Running Head: OBESITY AND DEPRESSION 1

The Comorbidity of Childhood Obesity and Depression

Stephanie Janzen
Disorders of Learning and Behaviour
EDPS 651
Dr. Brent Macdonald
OBESITY AND DEPRESSION 2

Obesity in adolescents is a growing concern in North America as currently 20 to 27% of children
and adolescents are now overweight (Erermis, Cetin, Tamar, Bukusoglu, Akdeniz, & Goksen, 2004).
The primary concern is that these children will experience medical issues later in life due to the extra
weight, such as diabetes and heart problems which will ultimately shorten their lifespan. This will
place a large burden on the health care system, which, is primarily why the government has an
investment in the health of todays children. But apart from the typical medical issues they face,
childhood obesity also is connected to psychopathology, the most correlated condition being that of
depression. In fact, because of the obvious societal and pathological links between the two, the
Surgeon General has identified pediatric obesity and depression as a major public health issue
(International Journal of Child Health & Human Development, 2008). The question that many medical
and psychological professionals are then confronted with is whether obesity causes many adolescents
to become depressed, or whether adolescents who are depressed have a greater chance of becoming
obese and how do we treat these two together?
Obesity and depression have repeatedly been described as being unidirectional in many
articles because despite the multitudes of studies done, researchers are still unsure as to which might
have more influence on the other. The general tendency is to agree that both share certain symptoms
that serve as a connection, and that obesity can in fact cause emotional distress leading to depression,
while at the same time those adolescents that are clinically depressed can also exhibit behaviours that
lead to excessive weight gain causing obesity.
Although obesity is rising in all age, ethnic, and racial groups as well as educational levels,
adolescents are experiencing the highest rate of increase (Goodman & Whitaker, 2002). In short,
people are considered obese when their body mass index (a measurement obtained by dividing a
person's weight in kilograms by the square of the person's height in meters) exceeds 30kg/m2.
Although the BMI range varies with the age and sex of the child, obesity in children and adolescents is
OBESITY AND DEPRESSION 3

defined as a BMI greater than the 95
th
percentile. In other words, a child is obese if their weight is
more than 20% higher than the ideal weight for a boy or girl of their age and height (Erermis et al.,
2004).
Childhood obesity is often called an epidemic in todays literature due to the growth rate. The
number of adolescents who are overweight has tripled since 1980 and the prevalence among younger
children has more than doubled. Although many blame it on modern technology, the number one
indicator of child obesity is parent obesity (Goodman et al., 2002). This indicates that diet, lifestyle
and behaviours that parents exhibit will more often than not; affect their children, especially in regards
to habit formation. Thus, the rate of adult obesity has a direct correlation on childhood obesity.
Diet has also changed over the last few decades. More adolescents are eating meals away from
home, consuming more sugared drinks, and snacking more frequently. Convenience is also a factor as
more adolescent are eating low-cost fast-food meals which are high in fat and calories (Education.com,
n.d.). Physical inactivity and sedentary behaviours also play a large role in obesity. Research indicates
that the decrease in daily energy expenditure may be an underlying factor as watching television, using
the computer, and playing video games occupies a large part of their leisure time. These technologies
are more commonplace and affordable as compared to ten years ago and are too easily accepted as
alternatives to exercise and physical activity (Goodman et al., 2002).
Physical environment also is a driver in rapid weight gain. In urban areas, space for outdoor
recreation may be scarce and crime may inhibit children from playing outside. Whereas in suburban
areas, the 'sprawl' can prevent people from walking or riding their bikes to destinations and force
greater dependence on cars. In fact, studies have shown that residents of the highest sprawling areas
are likely to weigh six pounds more an average than residents of the most compact areas (ASPE, n.d.).
As obese children are too young to experience the medical issues that usually arise later in life
due to excess weight, the first symptoms they experience tend to be emotional in nature. The social
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stigmatization associated with obesity typically includes embarrassment, shame, and guilt which can
eventually lead to psychopathology. Because of the stigma that comes with being obese, children can
also be the target of bullying or teasing which even further degrades their confidence. Such treatment
can make children draw away from their families and their peers and spend most of their time at home.
They develop a poor self-image and harbor thoughts of not being liked at all. Some avoid interactions
with peers of the same age and shy away from group activities. They prefer staying at home and begin
to internalize their feelings, all of which indicate early signs for depression (Goodman et al., 2002).
Within the context of the family, an obese child can experience increased depressive symptoms because
he or she can often become the focus of family conflicts. They can also be the recipient of subtle
hostility and rejection and be treated differently than their siblings.
Even though this association between obesity and depression has been found to be weak or
inconsistent in some epidemiological studies, the population based sample of obese children had more
psychiatric problems than the population-based sample of normal weight children. Also, further studies
have concluded that the longer a child is overweight, the more he is at risk for depression and other
mental health disorders (Lawson, 2003).
While excess weight has been identified as a precursor to depression, other studies have
suggested that binge eating is associated with psychiatric comorbidity in the obese rather than weight.
Binge eating in one study is defined as two episodes per week and then further classified into moderate
to severe binge eaters (Tanofsky-Kraff, Yanovski, Wilfley, Marmarosh, Morgan, & Yanovski, 2004).
The rationale being that binge eating exemplifies a loss of control while eating which leads to greater
body fat than those not experiencing loss of control. And that these children experiencing loss of
control had higher anxiety, more depressive symptoms and increased body dissatisfaction. Thus they
claim that such behaviours are a more reliable indicator of depression than just weight, as the results of
their study indicated that the severity of binge eating was linked to psychiatric disorders while the
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severity of obesity was not (Tanofsky-Kraff et al., 2004).
That being said, people who do exhibit such behaviours are typically doing so in order to deal
with negative emotions. Thus is it also possible that adolescents who are depressed engage in binge
eating as a coping mechanism, so that their sedentary tendencies and excess energy intake leads to
obesity (Friedman & Brownell, 1995). Thus binge eating still cannot explain the direction of the
relationship. What it does affect though is treatment and the sequence of interventions which may lead
to better outcomes.
Childhood and adolescent depression may not be widespread, but it is still a concern as there is
a 70% chance that children diagnosed with depression will experience it again within five years.
Furthermore, 50% of children with depression will have a recurrence as adults (Miller, 2011).
Depression is more prevalent among children who have attention, learning, conduct, or anxiety
disorders, yet it also tends to run in the family. In terms of gender, both boys are girls are at equal risk
for depression but during adolescences; girls are twice as likely as boys to develop it (Miller, 2011).
According to the DSM-IV, children must exhibit either a depressed mood or a loss of interest or
pleasure in normal activities. They will tend to try and avoid school, interactions with other children,
extracurricular activities etc. In terms of mood, it can be expressed as being irritable, behaving
recklessly, and reacting with anger or hostility. These symptoms must be present in the child for at
least two weeks and there must be a change in functioning prior to the expression of the symptoms
(Barkley & Mash, 2003). Due to the age, symptoms can often be hard to detect as children tend to
internalize their feelings and emotions more than adults.
Appetite change is also component of depression. While many tend to lose their appetite, there
is a subgroup of people who experience an increase in appetite, presumably to use food as a coping
mechanism (Reeve, Postolache, & Snitker, 2008). Those who are depressed, as previously mentioned,
tend to avoid social activities and thus tend to be more sedentary which ultimately contributes to
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gaining weight as well. A study done by Goodman and Whitaker (2002) confirmed this link by
concluding that depressed mood at baseline was associated with the development of obesity over one
year in those not yet obese at baseline. And among the initially obese adolescents, depressed mood was
associated with worsening obesity over the year.
As we can see, it is easy to understand how depression might lead to obesity and vice versa. But
beyond an explanation for the development of each, obesity and depression also share specific
symptoms that may serve as links between the two and thus serve as a basis for intervention. For
instance sleep or changes in sleep patterns is the most prevalent residual symptom of depression. At
the same time, overweight children are at risk for sleep apnea and obesity hypoventilation syndrome.
The pathological consequences of sleep deprivation serve as a link between the two as even in healthy
young adults, short term partial sleep deprivation results in increased insulin resistance (Reeve et al.,
2008). Sleep loss is also associated with increased hunger. Thus this increase in appetite and decrease
in insulin sensitivity is likely to exacerbate or at least sustain obesity.
Sedentary behaviour also serves as a link between the two. As mentioned previously,
technology is often blamed as being one of the leading causes of obesity, and indeed, TV viewing is the
strongest connection between a specific behaviour and obesity. Decreased motivation and incentive for
activities is also a core feature of depression. Therefore, an increase in sedentary behaviour may
contribute to worsening depression and obesity, thus serving as a link between both (Reeve et al.,
2008). In terms of intervention then, an increase in playtime of physical activity can improve mood
and self-esteem as well as energy expenditure.
Appetite and food intake is also another symptom that links depression and obesity. Appetite
change is an exclusive symptom criterion of depression that is not included in the diagnosis of anxiety,
trauma or other psychotic disorders, even including eating disorders (eating disorders require only a
change in food intake, not appetite). Food cravings may also develop in specific sub-types of
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depression such as seasonal affective disorder, where carbohydrate cravings seem to be common. Yet
indulging in such cravings only leads those individuals to feel worse rather than satiated. Those who
are obese obviously have an abnormal appetite, therefore in terms of intervention then for those who
are both obese and depressed, it is important to address their hyperphagia so that the effects of the
excess food do not exacerbate both conditions (Reeve et al., 2008).
Beyond such connections there is also a neuroendocrine process that mediates the association of
depression and obesity, known as the hypothalamic-pituitary-adrenal axis (HPA axis). The HPA axis is
a feed-back loop which signals the brain to release the hormones needed to respond to stress and to
regulate many body processes including digestion, the immune system, mood and emotions, sexuality,
and energy storage and expenditure. In short, when responding to stress, the hypothalamus releases
corticotrophin-releasing hormone (CRH). CRH then acts on the pituitary gland located right below the
brain, which triggers the release of the hormone adrenocorticotropic (ACTH) into the bloodstream.
The ACTH then signals the adrenal glands to release a number of hormonal compounds including
epinephrine, norepinephrine, and cortisol (Goodman et al., 2002).
During a stressful situation, adrenaline production has the effect of increasing alertness and
energy as well as metabolism by helping fat cells to release energy. Fat is also broken down to supply
the body with a rapid source of energy. Our appetite is also suppressed and the digestive system shuts
down temporarily. When the stressor has ended, the adrenaline dissipates and cortisol is released to
help restore homeostasis after stress. Cortisol is a steroid hormone that helps the body respond to
stress, both physical and emotional, but it also has other functions including converting fat, protein and
carbohydrates into energy. It also increases blood sugar levels, increases blood pressure and suppresses
the immune system. One of the ways it brings our body back to normal is by increasing our appetites
so that we can replace the carbohydrate and fat that we should have burned during the stressful period
(Goodman et al., 2002).
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Such a model is intended for those stressful situations which mandate a fight of flight response,
both of which require extreme energy expenditure. Yet rarely do todays situations require such
physicality. Our body assumes we have psychically exerted ourselves and so prompts us to restore our
reserves by eating a lot of carbohydrates or fatty food which can easily be stored into fat. Thus the
survival mechanism is causing our body to refuel when it does not need to (Lawson, 2003).
Consequently, sustained stress can cause people to overeat to renew energy with the result of gaining
excess weight.
Cortisol is associated particularly with abdominal weight as fat cells in those areas are more
sensitive to cortisol. These fat cells have more stress hormone receptors and thus are sensitive to
insulin and are also very effective in storing energy (Friedman, & Brownell, 1995). To confirm this
connection a study compared women who stored fat in their hips against those women who store fat
around their abdomens. They reported that the women with belly fat reported feeling more threatened
by stressful tasks and having more stressful lives. Testing also confirmed that they also produced
higher levels of cortisol. Therefore the researchers concluded that this high level of stress caused them
to store weight primarily around their waists (Lawson, 2003).
The endocrine system is also affected with those who are clinically depressed, as about one-half
will have an excess of cortisol in their blood. This link is believed to exist as cortisol levels tend to
return to normal once the depression disappears. We also know that for those who are depressed, the
hypothalamus may continuously influence the pituitary gland to produce CRH without regard to the
amount of cortisol that is in the blood. Other research indicates that the timing of the cortisol release
may be an issue. Normally, levels of this hormone peak in the morning, level off during the day, and
dip to a low during the night. Yet in people who are depressed, this cycle is interrupted so that they
might have a consistent secretion of cortisol at all times, or the highest amounts in the middle of the
night. This chronic elevation of cortisol has a negative effect on appetite so that depressed individuals
OBESITY AND DEPRESSION 9

are ingesting more food than necessary, leading to obesity (All About Depression, n.d.).
The neurotransmitter serotonin also serves as a connection between obesity and depression.
Brain serotonin is involved in the regulation of appetite, mood and other neuroendocrine functions.
Thus those suffering from low levels of serotonin might experience hyperphagia, depression and
perturbation of the pituitary adrenal axis. Consequently the connection is related to appetite, food
intake and food preference. For example, those who are suffering from Seasonal Affective Disorder
experience a decrease in serotonin levels and thus crave carbohydrates which have the effect of
increasing serotonin levels.
Serotonin selective reuptake inhibitors (SSRI's) are the most commonly prescribed medication
for pediatric depression but because it also affects appetites and cravings, it is hoped that it can also
have an effect on obesity as well. Specifically, the SSRI sibutramine has proven to be an efficient
remedy for the long-term treatment of obesity, whereas most other SSRI's are mainly used in the
treatment of depression and eating disorders (Hainer, Kabronova, Aldhoon, Kunesova, &
Wagenknecht, 2006).
It is also interesting to note that ADHD is also linked to obesity as their actions regarding food
are often controlled by their decrease in reward sensitivity. In other words, those with ADHD lack the
patience to think of the rewards that could be gained by engaging in or refraining in certain actions
(Friedman et al., 1995). For instance, if faced with a giant bowl of ice-cream, it is likely they will eat
the entire bowl simply because they like ice cream-rather than engage in any critical thinking
pertaining to the consequences of such actions. This is also called the dysfunctional capacity for self-
regulation in which they are unable to override their impulses and refrain from acting on undesired
behavioural tendencies.
ADHD also affects weight on a neuroendocrine level. Those with ADHD have a dopamine
dysfunction, dopamine being the neurotransmitter that mediates the rewarding affect. Therefore low
OBESITY AND DEPRESSION 10

dopamine activity may result in compensation by increasing food consumption. Furthermore, the
consumption of excess food is usually characterized by energy dense food which then activates the
dopamine pathway. This then leads to an excess intake of energy dense food which can potentially lead
to obesity (Friedman et al., 1995).
Despite the multitudes of studies pertaining to obesity and depression and how the two are
connected both in symptomology and on a neuroendocrine level, researchers are still unsure as to
which condition might have more impact on the other. Consequently, all we can conclude is that
obesity and depression often occur together and tend to aggravate one another to the point they become
inextricably linked. Therefore when determining intervention tactics, it is important to address both as
focuses on just one will most likely fail due to the exacerbating effects of the other. This means
focusing on medical interventions that pertain to the health risks and prevention of obesity while also
offering psychological interventions that serve to aid in the treatment of depression.




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