The effects of puberty on genetic risk for disordered eating: evidence for a sex difference.

Several twin studies document differences in genetic influences on disordered eating before and after puberty in girls (Culbert et al., 2009, Klump et al., 2003, Klump et al., 2007, Silberg and Bulik, 2005). Before puberty, genetic influences account for ~0% of the variability in disordered eating, whereas genetic factors account for over 50% during and after puberty (Culbert et al., 2009, Klump et al., 2003, Klump et al., 2007). Emerging data suggest that these developmental differences may be due to increases in ovarian hormones during puberty in girls. In particular, estrogen appears to moderate genetic influences on disordered eating, as there are no genetic influences on disordered eating symptoms (e.g., weight preoccupation, body dissatisfaction, binge eating) in twins with low estradiol levels during puberty, but significant genetic effects in twins with high estradiol levels (Klump et al., 2010). Collectively, these findings have led our team (Klump and Culbert, 2007, Klump et al., 2010) and others (Young, 2010) to speculate that ovarian hormones may “activate” genetic risk for disordered eating in girls during puberty. However, at least one additional piece of evidence is lacking – namely, are the same pubertal increases in genetic effects present in boys? Boys do not experience increases in ovarian hormones during puberty, as their pubertal development is driven by increases in testosterone. If pubertal increases in genetic effects are present in boys, then factors other than (or in addition to) ovarian hormones may drive increases in genetic effects in girls. Conversely, if pubertal increases in genetic effects are observed in girls only, then there would be additional, albeit indirect, evidence that sex-specific processes (e.g., ovarian hormones) differentially influence the magnitude of genetic risk across sex during puberty. No study has examined genetic influences on disordered eating in boys prior to puberty. Disordered eating is ~50% heritable in males in late adolescence (Baker et al., 2009) and young adulthood (Keski-Rahkonen et al., 2005, Reichborn-Kjennerud et al., 2003, Reichborn-Kjennerud et al., 2004, Slof-Op't et al., 2008, Tholin et al., 2005), an estimate on par with that for adult females (Bulik et al., 2000, Suisman and Klump, 2011). Thus, at least in late adolescence and adulthood, the magnitude of genetic influences on disordered eating appears to be similar in males and females. The next important step is to examine whether patterns of genetic effects are similar in males and females from pre-adolescence into adulthood. If ovarian hormones contribute to increases in genetic effects during puberty in girls, we would expect no effect of puberty on genetic risk in boys. Indeed, we would expect stable estimates of heritability across development since ovarian hormones do not play a major role in boys’ development. The aim of our study was to examine these possibilities by investigating differences in the magnitude of genetic influences in male twins during pre-puberty, puberty, and young adulthood. We further compared patterns of genetic effects in males to a sample of female twins who previously exhibited pubertal increases in genetic effects (see Culbert et al., 2009). The comparison of our male twins to an archival female group allowed us to directly examine sex differences in effects – without the females, we would be confined to visual comparisons of findings in male versus female twins rather than a quantitative test of sex differences.