Exogenous ovarian hormone exposure and risk for binge eating (#135)
Natural changes in ovarian hormones across the menstrual cycle predict increases in binge eating (Klump et al. (2013). The interactive effects of estrogen and progesterone on changes in emotional eating across the menstrual cycle. J Abnorm Psych). The riskiest hormonal milieu is the mid-luteal phase when estrogen and progesterone appear to drive binge eating via increases in genetic effects. Although these menstrual cycle studies are strong quasi-experimental designs, their exclusive focus on endogenous hormones limits their inferential power. An alternative design is to study the effects of exogenous hormones by examining twins taking birth control pills (BCPs) with hormonal combinations (estrogen and progesterone) that mimic the mid-luteal phase. The power of this approach lies in its ability to examine between-subject (binge eating in users vs. non-users), within-subject (changes in binge eating from inactive to active pills), and within-pair (differences in binge eating between co-twins discordant for BCPs) effects of exogenous hormones. The purpose of our pilot study was to explore all three exogenous hormone effects in 42 twins from the Michigan State University Twin Registry who were assessed for 45 days. Between-subjects, BCP twins exhibited higher rates of binge eating than the non-BCP twins. Within BCP subjects, significant increases in binge eating were observed when moving from the inactive to the active pill phase. Within discordant pairs, twins taking BCPs had higher rates of binge eating than their co-twins. These latter effects were much larger in fraternal than identical twin pairs, suggesting a genetically mediated effect of hormones. Taken together, data provide strong preliminary support for exogenous hormone effects on genetic risk for binge eating. Larger-scale studies are needed to replicate and confirm results, particularly given high rates of BCP use that may inadvertently increase risk for binge eating, especially in women who are genetically vulnerable to the phenotype.