Long-Term Skeletal Effects of Eating Disorders with Onset in Adolescence

Anorexia nervosa (AN), an eating disorder characterized by severe undernutrition and associated with hypogonadotropic hypogonadism, causes marked deficits in bone mass accrual when the disorder begins in the teenage years. Although bone mass accrual improves with weight gain and menstrual recovery,...

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Veröffentlicht in:Annals of the New York Academy of Sciences 2008-01, Vol.1135 (1), p.212-218
1. Verfasser: Misra, Madhusmita
Format: Artikel
Sprache:eng
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Zusammenfassung:Anorexia nervosa (AN), an eating disorder characterized by severe undernutrition and associated with hypogonadotropic hypogonadism, causes marked deficits in bone mass accrual when the disorder begins in the teenage years. Although bone mass accrual improves with weight gain and menstrual recovery, residual deficits persist. Women with a history of teenage onset of AN are more likely to be osteopenic than age‐matched women without this history, even after many years of weight and menstrual recovery. Non‐recovered women with persistent low weight and amenorrhea have continued decreases in bone density, with a high prevalence of both osteopenia and osteoporosis. Unlike anorexia nervosa, normal‐weight bulimia is not associated with low bone density, unless there is a past history of low weight or amenorrhea. A second possible skeletal effect of teenage‐onset anorexia nervosa is short stature. Duration of illness and time of onset of anorexia nervosa in relation to the pubertal growth spurt are likely important determinants of statural growth. Adolescent boys with anorexia nervosa are more likely than adolescent girls to have short stature, possibly because growth potential persists for two years longer in boys than in girls. Thus, many adolescent girls may have completed growth or be close to growth completion at the time that they develop anorexia nervosa, whereas adolescent boys may still have significant growth potential remaining. This remaining growth potential may be impaired as a consequence of low levels of insulin‐like growth factor‐I (IGF‐I) levels from persistent undernutrition.
ISSN:0077-8923
1749-6632
DOI:10.1196/annals.1429.002