Parental age at birth, telomere length, and autism spectrum disorders in the UK Biobank cohort.
Older parental age links to longer blood-cell telomeres in adults with ASD, complicating the usual ‘older parent, faster aging’ story.
01Research in Context
What this study did
The team looked at the adults with autism in the UK Biobank. They asked: does having ASD change telomere length, and does mom or dad’s age at birth matter?
Telomeres are tiny caps on chromosomes that shorten as we age. The scientists measured them from blood samples and compared adults with and without ASD.
What they found
Adults with ASD had the same average telomere length as other adults. But a surprise popped out: the older the parents were at birth, the longer the telomeres in the ASD group.
In plain words, being born to older parents did not speed up cell aging in autistic adults—it actually linked to younger-looking cells.
How this fits with other research
Shire et al. (2022) saw the opposite pattern in babies. Moms with faster “biologic age” had infants with slightly lower early cognitive scores. The new adult data flips the script: older calendar age at birth, not faster biologic age, tied to longer telomeres in ASD.
Gandhi et al. (2022) found autistic adults lose hippocampus volume faster, hinting at faster brain aging. Qiaofeng et al. now show their blood cells may age slower. Different tissues, different clocks—both papers remind us aging is not one-size-fits-all in ASD.
Supekar et al. (2017) showed comorbidity risk shifts with age. Adding telomere data gives us another biomarker to track as clients grow older.
Why it matters
When you see an adult client with ASD, don’t assume early health risk just because their parents were older. Longer telomeres might buffer some aging effects, yet brain studies still flag faster cognitive decline. Track both memory and medical comorbidities, not parental age alone.
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02At a glance
03Original abstract
Older parental age at birth is associated with increased risk of autism spectrum disorders (ASD) in offspring. Independently, shorter telomere length (TL) has also been shown to be associated with ASD in children. However, older paternal age at birth, with or without controlling for maternal age, has been associated with longer TL, a seemingly contradictory finding. Here, we conducted a retrospective cohort study among participants in the UK Biobank to disentangle associations between leukocyte TL and ASD status in adults, and the potential moderation by parental age on adult offspring's TL. Participants with ASD diagnosis (N = 87) with a mean age of 46.0 (SD 4.4) years were matched to participants without ASD diagnosis (N = 870) based on age, sex, ethnicity, education, household income, and assessment center. No statistically significant differences were seen in TL between participants with and without ASD when parental age at birth was not considered. However, there was a significant interaction between ASD diagnostic status and parental age on participants' TL, such that older paternal or maternal age at birth was more strongly associated with longer TL in participants with ASD. This study suggests that the shortened TL observed in children with ASD in previous research may partially depend on parental age at birth. Future studies tracking TL attrition before ASD diagnosis are warranted to depict temporal associations and the interacting effects of parental age at birth and ASD status on TL across the lifespan.
Autism research : official journal of the International Society for Autism Research, 2024 · doi:10.1002/aur.3258