Puberty is a time of sweeping biological and social change. Boys and girls who experience early and/or rapid puberty are at elevated risk for psychiatric and physical health problems, including substance use disorders, suicide, polycystic ovary syndrome (in females), and cardiovascular disease. Psychiatric disorders like major depressive disorder also become much more prevalent at puberty and may impede cognitive skill development . Considering the many negative implications of departures from the normal pubertal development, understanding the genetic and environmental regulators of puberty has become a topic of increasing urgency. Our research aims to identify specific and potentially modifiable environmental factors that influence pubertal timing and examine its association with children’s cognitive development and mental health, and we view genetic and epigenetic data as essential tools for accomplishing that goal.

Scientific progress on understanding genetic influences and epigenetic changes (including DNA methylation) at puberty has moved slowly. Previous studies looking at changes in DNA methylation across puberty have been conducted in very small samples; nevertheless, this previous work support the potential to develop an epigenetic clock for pubertal age, analogous to epigenetic clocks that exist for aging. However, generating a clock that is highly accurate and robust requires longitudinal DNA methylation data spanning the pubertal transition. We will substantially improve the rigor and reproducibility of previous research on the epigenetics of pubertal age by using a discovery sample that is substantially better-powered (the Texas Twin project) and by replicating results in an independent sample (ALSPAC). We can then examine potential environmental (e.g., family socioeconomic background) and genetic predictors (e.g., polygenic scores of reproductive phenotypes) of our epigenetic clock for pubertal age, as well as the cognitive and mental health sequelae of advanced epigenetic pubertal age.