Centenarian parentage tracks with delayed hypertension across three cohorts

What happened

Adults with at least one parent who lived to 100 showed a consistently lower age-associated risk of hypertension across three longitudinal cohorts, according to a study published August 26 in *JAMA Network Open*. The researchers also observed lower hazards for death and cardiovascular disease, although those meta-analysis findings no longer met conventional statistical significance after correction for multiple comparisons.

The hypertension result was more robust. Depending on which matched UK Biobank control group was included, centenarians’ offspring had a 32% to 33% lower hypertension hazard. They were also estimated to reach a standardized 40% hypertension event probability approximately 5.2 to 5.6 years later than controls.

These findings strengthen the case for studying exceptionally long-lived families to identify biological and environmental contributors to healthspan. They do not show that having a centenarian parent guarantees longer life, establish that inherited factors caused the differences, or identify an intervention that can reproduce them.

Three cohorts, different populations

The investigators harmonized time-to-event analyses from LonGenity, the New England Centenarian Study and UK Biobank. The principal LonGenity comparison included 245 centenarians’ offspring and 235 controls. The New England study included 1,082 centenarians’ offspring and 484 controls. In UK Biobank, 992 centenarians’ offspring were compared separately with two nonoverlapping matched control groups of 992 people each.

LonGenity enrolled older Ashkenazi Jewish adults in the New York City area from 2008 through 2024. The New England study began enrollment in 1995 and later expanded across the United States, with follow-up through 2024. UK Biobank enrolled adults in England, Scotland and Wales from 2006 to 2010 and linked outcomes through 2022.

For LonGenity and UK Biobank, the main exposure was having at least one parent reach 100, while controls had no parent survive beyond 85. The New England study used a different comparison group: spouses or unrelated people from the offspring generation whose parent died at 73.

The endpoints were age at death and age at reported or recorded diagnosis of hypertension, cardiovascular disease, stroke and cancer. Cox regression models accounted for sex and education, with sensitivity analyses incorporating available factors such as smoking, socioeconomic status, alcohol use, exercise and diet.

Strongest signal was hypertension

Across the three studies, centenarians’ offspring had lower estimated hazards for death, cardiovascular disease and hypertension. Meta-analysis estimates suggested a 39% to 42% lower death hazard and a 33% lower cardiovascular-disease hazard, depending on the UK control set.

However, the investigators tested several outcomes. After false-discovery-rate correction, the pooled mortality and cardiovascular-disease associations had adjusted P values of .07 and were no longer statistically significant at the prespecified .05 threshold. The pooled hypertension hazard remained significant after that correction, while the estimated hypertension-onset delay was borderline in one of the two UK matching analyses.

Cancer incidence did not differ significantly in any cohort. Stroke findings were inconsistent: reduced hazards appeared in LonGenity and the New England study, but the available events did not support a consistent three-cohort conclusion.

What the study cannot establish

This was an observational analysis, not a genetic experiment. Families share environments, behaviors, socioeconomic circumstances and early-life exposures as well as DNA. Statistical adjustment cannot eliminate residual confounding, particularly because childhood nutrition and other early exposures were unavailable.

Disease histories in LonGenity and the New England study were primarily self-reported, whereas UK Biobank incorporated linked health records. The cohorts were also predominantly White, limiting confidence that the estimates apply across populations. Healthy-volunteer selection and the requirement that parents survive long enough to define the exposure create additional potential biases, although the authors performed sensitivity analyses intended to address them.

The practical implication is therefore about research strategy, not personal prediction. Offspring of centenarians appear enriched for factors associated with delayed hypertension and possibly broader cardiovascular resilience. Determining how much comes from inherited biology, shared environments or their interaction will require more diverse cohorts, measured genetic and molecular data, and prospective validation.