (2006). Diagnosing major
depressive disorder. III. Can some symptoms be eliminated from the diagnostic crite-
ria? Journal of Nervous and Mental Disease, 194, 313–317.
Zuroff, D. C., Blatt, S. J., Sotsky, S. M., Krupnick, J. L., Martin, D. J., Sanislow, C. A., III, &
Simmens, S. (2000). Relation of therapeutic alliance and perfectionism to outcome in
brief outpatient treatment of depression. Journal of Consulting and Clinical Psychology,
68, 114–124.
Zweben, J. E., Cohen, J. B., Christian, D., Galloway, G. P., Salinardy, M., Parent, D., & Iguchi,
M. (2004). Psychiatric symptoms in methamphetamine users. American Journal of Addic-
tion, 13, 181–190.
Index
Abela, J. R. 202 Anouilh, Jean 65, 200
Abraham, Karl 153 anticonvulsive drugs 147–148
Abramson, Lyn Y. 70, 198, 203 antidepressive medications 37, 50, 51, 59,
abuse: parental 25, 107; emotional 83; physi- 106, 132, 135, 136, 138–150, 151, 164–166,
cal 82–83; sexual 83 169, 170–171, 179, 180, 183, 185, 186, 189,
activities, increasing pleasant 116 191, 193, 194; comparisons of effectiveness
acupuncture versus massage therapy 178 185, 186, 189, 191; comparisons in tolerabil-
adjective check list 17–18, 101 ity 139, 144; history of discovery 138–142;
adolescents: depression among 30, 37–41, increasing dose of 139, 185; newer 145–146;
86–87, 119; gender differences in manifes- sleep, effects on 55; time lag in effective-
tations 87; suicide among 39–40, 41, ness 141; use during pregnancy 150; use
149–150 with children 149–150
affectionless control 81–82 anxiety 47, 58–59, 71–72, 75, 82, 88, 93, 98,
African Americans, depression among 104, 105, 116, 158, 159, 174, 175, 177, 178,
33–34, 91, 137, 193 186, 188
age, depression and 27, 28, 35, 37–42, 47 appearance, improving 119–120
Agid, O. 201 Aretaeus 8
Agomelatine 55 Argyrapoulos, S. 199
Ainsworth, Mary D. S. 77–78, 79, 201 Aripiprazole 148, 149
Akiskal, H. S. 154, 198 Aro, A. R. 203
Alansky, Jennifer A. 201 Arroll, B. 204
alcohol dependence 34, 97–98 artificial light therapy 19, 20, 183–184
alcoholism: depression and 13, 60, 97–104, artists, depression among 8–9
106, 188; age of onset of the condition 100; Asian Americans, depression among 35–36,
gender differences 100; primary vs. second- 137
ary depression 98–102; psychological con- assertiveness training 117–118, 124
sequences 101–104; social consequences attachment 76–80, 83, 127, 158
101–104 attention, regulation of 173–174
Alegria, M. 204 attitudes, depression towards 28, 36, 137
Algood-Merten, Betty 203 Attributional Style Questionnaire 70–71
allegiance biases 160, 165, 173 attributional styles 70–71, 86
Alloy, L. B. 81, 82, 83, 201 atypical antipsychotics 148
alternative treatments, depression of 172–184 atypical depression 11, 14, 21, 143
Altman, Janet H. 64, 200 automatic thoughts 62–63, 70, 156–157
ambivalence 69, 112 availability, psychotherapist of 137
Amish, depression among 32
Amitriptyline 140 balance, keeping activities in 124–126, 195
amnesia, ECT induced 168, 169 Banks, S. 205
amygadala 48, 49, 58–59 Barcusa, S. L. 207
anaclitic depression 80 Barnes, P. 201
ancient world views, depression of 1 Barreto, R. M. 198
Anderson, I. M. 204 barriers, treatment to 137
anger 2, 68–70, 80–81, 82, 83, 87, 93, 105, Bass, Judith D. 81, 201
129, 153, 157, 159, 192; psychoanalytic view Bazner, E. 200
and depression 2, 68–70, 192 Beach, S. R. H. 142, 204
Angold, A. 198 Beauchemin, K. M. 200
231
232 Index
Beck, Aaron T. 8, 15, 60, 62, 67, 70, 156, 197, carbohydrate craving 21, 22
200, 205 Carey, Michael P. 198
Beck Depression Inventory 15, 41, 94, 99 Carter, F. A. 198
Becker, E. S. 197 Carver, Charles S. 66, 200
Beekman, A. T. 199 Caspi, A. 200, 202
behavior, changing 115–122 catastrophizing 86, 93
Bellak, Leopold 153–154, 205 Catrona, Carolyn 91, 202
Benassi, Victor A. 64, 200 Cerletti, Ugo 168
Benazon, N. R. 204 Cervantes 118
bereavement 10 Chabrol, H 199.
Berlioz, Hector 9 children: antidepressants, use in 149–150;
Bertolino, A. 200 depression in 30, 37–39, 75–87; subclinical
bibliotherapy 123–124, 188 depression in 39, 84
Bierut, L. J. 199 Childrens Depression Inventory 38–39,
Bifulco, A. 201, 202 85–86
Billings, Andrew G. 186, 207 Chinese-Americans, depression among
Bini, Lucio 168 35–36
biological clock 21, 54–55 Chiu, C-C 206
bipolar disorder 2, 8, 22–25, 27, 35, 36, 40, Christensen, Helen 124, 203
53, 105, 146–149, 182, 192; African Ameri- Church, N. F. 200
cans 34; age of onset 49; brain structure Ciccohetti, Dante 201
studies of 49; duration of cycles 23; med- circadian rhythms 21, 54–55
ications for 146–149, 194; prevalence of 29; citalopram 144
suicidal tendencies in 25; Type I versus Clark, David A. 202
Type II 24, 25; see also manic depression Clayton, A. H. 205
black and white thinking 66, 67, 156, 178 clinical depression versus depressed mood
black bile 1 5–6
Blatt, Sidney 80, 200, 201 Coats, K. I. 199
Blazer, Dan 198 cocaine dependence, depression and 105–106
Bliwise, Donald L. 200 Cofer, Dorcus H. 201
Bockting, C. L. 207 cognitive therapy or cognitive behavioral
body image 30, 119–120 therapy 8, 60, 96, 123–124, 156–158, 160,
body motion, constriction of 11 161, 164, 175, 188,189, 190
Bollini, P. 204 Cole, David 94, 202
Bond, M. 205 Coleg, E. A. 201
boundaries, respecting 131 Coleridge, Samuel Taylor 7
Bowlby, John 76, 77, 83, 89, 201, 202 Colla, J. 198
brain structure, depressed patients 48–49 college students: depression among 40–41;
Breslau, J. 198 stress among 40–41, 89–90, 94
Bridle, C. 205 combination treatment, drugs and psy-
brief dynamic therapies 153–154 chotherapy 138, 165–166
bright light therapy 19, 20, 183–184; appara- comorbid conditions, recurrence odds and
tus for 184; side effects of 184 186–187
Brooks-Gunn, J. 30, 198 comparative outcome studies, psychotherapy
Brown, Sandra A. 202 161–162
Browning, Elizabeth B. 151 comparing self with others 65, 113
Brunstein-Klomek, A. 205 compliance, patient with treatment 166
Buchwald, Alexander M. 200 composers, depression among 9
Bulmash, E. L 197 computer antidepressive programs 123–124
bupropion 145 concentration, diminished 5, 10, 12, 21, 24,
Burke, K. C. 199 37
Burns, David 123 confidence building activities 83–84
Butler, A. C. 205 confidence, self 64–65, 75, 76, 78, 79, 83, 84
Byron, Lord 8 Conte, Hope R 205
continuation and maintenance therapies 187,
Caccia, S. 206 189–191
Cade, John 146 continuation treatment, antidepressant med-
Cahn, B. Rael 174, 206 icines 185
Campbell, M. K. 206 Cook, Frederick A. 19, 197
Campbell, S. 199 coping, stress with 79, 87, 93–94, 96, 202
carbamazepine 148 Cornell, Dewey G. 197
Index 233
corrugator muscles 10 dysregulation 52, 54–55

cortisol, hypersecretion of 52–53, 91 dysthymic disorder 9, 27, 34, 35, 36, 40, 177
cost, treatment of 137, 166
Covington, M. B. 206 Earleywine, M. 203
Coyne, James C. 132, 204 eating disturbances 11, 21, 37, 38, 94, 134,
Cox, B. J. 200 140, 177
Cuijpers, P. 205 Egeland, Byron 198
cultural factors, seeking professional help in Egeland, Janice A 198
137 Ehlers, Cindy L. 54–55, 199
Crowe, Leif C. 97, 202 eicosapentaenoic acid (EPA) 181, 182
Einarson, T. R 204, 205
Dauber, Richard B. 197 elderly, depression among 42–44
Davis, Kenneth L. 52, 199 electroconvulsive therapy 168–171, 186
death of parent 80 Eliot, T. S. 8
defense mechanisms 74, 91, 115, 153 Elkin, I. 205
de Maat, S. M. 205 Ellis, Albert 67, 200
de Mello, M. F. 205 endogenous depression 9
denial, defense mechanism as 25, 36, 99, 153 endophenotypes 58
Denney, Douglas R. 200 Enns, H. W. 200
dependency relationships 65 Ernst, E 173, 206
Depression and Bipolar Support Alliance esccitalopram 144
(DBSA) 122–123, 131, 189 exercise, antidepressive effects of 119–120,
depression, prevalence of 26–28; increase in 131
27–29; within families 47–48 expression, sad 10, 24, 134, 187
Depue, Richard A. 23–24
DeRubeis, Robert J. 164, 205 facial expressions, perceptions of 62
desipramine 140 Fadden, G. 204
Deutsch, Albert 2 Fagot, B. I. 201
developmental tasks, adolescence in 87 failure, fear of 110, 111
Dexamethasone Suppression Test 52–63 Falret, J. P. 22, 198
DEX/CRH Test 53 family: negative effects on 132–133; support
Diagnostic and Statistical Manual of Mental by 28–29, 128–132
Disorders 9, 17, 20, 37, 38, 98, 99, 192, 197 family therapy 187
Dickens, Charles 9, 73 fatigue 10, 11–12
Dickerson, S. S. 199 Fava, M. 207
Dickinson, Emily 8 Fenichel, Otto 153
dimensional versus categorical view, depres- Field, T. 206
sion of 14, 15 Finucane, A. 206
Dingfelder, S. F. 200 Fitzgerald, F. Scott 9
discontinuation risks, cognitive therapies Fleet, Gordon L. 203
189 Floyd, M. 203
divorce, effects of 28, 40, 77, 80, 83, 88 Fluoxetine 143–144, 148; see also Prozac
docosahexaenoic acid (DHA) 181, 182 Fluvoxamine 144, 179
Doerfler, Leonard A. 198 Foa, E. B. 202
dopamine 142, 145 Fogel, J. 198
dothiepin 140 Folkenberg, J. 197
doxepin 140 Folkman, Susan 202
Dranovsky, A. 199 follow-up visits, psychotherapist to 190
dream analysis, therapy in 153 Ford, D. E 198
dreams, depression and 56; bipolar patients Forgas, Joseph P. 7, 197
56 Framptom, J. E. 204
drinking: as tension reliever 100–101; depres- Frangou, S. 207
sive effects of 101; expectations from 100–101 Frank, Ellen 54–55, 207
driving reactions, depression and 11 Frazier, J. A. 199
drug dependency, depression and 13, 25, free association, therapy in 153
104–108, 188 Freud, Sigmund 2, 12, 67, 69, 89, 152–154,
Duloxetine 145–146 197, 200, 202, 205
Dumais, A. 197 Friedman, R. A. 207
Dunn, A. L. 203
Durkheim, Emile 29, 198 Gallagher, W. 197
Dysfunctional Attitudes Scale 70 Galloway, G. P. 203
234 Index
Ganellen, Ronald J. 66, 200 Hispanic Americans, depression among

Gauguin, Paul 9 34–35, 137, 193
gender differences, depression in 29–33, 41, Hoberman, Harry M. 205
48, 87, 186, 193 Hoffman, K. B. 201
genes, depression and 47–48, 186–187 Holahan, Charles J. 202
George, William H. 97, 202 Hollon, Steven D. 200
Gjerde, Per F. 201 Holmes, A. 200
Gladstone, T. R. 201, 203 Holsinger, T. 206
Glasgiow, R. E. 203 Homish, G. 203
goals, setting reasonable 109–111 hopelessness 5, 25, 37, 65, 129
Goel, N. 207 hospitalization 41, 103, 129–130, 137, 148,
Goethe, Johann W. von 8, 197 167–168, 169
Goforth, H. W. 206 Hosteler, A. M. 198
Goldbart, J. 198 hypnosis 7
Goldsmith, H. H. 201 hypomania 22, 23, 146
Gonzales, Linda R 190, 205, 207
Gorman, J. 51, 199 Iacona, W. G. 207
Gotlib, I. H. 200 imaging studies 48–49, 51, 58–59; techniques
Grant, B. F. 198, 199, 202 used 46
Grenyer, B. F 201 Iminodibenzye 139–140
grief 10, 47, 158 Imipramine 140, 164
Griffiths, Kathleen M. 124, 203 immigrants versus native born, depression
group therapy 167 rates 33
Grozier, Sherilyn A. 66, 200 immune system 56–57
guilt 1, 10, 12, 71–72, 80, 90, 99, 129, 133, 197 improvement, meaning of 161
impulsivity 13, 72, 167
Haby, M. M. 205 inadequacy, feeling of 64, 68, 71–72
Hamilton, M. A. 197 indecision 12, 14, 99
Hamilton rating scale 15, 141, 160, 161 infections, susceptibility to 56–57
Hammen, Constance L. 31, 90, 92, 198, 202 inflation, importance of events 93, 112–113
Handel, George F. 9 insane asylums 2
Hankin, B. L. 198 insomnia, sleep onset 11, 54
Hariri, A. R. 58, 200 insulin induced seizures 168
Harkins, Kate 95, 202 interest, loss of 5, 8, 10, 99, 129, 134
Harkness, K. L. 202, 204 internal vs. external control of reinforcement
Harlow, Harry F 76–77, 201 63, 67, 86
Harris, A. H. S. 203 interpersonal psychotherapy 158–159, 160,
Hasin, D. S. 198, 199 164, 188
Hassler, G. 200 introjective depression 81
Hassles, daily 90 involutional melancholia 9
Hawkins, Wendy L 200 Iproniazid 142
Hawley, L. L 200, 207 Irons, C. 201
Hays, P. 200 irrational beliefs 67
Healy, David 139–140, 142 Isocarboxazid 142
Heiby, E. M. 114, 203
helplessness, learned 64–65, 83 Jacobson, Edith 153
Hemingway, Ernest 9 Jamison, Kay R. 8–9, 197
Hen, R. 199 Jarret, Robin B. 197
hereditary basis of depression 47–48, 128, Jewell, Donald S 125, 154–155
187, 193 Johnson, Mark H. 13, 197
heroin addiction 106–108; depression and 97, Joorman, J. 200
106–108; psychological consequences
106–108; social consequences 106–108 Kabat-Zinn, J. 175, 206
Hetherington, E. Mavis 201 Kallechstein, A. D. 203
Heuser, I. 199 Kaltenthaler, E. 203
Hewitt, Paul L. 122, 203 Kanner, A. D. 90, 202
Hibbeln, Joseph, R. 182, 206, 207 Karno, Marvin 198
Himmelfarb, Samuel A. 202 Karpman, Benjamin 106, 202
hippocampus 48–49 Kashani, Javad H. 37, 198
Hippocrates 1, 8, 176 Kashner, T. M. 189, 207
Hiroto, Donald 200 Kaslow, N. J. 201
Index 235
Kasper, S. 198 Lutz, David J. 99, 100, 202

Kathol, Roger G. 149 Luvox 144
Kazdin, Alan E 82–83, 151–152, 201, 205
Kearns, K. A. 201 MacGillivray, S. 204
Keats, John 8, 118 Magaro, Peter A. 13, 197
Keeler, Martin H. 203 Mahalik, James R. 125–126, 203
Kemeny, M. E. 202 Malm, H. 205
Kendall, P. C. 200 Manber, R. 206
Kendler, Kenneth S. 47–48, 199 manic depressive disorder 2, 9, 22–25, 46; see
Kerr, G. W. 204 also bipolar disorder
Kerr, Mary M. 39, 198 manic episodes 22–24, 27, 139, 146, 148, 184
Kessler, R. C 198, 199, 204, 206 Mann, John J. 199
Ketamine, adjunct to ECT as 170–171 Marcos, Luis R. 36, 198
Kieseppa, T. 199 marijuana, depressive reactions to 104–105
Kim, H. L. 206 marital therapy, depression for 131
Kistner, J. A. 201 Marwit, S. J. 203
Kivlighan, Dennis 125–126 masked depression 38
Klerman, Gerald 205 massage therapy 173, 176–179
Kline, Nate 142 Maugham, W. Somerset 128
Kocis, James H. 140, 204 Mazure, C. M. 202
Koizumi, Y. 203 McBride, C. 205
Koukopoulos, A. 198 McCabe, M. 203
Kovacs, M. 198 McCoy, S. J. 198
Kovess, V. 198 McCranie, Edward W. 81, 201
Kraepelin, Emil 2, 9, 197 McFarlane, J. W. 198
Kramer, Peter 144 McGirr, A. 197
Kramlinger, K. G. 198 McGrath, E. P. 201
Krohne, H. W. 202 McGuffin, P. 199
Kronmueller, K. T. 203 McGuire, P. A. 198
Kuhn, Roland 140 McLearn, K. T. 198
Kuhner, C. 204 McMain, S. F. 175, 206
Kunugi, H. 199 McMillan, Marcia J. 197
Kuo, P. H. 202 measuring depression 15–18
Kupfer, David 54–55, 199 medieval views, depression of 2
Kupka, R. W. 198 meditation 173–176
melancholia 1
Lam, R. W. 199, 207 Melartin, T. K. 207
Lamotrigine 148, 149 melatonin 21–22
Larson, R. W. 39, 198 Meller, William 199
Lau, Mark A. 175, 206 Melville, Herman 9
Lazarus, Richard S. 202 memories, early 82
Lee, Y. M. 206 memory, depression and 5, 13, 82
Lefkowitz, Monroe M. 38, 84, 198, 201 mental health care: seeking 134–137; for mi-
Leitenberg, Harold 85–86, 201 norities 35–36, 137
Lennartsson, C. 203 mental hospitals 167–168; past overcrowding
Lenze, E. J. 199 2
Lewinsohn, Peter M. 72, 201, 203 Mercer, S. W. 206
Lewy, A. J. 199 methamphetamine use, depression and 105
Libet, Julian M. 203 Metrazal induced seizures 168
life changes, major 87, 158–159, 193 Mexican-Americans, depression among 35
lifestyle, changes in 131, 188 Meyersburg, H. A. 71–72, 88, 202
Lincoln, Abraham 8 Michelangelo 9
Linde, K. 206 Mindfulness Based Cognitive Therapy
Lisanby, S. H. 206 (MBCT) 175–176
listening skills, improving 121–122, 130–131 mindfulness meditation 174–176
lithium 146–147, 149, 170, 171 mind-sets, measurement of 70–71
loneliness 40, 67, 86, 116, 120–121, 122, 158, minority groups, depression in 33–36
159 mistakes, living with 115
Looby, A. 203 Moclobemide 142
loss 2, 40, 41, 61, 69, 80, 83, 87, 88, 89, 93, Mojtabai, R. 204
153, 158, 192, 202 Molnar, B. E. 201
236 Index
Monoamine oxidase (MAO) 142 Ostberg, V. 203

Monoamine oxidase inhibitors (MAOIs) overdosing, antidepressants of 141
141–143; food restrictions 143; drug restric- overgeneralization 65–66, 70, 85–86, 112, 115,
tions 143; side effects 142; transdermal patch 156, 188, 193
143; treatment of atypical depression 143 Owens, M. J. 199
Monroe, Scott 95, 202
Montejo, A. L 204 Packard, E. 200
mood: induction, techniques of 7, 18; Palinkas, Lawrence A. 19, 20, 197
influence on thinking 7–8; measurement of Pandy, G. A. 199
17–18; rapid cycling 24, 25; sad, blue 5, 10, parent-child relationships 75–83, 127
24; swings 18–25 Parental Bonding Instrument 81, 82
mood GYM computer program 124, 188 Parker, G. 81, 201
mood stabilizing drugs 146–149 Paroxetine 144, 180
Moos, Rudolf H. 186, 202, 207 Parsons, Talcott 202
Mor, N. 200 patient attitudes in therapy 163
Moreno, R. A. 204, 206 Paxton, S. J. 203
Moyer, Christopher A. 206 Penninx, B. W. 199
Mourning and Melancholia 69, 89, 153 perfectionism 66–67, 70, 71–72, 113–114, 133,
Munsey, C. 203 156, 188, 194
Murray, A. D. 201 Peters, Stephanie 31, 198
Murrell, Stanley A. 202 Peterson, Christopher 200
Mylander, Maureen 125 Petty, S. C. 203
Phenelzine 142, 143
Nair, H. 201 physical abuse 82–83
Nathan, P. E. 203 physical complaints 8, 13, 14, 24, 36, 37, 56,
National Center for Complementary and Al- 93, 134
ternative Medicine 172, 173, 174 physicians, role in diagnosis 43, 143–135
Needles, Douglas 203 Pihl, R. O. 197
negative perspective 7–8, 14, 24, 60–63, 68, Pilowsky, D. J. 201
111, 117 pleasant activities, introduction of 116, 120,
Neighbors, H. W. 204 131, 195
Nelson, G. 201 Plosker, G. L. 204
Nemeroff, C. B. 199 Poe, Edgar Allan 8
Nemets, H. 207 Polich, John 174, 206
Neumeister, A. 199, 200 Pollock, Jackson 9
Neuringer, Charles 129, 204 Post, R. M. 198
neurons, generation of 48–49 postpartum depression 29–30, 70
neurotic depression 9 Potkin, S. G. 198
neurotransmitters 22, 46, 49–52, 128, 140, powerlessness, feelings of 43, 60, 63, 65,
142, 151, 193, 194 71–72
Nezu, Arthur M. 125, 203 pregnancy, antidepressant use during 145,
Nguyen, L. 206 150, 182
Nierenberg, A. A. 205 premenstrual depression 18–19, 29
Nietzel, Michael T. 205 Prescott, C. A. 199
NIMH Center for Epidemological Studies In- primary care physician, role of 134–137
ventory 15 Prisciandaro, J. J. 197
NIMH collaborative study 164 Pristein, M. J. 201
NIMH Interview Guide 26–27, 32 problem solving 93–94, 125
Norepinephrine 50, 51, 52, 140, 142 Prosen, H. 201
Nortriptyline 140 protective shield 63, 71–74
Nugent, J. F. 101–102, 203 Protriptyline 140
Prozac 143–144
Occupational Outlook Handbook 111 psychodynamic therapies 25, 152–155, 161
Oldenhinkel, A. J. 201 psychomotor agitation 10
Olfson, M. 204 psychotherapist, choosing a 162–163
O’Keeffe, Georgia 9 psychotherapy: 37, 67, 70, 71, 134–135, 136,
Olanzapine 148, 149 149, 151–161, 186, 188, 190, 191, 193, 194;
Omega-3 polyunsaturated fatty acids 181–183 cognitive-behavioral (or cognitive therapy)
optimism 73–74 8, 60, 96, 123–124, 156–158, 160, 161, 164,
Oquendo, M. A. 197 175, 188, 189, 190; common features of 152;
Ortega, A. N. 198 comparative outcome studies 161–162;
Index 237
comparisons with drugs 164–165; effective- sadness, prolonged 1, 5, 37

ness 160–165; interpersonal 158–159, 164, Safran, Jeremy D. 156–157, 205
190–191; involvement spouse of 131; moti- St. John, P. D. 198
vation for 154; patient characteristics as St. John’s wort 179–181
factor 163; psychodynamic 25, 152–155, 161; Salkovskis, P. 203
used with drugs 136, 138, 165–166; varieties Sargent, Marilyn 152, 199
of 151–152; versus medication 164–165 Schiefflen, Edward 198
psychotic features, depression with 148, 167, Schmidt, J. M. 197
171 Schmitz, J. M. 203
puberty, depression and 86 Schubert-Zsilavecz., M. 206
Schulz, V. 206
Quetiapine 148–149 Schumann, Robert 9
Quitkin, F. M. 204 Schwartz, G. E. 197
Scogin, Frank 123, 203
Radloff, L. S. 197 Seasonal Affective Disorder 19–22, 40, 54–55,
Rapaport, M. H. 204 183–184
rapid cycling 24, 25, 147–148 Sedler, M. J. 198
Rapp, Stephen R. 199 Segal, S. P. 198
rate, depression increasing 27–29 Selective memory 82
rationalization 73, 117 selective perception 62
reaction time, slowed 5, 8, 11, 24 selective serotonin reuptake inhibitors
reactions of others 131–132 (SSRIs) 143–145; adverse effects on sexual-
reactive depression 9 ity 144, 145; links to suicidal thinking in
reassurance seeking, excessive 87 children 145; reactions to discontinuation
recurrence of depression 14, 41, 62, 124, 138, 145; versus tricyclics 144
166, 185–191, 194; factors promoting 186– Selegiline 142, 143
187; odds of 18; prevention steps 188–191 self assessment 111–112
reframing maneuvers 73 self esteem 30, 31, 64, 65, 68, 73, 75, 79, 81,
regulator promoter area (5-HTTLPR) 83, 84, 85, 86, 87, 92–93, 110, 112, 119, 124,
58–59; short and long variants 58–59 153, 158, 159
reinforce self 114–115, 116 self focusing 13, 68
Reis, S. 201 self help manual 123, 126
rejection 30, 31, 32, 79, 80, 84, 85, 87 self report measures: depression 15–18, 27,
relapse versus recurrence 185–186 38, 99; for children 38–39
REM periods 54–55 self reproach 1, 12, 37, 40, 41, 67, 69, 71, 72,
Repetti, R. L. 201 73, 80, 85, 86, 90, 92, 115, 193
resistance to change, overcoming 116–118 Seligman, Martin E. P. 64, 70, 86, 200, 201
Restless Heart 65 Sen, S. 200
reuptake, neurons of 50, 51, 58, 140, 151 sensitization, following repeated depressive
Reynolds, William M. 40 episodes 95–96
Rinck, M 197 separation, child from mother 77–79, 80, 83
risk taking 110, 116 Serebruany, V. L. 205
Risperidone 148 serotonin 22, 50–51, 140, 142, 177, 178, 182;
Roberts, J. E. 197 link to suicide 149–150; transporter gene
Robbins, Paul R 14, 15, 19, 29, 40, 56, 69, 82, 58–59, 193
89, 94, 101–102, 109, 197, 198, 199, 200, 201, serotonin, noreprinephrine reuptake in-
202, 203 hibitors 145–146
Robins, Lee N. 198 Sertraline 144, 180
Rockhill, C. M. 201 severity depression, recurrence odds and
Rogers, Carl 151 186, 187
role playing 159 Shaffery, J. 199
role transitions 87, 89, 158–159 Shakespeare, William 8, 20, 197
romantic relationships, breakups in 89, 159 Shaw, Eric D. 153
Rosen, G. M. 203 Sherman, K. J. 206
Rosenthal, Norman E. 20, 207 Shrout, Patrick E. 202
Rost, K. 204 sick role 94–95
Rotter, Jullian B. 200 Siever, Larry J. 52, 198
rumination 13–14, 94 Simon, G. E. 204
rural vs. urban, depression in 32–33, 137 Sir, A. 205
Sirota, A. D. 197
Sabbatini, R. 206 Slangen, K. E. 202
238 Index
sleep disturbances 5, 10, 11, 13, 21, 54–56, 67, Surguiazde, S. A. 200
134, 140, 171, 192; antidepressant medicines surrogate mothers, chimpanzees 76–77
and 55; in seasonal affective disorder 21; Sweeney, P. D. 201
REM findings 54, 55; sleep onset insomnia symptoms of depression 9–15, 128
11 Szasz, Thomas 129, 204
small wins, strategy of 115–116 Szegedi, A. 206
Smith, J. A. 202
smothering 131 Takeuchi, D. T. 198
Snow, Peggy A. 99, 100, 202 Tanck, Roland H. 14, 19, 40, 62, 82, 89, 94,
Snowden, L. R. 198 197, 199, 200, 201, 202, 203
SNRIs 145–146 Taylor, S. 206
Snyder, C. R 73, 201 T-cell counts 57
social integration 29 Tchaikovsky, Peter 9
social relationships, improving 120–122 Teasdale, J. D. 206
social skills 84, 121–122 Teasdale, Sara 8
social support 13, 29, 32, 34, 35, 87, 94, 120– Teesson, M. 203
123, 127–133, 188–189; recurrence odds and Terman, Juian Su 183, 184, 207
188–189 Terman, Michael 183, 184, 207
Solkero, T. P. 197 Tesiny, Edward P. 38, 84, 198, 201
Sontrop, J. 206 Thase, M. E. 207
Sourander, A. 199 therapist: availability of 137; choosing 162–
Spaulding, J. L. 203 163; skill of 162
Spearing, M. 198 thought patterns: changing 156–158, 194; de-
specifiers, diagnosis in 14 pressive related 7–8, 14, 21, 24, 30, 60–63,
Spitz, Rene A. 77 68, 85–86, 156–158, 188, 193, 194
Stansfield, S. A. 203 Timbremont, B. 198
Steinbrueck, Susan M. 205 time, perception of 65
stigma, mental illness 36, 137 Tofranil 140
Stinson, F. S. 202, 203 tolerance, importance of 112–113, 114
Stoddard, J. J. 204 Tolstoy, Leo 9
strange situation 78–79 Toneatto, T. 206
stress: cognitive styles and 92; coping with Torrent, C. 198
79, 87, 93–94, 96, 202; depression, relation Touch Research Institute 177–179
to 88–96, 128, 137, 189, 193, 194, 195; early transcendental meditation 174
exposure to 75–77, 80–86; following de- transermal patch, MAO use for 143
pression 94–95; genetic factors in 58–59; in transference 153
adolescence 40, 86–87; in college 40–41, transporter, serotonin (5HTT) 58–59
89–90, 94; in job 33, 93, 111, 117, 194; in re- Tranylcypromine 142, 143
lationships 40, 88, 89, 112, 117, 127, 158, treatment shift, primary care physicians to
159; in urban areas 32, 33, 91; in women 135–136
30–31, 80; individual differences in 89, 90, tricyclics 139–141; overdosing risks 141
91–94; interpretation of 59; life changes Trivedi, M. H. 204
and 88–89, 91, 131, 158, 188; recurrence of Trowell, J. 205
depression 95–96; reducing stress at home Trude, S. 204
130; self-esteem as moderator 92–93; self- Tryptophan 50–51; deletion 51, 59
generated 90; social support for 89, 91, twin studies 47–48
95–96; socio-economic 91; uncontrollabil-
ity of 52, 90–91, 93 unconscious 12, 69, 152–153
stress management programs 95
Stroufe, L. A. 201 valproic acid 147–148, 149
Stuart, John 8 Valtonen, H. M. 198
Sublette, M. E. 207 Van Gogh, Vincent 9
subliminal perception, studies of 12 van Wijngaarden, B. 204
Sue, David 36, 137, 204 Veil, H. O. 204
Sue, Stanley 36, 137, 204 Velten, E. J. 197
suicide 5, 10, 13, 21, 26, 29, 37, 39–40, 41, 51, Venlafaxine 145–146
99, 103, 105, 107, 108, 129–130, 141, 149–150, victim mentality 68
155, 159, 167, 170, 171, 182, 184, 192, 199 Villanova, Peter 200
Summers, M. 198 Vincent, N. K. 200
Sund, A. M. 201 Vittengl, J. R. 207
support groups 122–123, 126, 194 Von Korff, M. 204
Index 239
Walker, J. R. 200 Whitman, Walt 8

Wall, J. H. 202 Whittington, C. J. 204
Wampold, B. E. 162, 205 Wilkinson , R. B. 203
Wang, C. E. 197 Wilson, S. 199
Wang, J. L. 199 Winquest, J. 200
Wang, P. S. 204 Winterborn, 1. R. 64, 200, 201
Wang, S. 206 Wong, David 144
Warren, M. P. 30, 198 worthlessness, feelings of 10, 13
Watson, S. 199 writers, depression among 8–9
Way, B. B. 205 Wurglics, M. 206
Wehr, Thomas A. 21, 198 Wurtman, Richard 1, 50, 129, 199
Weich, S. 198
Weick, Karl E. 124, 203 Yarrow, M. R. 204
weight, changes in 5, 10, 13, 14 Young, A. S. 204
Weisse, Carol 56–57, 200
Weissenburger, Jan E. 197 Zalsman, G. 200
Weissman, Myrna M. 70, 199, 200, 205 Zhang, A. Y. 198
Weniger, G. 197, 199 Zimmerman, Martin 14, 197
Wenzlaff, Richard M. 66, 200 Ziprasidone 148
Westermeyer, Joseph 207 Zurroff, D. C. 200
Whisky, E. 206 Zweben, E. 203

Understanding Depression - Robbins (2009)

Uploaded by

Copyright:

Available Formats

Understanding Depression - Robbins (2009)

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Understanding Depression - Robbins (2009)

Uploaded by

Copyright:

Available Formats

Coping with Stress:

The Psychology of Dreams (1988; paper 2005)

Anger, Aggression and Violence:

Adolescent Suicide (1998)

Romantic Relationships: A Psychologist

McFarland & Company, Inc., Publishers

¡. Depression, Mental — Popular works. I. Title.

British Library cataloguing data are available

©2009 Paul R. Robbins. All rights reserved

No part of this book may be reproduced or transmitted in any form

Cover art by Boris Zaysev (iStockphoto). Front cover by TG Design

Manufactured in the United States of America

McFarland & Company, Inc., Publishers

1. Depressed Mood and Depression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7

Chapter Notes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 197

When I had nearly completed my perusal of the recent scientiﬁc literature

With the continued inﬂux of new information about depression, it seemed

A grief without a pang, void, dark, and drear

Dickens, Ernest Hemingway, F. Scott Fitzgerald, Herman Melville, and Leo

Trouble in sleeping is another possible indication of depression. Obvi-

Thoughts of suicide are another sign of depression. Sometimes these

Not at All A Little Bit Deﬁnitely

Mood Swings in Clinical Depression

In recent years scientiﬁc studies carefully carried out in laboratories in

percent) noticed seasonal changes in their moods. About a quarter of those

I feel like I’m on top of the world

I can’t focus on anything for very long.

The authors then describe the behaviors of her depressive phases.

We shall now turn to the questions of how prevalent depression is in the

Sex Differences in Depression

Tracy tells a story of being in an unhappy marriage. She was married

Urban and Rural Comparisons

Depression in Members of Minority Groups

description of psychological states. An example of the error resulting from the

Age at Onset of Depression

Depression Among the Elderly

it is very clear that the problem of depression is widespread and probably

I remember looking through a textbook on abnormal psychology written

What happens when tryptophan is depleted in people who are not

these abnormalities in the neurotransmitters in depressed people are not fully

A Possible Biological Test for Depression

Depression and Sleep Patterns

Depression and the Immune System

responses using in vitro response to mitogins as a measure. Included in these

The Search for Genes That Underlie Depressive Disorders

activity of the amygadala when confronted with unsettling situations. People

Alan is a 20-year-old sophomore student at a suburban community col-

The Negative Perspective

doing psychoanalytic therapy. When he became convinced of the importance

depressed controls. There were consistent differences between the groups in

Some Depressive Thought Patterns

sergeant who tolerates no excuses, sees no extenuating circumstances and sees

Resentment and Anger

The Measurement of Mind-Sets

butable to one’s own actions (internal) or caused by external forces. Would

becomes an absolute, all-or-nothing issue, even, falling slightly short of the

The Protective Shield

tions, such as friendly, warm, communicates clearly, interested in other peo-