A large Norwegian birth cohort study has concluded that a child’s overall ADHD traits by mid-childhood are primarily driven by the child’s own genetics, with little evidence that parental genes shape development through the household environment.
Attention-deficit hyperactivity disorder is a neurodevelopmental condition characterised by patterns of inattention, hyperactivity and impulsivity. Decades of twin studies have shown ADHD to be highly heritable, indicating a major role for a child’s own DNA in the emergence of these traits.
Yet genetics and environment do not operate in isolation. Scientists have increasingly explored whether a person’s traits are shaped by the genes of those around them, particularly given that biological parents provide both DNA and rearing environments. When a parent’s genes influence the child’s environment, this indirect genetic effect, or genetic nurture, can blur the line between nature and nurture.
To untangle direct genetic effects from potential indirect influences, researchers led by Daniel L. Wechsler of King’s College London examined whether parents’ genetic profiles exert indirect effects on a child’s ADHD traits beyond the child’s own genetic risk.
The team used data from the Norwegian Mother, Father and Child Cohort Study, analysing genetic data from mother, father and child trios alongside parent-reported behavioural questionnaires. The study sought to map the total picture of ADHD traits across two developmental stages—early and mid-childhood.
The analysis, known as trio genome-wide complex trait analysis, assessed around a million genetic variations across the three family members. This method captures the cumulative influence of many genetic variations rather than focusing on a single gene or set of genes, allowing estimation of the child’s direct genetic effects alongside potential indirect effects from both parents.
At age five, the first large sample of 12,374 family trios yielded initial models where maternal indirect genetic effects appeared to account for roughly five per cent of variation in children’s ADHD traits, while the child’s direct genetic effects were estimated at under two per cent.
However, when the researchers applied more stringent statistical models, the results did not hold up. Model comparisons favoured a scenario in which neither direct nor indirect genetic effects were detectable at age five, with large margins of error preventing firm conclusions about any subtle influences.
These findings were unexpected given ADHD’s recognised heritability, and the authors suggested that the traits might not be fully measurable in five-year-olds. Another possibility is that a child’s own genetic propensities increasingly account for behavioural variation as they age; previous work using a larger sample from the same cohort had found direct genetic effects on specific traits like hyperactivity and inattention as early as age three.
A separate analysis on an overlapping sample of 12,714 family trios at age eight showed different initial signals. Early models indicated roughly equal contributions from the child’s own genes and the mother’s indirect genetic effects, each around eight per cent of variation.
Yet, in line with the earlier age, rigorous model comparisons at age eight pointed to the child’s direct genetics playing a role in ADHD traits, while there was no evidence of indirect genetic effects from either parent.
In total, across both ages the study did not find robust evidence that a mother’s or father’s genetic profile indirectly shapes a child’s overall ADHD traits through the environment. The results at age eight support the interpretation that a child’s own DNA is the primary driver of their ADHD traits by mid-childhood.
The researchers caution that the statistical models carried large margins of error, limiting definitive distinctions between direct and indirect effects in more complex models. They also note that focusing on total ADHD scores rather than dissecting specific behaviours might mask subtler genetic nurture effects observed in other studies.
Limitations include reliance on maternal reports and confinement to families of European ancestry, which may affect generalisability. The authors suggest that future work with even larger and more diverse samples could better isolate these intertwined genetic signals.
The study, titled Direct and Indirect Genetic Effects on Child ADHD Traits in Early and Mid-Childhood: Trio Genome-Wide Complex Trait Analyses in a Large Norwegian Birth Registry Cohort, is authored by Daniel L. Wechsler, Espen M. Eilertsen, Yasmin I. Ahmadzadeh, Rosa Cheesman, Nicoletta Adamo, Laurie J. Hannigan, Eivind Ystrom, and Tom A. McAdams.
