EATING DISORDER NOT OTHERWISE SPECIFIED

Is There a Place for Obesity in DSM-V?

nonhomeostatic overeating is beginning
Michael J. Devlin, MD* ABSTRACT
to mount, current evidence is mostly pre-
Objective: To revisit the merits and
liminary and indirect.
problems inherent in considering obe-
sity, or some aspect of obesity, as a men- Conclusion: An attempt to devise diag-
tal or behavioral disorder. nostic criteria based on the above mod-
els raises multiple difficulties, since the
Method: The author suggests shifting
phenomena central to each model are
the focus from the state of obesity to the
dimensional, common, and variably
process of nonhomeostatic overeating
associated with distress or dysfunction. A
that results in obesity. Studies are
detailed understanding of the neuro-
reviewed that pertain to various models
biological relationships among eating
of nonnormative overeating including
behavior, reward systems, and affect reg-
eating disorder models that stress the
ulation systems will enable a more
form of overeating, substance use disor-
meaningful consideration of these mod-
der models focusing on its consequences,
els and will facilitate specific treatment
and affect regulation or stress response
for disorders of overeating. V C 2007 by
models focusing on its function.
Wiley Periodicals, Inc.
Results: Studies focusing on abnormal
eating patterns, including binge eating Keywords: obesity; diagnosis; classifi-
and night eating suggest that such pat- cation; binge eating; night eating; emo-
terns may be related to the development tional eating; addiction
of obesity. While the literature pertaining
to substance use and other models of (Int J Eat Disord 2007; 40:S83–S88)

Introduction ing metabolic and activity-related components. A

The rise in obesity, both in the United States and
worldwide, is among the most remarkable and wor-
risome health-related trends of the latter portion of
the last century and the beginning of the current
one.1 As American psychiatry prepares to revise its
diagnostic classification system, it is an auspicious
moment to reexamine the relationship between the
phenomenon of obesity and the category of human
dysfunction that falls under the rubric of mental
and behavioral disorders.
Obesity, defined as an excess of body fat with body
mass index (BMI) greater than 30 kg/m2, is currently
and rightly considered a medical rather than a psy-
chiatric disorder. Nonetheless, obesity is without
question strongly influenced by behavior, in that it
represents an imbalance between energy intake in
the form of feeding and energy expenditure, includ-
Accepted 14 May 2007
*Correspondence to: Michael Devlin, New York State Psychiatric
Institute, Unit 116, 1051 Riverside Drive, New York, NY 10032.
E-mail: mjd5@columbia.edu
Department of Psychiatry, Columbia University College of Physi-
cians and Surgeons, New York, New York
Published online 7 August 2007 in Wiley InterScience
(www.interscience.wiley.com). DOI: 10.1002/eat.20430
VC 2007 Wiley Periodicals, Inc.
naı̈ve interpretation of this statement might suggest
that obese individuals are, in some sense, at fault for
their obesity in that they are eating excessively, or are
not sufficiently active. This interpretation underlies
much of the stigma that is still associated with obe-
sity.2 What such a moralistic view of obesity fails to
take into account is (1) the fact that appetitive
behaviors are strongly influenced by factors, genetic,
and environmental, that, at the very least, strongly
resist conscious control; and (2) the fact that obese
individuals who are maintaining their body weight
are eating an appropriate amount for their body
weight, just as individuals of varying size who main-
tain a normal healthy weight (reviewed in Ref. 3).
Under what circumstances, then, might obesity
be considered to reflect an underlying mental or
behavioral disorder? It is useful to distinguish the
trait of obesity vulnerability, which may reflect sev-
eral factors including one’s genetic endowment and
the time, place, and culture in which one lives, the
state of obesity, and the process of becoming obese
via energy consumption in excess of energy ex-
penditure, i.e., nonhomeostasis. While separable in
theory, these aspects are quite intertwined and all
are relevant to the problem of obesity. For example,
the combination of innate obesity vulnerability and

International Journal of Eating Disorders 40 S83–S88 2007—DOI 10.1002/eat S83

DEVLIN
obesity-promoting environment may drive a patho-
logical process of overeating that gives rise to the
fully realized state of obesity. Nonetheless, the pro-
cess of becoming obese may provide a useful focal
point for a classification system of behavioral disor-
ders. In particular, periods of energy nonhomeosta-
sis resulting from excessive food intake, not includ-
ing periods of normal growth, suggest the presence
of a process that may fit more comfortably into a
classification system of behavioral disorders than
simply the state of being obese.
Although obesity may develop at various stages
of development, and obesity occurring later in the
course of child and adolescent development is a
better predictor of adult obesity, most overweight
and obese individuals become so during adult-
hood.4 While recognizing that obesity is increas-
ingly common in children and adolescents5 and
fully worthy of diagnostic reconsideration in its
own right, this article focuses primarily on adult
obesity as an initial area for exploration of new
diagnostic models.
One immediately apparent difficulty with the
concept of nonhomeostatic overeating as an indi-
cator of pathology is the reality that, as demon-
strated in the CARDIA trial,6 significant weight gain
over the course of adult life is now normative,
reflecting in part the dramatic and well-docu-
mented secular trends in obesity during the late
20th and early 21st centuries. The rise in obesity
has resulted, at least in part, from cultural forces
that tend both to increase energy intake and
decrease energy expenditure, resulting in a mis-
match between the two. This may represent a cul-
tural disorder of sorts, but it cannot be considered a
psychiatric disorder. To constitute a meaningful be-
havioral disturbance, the phenomenon of nonho-
meostatic overeating must be understood as non-
normative, nonhomeostatic overeating, and the
challenge for nosologists is to define such overeat-
ing in a way that clearly differentiates it from the
norm. In addition, it might be argued that, to avoid
the ‘‘slippery slope’’ that leads to a dilution of the
concept of mental disorders and an overinclusive
DSM-V, a putative psychiatric disorder ought to
include more than a vaguely defined behavioral
disturbance linked to an adverse medical outcome.
The problem of identifying a well-defined psycho-
pathological process that reflects such non-
normative obesity-promoting overeating may be
approached from several vantage points: the tradi-
tional vantage point of the eating disorder (ED), the
increasingly popular vantage point of the substance
use disorder (SUD), and the vantage points of other
less well-explored models. For the purpose of illus-
S84 International Journal of Eating Disorders 40 S83–S88 2007—DOI 10.1002/eat
tration, a sample of obesity-related psychiatric dis-
order reflecting each orientation precedes the dis-
cussion of that model. Consideration of these vary-
ing constructs is followed by an overall discussion
of the particular challenges in developing diagnos-
tic criteria that are reliable, valid, and useful.
Nonhomeostatic Eating and EDs
Obesogenic Binge Eating Disorder
To date, most attempts to conceptualize obesity-
related behavioral disorders have focused on
abnormal patterns of eating, particularly binge eat-
ing disorder (BED) and night eating syndrome
(NES). Following the ED model, these proposed
syndromes focus primarily on a behavior, such as
binge eating, eating disproportionately at night, or
waking up to eat. Their status as mental or behav-
ioral disorders is bolstered by the presence of asso-
ciated distress and impairment, and in some cases
medical liabilities are associated with obesity.
Recent reviews have considered the relative merits
of these syndromes as potential disorders in a psy-
chiatric classification system.7,8 Of note is that,
while both patterns exist frequently in normal
weight as well as overweight or obese individuals,
clinical trials very often focus primarily on obese
samples, so much so that they are often thought of
as obesity-associated disorders.
If, as suggested earlier, the focus of obesity-associ-
ated behavioral diagnoses should be on the process
of weight gain, the legitimacy of these diagnoses as
obesity-associated behavioral disorders would hinge
importantly on the evidence that cause significant
nondevelopmentally appropriate weight gain. Evi-
dence that binge eating is causally associated with
an upward weight trajectory comes primarily from
longitudinal studies of eating and weight in adoles-
cent and young adult samples, along with recent
observations from BED and obesity treatment stud-
ies. In a community-based cohort study of 591
young adults, Hasler et al.9 found an association
between binge eating and both being overweight
and gaining weight over a 20-year period. Similarly,
Fairburn et al.10 studying the longitudinal course of
binge eating in the community over a 5-year period,
found that, while binge eating was strikingly unsta-
ble over time, the prevalence of obesity in the sam-
ple had nearly doubled by the end of the study. Sev-
eral studies of adolescents have reported associa-
tions between binge eating and upward weight
trajectory,11–14 although Stice et al.15 in a recent
study of 11- to 15-year-old girls observed over a

4-year period, did not find binge eating to be associ-
ated with obesity onset.
Indirect evidence from treatment studies also
suggests a link between binge eating and obesity
risk. The observation that binge cessation tends to
be associated with weight stabilization, while con-
tinued binge eating is associated with ongoing
weight gain has now been reported by several
groups.16–19 Data from the National Weight Control
Registry also suggest a deleterious effect of binge
eating on the maintenance of weight loss.20 Based
on these data, and the logical connection between
truly uncompensated binge eating and weight gain,
it is difficult to escape the conclusion that binge
eating is associated with weight gain and, in many
cases, ultimately contributes to the development of
obesity.
Less systematic information is available regarding
the association between NES and obesity. While NES
is traditionally thought of as an obesity-related eat-
ing pattern, and retrospective recall in clinical sam-
ples suggests that night eating may often precede
the onset of obesity,21 crosssectional community
studies have not borne out this association.22,23
Interestingly, in a psychiatric sample, NES was found
to be associated with both obesity and SUD.24 Longi-
tudinal community studies are needed to best
understand the relationship between NES and obe-
sity risk, and NES treatment studies with long-term
follow-up may shed light on the impact of stopping
night eating on subsequent weight trajectory.
It is important to note that both BED and NES
clearly exist in normal weight as well as overweight
or obese individuals and that weight status seems
to have little or no impact on clinical features or se-
verity.25–27 However, it is important to note that
these data are crosssectional and do not rule out
the possibility that normal weight individuals with
these disorders are on the way to become obese.
Even a clear lack of association between BED or
NES and obesity or weight gain, though, would not
necessarily argue against their status as meaningful
behavioral and mental disorders. In this case,
though, their status as significant disorders would
not rest on an association with nonhomeostatic
eating or obesity, but rather on distress or impair-
ment that is independent of obesity.
NonHomeostatic Eating and SUD
Obesogenic Food Abuse Disorder
Saper et al.28 make the distinction between
homeostatic and hedonic systems that control eat-
International Journal of Eating Disorders 40 S83–S88 2007—DOI 10.1002/eat
OBESITY IN DSM-V
ing, stating: ‘‘If feeding were controlled solely by
homeostatic mechanisms, most of us would be at
our ideal body weight, and people would consider
feeding like breathing or elimination, a necessary
but unexciting part of existence.’’ The fact that this
is not the case that suggests the important role of
reward systems in providing motivation for feeding,
and raise the possibility that excess energy con-
sumption may reflect a dysfunction in reward sys-
tems or in the interaction of reward mechanisms
and homeostatic mechanisms of feeding regula-
tion.
Significantly, a diagnosis based on the concept of
nonhomeostatic overeating as a dysfunction or
overuse of reward systems would not require an
abnormal eating pattern per se, but rather would
rest on the presence of excessive eating along with
some marker of dysfunctional use or overuse. One
such model, that of ‘‘food addiction,’’ rests on the
presence, among those exhibiting nonhomeostatic
eating or the remnant of such eating, of phenom-
ena associated with addictions such as tolerance,
withdrawal, and substance-seeking behaviors. The
presence of such parallels has been suggested by
both animal29,30 and human researchers,31 and has
found popularity with some who identify strongly
with the concept of eating ‘‘addictions,’’ as evi-
denced by popularity of groups such as Overeaters
Anonymous, that are based on an SUD model of
overeating. An emerging literature on reward
drive32 and sensitivity to reward33 suggests that a
‘‘personality trait rooted in the neurobiology of the
mesolimbic dopamine system’’34 may underlie
both SUDs and a predisposition toward overeating
and overweight.
An important conceptual foundation for the idea
of nonhomeostatic overeating as an addictive dis-
order analogous to SUDs is mounting evidence
that similar neuronal systems, including the nu-
cleus accumbens and its dopaminergic inputs as
well as endogenous opioid and serotonergic sys-
tems, are involved in motivation for eating and
substance use.35 Particularly, in the case of dopami-
nergic systems, human neurofunctional imaging
studies argue for a mechanistic overlap between
SUDs and severe obesity resulting from nonho-
meostatic eating.36 While a detailed review of these
systems is beyond the scope of this article, a sub-
stantial and mounting body of evidence supports
the contention that SUDs represent, at least in part,
a recruitment of neuronal systems that originally
evolved to subserve eating behavior.35,37 It is per-
haps understandable that our classification system
for mental and behavioral disorders has more eas-
ily recognized as pathological diversion of this sys-
S85
DEVLIN
tem to promote the use of substances not required
for life than the more subtly abnormal misuse or
overuse of a substance essential for life.
Other Models for Disorders of
Nonhomeostatic Eating
Obesogenic Emotional Eating Disorder
Other models related to the dysfunctional rein-
forcement of overeating have been suggested that
relate to, but are not precisely the same as, the food
addiction model. Affect regulation and stress
response models view overeating as a response to a
primary underlying problem in managing aversive
internal states or external conditions. In these
models, the emphasis, both in conceptualizing the
disorder and approaching its treatment is more on
the underlying problem than on the particular
behavior, in this case of overeating.
The affect regulation model proposed both in the
context of SUDs38 and of EDs39 views substance
use as a means of regulating emotions, particularly
negative affect. Approaches to the treatment of EDs
based largely on teaching affect regulation skills,
principally dialectical behavioral therapy (DBT)
have yielded promising results.40 A recent study
designed to experimentally test the validity of the
affect-regulation model for both bulimic and sub-
stance use psychopathology found that manipula-
tion of depression via short term cognitive behav-
ioral intervention led to a reduction in bulimic but
not in substance use symptoms.41 Although, this
study particularly examined bulimic eating symp-
toms, an affect-regulation model for nonhomeo-
static eating would rest not on the presence of any
particular eating pattern, but rather on the link
between negative affect and overeating. The con-
cept of emotional overeating as the central feature
of a form of obesity related to nonhomeostatic eat-
ing would of course be supported by evidence of an
association between emotional overeating and
BMI; at least one recent study failed to detect such
an association among overweight patients with
BED.42
An additional somewhat similar model is the
stress response model of binge eating described by
Gluck,43 which suggests that abnormal stress
responsivity contributes to obesity in vulnerable
individuals via exaggerated cortisol release that
may both drive binge eating and contribute directly
to central fat distribution. A variety of currently
available treatment interventions, including DBT,
mindfulness-based approaches, and even psycho-
S86 International Journal of Eating Disorders 40 S83–S88 2007—DOI 10.1002/eat
pharmacological treatments, may operate in part
by altering the response to stress. Again, although
this model has been proposed with respect to binge
eating, it could conceivably be extended to any
stress-related overeating, with the particular form
that the overeating takes being a secondary feature.
From Concept to Diagnosis
The models of nonhomeostatic overeating des-
cribed earlier differ importantly in their central
focus. ED models, and the diagnostic criteria that
attempt to operationalize these core diagnostic
concepts, focus on the form of the dysfunctional
behavior, whereas substance use models focus
more on the consequences of substance use, and
affect regulation or stress response models focus
on its function. For example, DSM-IV eating criteria
for BED and bulimia nervosa attempt to carefully
define what constitutes an eating binge and how
often eating binges must take place to meet crite-
ria, but are less specific about the consequences of
such behavior. In contrast, criteria for substance
abuse and dependence make little attempt to
quantify or characterize the pattern of substance
use (note that there is no binge drinking disorder,
even though binge drinking is a well-known pattern
of alcohol misuse), but describe in detail the be-
havioral consequences, in the case of abuse, or the
phenomena of tolerance and withdrawal, in the
case of dependence.
Adopting an EDs model for nonhomeostatic
overeating would raise several difficult problems. If
the core concept were simply eating sufficient to
bring about nondevelopmentally appropriate
weight gain, it would be necessary to quantify how
much weight gain, over what period of time, and in
what circumstances this would have to occur. For
example, would the commonly observed regain of
weight following a weight loss diet qualify? Would
weight gain resulting primarily from a decrease in
energy expenditure, voluntary or involuntary,
rather than a change in amount or pattern of eating
qualify? Would increased eating and weight gain
induced by medication be included? In addition,
the concepts of distress and impairment, consid-
ered to be central features differentiating normal
behavior from disordered behavior, would require
clarification in this context. Would an individual’s
distress, or lack thereof, regarding weight gain fac-
tor into the diagnosis? Would the onset or worsen-
ing of obesity constitute sufficient impairment to
merit consideration as a disorder? If not, as Tanof-
sky-Kraff and Yanovski44 suggest, nonhomeostatic

eating leading to obesity might constitute signifi-
cantly disordered eating without rising to the
threshold of an ED per se. The current solution,
restricting the diagnostic focus to abnormal pat-
terns of overeating that can be reliably identified,
has the advantage of relatively clear differentiation
from normal behavior, but may leave out a large
number of individuals whose nonhomeostatic eat-
ing does not fall into a clearly defined pattern.
Adopting a substance use model for nonhomeo-
static eating would solve certain of these problems,
but raise others. In particular, the fact that food is
necessary for life precludes an easy division of the
population into users and nonusers. Although, as
described above, researchers have begun to explore
such concepts as tolerance, withdrawal, and crav-
ing as they apply to food, these phenomena have
not yet been clearly defined or demonstrated in
this context. Thus a state of ‘‘food dependence’’
would, at this time, be difficult to characterize.
However, criterion A(7) for substance dependence,
‘‘the substance use is continued despite knowledge
of having a persistent or recurrent physical or psy-
chological problem that is likely to have been
caused or exacerbated by the substance,’’ may
apply, for example, to individuals with obesity and
diabetes mellitus who are not fully adherent to die-
tary recommendations. Regarding ‘‘food abuse,’’
current criteria for substance abuse may tend to ei-
ther be overinclusive or not applicable, depending
on the interpretation of the criterion. For example,
criterion A(2), ‘‘recurrent substance use in situa-
tions in which it is physically hazardous’’ might, if
broadly interpreted, characterize all consumption
of foods containing excessive amounts of unheal-
thy substances such as saturated fats or trans fats,
regardless of the situation. A similar problem exists
for nicotine use, a substance for which there is no
abuse diagnosis. A narrower interpretation of the
criterion might refer, for example, to the hazards of
driving an automobile while binge eating. This
would be closer to the spirit of the criterion as it
applies to substances of abuse, but departs from
the concept of the obesity-related hazards of non-
homeostatic eating. Criterion A(4), ‘‘continued sub-
stance use despite having persistent or recurrent
social or interpersonal problems caused or exacer-
bated by the effects of the substance’’ could simi-
larly include many individuals experiencing weight
gain, particularly in a culture in which overweight
is stigmatized.2
Affect regulation and stress response models for
nonhomeostatic overeating would also pose con-
siderable challenges. Although conjectures regard-
ing the function of unhealthy behaviors are com-
International Journal of Eating Disorders 40 S83–S88 2007—DOI 10.1002/eat
OBESITY IN DSM-V
monly part of the clinical description of behavioral
disorders, there are few precedents for criterion
sets for behavioral disorders based primarily on the
function of the behavior. In part, this may reflect
the difficulty in using self-report to definitively es-
tablish the function of a behavior. Additionally,
such phenomena as eating to relieve negative affect
or eating in response to stress exist across a spec-
trum of frequency and intensity, and it may be dif-
ficult to differentiate normal from abnormal pat-
terns of affect-related or stress-related eating. The
placement within DSM-V of an affect regulation-
centered overeating disorder would also be chal-
lenging, in that one could imagine its inclusion
with personality disorders, mood disorders,
impulse control disorders, or some other general
category of diagnostic entities.
Ultimately, a diagnosis based on underlying
pathophysiology will provide the best resolution to
these nosological dilemmas and the best founda-
tion for treatment. As we learn more about the neu-
robiological correlates of addictions in general,45 a
better understanding of how food interacts with
reward systems will be crucial in differentiating
normal food reward from food addiction, if such a
distinction even exists. Similarly, a psychobiologi-
cal understanding of the ways in which food intake
might modulate affect, or vice versa, would
undoubtedly be useful in considering questions
related to emotional eating as either a diagnosis in
its own right or a manifestation of an underlying
disorder of affect regulation. Understanding on this
level would be helpful in both identifying those
individuals for whom an obesity-related mental
and behavioral diagnosis would be meaningful,
and particularly for selecting a treatment that spe-
cifically targets the underlying problem. As we
approach the DSM-V, while we are closer than ever
before to understand nonhomeostatic eating and
obesity on this level, much remains to be done
before we can truly answer the questions of
whether, when, or how an obesity-related process
can meaningfully be considered and treated as a
behavioral or psychological disorder.
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