Differences in genetic and environmental influences on body weight and shape concerns across pubertal development in females.

The heritability of disordered eating increases during puberty; however, prior studies have largely examined a composite score of disordered eating, rather than specific symptoms. Body weight and shape concerns cut across all eating disorder diagnoses and are some of the strongest prospective risk factors for the development of eating disorders. Yet, little is known about potential developmental increases or decreases in genetic and environmental influences for these key symptoms. This study examined differences in genetic and environmental effects on a range of body weight and shape concerns during puberty and compared results to findings for overall levels of disordered eating symptoms. Participants were 926 same-sex female twins (ages 8-16) from the Michigan State University Twin Registry. Well-validated questionnaires were used to examine pubertal maturation, overall levels of disordered eating, and a range of cognitive body weight/shape constructs: body dissatisfaction, weight/shape concerns, and weight preoccupation. Findings for overall levels of disordered eating were very similar to those obtained in previous work, with significantly increased genetic effects in girls at more advanced pubertal development. Importantly, these same pubertal increases in genetic influences were observed for body dissatisfaction and weight/shape concerns. However, no pubertal moderation of genetic effects was observed for weight preoccupation; instead, pubertal moderation of nonshared and shared environmental effects was observed. Our findings point to differences in the extent to which genetic and environmental factors contribute to various cognitive body weight and shape symptoms during puberty.

Estrogen moderates genetic influences on binge eating during puberty: Disruption of normative processes?

Puberty is a critical period for changes in genetic effects for binge eating in girls. Previous twin studies show increases in genetic influences on binge eating from prepuberty (∼0%) to midpuberty and beyond (∼50%). However, little is known about the factors that drive these shifts in genetic effects. A small pilot study showed that pubertal activation of estrogen may contribute to increases in genetic influences, possibly via hormonally induced changes in gene expression. However, large-scale studies investigating hormone effects on genetic risk are lacking. Thus, the purpose of the present study was to examine the effects of estrogen on genetic influences for binge eating in 964 female twins (ages 8-16 years) from the Michigan State University Twin Registry. Binge eating was assessed with the Minnesota Eating Behaviors Survey, whereas afternoon saliva samples were assayed for estradiol levels using standard enzyme immunoassays. Twin moderation models showed substantial differences in genetic influences on binge eating across estradiol levels. Stronger genetic effects were observed at lower (rather than higher) estradiol levels, even when controlling for the effects of age, body mass index, the physical changes of puberty, and the onset of menses. Overall, findings suggest that comparatively lower levels of estradiol during this critical period may disrupt normative developmental processes and enhance genetic influences on binge eating. (PsycINFO Database Record