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There have been no systematic studies of abnormal eating attitudes or behavior in classical endocrine diseases such as excess or insufficient thyroid or adrenal states. Excess cortisol levels can be associated with depression, mania and organic mental syndromes and may result in a moderate weight gain. Patients with restrictive anorexia nervosa may have high blood cortisol levels related to increased corticotropic releasing factor (CRF) [80, 81]. Recent findings demonstrating GABA neuronal receptor activation by cortisol suggest CNS inhibitory and stimulatory potential for cortisol with implications for neurobiologic consequences in Cushing’s Syndrome, depression, and anorexia nervosa (hypercortisol states) [82]. Cushing’s patients may not manifest overtly abnormal eating behavior, however their eating habits may be similar to patients with mild obesity. A slight increase in appetite may be present. In Cushing’s disease, there may also be increased urinary-free cortisol which may not be present in either anorexia nervosa or depression. Cortisol, which has a catabolic effect and destroys tissues may possibly have a role in increased appetite to augment protein intake, restoring lost tissue and muscle mass.

A woman age 27-years-old, with a prior diagnosis of anorexia nervosa and a 54 percent loss of body weight, subsequently developed a pituitary corticotrophic cell adenoma with Cushing’s Syndrome alleviated by transsphenoidal surgery. Within two years of surgery in the absence of hypercortisolism, anorexia features reappeared [83] suggesting a common CRF-inducing mechanism.

In contrast to Cushing’s disease, cortisol insufficiency is found in Addison’s disease. These patients may have a seemingly normal appetite, but satiety occurs with minimal food ingestion. Exogenous steroids, when abruptly withdrawn, can produce a similar effect. Delayed gastric emptying seen in eating disorder patients may produce early satiety and feelings of fullness [84, 85]. These effects may persist after renutrition and may be related to gut neuroendocrine dysfunction.

Diabetes Mellitus coexisting with anorexia nervosa and bulimia has been frequently reported [86, 87, 88, 89, 90]. The prevalence of anorexia nervosa with Diabetes Mellitus ranged from zero percent [88] to 6.5 percent [91]. The presence of bulimia ranged from 6.5 percent [111] to 35 percent [143]. Rodin et al. [91] noted a six-fold increase for bulimia over the expected prevalence for nondiabetic individuals. Patients who failed to take their insulin developed glucosoria and thereby effected an indirect chemical method of "purging" [86]. The treatment of Diabetes Mellitus offers patients numerous opportunities to pursue their morbid goal of weight loss by dangerous maneuvers including surreptitious vomiting after bulimic episodes, adjustment of the insulin dose, failure to inject insulin and failure to provide urine samples [86, 92, 93]. Fairburn and Steel [94] noted that girls with anorexia nervosa could skillfully adjust their insulin dosage to match their reduced carbohydrate consumption.

Patients with growth hormone deficiency, which may occur in panhypopituitarism, may have diminished appetite [95]. This syndrome has been identified with non-organic failure to thrive and with maternal deprivation and may simulate idiopathic hypopituitarism. These children may show pica, eat from unusual places such as garbage cans and drink from toilets. They may steal food and polyphagia and polydipsia may alternate with vomiting and self-starvation. Patients may be overweight or underweight for their dwarfed height, but not emaciated. In contrast increased growth hormone levels may occur in malnutrition syndromes including kwashiorkor, marasmus and anorexia nervosa. When the patient is placed in a more normal environment, eating and drinking patterns normalize [96].


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