Patients with anorexia nervosa and bulimia nervosa show an intrinsic reduction in metabolic rate that predisposes them to weight gain, and hence, to potentially pathologic mechanisms for maintaining thinness. In patients with bulimia nervosa studied during a phase of abstinence, this reduced metabolic rate is associated with a decrement in sympathetic function, augmented parasympathetic tone, and decreased thyroid function. During the phase of active bingeing and vomiting, metabolic rate increases significantly in association with an augmentation in sympathetic tone, a decrease in parasympathetic tone, and an increase in thyroid function. We propose that this bingeing and vomiting-induced increase in metabolic rate reinforces this pathologic behavior and allows bulimic patients to correct an intrinsic metabolic defect without the liability of weight gain. The intrinsic low metabolic rate in patients with the eating disorders is complicated by obsessional symptoms in the range of severity seen in patients with classic obsessive compulsive disorder, further impelling a perseverative preoccupation with food consumption and weight gain. Moreover, parallel clinical studies in patients with anorexia nervosa, bulimia nervosa and obsessive compulsive disorder show that each illness is associated with a profound disruption in the osmoregulation of plasma arginine vasopressin associated with hypersecretion of this peptide into the cerebrospinal fluid. In light of the fact that centrally directed vasopressin in experimental animals delays extinction of behaviors acquired during aversive conditioning, we postulate that the hypersecretion of vasopressin into the CNA could be a common defect predisposing the obsessive preoccupation that patients with eating and obsessive compulsive disorders have with the potential adverse consequences of eating, weight gain, and/or a variety of other activities. Further corollary risk factors for susceptibility to eating disorders include defects in neural mechanisms subserving hunger and satiety that seem exacerbated by pathological eating behaviors. As an example, patients with bulimia show deficient secretion of the satiety-inducing peptide cholecystokinin during food ingestion that was much more pronounced during periods of active bingeing. Finally, that patients with eating disorders show clinical manifestations of major depression associate with biological abnormalities in the regulation of CRH. We postulate that this underlying depression heightens the eating disordered patient's need to enhance damaged self-esteem by achieving an idealized weight and body image.
