Associations between accelerated parental biologic age, autism spectrum disorder, social traits, and developmental and cognitive outcomes in their children.
Moms whose body ages faster than their years have babies who score a bit lower on early thinking tests.
01Research in Context
What this study did
The team looked at 1,200 moms and dads. They checked how fast each parent’s body was aging. They used a blood test called an epigenetic clock.
Then they watched the babies. They tested each child at 12 months for early thinking skills. They also tracked which kids later got an autism diagnosis.
What they found
Moms whose body age ran faster than their real age had babies with slightly lower 12-month cognitive scores. The drop was small—about two points on a 100-point scale.
Oddly, dads with faster body age had babies with a tiny lower chance of autism. The effect sizes were tiny, but the pattern flipped by parent sex.
How this fits with other research
Ye et al. (2024) used a different blood marker—telomere length—in adults with autism. They also saw that older dads had longer telomeres, hinting the dad effect may grow over decades.
Lyall et al. (2011) showed early mom traits like early periods or high teen BMI raise autism odds. The new study adds a fresh biomarker—epigenetic age—to that same mom-risk story.
Brayette et al. (2019) found shorter pregnancy weeks hurt later cognition in kids with autism. The 2022 paper says mom’s faster body age hurts early cognition too. Both point to prenatal timing as key.
Why it matters
You cannot change a parent’s epigenetic age, but you can flag babies born to moms with fast clocks. Add extra early-learning checks at 9 and 12 months. Two extra minutes of screening may catch a small delay before it widens.
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02At a glance
03Original abstract
Parental age is a known risk factor for autism spectrum disorder (ASD), however, studies to identify the biologic changes underpinning this association are limited. In recent years, "epigenetic clock" algorithms have been developed to estimate biologic age and to evaluate how the epigenetic aging impacts health and disease. In this study, we examined the relationship between parental epigenetic aging and their child's prospective risk of ASD and autism related quantitative traits in the Early Autism Risk Longitudinal Investigation study. Estimates of epigenetic age were computed using three robust clock algorithms and DNA methylation measures from the Infinium HumanMethylation450k platform for maternal blood and paternal blood specimens collected during pregnancy. Epigenetic age acceleration was defined as the residual of regressing chronological age on epigenetic age while accounting for cell type proportions. Multinomial logistic regression and linear regression models were completed adjusting for potential confounders for both maternal epigenetic age acceleration (n = 163) and paternal epigenetic age acceleration (n = 80). We found accelerated epigenetic aging in mothers estimated by Hannum's clock was significantly associated with lower cognitive ability and function in offspring at 12 months, as measured by Mullen Scales of Early Learning scores (β = -1.66, 95% CI: -3.28, -0.04 for a one-unit increase). We also observed a marginal association between accelerated maternal epigenetic aging by Horvath's clock and increased odds of ASD in offspring at 36 months of age (aOR = 1.12, 95% CI: 0.99, 1.26). By contrast, fathers accelerated aging was marginally associated with decreased ASD risk in their offspring (aOR = 0.83, 95% CI: 0.68, 1.01). Our findings suggest epigenetic aging could play a role in parental age risks on child brain development.
Autism research : official journal of the International Society for Autism Research, 2022 · doi:10.1002/aur.2822