Nutritional Dwarfing Anorexia Nervosa

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Nutritional dwarfing, an entity characterized by nutritional deprivation, body weight below 90% of ideal, growth retardation and growth failure, is associated with increased serum GH and decreased IGF-1 concentrations. The dissociation between GH and IGF-1 suggests that impaired somatic growth is related to reduced IGF-1 synthesis or action, whereas GH may mediate the metabolic adaptation to starvation through its effects on hepatic glucose production, lipolysis, and nitrogen conservation (22). In a recent study of 16 children with nutritional dwarfing, pubertal subjects had reduced mean 12-h GH concentrations in subjects (28). Spontaneous overnight GH secretion appears to be more sensitive to the effects of chronic undernutrition, and the pubertal subject is at particular risk for impaired GH secretion and potential compromise of final adult height. Despite these clinical findings, GH concentrations in a variety of malnourished states appears variable (28).

Anorexia nervosa, a psychiatric disease characterized by a disordered body image, severely limited caloric intake and body weight well below ideal, has been associated with elevated GH concentrations and a variable response to provocative stimuli (29). Studies using GHRH as a secretogogue demonstrate a variable GH response to food, in a manner similar to what has been observed in obese subjects, a group with unique neuroendocrine dynamics including blunted GH secretion.

Subjects with "fear of obesity," an eating disorder characterized by poor growth and delayed sexual development owing to caloric restriction over fear of becoming obese (30), is not associated with abnormal GH secretion. A spectrum of pituitary responsivity to stimuli was noted in nine subjects, distinct from that observed in anorexia nervosa and related to the degree of individual undernutrition (30,31).

In a study conducted in France (31), vitamin A and GH secretory status in 68 healthy, short prepubertal children was examined. Plasma vitamin A concentrations correlated positively (r = +0.64) with plasma GH during the night. Further, a group of 12 children with neurosecretory dysfunction and low vitamin A intake demonstrated significant increases in overnight GH secretion after 3 mo of supplemental vitamin A (31). The role of vitamin A and other fat-soluble vitamins as it relates to GH secretion needs to be further clarified; however, for subjects with cystic fibrosis or other forms of pancreatic insufficiency, this study provides additional support to the critical role nutrition plays in influencing GH secretory dynamics.

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