Biological programming of child mental health in early life: understanding mechanisms and their timing

Examine the prenatal and postnatal environment and the multifactorial causation of early-life child mental health conditions, particularly for ages 0–5 years.

We will identify key prenatal environmental exposures (e.g. chemical exposures, maternal nutrition, social adversity) and postnatal environmental exposures (e.g. screen-use behaviours), which are associated with child mental health outcomes at ages 2 and 4 years, and paediatric diagnostic outcomes for ASD, ADHD and anxiety at age 9 years.

Our team will add to our existing multi-omics data by undertaking whole-genome methylation of child buccal samples at age 4 years, which will allow an improved assessment of the impact and timing of early-life environment on the epigenetic programming of child mental health.
We will examine how adverse prenatal and postnatal environment increases child mental health risk through a priori biological pathways, using causal molecular mediation, with a focus on:

i. altered epigenetic programming

ii. inflammation and maternal immune activation

iii. disrupted oxidant/antioxidant metabolism

iv. endocrine (hormonal) disruption.

We will employ a life-course trajectory approach using available serial exposures, epigenetic, immune and metabolomic measures from age 28 weeks to age 4 years inclusive in mechanistic assessments examining mental health outcomes at ages 2, 4 and 9 years.