eating disorder research paper example

• Publications
• Published Papers, 2024

Published Papers by year

Walter Kaye and the UCSD Eating Disorders Research team have published over 250 papers on the neurobiology of eating disorders. These publications include behavioral, treatment, and cognitive neuroscience studies that have improved understanding of the clinical presentation, genetics, neurotransmitter systems, and neural substrates involved in appetite dysregulation and disordered eating. These studies are guiding the development of more effective, neurobiologically informed interventions.

• Change in motivational bias during treatment predicts outcome in anorexia nervosa
• Sophie R. Abber MS, Susan M. Murray PhD, Carina S. Brown MS, Christina E. Wierenga PhD
• doi: 10.1002/eat.24156. Epub 2024 February 01.
• Wiley Online Library
• The acceptability, feasibility, and possible benefits of a neurobiologically-informed 5-day multifamily treatment for adults with anorexia nervosa
• Christina E. Wierenga, Laura Hill, Stephanie Knatz Peck, Jason McCray, Laura Greathouse, Danika Peterson, Amber Scott, Ivan Eisler, Walter H. Kaye
• oi: 10.1002/eat.22876. Epub 2018 May 2.
• Research Program
• Current Research Studies
• Genetic Studies
• Participate in Our Studies

Eating Disorders Research Paper

Sample Eating Disorders Research Paper. Browse other research paper examples and check the list of research paper topics for more inspiration. iResearchNet offers academic assignment help for students all over the world: writing from scratch, editing, proofreading, problem solving, from essays to dissertations, from humanities to STEM. We offer full confidentiality, safe payment, originality, and money-back guarantee. Secure your academic success with our risk-free services.

The current system of psychiatric classification, the Diagnostic and Statistical Manual of Mental Disorders–Fourth Edition ( DSM-IV; American Psychiatric Association [APA], 1994), includes two official eating disorder (ED) syndromes: anorexia nervosa and bulimia nervosa, and a third (still provisional) diagnosis, binge-eating disorder. Binge-eating disorder, however, is likely to become officially recognized in future editions of the diagnostic manual and we therefore include it in this research paper. Anorexia, bulimia, and binge eating are polysymptomatic syndromes, defined by maladaptive attitudes and behaviors around eating, weight, and body image, including as well nonspecific disturbances of self-image, mood, impulse regulation, and interpersonal functioning. In this research paper, we review pathognomonic features of the EDs and findings on concurrent traits and comorbid psychopathology. We also discuss the putative set of factors, biological, psychological, and social (as well as eating-specific and more generalized) that may explain ED development.

Academic Writing, Editing, Proofreading, And Problem Solving Services

Get 10% off with 24start discount code, defining characteristics, anorexia nervosa.

Anorexia nervosa (AN) is defined by a relentless pursuit of thinness and a morbid fear of the consequences of eating (usually expressed as a dread of weight gain or obesity). The result is a willful (and often dramatic) restriction of food intake. The person with AN imposes upon herself a state of gradual weight loss and (sometimes) dangerous emaciation. (Recognizing different proportions of EDs among females and males, we use feminine personal pronouns. This convention is not intended to disregard eating syndromes in males.) At the core of such behavior appears to be a literal phobia of weight gain, so intense that the individual avoids behaviors (e.g., eating unfamiliar foods, eating without exercising) that could lead to weight gain and thus incrementally loses further weight.

Individuals with AN typically eat a restricted range of safe (usually low-calorie) foods or avoid social eating situations so that they will have full control over what, how much, and in what way they can eat. In some cases, anorexics purge after eating through vomiting, misuse of laxatives, or other means, due to fears that they may have overeaten. About half of sufferers eventually develop binge-eating episodes—that is, periodic dyscontrol over eating, or incapacity to satiate (DaCosta & Halmi, 1992). Consequently, a distinction is usually made between AN, restricting subtype, in which the sufferer limits food intake but does not engage in binge eating or purging (i.e., self-induced vomiting; misuse of laxatives, diuretics, or enemas), and AN, binge-eating/purging subtype, in which (as the label implies) binge or purge episodes are prominent.

Bulimia Nervosa

In apparent contrast to AN, the main feature of bulimia nervosa (BN) is binge eating (i.e., appetitive dyscontrol, vs. AN’s overcontrol). Bulimia nervosa is diagnosed in relatively normal or overweight individuals (not anorexics) who display recurrent eating binges, and who then compensate for overeating through self-induced vomiting, laxative misuse, intensive exercise, fasting, or other means. It is the combination of binge eating and compensation that define BN and that differentiates it from an apparently related syndrome, binge-eating disorder (which we will introduce shortly). In BN, binges are characterized by consumption, with a terrifying sense of dyscontrol, of sometimes massive quantities of calories. Binges can provoke profound feelings of shame, anxiety, or depression, and the bulimic’s sense of self-worth and well-being often shifts quite dramatically in concert with her sense of control around eating and body image. This lends to BN a characteristic unpredictability or lability, as people with this syndrome will shift rapidly (depending upon felt control over eating) from a sense of well-being, expansiveness, or excitability, to profound despair, irritability, and depression. Although the validity of BN as a unique diagnostic category seems well supported (Gleaves, Lowe, Snow, Green, & Murphy-Eberenz, 2000), the distinction (in DSM-IV criteria) between purging and nonpurging bulimic subtypes may be of dubious merit in identifying truly different populations of sufferers (Tobin, Griffing, & Griffing, 1997).

Binge-Eating Disorder and Eating Disorders Not Otherwise Specified

Other variations on EDs occur, classified in the DSM-IV system as eating disorder not otherwise specified (EDNOS). For example, anorexic-like weight preoccupations and pursuit of thinness in individuals who retain menses, are given the diagnosis of EDNOS. Most important of the EDNOS variants is, however, an apparently quite prevalent pattern characterized by recurrent eating binges in the absence of compensatory behaviors such as vomiting or fasting. This pattern, which (eventually) renders the sufferer overweight, is currently labeled binge-eating disorder (BED) . According to provisional criteria, defining characteristics include eating more rapidly than normal, eating until uncomfortably full, eating when not hungry, eating alone due to embarrassment around the quantity one eats, or feeling intense guilt, disgust, or depression after eating. In BED, binge episodes must be markedly distressing.

Compared to individuals with BN, BED patients are noted to binge over considerably longer periods of time (Fairburn, 1995), with individuals in some cases showing day-long binges. Eating in individuals with BED is noted to have a less desperate or driven character than in BN, and BED patients apparently consume more proteins than do bulimics, who preferentially binge on sweets or carbohydrates (Fitzgibbon & Blackman, 2000). In addition, BED subjects are reportedly more likely than bulimics to find the food on which they binge soothing or relaxing (Mitchell et al., 1999).

There has been controversy surrounding the BED diagnosis—a concern being that BED may not isolate a truly psychological or behavioral disturbance. However, data show obese people with BED to have more fear of weight gain, more body dissatisfaction, more problems of self-esteem and dysphoric mood, and poorer maintenance of weight loss (once achieved) than do non-BED obese people (Marcus, Wing, & Hopkins, 1988; Streigel-Moore, Wilson, Wilfley, Elder, & Brownell, 1998).Also lending credence to the validity of BED as a unique entity, data indicate taxonomic and genetic distinctiveness of the syndrome. A latent-class analysis applied in a large cohort of female twins ( N = 2,163) identified a distinct BED syndrome and showed greater resemblance for the syndrome among monozygotic versus dizygotic twins (Bulik, Sullivan, & Kendler, 1998).

The Restrictor-Binger Distinction

A distinction between restrictors (those anorexic patients who restrict food intake without binging and purging) and bingers (those ED patients, sometimes anorexic, sometimes bulimic, sometimes obese, who binge and purge) has been introduced by various theorists as an alternative to the formal anorexic-bulimic distinction (see DaCosta & Halmi, 1992). The restrictor-binger distinction has been thought to correspond to important phenomenological and etiological differences, including differences as to key personality features, family interaction styles, and associations with biological processes (all will be reviewed presently).

Where relevant, throughout this research paper, we will address and clarify the rationale for the restrictor-binger distinction concept.

Epidemiology

Anorexia nervosa and bulimia nervosa occur disproportionately, often in industrialized (vs. economically less developed) nations, but are otherwise reported to occur with surprisingly uniform prevalences in developed parts of Europe, Asia, and the Americas. Reported prevalences in school-aged females of strictly defined AN generally fall in the 0.5% to 1% range (Wakeling, 1996), and of BN generally in the 1% to 2% range (e.g., Garfinkel et al., 1995). However, it is probably fair to assume that in subthreshold forms, identified using less stringent diagnostic criteria, EDs occur in larger numbers (Garfinkel et al.). At least 10% of school-aged females in the industrialized world display partial anorexic or bulimic syndromes, associated with significant dietary, psychological, and medical distress.

Although a popular stereotype is the young adolescent AN sufferer, actual peak prevalences of EDs are observed in young adult women, reflecting the (unfortunate) tendency of EDs to run a chronic course and of BN to develop later in the life cycle (during the transition to adulthood). Although they occur about one-tenth as often in men as in women, classical anorexic and bulimic syndromes are also noted in males (e.g., Wakeling, 1996) and there are some indications to suggest that if ED prevalences are rising in any group, it is doing so especially among males. Eating disorders appear to occur less frequently in certain racial and ethnic groups, for example, among Black andAsian-AmericanversusWhitefemales(Crago,Shisslak,& Estes, 1996). A comparison of White, Hispanic, and Black adolescent females, both athletic ( N 571) and nonathletic ( N 463), for example, showed reliably lower rates of disordered eating in both of the Black female groups, compared to those obtained in White and Hispanic groups (Rhea, 1999). However, some findings suggest that Black women may yet be especially susceptible to certain aspects of eating disturbance: For example, a telephone-interview survey involving 1,628 Black and 5,741 White urban women found Blacks to report more fasting, abuse of laxatives or diuretics, and highfrequency binge eating than did the White women (StriegelMoore,Wilfley, Pike, Dohm, & Fairburn, 2000).

Although changes in diagnostic and record-keeping practices make it difficult to pin the issue down, evidence suggests an increasing ED incidence (Wakeling, 1996). Reviewing annual incidence rates for AN in the United States published between the early 1960s and the mid-1980s, Mitchell and Eckert (1987) concluded that there had been a progressive increase, from 0.35 to 4.06 per 100,000. Similarly, an incidence study in the Rochester, Minnesota, area concluded, after screening 2,806 medical records for new cases of AN, that there had been a long-term increase in AN, especially among 15- to 24-year-old females (Lucas, Crowson, O’Fallon, & Melton, 1999). In a similar vein, it is commonly believed that EDs are disorders of affluent, urban society. However, current data show surprisingly limited linkage to upper socioeconomic status, and unexpectedly high numbers of EDs found in rural communities suggest that EDs may not be as much an urban phenomenon as may once have been believed (Gard & Freeman, 1996).

Only limited epidemiological data are available for BED, given its more recent addition to the diagnostic nomenclature. Nonetheless, studies suggest a disturbingly common syndrome that may affect from 1% to 5% of the general population and about 8% of the population of obese people. In selected subgroups, such as obese people undergoing weight-loss treatment, BED prevalences apparently run as high as 30–50% (Spitzer et al., 1992). Intriguingly, data show BED to have a more even gender-based distribution than do other EDs, probably affecting 2 males for every 3 females (Streigel-Moore et al., 1998), and to affect a broader age group, with peak age being about 40 years, compared to 28 years for BN (Fitzgibbon & Blackman, 2000). Bingeeating disorder, therefore, seems to be less gender and age dependent than either AN or BN.

Comorbidity with Other Psychopathology

Paradoxically, it seems that if one assertion can be made about EDs, it is that they are not only about eating. Rather, EDs frequently co-occur with other forms of psychopathology, for example, mood, anxiety, substance-abuse, posttraumatic stress, and personality disorders.

Mood Disorders

Among comorbid tendencies noted in ED sufferers, comorbid mood disorders figure very prominently. Råstam (1992) reported a 40% rate for currently comorbid major depression in her anorexic sample, a 70% rate for overall mood disorders, and a rate of lifetime mood disorder in excess of 90%. A comparable, or perhaps even more pronounced, tendency toward comorbid mood disorder is noted in binge-purge syndromes. One study, comparing point prevalences of major depression across restricting and binging-purging anorexics, noted the disorder in about 30% of restrictors and in 53% of binger-purgers (Herzog, Keller, Sacks, Yeh, & Lavori, 1992). Other investigations have suggested that from 20% to more than 40% of bulimics are clinically depressed (Brewerton et al., 1995; Garfinkel et al., 1995).

Co-aggregation with other mood-disorder variants is also apparently considerable. A community study by Zaider, Johnson, and Cockell (2000) points to an important affinity between EDs and dysthymia, a milder chronic mood disturbance. In addition, evidence has shown a strong association of BN with seasonal affective disorder (SAD), implying cyclical season-dependent recurrences in depressed mood. In one study, 69% of BN patients were noted to show comorbid SAD (Levitan, Kaplan, Levitt, & Joffe, 1994). Furthermore, a study by our group demonstrated stronger SAD comorbidity in bulimic rather than anorexic ED variants. In a sample of 259 patients presenting at our specialized ED clinic, 27.0% were rated as showing SAD—71.4% diagnosed with BN, 18.6% with AN, and 10.0% with EDNOS (Ghadirian, Marini, Jabalpurlawa, & Steiger, 1999).

Various areas of etiological overlap can be postulated to explain eating disorder–mood disorder convergence. Both syndromes are believed to depend upon similar familial or developmental substrates (e.g., developmental neglect or familial overprotection), and both have been thought to have similar neurobiological substrates. Pertinent to questions of shared causality, a genetic-epidemiological study by Wade, Bulik, Neale, and Kendler (2000), involving 850 female twin pairs indicates that both genetic and environmental factors contribute significantly to shared risk for AN and major depression. Given the implication of serotonergic factors in mood disorders in general and in seasonality in particular, there is ample potential for serotonin-mediated crossover of risk for BN, mood disorders, and SAD—a notion that has been partially corroborated by findings showing serotonin abnormalities to be more pronounced in BN patients with a seasonal profile (Levitan et al., 1997).

Anxiety Disorders

Anxiety disorders in AN reportedly vary from 20% (Herzog et al., 1992) to more than 80% (Godart, Flament, Lecrubier, & Jeammet, 2000), and reported rates in BN vary from 13% (Herzog et al.) to about 60% (Garfinkel et al., 1995). Godart and colleagues reported 83% of persons with AN and 71% of those with BN to have at least one lifetime anxiety-disorder diagnosis. Most common among the conditions they studied was social phobia (present in 55% of anorexics and 59% of bulimics).

Although studies report generalized anxiety disorder, social and simple phobias, agoraphobia, panic disorder, and obsessive compulsive disorder (OCD) in the EDs, we pay particular attention to data on the convergence between OCD and the EDs. This is because the structure of the EDs so closely resembles that of OCD—intrusive obsessions with weight and body image that are appeased by apparently compulsive gestures, such as fasting or purging. Lifetime prevalences of OCD are reported to range from 15% to 70% in anorexics, and from 3% to 30% in bulimics. Thornton and Russell (1997) reported that OCD was more prevalent in 35 women with AN (27%) than in 33 women with BN (3%), suggesting stronger co-aggregation of OCD with anorexic ED variants. Arguing for a specific affinity, one study indicated that obsessive-compulsive symptoms in adolescent anorexics are more common than are depressive symptoms (Cassidy, Allsopp, & Williams, 1999). Arguing that OCD characteristics may constitute an equally common (and apparently stable) trait in those susceptible to BN, von Ranson, Kaye, Weltzin, Rao, and Matsunaga (1999) found scores measuring OCD to be higher in 31 active bulimics and 29 recovered bulimics (abstinent for more than 1 year) than in 19 healthy comparison women, with scores on measures of symmetry and exactness being as abnormal in recovered bulimics as they were in active cases.

Various additional studies have examined the temporal sequence of onset for anxiety and eating syndromes, testing the idea that in vulnerable individuals, EDs actually may evolve from anxiety disorders. Thornton and Russell (1997) and Godart et al. (2000) both concluded that anxiety disorders often precede ED onset, implying that an anxious (and often obsessive-compulsive) disposition predisposes to ED development—or may be a manifestation of an incipient ED.

Substance-Abuse Disorders

Studies consistently indicate bulimic ED variants to be more strongly associated with alcohol and chemical dependencies than is the AN-restrictive type (see Holderness, BrooksGunn, & Warren, 1994). Relevant findings show from 10% to 55% of women with BN to abuse substances, whereas from 25% to 40% of females with alcohol dependence show some form of (often bulimia-spectrum) ED. Schuckit and colleagues (1996) found BN, but not AN, to occur at a greaterthan-expected rate among alcoholic women. Corroborating the impression of syndrome-specific aggregation, a study implicating 1,031 adolescent girls and 888 adolescent boys showed binge eating, especially when associated with compensatory weight-control behaviors, to coincide with elevated substance abuse (Ross & Ivis, 1999). Not surprisingly, studies examining psychopathological implications of substance abuse in the EDs report that concurrent substance abuse predicts greater comorbidity. Lilenfeld and colleagues (1997), for example, found substance abusers in an eating disordered population to show significantly more social phobia, panic disorder, and personality disorders.

Holderness and colleagues (1994) discuss sources for etiological overlap between bulimic ED variants and substanceabuse disorders. A so-called addictive personality (one prone to misuse of substances) has been postulated to underlie both types of syndromes, but evidence of such a personality style is unconvincing. It remains viable to consider shared biological substrates underlying substance-abuse and binge-eating behaviors, mediated by shared genetic diathesis, or shared factors related to serotonin, endorphin, or other neurotransmitters or neurohormones.

Posttraumatic and Dissociative Disorders

Eating disorders are, in an alarming proportion of cases, associated with adverse (potentially traumatic) life experiences (Everill & Waller, 1995; Wonderlich, Brewerton, Jocic, Dansky, & Abbott, 1997)—a link that we discuss more fully in a later section on developmental factors. Consistent with such observations, findings have suggested a remarkable coincidence between EDs and posttraumatic stress disorder (PTSD). One study reported PTSD in about half of 294 women with AN, BN, or EDNOS (Gleaves, Eberenz, & May, 1998). Severity of PTSD, however, was not found to predict subtype or severity of ED symptoms, suggesting that trauma (and associated posttraumatic stress) may not specifically control eating symptoms. On a related theme, there is a sizable body of data addressing the connection between EDs and dissociative disorders. Characterized by disturbances in memory (e.g., amnesias), consciousness (e.g., problems of identity, or apparent fragmentation of the personality), and sensorimotor function (e.g., conversion-type symptoms), dissociative disorders are sometimes regarded as failed adaptive responses to traumatic stress. Applying the dissociative-disorder concept to EDs, several groups have noted that individuals with BN and BED both produce elevations, relative to normal subjects, psychiatric comparison subjects, and restrictor anorexics, on validated self-report instruments measuring dissociation (e.g., Vanderlinden,Vandereycken, van Dyk, &Vertommen, 1993). Likewise, one study reported that 29 obese women with BED showed significantly more dissociative symptoms on a selfreport questionnaire, and more traumatic experiences, than did 35 obese women with no binge-eating symptoms (Grave, Oliosi, Todisco, & Vanderlinden, 1997).

Although evidence suggests a link between dissociative phenomena and bulimic symptoms, the extent to which dissociative symptoms correspond to binge eating, per se, or to general psychopathological indicators that (only incidentally) co-occur with bulimic eating problems, remains to be established. Various relevant studies suggest that dissociation coincides more closely with nonspecific than eating-specific components of psychopathology in ED patients. For example, a study by Gleaves and Eberenz (1995) linked dissociative symptoms more closely to severity of anxiety and depressive symptoms than to bulimic or anorexic symptoms in 53 ED patients. Similarly, Demitrack, Putnam, Brewerton, Brandt, and Gold (1990) concluded that the propensity toward self-mutilation in BN patients is linked more strongly to dissociative pathology than to severity of eating symptoms. In contrast, indicating some degree of specificity in the dissociative disorder–eating disorder connection, Everill, Waller, and Macdonald (1995) found self-reported dissociation, and especially the style of absorption (e.g., daydreaming), to predict frequency of binging in 26 clinical BN sufferers; whereas Katz and Gleaves (1996), studying 52 females diagnosed as having either an ED with dissociation, ED alone, dissociation alone, or neither condition, found that even those ED patients who showed no comorbid dissociative disorder tended to display dissociative-spectrum psychopathology.

Various pathways might account for an etiological link, direct or indirect, between the EDs and traumatic events. Where traumata impact directly upon the body, intuition leads to consideration of relatively direct effects acting upon bodily experience, and in turn upon eating and weight-control behaviors. Alternatively, abusive experiences might impact upon regulation of self, mood, and impulse, and in these ways indirectly heighten the risk of maladaptive eating behavior or moderate the intensity of eating symptoms such as binging or purging. Full discussions of direct and indirect pathways thought to link trauma and EDs are available elsewhere (see Everill & Waller, 1995; Wonderlich et al., 1997). Our group has documented a tendency for more severely abused bulimics to show greater abnormalities on indices reflecting serotonin and cortisol function (Steiger, Gauvin, et al., 2001). Such results could imply neurobiological factors, associated with childhood abuse, that could heighten the risk of overreactivity to stress and of self- and appetitive dysregulation.

Personality Disorders

Among various comorbid propensities in the EDs, that with personality disorders is arguably the strongest (see Vitousek & Manke, 1994). A recent meta-analysis (Rosenvinge, Martinussen, & Ostensen, 2000) of 28 studies on this area of comorbidity represents well the general tendencies in findings. In particular, Rosenvinge and colleagues found a higher proportion (58%) of eating-disordered than of comparison women (28%) to have a personality disorder. Furthermore, whereasAN and BN patients were found to show comparable likelihood of DSM Cluster-C (anxious-fearful) personality disorders (45% and 44%, respectively), BN patients showed higher proportions of Cluster-B (dramatic-erratic) personality disorders (44% overall) and of borderline personality disorder (31%) than did AN patients or controls. Such findings are representative of themes noted in earlier reviews: Personality disorders are frequently present in anorexic and bulimic syndromes, and results imply differential co-aggregation of personality-disorder subtypes with restrictive and bulimic ED variants. Restrictive AN seems to be associated with a high concentration of anxious-fearful personality-disorder diagnoses (characterized by anxiousness, orderliness, introversion, and preference for sameness and control). Eatingdisorder variants characterized by binge-purge symptoms coincide with more heterogeneous personality-disorder subtypes than do restrictive forms, and more importantly, with more pronounced affinity for the dramatic-erratic personality disorders (characterized by prominent attention and sensation seeking, extraversion, mood lability, and proneness to excitability or impulsivity). In other words, the dietary overcontrol that characterizes restrictive AN seems to be paralleled by generalized overcontrol, as a personality or adaptive style, whereas the dietary dyscontrol that characterizes binge-purge syndromes seems, in many cases, to be paralleled by generalized dyscontrol.

Malnutrition can have adverse effects upon personality functioning (Keys, Brozek, Henschel, Mickelson, & Taylor, 1950).This raises the concern that apparent personality disturbances seen in ED sufferers (and, in turn, personality-disorder diagnoses) may reflect state disturbances associated with an active ED rather than trait tendencies. In other words, caution around the use of personality-disorder diagnoses in active ED patients is warranted. Nonetheless, various findings associate the EDs with stable underlying personality disturbances. One investigation reports 26% of women recovered from AN or BN to show some form of ongoing personality disorder, with Cluster-B personality disorders’being more closely associated with bulimic subtypes (Matsaunaga, Kaye, et al., 2000). Another study, comparing 51 weight-restored adolescent-onset anorexics to 51 matched comparison cases, concluded that anorexics often show persistent obsessions, compulsions, and social-interaction problems (Nilsson, Gillberg, Gillberg, & Råstam, 1999).

Contemporary etiological theory on the EDs invokes a multidimensional, biopsychosocial causality (Garfinkel & Garner, 1982; Striegel-Moore, Silberstein, & Rodin, 1986). In general form, such theory postulates that EDs implicate a collision among biological factors (e.g., heritable influences on mood, temperament, and impulse controls), social pressures (promoting body-consciousness or generalized selfdefinition problems), psychological tendencies (autonomy disturbances, perfectionism, preference for order and control, hypersensitivity to social approval), and developmental processes (conducive to self-image or adjustment problems). In the following sections, we review evidence pertaining to biological, psychological, and social factors that may act in ED development.

Psychological Factors

Developmental theories.

Psychological theories on ED development are very diverse. However, there is some consensus concerning convergence of psychological characteristics, developmental dynamics, and ED variants. Restrictive AN has been widely associated with traits of compliance and anxiousness in individuals who gravitate to orderliness or control, whereas bulimic subtypes of EDs (including AN, binge-purge subtype) have been linked to self-regulatory deficits, dramatic fluctuations in self-concept, and erratic efforts to regulate inner tensions. Early psychodynamic models interpreted anorexic symptoms as a defense against conflicting drives (e.g., sexual drives); eating was thought to invoke forbidden sexual fantasies, and food refusal to reduce associated anxiety (e.g., Waller, Kaufman, & Deutsch, 1940). Crisp (1980), in a related vein, formulated AN as a phobic-avoidance response, reinforced by a literal escape from maturational changes at puberty. In her conceptualization, Bruch (1973) emphasized maternal overinvolvement and failure to respond appropriately to the child’s self-affirming behaviors, believing such parenting problems to underlie autonomy deficits and pervasive feelings of ineffectiveness on the child’s part. Strober’s (1991) organismic -developmental paradigm again addressed pathological adaptations to adolescence, but emphasized an incompatibility between developmental imperatives surrounding puberty and a heritable temperament characterized by harm-avoidance, hyperreactivity to social approval, and preference for sameness . Related theories regard food refusal as a gesture of self-assertion, mounted by some children in the face of excessive familial controls or emotional overinvestment; in other words, as an adaptation to familial intrusions and overprotectiveness (e.g., Humphrey, 1991; Johnson, 1991).

From a developmental perspective, bulimic ED variants have been thought to be linked to family-wide interaction patterns tinged with greater hostility, neglect, criticism, rejection, and blaming (Humphrey, 1991; Johnson, 1991). For example, Johnson linked bulimic symptoms to parental neglect, in his view spanning a continuum from nonmalevolent forms (in families in which parents’ perfectionistic needs place excessive demands upon children) to malevolent forms (occurring in frankly chaotic or abusive families). Humphrey referred to family-wide deficits in nurturance and tension regulation and systems that ensnare members in mutually destructive, hostile, blaming projections. In both views, bulimic behaviors are conceived to play self- and mood-regulatory functions and to be metaphors for chaotic family interactions, tinged with desperate attempts to achieve closeness and hostile rejections.

Empirical Findings: Individual Psychological Characteristics

Empirical findings on personality and on cognitive and emotional functioning in individuals with EDs provide qualified support for tendencies outlined previously in the theoretical accounts.

Personality Characteristics. Early psychometric studies showed anorexic patients to be neurotic, socially anxious, and often depressed (Sohlberg & Strober, 1994). In addition, various findings pointed to a systematic co-aggregation between restrictor and binger-purger subtypes (on the one hand) and personality traits with an overcontrolled or dyscontrolled style (on the other)—the binger-purgers’being noted to show greater emotional lability, impulsivity, or oppositionality than the restrictors, and lesser extraversion and novelty seeking (risk taking). The same concept is reiterated, although imperfectly, in various contemporary studies. Findings with the Millon Clinical Multiaxial Inventory have, for example, suggested more schizoid or avoidant tendencies among restrictors and more histrionic tendencies among normal- or anorexic-weight bingers (Norman, Blais, & Herzog, 1993). With the Multidimensional Personality Questionnaire, Casper, Hedeker, and McClough (1992) found normal-weight bulimics to be less conforming and more impulsive than were either restrictor or binger-purger anorexics, but found the restrictors to show the greatest self-control, conscientiousness, and emotional inhibition. With the Tridimensional Personality Questionnaire, Bulik, Sullivan, Weltzin, and Kaye (1995) found normal-weight bulimics to be more novelty seeking than restrictor or binger anorexics, and restrictor anorexics to be more reward dependent than bulimic anorexics, but bulimic anorexics to be more harm avoidant than restrictors.

Taken together, available findings seem to support two theoretically important generalizations (seen also in data reviewed earlier on comorbid personality disorders): (a) Restrictive AN is associated with relatively circumscribed personality characteristics, with particular emphasis on traits of rigidity, emotional constriction, and compulsivity. (b) Binge-purge syndromes, on the other hand, are associated with relatively heterogeneous psychopathological characteristics that sometimes implicate greater behavioral disinhibition and affectivity. We illustrate this combination of tendencies in Figure 7.1, making the assumption that overcontrol and dyscontrol can be regarded as spanning a continuum along various theoretically related dimensions (e.g., compulsivity vs. impulsivity; preference for sameness vs. novelty seeking; introversion vs. extroversion; etc.). The figure depicts a tendency for there to be a circumscribed convergence, inrestrictive ED variants, of overcontrolled tendencies, but greater heterogeneity as to characteristics in bulimic (binge-purge) variants. Some bulimic cases show overcontrol, as has been associated with restrictive AN, but many others show marked erraticism and dyscontrol. Given trait heterogeneity among bulimics, theorists have proposed the existence of multiple pathways to bulimic eating disturbances, with some individuals being vulnerable due to underlying dysregulatory processes that manifest themselves in the form of mood and impulse dysregulation. What is believed is that, in some individuals, processes that correspond to generalized behavioral disinhibition may also underlie appetitive dysregulation (seeVitousek & Manke, 1994).

Specific Traits of Importance. Clinical observations consistently associate AN with specific personality traits, including perfectionism and impulsivity. For example, one study reported 322 anorexic women (restrictors and bingerpurgers alike) to have higher Multidimensional Perfectionism Scale scores than do 44 healthy control women, and notes a coincidence between degree of perfectionism and severity of eating symptomatology (Halmi et al., 2000). Perfectionism is also noted to be elevated in BN probands and their relatives (Lilenfeld et al., 2000), but not in individuals with BED (Fairburn et al., 1998). In addition, data show perfectionism to be evident in AN after long-term weight recovery (Srinivasagam et al., 1995), suggesting that the dimension may be an exophenotypic characteristic of AN. Following from this view, studies have attempted to link perfectionism causally to ED development. Perfectionism has been noted to be elevated premorbidly in those with AN and BN, compared to those with other mental disorder (Fairburn, Cooper, Doll, & Welch, 1999). However, assessed prospectively, perfectionism has not emerged as a predictor of individuals who, among healthy adolescents, would develop later ED symptoms (Calam & Waller, 1998).

We have already noted that bulimic patients can show remarkable propensities toward nonreflectiveness, behavioral disinhibition, self-harming behaviors, or other impulsive characteristics. Almost half of a cohort of normal-weight bulimics studied by Newton, Freeman, and Munro (1993), for example, met criteria for a multi-impulsive syndrome characterized by substance abuse, multiple overdoses, recurrent self-harm, sexual disinhibition, or shoplifting. Such findings corroborate the impression (described earlier) that impulse-control problems are prominent in many BN sufferers. Pronounced impulsivity in BN has been linked, in different reports, to more severe eating disturbances (binge eating, vomiting, laxative abuse, and drive for thinness), greater body-image problems, and greater generalized psychopathology—including substance abuse, self-injurious behaviors, and borderline traits (e.g., Wiederman & Pryor, 1996). However, impulsivity has not been shown to correspond to severity of bulimic symptoms in other studies (e.g., Wolfe, Jimerson, & Levine, 1994). In consequence, controversy remains around the question of whether impulsivity drives bulimic symptoms (and hence corresponds to their severity), or whether it should be regarded as an independent comorbid dimension that may heighten susceptibility but that is otherwise independent of symptom severity.

Gender Identifications. Given its gender distribution, there has been interest among ED theorists in variables reflecting gender-role adherence and gender identifications. Early findings suggested that eating-disordered women tended (in the most traditional sense of the term) to be hyperfeminine, or overidentified with traditional female roles (Sitnick & Katz, 1984).Arecent meta-analysis of 22 studies on the relationship between gender-role adherence and EDs provides modest corroboration of this proposal, finding clinical eating problems to be related positively with femininity and negatively with masculinity (Murnen & Smolak 1997).

Body-Image Perception. Given that the defining characteristics of AN and BN include disturbed body perception and experience, there has been a surprising degree of controversy around the body-image disturbance concept in the EDs. Although many empirical findings suggest overestimation of bodily proportions or unusually harsh attitudes toward body image in ED patients, many others suggest that eating-disordered individuals have body-image perceptions and attitudes that are quite normal (see Hsu & Sobkiewicz, 1991). Where abnormalities in bodily experience are identified, current findings tend to emphasize emotional and attentional factors and not perceptual ones (e.g., Carter, Bulik, Lawson, Sullivan, & Wilson, 1996). The actual origins of bodily disturbances in the EDs remain uncertain and have been postulated to reflect various factors; from social-learning influences, to effects of biological abnormalities that alter thought and perception, to the impact of body-relevant trauma.

Body Dysmorphic Disorder. Although its relationship to the EDs is uncertain, body-image disturbance is as much a central characteristic of body dysmorphic disorder (APA, 1994) as it is of EDs, and we therefore provide a special comment on this syndrome. Body dysmorphic disorder is defined by distress or functional impairment due to a preoccupation with a real (but minor) or an imagined physical defect. Because it involves an intense, distressing preoccupation (in this case with bodily characteristics) and the drive to correct perceived imperfections, it is often thought to represent a variant of OCD. Hence, one possible common pathway linking body dysmorphic disorder and eating disorders might be an underlying obsessive-compulsive structure. Regardless of whether this is true, body dysmorphic disorder appears to be prevalent in people with EDs, and it has been proposed that this convergence reflects common pathogenesis—especially at a neurobiological level (Olivardia, Pope, & Hudson, 2000)—and possible etiological convergence with OCD (see Widiger & Sankis, 2000). Consistent with the possibility of an ontological relationship, symptoms of body dysmorphic disorder have been reported to precede onset of anorexic symptoms in some anorexic patients. Indeed, some theorists have proposed that the thinness preoccupations seen in anorexic and bulimic women may represent gender-specific variants of the more generalized bodily preoccupations that manifest as body dysmorphic disorder—and which may be more focused upon fitness than on thinness among men (Widiger & Sankis, 2000). However, despite a common object of concern (i.e., the body), various differences are noted. Eating-disordered patients are noted to be mainly concerned about weight and body shape, whereas sufferers of body dysmorphic disorder have more diverse physical complaints and more pronounced negative self-evaluation and social avoidance due to appearance (Gupta & Johnson, 2000). Furthermore, EDs are, in at least some studies, noted to have broader implications for psychopathology. Hence, although speculations on commonalities remain appealing, it is premature to assume that EDs and body dysmorphic disorder are truly comparable syndromes at either phenomenological or etiological levels.

State versus Trait Issues on Personality Dimensions

Given the known effects of malnutrition (and other ED sequelae) upon the mental status, it is necessary, when studying affinities between psychological characteristics and eating disturbances, to differentiate stable,underlying traits from effects of being in an eating-disordered state . One approach to this question has been to assess characteristics in formerly eatingdisordered individuals after recovery. Certain tendencies have seemed to represent likely ED sequelae. For example, data have indicated recovered anorexics to display less harm avoidance and oppositionality and a more external locus of control than do actively ill anorexics (Bulik, Sullivan, Fear, & Pickering, 2000). Similarly, a study by our group showed rather marked illness-related sequelae (in the form of increased depression, anxiety, suicidality, interpersonal problems, and compulsivity in actively ill bulimics) that were not evident in recovered ones (Lehoux, Steiger, & Jabalpurlawa, 2000). In contrast, enduring traits of rigidity, overcautiousness, and obsessionality have been reported to persist (over several years) in recovered anorexics (Windauer, Lennerts, Talbot, Touyz, & Beumont, 1993), whereas enduring narcissistic disturbances are reported in recovered bulimics (Lehoux et al., 2000).

Binge Antecedents and Consequences

Cognitive components of dietary restraint—so-called restrictive eating attitudes (e.g., the belief that one should always eat low-calorie foods, or compensate when one eats more than usual)—are thought to make an important contribution to the development of disinhibited (binge-like) eating behaviors. Polivy and Herman’s (1985) restraint theory specifically postulates that chronic attitudinal restraint of eating potentiates the breakdown of cognitive controls upon appetitive behaviors, and eventual counterregulation (or overeating). It also proposes that counterregulation has specific cognitive and emotional triggers. An impressive catalogue of findings, derived mainly from laboratory studies in nonclinical populations, shows counterregulation of eating behavior to be induced (in attitudinally restrained eaters) by manipulations that generate (a) beliefs that one has exceeded an allowable calorie limit; (b) negative affects; (c) feelings of self-inadequacy; or (d) global disinhibition, as is induced following alcohol consumption. Clinicalexperiencedictatesthatallofthesefactorsarerelevant as binge precipitants in clinical BN patients.

The connection between binge eating and emotional factors deserves specific comment. Functional analyses of binge-eating antecedents (usually performed using on-line experience-sampling procedures) suggest that the proximal antecedents to binge episodes often include negative emotions (depression, anger, emptiness, worry), aversive social experiences, or negative self-perceptions (e.g., Polivy & Herman, 1993; Steiger, Gauvin, Jabalpurlawa, Séguin, & Stotland, 1999; Stickney, Miltenberger, & Wolff, 1999). Furthermore, data show that, compared with nonclinical dieters and nondieter controls, bulimic patients respond to laboratory stressors with increases in both hunger and the desire to binge (e.g., Tuschen-Caffier & Vogele, 1999). As for sequelae, binge episodes are reported to provide transient relief from negative feelings and thoughts and to decrease hunger and food cravings (e.g., Stickney et al.), but to heighten negative affect, poor self-esteem, and probability of further binge eating (Steiger, Gauvin, et al.) over the long term. Such consequences of binge-eating behaviors may be ingredients in the tendency for binge eating to become entrenched and self-perpetuating.

The preceding suggests that binge antecedents may include states characterized by caloric deprivation, negative affects, high social stress, and negative self-concepts. Intriguingly, available literature has also suggested that different antecedents may influence binge-eating behaviors in different individuals. In support, studies have documented a subgroup of binge eaters who deny dieting prior to the onset of eating binges (e.g., Borman Spurrel, Wilfley, Tanofsky, & Brownell, 1997). Moreover, Borman Spurrell et al. noted that people in whom binge eating preceded onset of dieting showed more evidence of personality pathology. These findings resonate with data from our research group, suggesting that restraint may be a weaker hour-to-hour antecedent to binge episodes in highly impulsive versus in less-impulsive bulimics (Steiger, Gauvin, et al., 1999). We interpret these findings as implying that processes associated with impulsivity may contribute directly to the propensity to binge. In this regard, it is noteworthy that some of our findings (described in the section titled “Neurobiology”) , have linked impulsivity in bulimics to greater disturbance of central serotonin mechanisms that are also thought to underlie problems with satiety mechanisms.

Cognitive Functioning

Anorexic and bulimic ED variants have both been linked to (generally mild) neuropsychological impairments associated with higher-level cognitive functions such as active memory, attention, and problem solving (e.g., Szmukler et al., 1992). In addition, some neuropsychological data corroborate the theme of general restrictor-binger differences. Blanz, Detzner, Lay, Rose, and Schmidt (1997) found that BN but notAN patients to show better nonverbal than verbal performance, and Toner, Garfinkel, and Garner (1987) indicated bulimic anorexics to be more likely than restrictor anorexics to commit errors of commission, suggesting problems with response inhibition. Studies that examine the prospective course of neuropsychological impairments in ED patients report improvements that coincide with ED-symptom remission for both AN (Szmukler et al.) and BN (Lauer, Gorzewski, Gerlinghoff, Backmund, & Zihl, 1999). However, some findings indicate alarmingly permanent structural and neuropsychological alterations (Lambe, Katzman, Mikulis, Kennedy, & Zipursky, 1997).

Family and Developmental Characteristics

Suggestive themes emerge in family findings pertaining to the EDs. However, there are several important limitations of the literature in this area: (1) Very few of the available studies apply appropriate psychiatric control groups to establish specificity of observed patterns to eating syndromes. (2) Studies rarely provide for corroboration, by family members, of observations from actively eating-disordered participants. (3) Even when systematic tendencies are identified (ED-specific or otherwise), there remains a need to clarify whether they express dynamic family patterns (transmitted via psychosocial pathways), or effects of temperamental traits (representing inherited tendencies). These concerns aside, available data have provided partial corroboration of developmental theories on EDs (reviewed earlier).

Studies on anorexic individuals and their relatives have provided general corroboration of the concepts of enmeshment, overprotection, separation problems, and conflict avoidance. Studies report anorexics’ families to limit members’ autonomy, or to show unusually low levels of conflict. Crisp, Hsu, Harding, and Hartshorn (1980) reported disturbed parent-child interactions in about half of 102 cases of AN, with enmeshment being the most commonly reported theme. Goldstein (1981), using coded records of parent-child interactions, discriminated families of hospitalized anorexics from those of hospitalized nonanorexics, on dimensions reflecting requests for protection and conflict avoidance. Similarly, families of anorexics have been noted to show unusually low expressed emotion, indicating low levels of conflictual or disapproving interactions (Hodes & leGrange, 1993). Such observations are compatible with the concept of an enmeshed or underseparated familial organization. However, Kog, Vertommen, and Vandereycken’s (1987) study of families with an eating-disordered daughter indeed identified a subset that displayed low conflict, although they found this pattern to coincide with bulimic ED variants as frequently as it did with restrictive ones. Their finding raises some doubts about the specificity of the conflict-avoiding, enmeshed family concept for AN.

Observational studies of families in which binge-purge syndromes develop have tended to corroborate the perspective that such syndromes coincide relatively more often with overt familial discord and hostility. For example, Sights and Richards (1984) noted bulimics’ families to display marked parent-daughter stress and rated bulimics’ mothers as being domineering and demanding. Similar themes are conveyed by Humphrey’s rather extensive observational work with eating-disordered families (see Humphrey, 1991). In studies comparing bulimic-anorexic mother-father-daughter triads to those of normal triads, her findings showed the bulimicanorexic families to be more blameful, rejecting, and neglectful, and less nurturant and comforting. Likewise, in a series of studies contrasting family processes in females with normal-weight bulimia, bulimic AN, restrictive AN, or no ED, Humphrey found the families of both bulimic subgroups to be prone to deficits in parental nurturance and (to some extent) empathy. In keeping with this notion, studies have indicated expressed emotion (i.e., open conflict and critical comments) to be greater in bingers’ than in restrictors’ families (Hodes & leGrange, 1993).

Data on family interaction patterns in BED are very rare, making it premature to draw conclusions. However, Hodges, Cochrane, and Brewerton (1998) obtained self-reports on family functioning in 23 anorexic-restrictor, 45 bulimic, 20 anorexic-binger, and 43 BED women. The BED patients reported less family cohesion than did anorexic ones and less familial expressiveness than did bulimic ones. The BED women also indicated their families to show less cohesion, expressiveness, independence, and intellectual-cultural and active-recreational pursuits than did women in a normal control group. Relative to the normal control women, BED patients reported their families to be higher on dimensions measuring conflict and control. In other words, BED patients seemed to be reporting a constellation of family interaction patterns that was at least partially reminiscent of those of BN patients.

Although there are systematic convergences between family interaction patterns (on the one hand) and ED subtypes (on the other), recent thinking on family factors in the EDs is close to abandoning the probably unrealistic notion that there may be ED-specific family interaction variants. Instead, theorists address more interesting questions about the possible modulating role of family functioning in the development and maintenance of eating symptoms. Schmidt, Humfress, and Treasure (1997) noted that severity of family dysfunction corresponds closely to severity of personality pathology in affected individuals, suggesting a modulating influence of family functioning enacted through concurrent psychopathological traits.

Psychosocial Induction

It is appealing to presume that the EDs depend upon psychosocial induction effects in which parents convey maladaptive concerns with body image, weight, and eating to their children. Indeed, in clinical populations, many studies report parents of ED sufferers to show abnormal eating and body-image attitudes (e.g., Hall & Brown, 1983). However, many others report an absence of differences between parents with and without eating-disordered daughters (e.g., Hall, Leibrich, Walkley, & Welch, 1986). At the same time, various findings are consistent with parental influences upon children’s eating behavior. Miller, McCluskey-Fawcett, and Irving (1993) compared perceptions of early mealtime experiences across normal eaters, repeat dieters, and bulimics, and found the bulimics to display more eating-related issues in the early family context. In a related vein, a recent study of 369 adolescent girls and their parents found that parents’ encouragements to daughters to lose weight were more significant as predictors of daughters’ dietary restraint than were parents’ own dietary restraint levels, and mothers’ encouragements were more influential than were fathers’ (Wertheim, 1999). Such findings may be sensitive to retrospective reporting biases but they are consistent with the idea that the family’s eating and body-image-relevant attitudes can convey risk for an ED.

Yet another source of parental influence over children’s eating patterns is suggested by data showing a disturbing degree of association between mothers’ EDs and feeding problems in children. Whelan and Cooper (2000) rated a filmed family meal in three groups of 4-year-olds: Children with feeding problems ( N 42), children with a nonfeeding form of disturbance (e.g., shyness or behavioral disturbance; N 79), and children with no disturbance ( N 29). They found mothers of children with feeding problems, when compared to mothers in the other two groups, to have higher rates of current and past EDs but not mood disorders.

On the basis of a review of studies concerning parent-child and familial attachment patterns in the EDs, Ward, Ramsay, Turnbull, Benedettini, and Treasure (2000) concluded that ED patients display pathological attachment tendencies. Various studies have indicated that individuals with anorexia, relative to healthy controls, report one or both parents to be less affectionate, empathic, caring, or protective (Rhodes & Kroger, 1992; Steiger, Van der Feen, Goldstein, & Leichner, 1989). Rhodes and Kroger found anorexic individuals to be anxious about parental separation and engulfment, whereas Armstrong and Roth (1989) found AN subjects to have more anxious attachments and separation depression than controls. While such findings are suggestive, we note that they do not necessarily imply ED-specific anomalies.

Data indicate parallel attachment problems in BN. Individuals with bulimia report themselves to form dependent or insecure attachments (Jacobsin & Robins, 1989), to be mistrustful of others, anxious about revealing imperfections, and fearful of intimacy (Pruitt, Kappins, & Gorman, 1992). An experience-sampling study by our group highlights the potential importance of relationship factors in BN, in that stressful social experiences emerged as relatively direct antecedents to binge episodes in actively bulimic women (Steiger, Gauvin, et al., 1999).

Childhood Sexual Abuse

Modal figures indicate roughly 30% of ED sufferers to report some form of unwanted sexual experience during childhood (e.g., Everill & Waller, 1995; Wonderlich et al., 1997). Given that they implicate such markedly disturbed bodily experience, it is enticing to think that EDs may be specifically (and causally) linked to body-relevant trauma occurring during childhood. However, it should be noted that observed rates of trauma in ED sufferers do not consistently exceed those obtained in females with other psychopathology, an implication that there is a strong but nonspecific association of the EDs with childhood trauma.

Data comparing prevalence of childhood sexual trauma in restricting and binging subgroups have suggested that bulimic ED variants might be associated with the more unfavorable developmental experiences. Schmidt et al. (1997), for example, conclude that findings have consistently associated childhood abuse more strongly with binge-purge than with restrictive ED variations. In keeping with the suggested tendency, Webster and Palmer (2000) found that women with bulimic symptomatology (but not restrictive AN) reported more troubled childhood experiences than did normal-eater comparison women, but reported experiences comparable to those of women with depression. Although such observations could reflect greater repression in restrictors, or protectiveness of the family, the trend in question would also be consistent with an overall portrait of the bulimic family as being the more destructive, abusive, or neglectful, rendering the child subject to a heightened risk of abuse. These data also reiterate the point made earlier about relative nonspecificity of the link between EDs and childhood abuse.

Community-survey data have corroborated the notion that BN coincides with relative elevations of victimization experiences. A telephone survey of 3,006 women linked history of forcible assault or rape to BN more than to BED or non–eating disordered status. Furthermore, in this study, reliance upon compensatory behaviors was associated with higher rates of victimization (Dansky, Brewerton, Kilpatrick, & O’Neil, 1997). Even if childhood traumata are more strongly linked to bulimic than to restrictive ED variants, however, this need not imply bulimia-specific pathogenic effects. Several studies in BN have noted that severity of childhood abuse predicts severity of personality pathology, impulsivity, dissociative potentials, and other forms of comorbid psychopathology more directly than it does severity of bulimic symptoms. For example, a study comparing 50 sexually abused versus 83 nonsexually abused eatingdisordered women showed elevations in the sexually abused women, not on ED symptoms, but on various self-reported personality dimensions: schizotypal, avoidant, schizoid, passive-aggressive, and borderline (Moreno, Selby, & Neal, 1998). One study of 44 former bulimics found that those with a history of sexual or physical abuse ( N 20) had more posttraumatic symptoms and more substance dependence (Matsunaga, Kaye, et al., 1999).

Sociocultural Context

Eating disorders occur disproportionately often in Western industrialized nations, implying that cultural ideals prevailing in the West may be conducive to ED development. It is obvious that Western social values to some extent equate slimness with cultural ideals of success, beauty, power, and self-control, and there is little doubt that such factors play some role in the development of clinical EDs (see Garfinkel & Garner, 1982). Changing ideals for female body shape are thought to be associated with the apparent increase in incidence of EDs that occurred in the West during the decades since 1960 (see the section titled “Epidemiology”). This period coincided with a dramatic shift in a cultural ideal—from a voluptuous form represented by such icons as Marilyn Monroe, Elizabeth Taylor, or Sophia Loren to a thin (and often relatively androgynous) ideal for female appearance that became popular in the early 1960s, and that remains prominent in celebrity and media images in the 2000s.Attesting to the importance of peer and pop culture influences in the development of maladaptive eating, a 1-year prospective study of 6,982 girls showed that measures of the felt importance of looking like the females that are seen on television, in movies, or in magazines predict the onset of regular vomiting or laxative abuse as a means of weight control (Field, Camargo, Taylor, Berkey, & Colditz, 1999). Further supporting the concept that social values pertinent to thinness have a causal role in EDs, the work of Garner and Garfinkel (see Garfinkel & Garner, 1982) shows AN to occur exceptionally often in individuals whose social milieu emphasizes weight control (e.g., ballet dancers, models, or athletes). In a related vein, various findings suggest that Western cultural values have a special role in generating risk for ED development. Davis and Katzman (1999) noted that level of eating and body-image concerns corresponded quite directly to the level of acculturation toAmerican values of Chinese university students studying in the United States. Likewise, Lake, Staiger, and Glowinski (2000) compared Australian-born and Hong Kong–born Australian university students on eating attitudes and body-shape perceptions, and found that Australian-born and Western-acculturated Hong Kong–born women showed greater body-image problems.

Although risk for EDs is certainly linked to Western social contexts, such social effects may yet have only a limited influence in ED etiology. For example, systematic cross-cultural research indicates anorexia-like syndromes, characterized by food refusal, to be prevalent in diverse (non-Western) contexts (Pate, Pumariega, Hester, & Garner, 1992), suggesting that anorexia-like syndromes may not be as culture-bound as once thought. A self-report assessment of attitudes toward eating among undergraduate women studying in Pennsylvania ( N = 111) and South Korea ( N = 115) showed similar percentages (21% and 18%, respectively) of respondents reporting elevations on an ED-screening instrument (Lippincott & Hwang, 1999). Indeed, some cross-cultural data reduce emphasis upon the role of cultural pressures favoring slimness in ED pathogenesis altogether. Lee, Ho, and Hsu (1993), for example, provided a well-constructed study of individuals with anorexia in Hong Kong—all of whom were clearly anorexic according to criteria reflecting self-imposed weight loss, resistance to others’ encouragements to eat, and amenorrhea (or loss of libido, in one male case). However, unlike individuals with anorexia encountered in American contexts, roughly 60% were noted to display no conscious fear of becoming fat. They justified their food refusal instead by stating a desire to avoid gastric bloating. Given similar findings from other Asian studies, Lee and colleagues proposed that fat phobia may be characteristic of weight-conscious Western societies but not definitive of AN at large.These findings imply that culture may exert pathoplastic effects that shape ultimate ED expression.

Other cross-cultural studies have reported an absence of cultural influences or culture-free universals that apply to the EDs. For example, bulimic tendencies and proneness to generalized impulse-control problems have been noted to coincide as much in Japanese samples as in Western cases (Matsunaga, Kiriike, et al., 2000). Similarly, cross-cultural data make a case that, regardless of cultural context, EDs and OCD converge (Matsunaga, Kiriike, et al., 1999). Emphasizing a universal importance of maladaptive family interactions as an ED correlate, one study has shown that the degree of maladaptive eating attitudes and behaviors in British Asian schoolgirls correlates with measures of familial overprotection and conflicts around socializing (Furnham & Husain, 1999).

Biological Factors

Family studies.

Findings from available family studies provide unequivocal support for the conclusion that there is familial aggregation for the EDs, a prerequisite if one assumes biological transmission. The largest case-controlled study available examined the prevalence of EDs among first-degree relatives of 300 probands with AN or BN (Strober, Freeman, Lampert, Diamond, & Kaye, 2000). This investigation found substantially higher risks for AN in female relatives of anorexic and bulimic probands (relative risks of 11.3 and 12.3, respectively) compared to those obtained in relatives of normaleater comparison subjects. A familial propensity was also indicated for BN, with relative risks of 4.2 for relatives of anorexic probands and 4.4 for bulimic probands, respectively. These findings suggest a strong family tendency for both anorexic and bulimic ED variants, but stronger aggregation for AN than for BN. Results of another recent family study have suggested that relatives of AN and BN probands both show similarly elevated risk for ED, withoutAN or BN specificity (Lilenfeld et al., 1998). These findings are consistent with familial transmission for a general factor that heightens susceptibility to EDs, but not specifically toAN or BN.

Cotransmission in Families With Other Syndromes

Family data need not imply disorder-specific transmission effects. Rather, they could reflect a liability that is conveyed by linkage within the family to another heritable disturbance or syndrome. Relationships of this type have been explored for the EDs with respect to various forms of psychopathology. Family studies suggest substantially higher rates of mood disorders, especially unipolar depression, among relatives of anorexic (e.g., Strober, Lampert, Morrell, Burroughs, & Jacobs, 1990) and bulimic (e.g., Logue, Crowe, & Bean, 1989) probands. However, when distinctions between ED probands with and without an ascertained history of mood disorder have been made, findings reveal increased risk of affective disorders in only the relatives of those ED probands who themselves suffer from mood disturbance (Lilenfeld et al., 1998; Strober et al.). In other words, while shared vulnerability factors may be implicated, there does not seem to be any simple or direct cotransmission for eating and affective disturbances.

Similarly, various studies have documented an increased rate of alcohol and drug abuse in ED patients and their relatives, especially in the relatives of bulimic probands (Lilenfeld et al., 1998). However, as noted for mood disorders, evidence on the co-aggregation of eating and substance-use disorders favors belief in independent transmission because only the relatives of ED probands who themselves abuse substances show consistently higher risk of substance-abuse problems (e.g., Lilenfeld et al.). Likewise, Lilenfeld and colleagues report that only eating-disordered probands who themselves show heightened OCD have family histories characterized by higher OCD prevalence. In other words, familial transmission of OCD appears also to occur independently of EDs.

In an intriguing contrast to the preceding, Lilenfeld and colleagues (1998) have also suggested shared familial transmission of obsessive-compulsive personality disorder (OCPD) with AN (but not BN). In their study, relatives of anorexic probands showed elevated OCPD, regardless of the presence of OCPD in the anorexic proband. Such findings are in keeping with the notion that there may be a relatively ANspecific transmission, within families, of personality traits of perfectionism, rigidity, and harm avoidance (i.e., OCPD) and risk for AN.

Twin Studies

Through comparison of concordance rates in genetically identical (i.e., monozygotic) versus nonidentical (i.e., dizygotic) twins, it becomes possible to isolate genetic factors that contribute to a disorder. Twin data can, furthermore (using behavioral-genetic models), be analyzed to tease apart the relative contributions of additive-genetic effects (i.e., inherited liabilities) , shared-environmental effects (i.e., liabilities resulting from such influences as general familyinteraction patterns, or the family’s socioeconomic status), and effects of the nonshared or individual-specific environment (i.e., liabilities related to having experienced childhood trauma, or having had a particular type of relationship with one parent). Various twin studies of EDs have now been completed, providing intriguing yet equivocal findings.

In a clinically ascertained sample of 31 monozygotic and 28 dizygotic anorexic twins, Treasure and Holland (1989) found substantially higher concordance in monozygotic than in dizygotic pairs (45% vs. 2%, respectively). Furthermore, when diagnostic criteria were narrowed to accept only restricting AN (i.e., excluding patients with binge or purge symptoms), differences between mono- and dizygotic twins became even more striking—with concordance increasing to 65% for monozygotic and falling to 0% for dizygotic. Such findings imply rather striking heritability for a restrictive AN factor, and based on their results, Treasure and Holland estimated a 70% liability for restrictive AN attributable to additive genetic effects. Raising controversy around such conclusions, however, Walters and Kendler (1995), in a population-based (vs. Clinically ascertained) sample, obtained no evidence of heightened risk for AN in monozygotic compared to dizygotic twins.

A reanalysis of combined data from the early-available twin studies on BN revealed 46% concordance for monozygotic twins versus 26% concordance for dizygotic twins, with an estimated 47% of the variance attributable to additive genetic effects, 30% to shared environment, and 23% to nonshared environment (Bulik, Sullivan, Wade, et al., 2000). Similarly, a population-based study of 2,163 female twins found concordance rates for BN to be 22.9% for monozygotic and 8.7% for dizygotic twins (Kendler et al., 1991), with an estimated 55% of variance from additive genetic effects, 0% from shared environment, and 45% from individual-specific environmental effects. Other studies have examined genetic effects acting upon more broadly defined (subthreshold) variants of BN. For example, Bulik, Sullivan, and Kendler (1998) estimated heritability of broadly defined BN to be 83% in a sample of 854 twin pairs, suggesting that BN is quite a heritable syndrome.

Genetic Linkage Studies

Genetic linkage studies seek to identify genes, in affected individuals and their relatives, that may underlie risk for a specific disorder. Studies aimed at candidate genes underlying ED vulnerability have focused on genes coding for dopamine, serotonin, and noradrenaline systems, under the assumption (which will be explained further) that these monoamines may regulate eating behavior. To date, relevant studies in anorexic samples have failed to find systematic linkage of particular variants of dopamine (Bruins-Slot et al., 1998) or 3 -adrenergic receptor (Hinney et al., 1997) genes in AN. The search for candidate genes within the serotonin (5-hydroxytryptamine, or 5HT) system has, however, yielded somewhat more promising results. Association has been reported between AN and a polymorphism (–1438G/A) in the promoter region of the 5HT 2A receptor (Enoch et al., 1998). Furthermore, this 5HT 2A finding has been found to be associated with both AN restrictor subtype and OCD, but not with bulimic ED variants. Together, such findings argue that the 5HT gene variation in question may correspond to both “anorexic” and “generalized” obsessions and compulsions.

Possible genetic substrates for BN are also identified. Levitan et al. (2000) reported an association between the C218 allele of the gene encoding for tryptophan hydroxylase (or TPH, the rate-limiting enzyme for 5HT synthesis) and BN. It is pertinent to note that Nielsen and colleagues (1998) reported a similar association, in male offenders, between a TPH gene variant (on the one hand) and suicidality and alcoholism (on the other hand), suggesting that this gene variant may correspond to an impulsive–behaviorally dysregulated phenotype. Such findings, viewed together, are consistent with the tendency of bulimic ED variants to be characterized by impulsivity and behavioral dyscontrol.

Neurobiology

The search for neurobiological agents that are implicated in the pathophysiology of EDs has led to the exploration of neurotransmitter, neuropeptide, and hormone systems involved in appetite, feeding behaviors, affect regulation, and temperament.

Neurotransmitters. Various monoamine neurotransmitters play a role in appetite regulation.Actions upon appetitive behaviors of noradrenaline and dopamine appear to include both excitatory and inhibitory effects upon feeding behavior, depending upon receptor sites stimulated. In contrast, serotonin (5HT), via its action on hypothalamic receptors, is believed to act mainly in the mediation of satiety.Animal and human studies indicate experimental manipulations that increase 5HT neurotransmission to lead to suppression of food intake, whereas antagonism of 5HT leads to hyperphagia (see Brewerton, 1995). We shall review the findings obtained for AN and BN in studies of each of these systems.

Several investigations have studied the noradrenergic system in AN. Anorexia nervosa has been associated with reduced concentrations of noradrenaline and its major metabolite, 3-methoxy-4-hydroxyphenylglycol (MHPG) in cerebrospinal fluid (CSF), as well as with increased density and sensitivity of platelet 2 -adrenergic receptors (see Fava, Copeland, Schweiger, & Herzog, 1989). However, after nutritional rehabilitation, CSF MHPG levels in women with AN are found to compare to those of control women (Kaye, Frank, & McConaha, 1999), suggesting that changes in the noradrenergic system may mainly constitute adaptations to starvation. Studies of dopamine activity in AN have yielded contradictory results. Kaye, Ebert, Raleigh, and Lake (1984) reported anorexic women to show lower CSF homovanillic acid (HVA, a dopamine metabolite) than did control women, and then, in a 1999 study, reported lower CSF HVA in a group of recovered anorexic restrictors and a tendency toward lower HVA in recovered anorexic bingers. Although such findings imply lowered dopamine activity in active or recovered AN, Johnston, Leiter, Burrow, Garfinkel, and Anderson (1984) found no differences when comparing HVA levels in women with anorexia to those in controls.

Studies of the serotonin system have revealed various 5HT abnormalities, consistent with reduced 5HT tone, in active anorexics, including (a) decreased platelet binding of serotonin uptake inhibitors (Weizman, Carmi, Tyano, Apter, & Rehavi, 1986); (b) blunted prolactin and cortisol responses to 5HT agonists and partial agonists (Monteleone, Brambilla, Bortolotti, La Rocca, & Maj, 1998); and (c) reduced CSF levels of 5HT metabolites (Kaye et al., 1984). Some investigators have reported normalization of prolactin response to a 5HT releasing agent, d-fenfluramine, in recovered anorexics (Ward, Brown, Lightman, Campbell, & Treasure, 1998), as might indicate a state-related 5HT abnormality. In contrast, Kaye, Gwirtsman, George, and Ebert (1991) found elevated CSF 5-hydroxyindoleacetic acid (or 5HIAA, a 5HT metabolite) in a sample of weight-restored anorexics. They interpreted this apparently anomalous finding as an indication that AN and associated traits (e.g., harm avoidance, perfectionism) may actually be linked to a primary state of increased 5HT tone that is then masked by malnutrition-induced reductions in 5HT activity during active stages of the disorder. Further work is needed to clarify this possibility.

As with AN, findings in BN have been consistent with decreased noradrenaline activity. For example, women with BN have been reported to show low resting levels of plasma noradrenaline (Kaye et al., 1990). Given a study reporting normal CSF MHPG levels in recovered bulimics, however, it appears that noradrenaline abnormalities in BN may need to be regarded as state-dependent effects (Kaye et al., 1998). Studies focused on dopaminergic activity in BN have documented low CSF HVA (a dopamine metabolite) in active BN (Jimerson, Lesem, Kaye, & Brewerton, 1992). However, again, one study reports normal CSF HVAlevels in recovered bulimics (Kaye et al., 1998).

More extensive than that in AN, study of the 5HT system in BN has consistently suggested reduced 5HT activity. Bulimia nervosa patients are noted to display (a) decreased CSF 5HIAA (Jimerson et al., 1992), (b) reduced platelet binding of 5HT uptake inhibitors (Steiger et al., 2000), and (c) blunted neuroendocrine responses to 5HT precursors and 5HT agonists or partial agonists (e.g., Levitan et al., 1997; Steiger, Koerner, et al., 2001). Such findings have been taken to suggest decreased brain 5HT turnover and down-regulation of postsynaptic 5HT receptors mediating neuroendocrine responses. Other studies have used dietary manipulations to explore links between 5HT levels and bulimic symptoms. For instance, tryptophan depletion, which lowers brain tryptophan and subsequent 5HT synthesis, has been shown to exacerbate bulimic symptoms in actively bulimic women (Kaye et al., 2000) and to lead to transient reappearance of bulimic symptoms in recovered bulimics (Smith, Fairburn, & Cowen, 1999). These results appear to reflect a particular vulnerability within the 5HT system of women at risk for BN and establishes a potential neurobiological substrate for antecedent effects of dieting in BN.

Given their marked co-aggregation, there has been an interest in the possibility that bulimic symptoms and impulsivity have a common serotonergic basis. In non–eating disordered populations,datadocumentaclearassociationbetweenimpulsivity and low 5HT (Coccaro et al., 1989). Paralleling such findings,Steiger,Koerner,etal.(2001b)foundcorrespondence between the extent of apparent reduction in 5HT activity and the severity of impulsive symptoms. Such findings imply that 5HT abnormalities may mediate both binge eating and impulsive symptoms, and may (in part) account for the frequent convergence of BN with problems of impulse regulation.

Appetite-Regulating Peptides and Hormones. Cholecystokinin (CCK), a peptide secreted by the gut, acts on the hypothalamus to produce satiety. Available data suggest low basal and postprandial (after-eating) plasma CCK in BN, but not in AN (Pirke, Kellner, Frie, Krieg, & Fichter, 1994). It is not known to what extent low CCK in BN may preexist disorder onset or may result from abnormal eating behaviors. Regardless, once established, low CCK could help perpetuate binge-eating behavior via its impact on satiety.

Leptin is a newly identified hormone secreted by fat cells. Leptin acts on the hypothalamus to regulate appetite and energy expenditure in accordance with fat stores. In active AN, findings have shown reductions in serum and CSF leptin levels corresponding to decreased body mass (Grinspoon et al., 1996). Findings have also shown restoration of normal levels upon weight recovery (Hebebrand et al., 1997). However, although low leptin levels in AN may, therefore, be partly attributable to low fat stores, one study found decreased leptin in restricting but not purging anorexics, despite equally low body weight in both groups (Mehler, Eckel, & Donahoo, 1999).Astudy of bulimic women has also reported low leptin levels, despite normal body weight (Monteleone, Di Lieto, Tortorella, Longobardi, & Maj, 2000). Leptin levels may, therefore, not be modulated by body weight alone, and further work is needed to investigate the full interplay that may exist between leptins and the EDs.

Neuroimaging Studies. Neuroimaging studies aim to establish structural or functional brain abnormalities and use techniques like computerized tomography (CT) and magnetic resonance imaging (MRI) to allow visualization of gross brain structure. Functional neuroimaging techniques, including positron emission tomography (PET) and proton magnetic resonance spectroscopy (H-MRS), are used to analyze specific chemical and electrical activity within the brain. With the use of CT and MRI, structural brain changes have been detected in both anorexic and bulimic patients. Findings include enlarged ventricles and sulcal widening, gray- and white-matter abnormalities, and lateralization of deficits (e.g., Hoffman et al., 1989). Reversible and irreversible components have been identified, including persistent graymatter (but not white-matter) volume deficits in weightrecovered anorexics (Lambe et al., 1997). Taken together, imaging studies suggest that many abnormalities constitute transient effects of nutritional deprivation, but that some may be disturbingly permanent sequelae.

An Integrated (Multidimensional) Etiological Concept

In a social context that equates thinness with many social values, it is not surprising to find that most people display bodyimage and diet consciousness, and that an alarming number of these persons (especially young women) progress to the development of full-blown EDs. However, as much as the EDs are defined by pathognomonic preoccupations with eating, weight-control, and body image, they are also polysymptomatic syndromes, invariably including characterological, affective, interpersonal, and self-regulatory disturbances. Syndromes with this degree of phenomenological complexity are likely to implicate diverse causal processes. An adequate etiological model for the EDs will need to account for roles of converging biological, psychological, familial, and sociocultural processes.

In attempting to understand ED etiology, we have often found it heuristic to contemplate two classes of causal agents, each having its own character and each (presumably) its own multiple (biopsychosocial) etiological agents. One factor relates to eating-specific aspects of disturbance (surrounding eating, weight, and body image); the other relates to more generalized vulnerabilities, psychopathology, or maladaptation. This proposal, that EDs implicate eating-specific and generalized components of pathology, was first addressed in the two-component model of eating disorders proposed by Garner, Olmstead, Polivy, and Garfinkel (1984). A basic aspect of this view is that eating-specific concerns are not sufficient to explain the development of clinical ED, and that the concurrent presence of a more generalized psychopathology, expressed through broad mood and behavioral dysregulation, is required. How might generalized and eating-specific factors interact in ED pathology? To reflect a diversity of possible pathways, we provide some illustrative examples.

• Constitutional vulnerabilities (e.g., inherited problems of serotonin neurotransmission) may, along with their predictable effects on mood and impulse regulation, confer vulnerability to disorders of satiation (and hence bulimic eating patterns) in individuals disposed by social or family pressures emphasizing thinness to restrict their food intake. This might, in part, explain an affinity of bulimic eating syndromes for manifestations including mood or impulse dyscontrol and, in part, findings showing BN to be associated with reduced serotonin functioning. In other words, BN may (at least sometimes) implicate a generalized (serotonin-linked) risk factor, related to susceptibility to impulsivenessandappetitivedysregulation,butwhatmight be needed to trigger the expression of this vulnerability is a specific pressure or encouragement toward dietary restraint.
• Given a social context that overvalues thinness and that links body-esteem to overall self-esteem (especially in women), generalized self-image problems in females (along with a propensity to be perfectionistic or overly sensitive to social approval) might indirectly heighten susceptibility to dieting and, eventually, to pathological eating practices. In this eventuality, one would expect (as tends to be the case) to find perfectionism, self-criticism, reward dependence, and related characteristics in ANprone individuals. We presume that such (generalized) tendencies heighten the likelihood that normal (eatingspecific) social concerns about slimness may be carried, in clinical ED sufferers, to the pathological extreme.
• Parental overprotection or overcontrol, while alone insufficient to explain ED development, might support the progression from compulsive dieting to frank eating obsession in the weight-conscious adolescent. Furthermore, the adolescent’s rejection of parental controls might, if the parents themselves showed propensities toward compulsiveness or anxious overcontrol, mobilize destructively intrusive overreactions on the part of the parents. The child’s further opposition would gradually feed into an escalating spiral of parental intrusiveness followed by angry oppositionality on the part of the affected child. Self-starvation seems, at least sometimes, to be mobilized as a weapon in such an escalation of conflict.

In each of the preceding examples, we assume that development of a clinical ED requires that thresholds be surpassed in key areas of vulnerability, some eating-specific, some more generalized. A main implication of this view is that diffuse psychopathology, while not representing an ED-specific ingredient, might be a manifestation of a process that serves to enhance risk of ED development. At the same time, it is also necessary to contemplate the full range of interactions (among biological, psychological, and social factors) that may occur once an ED has developed, such that increasingly more severe and more entrenched eating and generalized disturbances may ensue. Consider the following hypothetical examples.

In the first example, an insecure adolescent girl with an anxious, perfectionistic bent (prone to difficulties with establishing limits around her own performance) begins dieting to bolster her self-esteem. Weight loss produces various social rewards as peers and parents pay her more positive attention. However, dieting also leads to alteration of normal neurobiological systems (known sequelae of intensive dieting). One consequence can be an exacerbation of anxiety and obsessionality and, gradually, increasing preoccupation with thinness. Her natural tendency to demand too much of herself evolves, under new biological influences, into full-blown obsession—and intensive dieting gradually evolves into a full-blown ED.

Alternatively, consider the effects, in a second adolescent, in whom a very-destructive developmental environment characterized by parental hostility and physical abuse has (aside from having damaging effects upon her sense of selfworth) been a manifestation of a family wide tendency towards impulse dysregulation. Assume that the family tendency of impulse dysregulation may have been borne, in part, by genes that code for lowered serotonin synthesis and neurotransmission. For this girl, dieting to achieve a better selfimage (which would reduce brain serotonin activity even further) may not only lower the threshold for the expression of impulsive tendencies, but may lower the threshold for binge eating by creating impairment in satiety mechanisms. She might gradually develop binge eating, while at the same time becoming progressively more disinhibited, irritable, labile, and self-damaging. An implicit concept, especially important in designing eventual treatments, is that ED symptoms can become quite self-perpetuating, and in time, quite divorced from the psychobiological and sociocultural factors that may have originally contributed to the development of the disorder.

If ED etiology is as genuinely biopsychosocial as findings lead us to believe, then the study of eating disorders may inform theory on psychopathology in many ways, including the manner in which psychopathology can represent the activation of latent genetic vulnerabilities through specific environmental pressures; the manner in which latent traits and tendencies can be shaped by developmental experiences; and how maladaptive traits within the at-risk individual can mobilize destructive responses from the social environment. In addition, the EDs teach us to appreciate the ways in which socially prescribed responses (even those as apparently innocuous as a young girl’s dieting) can, in specifically vulnerable individuals, generate multiple and highly maladaptive repercussions that can come to broadly affect an individual’s global psychological development and functioning.

Bibliography:

• American Psychiatric (1994). Diagnostic and statistical manual of mental disorders (4th ed.). Washington, DC: Author.
• Armstrong, J., & Roth, D. M. (1989). Attachment and separation difficulties in eating disorders: A preliminary investigation. International Journal of Eating Disorders, 8, 141–155.
• Blanz, B. J., Detzner, U., Lay, B., Rose, F., & Schmidt, M. H. (1997). The intellectual functioning of adolescents with anorexia nervosa and bulimia nervosa. European Child and Adolescent Psychiatry, 6, 129–135.
• Borman Spurrel, E. B., Wilfley, D. E., Tanofsky, M. B., & Brownell, K. D. (1997). Age of onset for binge eating: Are there different pathways to binge eating? International Journal of Eating Disorders, 21, 55–65.
• Brewerton, T. D. (1995). Toward a unified theory of serotonin dysregulation in eating and related disorders. Psychoneuroendocrinology, 20, 561–590.
• Brewerton, T. D., Lydiard, R. B., Herzog, D. B., Brotman, A. W., O’Neil, P. M., & Ballenger, J. C. (1995). Comorbidity of Axis I psychiatric disorders in bulimia nervosa. Journal of Clinical Psychiatry, 56, 77–80.
• Bruch, H. (1973). Eating disorders: Obesity, anorexia nervosa and the person within . New York: Basic Books.
• Bruins-Slot, L., Gorwood, P., Bouvard, M., Blot, P., Ades, J., Feingold, J., Schwartz, J., & Mouren-Simeoni, M. (1998). Lack of association between anorexia nervosa and D3 dopamine receptor gene. Biological Psychiatry, 43, 76–78.
• Bulik, C. M., Sullivan, P. F., Fear, J. L., & Pickering, A. (2000). Outcome of anorexia nervosa: Eating attitudes, personality, and parental bonding. International Journal of Eating Disorders, 28, 139–147.
• Bulik, C. M., Sullivan, P. F., & Kendler, K. S. (1998). Heritability of binge-eating and broadly defined bulimia nervosa. Biological Psychiatry, 44, 1210–1218.
• Bulik, C. M., Sullivan, P. F., Wade, T. D., & Kendler, K. S. (2000). Twin studies of eating disorders: Areview. International Journal of Eating Disorders, 27, 1–20.
• Bulik, C. M., Sullivan, P. F., Weltzin, T. F., & Kaye, W. H. (1995). Temperament in eating disorders. International Journal of Eating Disorders, 17, 251–261.
• Calam, R., & Waller, G. (1998). Are eating disorders and psychosocial characteristics in early teenage years useful predictors of eating characteristics in adult years? A7-year longitudinal study. International Journal of Eating Disorders, 24, 351–362.
• Carter, F. A., Bulik, C. M., Lawson, R. H., Sullivan, P. F., & Wilson, J. S. (1996). Effect of mood and food cues on body image in women with bulimia and controls. International Journal of Eating Disorders, 20, 65–76.
• Casper, R. C., Hedeker, D., & McClough, J. F. (1992). Personality dimensions in eating disorders and their relevance for subtyping. Journal of the American Academy of Child and Adolescent Psychiatry, 31, 830–840.
• Cassidy, E., Allsopp, M., & Williams, T. (1999). Obsessivecompulsive symptoms at initial presentation of adolescent eating disorders. European Child & Adolescent Psychiatry, 8, 193–199.
• Coccaro, E. F., Siever, L. J., Klar, H. M., Maurer, G., Cochrane, K., Cooper, T. B., Mohs, R. C., & Davis, K. L. (1989). Serotonergic studies in patients with affective and personality disorders:
• Correlates with suicidal and aggressive behavior. Archives of General Psychiatry, 46, 587–599.
• Crago, M., Shisslak, C. M., & Estes, L. S. (1996). Eating disturbances among American minority groups: A review. International Journal of Eating Disorders, 19, 239–248.
• Crisp, A. H. (1980). Anorexia nervosa: Let me be . London: Academic Press.
• Crisp, A. H., Hsu, L., Harding, B., & Hartshorn, J. (1980). Clinical features of anorexia nervosa: A study of a consecutive series of 102 female patients. Journal of Psychosomatic Research, 24, 179–191.
• DaCosta, M., & Halmi, K. A. (1992). Classifications of anorexia nervosa: Question of subtypes. International Journal of Eating Disorders, 11, 305–313.
• Dansky, B. S., Brewerton, T. D., Kilpatrick, D. G., & O’Neil, P. M. (1997). The National Women’s Study: Relationship of victimization and posttraumatic stress disorder to bulimia nervosa. International Journal of Eating Disorders, 21, 213–228.
• Davis, C., & Katzman, M. A. (1999). Perfection as acculturation: Psychological correlates of eating problems in Chinese male and female students living in the United States. International Journal of Eating Disorders, 25, 65–70.
• Demitrack, M. A., Putnam, F. W., Brewerton, T. D., Brandt, H. A., & Gold, P. W. (1990). Relation of clinical variables to dissociative phenomena in eating disorders. American Journal of Psychiatry, 147, 1184–1188.
• Enoch, M. A., Kaye, W. H., Rotondo, A., Greenberg, B. D., Murphy, D. L., & Goldman, D. (1998). 5-HT 2A promoter polymorphism1438G/A, anorexia nervosa, and obsessive-compulsive disorder. Lancet, 351, 1785–1786.
• Everill, J., & Waller, G. (1995). Reported sexual abuse and eating psychopathology: A review of evidence for a causal link. International Journal of Eating Disorders, 18, 1–11.
• Everill, J., Waller, G., & Macdonald, W. (1995). Dissociation in bulimic and non-eating-disordered women. International Journal of Eating Disorders, 17, 127–134.
• Fairburn, C. G. (1995). Overcoming binge eating . New York: Guilford Press.
• Fairburn, C. G., Cooper, Z., Doll, H. A., & Welch, S. L. (1999). Risk factors for anorexia nervosa: Three integrated case-controlled comparisons. Archives of General Psychiatry, 56, 468–476.
• Fairburn, C. G., Doll, H. A., Welch, S. L., Hay, P. J., Davies, B. A., & O’Connor, M. E. (1998). Risk factors for binge eating disorders: A community-based study. Archives of General Psychiatry, 55, 425–432.
• Fava, M., Copeland, P. M., Schweiger, U., & Herzog, D. (1989). Neurochemical abnormalities of anorexia nervosa and bulimia nervosa. American Journal of Psychiatry, 146, 963–971.
• Field, A. E., Camargo, C. A., Taylor, C. B., Berkey, C. S., & Colditz, G. A. (1999). Relation of peer and media influences to the development of purging behaviors among preadolescent and adolescent girls. Archives of Pediatrics & Adolescent Medicine, 153, 1184–1189.
• Fitzgibbon, M. L., & Blackman, L. R. (2000). Binge eating disorder and bulimia nervosa: Differences in the quality and quantity of binge eating episodes. International Journal of Eating Disorders, 27, 238–243.
• Furnham, A., & Husain, K. (1999). The role of conflict with parents in disordered eating among British Asian females. Social Psychiatry & Psychiatric Epidemiology, 34, 498–505.
• Gard, M. C. E., & Freeman, C. P. (1996). The dismantling of a myth: A review of eating disorders and socioeconomic status. International Journal of Eating Disorders, 20, 1–12.
• Garfinkel, P., & Garner, D. (1982). Anorexia nervosa: A multidimensional perspective . New York: Brunner/Mazel.
• Garfinkel, P. E., Lin, E., Goering, P., Spegg, C., Goldbloom, D. S., Kennedy, S., Kaplan, A. S., & Woodside, D. B. (1995). Bulimia nervosa in a Canadian community sample: Prevalence and comparison of subgroups. American Journal of Psychiatry, 152, 1052–1058.
• Garner, D., Olmsted, M., Polivy, J., & Garfinkel, P. (1984). Comparison between weight preoccupied women and anorexia nervosa. Psychosomatic Medicine, 46, 255–266.
• Ghadirian, A. M., Marini, N., Jabalpurlawa, S., & Steiger, H. (1999). Seasonal mood patterns in eating disorders. General Hospital Psychiatry, 21, 354–359.
• Gleaves, D. H., & Eberenz, K. P. (1995). Correlates of dissociative symptoms among women with eating disorders. Journal of Psychiatric Research, 29, 417–426.
• Gleaves, D. H., Eberenz, K. P., & May, M. C. (1998). Scope and significance of posttraumatic symptomatology among women hospitalized for an eating disorder. International Journal of Eating Disorders, 24, 147–156.
• Gleaves, D. H., Lowe, M. R., Snow, A. C., Green, B. A., & MurphyEberenz, K. P. (2000). Continuity and discontinuity models of bulimia nervosa: A taxometric investigation . Journal of Abnormal Psychology, 109, 56–68.
• Godart, N. T., Flament, M. F., Lecrubier, Y., & Jeammet, P. (2000). Anxiety disorders in anorexia nervosa and bulimia nervosa: Comorbidity and chronology of appearance. European Psychiatry, 15, 38–45.
• Goldstein, H. J. (1981). Family factors associated with schizophrenia and anorexia nervosa. Journal of Youth and Adolescence, 10, 385–405.
• Grave,R.D.,Oliosi,M.,Todisco,P.,&Vanderlinden,J.(1997).Selfreported traumatic experiences and dissociative symptoms in obesewomenwithandwithoutbinge-eatingdisorder. EatingDisorders: The Journal of Treatment and Prevention, 5, 105–109.
• Grinspoon, S., Gulick, T., Askari, H., Landt, M., Vignati, L., Bowsher, R., Herzog, D., & Klibanski, A. (1996). Serum leptin levels in women with anorexia nervosa. Journal of Clinical Endocrinology and Metabolism, 81, 3861–3863.
• Gupta, M. A., & Johnson, A. M. (2000). Nonweight-related body image concerns among female eating-disordered patients and nonclinical controls: Some preliminary observations. International Journal of Eating Disorders, 27, 304–309.
• Hall, A., & Brown, L. B. (1983). A comparison of the attitudes of young anorexia nervosa patients and non-patients with those of their mothers. British Journal of Medical Psychology, 56, 39–48.
• Hall, A., Leibrich, J., Walkley, F., & Welch, G. (1986). Investigation of “weight pathology” of 58 mothers of anorexia nervosa patients and 204 mothers of schoolgirls. Psychological Medicine, 16, 71–76.
• Halmi, K. A., Sunday, S. R., Strober, M., Kaplan, A., Woodside, D. B., Fichter, M., Treasure, J., Berrettini, W. H., & Kaye, W. H. (2000). Perfectionism in anorexia nervosa: Variation by clinical subtype, obssessionality, and pathological behavior. American Journal of Psychiatry, 157, 1799–1805.
• Hebebrand, J., Blum, W. F., Barth, N., Coners, H., Englaro, P., Juul, A., Ziegler, A., Rascher, W., & Remschmidt, H. (1997). Leptin levels in patients with anorexia nervosa are reduced in the acute stage and elevated upon short-term weight restoration. Molecular Psychiatry, 2, 330–334.
• Herzog, D. B., Keller, M. B., Sacks, N. R., Yeh, C. J., & Lavori, P. W. (1992). Psychiatric comorbidity in treatment-seeking anorexics and bulimics. Journal of the American Academy of Child and Adolescent Psychiatry, 31, 810–818.
• Hinney, A., Lentes, K. U., Rosenkrantz, K., Barth, N., Roth, H., Ziegler, A., Henninghausen, K., Coners, H., Wurmser, H., Romer, J. K., Winnikes, G., Mayer, H., Herzog, W., Lehmkuhl, , Poustka, F., Schmidt, M. H., Blum, W. F., Pirke, K. M., Schafer, H., Greschik, K. H., Remschmidt, H., & Hebebrand, J. (1997). Beta 3-adrenergic receptor allele distributions in children, adolescents and young adults with obesity, underweight or anorexia nervosa. International Journal of Obesity Related Metabolic Disorders, 21, 224–230.
• Hodes, M., & leGrange, D. (1993). Expressed emotion in the investigation of eating disorders: A review. International Journal of Eating Disorders, 13, 279–288.
• Hodges, E. L., Cochrane, C. E., & Brewerton, T. D. (1998). Family characteristics of binge-eating disorder patients. International Journal of Eating Disorders, 23, 145–151.
• Hoffman, G. W., Ellinwood, E. H., Rockwell, W. J., Herfkens, R. J., Nishita, J. K., & Guthrie, L. F. (1989). Cerebral atrophy in bulimia. Biological Psychiatry, 25, 894–902.
• Holderness, C., Brooks-Gunn, J., & Warren, M. (1994). Comorbidity of eating disorders and substance abuse: Review of the litertaure. International Journal of Eating Disorders, 16, 1–34.
• Hsu, L. K. G., & Sobkiewicz, T. A. (1991). Body image disturbance: Time to abandon the concept for eating disorders. International Journal of Eating Disorders, 10, 15–30.
• Humphrey, L. L. (1991). Object relations and the family system: An integrative approach to understanding and treating eating disorders. In C. Johnson (Ed.), Psychodynamic treatment of anorexia nervosa and bulimia (pp. 321–353). New York: Guilford Press.
• Jacobsin, R., & Robins, C. J. (1989). Social dependency and social support in bulimic and nonbulimic women. International Journal of Eating Disorders, 8, 665–670.
• Jimerson, D. C., Lesem, M. D., Kaye, W. H., & Brewerton, T. D. (1992). Low serotonin and dopamine metabolite concentrations in cerebrospinal fluid from bulimic patients with frequent binge episodes. Archives of General Psychiatry, 49, 132–138.
• Johnson, C. (1991). Treatment of eating-disordered patients with borderline and false-self/narcissistic disorders. In C. Johnson (Ed.), Psychodynamic treatment of anorexia nervosa and bulimia (pp. 165–193). New York: Guilford Press.
• Johnston, J. L., Leiter, L. A., Burrow, G. N., Garfinkel, P. E., & Anderson, G. H. (1984). Excretion of urinary catecholamine metabolites in anorexia nervosa: Effect on body composition and energy intake. American Journal of Clinical Nutrition, 40, 1001–1006.
• Katz, B. E., & Gleaves, D. H. (1996). Dissociative symptoms with eating disorders: Associated feature or artifact of a comorbid dissociative disorder. Dissociation, 9, 28–36.
• Kaye, W. H., Ebert, M. H., Raleigh, M. H., & Lake, R. (1984). Abnormalities in CNS monoamine metabolism in anorexia nervosa. Archives of General Psychiatry, 41, 350–355.
• Kaye, W. H., Frank, G. K. W., & McConaha, C. (1999). Altered dopamine activity after recovery from restricting-type anorexia nervosa. Neuropsychopharmacology, 21, 503–506.
• Kaye, W. H., Gendall, K. A., Fernstrom, M. H., Fernstrom, J. D., McConaha, C. W., & Weltzin, T. E. (2000). Effects of acute tryptophan depletion on mood in bulimia nervosa. Biological Psychiatry, 47, 151–157.
• Kaye, W. H., Greeno, C. G., Moss, H., Fernstrom, J. D., Fernstrom, M. H., Lilenfeld, L. R, Weltzin, T. E., & Mann, J. (1998). Alterations in serotonin activity and psychiatric symptoms after recovery from bulimia nervosa. Archives of General Psychiatry, 55, 927–935.
• Kaye, W. H., Gwirtsman, H. E., George, D. T., & Ebert, M. H. (1991). Altered serotonin activity in anorexia nervosa after longterm weight restoration. Does elevated cerebrospinal fluid 5hydroxyindoleacetic acid level correlate with rigid and obsessive behavior? Archives of General Psychiatry, 48, 556–562.
• Kaye, W. H., Gwirtsman, H. E., George, D. T., Jimenson, D. C., Ebert, M. H., & Lake, R. (1990). Disturbances of noradrenergic systems in normal weight bulimia: Relationship to diet and menses. Biological Psychiatry, 27, 4–21.
• Kendler, K. S., Maclean, C., Neale, M. C., Kessler, R. C., Heath, A. C., & Eaves, L. J. (1991). The genetic epidemiology of bulimia nervosa. American Journal of Psychiatry, 148, 1627–1637.
• Keys, A., Brozek, J., Henschel, A., Mickelson, O., & Taylor, H. (1950). The biology of human starvation . Minneapolis: University of Minnesota Press.
• Kog, E., Vertommen, H., & Vandereycken, W. (1987). Minuchin’s psychosomatic family model revised: Aconcept validation study using a multitrait-multimethod apporach. Family Process, 26, 235–253.
• Lake, A. J., Staiger, P. K., & Glowinski, H. (2000). Effect of western culture on women’s attitudes to eating and perceptions of body shape. International Journal of Eating Disorders, 27, 83–89.
• Lambe, E. K., Katzman, D. K., Mikulis, D. J., Kennedy, S. H., & Zipursky, R. B. (1997). Cerebral gray matter volume deficits after weight recovery from anorexia nervosa. Archives of General Psychiatry, 54, 537–542.
• Lauer, C. J., Gorzewski, B., Gerlinghoff, M., Backmund, H., & Zihl, J. (1999). Neuropsychological assessments before and after treatment in patients with anorexia nervosa and bulimia nervosa. Journal of Psychiatry Research, 33, 129–138.
• Lee, S., Ho, P., & Hsu, L. K. G. (1993). Fat phobic and non-fat phobic anorexia nervosa: A comparative study of 70 Chinese patients in Hong Kong. Psychological Medicine, 23, 999–1017.
• Lehoux, P., Steiger, H., & Jabalpurlawa, S. (2000). State/trait distinctions in bulimic syndromes. International Journal of Eating Disorders, 27, 36–42.
• Levitan, R. D., Kaplan, A. S., Brown, G. M., Joffe, R. T., Levitt, A. J., Vaccarino, F. J., & Kennedy, S. (1997). Low plasma cortisol in bulimia nervosa patients with reversed neurovegetative symptoms of depression. Biological Psychiatry, 41, 366– 368.
• Levitan, R. D., Kaplan,A. S., Levitt,A. J., & Joffe, R.T. (1994). Seasonal fluctuations in mood and eating behavior in bulimia nervosa. International Journal of Eating Disorders, 16, 295–299.
• Levitan, R., Maselis, M., Kaplan, A., Basile, V., Kennedy, S., Lam, R., Vaccarino, F., Macciardi, F., & Kennedy, J. (2000, May). Serotonin genetic polymorphism in bulimia nervosa and seasonal affective disorder. Paper presented at the Ninth International Conference on Eating Disorders, New York.
• Lilenfeld, L. R., Kaye, W. H., Greeno, C. G., Merikangas, K. R., Plotnicov, K., Pollice, C., Rao, R., Strober, M., Bulik, C. M., & Nagy, L. (1997). Psychiatric disorders in women with bulimia nervosa and their first-degree relatives: Effects of comorbid substance dependence. International Journal of Eating Disorders, 22, 253–264.
• Lilenfeld, L. R., Kaye, W. H., Greeno, C. G., Merikangas, K. R., Plotnicov, K., Pollice, C., Rao, R., Strober, M., Bulik, C. M., & Nagy, L. (1998). A controlled family study of anorexia nervosa and bulimia nervosa: Psychiatric disorders in first-degree relatives and effects of proband comorbidity. Archives of General Psychiatry, 55, 603–610.
• Lilenfeld, L. R., Stein, D., Bulik, C. M., Strober, M., Plotnicov, K., Pollice, C., Rao, R., Merikangas, K. R., Nagy, L., & Kaye, W. H. (2000). Personality traits among currently eating disordered, recovered and never ill first-degree female relatives of bulimic and control women. Psychology Medicine, 30, 1399–1410.
• Lippincott, J. A., & Hwang, H. S. (1999). On cultural similarities in attitudes toward eating of women students in Pennsylvania and South Korea. Psychological Reports, 85, 701–702.
• Logue, C. M., Crowe, R. R., & Bean, J.A. (1989).Afamily study of anorexia nervosa. British Journal of Psychiatry, 30, 179–188.
• Lucas, A. R., Crowson, C. S., O’Fallon, W. M., & Melton, L. J. (1999). The ups and downs of anorexia nervosa. International Journal of Eating Disorders, 26, 397–405.
• Marcus,M.D.,Wing,R.R.,&Hopkins,J.(1988).Obesebingeeaters: Affect, cognitions and response to behavioral weight control. Journal of Consulting and Clinical Psychology, 13, 433–439.
• Matsunaga, H., Kaye, W. H., McConaha, C., Plotnicov, K., Pollice, C., & Rao, R. (2000). Personality disorders among subjects recovered from eating disorders. International Journal of Eating Disorders, 27, 353–357.
• Matsunaga, H., Kaye, W. H., McConaha, C., Plotnicov, K., Pollice, C., Rao, R., & Stein, D. (1999). Psychopathological characteristics of recovered bulimics who have a history of physical or sexual abuse. Journal of Nervous and Mental Disease, 187, 472–477.
• Matsunaga, H., Kiriike, N., Iwasaki, Y., Miyata, A., Matsui, T., Nagata, T., Yamagami, S., & Kaye, W. H. (2000). Multiimpulsivity among bulimic patients in Japan. International Journal of Eating Disorders, 27, 348–352.
• Matsunaga, H., Kiriike, N., Miyata, A., Iwasaki, Y., Matsui, T., Fulimtot, K., Kasai, S., & Kaye, W. H. (1999). Prevalence and symptomatology of comorbid obsessive-compulsive disorder among bulimic patients. Psychiatry and Clinical Neurosciences, 54, 661–666.
• Mehler, P. S., Eckel, R. H., & Donahoo, W. T. (1999). Leptin levels in restricting and purging anorectics. International Journal of Eating Disorders, 26, 189–194.
• Miller, D. A., McCluskey-Fawcett, K., & Irving, L. M. (1993). Correlates of bulimia nervosa: Early mealtime experiences. Adolescence, 28, 621–635.
• Mitchell, J. E., & Eckert, E. D. (1987). Scope and significance of eating disorders. Journal of Consulting and Clinical Psychology, 55, 628–634.
• Mitchell, J. E., Mussell, M. P., Peterson, C. B., Crow, S., Wonderlich, S. A., Crosby, R. D., Davis, T., & Weller, C. (1999). Hedonics of binge eating in women with bulimia nervosa and binge eating disorder. International Journal of Eating Disorders, 26, 165–170.
• Monteleone, P., Brambilla, F., Bortolototti, F., LaRocca, A., & Maj, M. (1998). Prolactin response to d-fenfluramine is blunted in people with anorexia nervosa. British Journal of Psychiatry, 172, 438–442.
• Monteleone, P., Di Lieto, A., Tortorella, A., Longobardi, N., & Maj, M. (2000). Circulating leptin in patients with anorexia nervosa, bulimia nervosa or binge-eating disorder: Relationship to body weight, eating patterns, psychopathology and endocrine changes. Psychiatry Research, 94, 121–129.
• Moreno, J. K., Selby, M. J., & Neal, S. (1998). Psychopathology in sexually abused and non-sexually abused eating-disordered women. Psychotherapy in Private Practice, 17, 1–9.
• Murnen, S. K., & Smolak, L. (1997). Femininity, masculinity, and disordered eating: A meta-analytic review. International Journal of Eating Disorders, 22, 231–242.
• Newton, J. R., Freeman, C. P., & Munro, J. (1993). Impulsivity and dyscontrol in bulimia nervosa: Is impulsivity an independent phenomenon or a marker of severity? Acta Psychiatrica Scandinavia, 87, 389–394.
• Nielsen, D., Virkkunen, M., Lappalainen, J., Eggert, M., Brown, G., Long, J., Goldman, D., & Linnoila, M. (1998). A tryptophan hydroxylase gene marker for suicidality and alcoholism. Archives of General Psychiatry, 55, 593–602.
• Nilsson, E. W., Gillberg, C., Gillberg, I. C., & Rastam, M. (1999). Ten-year follow-up of adolescent onset anorexia nervosa: Personality disorders. Journal of the American Academy of Child and Adolescent Psychiatry, 38, 1389–1395.
• Norman, D. K., Blais, D., & Herzog, D. (1993). Personality characteristics of eating-disordered patients as identified by the Millon Clinical Multiaxial inventory. Journal of Personality Disorders, 7, 1–9.
• Olivardia, R., Pope, H. G., Jr., & Hudson, J. I. (2000). Muscle dysmorphia in male weightlifters: A case-control study. American Journal of Psychiatry, 157, 1291–1296.
• Pate, J. E., Pumariega, A. J., Hester, C., & Garner, D. M. (1992). Cross-cultural patterns in eating disorders: A review. Journal of the American Academy of Child and Adolescent Psychiatry, 31, 802–809.
• Pirke, K. M., Kellner, M. B., Frie, E., Krieg, J.-C., & Fichter, M. M. (1994). Satiety and cholecystokinin. International Journal of Eating Disorders, 15, 63–69.
• Polivy, J., & Herman, C. P. (1985). Dieting and binging: A causal analysis. American Psychologist, 40, 193–201.
• Polivy, J., & Herman, C. P. (1993). Etiology of binge eating: Psychological mechanisms. In C. G. Fairbairn & G. T. Wilson (Eds.), Binge eating: Nature, assessment, and treatment (pp. 173–205). NewYork: Guilford Press.
• Pruitt,J.A.,Kappins,R.E.,&Gorman,P.W.(1992).Bulimiaandfear of intimacy. Journal of Clinical Psychology, 48, 472–476.
• Råstam, M. (1992). Anorexia nervosa in 51 Swedish adolescents: Premorbid problems and comorbidity. Journal of the American Academy of Child and Adolescent Psychiatry, 31, 819–829.
• Rhea, D. J. (1999). Eating disorder behaviors of ethnically diverse urban female adolescent athletes and non-athletes. Journal of Adolescence, 22, 379–388.
• Rhodes, B., & Kroger, J. (1992). Parental bonding and separationindividuationdifficultiesamonglateadolescenteatingdisordered women. Child Psychiatry & Human Development, 22, 249–263.
• Rosenvinge, J. H., Martinussen, M., & Ostensen, E. (2000). The comorbidity of eating disorders and personality disorders: A metaanalytic review of studies published between 1983 and 1998. Eating and Weight Disorders, 5, 52–61.
• Ross, H. E., & Ivis, F. (1999). Binge eating and substance use among male and female adolescents. International Journal of Eating Disorders, 26, 245–260.
• Schmidt, U., Humfress, H., & Treasure, J. (1997). The role of general family environment and sexual and physical abuse in the origins of eating disorders. European Eating Disorders Review, 5, 184–207.
• Schukit, M. A., Tipp, J. E., Anthenelli, R. M., Bucholz, K. K., Hesselbrock, V. M., & Nurnberger, J. I., Jr. (1996). Anorexia nervosa and bulimia nervosa in alcohol-dependent men and women and their relatives. American Journal of Psychiatry, 153, 74–82.
• Sights, J. R., & Richards, H. C. (1984). Parents of bulimic women. International Journal of Eating Disorders, 3, 3–13.
• Sitnick,T.,&Katz,J.(1984).Astudyofsexroleidentityandanorexia nervosa. International Journal of Eating Disorders, 3, 81–87.
• Smith, K. A., Fairburn, C. G., & Cowen, P. J. (1999). Symptomatic relapse in bulimia nervosa following acute tryptophan depletion. Archives of General Psychiatry, 56, 171–176.
• Sohlberg, S., & Strober, M. (1994). Personality in anorexia nervosa: An update and a theoretical integration. Acta Psychiatrica Scandinavica, 89 (Suppl. 378), 1–15.
• Spitzer, R. L., Devlin, M., Walsh, B. T., Hasin, D., Wing, R., Marcus, M., Stunkard, A., Wadden, T., Yanovski, S., Agras, S., Mitchell, J., & Nonas, C. (1992). Binge eating disorder: Amultisite field trial of diagnostic criteria. International Journal of Eating Disorders, 11, 191–203.
• Srinivasagam, N. M., Kaye, W. H., Plotnicov, K. H., Greeno, C., Weltzin, T. E., & Rao, R. (1995). Persistent perfectionism, symmetry, and exactness after long-term recovery from anorexia nervosa. American Journal of Psychiatry, 152, 1630–1634.
• Steiger, H., Gauvin, L., Israel, M., Koerner, Ng Ying Kin, N. M. K., Paris, J., & Young, S. N. (2001). Association of serotonin and cortisol indices with childhood abuse in bulimia nervosa. Archives of General Psychiatry, 58, 837–843.
• Steiger, H., Gauvin, L., Jabalpurlawa, S., Séguin, J. R., & Stotland, S. (1999). Hypersensitivity to social interactions in bulimic eating syndromes: Relationship to binge-eating. Journal of Consulting and Clinical Psychology, 67, 765–775.
• Steiger, H., Koerner, N. M., Engleberg, M., Israel, M., Ng Ying Kin, N. M. K., & Young, S. N. (2001). Self-destructiveness and serotonin function in bulimia nervosa. Psychiatry Research, 103, 15–26.
• Steiger, H., Leonard, S., Ng Ying Kin, N. M. K., Ladouceur, C., Ramdoyal, D., & Young, S. N. (2000). Childhood abuse and tritiated paroxetine binding in bulimia nervosa. Journal of Clinical Psychiatry, 61, 428–435.
• Steiger, H., Van der Feen, J., Goldstein, C., & Leichner, P. (1989). Defense styles and parental bonding in eating-disordered women. International Journal of Eating Disorders, 8, 131–140.
• Stickney, M. I., Miltenberger, R. G., & Wolff, G. (1999). A descriptive analysis of factors contributing to binge eating. Journal of Behavior Therapy and Experimental Psychiatry, 30, 177–189.
• Striegel-Moore, R. H., Silberstein, L. R., & Rodin, J. (1986). Toward an understanding of risk factors for bulimia. Amercan Psychologist, 41, 246–248.
• Striegel-Moore, R. H., Wilfley, D. E., Pike, K. M., Dohm, F. A., & Fairburn, C. G. (2000). Recurrent binge eating in blackAmerican women. Archives of Family Medicine, 9, 83–87.
• Striegel-Moore, R. H., Wilson, G. T., Wilfley, D. E., Elder, K. A., & Brownell, K. D. (1998). Binge eating in an obese community sample. International Journal of Eating Disorders, 23, 27–37.
• Strober, M. (1991). Disorders of the self in anorexia nervosa: An organismic-developmental paradigm. In C. Johnson (Ed.), Psychodynamic treatment of anorexia nervosa and bulimia (pp. 354–372). New York: Guilford Press.
• Strober, M., Freeman, R., Lampert, C., Diamond, J., & Kaye, W. (2000). Controlled family study of anorexia nervosa and bulimia nervosa: Evidence of shared liability and transmission of partial syndromes. American Journal of Psychiatry, 157, 393–401.
• Strober, M., Lampert, C., Morrell, W., Burroughs, J., & Jacobs, C. (1990).Acontrolledfamilystudyofanorexianervosa:Evidenceof familialaggregationandlackofsharedtransmissionwithaffective disorders. International Journal of Eating Disorders, 9, 239–253.
• Szmukler,G.I.,Andrewes,D.,Kingston,K.,Chen,L.,Stargatt,R.,& Stanley, R. (1992). Neuropsychological impairment in anorexia nervosa: Before and after refeeding. Journal of Clinical and Experimental Neuropsychology, 14, 347–352.
• Thornton, C., & Russell, J. (1997). Obsessive-compulsive comorbidity in the dieting disorders. International Journal of Eating Disorders, 21, 83–87.
• Tobin, D. L., Griffing, A., & Griffing, S. (1997). An examination of subtype criteria for bulimia nervosa. International Journal of Eating Disorders, 22, 179–186.
• Toner, B. B., Garfinkel, P. E., & Garner, D. M. (1987). Cognitive style of patients with bulimic and diet-restricting anorexia nervosa. American Journal of Psychiatry, 144, 510–512.
• Treasure, J. L., & Holland, A. J. (1989). Genetic vulnerability to eating disorders: Evidence from twin and family studies. In H. Remschmidt & M. H. Schmidt (Eds.), Anorexia nervosa (pp. 59–68). Toronto, Ontario, Canada: Hogrefe & Huber.
• Tuschen-Caffier, B., & Vogele, C. (1999). Psychological and physiological reactivity to stress: An experimental study on bulimic patients, restrained eaters and controls. Psychotherapy and Psychosomatics, 68, 333–340.
• Vanderlinden, J., Vandereycken, W., van Dyk, R., & Vertommen, H. (1993). Dissociative experiences and trauma in eating disorders. International Journal of Eating Disorders, 13, 187–194.
• Vitousek, K., & Manke, F. (1994). Personality variables and disorders in anorexia nervosa and bulimia nervosa. Journal of Abnormal Psychology, 103, 137–147.
• von Ranson, K. M., Kaye, W. H., Weltzin, T. E., Rao, R., & Matsunaga, H. (1999). Obsessive-compulsive disorder symptoms before and after recovery form bulimia nervosa. American Journal of Psychiatry, 156, 1703–1708.
• Wade, T. D., Bulik, C. M., Neale, M., & Kendler, K. S. (2000). Anorexia nervosa and major depression: Shared genetic and environmental risk factors. American Journal of Psychiatry, 157, 469–471.
• Wakeling, A. (1996). Epidemiology of anorexia nervosa. Psychiatry Research, 62, 3–9.
• Waller, J. V., Kaufman, M. R., & Deutsch, F. (1940). Anorexia nervosa: Apsychosomatic entity. Psychosomatic Medicine, 2, 3–16.
• Walters, E. E., & Kendler, K. S. (1995). Anorexia nervosa and anorexic-like syndromes in a population-based female twin sample. American Journal of Psychiatry, 152, 64–71.
• Ward, A., Brown, N., Lightman, S., Campbell, I. C., & Treasure, J. (1998). Neuroendocrine, appetitive and behavioral responses to d-fenfluramine in women recovered from anorexia nervosa. British Journal of Psychiatry, 172, 351–358.
• Ward, A., Ramsay, R., & Treasure, J. (2000). Attachment research in eating disorders. British Journal of Medical Psychology, 73, 35–51.
• Ward, A., Ramsay, R., Turnbull, S., Benedettini, M., & Treasure, J. (2000). Attachment patterns in eating disorders past in the present. International Journal of Eating Disorders, 28, 370–376.
• Webster, J. J., & Palmer, R. L. (2000). The childhood and family background of women with clinical eating disorders: A comparison with women with major depression and women without psychiatric disorder. Psychological Medicine, 30, 53–60.
• Weizman, R., Carmi, M., Tyano, S., Apter, A., & Rehavi, M. (1986). High affinity [3H]imipramine binding and serotonin uptake to platelets of adolescent females suffering from anorexia nervosa. Life Sciences, 38, 1235–1242.
• Wertheim, E. H. (1999). Relationships among adolescent girls’ eating behvaiors and their parents’ weight-related attitudes and behaviors. Sex Roles, 41, 169–187.
• Whelan, E., & Cooper, P. J. (2000). The association between childhood feeding problems and maternal eating disorder: A community study. Psychological Medicine, 30, 69–77.
• Widiger, T. A., & Sankis, L. M. (2000). Adult psychopathology: Issues and controversies. Annual Review of Psychology, 51, 377–404.
• Wiederman, M. W., & Pryor, T. (1996). Multi-impulsivity among women with bulimia nervosa. International Journal of Eating Disorders, 20 (4), 359–365.
• Windauer, U., Lennerts, W., Talbot, P., Touyz, S., & Beumont, P. (1993). How well are “cured” anorexia nervosa patients? An investigation of 16 weight-recovered anorexic patients. British Journal of Psychiatry, 163, 195–200.
• Wolfe, B. E., Jimerson, D. C., & Levine, J. M. (1994). Impulsivity ratings in bulimia nervosa: Relationship to binge eating behaviors. International Journal of Eating Disorders, 15, 289–292.
• Wonderlich, S. A., Brewerton, T. D., Jocic, Z., Dansky, B., & Abbott, D. W. (1997). Relationship of childhood sexual abuse and eating disorders. Journal of the American Academy of Child and Adolescent Psychiatry, 36, 1107–1115.
• Zaider, T. I., Johnson, J. G., & Cockell, S. J. (2000). Psychiatric comorbidity associated with eating disorder symptomatology among adolescents in the community. International Journal of Eating Disorders, 28, 58–67.

ORDER HIGH QUALITY CUSTOM PAPER

Home — Essay Samples — Nursing & Health — Public Health Issues — Eating Disorders

Essay Examples on Eating Disorders

What makes a good eating disorders essay topic.

When it comes to selecting a topic for your eating disorders essay, it's crucial to consider a multitude of factors that can elevate your writing to new heights. Below are some innovative suggestions on how to brainstorm and choose an essay topic that will captivate your readers:

- Brainstorm: Begin by unleashing a storm of ideas related to eating disorders. Delve into the various facets, such as causes, effects, treatment options, societal influences, and personal narratives. Ponder upon what intrigues you and what will engage your audience.

- Research: Embark on a comprehensive research journey to accumulate information and gain a profound understanding of the subject matter. This exploration will enable you to identify distinctive angles and perspectives to explore in your essay. Seek out scholarly sources such as academic journals, books, and reputable websites.

- Cater to your audience: Reflect upon your readers and their interests to tailor your topic accordingly. Adapting your subject matter to captivate your audience will undoubtedly make your essay more engaging. Consider the age, background, and knowledge level of your readers.

- Unveil controversies: Unearth the controversies and debates within the realm of eating disorders. Opting for a topic that ignites discussion will infuse your essay with thought-provoking and impactful qualities. Delve into various viewpoints and critically analyze arguments for and against different ideas.

- Personal connection: If you possess a personal connection or experience with eating disorders, contemplate sharing your story or delving into it within your essay. This will add a unique and personal touch to your writing. However, ensure that your personal anecdotes remain relevant to the topic and effectively support your main points.

Overall, a remarkable eating disorders essay topic should be meticulously researched, thought-provoking, and relevant to your audience's interests and needs.

Best Eating Disorders Essay Topics

Below, you will find a compilation of the finest eating disorders essay topics to consider:

1. The captivating influence of social media on promoting unhealthy body image. 2. Breaking free from stereotypes: Exploring eating disorders among male athletes. 3. The profound impact of diet culture on body image and self-esteem. 4. Unraveling the intricate link between eating disorders and the pursuit of perfection. 5. The portrayal of eating disorders in popular media: Dissecting the battle between glamorization and reality.

Best Eating Disorders Essay Questions

Below, you will find an array of stellar eating disorders essay questions to explore:

1. How does social media contribute to the development and perpetuation of eating disorders? 2. What challenges do males with eating disorders face, and how can these challenges be addressed? 3. To what extent does the family environment contribute to the development of eating disorders? 4. What role does diet culture play in fostering unhealthy relationships with food? 5. How can different treatment approaches be tailored to address the unique needs of individuals grappling with eating disorders?

Eating Disorders Essay Prompts

Below, you will find a collection of eating disorders essay prompts that will kindle your creative fire:

1. Craft a personal essay that intricately details your voyage towards recovery from an eating disorder, elucidating the lessons you learned along the way. 2. Picture yourself as a parent of a teenager burdened with an eating disorder. Pen a heartfelt letter to other parents, sharing your experiences and providing valuable advice. 3. Fabricate a fictional character entangled in the clutches of binge-eating disorder. Concoct a short story that explores their odyssey towards self-acceptance and recovery. 4. Construct a persuasive essay that fervently argues for the integration of comprehensive education on eating disorders into school curricula. 5. Immerse yourself in the role of a therapist specializing in eating disorders. Compose a reflective essay that delves into the challenges and rewards of working with individuals grappling with eating disorders.

Writing Eating Disorders Essays: Frequently Asked Questions

Below, you will find answers to some frequently asked questions about writing eating disorders essays:

Q: How can I effectively commence my eating disorders essay? A: Commence your essay with a captivating introduction that ensnares the reader's attention and provides an overview of the topic. Consider starting with an intriguing statistic, a powerful quote, or a personal anecdote.

Q: Can I incorporate personal experiences into my eating disorders essay? A: Absolutely! Infusing your essay with personal experiences adds depth and authenticity. However, ensure that your personal anecdotes remain relevant to the topic and effectively support your main points.

Q: How can I make my eating disorders essay engaging? A: Utilize a variety of rhetorical devices such as metaphors, similes, and vivid descriptions to transform your essay into an engaging masterpiece. Additionally, consider incorporating real-life examples, case studies, or interviews to provide concrete evidence and make your essay relatable.

Q: Should my essay focus solely on one specific type of eating disorder? A: While focusing on a specific type of eating disorder can provide a narrower scope for your essay, exploring the broader theme of eating disorders as a whole can also be valuable. Strive to strike a balance between depth and breadth in your writing.

Q: How can I conclude my eating disorders essay effectively? A: In your conclusion, summarize the main points of your essay and restate your thesis statement. Additionally, consider leaving the reader with a thought-provoking question or a call to action, encouraging further reflection or research on the topic.

Argumentative Essay on Eating Disorders

Eating disorders and methods of its treatment, made-to-order essay as fast as you need it.

Each essay is customized to cater to your unique preferences

+ experts online

The Correlation Between Social Media and The Development of Eating Disorders

The damages of eating disorders, stereotypes around eating disorders, anorexia – a growing issue in teenage girls, let us write you an essay from scratch.

• 450+ experts on 30 subjects ready to help
• Custom essay delivered in as few as 3 hours

Examining Eating Disorders and Social Learning Theory to Draw Useful Conclusions

Photoshopping images and how it impacts eating disorders, nutrition intervention for eating disorders, how beauty pageants can cause health difficulties, get a personalized essay in under 3 hours.

Expert-written essays crafted with your exact needs in mind

A Look into The Life of People with Anorexia Nervosa

Bulimia nervosa: causes, symptoms and treatment, the prevention and treatment of anorexia nervosa, food addiction: does it really exist, depiction of anorexia nervosa in the movie to the bone, a study of eating disorders in judaism and the impact of patriarchal values and pressures, the differences between anorexia and bulimia, social media as the reason of body dissatisfaction and eating disorders, the role of society in the development of anorexia in teen girls, exploring solutions for fighting the obesity epidemic, jane martin’s beauty, eating disorders in adolescents.

Eating disorders refer to a complex set of mental health conditions characterized by disturbances in one's eating behaviors and attitudes towards food, leading to severe consequences on an individual's physical and psychological well-being.

Anorexia Nervosa: Anorexia nervosa is a psychological disorder characterized by an intense fear of gaining weight and a distorted perception of one's body image. People with this disorder exhibit extreme food restriction, leading to significant weight loss and the possibility of reaching dangerously low levels of body weight. Anorexia nervosa is often accompanied by obsessive thoughts about food, excessive exercise routines, and a constant preoccupation with body shape and size. Bulimia Nervosa: Bulimia nervosa involves a cyclic pattern of binge eating followed by compensatory behaviors aimed at preventing weight gain. During binge episodes, individuals consume large quantities of food in a short period and experience a loss of control over their eating. To counteract the caloric intake, these individuals may resort to self-induced vomiting, excessive exercising, or the misuse of laxatives. It is important to note that unlike anorexia nervosa, individuals with bulimia nervosa typically maintain a body weight within the normal range or slightly above. Binge Eating Disorder: Binge eating disorder is characterized by recurrent episodes of consuming a significant amount of food in a short period, accompanied by a feeling of loss of control. Unlike other eating disorders, individuals with binge eating disorder do not engage in compensatory behaviors such as purging or excessive exercise.

Distorted Body Image: Individuals with eating disorders often have a distorted perception of their body, seeing themselves as overweight or unattractive, even when they are underweight or at a healthy weight. Obsession with Food and Weight: People with eating disorders may constantly think about food, calories, and their weight. They may develop strict rules and rituals around eating, such as avoiding certain food groups, restricting their intake, or engaging in excessive exercise. Emotional and Psychological Factors: Eating disorders are often associated with underlying emotional and psychological issues, such as low self-esteem, perfectionism, anxiety, depression, or a need for control. Physical Health: Eating disorders can have severe physical health consequences, including malnutrition, electrolyte imbalances, hormonal disruptions, gastrointestinal problems, and organ damage. These complications can be life-threatening and require medical intervention. Social Isolation and Withdrawal: Individuals struggling with eating disorders may experience a withdrawal from social activities, distancing themselves from others due to feelings of shame, guilt, and embarrassment related to their eating behaviors or body image. This social isolation can intensify the challenges they face and contribute to a sense of loneliness and emotional distress. Co-occurring Disorders: Eating disorders frequently co-occur with other mental health conditions, creating complex challenges for those affected. It is common for individuals with eating disorders to also experience anxiety disorders, depression, substance abuse issues, or engage in self-harming behaviors. The coexistence of these disorders can exacerbate the severity of symptoms and necessitate comprehensive and integrated treatment approaches.

Genetic and Biological Factors: Research suggests that there is a genetic predisposition to eating disorders. Individuals with a family history of eating disorders or other mental health conditions may be at a higher risk. Biological factors, such as imbalances in brain chemicals or hormones, can also contribute to the development of eating disorders. Psychological Factors: Psychological factors play a significant role in the development of eating disorders. Factors such as diminished self-worth, a relentless pursuit of perfection, dissatisfaction with one's body, and distorted perceptions of body image can play a significant role in the onset and perpetuation of disordered eating patterns. Sociocultural Influences: Societal pressures and cultural norms surrounding body image and beauty standards can contribute to the development of eating disorders. Media portrayal of unrealistic body ideals, peer influence, and societal emphasis on thinness can impact individuals' self-perception and increase the risk of developing an eating disorder. Traumatic Experiences: The impact of traumatic events, be it physical, emotional, or sexual abuse, can heighten the vulnerability to developing eating disorders. Such distressing experiences have the potential to instigate feelings of diminished self-worth, profound body shame, and a compelling desire to exert control over one's body and eating behaviors. Dieting and Weight-related Practices: Restrictive dieting, excessive exercise, and weight-focused behaviors can serve as triggers for the development of eating disorders. These behaviors may start innocently as an attempt to improve one's health or appearance but can spiral into disordered eating patterns.

Psychotherapy: Various forms of psychotherapy, such as cognitive-behavioral therapy (CBT), dialectical behavior therapy (DBT), and family-based therapy (FBT), are employed to address the underlying psychological factors contributing to eating disorders. These therapies aim to challenge distorted thoughts and beliefs about body image, develop healthier coping mechanisms, and improve self-esteem. Nutritional Counseling: Working with registered dietitians, individuals receive personalized guidance on developing a balanced and healthy relationship with food. Nutritional counseling focuses on establishing regular eating patterns, promoting mindful eating practices, and debunking harmful dietary myths. Medical Monitoring: This involves regular check-ups to assess physical health, monitor vital signs, and address any medical complications arising from the disorder. Medication: In some cases, medication may be prescribed to manage associated symptoms like depression, anxiety, or obsessive-compulsive disorder. Medications can complement therapy and help stabilize mood, regulate eating patterns, or address co-occurring mental health conditions. Support Groups and Peer Support: Joining support groups or engaging in peer support programs can provide individuals with a sense of community and understanding. Interacting with others who have faced similar challenges can offer valuable insights, encouragement, and empathy.

Films: Movies like "To the Bone" (2017) and "Feed" (2017) shed light on the struggles individuals with eating disorders face. These films delve into the psychological and emotional aspects of the disorders, emphasizing the importance of seeking help and promoting recovery. Books: Novels such as "Wintergirls" by Laurie Halse Anderson and "Paperweight" by Meg Haston offer intimate perspectives on the experiences of characters grappling with eating disorders. These books provide insights into the complexities of these conditions, including the internal battles, societal pressures, and the journey towards healing. Documentaries: Documentaries like "Thin" (2006) and "Eating Disorders: Surviving the Silence" (2019) offer real-life accounts of individuals living with eating disorders. These documentaries provide a raw and authentic portrayal of the challenges faced by those affected, raising awareness and encouraging empathy.

1. As per the data provided by the National Eating Disorders Association (NEDA), it is estimated that around 30 million individuals residing in the United States will experience an eating disorder during their lifetime. 2. Research suggests that eating disorders have the highest mortality rate of any mental illness. Anorexia nervosa, in particular, has a mortality rate of around 10%, emphasizing the seriousness and potential life-threatening nature of these disorders. 3. Eating disorders can affect individuals of all genders and ages, contrary to the common misconception that they only affect young women. While young women are more commonly affected, studies indicate that eating disorders are increasingly prevalent among men and can also occur in older adults and children.

The topic of eating disorders is of significant importance when it comes to raising awareness, promoting understanding, and addressing the challenges faced by individuals who experience these disorders. Writing an essay on this topic allows for a deeper exploration of the complexities surrounding eating disorders and their impact on individuals, families, and society. First and foremost, studying eating disorders is crucial for shedding light on the psychological, emotional, and physical aspects of these conditions. By delving into the underlying causes, risk factors, and symptoms, we can gain a better understanding of the complex interplay between biological, psychological, and sociocultural factors that contribute to the development and maintenance of eating disorders. Furthermore, discussing eating disorders helps to challenge societal misconceptions and stereotypes. It allows us to debunk harmful beliefs, such as the notion that eating disorders only affect a specific gender or age group, and instead emphasizes the reality that anyone can be susceptible to these disorders. Writing an essay on eating disorders also provides an opportunity to explore the impact of media, societal pressures, and body image ideals on the development of disordered eating behaviors. By analyzing these influences, we can advocate for more inclusive and body-positive narratives that promote self-acceptance and well-being. Moreover, addressing the topic of eating disorders is crucial for raising awareness about the available treatment options and support systems. It highlights the importance of early intervention, comprehensive treatment approaches, and access to mental health resources for those affected by these disorders.

1. American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). American Psychiatric Publishing. 2. Arcelus, J., Mitchell, A. J., Wales, J., & Nielsen, S. (2011). Mortality rates in patients with anorexia nervosa and other eating disorders: A meta-analysis of 36 studies. Archives of General Psychiatry, 68(7), 724-731. 3. Brown, T. A., Keel, P. K., & Curren, A. M. (2020). Eating disorders. In D. H. Barlow (Ed.), Clinical handbook of psychological disorders: A step-by-step treatment manual (6th ed., pp. 305-357). Guilford Press. 4. Fairburn, C. G., & Harrison, P. J. (2003). Eating disorders. The Lancet, 361(9355), 407-416. 5. Herpertz-Dahlmann, B., & Zeeck, A. (2020). Eating disorders in childhood and adolescence: Epidemiology, course, comorbidity, and outcome. In M. Maj, W. Gaebel, J. J. López-Ibor, & N. Sartorius (Eds.), Eating Disorders (Vol. 11, pp. 68-82). Wiley-Blackwell. 6. Hudson, J. I., Hiripi, E., Pope, H. G., & Kessler, R. C. (2007). The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication. Biological Psychiatry, 61(3), 348-358. 7. Jacobi, C., Hayward, C., de Zwaan, M., Kraemer, H. C., & Agras, W. S. (2004). Coming to terms with risk factors for eating disorders: Application of risk terminology and suggestions for a general taxonomy. Psychological Bulletin, 130(1), 19-65. 8. Keski-Rahkonen, A., & Mustelin, L. (2016). Epidemiology of eating disorders in Europe: Prevalence, incidence, comorbidity, course, consequences, and risk factors. Current Opinion in Psychiatry, 29(6), 340-345. 9. Smink, F. R. E., van Hoeken, D., & Hoek, H. W. (2012). Epidemiology of eating disorders: Incidence, prevalence and mortality rates. Current Psychiatry Reports, 14(4), 406-414. 10. Stice, E., Marti, C. N., & Rohde, P. (2013). Prevalence, incidence, impairment, and course of the proposed DSM-5 eating disorder diagnoses in an 8-year prospective community study of young women. Journal of Abnormal Psychology, 122(2), 445-457.

Relevant topics

• Drug Addiction
• Mental Health

By clicking “Check Writers’ Offers”, you agree to our terms of service and privacy policy . We’ll occasionally send you promo and account related email

No need to pay just yet!

We use cookies to personalyze your web-site experience. By continuing we’ll assume you board with our cookie policy .

• Instructions Followed To The Letter
• Deadlines Met At Every Stage
• Unique And Plagiarism Free

• Open access
• Published: 15 November 2022

Conceptualizing eating disorder recovery research: Current perspectives and future research directions

• Heather Hower 1 , 2 ,
• Andrea LaMarre 3 ,
• Rachel Bachner-Melman 4 , 5 ,
• Erin N. Harrop 6 ,
• Beth McGilley 7 &
• Therese E. Kenny 8  

Journal of Eating Disorders volume  10 , Article number:  165 ( 2022 ) Cite this article

4663 Accesses

3 Citations

6 Altmetric

Metrics details

How we research eating disorder (ED) recovery impacts what we know (perceive as fact) about it. Traditionally, research has focused more on the “what” of recovery (e.g., establishing criteria for recovery, reaching consensus definitions) than the “how” of recovery research (e.g., type of methodologies, triangulation of perspectives). In this paper we aim to provide an overview of the ED field’s current perspectives on recovery, discuss how our methodologies shape what is known about recovery, and suggest a broadening of our methodological “toolkits” in order to form a more complete picture of recovery.

This paper examines commonly used methodologies in research, and explores how incorporating different perspectives can add to our understanding of the recovery process. To do this, we (1) provide an overview of commonly used methodologies (quantitative, qualitative), (2) consider their benefits and limitations, (3) explore newer approaches, including mixed-methods, creative methods (e.g., Photovoice, digital storytelling), and multi-methods (e.g., quantitative, qualitative, creative methods, psycho/physiological, behavioral, laboratory, online observations), and (4) suggest that broadening our methodological “toolkits” could spur more nuanced and specific insights about ED recoveries. We propose a potential future research model that would ideally have a multi-methods design, incorporate different perspectives (e.g., expanding recruitment of diverse participants, including supportive others, in study co-creation), and a longitudinal course (e.g., capturing cognitive and emotional recovery, which often comes after physical). In this way, we hope to move the field towards different, more comprehensive, perspectives on ED recovery.

Our current perspectives on studying ED recovery leave critical gaps in our knowledge about the process. The traditional research methodologies impact our conceptualization of recovery definitions, and in turn limit our understanding of the phenomenon. We suggest that we expand our range of methodologies, perspectives, and timeframes in research, in order to form a more complete picture of what is possible in recovery; the multiple aspects of an individual’s life that can improve, the greater number of people who can recover than previously believed, and the reaffirmation of hope that, even after decades, individuals can begin, and successfully continue, their ED recovery process.

Plain English summary

How we research eating disorder (ED) recovery impacts what we know (perceive as fact) about it. In this paper we aim to provide an overview of the ED field’s current perspectives on recovery, discuss how our methodologies shape what is known about recovery, and suggest a broadening of our methodological “toolkits” in order to form a more complete picture of recovery. To do this, we (1) provide an overview of commonly used methodologies (quantitative, qualitative), (2) consider their benefits and limitations, (3) explore newer approaches, including mixed-methods, creative methods (e.g., Photovoice, digital storytelling), and multi-methods (e.g., quantitative, qualitative, creative methods, psycho/physiological, behavioral, laboratory, online observations), and (4) propose a potential future research model with a multi-methods design, incorporating different perspectives (e.g., increasing recruitment of diverse participants, including supportive others in study co-creation), and a longitudinal course (e.g., capturing cognitive recovery, which often comes after physical). In this way, we seek to expand our picture of what is possible in recovery; the multiple aspects of an individual’s life that can improve, the greater number of people who can recover than previously believed, and the reaffirmation of hope that, even after decades, individuals can begin and continue their ED recovery process.

How we research the process of eating disorder (ED) recovery impacts what we know (perceive as fact) about this process. Traditionally, research has focused more on the “what” of recovery (e.g., establishing criteria for recovery, connecting research and clinical experiences, reaching consensus definitions) than the “how” of recovery research (e.g., timing and framing of ED recovery items and measures, type of methodologies, triangulation of perspectives). Given that our “ways of looking” are inextricably tied to what we are looking at [ 1 ] it is important to step back and investigate how research methods shape what we can know about a phenomenon of interest. This exploration can offer insight into missing pieces of the analytic puzzle (e.g., the current gaps in our knowledge), and invite novel ways of researching ED recovery (e.g., incorporating different perspectives).

ED recovery research that is published in peer-reviewed journals most frequently uses quantitative (numerical, “objective”) Footnote 1 statistical methods, or qualitative (descriptive, “subjective”) interview methods, in order to convey their findings. In this paper, we provide an overview of commonly used methods and outline key analytic features of various types of analyses that fit within these broader method categories. We also present an examination of these commonly used methods, reflecting on the benefits and limitations of each, and what each allows us to know, or not know, about ED recovery. Following this overview, we explore mixed-methods (quantitative and qualitative), creative methods (e.g., Photovoice, digital storytelling), and multi-methods (e.g., quantitative, qualitative, creative methods, psycho/physiological, behavioral, laboratory, online observations), which may provide directions for future research, and enable new understandings of ED recovery.

Importantly, we are not suggesting that researchers abandon these commonly used quantitative or qualitative methods or that one approach is inherently better than others. Rather, we are recommending a broadening of our methodological “toolkits,” to increase the clarity of purpose of our studies, along with an alignment of the methods used. This may enable the development of more nuanced and specific insights about ED recoveries that take into account context, varied perspectives, and different positionalities. In this paper we thus aim to provide an overview of the ED field’s current perspectives on recovery, illuminate how those perspectives are necessarily informed by our methodological choices, and recommend broadening our methodological “toolkits” in order to form a more complete picture about what can be known as possible in recovery.

Ontological and epistemological stances in ED recovery research

The goal or purpose of ED recovery research depends largely on the ontological (the “what” of research) and the epistemological (the “how” of research) stances endorsed by the researcher [ 2 , 3 ]. This is often considered to be foundational in qualitative research, but is less frequently named in quantitative approaches. We give a brief overview of these stances here, because how a researcher views the world will inevitably impact the goal of the research and the methodological approaches used. In this way, we cannot present a discussion of recovery methodologies without also considering ontology and epistemology.

Ontological stance refers to what we believe can be known [ 4 , 5 ]. From a realist perspective, there is a single objective truth which exists [ 6 ]. On the other side, a relativist perspective suggests that there is no singular reality outside of human practices [ 7 ]. Researchers can therefore vary along this spectrum in terms of their assumptions about what knowledge exists.

Epistemology refers to how we can come to know this information [ 8 ]. For example, positivism argues that we can come to understand or know an objective reality through rigorous scientific practices [ 9 , 10 ]. This is the foundation of the scientific approach and what has often been referred to as the “hard sciences.” Recently, there has been a shift in which individuals from this perspective acknowledge that data collection and interpretation may be imperfect and influenced by researcher characteristics; what is now known as post-positivism [ 11 ].

Many of the quantitative approaches that will be discussed in this paper come from a post-positivist framework in that they assume there is an objective recovery “truth” that can be uncovered if we are rigorous in our approach and seek to minimize bias. On the other side, there are contextualist [ 12 ] and constructionist [ 13 ] epistemologies. Contextualism situates knowledge and the people who create it (e.g., participants, researchers) in a broader context, acknowledging that no one person can know everything. Constructionism argues that meaning is multiple, socially-constructed, and connected to wider systems of power. In this way, there is no one definition or understanding of a phenomenon.

The ontological/epistemological stance and research assumptions that dictate the approaches we take in turn inform debates on recovery. Those coming from different traditions will thus have different views of what can be known about the phenomenon. For example, the frames of (post)positivism typically underlie quantitative research, and researchers coming from this perspective have long been calling for a clear, consistent, and applicable definition of recovery (e.g., [ 14 , 15 , 16 , 17 ]). However, no overall consensus definition has been reached to date, which has several implications from a (post)positivist perspective. This lack of conceptual clarity, and between-study differences in measurement approaches, impact our ability to compare the findings between studies, including reported recovery rates, which can vary dramatically, depending upon the definitions and clinical groups used (e.g., [ 14 , 15 , 18 , 19 ]).

The belief that there is a need for a singular definition is one way of understanding the utility of recovery and may be useful for some groups. The intent of our paper, though, is not to provide a statement about what a consensus definition might be. Rather, we are offering a more diverse view of methodological perspectives (which stem from various ontological and epistemological stances) and ideas that might allow for forward movement in the field. In a dialectal format, this can involve both movement toward and away from consensus, including perspectives which do not seek to identify a single recovery definition. These paths are sometimes polarized, indicating that research aiming for (provisional) consensus is incompatible with research pushing into new areas. We suggest that both can be simultaneously pursued, acknowledging that one does not discount the other.

ED recovery research approaches: A brief overview

Quantitative research stemming from (post)positivist perspectives has tended to emphasize “objective” illness and recovery criteria that can be measured and compared in the lab/treatment, such as body mass index (BMI) (e.g., [ 20 ]), and behavioral/cognitive symptoms (e.g., [ 21 , 22 ]). For example, scores of validated ED measures such as the Eating Attitudes Test (EAT) [ 23 ] are frequently subdivided into “threshold” (criteria met for a probable clinical diagnosis) or “subthreshold” (diagnostic criteria unlikely to be met). Changes in measurable physical, behavioral, and symptomatic criteria are characteristic of the medical model of recovery, with a growing body of research suggesting that such approaches may not fit as well with lived experience perspectives [ 24 , 25 ].

In a systematic review of 126 studies looking at predictors of ED outcomes [ 26 ], symptom remission was used as a key outcome in over 80% of studies. This may differ from the “process” recovery criteria typically used in clinical settings, where the individual’s progress in therapy (e.g., how they navigate their recovery, showing improvements in not only symptoms, but also psychosocial functioning) may affect the extent to which they are deemed “recovered.”

A key element of these different definitions hinges on the extent to which symptom remission is considered an important first step in recovery. This point has often been promoted as self-evident, but is inconsistent with some orientations to recovery. For instance, a recovery model orientation, which has been noted to be potentially resonant with EDs (e.g., [ 27 ]) starts with an emphasis on a person’s goals and contexts, rather than assuming that symptom remission is a first step. This does not mean that “anything goes"; a recovery model promotes collaboration and discussion in exploring what recovery means and does for the person seeking it [ 28 , 29 ].

More recently, researchers have suggested that in alignment with this recovery model, it may be possible to continue to exhibit some symptoms (e.g., behaviors), but have improvement in other areas (e.g., improved psychosocial functioning, QOL), and still feel that one is in ED recovery (e.g., [ 27 , 29 , 30 , 31 , 32 , 33 , 34 , 35 ]). ED advocacy groups led by people with lived experience are also beginning to support approaches to harm reduction within ED recovery circles, such as those promoted by Nalgona Positivity Pride. Indeed, there are now several ED-specific, standardized measures of functioning and QOL that can provide more insight in this area, including the Eating Disorders Quality of Life (EDQOL) [ 36 ], Quality of Life for Eating Disorders (QOL ED) [ 37 ], Health-Related Quality of Life in Eating Disorders Questionnaire (HeRQoLED) [ 38 ], Eating Disorders Quality of Life Scale (EDQLS) [ 39 ], and, more recently, the Eating Disorders Recovery Questionnaire (EDRQ) [ 40 ]. In addition to assessing QOL from a quantitative perspective, QOL can also be explored qualitatively, allowing it to be contextualized against the landscape of participants’ lives.

What is considered to “matter” in ED recovery definitions thus far also differs to some extent according to who is asked. Researchers, clinicians, and people with lived experience (individuals and supportive others such as parents, family, partners, friends, mentors) may emphasize different criteria for ED recovery [ 41 ]. Further, these categories are not distinct; people may simultaneously occupy multiple positionalities at once, such as researchers and/or clinicians who also have lived experience of ED. While a consensus definition among clinicians is arguably becoming a more plausible goal [ 16 ], there may still be significant divergence of opinion between the larger clinical, research, and lived experience spaces [ 18 ]. Nevertheless, Bachner-Melman et al. [ 42 ] also found a broad area of overlap in the perspectives of people with lived experience of an ED, family members, and ED therapists, on what recovery encompasses. They proposed a questionnaire to measure four aspects of ED recovery that were agreed on by these overlapping perspectives: lack of symptoms, acceptance of self and body, social and emotional connection, and physical health [ 20 ].

Lived experience, including personally having lived with an ED, as well as being a “support” for someone with an ED (e.g., parents, family, partners, friends, mentors), necessarily informs a particular person’s ED recovery definition and provides an additional lens on the same construct. Thus, individuals who have lived through an ED may have a different view of recovery to that of their “supports” (e.g., improved psychosocial functioning, QOL, vs. medical stability, decreases in behaviors, and vice versa). However, the recovery priorities of individuals and “supports” may also align. For example, recent studies have indicated that both individuals and parents/families place high value on increased body acceptance and independence in the individual’s recovery process [ 43 , 44 ]. In addition, there is a relatively new resource for partners of those with ED, which focuses on understanding, supporting, and connecting with the partner on shared recovery goals [ 45 ]. In the book “Loving Someone with an Eating Disorder,” Dana Harron includes perspective-taking exercises to help the person understand their partner’s struggle, strategies for dealing with mealtime challenges, up-to-date facts about EDs, and self-care tips to help the person maintain healthy boundaries [ 45 ].

Conceptual and methodological challenges in ED recovery research

Related to the above, researchers face a number of conceptual and methodological questions when exploring ED recovery. For example, whether or not recovery should be considered per individual ED, or trans-diagnostically, is an important question in the recovery definition literature. Bardone-Cone et al. [ 15 ] suggest that a transdiagnostic approach is most appropriate, given that diagnoses can shift, and symptoms can fluctuate over time. Indeed, longitudinal studies have indicated that participants report receiving a single ED diagnosis at one point in time, however, over their lifetime, they would have met criteria for two, three, or four “different” ED diagnoses at different times (e.g., [ 46 ]). Anecdotally, our co-authors have also noted this when recruiting participants for research. Instead of necessitating an overall cessation of ED symptoms within one diagnostic category in the traditional categorical approach, a transdiagnostic approach could rather focus on improving the status of individual symptoms (e.g., frequency of restricting, binging) as a marker of individual “recovery.”

Beyond differences in being able to compare clinical groups across research findings, we might also consider who is most commonly included in these recovery studies (and who is not). There are many significant logistical barriers to receiving an ED diagnosis and related treatment worldwide. Indeed, practical barriers include: cost, insurance coverage, rurality, transportation, work or education schedules, and lack of available childcare, which disproportionately affects people from potentially disadvantaged groups (e.g., [ 47 , 48 , 49 , 50 ]). The process of recovery itself invokes privilege (e.g., who is able to be diagnosed, who has access to formal treatment, and who is recovering in the “right way”). For example, EDs may be missed, or diagnoses delayed, in those who do not fit the stereotypical picture of a person with an ED, including those in larger, or non-emaciated, bodies [ 51 , 52 ].

The majority of the studies thus far on ED recovery definitions are therefore composed predominantly of non-diverse participant samples who have the means to overcome the barriers to treatment access (i.e., predominantly White, thin, socioeconomically privileged, cisgender women, drawn primarily from clinical settings). Indeed, there has been comparatively little research on other populations with EDs (e.g., cis men, trans and nonbinary people, children, elders, higher weight individuals, individuals with binge eating disorder [BED], comorbidities, or late onset), as these groups often do not have access to the diagnoses and treatments that are the gateway to research study participation. These limitations determine whose recoveries we can learn about, and excludes other experiences [ 18 , 53 , 54 ].

Traditionally, those with lived experience have not been invited to co-design recovery research, limiting study participation and the diversity of representation. Even when recovery research includes non-clinical samples, methodology choices impact who is selected for participation. For example, studies that exclude potential participants with BMIs above certain levels (e.g., BMIs that are considered “overweight” or “obese”) exclude many ED recovery experiences automatically, limiting the view of what “recovery” looks like.

Additionally, the specific terminology of “recovery” may not resonate with all people experiencing life beyond an ED [ 55 ], causing some potential participants to self-select out of such studies. Some people with lived experience note that the term “recovery” is prescribed and carries preconceptions [ 56 , 57 ]. Indeed, there are nuances and connotations involved with the use of the word “recovery.” Some individuals may consider themselves “in recovery” (on a continuous journey), while others may consider themselves “recovered” (having moved past the ED completely). In this way, the meaning of “recovery” can indicate both a process and a state [ 58 ]. Stringent criteria for including people in studies as “recovered” may pre-define the group with whom recovery is being explored. Other terminology, such as severe and enduring anorexia nervosa (SEAN), and severe and enduring eating disorders (SEED), emphasize more chronic conditions. However, these terms are not always helpful for people experiencing longer-lasting ED, as they may insinuate that healthcare providers (or the patient) have given up hope for recovery [ 59 , 60 , 61 , 62 ].

Given that “recovery” as a term does not resonate with all [ 55 , 63 , 64 , 65 ], using other terms, including non-clinical ones (e.g., “getting better”, “healing”) to refer to these experiences may increase the diversity of experiences in the literature. As we will explain, these methodological features matter in recovery research because they significantly impact what we can know about ED recovery, and for whom.

Positioning ourselves

We come into this work from various vantage points; we name our positionalities here, since researchers’ subjectivity inevitably shapes their research and interpretations [ 66 ]. Engaging with the subjective, rather than presuming objectivity is the most ethical and effective stance in research, and can invite opportunities to uncover new and different knowledge [ 67 ]. The authors bring research and clinical lenses to bear on this work; some of us are primarily or exclusively researchers in the ED field, whereas others also practice clinically. We come from Global North countries, and all of us are White. We were thus trained in scientific traditions that privilege certain ways of knowing and doing that reflect the English and White dominant landscape of academia. While most of us benefit from thin privilege, able-bodied privilege, and cis-hetero privilege, our authorship team also includes those with non-binary, queer, fat, and chronically ill identities. Some of us have lived experience with ED, and have used this to inform our research and clinical practice. Some of us are newer to the ED field, whereas others have been working in the field for over 30 years. While we are different in some ways, our sameness centers around the academic privilege we have to access, interpret and navigate these literatures and their methodologies.

Overview and analysis of ED research methods

Below we provide an overview of the commonly used quantitative and qualitative research methods, along with tables that illustrate examples of the different types of analyses that fit within these broader methodological categories. We also analyze the benefits and limitations of each method, focusing on what we can learn from them and identifying relevant gaps in the literature.

Quantitative methods

As noted above, quantitative methods typically stem from a (post)positivist ontological/epistemological stance, which inherently affects how data are interpreted and understood. This is a core consideration of how we in turn can view the findings. This approach aims to provide “objective” results [ 68 ]; in this case, it is “recovery by the numbers.” It allows for the measurement of results through data, relying on a systematic approach of empirical investigation, and based on the assumption that there is a singular recovery definition which can be known. Researchers use statistical models, computational techniques, and mathematics to develop and test specific hypotheses. The types of quantitative analyses range from relatively simple descriptive/comparative measures to more complex multivariate measures and multi-level designs (which are all influenced by their study samples, assessments, and testable hypotheses). Data can be collected from the traditional in-person research study (or through video conferencing), or alternatively, from participant surveys (e.g., online, phone, mail, text).

Different types of quantitative methods have been employed in ED recovery research (see Table  1 ). Descriptive studies focus on the “how/what/when/where,” rather than the “why” (e.g., examining aspects of recovery definitions [ 69 ]), and comparative studies have a procedure to conclude that one variable is better than another (e.g., comparing different recovery definitions for agreement [ 70 ]). Univariate analyses examine the statistical characteristics of a single variable (e.g., dichotomous yes/no variable differences between recovery groups on a single measure [ 33 ], continuous range variable differences between recovery groups on multiple measures [ 71 ]), while bivariate analyses determine the empirical relationship between two variables (X and Y) (e.g., relationships between recovery attitudes and related variables [ 72 ]). Multivariate analyses aim to determine the best combination of all possible variables to test the study hypothesis (e.g., comparing recovery and healthy control groups across different recovery scores [ 73 ]).

According to (post)positivist stances, these quantitative methods have the anticipated or theoretical benefits of enabling researchers to reach higher sample sizes (increases generalizability), randomize participants (reduces bias), and replicate results (validates data). In practice, though, generalizability extends only to the sample that is recruited (as noted above, in most cases, thin, White women), and randomization within that sample thus does not increase the diversity of results. The relative focus on “novel” research means that replication studies are not conducted to the degree we would hope or expect.

In addition, quantitative methods limit what can be known about any particular individual. For example, numbers can tell us a person’s standardized assessment scores, but they do not include the detailed descriptions of the individual’s experiences. They also reduce recovery to a single experience which may overlook the tremendous diversity in lived experiences. Similarly, while statistical analyses can account for contextual confounding variables, they cannot tell us the broader factors which influence the delivery and the function of interventions.

Qualitative methods

Overall, qualitative methods offer the potential to engage deeply with phenomenon of interest, often stemming from non-positivist epistemological stances (e.g., constructionist, feminist). While qualitative methods are commonly critiqued for small sample sizes, in a qualitative paradigm, small samples allow researchers to dig into the nuances illustrated in participants’ stories, strengthening study findings. The aim of qualitative research is in-depth, contextualized analysis, rather than generalizations. Qualitative methods often, but not always, involve interacting directly with participants in the form of interviews or focus groups. However, qualitative research can also involve analyses of existing textual or image data, such as blog or social media posts, or news articles. A core feature of qualitative research is the researchers’ focus on exploring meaning in voiced or textual data, vs. using only quantitative measures.

Despite shared features, qualitative methods vary enormously in terms of data collection and analysis types. This is due in part to the differences in theoretical basis, epistemologies, ontologies, and paradigms that inform what meaning researchers perceive as possible to achieve. Some (e.g., [ 74 ]) draw on the concepts of “big Q” and “small q” to differentiate in broad terms between the qualitative methods [ 75 ]. Briefly, “big Q” methods invite and acknowledge researcher subjectivity, whereas “small q” approaches attempt to aim at more “objective interpretation,” [ 76 ], which is more similar to (post)positivist approaches. Further, “big Q” approaches tend to delve into the connections between knowledge production, analysis, and sociocultural contexts in which research takes place, whereas “small q” approaches tend to focus more on descriptive, groundwork-laying analysis for quantitative methods to provide generalizability [ 76 ]. Neither approach is inherently “better;” they are designed to achieve distinct findings.

Some of the qualitative methods that have been commonly used to explore ED recovery experiences are summarized in Table  2 . Note that these are not the only methods used. Some (particularly earlier) studies, describe their methods as “qualitative,” without specifying the exact type(s) of analysis. The differences between these various types of methods are at times subtle.

Discourse Analysis (DA) focuses on language not as just a route to content, but as powerful in and of itself (e.g., analysis of talk about recovery) [ 77 , 78 ]. Within DA, Linguistic Analysis adds a focus on language present in the text, with more of an emphasis on terms used, and their connotations (e.g., explorations of Internet message board communications about recovery) [ 79 ]. Also within DA, Narrative-Discursive Analysis adds a focus on social power (e.g., analysis of recovery interviews with a gender lens [ 80 ]), alongside an emphasis on stories (individual and broader, social stories). Narrative Approaches emphasize the story (e.g., analyses of participant writing, life-history), and situates recovery within the broader culture [ 31 , 81 , 82 , 83 , 84 ]). Phenomenological and Phenomenographic Approaches, including Interpretive Phenomenological Analysis (IPA) aim to get in “close” to participant embodied experiences (e.g., focus on recovery self-process in specific groups such as men, former patients, people in recovery from AN specifically [ 85 , 86 , 87 ]). Grounded Theory emphasizes context-specific “ground-up” theory developed from participant responses (e.g., development of cyclical, phase, and process models of recovery in/outside of treatment contexts [ 65 , 88 , 89 , 90 , 91 ]). Thematic Analysis (TA) is aimed at developing patterns/themes based on data (e.g., exploring patterns in experiences of recovery [ 92 , 93 , 94 ]) and can look quite different depending on the type of thematic analysis employed, ranging from more descriptive to more analytical. Content Analysis summarizes and organizes experiences amongst a particular group in a particular context (e.g., describing the content of interviews with specific groups, for example, athletes, or exploring the content of a particular stage of recovery, such as late-stage recovery [ 95 , 96 , 97 , 98 , 99 ]).

It is also possible to use different qualitative methods to explore similar phenomenon. For example, a constructivist grounded theory exploration of people who have received treatment for AN may focus on theorizing what ED recovery processes are occurring for this particular group [ 99 , 100 ]. An IPA of this same group, meanwhile, may emphasize the development of a set of themes relating to shared perspectives on what the experience felt like [ 101 , 102 ].

Qualitative methods can thus provide detailed descriptions of a wide diversity of lived experiences. This enables us to have a broader perspective of what is possible in recovery. Additionally, these methods allow us to consider the contextual factors which influence the delivery and the function of interventions. A potential further benefit is the individual’s own process of reflecting on their changes in recovery (via study participation), which may provide insight and encouragement for continuing on their path.

Critiques of qualitative methods tend to center around the concept of generalizability, though as noted this is not typically the goal of qualitative approaches. As noted above, quantitative studies, which typically focus on a person’s ED standardized assessment scores, and account for contextual confounding variables through statistical analyses, theoretically generate findings which can be applied to other populations from the study sample. However, as we have indicated, extrapolation of the results of mostly homogenous groups (e.g., predominantly White, thin, socioeconomically privileged, cisgender women, drawn primarily from clinical settings) falsely assumes that the course and outcomes will be the same for all.

Exploration of mixed-methods, creative methods, and multi-methods research

While ED recovery researchers have primarily conducted either quantitative or qualitative studies, some have integrated alternative or multiple methods in their designs. Below we explore some of these methods, which may enable new understandings of ED recovery. These include mixed-methods (usually a weaving of quantitative and qualitative), creative methods (e.g., Photovoice, digital storytelling), and multi-methods (e.g., complementary combinations of quantitative, qualitative, creative methods, psycho/physiological, behavioral, laboratory, online observations).

Mixed-methods (weaving of quantitative and qualitative)

It has been argued that mixed-methods allow us to weave together our quantitative and qualitative insights by acknowledging the benefits and limits of both designs. Cluster analysis intends to combine these methods with the goal of maximizing benefits [ 103 ]. For the qualitative aspects of the analysis, data is coded to themes using one of the qualitative methods, and each individual unit of data (e.g., person) is coded for the presence or absence of each theme. For the quantitative aspects of the analysis, data is plotted to identify different clusters of individuals, and then these clusters are interpreted via statistical methods. Cluster analysis aims to provide greater insight into groups of individuals, and potentially elucidate different clusters of “recovery definitions.” However, the qualitative analysis in this approach is inherently reductionistic (e.g., people are coded to create a quantitative measure), which aligns with the post-positivist stance associated with quantitative analyses. From this view, the approaches are not actually integrated; rather they are complimentary. Indeed, it may not be possible to truly integrate them when they emerge from different epistemological stances. We suggest, however, that integration is not needed.

Bachner-Melman et al. [ 42 ] used exploratory factor analysis to identify four factors that mapped onto ED recovery which had general agreement between participants with a lifetime ED diagnosis, healthy family members, and ED clinicians; (1) lack of symptomatic behavior, (2) acceptance of self and body, (3) social and emotional connection, and (4) physical health. These factors were then confirmed using confirmatory factor analysis. Utilizing more than one method thus expands our perspectives of ED recovery, allowing us to broaden our understanding of what can be known about recovery. Yet as noted above, we caution readers in viewing mixed-method approaches as an overall panacea; the approach tends to be more (post)positivist, and aims to quantify experiences, which may not be the goal for researchers from other stances. Again, this is not to say that the approach is without merit, but that it is important to acknowledge what it aims to do (or know).

Creative methods (photovoice, digital/verbal storytelling, collages, drawings)

Quantitative and qualitative methods are, of course, not the only options at the disposal of researchers interested in exploring ED recovery. Some researchers have elected to take creative approaches to research, seeking to explore recovery in different ways. Potentially, such methods enable researchers to “see” facets of recovery phenomenon that are less evident in methods that primarily hinge on either words or numbers [ 57 ]. To date, ED recovery researchers have used creative methods such as Photovoice [ 104 , 105 ], which aims to involve participants in the process of generating and analyzing research data [ 106 ]. This method may be particularly useful for generating disseminable results, with a view towards change in policy settings for the benefit of people in recovery [ 104 ].

Another creative method, digital storytelling [ 57 , 107 ], encourages participants to “story themselves” at a particular moment in time. This may enable the creation of more nuanced, rich, and person-centered depictions of recovery; the participant’s voice is centered in a way that may be less feasible in research that seeks to generate patterns across several participants’ accounts [ 107 ]. Like Photovoice, digital stories can also be used to work toward enhancing understandings of recovery amongst people who do not have lived experience (e.g., healthcare providers) [ 57 ].

Other creative methods include the use of collages, verbal storytelling, drawing,and more [ 108 , 109 , 110 ]. Placing the decision about which creative method to use in the hands of research participants may also enable a redressing of traditional power dynamics in research that position the researcher as the ultimate decision-maker [ 57 ].

Multi-methods (complimentary use of multiple methods)

Given that ED recovery is a complex phenomenon, one approach to exploring it is the use of a multi-method research design, including different complimentary types of analyses (e.g., quantitative, qualitative, creative methods, psycho/physiological, behavioral, laboratory, online observations), and ideally from different perspectives (e.g., individuals, “supports,” clinicians, researchers, policy makers, and other stakeholders). Broadening our methodological “toolkits” may allow for more nuanced and specific insights about ED recoveries, taking into account context, varied perspectives, and positionalities.

Several studies of ED symptom assessment have employed multi-method designs thus far, and each of these has the potential to contribute a piece of the “ED recovery puzzle.” For example, Stewart et al. [ 111 ] conducted a mixed method investigation of the experiences young people, parents, and clinicians had of online ED treatment during COVID-19. They used a mixed quantitative (Likert scale rating questions) and qualitative (free text entry questions) survey which they analyzed using a summary approach (quantitative) and reflexive thematic analysis (qualitative). Leehr and colleagues [ 112 ] analyzed binge eating episodes under negative mood conditions via electroencephalography (EEG) and eye tracking (ET) in a laboratory.

Bartholome et al. [ 113 ] combined standardized instrument interviews, laboratory investigations, and ecological momentary assessment (EMA) to collect data on binge eating episodes in participants with BED. In order to examine underlying mechanisms of the somatic sensation of “feeling fat,” Mehak and Racine [ 114 ] used multiple methods of self-reports, EMA, heart rate variability, laboratory measurements of BMI, dual energy X-ray absorptiometry (DEXA) scans, and clothing sizes.

Technological advances can offer more in-depth information about the recovery process, and could be utilized further in research studies. For example, EMA allows for moment by moment collection of data on phenomenon of interest. This can include biological functions (e.g., heart rate), as well as feelings and behaviors in an individual’s daily life. This approach provides a more “real time” look into experiences (versus having to recall such experiences later on in a survey, or in an interview). In the case of ED recovery, future research can explore the answer to the question of what “active” recovery looks like on a daily basis for individuals via EMA (e.g., what challenges do individuals encounter; how does it impact their behavior/feelings?).

Other technological laboratory tools, such as fMRI, DEXA, and other scanning techniques, can add visual information about the current physical state of recovery (and any related functional “scars” from the ED). It may be helpful in future studies to provide this feedback so individuals can have an accurate picture of the medical status of their body, and make adjustments (e.g., take Vitamin D to increase bone density).

Additional methodological approaches/considerations

Co-design with different perspectives in ed recovery research.

We believe it will be helpful to incorporate different perspectives in ED recovery research for many reasons. For example, expanding who is included in our studies, what identities are represented, and those with both formal and informal treatment, will increase the participant representation, relevance, and generalizability of the findings [ 53 ]. This in turn will allow us to know more about the process of recovery for different individuals and groups, and will broaden our conceptualization of the phenomenon. Ideally, future research will include individuals with lived experiences and their “supports” (e.g., parents, families, partners, friends, mentors), as well as clinicians and researchers, in co-designing studies that could identify and assess aspects of ED recovery that are important to all of the constituents.

Longitudinal research design

We also underscore the need for an extended duration of studies in order to better understand the longitudinal course and outcome of individuals in ED recovery. This design will allow us to compare recovery operalizations vs. subsequent relapse rates, to track how perspectives of recovery develop and change over time (via quantitative, qualitative and mixed-method measures), and how these in turn affect an individual’s identity (e.g., [ 15 ]).

There are several areas of potential future longitudinal research. For example, follow-up on cognitive recovery (which we know tends to occur later (e.g., [ 43 ]), and how related timelines for this may impact subsequent relapse rates, tracking recovery changes over time with mixed or multi-methods designs in underrepresented populations (e.g., Atypical Anorexia (AAN) [ 115 ]), and holding on to hope, with more longitudinal data indicating that recovery is possible, even after decades (e.g., [ 59 ]).

Future research directions

Based on the above studies, we suggest some potential areas for future research, ideally incorporating multi-method designs to provide different perspectives on ED recovery. Recently, several themes have been identified in the literature as promising lines of research that may improve our understanding of ED, and increase the clinical application of findings.

Predictors of outcomes

Within quantitative research, Bardone-Cone et al. [ 15 ] note that predictors of outcomes, biological/neuropsychological techniques, and a focus on the SEAN population are newer, more nuanced, areas of investigation. In their systematic review and meta-analysis of predictors of ED treatment outcomes (at end of treatment [EoT], and follow-up), Vall and Wade [ 26 ] reported that the most robust predictor at both time frames was greater symptom change earlier in treatment. Other baseline predictors of better outcomes included: higher BMI, fewer binge/purge behaviors, more functional relationships (e.g., with family, friends), and greater motivation to recover. Of note, it is important to understand that higher BMI is in the context of a “higher” thin BMI, as most people with BMI > 25 are not included in studies of recovery. This is another example of how our methods and design choices impact what we can know.

Relatedly, one potential area for future ED quantitative predictor research is to build a Risk Calculator (RC), which is a statistical tool that identifies risk factors, and determines how likely an event is to happen for a particular person [ 116 ]. Physicians have used RCs clinically across an array of medical conditions, including stroke [ 117 ] and cancer [ 118 ]. There has been a recent turn toward integrating RCs into charting psychiatric disorder outcomes and treatment approaches; they have been used for psychosis [ 116 ], depression [ 119 ], and bipolar disorder [ 120 , 121 , 122 , 123 ]. This same technique could be applied to build a RC for personalized risk of ED onset/relapse, utilizing variables collected in research/treatment. A statistical combination of factors that reliably predict the non-occurrence of ED relapse could be a valuable addition to, predictor of, or even criterion, for full recovery. As part of these research initiatives, it will be important for researchers to employ diverse and longitudinal methods in order to obtain long-term, dynamic data.

In line with this, narrative qualitative analysis may be useful in elucidating predictors/risk factors for individuals. In this way, the (narrative) story that the person tells themselves about their recovery, and what was helpful to them, also has importance alongside any quantitative measures. Indeed, this perspective perhaps has more personal meaning, especially in contexts where minute changes identifiable through quantitative studies may be less relevant in the daily lives of their ED recovery.

Biological and neurological markers

Recent developments in the understanding of biological and neurological markers have enabled us to parse out what features may be involved with the ED “state” (which resolves with recovery), what features may onset premorbid to the ED (and will potentially continue after recovery), and what features may be “scars” (consequences of the ED). In their functional Magnetic Resonance Imaging (fMRI) study on participants who had recovered from AN, Fuglset et al. [ 124 ] reported increased activation in visual processing regions in anticipation of seeing images of food, with corresponding reduced activation in decision-making regions. While they found some normalization of the brain regions during recovery, other differences related to longer periods of starvation that appear later in life remained (residual “scars”).

Future quantitative research which incorporates longitudinal designs following the same participant cohort may elucidate more closely the timepoints during which the “state” and “scar” markers begin to emerge, in order to provide earlier interventions. In this instance, qualitative longitudinal studies could be beneficial here too. For example, participant narrative descriptions of ongoing biological changes in their recovery (e.g., feeling hungrier, not being able to tolerate hunger as well) not only reaffirm that people are noticing these internal bio markers, but provide the opportunity for them to discuss their day to day experiences of these lasting changes.

Recovery criteria

From a post-positivist perspective, there has been a longstanding call for standardized ED recovery criteria, typically involving weight, behavioral, and cognitive criteria (e.g., [ 14 , 15 , 16 , 17 ]). Drawing from the above, we suggest that research looking into recovery criteria may benefit from more diverse methodological approaches which pull from a variety of sources (e.g., clinicians, researchers, individuals with lived experience). For example, BMI has historically been used as an indicator of recovery status because it is readily obtained by ED researchers (and clinicians). While weight monitoring can be helpful in specific cases (e.g., those who are severely underweight or have lost a lot of weight in a short period of time), it is limited in use. Namely, BMI is insufficient to determine medical stabilization, it fails to take into account individual differences, and it can have negative impacts on treatment when individuals are discharged on the basis of weight alone [ 125 ]. Given these concerns, future research could discontinue the use of BMI as the “core” recovery criterion, as suggested by Kenny and Lewis [ 126 ], and instead focus on other variables that are more indicative of recovery over follow-up (e.g., Vall and Wade’s systematic review and meta-analysis findings of early symptom change during treatment as the most robust predictor of outcomes) [ 26 ].

Similarly, standardized assessments (e.g., EDE-Q, EDE, ED-LIFE) have been the “go-to” for assessing recovery outcomes in comparison to statistical norms. However, these measures are often developed by clinicians/researchers (thus reflecting what they feel is important in recovery) and in line with particular therapeutic modalities (e.g., the EDE-Q has a cognitive orientation). Thus, scores on these measures may not always match the person’s particular recovery aims and goals, nor the relative importance of particular behaviors in their lives. Employing these measures as a part of multi-methods designs with other types of assessments for comparison may offer the potential to think differently about these measures, and their role in assessing outcomes. We also suggest the need for measures co-designed with folks with lived experience and which reflect the diverse recovery elements described in qualitative studies (e.g., [ 33 ]).

The recovery process

Future research could compile more comprehensive lived experience narratives of changes in thought patterns through the recovery journeys (e.g., descriptions of how the “ED” voice began to leave, if ED voice is a relevant construct for the person), which could provide a more realistic timeline of this portion of the process for individuals and their “supports.” To begin to employ these kinds of measures in a way that opens up new possibilities, it would also be important to explore whether the ED-related ideas being measured resonate with the person whose recovery is being explored. Co-design processes may also be particularly relevant here, inviting people in recovery to be a part of research teams and take a role in determining the kinds of measures that could be used to assess recovery.

As years of ED behaviors and thoughts tend to impair different areas of psychosocial functioning (e.g., relationships, school/work, recreation, household duties), improvement in these areas, along with related QOL, tends to also lag behind physical recovery (e.g., [ 43 ]). Future research could further elaborate the timelines for which recovery in the different areas occurs, both from a group (e.g., through life story, narrative, or thematic analysis), and an individual (e.g., personal recording of recovery progress, case study approach) level. This approach offers a shift in methodological perspective, providing opportunity to conceptualize recovery differently.

Other areas for future consideration

Several studies (and informal support groups) have successfully employed recovered mentors, providing hope in recovery (e.g., [ 127 ]). Future research could examine more of the nuances of the mentorship role, including the characteristics of the mentor, the stage of recovery that the individual is in, and the dynamics of the mentor relationship. Further, taking a truly co-designed approach and, in particular, working with those who have not been included and heard in either treatment or research (not only more diverse participants, but their “supports,” including mentors), could offer new insight into recovery processes. Indeed, going forwards, we need to conduct our research differently if we want to incorporate the perspectives of those that we do not usually hear from.

Another area of study has developed around online (e.g., social media) use among those who are at risk for developing an ED, struggling with an ED, and those who are on the path to ED recovery. Analyses of online websites, blogs, and social media posts, along with their related potentially triggering content, have been conducted (e.g., [ 128 ]). However, on a positive note, this medium allows us to explore other methodological possibilities, including potentially focusing on reducing participant burden, and engaging with content from spaces where people are more “organically” describing these experiences, to get a sense of recovery outside of a clinical perspective. One possibility for future research is to combine the use of EMA with exposure to a range of different ED blog content (e.g., from triggering to supportive posts), in order to provide more proximal individual reaction information (e.g., EMA before exposure, EMA at exposure time, EMA after exposure time).

Proposed future research model: Dialectical movement towards and away from a consensus

The aim of this paper is to offer a more diverse view of methodological perspectives (which stem from various ontological and epistemological stances) and ideas that might allow for forward movement in the field. As noted above, in a dialectal format, this can involve both movement toward and away from a consensus, including perspectives which do not seek to identify a single recovery definition. We believe that both can be simultaneously pursued, acknowledging that one does not discount the other. We have outlined several potential areas to explore which do not necessarily depend upon a consensus definition. Here, for balance, we would like to propose a future research model that could guide us in a direction that may eventually lead to a consensus definition–or definition s . In effect, we are advocating for: (1) transparency in researchers’ epistemological stances; (2) more varied approaches to research in order to “see” different aspects of recovery experiences; and (3) collaboration between researchers and other stakeholders to generate new methodological approaches and insights about recovery.

Our proposed future research model is detailed in Table  3 . Based upon the studies we cited above, we suggest a multi-methods design (e.g., quantitative, qualitative, creative methods, psycho/physiological, behavioral, laboratory, online observations), which incorporates different perspectives (e.g., expanding recruitment of participants that have been less represented in the literature, including “supportive” others), and extends the duration of studies to provide a more longitudinal outlook (e.g., capturing cognitive recovery, and improvement in psychosocial functioning/QOL, which often comes later, and noting how definitions of recovery may change over time for people). In this way, we hope to move the field towards different, more nuanced, and comprehensive perspectives on ED recovery.

In conclusion, we would like to encourage a creative, transparent, and thoughtful approach to ED recovery methodology, that considers what each of the methods allows us to engage with, or not, as the case may be. What we can (and do) know about recovery is intricately tied to our methodological and study design choices, which all have limits. Within this context, while there is a benefit to current pushes in the field to “come to consensus,“ these consensus definitions will necessarily leave out some people and experiences. This is especially the case for those who have not been meaningfully included in the research we have conducted to reach this consensus (e.g., people with lived experience, “non-traditional” patients, patients without access to treatment). Since there are so many different facets of recovery experiences, using different methodologies is imperative to develop a more complete understanding.

Indeed, it is important to acknowledge how the centrality of the method that is chosen to define ED recovery in turn influences how researchers and clinicians understand recovery, and how one moves towards it. New insights into recovery processes may depend on new methods of investigation. Thus, we suggest that some potential areas for future research ideally employ multi-method designs (e.g., quantitative, qualitative, creative methods, psycho/physiological, behavioral, laboratory, online observations), incorporate different perspectives (e.g., expanding recruitment of participants that have been less represented in the literature, including supportive others) and extend the duration of studies to provide a more longitudinal outlook (e.g., capturing cognitive recovery, which often comes later, and noting how definitions of recovery may change over time for people). In this way, we hope to move the field towards different, more nuanced, and comprehensive perspectives on ED recovery.

Availability of data and materials

Not applicable.

There are debates about the degree to which research can ever be truly objective or whether this is desirable. Here, we use objective and subjective in quotation marks to signal broader perceptions about these processes.

Abbreviations

Anorexia nervosa

Binge eating disorder

Body mass index

Bulimia Nervosa

Connectedness, hope and optimism, identity, meaning in life, empowerment

Dual energy X-ray absorptiometry

Eating attitudes test

• Eating disorders

Eating Disorders Recovery Endorsement Questionnaire

Eating Disorders Recovery Questionnaire

Eating Disorders Quality of Life Scale

Eating Disorders Quality of Life

Electroencephalography

Ecological momentary assessment

Eye tracking

Functional magnetic resonance imaging

Generalized estimating equations

Health-Related Quality of Life in Eating Disorders Questionnaire

Hierarchical linear models

Interpretive phenomenological analysis

Multivariate analysis of variance

National Institutes of Health

Risk calculator

Substance Abuse and Mental Health Services Administration

Severe and enduring anorexia nervosa

Severe and enduring eating disorder

Quality of life for eating disorders

Barad K. Meeting the Universe Halfway. Durham: Duke University Press; 2007.

Book   Google Scholar  

Slevitch L. Qualitative and quantitative methodologies compared: ontological and epistemological perspective. J Qual Assur Hosp Tour. 2011;12(1):73–81.

Article   Google Scholar  

Tuli F. The basis of distinction between qualitative and quantitative research in social science: reflection on ontological, epistemological and methodological perspectives. Ethiop J Educ Sci. 2010;6(1).

Duncan C, Cloutier JD, Bailey PH. Concept analysis: the importance of differentiating the ontological focus. J Adv Nurs. 2007;58(3):293–300.

Article   PubMed   Google Scholar  

Hofweber T. Logic and ontology. In: Zalta EN, editor. The Stanford encyclopedia of philosophy. Stanford: The Metaphysics Research Lab, Center for the Study of Language and Information; 2021.

Google Scholar  

Hupcey JE, Penrod J. Concept analysis: examining the state of the science. Res Theory Nurs Pract. 2005;19(2):197–208.

Wilson J. Thinking with concepts. Cambridge: Cambridge University Press; 1963.

Setup M, Ram N. Epistemology. In: Zalta EN, editor. The Stanford encyclopedia of philosophy. Stanford: The Metaphysics Research Lab, Center for the Study of Language and Information; 2020.

Macionis JJ, Gerber LM, Sociology (7th Canadian). Pearson, Canada: Pearson Canada; 2011.

Larrain J. The concept of ideology. London: Hutchison; 1979.

Phillips DC, Burbules NC. Postpositivism and educational research. Lanham & Boulder: Rowman & LIttlefield Publishers; 2000.

Stanley J. Knowledge and practical interests. New York: Oxford University Press; 2005.

Cakir M. Constructivist approaches to learning in science and their implications for science pedagogy: a literature review. Int J Environ Sci Educ. 2008;3(4):193–206.

Bardone-Cone AM, Harney MB, Maldonado CR, Lawson MA, Robinson DP, Smith R, et al. Defining recovery from an eating disorder: conceptualization, validation, and examination of psychosocial functioning and psychiatric comorbidity. Behav Res Ther. 2010;48(3):194–202.

Bardone-Cone AM, Hunt RA, Watson HJ. An overview of conceptualizations of eating disorder recovery, recent findings, and future directions. Curr Psychiatry Rep. 2018;20(9):79.

Wade TD, Lock J. Developing consensus on the definition of remission and recovery for research. Int J Eat Disord. 2020;53(8):1204–8.

Attia E, Blackwood KL, Guarda AS, Marcus MD, Rothman DJ. Marketing residential treatment programs for eating disorders: a call for transparency. Psychiatr serv. 2016;67(6):664–6.

McGilley BS.  J. Recipe for recovery: necessary ingredients for the client’s and clinician’s Success. In: Maine M, Bunnell, editors. New York: Elsevier; 2010.

Noordenbos G. Which criteria for recovery are relevant according to eating disorder patients and therapists? Eat Disord. 2011;19(5):441–51.

Solmi M, Wade TD, Byrne S, Del Giovane C, Fairburn CG, Ostinelli EG, et al. Comparative efficacy and acceptability of psychological interventions for the treatment of adult outpatients with anorexia nervosa: a systematic review and network meta-analysis. Lancet Psychiatry. 2021;8(3):215–24.

Treasure J, Duarte TA, Schmidt U. Eating disorders. Lancet. 2020;395(10227):899–911.

Waller G, Raykos B. Behavioral interventions in the treatment of eating disorders. Psychiatr Clin North Am. 2019;42(2):181–91.

Garner DM, Garfinkel PE. The eating attitudes test: an index of the symptoms of anorexia nervosa. Psychol Med. 1979;9(2):273–9.

Kenny TE, Trottier K, Lewis S. Lived experience perspectives on a model of eating disorder recovery in a sample of predominantly white women: a mixed method study. J Eat Disord. 2022;10(1):1–19.

McDonald S, Williams AJ, Barr P, McNamara N, Marriott M. Service user and eating disorder therapist views on anorexia nervosa recovery criteria. Psychol Psychother. 2021;94(3):721–36.

Article   PubMed   PubMed Central   Google Scholar  

Vall E, Wade TD. Predictors of treatment outcome in individuals with eating disorders: a systematic review and meta-analysis. Int J Eat Disord. 2015;48(7):946–71.

Dawson L, Rhodes P, Touyz S. “Doing the impossible”: the process of recovery from chronic anorexia nervosa. Qual Health Res. 2014;24(4):494–505.

Anthony WA. Recovery from mental illness: the guiding vision of the mental health service system in the 1990s. Psychosoc Rehabilit J. 1993;24(9):159–68.

Wetzler S, Hackmann C, Peryer G, Clayman K, Friedman D, Saffran K, et al. A framework to conceptualize personal recovery from eating disorders: a systematic review and qualitative meta-synthesis of perspectives from individuals with lived experience. Int J Eat Disord. 2020;53(8):1188–203.

Jarman M, Walsh S. Evaluating recovery from anorexia nervosa and bulimia nervosa: integrating lessons learned from research and clinical practice. Clin Psychol Rev. 1999;19(7):773–88.

Dawson L, Rhodes P, Touyz S. Defining recovery from anorexia nervosa: a Delphi study to determine expert practitioners’ views. Adv Eat Disord: Theory Res Pract. 2015;3:165–76.

’t Slof-OpLandt MCT, Dingemans AE, de la Torre YRJ, van Furth EF. Self-assessment of eating disorder recovery: absence of eating disorder psychopathology is not essential. Int J Eat Disord. 2019;52(8):956–61.

de Vos JA, Radstaak M, Bohlmeijer ET, Westerhof GJ. Having an eating disorder and still being able to flourish? Examination of pathological symptoms and well-being as two continua of mental health in a clinical sample. Front Psychol. 2018;9:2145.

Emanuelli F, Waller G, Jones-Chester M, Ostuzzi R. Recovery from disordered eating: sufferers’ and clinicians’ perspectives. Eur Eat Disord Rev. 2012;20(5):363–72.

Noordenbos G, Seubring A. Criteria for recovery from eating disorders according to patients and therapists. Eat Disord. 2006;14(1):41–54.

Engel SG, Wittrock DA, Crosby RD, Wonderlich SA, Mitchell JE, Kolotkin RL. Development and psychometric validation of an eating disorder-specific health-related quality of life instrument. Int J Eat Disord. 2006;39(1):62–71.

Abraham SF, Brown T, Boyd C, Luscombe G, Russell J. Quality of life: eating disorders. Aust N Z J Psychiatry. 2006;40(2):150–5.

Las Hayas C, Quintana JM, Padierna A, Bilbao A, Munoz P, Madrazo A, et al. The new questionnaire health-related quality of life for eating disorders showed good validity and reliability. J Clin Epidemiol. 2006;59(2):192–200.

Adair CE, Marcoux GC, Cram BS, Ewashen CJ, Chafe J, Cassin SE, et al. Development and multi-site validation of a new condition-specific quality of life measure for eating disorders. Health Qual Life Outcomes. 2007;5:23.

Bachner-Melman R, Lev-Ari L, Zohar AH, Linketsky M. The Eating Disorders Recovery Questionnaire: psychometric properties and validity. Eat Weight Disord. 2021;26(8):2633–43.

Noordenbos G. When have eating disordered patients recovered and what do the DSM-IV criteria tell about recovery? Eat Disord. 2011;19(3):234–45.

Bachner-Melman R, Lev-Ari L, Zohar AH, Lev SL. Can recovery from an eating disorder be measured? Toward a standardized questionnaire. Front Psychol. 2018;9:2456.

Accurso EC, Sim L, Muhlheim L, Lebow J. Parents know best: caregiver perspectives on eating disorder recovery. Int J Eat Disord. 2020;53(8):1252–60.

Richmond TK, Woolverton GA, Mammel K, Ornstein RM, Spalding A, Woods ER, et al. How do you define recovery? A qualitative study of patients with eating disorders, their parents, and clinicians. Int J Eat Disord. 2020;53(8):1209–18.

Harron D. Loving Someone with an Eating Disorder. Oakland: New Harbinger Publications, Inc.; 2019.

Milos G, Spindler A, Schnyder U, Fairburn CG. Instability of eating disorder diagnoses: prospective study. Br J Psychiatry. 2005;187:573–8.

Becker AE, Franko DL, Speck A, Herzog DB. Ethnicity and differential access to care for eating disorder symptoms. Int J Eat Disord. 2003;33(2):205–12.

Cachelin FM, Rebeck R, Veisel C, Striegel-Moore RH. Barriers to treatment for eating disorders among ethnically diverse women. Int J Eat Disord. 2001;30(3):269–78.

Cachelin FM, Striegel-Moore RH. Help seeking and barriers to treatment in a community sample of Mexican American and European American women with eating disorders. Int J Eat Disord. 2006;39(2):154–61.

Ali K, Farrer L, Fassnacht DB, Gulliver A, Bauer S, Griffiths KM. Perceived barriers and facilitators towards help-seeking for eating disorders: a systematic review. Int J Eat Disord. 2017;50(1):9–21.

Lebow J, Sim LA, Kransdorf LN. Prevalence of a history of overweight and obesity in adolescents with restrictive eating disorders. J Adolesc Health. 2015;56(1):19–24.

Harrop EN, Mensinger JL, Moore M, Lindhorst T. Restrictive eating disorders in higher weight persons: a systematic review of atypical anorexia nervosa prevalence and consecutive admission literature. Int J Eat Disord. 2021;54(8):1328–57.

Egbert AH, Hunt RA, Williams KL, Burke NL, Mathis KJ. Reporting racial and ethnic diversity in eating disorder research over the past 20 years. Int J Eat Disord. 2022;55(4):455–62.

Mikhail ME, Klump KL. A virtual issue highlighting eating disorders in people of black/African and indigenous heritage. Int J Eat Disord. 2021;54(3):459–67.

Conti JE. Recovering identity from anorexia nervosa: women’s constructions of their experiences of recovery from anorexia nervosa over 10 years. J Constructivist Psychol. 2018;31(1):72–94.

Kenny TE, Thomassin K, Trottier K, Lewis SP. Views on the term ‘recovery’ in a sample of primarily white treatment-experienced women with lived eating disorder experience. Int J Eat Disord. Under Review.

LaMarre A, Rice C. Healthcare providers’ engagement with eating disorder recovery narratives: opening to complexity and diversity. Med Humanit. 2020;47:78–86.

Fava GA. The concept of recovery in affective disorders. Psychother Psychosom. 1996;65(1):2–13.

Eddy KT, Tabri N, Thomas JJ, Murray HB, Keshaviah A, Hastings E, et al. Recovery from anorexia nervosa and bulimia nervosa at 22-year follow-up. J Clin Psychiatry. 2017;78(2):184–9.

Dawson L, Rhodes P, Touyz S. The recovery model and anorexia nervosa. Aust N Z J Psychiatry. 2014;48(11):1009–16.

Touyz S, Hay P. Severe and enduring anorexia nervosa (SE-AN): in search of a new paradigm. J Eat Disord. 2015;3:26.

Calugi S, Milanese C, Sartirana M, El Ghoch M, Sartori F, Geccherle E, et al. The eating disorder examination questionnaire: reliability and validity of the Italian version. Eat Weight Disord. 2017;22(3):509–14.

LaMarre A, Rice C, Rinaldi J tracing fatness through the eating disorder assemblage. Thickening fat, 1st Edition: Routledge; 2019. pp. 64–76.

Shohet MN, Anorexia. “Full” and “struggling.” Genres  Recover Ethos. 2008;35(3):344–82.

Musolino C, Warin M, Wade T, Gilchrist P. Developing shared understandings of recovery and care: a qualitative study of women with eating disorders who resist therapeutic care. J Eat Disord. 2016;4:36.

Malterud K. Qualitative research: standards, challenges, and guidelines. Lancet. 2001;358(9280):483–8.

Gough B, Madill A. Subjectivity in psychological science: from problem to prospect. Psychol Methods. 2012;17(3):374–84.

Matthews B, Ross L. Research methods. a practical guide for the social sciences. Harlow: Pearson Education; 2010.

Couturier J, Lock J. What is recovery in adolescent anorexia nervosa? Int J Eat Disord. 2006;39(7):550–5.

Ackard DM, Richter SA, Egan AM, Cronemeyer CL. What does remission tell us about women with eating disorders? Investigating applications of various remission definitions and their associations with quality of life. J Psychosom Res. 2014;76(1):12–8.

Cogley CB, Keel PK. Requiring remission of undue influence of weight and shape on self-evaluation in the definition of recovery for bulimia nervosa. Int J Eat Disord. 2003;34(2):200–10.

Dimitropoulos G, McCallum L, Colasanto M, Freeman VE, Gadalla T. The effects of stigma on recovery attitudes in people with anorexia nervosa in intensive treatment. J Nerv Ment Dis. 2016;204(5):370–80.

Bachner-Melman R, Zohar AH, Ebstein RP. An examination of cognitive versus behavioral components of recovery from anorexia nervosa. J Nerv Ment Dis. 2006;194(9):697–703.

Braun VC, Can V. I use TA? Should I use TA? Should I not use TA? Comparing reflexive thematic analysis and other pattern-based qualitative analytic approaches. Couns Psychother Res. 2021;21(1):37–47.

Kidder LH, Fine M. Qualitative and quantitative methods: when stories converge. Eval Policy. 1987;1987(35):57–75.

Clarke V. Navigating the messy swamp of qualitative research: are generic reporting standards the answer? In: Levitt HM, editor. Reporting qualitative research in psychology: how to meet APA Style journal article reporting standards, revised edition. Washington: American Psychological Association; 2020.

Hardin PK. Social and cultural considerations in recovery from anorexia nervosa: a critical poststructuralist analysis. ANS Adv Nurs Sci. 2003;26(1):5–16.

Keski-Rahkonen A, Tozzi F. The process of recovery in eating disorder sufferers’ own words: an Internet-based study. Int J Eat Disord. 2005;37(Suppl):S80-6 discussion S7-9.

Maison H, Bailey L, Clarke S, Treasure J, Anderson G, Kohn M. Un/imaginable future selves: a discourse analysis of in-patients’ talk about recovery from an eating disorder. Eur Eat Disord Rev. 2011;19(a):25–36.

Moulding N. Gendered intersubjectivities in narratives of recovery from an eating disorder. J Women Soc Work. 2016;31(1):70–83.

LaMarre A, Rice C. Normal eating is counter-cultural: embodied experiences of eating disorder recovery. J Commun Appl Soc Psychol. 2016;26:136–49.

Matusek JA, Knudson RM. Rethinking recovery from eating disorders: spiritual and political dimensions. Qual Health Res. 2009;19(5):697–707.

Patching J, Lawler J. Understanding women’s experiences of developing an ED and recovery: a life-history approach. Nurs Inq. 2009;12(1):10–21.

Redenbach J, Lawler J. Recovery from disordered eating: what life histories reveal. Contemp Nurse. 2003;15(1–2):148–56.

Bjork T, Wallin K, Pettersen G. Male experiences of life after recovery from an eating disorder. Eat Disord. 2012;20(5):460–8.

Bjork T, Ahlstrom G. The patient’s perception of having recovered from an eating disorder. Health Care Women Int. 2008;29(8):926–44.

Jenkins J, Ogden J. Becoming ‘whole’ again: a qualitative study of women’s views of recovering from anorexia nervosa. Eur Eat Disord Rev. 2012;20(1):e23–31.

D’Abundo M, Chally P. Struggling with recovery: participant perspectives on battling an eating disorder. Qual Health Res. 2004;14(8):1094–106.

Krentz A, Chew J, Arthur N. Can J Couns. 2005;39(2):118–35.

Lamoureux MMH, Bottorff JL. “Becoming the real me”: Recovering from anorexia nervosa. Heatlh Care for Women International. 2005;26:170–88.

Woods S. Untreated recovery from eating disorders. Adolescence. 2004;39(154):361–71.

PubMed   Google Scholar  

Hay PJ, Cho K. A qualitative exploration of influences on the process of recovery from personal written accounts of people with anorexia nervosa. Women Health. 2013;53(7):730–40.

LaMarre A, Rice C. Hashtag recovery: #eating disorder recovery on instagram. Soc Sci. 2017;6(3):68.

Lord VM, Reiboldt W, Gonitzke D, Parker E, Peterson C. Experiences of recovery in binge-eating disorder: a qualitative approach using online message boards. Eat Weight Disord. 2018;23(1):95–105.

Arthur-Cameselle JN, Quatromoni PA. A qualitative analysis of female college athletes’ eating disorder recovery experiences. Sport Psychol. 2014;28:334–46.

Lindgren BM, Enmark A, Bohman A, Lundstrom M. A qualitative study of young women’s experiences of recovery from bulimia nervosa. J Adv Nurs. 2015;71(4):860–9.

Nilsson K, Hagglof B. Patient perspectives of recovery in adolescent onset anorexia nervosa. Eat Disord. 2006;14(4):305–11.

Pettersen G, Thune-Larsen KB, Wynn R, Rosenvinge JH. Eating disorders: challenges in the later phases of the recovery process: a qualitative study of patients’ experiences. Scand J Caring Sci. 2013;27(1):92–8.

Charmaz K. The power of constructivist grounded theory for critical inquiry. Res Methods Eval. 2016;23(1):34–45.

Williams K, King J, Fox JR. Sense of self and anorexia nervosa: a grounded theory. Psychol Psychother. 2016;89(2):211–28.

Smith JA. Reflecting on the development of interpretive phenomenological analysis and its contribution to qualitative research in psychology. Qual Res Psychol. 2008;1(1):39–54.

Fox AP, Larkin M, Leung N. The personal meaning of eating disorder symptoms: an interpretative phenomenological analysis. J Health Psychol. 2011;16(1):116–25.

Henry D, Dymnicki AB, Mohatt N, Allen J, Kelly JG. Clustering methods with qualitative data: a mixed-methods approach for prevention research with small samples. Prev Sci. 2015;16(7):1007–16.

Saunders JF, Eaton AA. Social comparisons in eating disorder recovery: using photovoice to capture the sociocultural influences on women’s recovery. Int J Eat Disord. 2018;51(12):1361–6.

Saunders JF, Eaton AA, Aguilar S. From self(ie)-objectification to self-empowerment: the meaning of selfies on social media in eating disorder recovery. Comput Human Beh. 2020;111:106420.

Wang C, Burris MA. Photovoice: concept, methodology, and use for participatory needs assessment. Health Educ Behav. 1997;24(3):369–87.

LaMarre A, Rice C. Embodying critical and corporeal methodology: digital storytelling With young women in eating disorder recovery. Forum Qual Soc Res. 2016;17:2.

Bartel H. A ‘Girls’ Illness?’ Using narratives of eating disorders in men and boys in healthcare education and research. In: Arts based health care research: a multidisciplinary perspective. Cham: Springer; 2022. p. 69-84.

Proszynski J. Interior designs: demolition and reconstruction of the self in eating disorder recovery through transformable collage book making (Doctoral dissertation, Pratt Institute). 2022.

Marzola E, Abbate-Daga G, Gramaglia C, Amianto F, Fassino S, Mobini S (ReviewingEditor). A qualitative investigation into anorexia nervosa: The inner perspective. Cogent Psychol 2015;2:1. https://doi.org/10.1080/23311908.2015.1032493 .

Stewart C, Konstantellou A, Kassamali F, McLaughlin N, Cutinha D, Bryant-Waugh R, et al. Is this the ‘new normal’? A mixed method investigation of young person, parent and clinician experience of online eating disorder treatment during the COVID-19 pandemic. J Eat Disord. 2021;9(1):78.

Leehr EJ, Schag K, Dresler T, Grosse-Wentrup M, Hautzinger M, Fallgatter AJ, et al. Food specific inhibitory control under negative mood in binge-eating disorder: Evidence from a multimethod approach. Int J Eat Disord. 2018;51(2):112–23.

Bartholome LT, Raymond NC, Lee SS, Peterson CB, Warren CS. Detailed analysis of binges in obese women with binge eating disorder: Comparisons using multiple methods of data collection. Int J Eat Disord. 2006;39(8):685–93.

Mehak A, Racine SE. Understanding “feeling fat” and its underlying mechanisms: the importance of multimethod measurement. Int J Eat Disord. 2020;53(9):1400–4.

Harrop E. “Maybe i really am too fat to have an eating disorder”: A mixed methods study of weight stigma and healthcare experiences in a diverse sample of patients with atypical anorexia (Doctoral dissertation). Seattle: University of Washington; 2020.

Fusar-Poli P, Rutigliano G, Stahl D, Davies C, Bonoldi I, Reilly T, et al. Development and validation of a clinically based risk calculator for the transdiagnostic prediction of psychosis. JAMA Psychiatry. 2017;74(5):493–500.

Nobel L, Mayo NE, Hanley J, Nadeau L, Daskalopoulou SS. MyRisk_stroke calculator: a personalized stroke risk assessment tool for the general population. J Clin Neurol. 2014;10(1):1–9.

Gail MH, Brinton LA, Byar DP, Corle DK, Green SB, Schairer C, et al. Projecting individualized probabilities of developing breast cancer for white females who are being examined annually. J Natl Cancer Inst. 1989;81(24):1879–86.

Perlis RH. Pharmacogenomic testing and personalized treatment of depression. Clin Chem. 2014;60(1):53–9.

Hafeman DM, Merranko J, Goldstein TR, Axelson D, Goldstein BI, Monk K, et al. Assessment of a person-level risk calculator to predict new-onset bipolar spectrum disorder in youth at familial risk. JAMA Psychiatry. 2017;74(8):841–7.

Birmaher B, Merranko JA, Goldstein TR, Gill MK, Goldstein BI, Hower H, et al. A risk calculator to predict the individual risk of conversion from subthreshold bipolar symptoms to bipolar disorder I or II in youth. J Am Acad Child Adolesc Psychiatry. 2018;57(10):755–63 e4.

Birmaher B, Merranko JA, Gill MK, Hafeman D, Goldstein T, Goldstein B, et al. Predicting personalized risk of mood recurrences in youths and young adults with bipolar spectrum disorder. J Am Acad Child Adolesc Psychiatry. 2020;59(10):1156–64.

Goldstein TR, Merranko J, Hafeman D, Gill MK, Liao F, Sewall C, et al. A risk calculator to predict suicide attempts among individuals with early-onset bipolar disorder. Bipolar Disord. 2022.

Fuglset TS, Landro NI, Reas DL, Ro O. Functional brain alterations in anorexia nervosa: a scoping review. J Eat Disord. 2016;4:32.

Phillipou A, Beilharz F. Should we shed the weight criterion for anorexia nervosa? Aust N Z J Psychiatry. 2019;53(6):501–2.

Kenny TE, Lewis SP. Reconceptualizing recovery: integrating lived experience perspectives into traditional eating disorder recovery frameworks. Psychiatr Serv. 2021;72(8):966–8.

Ramjan LM, Hay P, Fogarty S. Benefits of a mentoring support program for individuals with an eating disorder: a proof of concept pilot program. BMC Res Notes. 2017;10(1):709.

Wolf M, Thies F, Kordy H. Language use in eating disorder blogs: psychological implications of social online activity. J Lang Soc Psychol. 2013;32(2):212–26.

Download references

Acknowledgements

The authors wish to thank our colleagues in ED recovery.

None received.

Author information

Authors and affiliations.

Department of Psychiatry, Eating Disorders Center for Treatment and Research, University of California at San Diego School of Medicine, 4510 Executive Drive, San Diego, CA, 92121, USA

Heather Hower

Department of Health Services, Policy, and Practice, Hassenfeld Child Innovation Institute, Brown University School of Public Health, 121 South Main Street, Providence, RI, 02903, USA

School of Psychology, Massey University, North Shore, Private Bag 102-904, Auckland, 0632, New Zealand

Andrea LaMarre

Clinical Psychology Graduate Program, Ruppin Academic Center, 4025000, Emek-Hefer, Israel

Rachel Bachner-Melman

School of Social Work, Hebrew University of Jerusalem, Mt. Scopus, 9190501, Jerusalem, Israel

Graduate School of Social Work, University of Denver, 2148 S High Street, Denver, CO, 80208, USA

Erin N. Harrop

University of Kansas School of Medicine, 1010 N Kansas St, Wichita, KS, 67214, USA

Beth McGilley

Department of Psychology, Clinical Child and Adolescent Psychology, University of Guelph, 50 Stone Road East, Guelph, ON, N1G 2W1, Canada

Therese E. Kenny

You can also search for this author in PubMed   Google Scholar

Contributions

HH contributed to the conceptualization of the manuscript, the writing and editing of the abstract, introduction, quantitative text and table, mixed-methods, creative methods, multi-methods, future research, and conclusions sections, EndNote reference library/citations, formatting of the manuscript, and overall final revisions. AL contributed to the conceptualization of the manuscript, the writing and editing of the abstract, introduction, qualitative text and table, mixed-methods, creative methods, and conclusion sections, and overall final revisions. RBM contributed to the conceptualization of the manuscript, the writing and editing of the abstract, introduction, quantitative, and qualitative sections, and overall final revisions. EH contributed to the conceptualization of the manuscript, the writing and editing of the abstract, introduction, qualitative text and table sections, and overall final revisions. BM contributed to the conceptualization of the manuscript, the writing and editing of the abstract, introduction, qualitative, and mixed-methods sections, and overall final revisions. TK contributed to the conceptualization of the manuscript, the writing and editing of the epistemology and ontology sections, and discussion of these concepts through other sections, as well as overall final revisions. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Heather Hower .

Ethics declarations

Ethics approval and consent to participate, consent for publication, competing interests.

RBM is a Senior Editor of this Journal. All other authors declare that they have no competing interests.

Additional information

Publisher’s note.

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ . The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/ ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Cite this article.

Hower, H., LaMarre, A., Bachner-Melman, R. et al. Conceptualizing eating disorder recovery research: Current perspectives and future research directions. J Eat Disord 10 , 165 (2022). https://doi.org/10.1186/s40337-022-00678-8

Download citation

Received : 05 September 2022

Accepted : 25 October 2022

Published : 15 November 2022

DOI : https://doi.org/10.1186/s40337-022-00678-8

Share this article

Anyone you share the following link with will be able to read this content:

Sorry, a shareable link is not currently available for this article.

Provided by the Springer Nature SharedIt content-sharing initiative

• Quantitative research
• Qualitative research
• Multi-methods research

Journal of Eating Disorders

ISSN: 2050-2974

• General enquiries: [email protected]

Cookie Acceptance Needed

This website would like to use cookies to collect information to improve your browsing experience. Please review our Privacy Statement for more information. Do you accept?

Accept Deny

• News |  
• Articles |  
• Body image research to practice

Customized care: Auburn University body image research sets new standard for person-centered treatment

From research to treatment, students and faculty at Auburn University are leading the charge to dispel stereotypes about eating disorders. Their work lays a foundation for a new clinical model, one that understands that eating disorders can happen to anyone, and through that understanding, prepares clinicians to better help everyone.

Assistant Professor of Psychological Sciences Tiffany Brown leads the Appearance Concerns, Eating, Prevention and Treatment (ACCEPT) Lab and co-directs the Auburn Eating Disorders Clinic (AEDC). Through both, she leads a cyclical effort to investigate, test and improve eating disorders treatment.

"The really exciting thing for me as both a clinician and then also a researcher, an academic, is being able to integrate what we're finding out in research about risk for eating disorder behaviors within diverse groups," Brown said. "We can then actually apply that or target some of those factors in treatment."

Culturally informed research

The ACCEPT Lab researches the factors behind negative body image and eating disorders across traditionally underserved populations. Recent psychology graduate and research assistant Minh Le's '24 work focused on how identity-related stress affects body dissatisfaction, including in populations across racial groups and the LGBTQ+ community.

Le said Brown helped him translate his hope for positive change into deliverable results that will benefit future researchers and clinicians. For example, Le's study revealed that stress around hiding sexual identity can predict body dissatisfaction in Asian individuals.

"My initial process of wanting to do this project was me being a part of a minority group and also the LGBTQ+ community. I really saw a difference between individuals that I have met in my life, and I wanted to see if there was an impact on body dissatisfaction," Le said. "I saw in my experiences that there is a sense of shame and dishonor whenever you are seen outside of the 'normal' group within Asian cultures. So, I see why it makes sense that sexual orientation concealment would be the highest predictor for it."

Graduate research assistant and clinical psychology student Marley Billman Miller also studies body dissatisfaction with an intersectional lens. Her latest work studied how race, gender and sexuality interacts with body image and eating disorders.

She found that while BIPOC (Black, Indigenous or other people of color) men have low rates of body dissatisfaction, they reported higher rates of eating disorder behavior. Those behaviors included purging and excessive exercise, which may be considered atypical if research is only limited to body dissatisfaction as the driving force behind eating disorders.

Billman Miller said these findings are important because while stereotypes around eating disorders are changing, treatment is slower to develop.

"My hope for the future is that more representation is seen in clinical trials and better adaptations are made to the existing, evidence-based treatments," Billman Miller said. "What we know is even our best treatments are only meeting the needs of about 50% of our patients, so if we incorporate more representation within our clinical trials or adapt our existing evidence-based treatments for those groups, we'll see better outcomes for everybody."

Evidence backed treatment

Research from the ACCEPT Lab applies directly to developing informed treatments for AEDC patients. The AEDC, co-directed by Brown and Associate Professor April Smith , treats a variety of eating disorders across the lifespan.

Billman Miller, who came to Auburn after serving as a clinical research coordinator at the Penn State College of Medicine, said that direct link between research and treatment drew her to Auburn's doctoral program.

"Knowing that we had an in-house training clinic, where I could work directly with individuals who were struggling with eating disorders, was a huge draw, as well as the ample opportunities to get involved with both research and clinical work," Billman Miller said. "Auburn does a great job of balancing the two, so I knew I'd come out a very well-rounded researcher and clinician at the end of my training."

Graduate students both conduct research and serve as clinicians in the AEDC. They also help undergraduate researchers address the gap between body image literature and treatment.

Brown said undergraduate and graduate students bring a variety of perspectives to challenging the one-size-fits-all approach to eating disorder treatment.

"One of the things we're trying to do with both the ACCEPT Lab and then also the AEDC is to help provide affirmative care for LGBTQ folks. Specifically, our research is currently focused on developing more specific treatments that target unique risk factors for LGBTQ individuals with an eating disorder," Brown said. "For men, both in the ACCEPT Lab and at the AEDC, we're really trying to develop and deliver prevention and treatment programs that focus on both traditional and male-specific body image and eating disorder concerns."

Lifesaving results

Research and treatment for eating disorders, which are the deadliest among mental health conditions, is underfunded compared to other psychological disorders. While Auburn faculty and students treat as many people as possible, their efforts also contribute to preventative measures.

Through the research collected in the ACCEPT Lab and the AEDC, Auburn has developed and delivered programs to prevent body dissatisfaction and eating disorders before they start. One of those interventions focused on improving body image concerns for young men.

Le served as an interventionist during the program and said his work around body image has completely changed the trajectory of his psychology career.

"Initially I didn't really know where I wanted to go or what I had to do for it, but joining this lab has set so many foundations for me to know what my path is, what my goal is at the end," Le said. "I really hope to see a bigger understanding of how to accommodate each person's need, depending on their backgrounds, depending on their identities, that we do focus on what is the most important part of helping these individuals rather than just finding out what's wrong."

The demand for high-quality, research-informed eating disorders treatment in Alabama is high. The AEDC is uniquely positioned to deliver specialized care, but currently has a waitlist to manage its patient load. Further, it follows a sliding scale model for treatment cost, meaning patients can receive treatment at a more affordable rate than other clinics.

Brown said the self-funded clinic hopes to expand services to care for even more patients in the future.

"We had a waitlist basically within a week of opening, which both shows a huge need in the community here for eating disorder treatment, but also shows that we weren't able to fully care for everybody who was coming in and needing treatment," Brown said. "One of the really great things with having increased support from the university and donors is we've been able to expand our services further."

Since the AEDC opened in 2022, support from the Auburn Family has helped the clinic double its patient capacity by hiring two full-time graduate clinicians and assisting its low-income patients by covering treatment costs.

To give or learn more about how your support makes a difference, visit the AEDC website .

Tags: Students Faculty Research Community and Outreach Psychological Sciences

Related Articles

Auburn professor receives Fulbright Specialist Award to teach medical speech-language pathology in Bulgaria

Auburn public relations students attend PRSSA ICON conference

Auburn professors talk about importance of mental health in wake of Osaka’s French Open withdrawal

Is the US moving toward a cashless society?

Auburn students living examples of creed at work through diversity, equity, inclusion efforts

Eight CLA students receive awards at annual Student Research Symposium

Newsletter signup.

Diet Review: MIND Diet

Finding yourself confused by the seemingly endless promotion of weight-loss strategies and diet plans?  In this series , we take a look at some popular diets—and review the research behind them.

What Is It?

The Mediterranean-DASH Diet Intervention for Neurodegenerative Delay, or MIND diet, targets the health of the aging brain. Dementia is the sixth leading cause of death in the United States, driving many people to search for ways to prevent cognitive decline. In 2015, Dr. Martha Clare Morris and colleagues at Rush University Medical Center and the Harvard Chan School of Public Health published two papers introducing the MIND diet. [1,2] Both the Mediterranean and DASH diets had already been associated with preservation of cognitive function, presumably through their protective effects against cardiovascular disease, which in turn preserved brain health.

The research team followed a group of older adults for up to 10 years from the Rush Memory and Aging Project (MAP), a study of residents free of dementia at the time of enrollment. They were recruited from more than 40 retirement communities and senior public housing units in the Chicago area. More than 1,000 participants filled out annual dietary questionnaires for nine years and had two cognitive assessments. A MIND diet score was developed to identify foods and nutrients, along with daily serving sizes, related to protection against dementia and cognitive decline. The results of the study produced fifteen dietary components that were classified as either “brain healthy” or as unhealthy. Participants with the highest MIND diet scores had a significantly slower rate of cognitive decline compared with those with the lowest scores. [1] The effects of the MIND diet on cognition showed greater effects than either the Mediterranean or the DASH diet alone.

How It Works

The purpose of the research was to see if the MIND diet, partially based on the Mediterranean and DASH diets, could directly prevent the onset or slow the progression of dementia. All three diets highlight plant-based foods and limit the intake of animal and high saturated fat foods. The MIND diet recommends specific “brain healthy” foods to include, and five unhealthy food items to limit. [1]

The healthy items the MIND diet guidelines* suggest include:

• 3+ servings a day of whole grains
• 1+ servings a day of vegetables (other than green leafy)
• 6+ servings a week of green leafy vegetables
• 5+ servings a week of nuts
• 4+ meals a week of beans
• 2+ servings a week of berries
• 2+ meals a week of poultry
• 1+ meals a week of fish
• Mainly olive oil if added fat is used

The unhealthy items, which are higher in saturated and trans fat , include:

• Less than 5 servings a week of pastries and sweets
• Less than 4 servings a week of red meat (including beef, pork, lamb, and products made from these meats)
• Less than one serving a week of  cheese and fried foods
• Less than 1 tablespoon a day of butter/stick margarine

*Note: modest variations in amounts of these foods have been used in subsequent studies. [9,10]

This sample meal plan is roughly 2000 calories, the recommended intake for an average person. If you have higher calorie needs, you may add an additional snack or two; if you have lower calorie needs, you may remove a snack. If you have more specific nutritional needs or would like assistance in creating additional meal plans, consult with a registered dietitian. 

Breakfast: 1 cup cooked steel-cut oats mixed with 2 tablespoons slivered almonds, ¾ cup fresh or frozen blueberries, sprinkle of cinnamon

Snack: 1 medium orange

• Beans and rice – In medium pot, heat 1 tbsp olive oil. Add and sauté ½ chopped onion, 1 tsp cumin, and 1 tsp garlic powder until onion is softened. Mix in 1 cup canned beans, drained and rinsed. Serve bean mixture over 1 cup cooked brown rice.
• 2 cups salad (e.g., mixed greens, cucumbers, bell peppers) with dressing (mix together 2 tbsp olive oil, 1 tbsp lemon juice or vinegar, ½ teaspoon Dijon mustard, ½ teaspoon garlic powder, ¼ tsp black pepper)

Snack: ¼ cup unsalted mixed nuts

• 3 ounces baked salmon brushed with same salad dressing used at lunch
• 1 cup chopped steamed cauliflower
• 1 whole grain roll dipped in 1 tbsp olive oil

Is alcohol part of the MIND diet?

Wine was included as one of the 15 original dietary components in the MIND diet score, in which a moderate amount was found to be associated with cognitive health. [1] However, in subsequent MIND trials it was omitted for “safety” reasons. The effect of alcohol on an individual is complex, so that blanket recommendations about alcohol are not possible. Based on one’s unique personal and family history, alcohol offers each person a different spectrum of benefits and risks. Whether or not to include alcohol is a personal decision that should be discussed with your healthcare provider. For more information, read Alcohol: Balancing Risks and Benefits .

The Research So Far

The MIND diet contains foods rich in certain vitamins, carotenoids, and flavonoids that are believed to protect the brain by reducing oxidative stress and inflammation. Although the aim of the MIND diet is on brain health, it may also benefit heart health, diabetes, and certain cancers because it includes components of the  Mediterranean  and  DASH  diets, which have been shown to lower the risk of these diseases.

Cohort studies

Researchers found a 53% lower rate of Alzheimer’s disease for those with the highest MIND diet scores (indicating a higher intake of foods on the MIND diet). Even those participants who had moderate MIND diet scores showed a 35% lower rate compared with those with the lowest MIND scores. [2] The results didn’t change after adjusting for factors associated with dementia including healthy lifestyle behaviors, cardiovascular-related conditions (e.g., high blood pressure, stroke, diabetes), depression, and obesity, supporting the conclusion that the MIND diet was associated with the preservation of cognitive function.

Several other large cohort studies have shown that participants with higher MIND diet scores, compared with those with the lowest scores, had better cognitive functioning, larger total brain volume, higher memory scores, lower risk of dementia, and slower cognitive decline, even when including participants with Alzheimer’s disease and history of stroke. [3-8]

Clinical trials

A 2023 randomized controlled trial followed 604 adults aged 65 and older who at baseline were overweight (BMI greater than 25), ate a suboptimal diet, and did not have cognitive impairment but had a first-degree relative with dementia. [9] The intervention group was taught to follow a MIND diet, and the control group continued to consume their usual diet. Both groups were guided throughout the study by registered dietitians to follow their assigned diet and reduce their intake by 250 calories a day. The authors found that participants in both the MIND and control groups showed improved cognitive performance. Both groups also lost about 11 pounds, but the MIND diet group showed greater improvements in diet quality score. The authors examined changes in the brain using magnetic resonance imaging, but findings did not differ between groups. [10] Nutrition experts commenting on this study noted that both groups lost a similar amount of weight, as intended, but the control group likely improved their diet quality as well (they had been coached to eat their usual foods but were taught goal setting, calorie tracking, and mindful eating techniques), which could have prevented significant changes from being seen between groups. Furthermore, the duration of the study–3 years–may have been too short to show significant improvement in cognitive function.

The results of this study showed that the MIND diet does not slow cognitive aging over a 3-year treatment period. Whether the MIND diet or other diets can slow cognitive aging over longer time periods remains a topic of intense interest.

Other factors

Research has found that greater poverty and less education are strongly associated with lower MIND diet scores and lower cognitive function. [11]

Potential Pitfalls

• The MIND diet is flexible in that it does not include rigid meal plans. However, this also means that people will need to create their own meal plans and recipes based on the foods recommended on the MIND diet. This may be challenging for those who do not cook. Those who eat out frequently may need to spend time reviewing restaurant menus.
• Although the diet plan specifies daily and weekly amounts of foods to include and not include, it does not restrict the diet to eating only these foods. It also does not provide meal plans or emphasize portion sizes or exercise .

Bottom Line  

The MIND diet can be a healthful eating plan that incorporates dietary patterns from the Mediterranean and DASH , both of which have suggested benefits in preventing and improving cardiovascular disease and diabetes , and supporting healthy aging. When used in conjunction with a balanced plate guide , the diet may also promote healthy weight loss if desired. Whether or not following the MIND diet can slow cognitive aging over longer time periods remains an area of interest, and more research needs to be done to extend the MIND studies in other populations.

• Healthy Weight
• The Best Diet: Quality Counts
• Healthy Dietary Styles
• Other Diet Reviews
• Morris MC, Tangney CC, Wang Y, Sacks FM, Barnes LL, Bennett DA, Aggarwal NT. MIND diet slows cognitive decline with aging. Alzheimer’s & dementia . 2015 Sep 1;11(9):1015-22.
• Morris MC, Tangney CC, Wang Y, Sacks FM, Bennett DA, Aggarwal NT. MIND diet associated with reduced incidence of Alzheimer’s disease. Alzheimer’s & Dementia . 2015 Sep 1;11(9):1007-14.
• Dhana K, James BD, Agarwal P, Aggarwal NT, Cherian LJ, Leurgans SE, Barnes LL, Bennett DA, Schneider JA. MIND diet, common brain pathologies, and cognition in community-dwelling older adults. Journal of Alzheimer’s Disease . 2021 Jan 1;83(2):683-92.
• Cherian L, Wang Y, Fakuda K, Leurgans S, Aggarwal N, Morris M. Mediterranean-Dash Intervention for Neurodegenerative Delay (MIND) diet slows cognitive decline after stroke. The journal of prevention of Alzheimer’s disease . 2019 Oct;6(4):267-73.
• Hosking DE, Eramudugolla R, Cherbuin N, Anstey KJ. MIND not Mediterranean diet related to 12-year incidence of cognitive impairment in an Australian longitudinal cohort study. Alzheimer’s & Dementia . 2019 Apr 1;15(4):581-9.
• Melo van Lent D, O’Donnell A, Beiser AS, Vasan RS, DeCarli CS, Scarmeas N, Wagner M, Jacques PF, Seshadri S, Himali JJ, Pase MP. Mind diet adherence and cognitive performance in the Framingham heart study. Journal of Alzheimer’s Disease . 2021 Jan 1;82(2):827-39.
• Berendsen AM, Kang JH, Feskens EJ, de Groot CP, Grodstein F, van de Rest O. Association of long-term adherence to the mind diet with cognitive function and cognitive decline in American women. The journal of nutrition, health & aging . 2018 Feb;22(2):222-9. Disclosure: Grodstein reports grants from International Nut Council, other from California Walnut Council, outside the submitted work.
• Chen H, Dhana K, Huang Y, Huang L, Tao Y, Liu X, van Lent DM, Zheng Y, Ascherio A, Willett W, Yuan C. Association of the Mediterranean Dietary Approaches to Stop Hypertension Intervention for Neurodegenerative Delay (MIND) Diet With the Risk of Dementia. JAMA psychiatry . 2023 May 3.
• Liu X, Morris MC, Dhana K, Ventrelle J, Johnson K, Bishop L, Hollings CS, Boulin A, Laranjo N, Stubbs BJ, Reilly X. Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) study: rationale, design and baseline characteristics of a randomized control trial of the MIND diet on cognitive decline. Contemporary clinical trials . 2021 Mar 1;102:106270. Disclosure: several corporations generously donated mixed nuts (International Tree Nut Council Nutrition Research and Education Foundation), peanut butter (The Peanut Institute), extra virgin olive oil (Innoliva-ADM Capital Europe LLP), and blueberries (U.S. Highbush Blueberry Council). These items will be distributed to those participants who are randomized to the MIND diet arm.
• Barnes LL, Dhana K, Liu X, Carey VJ, Ventrelle J, Johnson K, Hollings CS, Bishop L, Laranjo N, Stubbs BJ, Reilly X. Trial of the MIND Diet for Prevention of Cognitive Decline in Older Persons. New England Journal of Medicine . 2023 Jul 18.
• Boumenna T, Scott TM, Lee JS, Zhang X, Kriebel D, Tucker KL, Palacios N. MIND diet and cognitive function in Puerto Rican older adults. The Journals of Gerontology: Series A . 2022 Mar;77(3):605-13.

Last reviewed August 2023

Terms of Use

The contents of this website are for educational purposes and are not intended to offer personal medical advice. You should seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. The Nutrition Source does not recommend or endorse any products.

An official website of the United States government

The .gov means it’s official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

• Publications
• Account settings

Preview improvements coming to the PMC website in October 2024. Learn More or Try it out now .

• Advanced Search
• Journal List
• Indian J Psychol Med
• v.41(4); Jul-Aug 2019

Eating Disorders: An Overview of Indian Research

Sivapriya vaidyanathan.

Department of Psychiatry, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India

Pooja Patnaik Kuppili

1 Department of Psychiatry, All India Institute of Medical Sciences, Jodhpur, Rajasthan, India

Vikas Menon

There has been sporadic research on eating disorders in India, with no published attempt to collate and summarize the literature landscape. Hence, the present narrative review aims to summarize Indian work related to eating disorders, discern current trends, and highlight gaps in research that will provide directions for future work in the area. Electronic search using the MEDLINE, Google Scholar, and PsycINFO databases was done to identify relevant peer-reviewed English language articles, in October 2018, using combinations of the following medical subject headings or free text terms: “eating disorders,” “anorexia nervosa,” “bulimia,” “treatment,” “epidemiology,” “co-morbidity,” “management,” “medications,” “behavioral intervention,” and “psychosocial intervention.” The data extracted from studies included details such as author names, year, from which of the states in India the work originated, type of intervention (for interventional studies), comparator (if any), and major outcomes. There is increasing research focused on eating disorders from India over the last decade, but it continues to be an under-researched area as evidenced by the relative paucity of original research. The cultural differences between east and west have contributed to variations in the presentation as well as challenges in the diagnosis. Hence, there is a need for the development of culturally sensitive instruments for diagnosis, as well as generating locally relevant epidemiological data about eating disorders from community and hospital settings.

The earliest description of an eating disorder (ED)-like syndrome appears in a treatise by Morton (1694), under the section “Nervous Consumption,” where the author talks about two adolescents who presented with loss of appetite, extreme fasting, weight loss, and their treatment and outcome.[ 1 ] Historical reports point to the existence of ED even in the 17 th century, referred to as “holy anorexia.” However, one of the first scientific reports of this condition, in the late 19 th century, was by William Gull who is credited with coining the term anorexia nervosa (AN).[ 2 ] In India, the occurrence of ED was not reported until the late 20 th century.[ 3 ] Perhaps, media-related glorification of “size zero” body type and culturally sanctioned drive for thinness, body shaming, and dissatisfaction have contributed to the recent upsurge of ED cases.[ 4 , 5 , 6 ] Traditionally, these parameters have been less of a concern in India than other countries.[ 4 ] Yet, another reason for the recent increase in the incidence of ED such as bulimia nervosa (BN) and binge eating disorder (BED) is more easy access to media outlets promoting unhealthy body types and higher socioeconomic status of people.[ 7 , 8 ]

Notwithstanding its increasing prevalence rates, ED continues to be an area that is under-reported and under-researched. There are several reasons why ED must be given increasing focus in health care research and policy planning in today's scenario. AN, a prototype ED, has the highest mortality rate among mental health disorders.[ 9 , 10 ] The economic and social impact of ED was estimated to be upwards of $15 billion (INR 1057.8 billion) in 2012, which is comparable to the productivity impact of anxiety and depression, estimated at $17.9 billion (INR 1262.3 billion) in 2010.[ 9 ] Though, relatively rare in the general population, the individual impact of ED can be quite debilitating and long-term treatments are often expensive. ED have high rates of psychiatric and medical co-morbidity.[ 9 , 10 , 11 , 12 ]

Though there has been sporadic research on ED in India, there has been no attempt to collate and summarize the literature landscape. We undertook the present narrative review with the objectives of summarizing Indian work related to ED, discern current trends, and highlight gaps in research that will provide directions for future work in the area. These would potentially answer key questions on the clinical presentation and trajectories of ED in our setting.

METHODOLOGY

Search strategy and study selection.

Electronic search using the MEDLINE, Google Scholar, and PsycINFO to identify relevant peer-reviewed English language articles was carried out to include articles between April 1967 to October 2018. We used random combinations of the following medical subject headings or free text terms: “eating disorders,” “anorexia nervosa,” “bulimia,” “treatment,” “epidemiology,” “co-morbidity,” “management,” “medications,” “behavioral intervention,” and “psychosocial intervention.”

This being a narrative review and because research on ED in India is relatively sparse, we included all types of research reports, including case reports, to gain a true picture of the research landscape. The initial search yielded 84 articles. From the initial search, 39 articles were relevant and therefore selected for inclusion in the review. The full text of these articles was retrieved electronically. Additionally, the reference section of all articles was manually screened to identify potentially relevant articles. We only selected articles describing research from India. There was no restriction on the date of publication. Citation indexing services and gray literature such as conference proceedings were not included in the present review.

Data extraction

The data extracted from studies included details such as author names, year, from which of the states in India the work originated, type of intervention (for interventional studies), comparator (if any), and major outcomes.

A major part of the literature on ED from India is derived from case reports and case series ( n = 24). In comparison, there are 15 original studies summarized in Table 1 .

Summary of original studies on eating disorders in India

AN – Anorexia nervosa; BDI – Beck’s Depression Inventory; BED – Binge eating disorder; BITE – Bulimia investigatory test; BSQ – Body shape questionnaire; BN – Bulimia nervosa; DSM-IV – Diagnostic and Statistical Manual of Mental Disorders Version IV; DSM-III – Diagnostic and Statistical Manual of Mental Disorders Version III; EAT – Eating attitudes test; EDS – Eating distress syndrome; ICD-10 – International Classification of Diseases; QOL EDs – Quality-of-life for eating disorders questionnaire; SCOFF – Sick, Control, One-stone (14 lbs/6.5 kg), Fat, Food; SRQ – Self-report questionnaire; SQ-EDS – Screening questionnaire for eating distress syndrome

The earliest reports of ED date back to 1966. The case was of AN in a 42-year-old female with episodes of compulsive fasting for 2 years. The patient was treated with 100 mg chlorpromazine, 100 ml of 25% glucose with vitamin C 500 mg intravenously, 10 injections of liver extract 2 ml intramuscularly biweekly, and 9 sessions of electroconvulsive treatment. After 46 days of intensive pharmacotherapy and supportive psychotherapy, she showed improvement and was kept in close follow up.[ 3 ] Following this, there has been increasing reports of ED cases in the last two decades. Majority of the cases were of AN, especially restrictive subtype. The typical profile of cases described from India is of adolescent females,[ 26 , 27 , 28 , 29 , 30 , 31 ] belonging to Hindu religion,[ 29 , 31 , 32 ] and coming from an upper- or middle-socioeconomic background[ 26 , 27 , 28 , 29 , 31 , 33 ] In contrast, there are only four cases of male AN reported.[ 27 , 34 ] There is a single case report of AN described in a pair of monozygotic twins too.[ 35 ]

Cases of AN have been described in Indian adolescents belonging to Sikh religions, living in the United Kingdom.[ 34 ] The symptoms of AN were found to flare up after being teased by peers about weight which was followed by concerns about weight gain, in the majority of cases.[ 27 , 29 ] There is also a case of AN which had atypical features such as denial of fears of weight gain.[ 36 ] One report of disordered eating described a young female, in whom “not eating” was conceptualized as a resistance to the patriarchal system and this highlights the role of Indian sociocultural factors for developing an ED.[ 37 ]

Bradycardia, hypotension, anemia, and dyselectrolytemia have been reported at the time of presentation to a psychiatrist.[ 27 , 28 , 38 ] Wernicke–Korsakoff syndrome was the presenting symptom for a 39-year-old female who had AN from adolescence.[ 39 ] Surreptitious use of metformin, with episodes of hypoglycemia, was the presenting symptom in another case of AN in a 21-year-old female.[ 33 ] Though the nature of psychiatric co-morbidity has not been described, psychiatric co-morbidity was noted in all the cases of a case series.[ 27 ] Obsessive traits of symmetry and order,[ 32 ] obsessive compulsive disorder (OCD),[ 40 ] and major depressive disorder have been reported as co-morbidities.[ 33 ] Menstrual abnormalities and poorly developed secondary sexual characteristics have been noted in the majority of cases.[ 26 , 27 , 28 , 32 , 41 ]

There have been only five cases of BN reported till date.[ 42 , 43 , 44 , 45 , 46 ] Two of the cases were females: one was a 22-year-old medical student, with the onset of symptoms around 13 years of age, with binging and purging with isabgol husk and consumption of orlistat.[ 44 , 45 ] The other three cases were atypical, with an absence of concerns for body weight or body image, along with an absence of concurrent use of diuretics or laxatives in a 37-year-old male,[ 46 ] 15-year-old female,[ 43 ] and a 24-year-old female.[ 42 ]

Cases of ED have been described occurring co-morbid to physical illnesses such as systemic lupus erythematosus[ 26 ] and secondary to traumatic brain injury[ 31 ] or due to an adverse drug reaction to zolpidem consumption termed as a nocturnal sleep-related ED.[ 47 ] Further, AN has been found to mask physical illnesses such as carcinoma.[ 48 ] Treatment described in these cases included comprehensive treatment involving mental health professionals and dieticians.[ 26 , 27 ]

Majority of cases were managed in the in-patient setting.[ 3 , 26 , 27 ] In AN, high-calorie high-protein diet has been advised, with careful monitoring for re-feeding syndrome.[ 26 , 27 ] In the 1960s, chlorpromazine and modified insulin therapy were the treatment options used.[ 3 ] Cyproheptadine in combination with chlorpromazine,[ 26 ] combination of cyproheptadine and olanzapine,[ 41 ] mirtazapine,[ 27 ] risperidone,[ 27 ] trazodone,[ 27 ] citalopram,[ 27 ] and fluoxetine at 20 mg/day[ 28 ] have been used for treatment of AN. Combinations of olanzapine and fluvoxamine or olanzapine and fluoxetine have been used in cases of AN with obsessive traits and OCD, respectively.[ 32 , 40 ] Sertraline[ 42 ] and fluoxetine at low dose of 20 mg/day[ 44 ] as well as at 80 mg/day[ 42 ] has been described in the management of BN, with good response.

The non-pharmacological therapy of ED included family therapy, cognitive behavioral therapy (CBT), supportive psychotherapy, contingency management, hypnotherapy, and play therapy.[ 26 , 27 , 29 , 31 , 42 , 43 , 44 , 49 ] High-frequency repetitive transcranial magnetic stimulation (rTMS) over the left dorsolateral prefrontal cortex was given as augmentation strategy in a 23-year-old female who earlier had only a partial response to antidepressants as well as atypical antipsychotics and CBT. rTMS was found to improve attitude toward body weight and body shape, with an improvement of weight.[ 38 ]

This review attempted to summarize the Indian research on ED. The literature is largely comprised of case reports, as noted in the previous reviews.[ 50 , 51 ] However, there has been an increase in the number of published original research articles over the last 5–6 years. There are no studies available which determined the prevalence of ED from the community setting. There is a single hospital-based retrospective review, which reported a prevalence of 1.25% for ED.[ 16 ] Of them, almost 85% had psychogenic vomiting and about 15% had AN. This is in contrast to the international literature, wherein the frequency of occurrence of BN and BED is more common than that of AN. A meta-analysis of 15 studies from various settings reported that the estimated lifetime prevalence of any ED was 1.01%, and those of AN, BN, and BED were 0.21%, 0.81%, and 2.22%, respectively.[ 52 ] BED had the highest point prevalence of ED, followed by BN and AN, among young females across China, Japan, Africa, and Latin America.[ 53 ] In comparison, in the Indian setting, there are no cases reported of BED, and only five cases have been reported of BN.[ 42 , 43 , 44 , 45 , 46 ] Further, the two-step assessment (initial screening by self-rated questionnaire, followed by assessment by semi-structured or diagnostic interview) is the standard procedure followed globally. However, there is a single study using the two-step procedure and found no cases.[ 14 ] Majority of the Indian studies used only the screening, self-rated assessment. The frequency of disordered eating/probable ED ranged from 4 to 45.4%.[ 18 , 25 ]

It is possible that subsyndromal ED cases may not be captured by a self-rated assessment. Two studies reported the prevalence of eating distress syndrome (EDS) to be 11% and 14.8%.[ 14 , 15 ] EDS refers to subsyndromal forms of AN or BN, with patients having distressing and conflicting thoughts about body shape and eating habits. EDS is characterized by strict dieting, and bingeing in a few cases, with no significant weight loss or behaviors such as resorting to severe measures of weight loss such as diet pills, starvation, purging, or vomiting.[ 14 ] However, there has been practically no Indian research on EDS in the last 20 years.

There are several methodological issues in Indian studies which need to be addressed. Firstly, many of the studies have employed convenient sampling on medical and nursing students.[ 14 , 15 , 18 , 22 , 24 , 25 ] This may lead to selection bias and such samples may not be truly representative of the population at large. However, this practice of studying medical students is popular worldwide. The rationale given to support this being the “stressful” nature of medical training, which could be a risk factor for ED.[ 54 , 55 , 56 ] But this may also imply that the prevalence rates obtained in these studies may be an inflated figure.

Secondly, in the measurement of the frequency of disordered eating, it was found to be higher as per the Sick, Control, One-stone, Fat, Food questionnaire (SCOFF) compared to the Eating Attitudes Test-26 item (EAT-26) questionnaire.[ 23 , 25 ] The frequency with SCOFF ranged from 17.2% in women to 45.4% in men, and the frequency with EAT-26 ranged from 4% to 31%.[ 6 , 18 , 24 , 25 ] Thirdly, there are limitations in the translation and implementation of the questionnaires in a setting like India that has such linguistic diversity. Though the EAT-26 questionnaire has been translated into Hindi, the cut-off score for the Hindi version has not been defined.[ 24 ] Also, the rationale for using the same cut-off of the English version in the Kannada version is not clear.[ 6 ] Hence, due to cultural differences between the western and Indian settings, there is a definite need for the development of culturally sensitive scales for screening ED.

Culture bears a strong influence on the presentation of ED in India. One unique point noted in the Indian presentations of ED is relative lack of concern for body fat/shape. This has been termed as “Non-fat phobic” variant of AN.[ 50 ] This has been described in Hong Kong as well. In this form, food restriction is attributed to somatic complaints such as abdominal bloating, pain, and lack of appetite, rather than concern for body fat. Similar atypical features have been noted in cases of BN too from India. Also, the concept of EDS is in accordance with this concept.[ 50 , 57 ] Further, food restriction is culturally sanctioned in Indian culture when one is unwell, for “cleansing the bowel.”[ 36 ] However, several recent studies show an association between perception of body shape and higher scores on EAT-26.[ 18 , 22 , 24 ] This could be explained by the ongoing rapid societal transitions in India and the increasing influence of western ideals.

At least 50% of patients with an ED are known to have a psychiatric co-morbidity, with depression being the most common.[ 58 , 59 ] In contrast, a few cases had syndromal co-morbidity.[ 27 , 40 ] The principles of management of ED adopted in India is similar to the west. Most reports of AN and BN describe using a combination of pharmacotherapy and psychotherapy. Selective serotonin reuptake inhibitors (SSRIs), second-generation antipsychotics, and cyproheptadine have been found to be effective for AN.[ 60 ] Patients with BN were treated with 20–80 mg/day of fluoxetine in the case reports.[ 42 , 44 ] In contrast, globally, a higher dose of SSRIs, especially fluoxetine, has been found to be effective in cases of BN.[ 61 ] Psychotherapeutic approaches used in the Indian setting, such as family-based therapy and CBT, therapy match global practices.[ 62 ]

To conclude, there is increasing research focus on ED from India over the last two decades. Lower prevalence of ED could be the reason for the relative paucity of studies. But, with the increasing impact of westernization of society, ED merit renewed focus. The cultural differences between east and west have contributed to variations in presentation as well as challenges in diagnosis. Hence, there is a need for the development of culturally sensitive instruments for diagnosis as well as generating locally relevant epidemiological data about ED from the community and hospital settings.

Financial support and sponsorship

Conflicts of interest.

There are no conflicts of interest.