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The Biological Viewpoint

The traditional biological viewpoint focuses on mental disorders as diseases, many of the
primary symptoms of which are cognitive, emotional or behavioral. The major biomedical
breakthrough wherein general paresis initially thought to be a specific type of mental disorder
characterized by paralysis and insanity and causing death within two to five years, was found to
be linked to syphilis of the brain, provided a major impetus to the biological viewpoint. Under
this viewpoint, mental disorders are viewed as disorders of the central and autonomic nervous
systems and/or the endocrine system that are either inherited or caused by some pathological
process. At one time, people adopting the biological approach hoped to find simple biological
explanations for mental disorders. Today, however most clinical psychologists and psychiatrists
recognize the complexity of such explanations and acknowledge the role of psychosocial and
socio-cultural causal factors along with biological factors, both in terms of their independent
effects as also their capacity to cause each other.

Biological Causal Factors:

Biological causal factors in the development of mental disorders are on a broad basis divided
into four categories. These include - a) neurotransmitter and hormonal imbalances in the brain, b)
genetic vulnerabilities, c) temperament and d) brain dysfunction and neural plasticity or the
flexibility of the brain in making changes in organization or function in response to various
factors. Each of these categories encompasses a number of conditions that influence the quality
and functioning of our body and behavior and can possibly lead to maladaptive behavior. They
are often not independent of each other and often occur in varying combinations in different
people.

Neurotransmitter imbalances

The effective communication between neurons or nerve cells is essential for adequate brain
functioning. The site of the communication between the axon of one neuron and the dendrites or
cell body of another neuron is the synapse – a tiny fluid filled space between the neurons. Inter-
neuronal transmissions are accomplished by neurotransmitters or chemical substances that are
released into the synapse by the presynaptic neuron when a nerve impulse occurs. There are
many different kinds of neurotransmitters. Some increase the possibility that the postsynaptic
neuron will fire or produce an impulse, whereas others inhibit this possibility. Whether the neural
message is successfully transmitted to the postsynaptic neuron also depends among other things,
on the concentration of certain neurotransmitters within the synapse. The belief that
neurotransmitter imbalances in the brain can result in abnormal behavior is one of the basic
tenets of the biological perspective today, although today most researchers agree that this is only
part of the causal pattern involved in the etiology of most disorders. Sometimes psychological
stress can also bring on neurotransmitter imbalances. Neurotransmitter imbalances can be created
in a variety of ways –

1) There may be excessive production and release of the neurotransmitter substance into the
synapses, causing a functional excess in the levels of that neurotransmitter.
2) There may be dysfunctions in the normal processes by which neurotransmitters once
released into the synapse are deactivated. Ordinarily, this deactivation occurs through the
re-uptake of the released neurotransmitter from the synapse into the axon-ending or
through a process of degradation by certain enzymes present in the synapse and in the
presynaptic axon-ending.
3) A third cause of neurotransmitter imbalance may be problems with receptors in the
postsynaptic neuron which may either be abnormally sensitive or insensitive.

Neurons sensitive to a particular neurotransmitter tend to cluster together forming neural paths
between different parts of the brain known as chemical circuits. Different disorders are believed
to stem from neurotransmitter imbalances and chemical circuit dysfunctions in various brain
areas, and medications used to treat these disorders tend to operate by correcting these
imbalances. For example, the anti-depressant Prozac slows down the re-uptake of the
neurotransmitter serotonin thus prolonging the presence of serotonin in the synapse.
 Neurotransmitter imbalances are implicated as one of the major biological causal factors
for psychological disorders

Among the hundreds of neurotransmitters that have been discovered to date, four different kinds
of neurotransmitters have been extensively studied in relation to psychopathology. These include
–Norepinephrine, Dopamine, Serotonin (all three of which are monoamines), and Gamma
Aminobutyric Acid (GABA). Norepinephrine is seen to play an important role in acute stress
reactions in emergency situations. Dopaminehas been implicated in schizophrenia as well as
addictive disorders and Serotonin has been found to have important effects on the way we think
and process environmental information as well as on our behavior and moods. Serotonin thus
seems to play an important role in emotional disorders such as anxiety, depression as well as
suicide. GABA is strongly implicated in reducing anxiety as well as other emotional states
characterized by high arousal.

Hormonal imbalances

Some forms of psychopathology have also been linked to hormonal imbalances. Hormones are
chemical messengers secreted by a set of endocrine glands in our body. Each of the endocrine
glands produces and releases its own set of hormones which travel through the bloodstream and
affect various parts of our brain and body. Our central nervous system is linked to the endocrine
system and hence this linkage is often expressed in terms of the neuroendcorine system. The
linkage occurs by the effects of the hypothalamus on the pituitary gland which is the master
gland of the body producing a variety of hormones that regulate and control other endocrine
glands.

The Endocrine Glands

An important set of interactions particularly implicated in the development of psychopathology

is the hypothalamic-pituitary-adrenal-cortical axis. Activation of this axis involves the release of
corticotrophin-releasing hormone (CRH) from the hypothalamus to the pituitary. In response to
CRH, the pituitary releases the adrenocorticotrophic hormone (ACTH) which stimulates the
adrenal gland to produce epinephrine and the stress hormone cortisol which mobilizes the body
to deal with stress. Cortisol in turn provides negative feedback to the hypothalamus and pituitary
to decrease their release of CRH and ACTH which in turn reduces epinephrine and cortisol
levels. This feedback system operates just as a thermostat does to regulate temperature.
Malfunctioning of this negative feedback system has been implicated in various forms of
psychopathology such as depression and post-traumatic stress disorder.

The HPA Axis

Sex hormones are produced by the gonadal glands (for example the male hormones or
androgens), and an imbalance in these can also contribute to maladaptive behavior. Gonadal
hormonal influences on the developing nervous system also seem to contribute to the differences
between behavior in males and females.

Genetic vulnerabilities

Chromosomes are chain-like structures within a cell nucleus that contain genes. Genes consist of
very long molecules of DNA and are at present at various locations on chromosomes. Genes are
the carriers of genetic information that we inherit from our parents and our ancestors. Although
neither behavior nor mental disorders are determined exclusively by genes, there is substantial
evidence that most mental disorders show at least some genetic influence ranging from small to
large. Some of these genetic influences such as broad temperamental features or certain genetic
abnormalities are first apparent in newborns and children, other sources of genetic vulnerability
do not manifest themselves until adolescence and adulthood when most mental disorders appear
for the first time.

Normal human cells have 46 chromosomes containing genetic material that determines heredity
and potentialities for development and behavior throughout a lifetime. Of these 23 pairs of
chromosomes, one of each pair comes from the mother and the other from the father. 22 of the
chromosome pairs determine by their biochemical action the individual’s general anatomical and
other physiological characteristics. The remaining pair, the sex chromosomes, determine the
individual’s sex.In a female, both of the sex chromosomes are X chromosomes. In a male, the
combination is XY, with the chromosome coming from the mother and Y from the father.

Abnormalities in the structure or number of chromosomes are associated with major defects or
disorders. For example, Down syndrome is a type of mental retardation cause by a trisome in
chromosome 21. Anomalies may also occur in the sex chromosomes producing a variety of
complications such as ambiguous sexual characteristics that may predispose a person to develop
abnormal behavior. Fortunately, advances in developmental genetics and other related areas have
enabled the detection of chromosomal abnormalities even before birth, thus making it possible to
study their effects on future development and behavior.

Most personality traits and mental disorders, however, are not affected by chromosomal
abnormalities per se but rather are affected by abnormalities in some of the genes on the
chromosomes. Although researchers posit that the gene for a particular disorder has been
discovered, vulnerabilities to mental disorders are almost always polygenic or influenced by
multiple genes. A genetically vulnerable person usually inherits a large number of genes that
collectively represent faulty heredity and operate together in some additive or interactive fashion.
These faulty genes may lead to abnormalities in the central nervous system, to errors in the
regulation of brain chemistry and hormonal balance, or to excesses or deficiencies in the
reactivity of the autonomic nervous system which mediates many of our emotional responses.

However, in the field of abnormal psychology, genetic influences rarely express themselves in a
simple and straightforward manner. Gene expression is normally not a simple outcome of
information encoded in DNA but is the end product of an intricate process that may be
influenced by internal or intrauterine and external environment. For instance, genes can actually
be “turned on” and “turned off” in response to environmental influences such as stress. The
specific features of genetic endowment vary widely and no two humans ever begin life with the
same endowment, except for identical twins. Thus heredity not only determines the potentialities
for development but is also an important source of individual differences.

Genotypes and Phenotypes

What heredity does is not to fully determine human behavior but the ranges within which
behavior can be modified by environmental or experiential influences. For example, a child born
with an introverted disposition may never become truly extroverted because this range of his
disposition is determined by heredity. However, depending upon his environmental experiences,
he may become more introverted or less introverted. A person’s total genetic endowment is
referred to as his or her genotype. The observed structural and functional characteristics that
result from an interaction of the genotype and the environment are referred to as a person’s
phenotype. In some cases, genotypic vulnerability does not exert its influence on the phenotype
until much later in life. In other cases, the genotype may shape the environmental experiences a
child has, thus influencing the phenotype in an important way.

The genotype may have what is termed a passive effect on the environment resulting from the
genetic similarity of parents and children. For example, highly intelligent parents may provide a
highly stimulating environment for their child, thus creating an environment which will interact
in a positive way with the child’s genetic endowment for high intelligence. The child’s genotype
may also evoke particular types of reactions from the social and physical environment – the
evocative effect, for example, a child genetically predisposed to aggressive behavior may be
rejected by his or her peers in early grades because of the aggressive behavior. Such rejections
may lead the child to associate with similarly aggressive and delinquent peers in later grades,
leading to the development of a full-blown pattern of aggression and delinquency in adolescence.
Thirdly, a child’s genotype may play a more active role in shaping the environment – the active
effect. In this case, the child seeks to build an environment that is supportive to his genotype – a
phenomenon known as niche-building. For instance, extraverted children may seek out the
company of others, thereby enhancing their own tendencies to be sociable.
Apart from the genotype-environment correlations where genes affect the quality of a child’s
exposure to the environment, there are also genotype-environment interactions. In genotype-
environment interactions, people with different genotypes are differentially sensitive to their
environments. One important example is the PKU-induced mental retardation. People with
genetic vulnerability to PKU react very differently to common foods with phenylalanine than do
normal children, because they cannot metabolise the phenylalanine, and as its metabolic products
build up, they damage the brain. Fortunately, this mental retardation can be prevented by
eliminating foods with phenylalanine in the child’s diet until about ages five or six.

Similarly research has shown that people at a genetic risk for depression were more likely to
respond to stressful events by becoming depressed as compared to people without the genetic
risk factors and experiencing the same stressful life events.

Methods for studying genetic influences

Most of the information that we currently have about the role of genetic factors in mental
disorders is based not on the studies of genes but on the studies of people who are related to each
other. Three primary methods traditionally used in behavior genetics or the field that focuses on
studying the heritability of mental disorders and other aspects of psychological functioning
include –

1) The family history or pedigree method – where the investigator observes samples of
relatives of each subject (carrier of the trait or disorder in question) to see whether the
incidence of the disorder increases in proportion to the degree of hereditary relationship
as compared to the incidence of the trait in the normal population. However, a major
limitation is that people who are closely related genetically also share more similar
environments making it difficult to disentangle genetic and environmental effects.
2) The twin method– seeks to study the concordance rates of mental disorders between
identical or monozygotic twins and non-identical or dizygotic twins. The underlying
assumption is that, if a given disorder or trait is completely heritable, the concordance
rate or percentage of identical twins sharing the disorder would be 100%. Research does
reveal that while there are no forms of psychopathology where the concordance rates for
identical twins are this high, and so no mental disorders are completely heritable, yet the
 concordance rates for identical twins is much higher as compared to non-identical twins
in some common and severe forms of psychopathology. Some researchers argue that the
high concordance rates are not conclusive evidence of genetic contribution, because it is
always possible that identical twins are treated more similarly by their parents and have
more similar environments as compared to non-identical twins. An ideal study of genetic
factors in psychopathology using twin method would involve studying identical twin who
have been reared apart in significantly different environments. Unfortunately, finding
such twins is extremely difficult and so only few small studies have been done.
3) Adoption method – In one variation of this method, biological parents of individuals who
have a given disorder and who were adopted shortly after birth, are compared with the
biological parents of individuals without the disorder, who were also adopted shortly
after birth. If there is a genetic influence, one expects to find higher rates of the disorder
in the biological relatives of those with the disorder than those without. In another
variation of the adoption method, researchers compare the rates of disorder in the adopted
offspring of biological parents who have a disorder with the rates of disorder in adopted
offspring of normal biological parents. If there is a genetic influence, higher rates of
disorder should be seen in the adopted offspring of biological parents having the disorder.

Although pitfalls arise in the interpretation of each of these methods, if the results form
studies using all three strategies converge, one can draw reasonably strong conclusions about
the genetic influence of a disorder.
 The family history method, the adoption method and the twin method are three of the most
popular and effective means of studying genetic influences.

Linkage Analysis-Association Studies

Recent molecular genetic measures used to study genetic influences on mental disorders include
linkage analysis and association studies.

Linkage analysis capitalizes on several currently known locations on chromosomes of genes for other
inherited physical characteristics or biological processes such as eye color, blood group etc. For
example researchers may conduct a large pedigree study on schizophrenia, looking at all known
relatives of the person with schizophrenia, going back several generations. At the same time they may
keep track of something like the eye color of each individual and his diagnostic status on
schizophrenia. Eye color may be selected as a known genetic marker located on a particular
chromosome. If researchers found that familial patterns of schizophrenia were closely linked with
familial patterns for eye color in the same pedigree, they could infer that the gene affecting
schizophrenia must be located very nearby on the chromosome containing the genetic marker for eye
color. Linkage analysis studies have most successful in locating genes for single-gene brain disorders
such as Huntington’s disease, while results in the areas of other mental disorders have remained
inconclusive.

Association studies begin with a large group of individuals both with and without the disorder.
Researchers then compare the frequencies of certain genetic markers known to belocated on
certain chromosomes such as eye color, blood group etc. in people with and without the
disorder.If one or more of such genetic markers occur with a markedly higher frequency in those
with the disorder the searchers conclude that the one or more of the genes for this disorder must
be located in the same chromosome.

Considerable excitement surrounds linkage analysis and association studies because

identification of the location of genes for certain disorders could provide promising leads for new
forms of treatment and prevention of those disorders.

Temperament

Temperament refers to a child’s reactivity and characteristic ways of self-regulation. Babies who
differ in temperament show differences in their characteristic emotional and arousal responses to
various stimuli, and in their tendency to approach, attend to, or withdraw from certain situations.
For example, some babies are startled by slight sounds or cry when sunlight hits their faces;
others are more communicative, vigorous and outgoing, while some others are seemingly
insensitive to such stimulation. Temperament and temperament related behaviours are strongly
influenced by genetic factors, but prenatal and postnatal environmental factors also play a major
role.

Our early temperament is thought to be the basis from which our personality develops. Starting
at about two to three months of age, approximately five dimensions of temperament can be
identified. These are – fearfulness, irritability and frustration, positive affect, activity level, and
attentional persistence, although some of these emerge later than the others. These early
temperamental dimensions are believed to be related to three important dimensions of adult
personality: neuroticism or negative emotionality, extraversion or positive emotionality, and
constraint which includes conscientiousness and agreeableness. The infant dimensions of
fearfulness and irritability correspond to the adult dimension of neuroticism. The infant
dimensions of positive affect and activity level tend to correspond to the adult dimension of
extraversion, and the infant dimension of attentional persistence seems to be related to the adult
dimension of constraint or control. At least some aspects of temperament show a moderate
degree of stability from the first year of life through at least middle childhood, although
temperament can also change.

Temperament may involve a number of gene-environment correlations. For example, a child

with a fearful temperament is more likely to have opportunities for the classical conditioning of
fear to situations in which fear is provoked, and later the child may avoid those feared situations
and may even go on to fear a large number of social situations in the same manner as he grows
up. Similarly, a child with a low threshold for stimulation may keep the level of stimulation low,
whereas a child with a high need for stimulation may do things to increase excitement.

Our temperament can have a consistent impact on our behavior and can also lead to
maladaptive behavior patterns

Temperament can set the stage for the development of various forms of psychopathology. For
example, children with fearful temperaments tend to be behaviorally inhibited and stand the risk
of developing anxiety disorders in later childhood and adulthood, especially when the trait is
stable. On the other hand, children who are highly extraverted and uninhibited, showing little
fear of anything, may have difficulty in learning moral standards for behavior from parents or
society. Research shows such children to have more aggressive and delinquent behavior patterns
in early adolescence. If these personality ingredients are combined with other temperamental
factors such as high levels of hostility and unfavourable environmental factors such as distant
family relationships and lack of parental guidance and understanding, the stage could be set for
the development of conduct disorder or anti-social personality disorder.

Brain dysfunction and neural plasticity

Recent advances in the understanding of how subtle deficiencies of brain structure or function
are involved in many mental disorders through the use of sophisticated neuroimaging techniques,
have shown that genetic programmes for brain development are not so rigid and deterministic as
one’s belief. There is considerable neural plasticity, that is, the flexibility of the brain in making
changes in organization and/or function in response to prenatal and postnatal experiences, stress,
diet, disease, drugs, maturation, etc. Existing neural circuits can be modified, or new neural
circuits can be generated. The effects of these can either be beneficial or detrimental to the
animal or person, depending upon the circumstances.

One example of the positive effects of prenatal experiences is an experiment in which pregnant
rats housed in complex enriched environments had offspring that responded less to brain injury
that occurred early in development. One example of the negative effects of prenatal experiences
is another experiment in which pregnant monkeys that were exposed to unpredictable loud
sounds had infants that were jittery an showed neurochemical abnormalities, such as elevated
levels of circulating catecholamines.

Environmental events that occur postnatally can also affect brain development. For example, the
formation of new neural connections or synapses after birth is dramatically affected by the
experiences of a young organism. For instance, rats reared in enriched environments as opposed
to isolation showed heavier and thicker cell development in certain regions of the cerebral
cortexas well as more synapses per neuron. Similar yet less extensive changes occur in older
animals exposed to enriched environments, and hence neural plasticity continues to some extent
throughout the lifespan.
Brain plasticity refers to the flexibility of the brain in making changes in organization and
function in response to prenatal and postnatal events

The early implications of such experiments seem to suggest that human infants should be
exposed to highly enriched environments. However, subsequent work shows that normal rearing
conditions with caring parents are perfectly adequate. However, unstimulating deprived
environments can cause retarded development.

With the work on neural and behavioural plasticity and genotype-environment correlations,
psychopathologists today devote increasing attention to a developmental systems approach. This
approach acknowledges not only that genetic activity influences neural activity, which in turn
influences behavior, which in turn influences the environment, but also that these influences are
essentially bidirectional.

Although, the recognition of biological causal factors in mental disorders have often led to an
ignorance of vital psycho-social and socio-cultural triggers of mental illness, the discovery of
biological viewpoints and causal factors have no doubt also had a profound positive effect on the
way we think about human behavior and mental disorders. It has led us to recognize the
important role of biochemical factors and innate characteristics, many of which are genetically
determined, in both normal and abnormal behavior. Biological causation evidences have also led
to the discovery and use of drugs that can dramatically alter the severity and course of several
mental disorders especially the more severe ones such as schizophrenia.