A large study of families suggests that a child’s overall attention-deficit hyperactivity disorder traits are primarily driven by their own genetics by mid-childhood, rather than by the indirect environmental influence of their parents’ genes. Researchers found a lack of evidence for parental genetic nurture effects at both age five and age eight, though they note that statistical limitations might obscure more subtle influences. The research was published in Behavior Genetics.
Attention-deficit hyperactivity disorder, or ADHD, is a neurodevelopmental condition involving patterns of inattention, hyperactivity, and impulsivity. Decades of twin studies indicate that ADHD is highly heritable. This means a child’s own DNA plays a major role in whether they develop these behavioral traits.
However, genetic and environmental factors do not operate in isolation. In recent years, scientists have focused on how an individual’s traits might be shaped by the genes of the people around them. Because biological parents provide both their children’s DNA and their rearing environment, it is notoriously difficult to separate nature from nurture.
When parents’ genes influence their child’s environment, this process is known as an indirect genetic effect, or genetic nurture. For instance, a parent’s genetic makeup might influence their patience, parenting style, or the general household environment they create. This environment then affects the child’s development, meaning the parent’s genes have shaped the child’s traits from the outside in.
When indirect genetic effects are not accounted for, researchers risk overestimating the direct impact of a child’s own DNA. To better understand the origins of ADHD traits, researchers set out to untangle these direct and indirect genetic influences. Daniel L. Wechsler, a researcher at King’s College London, led a team to investigate whether parents’ genetic profiles exert indirect effects on a child’s ADHD traits over and above the child’s own direct genetic risks.
The researchers also wanted to see how these influences might shift as children grow. Previous research has explored these dynamics for specific traits like hyperactivity at single time points. The current project instead focused on overall ADHD scores across two distinct developmental stages, early and mid-childhood.
Wechsler and his colleagues utilized data from the Norwegian Mother, Father and Child Cohort Study, a population-based registry. They analyzed genetic data from mother, father, and child trios alongside survey data. The questionnaires asked parents to rate the frequency of specific behaviors, such as difficulty paying attention to tasks or acting without thinking.
A method called trio genome-wide complex trait analysis was used to examine around a million genetic variations across all three family members. These genetic variations, known as single-nucleotide polymorphisms, are tiny changes in the genetic code that can influence various physical and behavioral traits. Humans share the vast majority of their DNA, but these small variations make each person unique.
Unlike some genetic approaches that only look at specific genes tied to a known condition, this method captures the cumulative influence of all measured genetic variations. By modeling the genetic data from the whole family at once, the researchers could estimate the child’s direct genetic effects alongside the cumulative indirect environmental effects of both parents’ genes.
The first analysis focused on a large study sample of 12,374 family trios when the children were five years old. The initial statistical models at this age suggested that maternal indirect genetic effects accounted for nearly five percent of the variation in children’s ADHD traits. At the same time, the child’s direct genetic effects appeared to account for less than two percent.
However, when the researchers tested these findings against more stringent statistical models, the results failed to hold up. The model comparisons ultimately favored a scenario in which neither direct nor indirect genetic effects were present at age five. Large margins of error in the data prevented the team from confirming specific genetic effects at this age.
This lack of measurable direct genetic influence at early childhood was unexpected. ADHD is widely recognized as highly heritable, even in young children. The researchers suggested that ADHD traits might not fully manifest in a measurable way for many children by age five.
Alternatively, it is possible that children’s individual genetic propensities simply account for more variation in their behavior as they grow older. This pattern has been observed in other developmental traits, where the influence of a child’s own genetics becomes more apparent over time. In previous research utilizing an even larger sample of the same cohort, scientists found evidence for direct genetic effects on specific traits like hyperactivity and inattention as early as age three.
Next, the team conducted a similar analysis on an overlapping large study sample of 12,714 family trios when the children were eight years old. The preliminary models for this mid-childhood stage showed increased genetic influence overall. These early estimates pointed to roughly equal contributions, with the child’s own genes and the mother’s indirect genetic effects each accounting for about eight percent of the variation.
Once again, the researchers applied rigorous model comparisons to see which scenario best fit the data. At age eight, the most accurate model indicated that the child’s direct genetics played a role in their ADHD traits. This model, however, showed no evidence of indirect genetic effects from either parent.
Across both age groups, the team found no robust evidence that a mother or father’s genetic profile indirectly influences a child’s overall ADHD traits through the environment. The results at age eight suggest that a child’s own DNA is the primary biological driver of their overall ADHD traits by mid-childhood.
While the results appear to rule out genetic nurture for total ADHD traits, the researchers caution against drawing absolute conclusions. The statistical models were hampered by large margins of error, meaning the results were not statistically significant enough to firmly distinguish direct from indirect effects in the more complicated models. The study might simply have lacked the mathematical power to detect subtle indirect influences.
The decision to analyze total ADHD scores rather than breaking them down into specific categories might have also obscured important details. Past studies have successfully detected indirect genetic effects on specific behaviors like hyperactivity and inattention. This suggests that genetic nurture might operate on certain specific behaviors rather than the overarching condition.
Another limitation is that the survey data relied solely on the mothers’ assessments of their children. Mothers’ ratings could be influenced by their own perceptions or biases based on their specific interactions with the children. Utilizing teacher reports or formal clinical diagnoses could provide a more rounded perspective in future investigations.
Additionally, the genetic data came exclusively from families of European ancestry. This demographic focus limits how well the findings might apply to more diverse populations worldwide. Future research could benefit from even more massive study samples across diverse demographics to better separate these intertwined genetic signals.
The study, “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,” was authored by Daniel L. Wechsler, Espen M. Eilertsen, Yasmin I. Ahmadzadeh, Rosa Cheesman, Nicoletta Adamo, Laurie J. Hannigan, Eivind Ystrom, and Tom A. McAdams. Their work adds new context to the ongoing scientific effort to untangle the developmental roots of behavioral traits.