Aims

Early puberty is associated with poor mental health outcomes in adolescence, from diminished mental wellbeing to psychopathology, especially amongst females. Explanations for this observed association predominantly centre on developmental mismatching of cognitive and emotional capacities and social engagement with older rather than same age peers. Research in this area has, however, largely neglected to examine the extent to which mental health issues precede premature pubertal development.

Life history theory considers early pubertal development to be an adaptive response to early environmental adversity, including factors such as familial discordance, hostile or neglectful parenting and low resource stability including family economic hardship. These social determinants of early puberty are also known to be related to behavioural problems and psychosocial difficulties (e.g., Boe et al., 2012). The inter-related nature of these outcomes and their timing require further exploration. Relevant longitudinal research in this context (Mensah et al., 2013) has recently revealed psychosocial and behavioural adjustment issues among four year-olds that go on to experience premature puberty. Utilisation of ALSPAC data will enable further generalisation of this research. We aim to follow up and extend research in this area by examining the extent to which psychological health, health-related behaviour, neurodevelopmental disorders and cognitive abilities in early childhood vary according to subsequent pubertal timing.

Pubertal timing is strongly controlled by genetic factors (heritability of menarcheal timing is estimated to be as high as 74%; He & Murabito, 2014). Both genome-wide association studies and candidate approaches have identified these factors which are among the most robust findings in the field of complex trait genetics. We would like to include genetic variants in our analysis to control for genetic influences and also test whether genes associated with pubertal timing in boys and girls could be directly implicated in related psychological and behavioural phenotypes. Interestingly one of the genes identified, CYP19A1, has also been implicated in dyslexia, a common neurodevelopmental phenotype. For this reason, we would like to include reading-related measures in our dataset. Also pertinent to this context are findings of sex differences in neurodevelopmental disorders (e.g., Willcutt & Pennington, 2000). We aim to examine potential environmental and genetic factors which may contribute to gender differences in prevalence rates.

This project builds on a collaboration between research groups in the School of Medicine, University of St Andrews, which is focusing on a wider project on the determinants and consequences of early pubertal timing. Professor Candace Currie currently acts as International Coordinator of the 43-country Health Behaviour in School-aged Children (HBSC) study and directs the Child and Adolescent Health Research Unit (CAHRU) in St Andrews. Professor Currie has a strong track record in fields of puberty and adolescent health and has been an active researcher in these areas for over 20 years. Dr Silvia Paracchini is a Royal Society University Research Fellow and an active researcher in the field of neurodevelopmental genetics. She has extensive experience in working with cognitive measures from the ALSPAC dataset. Dr Ross Whitehead is a Research Fellow with the Scottish HBSC team and has backgrounds in cognitive neuroscience and the evolution of human behaviour. As part of our collaborative project, we will extend our analysis to other relevant existing cohorts such as the 'Generation Scotland' study, which allows retrospective investigation into some of the above research questions