Eating disorders and their core symptoms (e.g. binge eating, weight/shape concerns) become prominent during puberty and disproportionately affect females. This review evaluates evidence for phenotypic and genetic effects of sex… Click to show full abstract
Eating disorders and their core symptoms (e.g. binge eating, weight/shape concerns) become prominent during puberty and disproportionately affect females. This review evaluates evidence for phenotypic and genetic effects of sex steroid hormones on differential vulnerability to eating pathology. Accumulating data suggest that perinatal testosterone exerts an initial bout of protection that decreases risk for eating pathology in males, relative to females. The subsequent exposure to circulating androgens (e.g. testosterone), during puberty and adulthood, appears to provide additional protective effects that serve to further reduce risk for eating pathology in most males. Conversely, the absence of perinatal testosterone, coupled with low pubertal estradiol and the post-pubertal cyclical circulation of ovarian hormones, creates hormonal milieus that enhance eating pathology in vulnerable females.
               
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