“…For example, in restrictive eating disorders such as anorexia nervosa, chronic starvation may lead to hypothalamic amenorrhea with hypoestrogenemia, low testosterone levels, hypercortisolemia, growth hormone resistance (high growth hormone, but low downstream IGF‐1 levels), and altered secretion of appetite‐regulating hormones (e.g., low anorexigenic hormones leptin and oxytocin; high orexigenic ghrelin [Culbert, Racine, & Klump, ; Misra & Klibanski, ] and AGRP [Merle et al, ]). While many hormonal alterations in response to low‐weight are adaptive (i.e., to stimulate food consumption and/or conserve limited resources) and resolve with weight restoration, evidence of seemingly paradoxical hormone levels in some cases (e.g., high levels of anorexigenic PYY) and persistent abnormalities after weight gain (e.g., in PYY [Misra et al, ; Nakahara et al, ; Pfluger et al, ]), ghrelin (Holsen, Lawson, Christensen, Klibanski, & Goldstein, ; Nakahara et al, ), oxytocin (Afinogenova et al, ), hypothalamic–pituitary–adrenal axis (e.g., cortisol) (Grinspoon et al, ; Lawson et al, ; Mayer et al, ) argue for a potential etiologic role versus scar or delayed recovery from chronic starvation, or effects of residual psychopathology (Misra & Klibanski, ). Endocrine changes, including reproductive dysfunction, activation of the hypothalamic–pituitary–adrenal axis, and differences in secretion of appetite‐regulating hormones, have also been demonstrated in other eating disorders, such as bulimia nervosa and binge‐eating disorder (Culbert et al, ; Poyastro Pinheiro et al, ).…”