Nutrition in early life interacts with genetic risk to influence preadult behaviour in the Raine Study

TL;DR

The study finds that early nutrition and genetic risk interact to influence child behavior, with diet and breastfeeding effects varying based on genetic predispositions.

Contribution

The study provides novel evidence that early nutrition interacts with psychiatric genetic risk to influence child behavior.

Findings

Longer breastfeeding reduced behavioral problems in children with higher chronic pain genetic risk.

A healthier diet at age 1 reduced behavioral problems in children with lower ADHD genetic risk.

Plant-based food consumption appears to drive the beneficial diet-behavior association.

Abstract

Early life nutrition is associated with child behaviour; however, the interplay with genetic vulnerability is understudied. We hypothesised that psychiatric genetic risk interacted with early nutrition to predict behavioural problems in childhood and adolescence.

The Raine Study participants with genetic information aged 2–17 were repeatedly evaluated with the child behaviour checklist total problems score (CBCLTOT). Breastfeeding duration was recalled at age 1, 2 and 3 follow-up, and toddler diet derived by an age-1 24-h maternal recall (EAT1, scale 0–70, SD 10, higher scores proxying healthy diet). We derived polygenic scores (PGS) impacting general psychopathology: attention-deficit hyperactivity disorder (ADHD), depression, chronic multisite pain (CMSP), total behaviour problems and birthweight. In confounder-adjusted mixed-effects models of CBCLTOT throughout follow-up we examined nutrition-by-PGS interactions.

In 1393 participants, a borderline signal suggests that 1 month longer breastfeeding reduces CBCLTOT by −0.108 (95% CI [−0.184, −0.0289]) exclusively in individuals with a higher CMSP PGS (Interaction p = 0.03). In 1310 participants, a strong signal suggests that 1 EAT1 point increase results in a reduced CBCLTOT by 0.121 points (95% CI [−0.171, −0.0704]) exclusively in individuals with a lower ADHD PGS (Interaction p = 0.0005). Post hoc analysis suggests that plant-based food consumption drives the favourable EAT1-CBCLTOT association.

Nutrition in early life and psychiatric genetic risk may interact to determine lasting child behaviour. Contrary to our hypothesis, we find dietary benefits in individuals with lower ADHD PGS, necessitating replication. We also highlight the possibility of including genetics in early nutrition intervention trials for causal inference.

Byg et al. examine whether psychiatric genetic risk interacts with early nutrition to influence child behaviour in pre-adulthood measured using the repeated Child Behaviour Checklist (CBCL). They find nutrition in early life and psychiatric genetic risk may interact to determine longer term child behaviour.

It has been proposed that both early nutrition and genetic risk influence behaviour in childhood and adolescence. However, the interplay between the two remains poorly understood. We examined the interaction between genetic and early nutritional data with repeated parent ratings of behaviour from birth until age 17 years in Australian children. We saw fewer behavioural problems in those with a healthy diet at one year of age if the children had a low risk of developing ADHD based on their genetics. In contrast, longer breastfeeding duration primarily reduced behavioural problems in those with a higher risk of chronic pain based on their genetics. Our results suggest that tailoring early nutrition based on genetic risk could reduce pre-adult behaviour problems. However this association should be further tested in clinical studies.

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