Endocrine consequences of anorexia nervosa

Abstract

Summary Anorexia nervosa (AN) is prevalent in adolescents and young adults, and endocrine changes include hypothalamic amenorrhea, a nutritionally acquired growth hormone resistance with low insulin like growth factor-1 (IGF-1), relative hypercortisolemia, decreases in leptin, insulin, amylin and incretins, and increases in ghrelin, PYY and adiponectin. These changes in turn have deleterious effects on bone, and may affect neurocognition, anxiety, depression and eating disorder psychopathology. Low bone density is particularly concerning; clinical fractures occur and changes in both bone microarchitecture and strength estimates have been reported. Recovery causes improvement of many, but not all, hormonal changes, and deficits in bone accrual may persist despite recovery. Physiologic, primarily transdermal, estrogen replacement increases bone density in adolescents, although catch-up is incomplete. In adults, oral estrogen co-administered with rhIGF-1 in one study, and bisphosphonates in another increased bone density, though not to normal. More studies are necessary to determine the optimal therapeutic approach in AN.

The dietary protein, IGF-I, skeletal health axis

“…Nevertheless, protein depletion associated with low lean body mass has been clearly identified in anorexia nervosa patients [95]. This finding is in agreement with the decreased serum level of IGF-I found in this disease (for recent reviews see [96,97]) as well as in experimental isocaloric protein depletion [12]. Refeeding anorexia nervosa patients with a diet of which 20% of energy was provided by protein significantly increases both lean body mass -when rightly calculated in absolute value and not related to body weight -and total body protein [95].…”

Adipokine profile in patients with anorexia nervosa

“…To date, no genetic mechanisms underlying AN have been established [9]. Previous studies examined the interactions between anorexia nervosa and orexigenic and anorexigenic factors, as well as other peptides and hormones in the control of eating behaviour and energy metabolism in severe undernutrition [10][11][12][13][14]. Most papers focused on adipokine evaluation in malnourished AN individuals, without any assessment after long-term refeeding.…”

Insulin-like Growth Factors in a clinical setting: Review of IGF-I

“…A model situation is the psychological disorder; anorexia nervosa. GH and also in parallel, IGF-I decreases with the disease progression as an effect of starvation on receptor function 19 . This phenomenon includes hypothalamic amenorrhea, relative hypercortisolemia, reduced stimulated levels of leptin, insulin, amylin and incretins (glucagon-like polypeptide-1, glucose-dependent insulinotropic polypeptide), and conversely increased levels of adiponectin, ghrelin and peptide YY.…”

“…Serious complications of anorexia nervosa include changes in bone microarchitecture with bone mineral density reduction, increased risk of fracture, neuro-cognitive impairment and the development of anxiety and depression. This could be seen as an indication for combined estrogen and IGF-I treatment in patients suffering from anorexia nervosa or those recovering from this condition [19][20][21][22] . The opposite situation is the overproduction of GH, with elevated IGF-I levels, in acromegaly.…”