The ASAM Principles of Addiction Medicine 5th Edition

92. Co-Occurring Addiction and Eating Disorders

Lisa J. Merlo, PhD, MPE, Kevin Wandler, MD, and Mark S. Gold, MD, FASAM












This chapter describes commonalities between and comorbidity of addiction disorders and disturbances in eating. Anorexia nervosa (AN), bulimia nervosa (BN), binge eating disorder (BED), and obesity are serious clinical conditions with significant medical and psychological consequences. In addition, subclinical presentations of these disorders are common. There are many similarities between obesity, eating disorders, and traditional addiction disorders (i.e., addiction to alcohol and/or drugs), and these disorders are frequently comorbid. Eating disorders can trigger addiction disorder relapses or binges and vice versa. Addiction clinicians must prevent hyperphagia, overeating, and obesity as part of the comprehensive treatment of addiction disorders. Comorbidity among addiction disorders and diseases of eating complicates the assessment, diagnosis, treatment, and long-term recovery processes for both conditions.



Addiction has been summarized by the three Cs: compulsive use, loss of control, and repetition despite adverse consequences. Many eating disorders can be similarly described (1) and for this reason have often been labeled as a form of behavioral addiction. Indeed, the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) (2) criteria for substance dependence have been applied to food (as a potential substance of abuse), in order to propose diagnostic criteria for the construct of “food addiction” (3,4). Using such methods, clinical and research evidence has demonstrated that pathologic attachment to food (particularly foods high in sugar and fat) is similar to a drug use disorder in virtually all spheres, including neurobiologic (28). Specifically, both animal (9) and human (10,11) researchers have documented down-regulation of dopamine receptors among obese subjects, suggesting that deficits in the neurobiologic reward mechanisms may be associated with compulsive eating, just as with compulsive drug use. Results of a functional magnetic resonance imaging (fMRI) study comparing scores on a measure of food addiction with brain activity also suggested that neural activation patterns are similar for individuals who demonstrate addictive behavior toward either food or drugs (12).

Further, just as recent research has expounded on the importance of a fourth C—craving—in addiction disorders such as alcohol dependence (13), food craving has been associated with eating disturbance, particularly as observed in cases of food addiction (14). Whereas addictions can be understood as an individual’s biologic sensitivity and pathologic attachment to drugs or alcohol, eating disorders can be similarly described as a pathologic relationship with food.

Eating Disorders

The eating disorders comprise a category of psychiatric illnesses characterized by disturbed eating patterns and dysfunctional attitudes related to food, eating, and body shape. The DSM-IV-TR (2) lists three separate eating disorders with specific criteria to differentiate them: anorexia nervosa (AN), bulimia nervosa (BN), and eating disorder not otherwise specified (EDNOS). Symptoms of both AN and BN are rooted in disturbed body image and concerns related to consequences of gaining weight. EDNOS describes a sub-clinical presentation of either one of the other two disorders or BED, which will be described later. More recently, researchers have proposed adding obesity or “food addiction” to future editions of the DSM (15,16).

Anorexia Nervosa

AN may be the most widely recognized eating disorder, though it is not well understood by the general public. Readers are referred to the current Diagnostic and Statistical Manual of Mental Disorders for a full listing of diagnostic criteria. In general, individuals with AN are characterized by extremely low body weight for their age and height, making their disorder difficult to conceal. Like individuals with addiction disorders, they are often adamant in their denial of the disorder (17) and may go to great lengths in an attempt to mask their impairment. For example, individuals with AN may attempt to surreptitiously increase their weight for weighins using weights, heavy clothing, or water loading (18), or they may hide their symptoms (e.g., by avoiding eating around other people, wearing baggy clothing to hide their emaciated frame, creating/eating elaborate meals when there are witnesses). Just as an individual with alcohol abuse/dependence may boast about high tolerance, individuals with AN rarely have insight into their problem and frequently note significant weight loss as an achievement, despite the medical complications associated with their condition. Associated physical symptoms (which may initially provide the impetus for seeking treatment) include constipation, cold intolerance, lethargy, and in some cases lanugo (fine body hair that develops along the midsection and appendages). AN can result in significant medical complications, including hypothalamic–pituitary–adrenal axis dysfunction, pubertal delay or interruption, growth retardation, bone mass reduction, and osteopenia/osteoporosis. Other possible symptoms include bradycardia, hypotension, cardiac arrhythmias, mitral valve prolapse, metabolic alkalosis or acidosis, hypokalemia, hypoglycemia, leukopenia, anemia, carotenemia, acrocyanosis, thrombocytopenia, peripheral neuropathy, hypothermia, dehydration, hair loss, and dry skin (1921). Similar to addiction populations, the mortality rate for individuals with AN is extremely high. In one longitudinal study, 7% of individuals with AN had died after 8 years (22). Another study involving AN patients with a comorbid alcohol use disorder found nearly 10% of patients died within the 8-year study period (23). Rates of completed suicide in this population range from 0.9% to 6.3% (24). This completion rate is one of the highest of any psychiatric illness (25).

Bulimia Nervosa

The diagnostic criteria for BN are outlined in the current Diagnostic and Statistical Manual of Mental Disorders. BN differs from AN in that markedly low body weight is not a required symptom, but presence of binge eating and compensation for bingeing are necessary for the diagnosis. Compensatory actions involve purging by self-induced vomiting in approximately 90% of BN cases. Compensatory behaviors may also include misuse of laxatives, diuretics, and/or enemas; excessive exercise; periods of fasting; or severe caloric restriction. Because of the frequency of vomiting, it is common for dental enamel to show significant erosion (26). Other significant medical complications associated with BN include fluid and electrolyte abnormalities (e.g., hypokalemia, metabolic alkalosis or acidosis), cardiac arrhythmias, parotid enlargement, submandibular adenopathy, menstrual irregularity, constipation, and reproductive problems (21,27).

Binge Eating Disorder

Diagnostic criteria for BED are also listed in the current edition of the Diagnostic and Statistical Manual of Mental Disorders. The extant literature related to BED is growing rapidly. Though it is similar to BN, in that regular binge eating occurs, the key distinction is that individuals with BED do not engage in compensatory behavior for their overeating. Binge eating episodes share many characteristics in common with binge drinking episodes, such as eating rapidly, eating more than intended (e.g., eating until uncomfortably full or bingeing when not hungry), eating alone (often owing to embarrassment or shame regarding the excessive food intake), and feeling disgusted, guilty, or depressed after binge eating. Some have suggested that BED may reflect the consequences of food addiction (28,29). Studies have demonstrated that 40.5% to 56.8% of BED patients can be classified as food addicted (3,30), and 72.2% of obese individuals with food addiction were diagnosed with BED (31). Some report feelings of dissociation during episodes of binge eating, and most with BED view their binge eating as unwanted and distressing. Approximately 20% of individuals with BED are overweight, and approximately 70% are obese (32). Additionally, 30% of individuals who are obese are diagnosed with BED (33). The most common medical complications associated with BED result from consequences of morbid obesity, including hypertension, type II diabetes, cardiovascular disease and stroke, osteoarthritis, increased risk for cancer, chronic muscular pain, joint pain, gastrointestinal problems including irritable bowel syndrome, and early menarche (3436).


Though not included in the DSM, obesity represents another serious condition related to a disturbance in eating. Generally, a diagnosis of obesity is made on the basis of an individual’s body mass index (BMI) score. BMI is calculated by dividing weight in kilograms by height in meters squared. Standard cutpoints are used to determine whether the individual falls within a healthy weight range (i.e., underweight = BMI < 18.5, normal weight = BMI 18.5 to <25, overweight = BMI ≥ 25 to 30, and obese = BMI ≥ 30). BMI from 30 to 35 is considered stage 1 obesity, from 35 to 40 is stage 2 obesity, and over 40 is stage 3 obesity (also called morbid obesity). As mentioned previously, obesity is associated with multiple serious health problems.


General Population

Although eating disorders are most common in Western society, there is evidence of their existence across many cultures (37,38). In general, the prevalence of eating disorders is higher in urban environments (39). Though AN occurs relatively equally among areas of diverse urbanization levels, BN appears to be much more common in cities than in rural areas (40). In addition, upward mobility within the social system is associated with increased risk for eating disorders across various cultures (4144). As with addiction disorders, heritability appears to be an important factor in the development of eating disorders, with genes accounting for 58% to 71% of the variance for AN (45) and 30% to 83% of the variance for BN (46,47). Unlike addiction disorders, it is commonly accepted that the prevalence of eating disorders is much higher in females, with the incidence of eating disorders in males being approximately one-tenth that of females. However, it is likely that eating disorders have been underdiagnosed among boys and men.

Like addiction disorders, eating disorders are often described as diseases of pediatric origin. Symptom onset rarely occurs past the age of 40 years (2), and point prevalence rates are much higher during adolescence and early adulthood. For example, the prevalence of subclinical AN among girls ages 16 to 25 is estimated to be approximately 10% (48). Recent studies have determined the lifetime prevalence of AN in females to be between 0.9% and 1.9% and have found the lifetime prevalence of AN in males to be between 0.29% and 0.3% (4951). With regard to BN, recent research has demonstrated the lifetime prevalence of BN to be higher than that of AN, at 1.5% to 2.9% in females and approximately 0.5% in males (49,51). The onset of BN occurs most commonly between the ages of 14 and 22 (49). Finally, recent studies have suggested that BED is the most common of these eating disorders, with lifetime prevalence rates of 1.9% to 3.5% in females and 0.3% to 2.0% in males (49,51,52). The estimated 12-month and lifetime prevalence of BED greatly exceeds the prevalence of both AN and BN (49,53), reaching up to 1.2% for the previous 12 months, and the prevalence of subclinical binge eating symptoms is even higher, with rates of 2.1% for the previous 12 months and 4.5% for lifetime occurrence (49). Among the American Latino population, up to 5.61% of individuals demonstrate some binge eating behavior during their lifetime (54). Given that underreporting is typical in the measurement of disordered eating, the prevalence of BED may be as high as 6% among Americans (55). BED onset typically occurs later than AN or BN and most frequently in the early to mid-20s, though many patients do not present for treatment until their 40s (56,57).

With regard to obesity, the problem extends across all ages, and the number of obese individuals has more than tripled in the last 50 years (58). As of 2004, 31.1% of American adults aged 20 or older are obese (i.e., BMI ≥ 30), and an additional 2.8% are morbidly obese (i.e., BMI ≥ 40) (59). Among pediatric populations, the proportion of children ages 6 to 11 years meeting criteria for obesity has more than doubled since 1970 (60). And finally, even half of the economically disadvantaged nations studied in sub-Saharan Africa, Latin America, the Caribbean, East and South Asia, Central Asia, North Africa, and the Middle East currently have rates of overweight/obesity (i.e., BMI ≥ 25) that exceed rates of underweight (61).

Much as the prevalence of substance use exceeds the prevalence of substance abuse or dependence, more individuals display subclinical eating disturbances than a clinically diagnosable eating disorder. These symptoms often include patterns of disordered eating and body image concerns. For example, a recent study of middle and high school students demonstrated that 41.5% of females and 24.9% of males had body shape perception disturbance, 36.4% of females and 23.9% of males had undue influence of weight on self-esteem, and 9.4% of females and 13.5% of males were engaging in compensatory behavior to control their weight (52). Among college students, 16.3% of females and 9.2 % of males in one study reported binge eating; 18.6% of females and 5.2% of males reported using laxatives, diet pills, or diuretics to facilitate weight loss; and 17.4% of females and 10.4% of males reported that eating and weight concerns significantly interfered with their academic performance (62). Results of another study suggested that 12% of male college students are dissatisfied with their body shape and 9% engage in disordered eating behaviors (63). Similarly, among pre-and early perimenopausal women without diagnosed eating disorders, approximately 29.2% report dissatisfaction with their eating patterns, 11% report regular binge eating, and 9.2% report a strong fear of gaining weight (64).

Addiction Treatment Populations

It is particularly important for addiction clinicians to be familiar with the eating disorders and obesity, as these disorders display relatively high comorbidity with addiction disorders (65,66). Drug use, abuse, and dependence can have dramatic and consistent effects on eating. In addition, certain addiction disorders appear to co-occur with specific diseases of eating. Treating one may exacerbate the other, but ignoring one may cause a new life-threatening disease to emerge; thus, careful consideration to co-occurring eating disorders must be part of the comprehensive care of addiction disorders and vice versa. Among individuals receiving treatment for an addiction disorder, approximately 0.02% to 3.4% also currently suffer from a current eating disorder (67,68). Further, results of the National Comorbidity Survey Replication study suggested that lifetime co-occurrence of alcohol use disorders and eating disorders ranges from 25% to 24%, whereas lifetime co-occurrence between drug use disorders and eating disorders is 18% to 26% (49). Between 2% and 41% of substance abuse patients have a lifetime history of eating disorder behaviors (69). It has been estimated that 17% to 25% of women with eating disorders have a lifetime history of an addiction disorder (23,70). Among adolescents being treated for eating disorders, approximately 35% display risky substance use, with rates of addiction disorders estimated at 1.1% for alcohol, 3.2% for cannabis, 1.1% for other drugs, and 14.7% for tobacco (71).

Specifically, results of several studies demonstrate that binge eating is frequently associated with excessive alcohol consumption (7274). Indeed, up to 57% of men and 28% of women with BED meet criteria for an addiction disorder (75). Thus, any BED diagnosis should raise questions regarding alcohol use and vice versa. Some research suggests that levels of BN are also significantly higher among women abusing alcohol than those in the general population, with greater than two-thirds identifying themselves as “binge eaters” with or without purging (76). There is anecdotal evidence suggesting that individuals with a history of overeating may develop alcohol or drug abuse after improving their eating habits (e.g., following bariatric surgery). In addition, animal research has demonstrated that abstaining from alcohol may promote bingeing on sugary foods, whereas restricting sugary food intake may promote excessive alcohol consumption (77). Human studies have further demonstrated that weight gain frequently occurs after treatment and recovery from addiction disorders (7880). However, in the absence of BED, obesity may actually serve a protective function against development of an addiction disorder. Research has demonstrated that, as BMI increases, the percentage of women who have consumed alcohol or smoked marijuana in the previous year decreases significantly (8183).

Conversely, dieting and purging are frequently associated with the use of cocaine and other stimulants (73,74,84,85). Whereas individuals with food-restricting habits are less likely to abuse stimulants than individuals who binge or purge, they still display increased use of stimulants compared to the general population (73). In fact, results of one study demonstrated that 32% of individuals seeking treatment for cocaine abuse/dependence met criteria for either AN or BN (85). AN patients also frequently abuse prescription and over-the-counter medication and may use drugs to suppress their appetite in order to lose weight. For example, particularly among college students, psychostimulants are misused for weight management as well as for prolonged study sessions or reversing the effects of cannabis smoking on new learning (86). Abuse of caffeine and laxatives is common in all forms of eating disorders (87). In addition, many chronic tobacco smokers cite fear of weight gain as a deterrent to their efforts at smoking cessation (88), and presence of an eating disorder may impede treatment efforts in this arena. However, female adolescents with restricting habits are actually less likely to use tobacco, alcohol, and marijuana than are individuals in the general population (87).

Psychiatric Treatment Populations

Individuals with eating disorders frequently display other psychiatric disorders as well. For example, Blinder et al. (74) recently demonstrated that up to 97% of females treated for anorexia had experienced one or more comorbid psychiatric diagnoses in their lifetime. The rates of psychiatric comorbidity among individuals with AN and BN are not significantly different. The most common Axis I psychiatric comorbidities among individuals with AN are mood disorders, particularly depression, with approximately 94% of AN patients meeting criteria for a depressive disorder (74). Between 56% and 66% of those with an eating disorder experience one or more anxiety disorders (74,89). Obsessive–compulsive disorder is the most common comorbid anxiety disorder, with a prevalence rate between 29.5% and 41% among individuals with AN or BN (8991). Social phobia is the next most common, with a 20% rate of comorbidity (89,92). Finally, Axis II disorders are extremely common among individuals with eating disorders. Research has demonstrated that approximately 68% of patients meet diagnostic criteria for one or more personality disorders (91), though rates vary between 21% and 97% (93). Patients with AN most commonly display cluster C (anxious/avoidant) personality disorders, whereas those with BN are more likely to display cluster B (dramatic/ erratic) personality disorders (93). Finally, individuals with BED are three times more likely to suffer from major depressive disorder than are individuals from the general population (94), and Axis II comorbidities are frequently associated with the severity of binge eating (75). Obesity is also associated with increased psychiatric conditions, including major depressive disorder and generalized anxiety disorder (95).

Primary Care or Other Health Care Populations

Within a family practice setting, the prevalence of AN is estimated to be between 4.2% and 6.3%, and the prevalence of BN is estimated to be between 6.3% and 12.2% (40,96,97). However, rates vary among members of different groups. For example, among female adolescents with Type I diabetes, up to one-third of patients exhibit disordered eating behaviors or eating disorders (98). With regard to BED, the prevalence is approximately 5% to 30% among obese individuals (99,100). In fact, there is almost a fivefold increase in risk for BED among individuals whose BMI is at least 40 compared to those whose BMI is within the normal range, and the risk for displaying subclinical binge eating behavior shows the same trend (101). Heredity may play a role in the development of BED, as 20.2% of individuals who are related to an overweight or obese person with BED also develop BED, compared to only 9.6% of individuals who are related to an overweight or obese person without BED. Relatives of the BED group are also more likely to have higher current BMI and elevated rates of obesity (101). In addition, among female athletes, rates of subclinical eating disorders range from 15% to 32% (102), and these symptoms also commonly occur among male athletes. Participation in aesthetic sports (e.g., ballet, gymnastics, figure skating) or sports in which “making weight” is required (e.g., wrestling, horse racing) results in increased risk for disordered eating (103).


Identifying Eating Disorders

Unfortunately, with the exception of obesity, the detection of eating disorders can be difficult. In fact, research suggests that more than half of individuals with an eating disorder go undiagnosed (4,104). Even an obesity diagnosis must be made by the physician taking an accurate weight on a reliable scale and measuring the patient’s height without shoes. In addition, just as addiction disorder patients are unlikely to self-refer for treatment, eating disorder patients often resist acknowledging their symptoms and impairment and are often in extreme denial of their illness. They may deny their hunger or attempt to hide their eating disturbances, even when referred for treatment by a parent or friend. When self-referred, individuals with AN may neglect to mention their disordered eating, instead presenting with nonspecific symptoms such as fatigue, lack of energy, or dizziness (105), or associated complaints such as intolerance to cold, throat or abdominal pain, digestive problems, heart palpitations, or changes in drinking or urination (106). In addition, several medical disorders share symptoms with eating disorders, complicating the diagnostic process. For example, hyperthyroidism, diabetes, tumors, gastrointestinal disorders (e.g., inflammatory bowel disease), nutrient malabsorption, immunodeficiency, chronic infections, and Addison disease may all result in weight changes and associated symptoms (106).

Eating Disorders in Addiction Disorder Patients

Among addiction disorder patients, detection of eating disorders may be particularly difficult, as substance abuse can lead to symptoms similar to those seen in AN, BN, BED, and even obesity. For example, alcohol-related disorders can include vomiting (as seen in AN and BN) and lethargy (as seen in AN, BN, BED, and obesity). Use of amphetamines, methamphetamine, cocaine, MDMA (3-4 methylenedioxy-methamphetamine), and opiates can result in decreased eating and significant weight loss (as in AN), whereas marijuana use may result in binge eating (as in BN, BED, and obesity). In particular, MDMA has attracted some college students who use doses that are markedly lower than those used as part of the club or party scene (107). As a result, eating disorder symptoms may be written off as secondary to the addiction disorder if a careful assessment is not performed. Regardless of whether an eating disorder is initially suspected, addiction clinicians should specifically inquire about eating disturbances, as well as weight-related drug misuse or abuse (e.g., use of “diet pills,” laxatives, stimulants). Individuals with eating disorders are unlikely to offer this information spontaneously, but presence of a comorbid eating disorder may affect decisions regarding clinical care.

Ideally, all substance-misusing, substance-abusing, and substance-dependent patients should be evaluated for comorbid psychiatric disorders and diseases of eating. All patients would benefit from an analysis of diet, exercise, eating behaviors (108), and BMI. In particular, patients undergoing treatment for alcohol abuse/dependence should always be evaluated for binge eating symptoms; those in treatment for stimulant abuse/dependence should always be assessed for purging behaviors and excessive dieting; and patients abusing caffeine or laxatives should always undergo a general eating disorder screening. The addiction clinician should also routinely include an assessment of current and past eating habits when recording a medical history, in order to obtain a comprehensive understanding of the patient and be alert to signs of an underlying or comorbid eating disorder. In addition, as treatment for the addiction disorder progresses, the patient’s weight and BMI should be monitored to track significant gain or loss. Many instruments are available to assist with eating disorder screening and assessment. Addiction clinicians may find it helpful to use these questionnaires in their initial evaluation and intermittently throughout treatment. Some example questionnaires are listed below.


Yale Food Addiction Scale

The Yale Food Addiction Scale (YFAS) was developed to apply the DSM-IV-TR criteria for substance abuse to food (108). It can be used to screen for possible food addiction among patients. The YFAS includes items assessing symptomatic behaviors and one section to assess problem foods. Respondents use a yes/no format to identify psychological and physical problems and a 4-point scale ranging from “never” to “daily” to rate the frequency of each behavior. Gearhardt et al. (12) validated the YFAS in an fMRI study that showed elevated “food addiction” scores were associated with similar patterns of neural activation as seen in patients with substance dependence. A positive screen on the YFAS may identify patients who are food addicts, even if they are not necessarily obese. The YFAS has been validated for use with adults and takes less than 10 minutes to complete.

Eating Disorders Inventory—Third Edition

The Eating Disorders Inventory—Third Edition (EDI-3) (109) has established psychometric properties (110,111) and is the most widely used self-report measure of disordered eating and related symptoms of AN and BN. This measure can be used to assist in the diagnosis of an eating disorder. The 91 items are scored using a forced choice format. The EDI-3 contains 12 subscales assessing specific eating disorder symptoms (e.g., drive for thinness, body dissatisfaction, bulimia) and related psychological constructs (e.g., ineffectiveness, perfectionism). It is appropriate for individuals 12 and older and can be completed in about 20 minutes.

Eating Disorder Diagnostic Scale

The Eating Disorder Diagnostic Scale (EDDS) (112) is a 19-item self-report questionnaire that assesses eating disorder symptoms over the previous 3 months. It is useful in differential diagnosis for AN, BN, and BED and requires about 5 minutes to complete. Most items are scored using a 7-point Likert-type scale. Items assessing overeating and loss of control are structured with an initial yes/no question with follow-up frequency assessment when appropriate. The authors have developed algorithms to determine whether diagnostic criteria are met for AN, BN, and/or BED. The EDDS has demonstrated excellent psychometric properties.

Eating Disorder Examination Questionnaire

The Eating Disorder Examination Questionnaire (EDE-Q) (113) is a self-report measure that was based on the EDE interview. The EDE-Q assesses disordered eating behaviors and attitudes over the previous 4 weeks, in order to assist with diagnosis of AN and BN. Like the interview version, the EDE-Q attempts to discriminate between objective and subjective bulimic episodes. The EDE-Q contains 36 items that are scored using a 7-point forced choice scale. It has demonstrated good psychometric properties and takes about 10 minutes to complete.

Bulimia Test—Revised

The Bulimia Test—Revised (BULIT–R) (114) is a 36-item self-report measure of BN symptoms (e.g., binge eating, compensatory behaviors, and body shape disturbance). It can be used specifically to assist with the diagnosis of BN and can be completed in 5 to 10 minutes. Items are scored using a 5-point Likert-type scale. Reliability and validity have been well established, and the BULIT–R has been used with both clinical and nonclinical populations (115). The BULIT–R is recommended for individuals 16 and older.

Binge Eating Scale

The Binge Eating Scale (BES) (116) is a 16-item measure used to assess binge eating symptoms and assist with diagnosis of BED. Eight items measure behavioral symptoms, and eight items measure feelings and cognitions related to binge eating symptoms. For each item, respondents choose from four statements to determine which statement describes them best. The BES has strong psychometric properties and published cutoffs to determine whether an individual displays clinically significant binge eating symptoms. This measure can be completed in less than 5 minutes.

Night Eating Symptom Scale

The Night Eating Symptom Scale (NESS) (117) is a self-report instrument that contains 12 items specifically assessing symptoms of night eating syndrome (i.e., overeating during the nighttime hours), such as percentage of food consumed after supper and frequency of nighttime snacking. It takes less than 5 minutes to complete, but does not specifically assess symptoms of AN, BN, BED, or obesity. Items are rated on a 5-point scale. The NESS has demonstrated treatment sensitivity, but its psychometric properties have not been reported.

Eating Behaviors Questionnaire

The Eating Behaviors Questionnaire (EBQ) (118) is a 20-item self-report measure that was developed to assess for symptoms of food addiction. Both child and adult versions are available. Items were developed based on modified DSM-IV-TR criteria for substance use disorders and include assessment of tolerance and cravings, as well as distress and impairment related to excessive food consumption. For each item, respondents use a 6-point scale ranging from “never” to “always” to describe their experience of each symptom. The measure can be completed in 5 to 10 minutes, but psychometric properties have not been established.

If a patient obtains a positive score on an eating disorder screening questionnaire, the addiction clinician should evaluate further to determine whether immediate eating disorder intervention is necessary. For example, it is important to note that there can be symptom overlap between eating disorders and addiction disorders (weight loss, lethargy, changes in eating habits, etc.), and these symptoms do not necessarily signify a comorbid eating disorder unless the associated symptoms (e.g., body image disturbance, concerns about gaining weight, lack of control over eating) are also present.


Like addiction treatment, the treatment of eating disorders can be a long and arduous process marked by alternating periods of relapse and recovery.

Acute Treatment

For serious cases, and particularly for adolescent patients, treatment may commence on a coerced or even involuntary basis through enrollment in an inpatient or residential program. A focus on refeeding takes precedence in order to medically stabilize the patient and restore cognitive functioning so that he or she is able to participate in the treatment process.

Subacute Treatment

As with addiction treatment, the patient is more likely to be successful if he or she agrees to treatment and is motivated to change his or her behavior. As a result, motivational interviewing interventions may be useful in helping the patient to recognize the need for treatment and to increase his or her willingness to enter and participate in a treatment program (119,120).

Long-Term Treatment

Management of an eating disorder typically involves a multidisciplinary team and includes psychosocial, behavioral, and pharmacologic interventions. Psychotherapy often includes both individual sessions and family sessions. Depending on the severity of symptoms and presence of comorbid addiction or psychiatric disorders, treatment may be administered in outpatient, partial hospitalization, inpatient, or residential settings. No matter the treatment milieu or modality, development of a treatment contract specifying goals and expectations related to each disorder may be beneficial.


Acute Biologic Management of AN

Generally, patients who are considered medically or psychiatrically unstable are referred for inpatient care (121). Individuals with comorbid addiction disorders may also be referred for more intensive treatment owing to the increased psychological strain associated with attempting to simultaneously abstain from two maladaptive coping mechanisms (i.e., substance use and disordered eating or purging) and the increased medical risks associated with these conditions. Whether the patient has a comorbid addiction disorder or not, the medical management of AN begins with a comprehensive medical and neurologic evaluation and treatment of medical comorbidities. Rehydrating and refeeding safely are the keys to the medical intervention. While the establishment of weight gain is a goal, it is important to be certain that an electrolyte, cardiac, or other disease does not kill the patient or compromise the patient’s ability to be treated or recover.

Subacute Biologic Management of AN

In cases of comorbid AN and addiction disorders, once medical issues are resolved, it is generally recommended that addiction treatment take priority unless the patient is at immediate medical risk due to malnutrition. Once the patient achieves stable sobriety, the treatment for AN may begin. Individuals with AN are generally terrified of gaining weight (much as the addict may be terrified of living without his drug of choice), so weight gain should be implemented gradually (e.g., 0.5 to 1.0 pound per week). The American Dietetic Association recommends nutrition intervention and nutritional counseling by a registered dietician as an integral part of treatment for AN (122). Thus, every addiction counselor should establish contact with a credible referral source to assist with this component of treatment. Referral to a mental health professional who specializes in eating disorders may also be beneficial for many patients. Among adolescents, weight gain may best be achieved using a family intervention referred to as the Maudsley method. This approach involves encouraging parents to take an active role in promoting their child’s weight regain (123). However, neither this method nor other forms of family therapy are generally efficacious for adult patients with AN (124,125). Nutritional rehabilitation and weight restoration treatment for adult patients and some adolescents generally consist of utilizing behavioral reinforcement to reward eating. It has been suggested that parenteral nutrition and nasogastric feeding be avoided, if possible, owing to concerns that the patient may relapse or develop other symptoms (e.g., purging) to compensate for her or his weight gain (126). However, there is some evidence that nocturnal nasogastric feeding may increase weight gain (127).

Long-Term Biologic Management of AN

The process of gaining weight is often very stressful for patients with AN, and the addiction clinician may wish to monitor the patient more closely during the weight restoration period to assess for signs of addiction relapse. Thus far, no pharmacologic treatments have proven effective in treatment of the primary symptoms of AN (124,128). However, selective serotonin reuptake inhibitors (SSRIs) may help to decrease associated symptoms such as depression, obsessive– compulsive symptoms, and lack of interoceptive awareness (129,130). Like parenteral feeding, it is recommended that medications to promote weight gain be used judiciously in order to avoid overwhelming the patient. However, use of calcium supplements and a multivitamin is recommended (131). Oral contraceptives or hormone replacement therapy may be prescribed to help regulate the menstrual cycle, mitigate effects of hypoestrogenemia, and minimize bone loss (132,133). Some patients with a comorbid addiction disorder may prefer to avoid prescription medications in order to maintain their focus on sobriety from all mood-altering drugs. Benzodiazepines are often wrongly prescribed to patients with AN to help them remain calm at meal time so they may eat more. Benzodiazepines are not indicated for the treatment of any eating disorder and should be tapered and discontinued during the course of their addiction disorder treatment.

Acute Biologic Management of BN

Management of medical complications associated with BN may be necessary. For example, estrogen replacement may be indicated to combat hypothalamic hypogonadism. Physicians should monitor patients with BN to assess for fluid and electrolyte abnormalities, cardiac arrhythmias, gastrointestinal symptoms, and reproductive problems. BN patients with comorbid addiction disorders are more likely to have medical complications; a general medical workup may be indicated for these patients.

Subacute Biologic Management of BN

As in AN, patients with BN who have a comorbid addiction disorder should be treated first for their addiction. Once in stable sobriety, biologic management of BN generally involves medication with an SSRI. Specifically, fluoxetine has demonstrated efficacy in reducing the core symptoms of BN and has been shown to lower treatment dropout rates (134,135). The suggested dosage is approximately 60 mg/d. Other medications with demonstrated efficacy include desipramine, up to 300 mg/d (136,137); imipramine, up to 300 mg/d (138,139); and topiramate, titrated from 25 mg/d up to 250 mg/d or 400 mg/d (140,141).

Long-Term Biologic Management of BN

With any medication, it is recommended that pharmacotherapy be combined with cognitive–behavioral therapy (CBT), as described later (141145). Individuals with a comorbid addiction disorder who prefer not to take prescription medication should be referred directly for CBT for BN. Among those who are willing to take medications, pharmacotherapy for comorbid psychiatric conditions should also be considered. Given the detrimental effects of digestive juices on tooth enamel and oral health, a dental exam is recommended for patients with BN who engage in purging through vomiting (143), as well as those with the binge–purge subtype of AN.

Biologic Management of BED

Though there is currently no treatment for BED approved by the Food and Drug Administration (FDA), experimental treatments of binge eating with various pharmacologic agents have provided positive results. After the BED patient with comorbid addiction achieves sobriety, there are several options for medication management to assist with BED symptoms. For example, several SSRIs (e.g., sertraline, 50 to 200 mg/d; fluvoxamine, 50 to 300 mg/d; fluoxetine, 20 to 80 mg/d; and citalopram, 20 to 60 mg/d) have demonstrated efficacy (146149). In addition, as with binge drinking, topiramate (50 to 600 mg/d) has shown utility in decreasing the number of binge eating episodes per week, decreasing BMI, and shortening the time to recovery (150). Similar to treatment of AN and BN, pharmacologic treatment of comorbid psychiatric conditions in BED patients may be warranted if permitted within the patient’s sobriety goal. Finally, given that overweight and obesity may be consequences of BED, additional medical management may be necessary to prevent or treat associated conditions (e.g., hypertension, type II diabetes, hypercholesteremia, hyperlipidemia).

Acute Biologic Management of Obesity

Treating obesity is very difficult and complex because of the short and long feedback loops and the importance of eating to survive (151).

Biologic management of obesity is generally considered a three-tiered approach that begins with changes in diet and increased exercise. If additional assistance is needed, medications can be added, or surgery can be considered. When patients display morbid obesity, particularly with additional risk factors such as hypertension and type II diabetes, Roux-en-Y gastric bypass surgery or lap-band surgery may be performed. Research has demonstrated that these surgeries result in sustained weight loss with decreased prevalence of health conditions (e.g., type II diabetes) related to obesity (152154). Unfortunately, though these surgeries can be lifesaving for many patients, they are associated with risk of rehospitalization (e.g., due to ventral hernia repair and gastric revision) (155) and early mortality, particularly in elderly patients (156). In addition, bariatric surgery should not be considered without a full psychiatric evaluation, including an addiction disorder assessment, as psychiatric and substance use comorbidities are common among bariatric surgery candidates (157) and can affect the success of surgery. Clinical evidence suggests that individuals who undergo bariatric surgery may be at increased risk of developing addictions post-surgery, and patients with a history of addiction disorders may be particularly at risk, as alcohol absorption and metabolism is considerably changed after bariatric surgery (158,159)

Subacute Biologic Management of Obesity

If bariatric surgery is not yet indicated, antiobesity medication may be utilized. Antiobesity medications have had a rich though mixed history due to side effects, with many medications withdrawn from the market (160). Until recently, only three drugs were approved by the FDA for weight loss; two of them (phentermine and diethylpropion) are appetite suppressants for short-term (i.e., less than a year) use only. Orlistat, a fat inhibitor, has a mechanism similar to that of Antabuse, wherein individuals taking orlistat experience severe gastrointestinal symptoms after eating a high-fat meal (147,149).

Given the need for effective obesity treatments, several new antiobesity medications have recently been introduced, though long-term data are needed to fully understand their efficacy and potential side effects (161). For example, one experimental medication for the treatment of obesity combines the FDA-approved medications bupropion SR and naltrexone SR. This sustained-release medication is currently in Phase III clinical trials (160). Bupropion and naltrexone have each demonstrated effectiveness in promoting weight loss (162). In addition, research comparing the bupropion SR/ naltrexone SR combination pill plus diet modification and exercise against a placebo pill plus diet modification and exercise demonstrated positive results (163). Lorcaserin, which was recently approved by the FDA, is a selective serotonin receptor agonist that is believed to suppress appetite signals in order to promote weight loss (164). This medication has been associated with improved weight loss in trials involving overweight and obese patients, including those with Type II diabetes (165,166). Finally, another newly approved medication combines the drugs phentermine (an appetite suppressant) and topiramate XR (an anticonvulsant with weight loss side effects) as a treatment for obesity (167). This medication has demonstrated efficacy in promoting weight loss, but the FDA recommends monitoring patients for cardiovascular risk, with an indication against use by pregnant women (168).

Long-Term Biologic Management of Obesity

Lifestyle changes including improved diet and increased exercise are recommended for long-term management of obesity. These interventions are recommended for all obese patients, including those who are prescribed antiobesity medication or undergo bariatric surgery.


Acute Psychological Management

As in treatment for addiction disorders, for all eating disorder patients, behavioral intervention strategies can be extremely useful. Many of the same issues arise during therapy for addiction disorders and eating disorders. Thus, participation in addiction treatment may provide a strong foundation from which to work toward management of disordered eating symptoms as well. For example, learning better ways to communicate with family and handle conflict may reduce the need for maladaptive coping through both substance use and disordered eating. Practicing these strategies during addiction treatment may give the patient confidence to implement similar strategies in order to manage the eating disorder symptoms. For example, establishing a daily routine, self-monitoring using a food journal, developing structured meal times, ensuring the availability of nutritious and “safe” foods, and limiting exposure to triggers for bingeing or purging can be effective ways to promote recovery from an eating disorder.

Specifically for AN patients, both family therapy and individual therapy have demonstrated efficacy, though family therapy may be particularly beneficial for younger patients (169,170). CBT has consistently been shown to reduce the risk for relapse and improve outcome for AN patients (123,171,172). Again, many of the skills developed during CBT for an addiction disorder can be easily transferred to eating disorder treatment (e.g., challenging dysfunctional cognitions, behavioral experiments). As stated previously, management of BN is generally enhanced by combining pharmacotherapy with CBT. CBT is currently recommended as the first-line treatment for BN, given its demonstrated efficacy in multiple trials (173175). As with AN, treatment for BN should commence once sobriety is attained. CBT can be administered either individually or in a group setting and is generally included as part of both residential and outpatient treatment programs. Among BED patients without comorbid addiction disorders, psychotherapy appears to be most successful when administered as either individual or group CBT (124), though interpersonal psychotherapy has also demonstrated efficacy (176,177). With regard to obesity symptoms, behavioral weight loss strategies have demonstrated positive outcomes in the short term, particularly with regard to weight loss (178); however, CBT appears to be a superior treatment for the symptoms of BED over time (179). Again, when the eating disorder patient has a comorbid addiction disorder, it is important to continue monitoring the patient closely in order to be vigilant for signs of relapse. Therapy should focus on developing new adaptive coping skills to replace the addiction and eating disorder symptoms.

Subacute Psychological Management

Social support can be beneficial to individuals as they undergo treatment and recovery. As in addiction treatment, group therapy may be an appropriate and useful component of a comprehensive program. Patients can learn that they are not alone in their struggles with disordered eating, share their challenges and successes, and learn from one another’s experiences. However, for individuals admitted to treatment involuntarily (and particularly those with AN), group therapy may be contraindicated. In some cases, this may lead to competition among the patients to be the “thinnest” in the group or sharing of maladaptive strategies to continue losing weight.

Eating disorders occur frequently within close-knit groups (e.g., “cliques” of friends, sports teams, sororities), particularly among adolescent females and young adults (180,181). Socially valued behaviors (e.g., food restriction) appear to increase with social proximity, whereas nonvalued behaviors (e.g., binge eating, purging) appear to decrease (182). However, levels of binge eating appear to grow more similar among females as their friendship grows closer (183). As a result, large-scale prevention and intervention programs are important and can be effective in managing the incidence and prevalence of AN, BN, and BED (184,185).

Long-Term Psychological Management

Among motivated individuals, and particularly those who have participated successfully in Alcoholics Anonymous (AA) or Narcotics Anonymous, referral to a 12-step program for eating disorders may be beneficial. Eating Disorders Anonymous (EDA) follows many of the tenets of AA (e.g., 12 steps and 12 traditions), but—given that food is necessary for survival—it focuses on “balance” rather than “abstinence” as the goal. Eating disorder symptoms (e.g., restricting, bingeing, purging) are viewed as ways of coping with stress, so the program focuses more on developing alternate adaptive coping strategies rather than focusing on eating habits per se. EDA participants are encouraged to work with a sponsor or “buddy” on their path to recovery. Similarly, Overeaters Anonymous (OA) is a 12-step fellowship program following in the tradition of AA. OA meetings focus primarily on the needs of individuals with compulsive eating or binge eating symptoms. It may be particularly useful for individuals who appear to suffer from a food addiction. OA participants view overeating as similar to an alcohol or drug addiction and work toward the goal of abstaining from overeating. Like EDA and other 12-step groups, OA stresses the importance of anonymity within the group as well as fellowship and spirituality on the road to recovery.


Comorbid Addiction Disorders

Comorbidity of addiction and eating disorders may negatively affect treatment prognosis (186), though many publicly funded addiction treatment programs are not able to admit/treat all patients with comorbid eating disorders (187). In fact, eating disorder symptoms may serve as a coping mechanism for some patients with addiction disorders. Thus, as described previously, it is typically recommended that individuals be treated first for their addiction disorder. In addition, when substance abuse is comorbid with AN, it is generally suggested that treatment occur in a residential treatment facility where both issues can be addressed (188). Recovery rates for AN with comorbid substance abuse, especially alcohol abuse, are generally poor; indeed, suffering from these conditions in combination is a strong predictor of fatal outcome (37,189). On the other hand, though studies have shown that BN patients with a comorbid addiction disorder have treatment outcomes similar to those without a history of substance abuse (23,190), addiction patients with bingeing symptoms may have a worse outcome than those without bingeing (191). Individuals who suffer from BED with a comorbid addiction disorder generally show outcomes similar to those without an addiction disorder (75).

General Recovery Rates

Research has demonstrated recovery rates for eating disorders to be between approximately 40% and 94%, with better recovery rates and outcome for BN than for AN (192194). BN generally is not fatal, whereas the mortality rate for those with AN is about 10% (2). In terms of general treatment prognosis, about half of individuals with AN have good outcomes, approximately 30% display intermediate outcomes, and one in five individuals with AN has a poor outcome. With regard to BN, about 45% of patients display a good outcome, 18% have an intermediate outcome, and 21% have a poor outcome (92). Among BED patients, there is some evidence that the disorder will spontaneously remit over time (195), though other research has suggested a more chronic nature, particularly among patients who are older, who are more obese, and who meet full diagnostic criteria (196). As is seen among individuals recovering from addiction disorders, the vacillation between dieting (i.e., “abstinence”) and overeating (i.e., “active use”) is common among individuals struggling with obesity or BED (197).

Disordered Eating after Addiction Treatment

After treatment for an addiction disorder, some individuals who are abstaining from drug or alcohol use may compensate for this lack of chemical reinforcement by overeating. Preliminary research has demonstrated significant weight gain among a group of adolescents who completed treatment and maintained abstinence from substances of abuse (78). More research is currently underway to examine this phenomenon among adult patients. In addition, one study has documented the significant rates of past addiction disorders among extremely obese individuals considering bariatric surgery. Kalarchian et al. (198) reported that one-third of these individuals were in recovery from an addiction disorder, whereas fewer than 2% had a current diagnosis. Though information was not available regarding their weight at the time of active substance abuse, clinical experience suggests that many of these individuals became obese after treatment for their addiction disorders. In addition, presence of an eating disorder is associated with increased risk for a relapse to substance use. Individuals who are attempting to manage their disordered eating symptoms may turn to drugs or alcohol as an alternate coping strategy. As a result, the addiction clinician should be vigilant to symptoms of overeating or disordered eating among substance use disorder patients and should provide all patients with preventative counseling and referral to a registered dietitian.


As mentioned previously, further research is needed to explore and evaluate the concept of obesity as a consequence of a food addiction. Though various authors have written to support or refute this topic (58,28,199,200), larger controlled and prospective studies are needed to determine the indicators of food addiction and its similarities and dissimilarities with other addictions. In addition, obesity and food addiction may warrant consideration for inclusion in future revisions of the DSM (15,16).

Finally, as research data accumulate demonstrating the similarities among the various eating disorders and addiction disorders, the addiction clinician will likely need to gain further experience with the identification and treatment of these serious diseases. Future work might focus on the development of additional brief screening devices (e.g., a “CAGE”-type questionnaire for eating disorders) as well as alternate treatment strategies built on the principles developed within the field of addiction medicine. For example, eating disorder treatments may increasingly capitalize on methods such as contingency management, pharmacotherapies, and long-term residential care for eating disorders and obesity. Addiction clinicians and eating disorder specialists would likely benefit from opportunities to network and share methods and ideas in order to maximize care for these commonly comorbid disorders.


Eating disorders (e.g., AN, BN, and BED) are serious conditions that necessitate timely detection and intervention. These disorders have both psychological and medical consequences that can be life threatening. Comorbidity with addiction disorders is common, and it is recommended that all individuals undergoing treatment for an addiction disorder be screened for disordered eating behaviors. When present, serious disordered eating symptoms may complicate treatment for addiction disorders. Individuals should be medically stabilized before beginning addiction treatment. However, once stable, treatment should focus on recovery from the addiction disorder before treatment for the eating disorder commences. Eating disorders and addiction disorders share many similarities with regard to underlying psychopathology and lack of adaptive coping skills. Treatments for both disorders are frequently complementary. Skills learned in the management of an addiction disorder can often be applied to the management of eating disorders and vice versa.


1.Volkow ND, Wise RA. How can drug addiction help us understand obesity? Nat Neurosci 2005;8:555–560.

2.American Psychiatric Association. Diagnostic and statistical manual of mental disorders, 4th ed. Washington, DC: American Psychiatric Association, 2000.

3.Cassin SE, von Ranson KM. Is binge eating experienced as an addiction? Appetite 2007;49:687–690.

4.Gearhardt AN, Corbin WR, Brownell KD. Food addiction: an examination of the diagnostic criteria for dependence. J Addict Med 2009;3:1–7.

5.Wang G, Volkow ND, Thanos PK, et al. Similarity between obesity and drug addiction as assessed by neurofunctional imaging: a concept review. J Addict Dis 2004;23:39–53.

6.Gold MS, Frost-Pineda K, Jacobs WS. Overeating, binge eating, and eating disorders as addictions. Psychiatr Ann 2003;33:117–122.

7.Avena NM, Bocarsly ME, Hoebel BG, et al. Overlaps in the nosology of substance abuse and overeating: the translational implications of “food addiction”. Curr Drug Abuse Rev2011;4:133–139.

8.Avena NM, Gold JA, Kroll C, et al. Further developments in the neurobiology of food and addiction: update on the state of the science. Nutrition 2012;28:341–343.

9.Johnson PM, Kenny, PJ. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nat Neurosci 2010;13:635–641.

10.Volkow ND, Wang GJ, Telang F, et al. Low dopamine striatal D2 receptors are associated with prefrontal metabolism in obese subjects: possible contributing factors. Neuroimage2008;42:1537–1543.

11.Stice E, Spoor S, Bohon C, et al. Relation of reward from food intake and anticipated food intake to obesity. A functional magnetic resonance imaging study. J Abnorm Psychol2008;117:924–935.

12.Gearhardt AN, Yokum S, Orr PT, et al. Neural correlates of food addiction. Arch Gen Psychiatry 2011;68:808–816.

13.Kenna GA, Swift RM, Hillemacher T, et al. The relationship of appetitive, reproductive and posterior pituitary hormones to alcoholism and craving in humans. Neuropsychol Rev2012;22(3):211–228.

14.Meule A, Kubler A. Food cravings in food addiction: the distinct role of positive reinforcement. Eat Behav 2012;13:252–255.

15.Moreno C, Tandon R. Should overeating and obesity be classified as an addictive disorder in DSM-5? Curr Pharm Des 2011;17:1128–1131.

16.Volkow ND, O’Brien CP. Issues for DSM-5: should obesity be included as a brain disorder? Am J Psychiatry 2007;164:708–710.

17.Couturier J, Lock J. Denial and minimization in adolescents with anorexia nervosa. Int J Eat Disord 2006;39:212–216.

18.Kreipe RE, Birndorf SA. Eating disorders in adolescents and young adults. Med Clin North Am 2000;84:1027–1049.

19.Katzman DK. Medical complications in adolescents with anorexia nervosa: a review of the literature. Int J Eat Disord 2005;37(Suppl):S52–S59.

20.Miller KK, Grinspoon SK, Ciampa J, et al. Medical findings in outpatients with anorexia nervosa. Arch Intern Med 2005;165:561–566.

21.Cartwright MM. Eating disorder emergencies: understanding the medical complexities of the hospitalized eating disordered patient. Crit Care Nurs Clin North Am 2004;16:515–530.

22.Eddy KT, Keek PK, Dorer DJ, et al. Longitudinal comparison of anorexia nervosa subtypes. Int J Eat Disord 2002;31:191–201.

23.Franko DL, Dorer DJ, Keel PK, et al. How do eating disorders and alcohol use disorder influence each other? Int J Eat Disord 2005;38:200–207.

24.Franko DL, Keel PK. Suicidality in eating disorders: occurrence, correlates, and clinical implications. Clin Psychol Rev 2006;26: 769–782.

25.Neumarker K. Mortality rates and causes of death. Eur Eat Disord Rev 2000;8:181–187.

26.Rytomaa I, Jarvinen V, Kanerva R, et al. Bulimia and tooth erosion. Acta Odontol Scand 1998;56:36–40.

27.Mehler PS, Crews C, Weiner K. Bulimia: medical complications. J Womens Health 2004;13:668–675.

28.Avena NM, Rada P, Hoebel BG. Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev 2008;32:20–39.

29.Rada P, Avena NM, Hoebel BG. Daily binging on sugar repeatedly releases dopamine in the accumbens shell. Neuroscience 2005;134:737–744.

30.Gearhardt AN, White MA, Masheb RM, et al. An examination of the food addiction construct in obese patients with binge eating disorder. Int J Eat Disord 2012;45:657–663.

31.Davis C, Curtis C, Levitan RD, et al. Evidence that “food addiction” is a valid phenotype of obesity. Appetite 2011;57:711–717.

32.Gruzca RA, Przybeck TR, Cloninger CR. Prevalence and correlates of binge eating disorder in a community sample. Compr Psychiatry 2007;48:124–131.

33.Pagoto S, Bodenlos JS, Kantor L, et al. Association of major depression and binge eating disorder with weight loss in a clinical setting. Obesity 2007;15:2557–2559.

34.Bulik CM, Reichborn-Kjennerud T. Medical morbidity in binge eating disorder. Int J Eat Disord 2003;34:S39–S46.

35.Raman RP. Obesity and health risks. J Am Coll Nutr 2002;21:S134–S139.

36.Pi-Sunyer FX. The medical risks of obesity. Obes Surg 2002;12:S6–S11.

37.Keel PK, Klump KL. Are eating disorders culture-bound syndromes? Implications for conceptualizing their etiology. Psychol Bull 2003;129:747–769.

38.Anderson-Fye EP, Becker AE. Cultural aspects of eating disorders across cultures. In: Thompson JK, ed. The handbook of eating disorders and obesity. London, UK: Wiley, 2003.

39.Hoek HW, Bartelds AI, Bosveld JJ, et al. Impact of urbanization on detection rates of eating disorders. Am J Psychiatry 1995;152:1272–1278.

40.Hoek HW. The incidence and prevalence of anorexia nervosa and bulimia nervosa in primary care. Psychol Med 1991;21:455–460.

41.Silber TJ. Anorexia nervosa in blacks and Hispanics. Int J Eat Disord 1986;5:121–128.

42.Yates A. Current perspectives on the eating disorders: I. history, psychological and biological aspects. J Am Acad Child Adolesc Psychiatry 1989;28:813–828.

43.Soomro GM, Crisp AH, Lynch D, et al. Anorexia nervosa in ‘nonwhite’ populations. Br J Psychiatry 1995;167:385–389.

44.Becker AE, Burwell R, Gilman S, et al. Disordered eating behaviors and attitudes follow prolonged exposure to television among ethnic Fijian adolescent girls. Br J Psychiatry2002;180:509–514.

45.Klump KL, Miller KB, Keel PK, et al. Genetic and environmental influence on anorexia nervosa syndromes in a population-based twin sample. Psychol Med 2001;31:737–740.

46.Kendler KS, Walters EE, Neale MC, et al. The structure of the genetic and environmental risk factors for six major psychiatric disorders in women: phobia, generalized anxiety disorder, panic disorder, bulimia, major depression, and alcoholism. Arch Gen Psychiatry 1995;52:374–383.

47.Bulik CM, Sullivan PF, Kendler KS. Heritability of binge-eating and broadly defined bulimia nervosa. Biol Psychiatry 1998;44:1210–1218.

48.Walsh JM, Wheat ME, Freund K. Detection, evaluation, and treatment of eating disorders: the role of the primary care physician. J Gen Intern Med 2000;15:577–590.

49.Hudson JI, Hiripi E, Pope HG Jr, et al. The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication. Biol Psychiatry 2007;61:348–358.

50.Bulik CM, Sullivan PF, Tozzi F, et al. Prevalence, heritability, and prospective risk factors for anorexia nervosa. Arch Gen Psychiatry 2006;63:305–312.

51.Wade TD, Bergin JL, Tiggemann M, et al. Prevalence and long-term course of lifetime eating disorders in an adult Australian twin cohort. Aust N Z J Psychiatry 2006;40:121–128.

52.Ackard DM, Fulkerson JA, Neumark-Sztanier D. Prevalence and utility of DSM-IV eating disorder diagnostic criteria among youth. Int J Eat Disord 2007;40:409–417.

53.Hoek H, van Hoeken, D. Review of the prevalence and incidence of eating disorders. Int J Eat Disord 2003;34:383–396.

54.Alegria M, Woo M, Cao Z, et al. Prevalence and correlates of eating disorders in Latinos in the United States. Int J Eat Disord 2007;40:515–521.

55.Grucza R, Przybeck TR, Cloninger CR. Prevalence and correlates of binge eating disorder in a community sample. Compr Psychiatry 2007;48:124–131.

56.Mussel MP, Mitchell JE, Weller CL, et al. Onset of binge eating, dieting, obesity, and mood disorders among subjects seeking treatment for binge eating disorder. Int J Eat Disord1995;17:395–401.

57.Spurrell EB, Wilfley DE, Tanofsky MB, et al. Age of onset for binge eating: are there different pathways to binge eating? Int J Eat Disord 1997;21:55–65.

58.Parikh N, Pencina MJ, Wang TJ, et al. Increasing trends in incidence of overweight and obesity over 5 decades. Am J Med 2007;120:242–250.

59.Ogden C, Carroll MD, Curtin LR, et al. Prevalence of overweight and obesity in the United States, 1999–2004. JAMA 2006;295:1549–1555.

60.National Center for Chronic Disease Prevention and Promotion. Defining overweight and obesity, 2004. obesity/trend/index.htm, accessed December 4, 2008.

61.Mendez M, Monteiro CA, Popkin BM. Overweight exceeds underweight among women in most developing countries. Am J Clin Nutr 2005;81:714–721.

62.Hoerr SL, Bokram R, Lugo B, et al. Risk for disordered eating relates to both gender and ethnicity for college students. J Am Coll Nutr 2002;21:307–314.

63.O’Dea JA, Abraham S. Eating and exercise disorders in young college men. J Am Coll Health 2002;50:273–278.

64.Marcus MD, Bromberger JT, Wei HL, et al. Prevalence and selected correlates of eating disorder symptoms among a multiethnic community sample of midlife women. Ann Behav Med2007;33:269–277.

65.Jonas JM, Gold MS. Naltrexone treatment of bulimia: clinical and theoretical findings linking eating disorders and substance abuse. Adv Alcohol Subst Abuse 1988;7:29–37.

66.Root TL, Pinheiro AP, Thornton L, et al. Substance use disorders in women with anorexia nervosa. Int J Eat Disord 2010;43:14–21.

67.Hasin D, Sarnet S, Nunes E, et al. Diagnosis of comorbid psychiatric disorders in substance users assessed with the psychiatric research interview for substance and mental disorders for DSM-IV. Am J Psychiatry 2006;163:689–696.

68.Castel S, Rush B, Urbanoski K, et al. Overlap of clusters of psychiatric symptoms among clients of a comprehensive addiction treatment service. Psychol Addict Behav 2006;20:28–35.

69.Holderness CC, Brooks-Gunn J, Warren MP. Co-morbidity of eating disorders and substance abuse: review of the literature. Int J Eat Disord 1994;16:1–34.

70.Herzog DB, Franko DL, Dorer DJ, et al. Drug abuse in women with eating disorders. Int J Eat Disord 2006;39:364–368.

71.Castro-Fornieles J, Díaz R, Goti J, et al. Prevalence and factors related to substance use among adolescents with eating disorders. Eur Addict Res 2010;16(2):61–68.

72.Piran N, Robinson SR. Associations between disordered eating behaviors and licit and illicit substance use and abuse in a university sample. Addict Behav 2006;31:1761–1775.

73.Conason AH, Sher L. Alcohol use in adolescents with eating disorders. Int J Adolesc Med Health 2006;18:31–36.

74.Blinder BJ, Cumella EJ, Sanathara VA. Psychiatric comorbidities of female inpatients with eating disorders. Psychosom Med 2006;68:454–462.

75.Wilfley DE, Friedman MA, Dounchis JZ, et al. Comorbid psychopathology in binge eating disorder: relation to eating disorder severity at baseline and following treatment. J Consult Clin Psychol2000;68:641–649.

76.Stewart S, Brown, CG, Devoulyte, K, et al. Why do women with alcohol problems binge eat? Exploring connections between binge eating and heavy drinking in women receiving treatment for alcohol problems. J Health Psychol 2006;11:409–425.

77.Avena NM, Carrillo CA, Needham L, et al. Sugar-dependent rats show enhanced intake of unsweetened ethanol. Alcohol 2004;34:203–209.

78.Hodgkins CC, Jacobs WS, Gold MS. Weight gain after adolescent drug addiction treatment and supervised abstinence. Psychiatr Ann 2003;33:112–116.

79.Koopmann A, Dinter C, Grosshans M, et al. Psychological and hormonal features of smokers at risk to gain weight after smoking cessation–results of a multicenter study. Horm Behav2011;60:58–64.

80.Neale J, Nettleton S, Pickering L, et al. Eating patterns among heroin users: a qualitative study with implications for nutritional interventions. Addiction 2012;107:635–641.

81.Kleiner KD, Gold MS, Frost-Pineda K, et al. Body mass index and alcohol use. J Addict Dis 2004;23:105–118.

82.Warren M, Frost-Pineda K, Gold MS. Body mass index and marijuana use. J Addict Dis 2005;24:95–100.

83.Gold MS. From bedside to bench and back again: a 30-year saga. Physiol Behav 2011;104:157–161.

84.Piran N, Robinson S. The association between disordered eating and substance use and abuse in women: a community-based investigation. Women Health 2006;44:1–20.

85.Jonas JM, Gold MS, Sweeney D, et al. Eating disorders and cocaine abuse: a survey of 259 cocaine abusers. J Clin Psychiatry 1987;48:47–50.

86.Teter CJ, McCabe SE, LaGrange K, et al. Illicit use of specific prescription stimulants among college students: prevalence, motives, and routes of administration. Pharmacotherapy2006;26:1501–1510.

87.Stock SL, Goldberg E, Corbett S, et al. Substance use in female adolescents with eating disorders. J Adolesc Health 2002;31:176–182.

88.Pomerleau CS, Zucker AN, Stewart AJ. Characterizing concerns about postcessation weight gain: results from a national survey of women smokers. Nicotine Tob Res 2001;3:51–60.

89.Kaye WH, Bulik CM, Thornton L, et al. Comorbidity of anxiety disorders with anorexia nervosa and bulimia nervosa. Am J Psychiatry 2004;161:2215–2221.

90.Milos G, Spindler A, Ruggiero G, et al. Comorbidity of obsessive-compulsive disorders and duration of eating disorders. Int J Eat Disord 2002;31:284–289.

91.Milos G, Spindler A, Schnyder U. Psychiatric comorbidity and Eating Disorder Inventory (EDI) profiles in eating disorder patients. Can J Psychiatry 2004;49:179–184.

92.Herzog DB, Nussbaum KM, Marmor AK. Comorbidity and outcome in eating disorders. Psychiatr Clin North Am 1996;19:843–859.

93.Westen D, Harnden-Fischer J. Personality profiles in eating disorders: rethinking the distinction between axis I and axis II. Am J Psychiatry 2001;158:547–562.

94.Telch CF, Stice E. Psychiatric comorbidity in women with binge eating disorder prevalence rates from a non-treatment seeking sample. J Consult Clin Psychol 1998;66:768–776.

95.Kasen S, Cohen P, Chen H, et al. Obesity and psychopathology in women: a three decade prospective study. Int J Obes (Lond) 2007;32:558–566.

96.Currin L, Schmidt U, Treasure J, et al. Time trends in eating disorder incidence. Br J Psychiatry 2005;186:132–135.

97.Turnbull S, Ward A, Treasure J, et al. The demand for eating disorder care: an epidemiological study using the general practice research database. Br J Psychiatry 1996;169:705–712.

98.Rodin G, Craven J, Littlefield C, et al. Eating disorders and intentional insulin undertreatment in adolescent females with diabetes. Psychosomatics 1991;32:171–176.

99.Bruce B, Agras WS. Binge eating in females: a population-based investigation. Int J Eat Disord 1992;12:365–373.

100.Bruce B, Wilfley DE. Binge eating among the overweight population: a serious and prevalent problem. J Am Diet Assoc 1996;96:58–61.

101.Hudson J, Lalonde JK, Berry JM, et al. Binge-eating disorder as a distinct familial phenotype in obese individuals. Arch Gen Psychiatry 2006;63:313–319.

102.Beals KA, Manore MM. Disorders of the female athlete triad among collegiate athletes. Int J Sport Nutr Exerc Metab 2002;12:281–293.

103.Reinking MF, Alexander LE. Prevalence of disordered-eating behaviors in undergraduate female collegiate athletes and nonathletes. J Athl Train 2005;40:47–51.

104.Becker AE, Grinspoon SK, Klibanski A, et al. Eating disorders. N Engl J Med 1999;340:1092–1098.

105.Mehler PS. Diagnosis and care of patients with anorexia nervosa in primary care settings. Ann Intern Med 2001;134:1048–1059.

106.Pritts SD, Susman J. Diagnosis of eating disorders in primary care. Am Fam Physician 2003;67:297–304.

107.Strote J, Lee JE, Wechsler H. Increasing MDMA use among college students: results of a national survey. J Adolesc Health 2002;30:64–72.

108.Gearhardt AN, Corbin WR, Brownell KD. Preliminary validation of the Yale Food Addiction Scale. Appetite 2009;52:430–436.

109.Garner DM. Eating disorder inventory-3. In: Professional manual. Lutz, FL: Psychological Assessment Resources, 2004.

110.Cumella EJ. Review of the eating disorder inventory-3. J Pers Assess 2006;87:116–117.

111.Clausen L, Rosenvinge JH, Friborg O, et al. Validating the eating disorder inventory-3 (EDI-3): a comparison between 561 female eating disorders patients and 878 females from the general population. J Psychopathol Behav Assess 2011;33:101–110.

112.Stice E, Telch CF, Rizvi SL. Development and validation of the Eating Disorder Diagnostic Scale: a brief self-report measure of anorexia, bulimia, and binge eating disorder. Psychol Assess 2000;12:123–131.

113.Fairburn CG, Beglin SJ. Assessment of eating disorders: interview or self-report questionnaire? Int J Eat Disord 1994;16:363–370.

114.Thelen MH, Farmer J, Wonderlich S, et al. A revision of the Bulimia Test: the BULIT-R. Psychol Assess 1991;3:119–124.

115.Williamson DA, Anderson DA, Jackman LP, et al. Assessment of eating disordered thoughts, feelings, and behaviors. In: Allison DB, ed. Handbook of assessment methods for eating behaviors and weight-related problems. Thousand Oaks, CA: Sage, 1995.

116.Gormally J, Black S, Daston S, et al. The assessment of binge eating severity among obese persons. Addict Behav 1982;7:47–55.

117.O’Reardon JP, Stunkard AJ, Allison KC, Clinical trial of sertraline in the treatment of night eating syndrome. Int J Eat Disord 2004;35:16–26.

118.Merlo LJ, Klingman C, Malasanos TH, et al. Exploration of food addiction in pediatric patients: a preliminary investigation. J Addict Med 2007;3:26–32.

119.Dunn EC, Neighbors C, Larimer ME. Motivational enhancement therapy and self-help treatment for binge eaters. Psychol Addict Behav 2006;20:44–52.

120.Macdonald P, Hibbs R, Corfield F, et al. The use of motivational interviewing in eating disorders: a systematic review. Psychiatry Res 2012;200(1):1–11.

121.American Psychiatric Association. Practice guidelines for the treatment of patients with eating disorders revisions. Am J Psychiatry 2000;157:1–39.

122.American Dietetic Association. Position of the American Dietetic Association: nutrition intervention in the treatment of anorexia nervosa, bulimia nervosa, and other eating disorders. J Am Diet Assoc2006;106:2073–2082.

123.LeGrange D. The Maudsley family-based treatment for adolescent anorexia nervosa. World Psychiatry 2005;4:142–146.

124.Bulik CM, Berkman ND, Brownley KA, et al. Anorexia nervosa treatment: a systematic review of randomized controlled trials. Int J Eat Disord 2007;40:310–320.

125.Wilson GT. Psychological treatment of eating disorders. Annu Rev Clin Psychol 2005;1:439–465.

126.Tiller J, Schmidt U, Treasure J. Compulsory treatment for anorexia nervosa: compassion or coercion? Br J Psychiatry 1993;162: 649–680.

127.Robb AS, Silber TJ, Orrell-Valente JK, et al. Supplemental nocturnal nasogastric refeeding for better short-term outcome in hospitalized adolescent girls with anorexia nervosa. Am J Psychiatry2002;159:1347–1353.

128.Becker AE. Outpatient management of eating disorders in adults. Curr Womens Health Rep 2003;3:221–229.

129.Santonastaso P, Friederici S, Favaro A. Sertraline in the treatment of restricting anorexia nervosa: an open controlled trial. J Child Adolesc Psychopharmacol 2001;11:143–150.

130.Fassino S, Leombruni P, Daga G, et al. Efficacy of citalopram in anorexia nervosa: a pilot study. Eur Neuropsychopharmacol 2002;12:453–459.

131.Berger MM, Shenkin A. Vitamins and trace elements: practical aspects of supplementation. Nutrition 2006;22:952–955.

132.Cumming DC. Exercise-associated amenorrhea, low bone density and estrogen replacement therapy. Arch Intern Med 1996;156:2193–2195.

133.Klibanski A, Biller BMK, Schoenfield DA, et al. The effects of estrogen administration on trabecular bone loss in young women with anorexia nervosa. J Clin Endocrinol Metab1995;80:898–904.

134.Berkman ND, Bulik CM, Brownley KA, et al. Management of eating disorders. Evid Rep Technol Assess 2006;135:1–166.

135.Goldstein DJ, Wilson MG, Thompson VL, et al. Long term fluoxetine treatment of bulimia nervosa. Br J Psychiatry 1995;166:660–666.

136.Walsh BT, Wilson GT, Loeb KL, et al. Medication and psychotherapy in the treatment of bulimia nervosa. Am J Psychiatry 1997;154:523–531.

137.Walsh BT, Hadigan CM, Devlin MJ, et al. Long-term outcome of antidepressant treatment for bulimia nervosa. Am J Psychiatry 1991;148:1206–1212.

138.Agras WS, Rossiter EM, Arnow B, et al. Pharmacologic and cognitive behavioral treatment for bulimia nervosa: a controlled comparison. Am J Psychiatry 1992;149:82–87.

139.Mitchell JE, Pyle R, Eckert ED, et al. A comparison study of antidepressants and structured group psychotherapy in the treatment of bulimia nervosa. Arch Gen Psychiatry1990;47:149–157.

140.Nickel C, Tritt K, Muehlbacher M, et al. Topiramate treatment in bulimia nervosa patients: a randomized, double-blind, placebo-controlled trial. Int J Eat Disord 2005;38:295–300.

141.Hoopes SP, Reimherr FW, Hedges DW, et al. Treatment of bulimia nervosa with topiramate in a randomized, double-blind, placebo-controlled trial. Part 1: improvement in binge and purge measures. J Clin Psychiatry 2003;64:1335–1341.

142.Hay PJ, Backaltchuk J. Extracts from “clinical evidence”: bulimia nervosa. BMJ 2001;323:33–37.

143.Hay PJ. Understanding bulimia. Aust Fam Physician 2007;36: 708–712.

144.Ramoz N, Versini A, Gorwood P. Eating disorders: an overview of treatment responses and the potential impact of vulnerability genes and endophenotypes. Expert Opin Pharmacother2007;8:2049–2044.

145.Whittal ML, Agras WS, Gould RA. Bulimia nervosa: a meta-analysis of psychosocial and pharmacological treatments. Behav Ther 1999;30:117–135.

146.McElroy SL, Hudson JI, Malhotra S, et al. Citalopram in the treatment of binge-eating disorder: a placebo-controlled trial. J Clin Psychiatry 2003;64:807–813.

147.Hudson JI, McElroy SL, Raymond NC, et al. Fluvoxamine in the treatment of binge-eating disorder: a multicenter placebo-controlled, double-blind trial. Am J Psychiatry 1998;155:1756–1762.

148.Arnold LM, McElroy SL, Hudson JI, et al. A placebo-controlled, randomized trial of fluoxetine in the treatment of binge-eating disorder. J Clin Psychiatry 2002;63:1028–1033.

149.McElroy SL, Casuto LS, Nelson EB, et al. Placebo-controlled trial of sertraline in the treatment of binge eating disorder. Am J Psychiatry 2000;157:1004–1006.

150.McElroy SL, Hudson JI, Capece KB, et al. Topiramate for the treatment of binge-eating disorder associated with obesity: a placebo-controlled study. Biol Psychiatry 2007;61:1039–1048.

151.Valentino MA, Lin JE, Waldman SA. Central and peripheral molecular targets for antiobesity pharmacotherapy. Clin Pharmacol Ther 2010;87:652–662.

152.Ben-David K, Rossidis G. Bariatric Surgery: indications, safety and efficacy. Curr Pharm Des 2011;17:1209–1217.

153.Mingrone G, Panunzi S, De Gaetano A, et al. Bariatric surgery versus conventional medical therapy for type 2 diabetes. N Engl J Med 2012;366:1577–1585.

154.Schauer PR, Kashyap SR, Wolski K, et al. Bariatric surgery versus intensive medical therapy in obese patients with diabetes. N Engl J Med 2012;366:1567–1576.

155.Birkmeyer NJ, Dimick JB, Share D, et al. Hospital complication rates with bariatric surgery in Michigan. JAMA 2010;304:435–442.

156.Maciejewski ML, Livingston EH, Smith VA, et al. Survival among high-risk patients after bariatric surgery. JAMA 2011;305: 2419–2426.

157.Rosenberger PH, Henderson KE, Grilo CM. Psychiatric disorder comorbidity and association with eating disorders in bariatric surgery patients: a cross-sectional study using structured interview-based diagnosis. J Clin Psychiatry 2006;67:1080–1085.

158.Maluenda F, Csendes A, De Aretxabala X, et al. Alcohol absorption modification after a laparoscopic sleeve gastrectomy due to obesity. Obes Surg 2010;20:744–748.

159.Woodard GA, Downey J, Hernandez-Boussard T, et al. Impaired alcohol metabolism after gastric bypass surgery: a case-crossover trial. J Am Coll Surg 2011;212:209–214.

160.Powell AG, Apovian CM, Aronne, LJ. New drug targets for the treatment of obesity. Clin Pharmacol Ther 2011;90:40–51.

161.Heal DJ, Gosden J, Smith SL. What is the prognosis for new centrally-acting anti-obesity drugs? Neuropharmacology 2012;63:132–146

162.Plodkowski RA, Nguyen Q, Sundaram U, et al. Bupropion and naltrexone: a review of their use individually and in combination for the treatment of obesity. Expert Opin Pharmacother2009;10: 1069–1081.

163.Sinnayah P, Wallingford N, Evans A, et al. Bupropion and naltrexone interact synergistically to decrease food intake in mice. Obesity 2007;15:A179.

164.Hurren KM, Berlie HD. Lorcaserin: an investigational serotonin 2C agonist for weight. Am J Health Syst Pharm 2011;68(21): 2029–2037.

165.Fidler MC, Sanchez M, Raether B, et al. A one-year randomized trial of lorcaserin for weight loss in obese and overweight adults: the BLOSSOM trial. J Clin Endocrinol Metab2011;96:3067–3077.

166.O’Neil PM, Smith SR, Weissman NJ, et al. Randomized Placebo-controlled clinical trial of lorcaserin for weight loss in type 2 diabetes mellitus: the BLOOM-DM study. Obesity2012;20:1426–1436.

167.Gadde KM, Allison DB, Ryan, DH, et al. Effects of low-dose, controlled-release, phentermine plus topiramate combination on weight and associated comorbidities in overweight and obese adults (CONQUER): a randomised, placebo-controlled, phase 3 trial. Lancet 2011;377:1341–1352.

168.Salazar S. Assessment and management of the obese adult female: a clinical update for providers. J Midwifery Womens Health 2006;51:202–207.

169.Robin AR, Siegal PT, Koepke T, et al. Family therapy versus individual therapy for adolescent females with anorexia nervosa. J Dev Behav Pediatr 1994;15:111–116.

170.Eisler I, Dare C, Russell GF, et al. Family and individual therapy in anorexia nervosa: a 5-year follow-up. Arch Gen Psychiatry 1997;54:1025–1030.

171.McIntosh VV, Jordan J, Carter FA, et al. Three psychotherapies for anorexia nervosa: a randomized, controlled trial. Am J Psychiatry 2005;162:741–747.

172.Pike KM, Walsh BT, Vitousek K, et al. Cognitive behavior therapy in the posthospitalization treatment of anorexia nervosa. Am J Psychiatry 2003;160:2046–2049.

173.Fairburn CG, Jones R, Peveler RC, et al. Psychotherapy and bulimia nervosa: the longer-term effects of interpersonal psychotherapy, behavior therapy, and cognitive behavior therapy. Arch Gen Psychiatry1993;50:419–428.

174.Goldbloom DS, Olmstead M, Davis R, et al. A randomized controlled trial of fluoxetine and cognitive behavioral therapy for bulimia nervosa: short term outcome. Behav Res Ther1997;35:803–811.

175.Lewandowski LM, Gebing TA, Anthony JL, et al. Meta-analysis of cognitive behavioral treatment studies for bulimia. Clin Psychol Rev 1997;17:703–718.

176.Wilfley DE, Agras WS, Telch CF, et al. Group cognitive behavioral therapy and group interpersonal psychotherapy for the nonpurging bulimic individual: a controlled comparison. J Consult Clin Psychol1993;61:296–305.

177.Wilfley DE, Welch RR, Stein RI, et al. A randomized comparison of group cognitive behavioral therapy and group interpersonal psychotherapy for the treatment of overweight individuals with binge eating disorder. Arch Gen Psychiatry 2002;59:713–721.

178.Nauta H, Hospers H, Kok G, et al. A comparison between a cognitive and a behavioral treatment for obese binge eaters and obese non-binge eaters. Behav Ther 2000;31:441–461.

179.Nauta H, Hospers H, Jansen A. One-year follow-up effects of two obesity treatments on psychological well-being and weight. Br J Health Psychol 2001;6:271–284.

180.Paxton SJ, Schutz HK, Wertheim EH, et al. Friendship clique and peer influences on body image concerns, dietary restraint, extreme weight-loss behaviors, and binge eating in adolescent girls. J Abnorm Psychol 1999;108:255–266.

181.Sundgot-Borgen J. Eating disorders among male and female elite athletes. Br J Sports Med 1999;33:434.

182.Meyer C, Waller G. Social convergence of disturbed eating attitudes in young adult women. J Nerv Ment Dis 2001;189:114–119.

183.Crandall CS. Social contagion of binge eating. J Pers Soc Psychol 1988;55:588–598.

184.Becker CB, Smith LM, Ciao AC. Peer-facilitated eating disorder prevention: a randomized effectiveness trial of cognitive dissonance and media advocacy. J Counsel Psychol2006;53:550–555.

185.Becker CB, Smith LM, Ciao AC. Reducing eating disorder risk factors in sorority members: a randomized trial. Behav Ther 2005;36:245–253.

186.Bonfà F, Cabrini S, Avanzi M, et al. Treatment dropout in drug-addicted women: are eating disorders implicated? Eat Weight Disord 2008;13:81–86.

187.Gordon SM, Johnson JA, Greenfield SF, et al. Assessment and treatment of co-occurring eating disorders in publicly funded addiction treatment programs. Psychiatr Serv2008;59:1056–1059.

188.Woodside BD, Staab R. Management of psychiatric comorbidity in anorexia nervosa and bulimia nervosa. CNS Drugs 2006;20:655–663.

189.Herzog DB, Greenwood DN, Dorer DJ, et al. Mortality in eating disorders: a descriptive study. Int J Eat Disord 2000;28:20–26.

190.Mitchell JE, Pyle R, Eckert ED, et al. The influence of prior alcohol and drug abuse problems on bulimia nervosa treatment outcome. Addict Behav 1990;15:169–173.

191.Cohen LR, Greenfield SF, Gordon S, et al. Survey of eating disorder symptoms among women in treatment for substance abuse. Am J Addict 2010;19:245–251.

192.Couturier J, Lock J. What is recovery in adolescent anorexia nervosa? Int J Eat Disord 2006;39:550–555.

193.Katz JL. Eating disorders: a primer for the substance abuse specialist. J Subst Abuse Treat 1990;7:143–149.

194.Fichter MM, Quadflieg N. Twelve-year course and outcome of bulimia nervosa. Psychol Med 2004;34:1395–1406.

195.Fairburn CG, Brownell K, Cooper Z, et al. The natural course of bulimia nervosa and binge eating disorder in young women. Arch Gen Psychiatry 2000;57:659–665.

196.Pope HG, Lalonde JK, Pindyck LJ, et al. Binge eating disorder: a stable syndrome. Am J Psychiatry 2006;163:2181–2183.

197.Jeffery RW, Drewnowski A, Epstein LH, et al. Long-term maintenance of weight loss: current status. Health Psychol 2000;19:5–16.

198.Kalarchian MA, Marcus MD, Levine MD, et al. Psychiatric disorders among bariatric surgery candidates: relationship to obesity and functional health status. Am J Psychiatry2007;164:328–334.

199.Wilson GT. Eating disorders, obesity and addiction. Eur Eat Disord Rev 2010;18:341–351.

200.Liu Y, von Deneen KM, Kobeissy FH, et al. Food addiction and obesity: evidence from bench to bedside. J Psychoactive Drugs 2010;42:133–145.