Disease-risk variants linked to more children and shorter lives
An observational analysis of human genetic data across 62 diseases found signs that natural selection may have favored risk variants also linked to having more children.
Limit: Number of children was a proxy for reproductive success
Edited by Boris Djordjevic · AgingResearch.News
Researchers conducted an observational analysis of genetic data from people of predominantly European ancestry, covering 62 diseases, lifespan and number of children. Longevity estimates used nearly one million parental lifespans from about 450,000 UK Biobank participants. On average, disease-risk variants—differences in DNA—were associated with shorter lives and more children.
Variants linked to both disease risk and more children appeared to have been favored by natural selection over the past 50,000 years. Mendelian randomization, a method using genetic variants to assess relationships between traits, also linked inherited disease risk to shorter lifespan, but found no robust evidence for an effect on fertility. Among UK Biobank participants with high combined genetic disease risk, affected people had more children than unaffected people for most diseases. Early-onset diseases showed the opposite pattern.
Why it matters
The authors said trade-offs between reproduction and lifespan could help explain why disease-risk variants persist across generations.
Caveats
These observational genetic analyses cannot establish cause and effect, and number of children served as a proxy for reproductive success. The findings may not extend beyond the predominantly European-ancestry populations studied.
The paper
Universitat Pompeu Fabra
Nature Ecology & Evolution, Jul 21, 2026, Open access
