The Eating Disorders Work Group of the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition Task Force was given the charge of considering whether obesity is a mental disorder that should be included.
There were several reasons for considering the salience of obesity for the psychiatric nomenclature. First, phenotypic similarities in the behaviors associated with obesity and both eating disorders and substance use disorders, as well as findings documenting different brain responses to food-related cues in lean and obese individuals,1 have led to consideration of obesity as a mental disorder.
Next, there is growing evidence documenting a relation between obesity and numerous psychiatric disorders.2–4 Finally, increasing concern about the association of psychotropic drugs with weight gain and increases in cardiometabolic risk has led to enhanced awareness of obesity in psychiatry.5 Nevertheless, there currently is insufficient evidence to include obesity in DSM-5. In the sections that follow, we outline research findings that informed the decision making of the Eating Disorders Work Group.
Characteristics of Obesity
Obesity refers to an excess of body fat. In the broadest sense, obesity is caused by a long-term imbalance between energy intake and energy expenditure resulting in the storage of non-essential lipids in adipose cells. There is no clear demarcation between normal and abnormal levels of body fat, and obesity is most commonly estimated by various proxies. Currently, body mass index (BMI), which is a ratio of weight to height that is calculated by weight in kilograms divided by height in meters squared, is used most commonly to define obesity operationally. BMI is strongly associated with adiposity and obesity-related morbidity, and category thresholds have been established (BMI < 18.5 – underweight; BMI 18.5–24.9 – normal weight; BMI 25–29.9 – overweight; BMI > 30 – obese).6
Since the middle of the 20th century, rates of obesity in the United States have increased dramatically in men and women, and in all racial/ethnic and socioeconomic groups. There is some evidence that the striking increases in obesity have leveled off; nevertheless, the prevalence of obesity in the US in 2009–2010 was 35.5% in adult men and 35.8% among adult women, and there is no indication that prevalence is decreasing.7
Obesity has profound medical consequences8 and is associated with cardiovascular disease, hypertension, type 2 diabetes, and certain types of cancer. Obesity also is related to psychosocial impairments and poorer quality of life. Health care costs associated with obesity were estimated to account for 9.1% of US medical expenses in 1998,9 and if current trends continue, obesity will account for 16% of US health care expenditures by 2030.10
The substantial personal and societal burden incurred by obesity has led The Obesity Society to declare on utilitarian grounds that obesity is a disease in order to promote research, reduce stigma, and facilitate professional care.11 Indeed, in light of the medical morbidity and costs associated with obesity, research focusing on the causes, consequences, and treatment of obesity is a public health priority.
Etiology of Obesity
The causes of obesity are incompletely understood. At a population level, many epidemiologists have concluded that the increased prevalence of obesity may be due primarily to modest increases in calorie intake and decreases in physical activity that have led to overall upward shifts in population weights.12 At an individual level, however, there is agreement that causes are heterogeneous and involve an intricate interplay among genetic, individual, environmental, and societal factors.13 Research in obesity has increased exponentially with work across multiple levels of analysis from the molecular to the macroeconomic.
Findings suggest that obesity results from varying alterations of complex internal and environmental milieus that interact to result in a diversity of phenotypes. In light of the multiple pathways to obesity, the DSM-5 Eating Disorders Work Group concluded that there is little evidence to support the conclusion that obesity per se is a mental disorder.14 Nevertheless, it certainly is possible that particular obesity phenotypes are the consequence of mental disorder.
Behavioral Phenotypes of Obesity
Obesity and Binge Eating
In a paper examining the potential role for obesity-related diagnoses in the DSM-5, Devlin15 proposed eating disorders (EDs), in particular binge eating disorder (BED), or substance use disorders (SUDs) as two models for including obese phenotypes characterized by “non-normative obesity-promoting overeating.” BED, which has been recommended for inclusion in the DSM-5 as an ED, is characterized by persistent and frequent ingestion of large amounts of food coupled with a loss of control over the aberrant eating, which are associated with clinically significant distress and dysfunction.
Available evidence has indicated that recurrent binge eating is associated with weight gain.16 Moreover, there is a strong relationship between BED and obesity in clinical and community samples, as well as an association between severity of binge eating and degree of overweight.17 Thus, there already is a diagnosis in the DSM for an obesity phenotype characterized by aberrant eating. Nevertheless, it is important to recognize that not all individuals with BED are obese, and conversely, the vast majority of obese individuals do not have BED. Thus, inclusion of BED in the DSM-5 will not address the question of obesity as a psychiatric disorder completely.
Obesity as an SUD
An alternate conceptualization would be to classify obesity as an SUD based on phenotypic similarities between drug-seeking in individuals who are addicted to drugs and food-seeking in obese individuals, who ostensibly are addicted to food. In an addiction model of obesity, certain foods, in particular those that are highly palatable, are theorized to co-opt central reward neuro-circuitry in a manner analogous to that seen in other SUDs.18
Observers have noted evidence of compulsive food-seeking and the development of tolerance, withdrawal, and loss of control over eating in obese individuals, with persistence of overeating despite adverse consequences for the individual.19
However, considering obesity as an SUD is problematic for several reasons, including that food, unlike drugs of abuse, is necessary for survival, and there is no compelling evidence of human withdrawal symptoms from foods. In addition, not all obese individuals report patterns of behavior consistent with food addiction or substance abuse.
A more nuanced stance might be to consider whether the concept of food addiction is most salient for individuals with clearly aberrant eating, ie, those with BED. Nevertheless, not all individuals with BED are phenotypically similar to those with SUD,20 and there are compelling arguments that models utilizing clinical phenomenology of EDs or SUDs to conceptualize psychiatric phenotypes of obesity are too imprecise to evaluate critically.21
Advances in understanding are likely to emerge from work examining the neurobiology of obese phenotypes across these psychiatric disorders. For example, there has been an explosion of work in neuroscience, particularly from studies utilizing functional neuroimaging, which has focused on the potential dysfunction of central pathways that may be involved in obesity-related eating behavior.
The notion that obesity may be understood in the context of the neurobiological framework of addiction, if not as a SUD per se, has gained increasing attention. In particular, Volkow and colleagues,18 informed by work in animal and human models of addiction, have posited that in vulnerable people (by virtue of genetic liability or other individual factors), reinforcers in the form of food or drugs become overvalued relative to other reinforcers as a result of conditioned learning.
Then, an elevated expected or anticipated reward from food or drugs over-activates memory and reward circuits and inhibits cognitive control circuitry, which in turn, leads to an inability to self-manage the drive to consume drugs or foods.
Support for various components of the model come from burgeoning evidence documenting differences between obese and lean individuals in neural responding in pathways that involve reward sensitivity, conditioned learning and cognitive control, as well as data that elucidate how hypothalamic neuropeptides that regulate energy balance affect the activity of dopamine cells in reward pathways.22
Nevertheless, numerous questions remain. There is little evidence that differences in neural activation in response to food-related or non–food-related reward are directly associated with the onset or maintenance of obesity or in vivo eating behavior.14 Moreover, findings from functional neuroimaging studies have not been consistent, which may be due to the highly heterogeneous nature of obesity, or the need for more precise tools to measure potential differences in responding and more sophisticated characterizations of potentially aberrant human eating behavior.21
Comorbid Psychiatric Disorders and Obesity
The relation between obesity and psychiatric disorder is not limited to EDs and SUDs. A growing body of evidence from epidemiologic and community samples has documented a relationship between obesity and other psychiatric disorders, including mood and anxiety disorders,23 as well as personality disorder.24 Moreover, developing evidence has suggested a relationship between obesity and attention-deficit/hyperactivity disorder (ADHD)2 and posttraumatic stress disorder.3
The exact causes for the comorbidity of obesity and non-eating or substance-related mental disorders remain unknown. However, there are several possible explanations. For example, obesity shares a number of symptomatic features in common with mood disorders, including increased appetite, decreased activity levels, and sleep disturbance. Indeed, changes in weight status or eating behavior are included in the current DSM criteria for major depressive episodes, dysthymia, and borderline personality disorder.25
Obesity also shares a number of correlates in common with mental disorders in addition to those noted with regard to EDs and SUDs, including hypothalamic-pituitary-adrenal (HPA) axis dysregulation and environmental precipitants such as childhood trauma. Thus, it is possible that increased adiposity in psychiatric patients may signal the presence of clinically relevant third variables that might have relevance for course or outcome.
The ubiquity of the relationships between obesity and numerous psychiatric disorders highlights both the heterogeneity of obesity and the limitations inherent in descriptive diagnostic categories.
The current understanding of mental disorder encompasses multiple levels of analysis, including genetics, brain circuitry, and behavioral factors, and does not always correspond clearly to the current symptom-based psychiatric nosology. This has led to increased interest in efforts to examine conceptually relevant dimensions associated with psychiatric disorder that will guide investigations designed to identify meaningful distinctions and similarities across the range of psychiatric diagnoses. This approach is exemplified by the National Institute of Mental Health (NIMH) Research Domain Criteria (RDoC) project.26
Thus, a more complete understanding of the relationships among eating pathology, obesity and the range of psychiatric disorders is likely to involve examination of these phenomena across psychiatric classes to identify neurobiological factors that underlie phenotypic similarities (eg, binge eating in mood disorder, BED, and borderline personality disorder) and distinguish lean from obese individuals. As there is complexity and redundancy of central and peripheral mechanisms involved in the regulation of energy, this will require additional studies focusing on the neurobiology of reward, but also broadening the investigative focus to examine patterns of responding in other disorders where obesity and aberrant eating are common.
Such studies will need to include other relevant domains of neural responding such as those involved in threat or arousal systems that govern sleep. In addition, these data will need to be integrated with findings that explicate the homeostatic systems involved with energy regulation (ie, hunger and satiety) and their interaction with central systems implicated in psychiatric disorder.
Overall, the research designed to elucidate the role and function of central mechanisms associated with psychiatric and obese phenotypes shows great promise for promoting understanding of the relationship between obesity and psychiatric dysfunction. However, the complex and heterogeneous nature of this relationship highlights the problems of including obesity as a distinct disorder in DSM-5.
Psychotropic Drugs and Obesity
An additional factor that has prompted interest in the salience of obesity to psychiatry is the effect of psychotropic drugs on body weight. Many psychiatric medications available currently are associated with weight gain,5 but there has been a particular focus on the potential iatrogenic effects of second-generation antipsychotic agents, especially clozapine and olanzapine.27 Medication-induced weight gain has been linked to noncompliance with treatment and the development of obesity and its related comorbidities.28 However, because psychiatric medications affect multiple and diverse aspects of central functioning, there is no single cause of psychotropic-associated weight gain.29 There also is marked variation in medication-induced weight gain across patients.
Future research may help to identify patients at highest risk for significant weight gain and metabolic risk. For example, a recent study documented that a locus near the melanocortin 4 receptor gene was associated with extreme weight gain from second-generation antipsychotic medications.30
In light of the potential effects of psychiatric medications on the development of obesity and associated medical comorbidities, it is critical that clinicians select medications carefully and monitor side effects closely. Moreover, it is advisable to include BMI as an index of adiposity in the assessment and management of all psychiatric illnesses. Referral for additional medical assessment is recommended for individuals with marked increases in weight during treatment.
In summary, the Eating Disorders Work Group concluded that obesity should not be included in DSM-5. Obesity is a heterogeneous condition with a complex and incompletely understood etiology, and thus cannot be considered a mental disorder per se. There may be obesity phenotypes that are caused by mental disorder, but research focusing on the role of neural mechanisms in the onset and maintenance of obesity and obesity-related behaviors (eg, overeating) is in its infancy.
Future work focusing on conceptually relevant biological dimensions that may underlie both obesity and psychiatric disorders could shed light on the role of mental dysfunction in the expression of psychiatrically relevant obesity subtypes. Nevertheless, obesity is associated with numerous psychiatric disorders, and several classes of psychotropic medications are associated with weight gain, metabolic risk factors, and obesity. Consequently, clinicians are advised to monitor weight and BMI closely and to consider the salience of overeating and weight-related issues in patients with psychiatric disorders.
- Stice E, Spoor S, Ng J, Zald DH. Relation of obesity to consummatory and anticipatory food reward. Physiol Behav. 2009;97(5):551–560. doi:10.1016/j.physbeh.2009.03.020 [CrossRef]
- Pagoto SL, Curtin C, Lemon SC, et al. Association between adult attention deficit/hyperactivity disorder and obesity in the US Population. Obesity (Silver Spring). 2009;17(3):539–544. doi:10.1038/oby.2008.587 [CrossRef]
- Pagoto SL, Schneider KL, Bodenlos JS, et al. Association of post-traumatic stress disorder and obesity in a nationally representative sample. Obesity (Silver Spring). 2012;20(1):200–205. doi:10.1038/oby.2011.318 [CrossRef]
- Allison DB, Newcomer JW, Dunn AL, et al. Obesity among those with mental disorders: a National Institute of Mental Health meeting report. Am J Prev Med. 2009;36(4):341–350. doi:10.1016/j.amepre.2008.11.020 [CrossRef]
- Schwartz TL, Nihalani N, Virk S, Jindal S, Chilton M. Psychiatric medication-induced obesity: treatment options. Obes Rev. 2004;5(4):233–238. doi:10.1111/j.1467-789X.2004.00149.x [CrossRef]
- National Institutes of Health. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults–The Evidence Report. National Institutes of Health. Obes Res. 1998;6(Suppl 2):51S–209S.
- Flegal KM, Carroll MD, Kit BK, Ogden CL. Prevalence of obesity and trends in the distribution of body mass index among US adults, 1999–2010. JAMA. 2012;307(5):491–497. doi:10.1001/jama.2012.39 [CrossRef]
- Bray GA. Medical consequences of obesity. J Clin Endocrinol Metab. 2004;89(6):2583–2589. doi:10.1210/jc.2004-0535 [CrossRef]
- Finkelstein EA, Fiebelkorn IC, Wang G. National medical spending attributable to overweight and obesity: how much, and who’s paying?Health Aff (Millwood). 2003;Suppl Web Exclusives:W3-219–226. doi:10.1377/hlthaff.w3.219 [CrossRef]
- Wang Y, Beydoun MA, Liang L, Caballero B, Kumanyika SK. Will all Americans become overweight or obese? estimating the progression and cost of the US obesity epidemic. Obesity (Silver Spring). 2008;16(10):2323–2330. doi:10.1038/oby.2008.351 [CrossRef]
- Allison DB, Downey M, Atkinson RL, et al. Obesity as a disease: a white paper on evidence and arguments commissioned by the Council of the Obesity Society. Obesity (Silver Spring). 2008;16(6):1161–1177. doi:10.1038/oby.2008.231 [CrossRef]
- Sturm R. Increases in morbid obesity in the USA: 2000–2005. Public Health. 2007;121(7):492–496. doi:10.1016/j.puhe.2007.01.006 [CrossRef]
- Bray GA, Champagne CM. Beyond energy balance: there is more to obesity than kilocalories. J Am Diet Assoc. 2005;105(5 Suppl 1):S17–23. doi:10.1016/j.jada.2005.02.018 [CrossRef]
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- Devlin MJ. Is there a place for obesity in DSM-V?Int J Eat Disord. 2007;40(Suppl):S83–88. doi:10.1002/eat.20430 [CrossRef]
- Wonderlich SA, Gordon KH, Mitchell JE, Crosby RD, Engel SG. The validity and clinical utility of binge eating disorder. Int J Eat Disord. 2009;42(8):687–705. doi:10.1002/eat.20719 [CrossRef]
- Hudson JI, Hiripi E, Pope HG Jr., Kessler RC. The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication. Biol Psychiatry. 2007;61(3):348–358. doi:10.1016/j.biopsych.2006.03.040 [CrossRef]
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- Grosshans M, Vollmert C, Vollstadt-Klein S, et al. Association of leptin with food cue-induced activation in human reward pathways. Arch Gen Psychiatry. 2012;69(5):529–537. doi:10.1001/archgenpsychiatry.2011.1586 [CrossRef]
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- Virk S, Schwartz TL, Jindal S, Nihalani N, Jones N. Psychiatric medication induced obesity: an aetiologic review. Obes Rev. 2004;5(3):167–170. doi:10.1111/j.1467-789X.2004.00141.x [CrossRef]
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