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Your Parents’ DNA May Shape Your Traits in Ways You Didn’t Directly Inherit

In A Nutshell

  • A study of roughly 30,000 families found that parental genes can influence children’s height, weight, and school performance even through DNA that was never passed down, by shaping the environment a child grows up in.
  • Whether a gene variant came from mom or dad also matters, with the same variant capable of producing different effects depending on its origin, a phenomenon found to be far more widespread than previously mapped.
  • When parental environmental and parent-of-origin effects are combined, their total influence rivals that of the DNA a child directly inherits.
  • Standard genetic research tools were found to overestimate a child’s direct genetic influence while underestimating these broader parental effects, pointing to a need for more sophisticated methods.

Genes don’t tell the whole story of why traits run in families. A new study of roughly 30,000 families found that a parent’s DNA may shape children’s height, body weight, and school performance not only through the genes passed down at conception, but through the environment those genes help create. Moreover, which parent a gene comes from can change what it actually does in the child who inherits it.

Published in Cell Genomics, the research found both of these forces are substantially larger than standard genetic studies have been capturing. Together, they rival the direct effect of a child’s own inherited DNA, a finding that points to a significant blind spot in how scientists have been reading the genome.

Parental DNA Linked to Children’s Height, Weight, and School Scores

To understand why this matters, consider what genes actually do inside a family. A child inherits one copy of each gene from mom and one from dad. Standard genetics says those inherited copies drive the child’s biology. But families do not operate in a vacuum. Parents act on their own genetic tendencies every day, and those actions may shape the world their children grow up in.

Until now, measuring those overlapping influences was extremely difficult. The new study introduced JODIE, a statistical tool designed to separate three distinct genetic forces at once: the effect of a child’s own inherited DNA, the effect of the mother’s genes on the child’s environment, and the effect of the father’s genes on the child’s environment. It also tracked a fourth force, parent-of-origin effects, tied to a process in which one parent’s copy of a gene is switched on while the other parent’s copy stays silent.

Previous methods had struggled with a particular wrinkle: people tend to have children with partners who are genetically similar to them. That pattern creates statistical echoes that can make a child’s own DNA look more influential than it really is, while obscuring the parent-of-origin contribution. JODIE was built to correct for this.

Data came from the Norwegian Mother, Father, and Child Cohort and the Estonian Biobank, covering three traits: height, body weight relative to height, and childhood educational test scores. Educational scores were measured around age 10 in the Norwegian children; height and body weight measures from Norway came from children ages 7 to 8, while Estonian data covered adults.

parent dna
A new study finds parental genes may shape children’s traits through environment and gene origin, not just inherited DNA. (Image by StudyFinds)

Mom’s and Dad’s Genes Each Contribute Roughly Equally to Indirect Effects

A child’s own inherited DNA remained the strongest single driver of all three traits. But when the indirect effects from both parents are combined with the parent-of-origin effects, their total is comparable to the direct effects, too large to treat as background noise.

For height and educational scores, the genome regions where a child’s own genes act tend to overlap with the regions where parental genes exert their environmental influence. Maternal and paternal contributions were roughly equal in size.

Researchers identified specific locations across the genome tied to each trait: 276 linked to height, 15 to body weight, and 11 to childhood test scores. Most held up when checked against independent data from the UK Biobank and the Generation Scotland study. Notably, these locations were spread across the genome rather than concentrated in regions already known for parent-of-origin switching, pointing to a broader role for this phenomenon than previously understood.

A few locations stood out. One near a gene involved in brain and facial development was linked to childhood educational scores. Another, inside a gene active in sperm-producing cells, was associated with height, a detail the researchers flagged as potentially relevant to how fathers pass chemical markers alongside their DNA. A third, near a gene showing activity in testis tissue, was connected to body weight.

Why Standard Genetic Studies May Miss Part of the Picture

In the study’s simulations, several commonly used approaches became biased under the more complex family scenarios JODIE was designed to handle. They overestimated how much a child’s own DNA was responsible for a given trait while underestimating the parent-of-origin contribution. A common shortcut of estimating missing parental DNA rather than collecting it directly also systematically underestimated indirect parental effects.

That matters because standard genetic studies, the kind that scan millions of people’s DNA to find which variants predict disease or ability, treat a person’s genome as if it acts alone. This research adds statistical evidence to a growing body of work suggesting that assumption is incomplete.

Study authors caution that 30,000 family trios is not enough to draw the full map, and that larger, more diverse datasets will be needed to confirm how these effects work across populations.

A child’s genetic story does not begin and end with the DNA they carry. A parent’s genes may be shaping the home, the habits, and the circumstances that steer who that child becomes, whether or not a single strand of that DNA was ever passed along.


Paper Notes

Limitations

The authors identify several limitations directly in the paper. Sample sizes of approximately 30,000 trios, while the largest family-based cohorts available for this analysis, are described as insufficient to map large numbers of genetic locations or to build genetic predictors with high accuracy. The estimates of variance attributable to parental genetic effects may reflect some combination of real indirect genetic effects and population stratification, meaning differences in ancestry across groups could contribute to the results, though the authors provide analysis suggesting population stratification alone cannot explain the magnitudes observed. Without data on grandparents or broader family members, parental indirect genetic effects cannot be interpreted as definitively causal in the parents themselves. Parent-of-origin effects are acknowledged as particularly difficult to detect and interpret, as imprinting can vary by tissue type, developmental stage, and environmental factors such as nutrition, making effects variable across populations. The authors further note that highly parameterized statistical models applied to observational data may always carry alternative interpretations, and that other models making different assumptions could also be applied to the same data.

Funding and Disclosures

According to the paper, this work was funded by an SNSF Eccellenza Grant to Matthew R. Robinson (grant PCEGP3-181181) and by core funding from the Institute of Science and Technology Austria. The Norwegian Mother, Father, and Child Cohort Study is supported by the Norwegian Ministry of Health and Care Services and the Ministry of Education and Research. Co-author Olivier Delaneau is currently an employee of Regeneron Pharmaceuticals Inc. No other conflict-of-interest disclosures were identified.

Publication Details

Paper title: Separating direct, indirect, and parent-of-origin genetic effects in the human population | Authors: Ilse Krätschmer, Laura Hegemann, Robin J. Hofmeister, Elizabeth C. Corfield, Mahdi Mahmoudi, Olivier Delaneau, Ole A. Andreassen, Archie Campbell, Caroline Hayward, Estonian Biobank Research Team, Riccardo E. Marioni, Eivind Ystrom, Alexandra Havdahl, and Matthew R. Robinson | Journal: Cell Genomics, Volume 6, July 8, 2026 | DOI: https://doi.org/10.1016/j.xgen.2026.101277 | Corresponding authors: Ilse Krätschmer ([email protected]), Alexandra Havdahl ([email protected]), and Matthew R. Robinson ([email protected]) | Access: Open access under CC BY-NC-ND license

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