Prenatal testosterone may masculinize (i.e., lower) risk for disordered eating and account for sex differences in prevalence, yet how these effects emerge and whether these effects remain static across development is unknown. Opposite-sex (OS) twins provide a natural design to investigate such effects, as OS female twins are thought to be exposed to elevated testosterone in utero from their male co-twin. Although OS female twins have shown masculinized disordered eating relative to other females, findings have been mixed. The current research used a series of studies to investigate whether there are developmental differences in the masculinizing/protective effects of prenatal testosterone exposure in risk for disordered eating. Study 1 examined whether age moderates the masculinizing effects of prenatal testosterone on disordered eating. OS female twins have shown masculinized disordered eating in early young adulthood, but these effects have not been robustly observed in other time periods, e.g., mid-to-late adolescence or mid-to-late young adulthood. Participants included 764 male and female twins (ages 15-30) and 74 non-twin females (ages 15-23) from the Michigan State University Twin Registry (MSUTR). Two well-validated measures (i.e., Minnesota Eating Behaviors Survey and the Eating Disorder Examination Questionnaire) were used to assess several disordered eating symptoms. Results indicated no evidence for masculinization of disordered eating in OS female twins during mid-to-late adolescence (ages 15-20). In contrast, OS female twins showed substantially masculinized levels of disordered eating across several scales in early young adulthood (ages 21-23). Masculinization of disordered eating in OS female twins also appeared to be present in mid-to-late young adulthood (ages 24-30), but effects were weaker and more variable across disordered eating scales. These findings suggest developmental windows of expression for the protective effects of prenatal testosterone on disordered eating, with effects strongest under "average" risk periods (i.e., young adulthood) and attenuated under higher risk periods (i.e., mid-to-late adolescence, the peak period for eating disorder onset). Study 2 was a translational extension of study 1 that aimed to determine if prenatal testosterone's masculinizing effects on disordered eating only become prominent during young adulthood (as observed in study 1), or whether, as predicted by animal data, masculinization effects emerge with puberty. In female animals, early testosterone exposure decreases sensitivity to ovarian hormones during and after puberty. Thus, one potential mechanism for prenatal testosterone's effects on disordered eating may be via decreased sensitivity to the activating effects of ovarian hormones on disordered eating risk. Study 2 examined whether puberty underlies the emergence of prenatal testosterone's masculinization of disordered eating, independent of the confounding effects of several other factors (e.g., adiposity, mood, autonomy, being reared with a brother). Participants included 394 male and female twins and 63 non-twin females (ages 10-15) from the MSUTR. Well-validated measures assessed disordered eating, pubertal status, mood symptoms, and autonomy difficulties. Body mass index was used as a marker of adiposity. Disordered eating did not differ amongst twin types in pre-early puberty, whereas OS female twins fell intermediate to males and SS female twins on levels of disordered eating during mid-late puberty. Masculinization effects in mid-late pubertal OS female twins were not accounted for by adiposity, mood symptoms, autonomy difficulties or being reared with a brother. Taken together, findings indicate that other key factors (e.g., sensitivity to circulating gonadal hormones) likely underlie prenatal testosterone's protective effects on disordered eating.
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