Eating Disorders (Anorexia Nervosa, Bulimia Nervosa, Binge Eating Disorder) involve disturbances in eating patterns and body weight/shape concerns. Each disorder shares body image disturbance and carries significant medical morbidity. Treatment requires comprehensive biopsychosocial intervention addressing eating, cognitions, emotions, and medical complications.
From your DSM-5 training, you know that psychiatric diagnosis requires both symptom criteria and functional impairment. Eating disorders are among the most medically dangerous psychiatric conditions — anorexia nervosa has the highest mortality rate of any psychiatric disorder, primarily through cardiac arrest, electrolyte imbalance, and suicide. Understanding each disorder requires distinguishing the specific behavioral pattern, the cognitive features, and the physiological consequences.
Anorexia Nervosa (AN) is defined by severe restriction of caloric intake, a significantly low body weight, intense fear of gaining weight, and disturbed body image — specifically, the experience of being "fat" at objectively dangerous levels of underweight. There are two subtypes: restricting (pure caloric restriction) and binge-purge type (restriction punctuated by episodes of bingeing and purging). The cognitive core is weight and shape overvaluation: self-worth is evaluated almost entirely through control of eating and body weight, making the restriction ego-syntonic — patients often don't want to change because thinness feels like an achievement, not a problem. This ego-syntonic quality distinguishes AN from most other psychiatric disorders and makes engagement in treatment uniquely difficult. Medical complications of malnutrition are widespread: bradycardia, hypotension, osteoporosis, lanugo (fine body hair), and electrolyte abnormalities (hypokalemia is the primary cause of fatal arrhythmias).
Bulimia Nervosa (BN) involves repeated cycles of binge eating (eating a large amount of food in a discrete period with a subjective sense of loss of control) followed by compensatory behaviors to prevent weight gain — typically self-induced vomiting, but also laxative misuse, fasting, or excessive exercise. Unlike AN, people with BN are typically at normal or above-normal weight; their disorder is hidden. The medical consequences flow from the purging: dental enamel erosion from stomach acid, parotid gland hypertrophy (chipmunk cheeks), Russell's sign (calluses on knuckles from inducing vomiting), and hypokalemia. Binge Eating Disorder (BED), the most prevalent eating disorder, involves recurrent bingeing without compensatory behaviors and is associated with obesity, shame, and distress — but the medical risk profile differs from AN and BN.
All three disorders share a cognitive feature: body image disturbance, in which perception or evaluation of one's body is persistently inaccurate and negatively valenced. But the mechanism differs. In AN, patients often literally perceive themselves as larger than they are (perceptual distortion). In BN and BED, the distortion is more evaluative — the body is experienced as unacceptable, inadequate, or shameful. Treatment approaches therefore address both behavioral change (normalized eating patterns, elimination of compensatory behaviors) and cognitive change (challenging overvaluation of weight and shape, addressing perfectionism and low self-esteem). Family-based treatment is first-line for adolescent AN, given the ego-syntonic nature that limits individual engagement. Enhanced CBT (CBT-E) is first-line for adults with BN and BED. SSRIs have evidence for BN (reducing binge-purge frequency) but are not sufficient as standalone treatment for AN.