* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download Chapter 22
Kleptomania wikipedia , lookup
Reactive attachment disorder wikipedia , lookup
Anxiety disorder wikipedia , lookup
Personality disorder wikipedia , lookup
Major depressive disorder wikipedia , lookup
Glossary of psychiatry wikipedia , lookup
Controversy surrounding psychiatry wikipedia , lookup
Substance use disorder wikipedia , lookup
Factitious disorder imposed on another wikipedia , lookup
Emergency psychiatry wikipedia , lookup
Bipolar II disorder wikipedia , lookup
Autism spectrum wikipedia , lookup
Separation anxiety disorder wikipedia , lookup
Abnormal psychology wikipedia , lookup
Mental disorder wikipedia , lookup
Panic disorder wikipedia , lookup
History of psychiatry wikipedia , lookup
Obsessive–compulsive personality disorder wikipedia , lookup
Causes of mental disorders wikipedia , lookup
Bipolar disorder wikipedia , lookup
Excoriation disorder wikipedia , lookup
Dissociative identity disorder wikipedia , lookup
History of mental disorders wikipedia , lookup
Spectrum disorder wikipedia , lookup
Schizoaffective disorder wikipedia , lookup
Depersonalization disorder wikipedia , lookup
Antisocial personality disorder wikipedia , lookup
Classification of mental disorders wikipedia , lookup
Child psychopathology wikipedia , lookup
Rumination syndrome wikipedia , lookup
Asperger syndrome wikipedia , lookup
Generalized anxiety disorder wikipedia , lookup
Diagnostic and Statistical Manual of Mental Disorders wikipedia , lookup
Narcissistic personality disorder wikipedia , lookup
Conversion disorder wikipedia , lookup
Conduct disorder wikipedia , lookup
Eating Disorders Chapter 22 Eric Stice and Cara Bohon HISTORICAL CONTEXT Anorexia nervosa was first recognized as a psychiatric disorder more than a century ago. Stunkard (1959) first described binge eating disorder half a century ago among overweight individuals. Binge eating disorder has not yet been recognized as a diagnostic entity but considerable research has led to the likely inclusion of the disorder in the next edition of the DSM. Bulimia nervosa was recognized as a psychiatric disorder in the late 1970s. DIAGNOSTIC ISSUES AND DSMIV CRITERIA Anorexia Nervosa Weight loss or failure to gain weight (with weight less than 85% of what would be expected for height, age, and developmental level) Intense fear of gaining weight or of becoming fat despite a low body weight Disturbed perception of weight and shape An undue influence of weight or shape on self-evaluation or a denial of the seriousness of the illness Amenorrhea in postmenarcheal females Bulimia Nervosa Marked by recurrent episodes (at least twice weekly for 3 months) of consumption of unusually large amounts of food (coupled with a sense that the eating is out of control) Recurrent (at least twice weekly for 3 months) compensatory behaviors to prevent weight gain (e.g., self-induced vomiting, laxative/diuretic abuse, fasting, or excessive exercise) Undue influence of weight and shape on self-evaluation DIAGNOSTIC ISSUES AND DSMIV CRITERIA Binge Eating Disorder Binge eating disorder is listed in the DSM-IV (American Psychiatric Association, 2000) as a provisional eating disorder requiring further study, exemplifying an eating disorder not otherwise specified (EDNOS). This eating disorder involves: • Repeated episodes (at least 2 days per week for 6 months) of uncontrollable binge eating characterized by certain features (e.g., rapid eating, eating until uncomfortably full, eating alone because of embarrassment, and feeling guilty or depressed after overeating) • Marked distress regarding binge eating • The absence of regular compensatory behaviors (e.g., monthly vomiting for weight control) DIAGNOSTIC ISSUES AND DSMIV CRITERIA Eating Disorder Not Otherwise Specified (ED- NOS) The DSM-IV currently describes five symptom presentations in addition to binge-eating disorder as examples of Eating Disorder Not Otherwise Specified (EDNOS): • • • • • Anorexia nervosa with menses present Anorexia nervosa with normal weight Low-binge frequency bulimia nervosa Chewing and spitting food repeatedly Purging disorder (the regular use of inappropriate compensatory behavior after eating food that would not be considered a binge episode) PREVALENCE Between 0.9% and 2.0% of girls and women and between 0.1% and 0.3% of boys and men experience anorexia nervosa during their lifetimes (Hudson, Hiripi, Pope, & Kessler, 2007; Lewinsohn Striegel-Moore, & Seeley, 2000). Bulimia nervosa afflicts between 1.1% and 4.6% of girls and women and between 0.1% and 0.5% of boys and men during their lifetimes (Garfinkel et al., 1995; Hudson et al., 2007). Binge eating disorder afflicts between 0.2% and 3.5% of girls and between 0.9% and 2.0% of boys and men during their lifetimes (Hoek & van Hoeken, 2003; Hudson et al., 2007). RISK FACTORS, PROTECTIVE FACTORS, AND ETIOLOGIC FORMULATIONS Anorexia Nervosa Picky eating and digestive problems in early childhood Premature birth and cephalhematoma Infant feeding problems Maternal depressive symptoms Thin-ideal internalization and body dissatisfaction Depressive symptoms and psychological disturbances High self-esteem and higher maternal body mass index appear to be protective factors. RISK FACTORS, PROTECTIVE FACTORS, AND ETIOLOGIC FORMULATIONS Bulimia Nervosa Binge Eating Disorder Body dissatisfaction Initial elevations in body mass Preoccupation with thinness Perceived pressure for by family members and peers Dietary restraint Negative affect Deficits in social support Substance abuse Elevated body mass Early feeding problems thinness Body dissatisfaction Dietary restraint Negative affect Tendency to eat in response to negative emotions Depressive symptoms GENETIC AND OTHER BIOLOGICAL FACTORS Heritability Relatives of individuals with eating disorders are at elevated risk for eating pathology (Strober et al., 2000). Genetic studies Evidence suggesting a genetic basis for anorexia and bulimia nervosa has emerged from molecular genetics studies but almost no reliable findings have emerged from genetic research on eating disorders. GENETIC AND OTHER BIOLOGICAL FACTORS Neuroendocrine and neurohormonal factors Serotonergic Histamergic Various peptidergic systems Brain structure and functioning studies Gray and white matter loss Increased ventricular size Increased cerebrospinal fluid volume Enlarged sulci DEVELOPMENTAL PROGRESSION Anorexia Nervosa Two peak periods of risk for anorexia nervosa onset: Around ages 14 and 18 (APA, 2000). Among adolescents with anorexia nervosa: • 50% to 70% will recover • 20% will show improvement but will exhibit residual symptoms • 10% to 20% will develop a chronic course (Berkman et al., 2006; Wilson et al., 2003). Course of illness is on average 10 years (Strober, Freeman, & Morrell, 1997). Approximately 6% of patients diagnosed with this disorder die per decade of illness. The suicide rate for anorexia nervosa is 57 times higher than in the general population (Keel et al., 1997). DEVELOPMENTAL PROGRESSION Bulimia Nervosa Peak period of risk for onset for bulimia nervosa is between 14 and 19 years of age for females (Lewinsohn et al., 2000; Stice et al., 2009). Community-recruited samples suggest that bulimia nervosa typically shows a chronic course characterized by periods of recovery and relapse (Bohon, Stice, & Burton, 2009). Studies have suggested that both diagnosable and subthreshold bulimia nervosa are associated with future onset of: • • • • • • Depression Suicide attempts Anxiety disorders Substance abuse Obesity Health problems (Fairburn, 2000; Johnson et al., 2002; Stice, Cameron, Killen, Hayward, & Taylor, 1999; Stice, Hayward, Cameron, Killen, & Taylor, 2000; Striegel-Moore, Seeley, & Lewinsohn, 2003). COMORBIDITY Anorexia Nervosa Adolescent comorbidity: • Dysthymia, bipolar disorder, agoraphobia, simple phobia, marijuana dependence, and oppositional defiant disorder Anxiety disorders often predate the eating disorder, and depression often persists postrecovery (Kaye, Bulik, Thornton, et al., 2004; Sullivan, Bulik, Fear & Pickering, 1998). Bulimia Nervosa Adolescent comorbidity: • Major depression, dysthymia, bipolar disorder, agoraphobia, social phobia, alcohol dependence, marijuana dependence, and conduct disorder, but not with current simple phobia, overanxious disorder, panic disorder, posttraumatic stress disorder, generalized anxiety disorder, obsessive-compulsive disorder, oppositional defiant disorder, attention deficit hyperactivity disorder, or other substance use disorders (Stice & Peterson, 2007). COMORBIDITY Binge Eating Disorder The National Comorbidity Survey Replication found that 78.9% of respondents with binge eating disorder met criteria for at least one DSM-IV disorder, although no particular disorder stood out as being more common than others among those with binge eating disorder (Hudson et al., 2007) SEX DIFFERENCES and CULTURAL CONSIDERATIONS Female to male sex ratios of the prevalence of anorexia nervosa and bulimia nervosa are approximately 10:1 (APA, 2000). Striegel-Moore et al. (2005) noted different patterns of eating disorder symptoms across ethnic/racial groups, reporting that binge eating in the absence of purging was more common in African American women, whereas purging in the absence of binge eating was more common in Caucasian women. Several studies have found no racial or ethnic differences in the prevalence of recurrent binge eating, eating disorder symptoms, or risk factors for eating disorders (Smith et al., 1998). One consistent difference is that African Americans report less body image dissatisfaction than their white counterparts.(Kronenfeld, RebaHarrelson, Von Holle, Reyes, & Bulik, 2010). SYNTHESIS AND FUTURE DIRECTIONS Developmental processes that give rise to eating disorders are currently incomplete. Another key gap in the literature regards maintaining factors—either psychosocial or biological—that perpetuate eating-disordered behaviors once they emerge. An improved understanding of risk factors is essential for the design of more effective prevention programs, and improved understanding of maintenance factors is vital for the development of more effective treatment interventions.