Depression and Obesity
Albert J. Stunkard, Myles S. Faith, and Kelly C. Allison
The prevalence of depression (10%) and overweight
(65%) indicates that there is a probability that they will
co-occur, but are they functionally related? This report
used the moderator/mediator distinction to approach this
question. Moderators, such as severity of depression,
severity of obesity, gender, socioeconomic status (SES),
gene-by-environment interactions and childhood experi-
ences, specify for whom and under what conditions effects
of agents occur. Mediators, such as eating and physical
activity, teasing, disordered eating and stress, identify why
and how they exert these effects. Major depression among
adolescents predicted a greater body mass index (BMI ⫽
kg/m2) in adult life than for persons who had not been
depressed. Among women, obesity is related to major
depression, and this relationship increases among those of
high SES, while among men, there is an inverse relation-
ship between depression and obesity, and there is no
relationship with SES. A genetic susceptibility to both
depression and obesity may be expressed by environmen-
tal influences. Adverse childhood experiences promote the
development of both depression and obesity, and, presum-
ably, their co-occurrence. As most knowledge about the
relationship between these two factors results from re-
search devoted to other topics, a systematic exploration of
this relationship would help to elucidate causal mecha-
nisms and opportunities for prevention and treatment.
Biol Psychiatry 2003;54:330 –337 © 2003 Society of Bi-
ological Psychiatry
Key Words: Depression, obesity, comorbidity, mediators,
moderators, stress
Introduction
O besity is a very common disorder: 65% of Americans
are considered overweight or obese (Flegal et al
2002). There is thus a strong probability that they will
occur together with major depression, for which the
prevalence has been estimated at 10% (Kessler et al 1994).
However little is known about the relationship between the
From the Weight and Eating Disorders Program, Department of Psychiatry,
University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania.
Address reprint requests to Dr. Albert Stunkard, Department of Psychiatry,
University of Pennsylvania, 3535 Market Street, Room 3025, Philadelphia, PA
19104-3309
Received November 25, 2002; revised March 17, 2003; revised June 3, 2003; accepted
June 6, 2003.
© 2003 Society of Biological Psychiatry
two disorders and there has been little systematic research
on the topic. They have been studied as two largely
independent disorders and investigators in the two fields
have had little contact. For years it has been assumed that
any relationship of obesity to depression in the general
population is largely coincidental.
Part of the problem in associating depression and
obesity is derived from the many differences between
treatment-seeking obese persons and nontreatment-seek-
ing obese persons (community samples) (Fitzgibbon et al
1993). Despite uncertainty regarding the relationship in
community studies, relationships between obesity and
psychopathology have been found among obese persons
seeking treatment. This report will explore the nature of
this relationship, making use of the framework provided
by the moderator/mediator distinction. This distinction,
first utilized in the social psychological literature by Baron
and Kenny (1986), is attracting increasing attention in
treatment studies in psychiatry (Kraemer et al 2002).
Moderators specify for whom and under what conditions
agents exert their effects; mediators identify why and how
they exert their effects. Moderators always precede what
they moderate, which, in turn, precedes the outcome;
mediators always come between what they mediate and
the outcome. In this review, moderators are defined as
variables on which the obesity-depression covariation is
conditional, whereas mediators bridge the causal relation-
ship between obesity and depression.
The critical role of theory in distinguishing those
variables that are moderators as opposed to mediators
cannot be overstated. Variables that are conceptualized as
moderators in one researcher’s framework may be con-
ceptualized as mediators in another researcher’s frame-
work. Perhaps the one exception to this note is DNA and
genetic polymorphisms, which would almost naturally
seem to function as moderators rather than mediators.
Even here, however, the picture is not entirely clear as the
process of gene transcription can be influenced by envi-
ronmental conditions (Plomin and Crabbe 2000). Hence,
the putative moderators and mediators listed in this do-
main—as in any other—are not written in stone. Arguably
no single study can “resolve” such issues, in contrast to the
cumulative database gleaned from multiple studies that
replicate findings. The ultimate value of adopting a mod-
erator/mediator framework, compared to not adopting
0006-3223/03/$30.00
doi:10.1016/S0006-3223(03)00608-5
Depression and Obesity
Table 1. Potential Moderators and Mediators of Depression
and Obesity
Moderators Mediators
Severity of Depression Eating and Physical Activity
Severity of Obesity Teasing
Gender Disordered Eating
Socioeconomic Status Stress
Gene-Environment Interactions
Adverse Childhood Experience
such a framework, can be evaluated by the knowledge
base and clinical innovations stimulated by such a frame-
work.
The present review article is, by necessity, a brief one in
light of the existing data. There are numerous inconsisten-
cies in the literature which, according to Friedman and
Brownell (1995), stem in large part from considerable
study heterogeneity. The moderators and mediators illus-
trated herein are not presented with definitive certainty but
rather as putative pathways to be tested in subsequent
research. The ultimate identification of “true” moderators
and mediators is of utmost clinical importance. Identifying
moderators such as gender, ethnicity, or age would pin-
point those obese individuals among whom depression is
more likely to occur and who may be the most appropriate
candidates for psychiatric treatment. Similarly, identifica-
tion of “true” mediators (whether they be they physiologic
and behavioral) would lead to better pharmacological and
lifestyle interventions as causal pathways are delineated.
Moderators and Mediators
A list of potential moderators and mediators is shown in
Table 1.
Potential Moderating Variables
SEVERITY OF DEPRESSION. The first variable that
might moderate the relationship between depression and
obesity is depression itself. That is, the development of an
obesity-depression comorbidity may be most likely among
those individuals who are more depressed at baseline. At
least one prospective study has shown that the presence of
clinical depression predicts the development of obesity.
Pine et al (2001) found that major depression among 6
to19 year olds predicted a greater body mass index (BMI
⫽ kg/m2) in adult life than that of persons who had not
been depressed (BMI of 26.1 vs. 24.2). At the same time,
numerous other studies have failed to detect an association
between subclinical depression levels and obesity (Fried-
man and Brownell 1995). Hence, associations between
obesity and depression may be most likely among those
experiencing more significant depression levels.
BIOL PSYCHIATRY 331
2003;54:330 –337
Figure 1. Relationship of BMI to major depression among boys
and girls aged 15 to 19 years. There is little difference in the
prevalence of major depression as a function of BMI until the 95
percentile is reached. Here, however, the prevalence of major
depression (20% for boys, 30% for girls) is unusually high for
adolescents. Reproduced from Martin and Moore, personal
communication, April 24, 2002. Data are used with permission
from Shape Up America! (www.shapeup.org). BMI, body mass
index.
SEVERITY OF OBESITY. There is evidence that the
association between depression and obesity may be stron-
gest among the most obese individuals. An example is
illustrated in Figure 1, from “Shape Up America!” in the
National Health and Nutrition Examination Survey
(NHANES)-III data, which shows the relationship be-
tween severity of obesity and the prevalence of major
depression (Martin and Moore, personal communication,
April 24, 2002). Among the leanest adolescents, aged 15
to 19, depression was uncommon and, in fact, not present
among the leanest boys. Among the most obese subjects,
in the 95 to 100 percentile, the prevalence of major
depression increased to highly significant levels (20% for
boys and 30% for girls). Thus, the relationship between
body weight and depression levels depended on the degree
of obesity.
GENDER. Several studies report that the relationship
between obesity and depression differs for men and
women. Istvan et al (1992), for example, showed a
positive relationship between depression and obesity
among women but not among men. Similarly, Faith et al
(2001) found a positive relationship between neuroticism
and BMI in women but not in men. Another striking
example of the different relationship between depression
and obesity among men and women is shown in Table 2
from Carpenter et al (2000). Table 2 shows that obesity in
women was associated with a 37% increase in major
depression whereas among men, obesity was associated
with a 37% decrease in major depression.
SOCIOECONOMIC STATUS. The relationship between
depression and obesity appears to differ across socioeco-
332 BIOL PSYCHIATRY
2003;54:330 –337
Table 2. Adjusted Odds Ratiosa for the Categorical and
Continuous Weight-by-Gender Interactions
Major Depressionb
Continuous Weight (BMI)c
Men
Women
Obese vs. Average Weight
Men
Women
Data taken in part from Carpenter et al 2000.
OR, odds ratio; CI, confidence interval.
a
All ORs are adjusted for race, age, education, past year income, self-reported
disease history, and the race-by-weight interaction term.
b
OR (95% CI).
c
Odds ratios are presented for a 10-unit change in body mass index (BMI).
nomic status (SES) levels (Faith et al 2002). Figure 2,
adapted from data in the Midtown Manhattan Study
(Moore et al 1962), shows that the difference in percent
depressed between obese and normal weight men was not
related to their SES. Among women, however, SES
predicted the nature of the relationship between depression
and obesity. Being obese was associated with greater
depression among women of high SES but with reduced
depression among women of low SES. Carpenter et al
(2000) found similar relationships among both Caucasian
and African American women.
GENE-ENVIRONMENT INTERACTIONS. The predispo-
sition to both depression and obesity may coexist in the
genomes of some persons but not others, or under appro-
priate environmental conditions. That is, certain genotypes
or environmental factors may give rise to a relationship
between obesity and depression. This possibility is de-
picted in Figure 3 in which BMI-depression covariation
might be attributable to a common set of underlying genes
and common environmental factors. Although this figure
does not fully explain the physiologic pathways linking
obesity and depression, the model has been used as an
empirical framework by Kendler et al (1995) in their
Figure 2. Difference in depression prevalence as a function of
gender and socioeconomic status (SES) in the Midtown Manhat-
tan Study (adapted from Moore et al 1962).
A.J. Stunkard et al
.55 (.48, .63)
1.22 (1.06, 1.40)
.63 (.60, .67)
1.37 (1.09, 1.65)
Figure 3. Pictorial representation of “genetic correlation” and
“environmental correlation” between depression and obesity.
The former refers to a correlation induced by a common set of
genes that promote both depression and obesity. The latter refers
to a correlation that is induced by common life experiences that
also promote both conditions.
studies of genetic epidemiology. Evidence for a genetic
correlation can be estimated from path coefficients a and
b. Evidence for an “environmental correlation” can be
estimated from path coefficients c and d. Using these
models, Kendler and colleagues found that a common set
of genes underlies major depression and alcoholism, while
a different set of genes underlies phobia, generalized
anxiety disorder, panic disorder and bulimia nervosa
(Kendler et al 1995). Evidence for a comparable genetic
correlation between depression and body weight has also
been reported (Faith et al 2002).
A potential candidate gene for a genetic correlation
between body weight and depression was reported by
Comings et al (1996) at locus ObD7s 1875, which is near
the OB gene on chromosome seven. This gene, related to
body weight, may also confer differences in levels of
depression. Clearly, the ultimate goal of identifying ge-
netic moderator variables is to better delineate physiologic
pathways linking these disorders.
It should be noted that some research suggests an
association between syndrome X and depression. For
example, Ketterer et al (1996) reported greater depression
symptoms among adult males with syndrome X than
among males who had histories of positive angiograms or
control males with no manifest history of atherosclerotic
disease. Given the increasing research into syndrome X,
its association with depression will be an important re-
search area in the future. The genetic basis for the
clustering of obesity, insulin-resistance and hypertension
in syndrome X (Kissebah et al 2000) may serve as a useful
model in the study of potential common genetic pathways
for obesity and depression.
Depression and Obesity
ADVERSE CHILDHOOD EXPERIENCES. The develop-
ment of an association between obesity and depression
may depend upon exposure to adverse childhood experi-
ences. A series of studies have shown that exposure to
childhood adversities is associated with increased obesity.
Although these studies did not examine obesity-depression
comorbidity per se, we propose that these life experiences
may function as moderators that promote both disorders.
Lissau and Sorensen (1994), in a prospective study in
Copenhagen, found a striking relationship between child-
hood neglect and adult obesity. Children (n ⫽ 756)
selected by their teachers as being “neglected” at age 10
were 7.1 times more likely to be obese at age 20 (p ⬍
.0001) than those not selected, while those identified as
“dirty and neglected” had a risk ratio for adult obesity of
9.8 (p ⬍ .0001). Felitti and colleagues (1998) (Felitti
1991, 1993; Williamson et al 2002) have proposed that
childhood abuse is associated with adult obesity. A study
of 13,177 members of a health maintenance organization
inquired into a history of abuse: sexual, verbal, physical,
and fear of physical abuse (Williamson et al 2002). This
history was related to the BMI of the subjects at an
average age of 55.7 years. Exposure to all four types of
abuse at the greatest level of severity resulted in a relative
risk for a BMI ⱖ 30 and ⱖ 40 of 1.46 (1.16 –1.85) and
2.54 (1.21–3.35). In a study of another population (Felitti
et al 1998), a similar high level of childhood abuse was
associated with a relative risk of 4.6 (3.8, 5.6) for clinical
depression. Regarding treatment, King et al (1996) re-
ported that 22 obese women who had been sexually
abused in childhood or adolescence lost significantly less
weight (15.3 ⫾ 10.1kg) than 22 nonsexually abused
women in the same weight reduction program (23.5 ⫾ 8.8
kg; p ⬍ .01).
As reviewed by Harris (2001), a mounting literature
implicates early childhood adversities and their probable
long-term impact on the development of depression. More
specifically, these studies speak to the detrimental effects
of powerlessness, loss, and humiliation as contributing
pathways to depression onset. For example, girls who
were exposed to physical or sexual abuse were signifi-
cantly more likely to experience depressive symptoms
compared to girls who were not exposed in a national
sample (Diaz et al 2002). Indeed, history of childhood
abuse predicted ACTH-response during a laboratory cor-
tisol test among a sample of adult women (Heim et al
2002). Although obesity measures have been traditionally
neglected from this literature, their incorporation in future
studies would be most valuable.
Potential Mediating Variables
EATING AND PHYSICAL ACTIVITY. Among the most
important determinants of obesity are eating and physical
BIOL PSYCHIATRY 333
2003;54:330 –337
activity, and both may play an important part in linking
depression with obesity. Although the DSM-IV finds both
overeating, with weight gain, and undereating, with weight
loss, among the diagnostic criteria for major depression
(American Psychiatric Association 2000), the study of
eating and physical activity as potential mediators of
depression and obesity has been limited. There is reason to
predict this relationship. For example, physical inactivity
not only characterizes many depressed persons (Paluska
and Schwenk 2000), but also predicts weight gain and
physical activity has been used with some success in the
treatment of depression (Babyak et al 2000).
Limitations to the validity of measures of food intake
and physical activity in the community have hindered
existing research. Nevertheless simple measures such as
parents’ reports of their infants’ food intake can yield
results that appear to be valid when assessed with the aid
of more sophisticated measurement techniques (Stunkard
et al 1999). And other more sophisticated techniques are
also becoming increasingly available. Among them are the
doubly labeled water technique for measurement of total
energy expenditure (Schoeller 1999), actigraphy to mea-
sure physical activity accurately enough to determine
sleep onset and offset (Pollack et al 2001) and television
“time loggers” to measure the amount of time that a
television set has been activated (Faith et al 2001).
TEASING. Everyone has had experience with the effects
of teasing upon the confidence and self esteem of people,
and many of us have experienced this problem in our own
lives. Obese persons, from childhood on, are subject to
such verbal abuse and its effects have been documented in
the significantly greater rate of depression experienced by
obese persons (Thompson et al 1999). An instructive
3-year prospective study of adolescents demonstrated how
teasing mediated the relationship between obesity and
subsequent levels of depression (Thompson et al 1995).
The obesity status of these adolescents elicited teasing,
which, in turn, elicited depression through their increased
dissatisfaction with their appearance. Jackson et al (2000)
also reported that those obese women with binge eating
disorder (BED) who experienced teasing about their ap-
pearance developed bodily dissatisfaction and depression.
DISORDERED EATING. Disordered eating may mediate
the relationship between depression and obesity, such that
experience of binge eating (and its associated feelings of
uncontrollable eating) may promote depression. BED was
defined in the initial descriptions as characterized by
“recurrent episodes of binge eating associated with sub-
jective and behavioral indicators of impaired control over,
and a significant distress about, the binge eating, without
the presence of inappropriate compensatory behaviors”
(Spitzer et al 1992, 1993). From the first descriptions,
334 BIOL PSYCHIATRY
2003;54:330 –337
BED has been strongly associated with depression (Mar-
cus et al 1996; Mitchell and Mussell 1995; Yanovski
1993). Among persons suffering from BED, 54% were
diagnosed with a history of major depressive disorder
compared to 14% of nonbinge eating obese persons
(Yanovski 1993). Sherwood et al (1999) showed that
improvements in binge eating status predicted greater
weight loss in treatment through a pathway that involved
depression.
Data also suggest that obese persons suffering from the
night eating syndrome (NES) may be at increased risk for
depression in part because of their deranged eating pat-
terns. They manifest morning anorexia, evening hyperpha-
gia, insomnia, and night time awakenings to eat (Stunkard
et al 1955). In one study, 44% of night eaters had a history
of major depressive disorder compared to 18% of noneat-
ing disordered obese persons (Stunkard et al, unpublished
data). Patients with the NES show levels of depression that
are consistently higher than they are among control pa-
tients matched for weight and age (Gluck et al 2001;
Allison et al, unpublished data). A particularly interesting
characteristic of the depression exhibited by night eaters is
its distinctive circadian quality. Thus, among these pa-
tients depressive mood is minimal in the morning, rises
during the afternoon and evening, and reaches its peak late
at night in conjunction with the most intense hyperphagia
(Birketvedt et al 1999). Obese persons suffering from the
NES have higher levels of depression than obese control
subjects (Gluck et al 2001; Stunkard et al, unpublished
data).
STRESS. Depressed individuals may experience in-
creased stress that, in turn, may promote obesity in certain
individuals. The influence of stress upon obesity is exerted
via both psychological and physiologic mechanisms. At-
tention to a healthy diet and adequate physical activity are
key elements in preventing obesity and in controlling it
once it has begun. One of the primary influences of stress
is to disrupt these habits and these concerns, fostering the
development of obesity. Similarly, stress leads to depres-
sion via psychological routes, as shown in the stunning
impact of bereavement, marital separation and job loss.
A physiologic mechanism whereby stress may impact
both depression and obesity is via its action on the
hypothalamic-pituitary-adrenal (HPA) axis, with activa-
tion at all levels of the axis. Elevated levels of cortisol,
indicating HPA activation, are not uncommon among
obese persons and are believed to give rise to so-called
abdominal obesity—fat primarily within the abdominal
wall. This fat distribution is notable for its malign associ-
ation with many bodily functions. Activation of the HPA
axis in depression appears to be responsible for the small
but statistically significant associations between depres-
sion and abdominal body fat (Bjorntorp and Rosmond
A.J. Stunkard et al
Table 3. Effects of Pharmacotherapy for Depression on
Weight
Medication Effect on Weight
Tricyclics Most produce weight gain
SSRIs:
Citalopram, fluoxetine, fluvoxamine, Neutral
and sertraline
Paroxetine Gain
Buproprion Loss
Mirtazapine Gain
Venlafaxine Neutral
Table compiled with permission from Sifton 2002 and Fuller and Sajatovic
2003.
SSRI, selective serotonin reuptake inhibitor.
2000; Larsson et al 1989). Rosmond and Bjorntorp (1998)
identified a group of subjects whom they termed “anxio-
depressive” who scored high on measures of psychologi-
cal disturbance. These authors found that nonresponse to
the Dexamethasone Suppression Test, indicative of ele-
vated HPA axis activity was significantly associated with
BMI (p ⫽ .03), waist-to-hip ratio (p ⫽ .008) and sagittal
diameter (p ⫽ .05).
A similar finding was noted in obese persons suffering
from the NES (Stunkard et al 1955). In controlled meta-
bolic studies, serum cortisol was significantly higher
among persons suffering from this disorder than among
matched control subjects (Birketvedt et al 1999) as was
serum ACTH (Stunkard et al, unpublished data).
Treatment of Obese Patients with
Depression
There is a fascinating relationship between the treatment
of depression in the presence of obesity, and vice versa.
Treatment of obesity often leads to a decrease in depres-
sion. The most striking such example is the dramatic
improvement in mood that accompanies the large weight
losses achieved by gastric bypass surgery (Waters et al
1991; Dymek et al 2001). In the case of modest weight
loss, the reduction in depression tends also to be modest
(Gladis et al 1998).
In contrast to the favorable results of the treatment of
obesity on depression, the treatment of depression can
have a negative effect on obesity. Rarely has treatment of
depression had a stronger impact upon another disorder
than it does on obesity. Table 3 shows the effects of
pharmacotherapeutic agents for depression on body
weight. Traditional tricyclic antidepressants have long
been known to produce weight gain. The advent of the
selective serotonin reuptake inhibitors (SSRIs) has had a
salutary effect on this problem. Most of the SSRIs do not
cause weight gain and have therefore led to better adher-
ence to therapy than was the case when tricyclic antide-
Depression and Obesity
Table 4. Effects of Pharmacotherapy for Bipolar Disorder on
Weight
Medication Effect on Weight
Lithium
Valproate
Olanzapine
Carbamazepine
Lamotrigine
Topiramate
Table compiled with permission from Sifton 2002 and Fuller and Sajatovic
2003.
pressants were the mainstay of treatment. Finally, it should
be noted that cognitive-behavioral therapies (CBT) for
adult depression has been shown to be effective for many
individuals. Indeed, as part of the National Institute of
Mental Health Treatment of Depression Collaborative
Program, investigators compared the effectiveness of
CBT, interpersonal therapy, and imipramine treatments
among 65 outpatients with early onset chronic depression
(Agosti and Ocepek-Welikson 1997). Results indicated
that improvements in depression did not differ signifi-
cantly among the three groups. At the same time, to our
knowledge, there are no published data addressing con-
comitant weight changes associated with CBT interven-
tion for depression.
The problem of weight gain with pharmacotherapy for
bipolar disorder is very serious (Table 4). Some of the
newer agents for the treatment of bipolar disorder produce
weight gains so large as to cause therapy to be interrupted.
There can hardly be a more urgent need in all of pharma-
cotherapy than for the development of agents for bipolar
disorder that do not cause large weight gains.
Recommendations for Future Research
We suggest that future studies invoke a moderator/medi-
ator framework for better understanding the relationship
between obesity and depression. We have reviewed some
putative variables in this report, although the limited data
currently available suggests that these should be inter-
preted cautiously and used as illustrators to stimulate
future research. In addition, many other substantive issues
related to obesity/depression covariation deserve attention.
For example, an understanding of social pressures for
thinness and obesity and their consequences in favorable
or unfavorable effects on mood would advance our under-
standing of these relationships and could also be useful in
developing programs for the prevention of obesity and its
deleterious impact on mood. It is time to update the 1962
database relating SES, obesity and mood (Moore et al
1962). Research on the role of neglect and subsequent
weight gain deserves greater attention.
BIOL PSYCHIATRY 335
2003;54:330 –337
A pertinent clinical issue that deserves attention is the
development of antidepressant medication that does not
stimulate eating and weight gain. The issue is important
for the treatment of unipolar depression but it is urgent for
Gain
Gain the treatment of bipolar disorder. As noted above, most
Gain medications for bipolar disease lead to weight gain of such
Neutral a degree as to seriously interfere with treatment, not to
Neutral mention the serious consequences of the weight gain.
Loss
Although very little research has examined the relation-
ship between “atypical depression” and obesity, this may
be an important direction for future research. Atypical
depression is associated with hyperphagia in some re-
search (Posternak and Zimmerman 2001).
One of the most important long-term research needs is
for better understanding of genes that promote both
depression and obesity. Research along these lines is
already well under way and its importance cannot be
overestimated.
Aspects of this work were presented at the conference, “The Diagnosis
and Treatment of Mood Disorders in the Medically Ill,” November
12–13, 2002 in Washington, DC. The conference was sponsored by the
Depression and Bipolar Support Alliance through unrestricted educa-
tional grants provided by Abbott Laboratories, Bristol-Myers Squibb
Company, Cyberonics, Inc., Eli Lilly and Company, Forest Laboratories,
Inc., GlaxoSmithKline, Janssen Pharmaceutica Products, Organon Inc.,
Pfizer Inc, and Wyeth Pharmaceuticals.
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