Long-Lived Parents May Signal Slower Biological Ageing, Swedish Study Finds

How long your parents lived may reveal more about your own biology than any genetic test currently on the market. That is the striking implication of a new study from the University of Gothenburg, published in GeroScience, which followed more than 1,100 Swedish 70-year-olds over six years and compared two very different ways of measuring inherited longevity: the ages to which their parents survived, and modern polygenic longevity scores built from millions of genetic variants. The results suggest that simply asking patients how old their parents were when they died could serve as a cheap, powerful screening tool for identifying who is ageing fastest and who is most at risk of age-related disease.

The research draws on the Gothenburg H70 Birth Cohort Study, one of the longest-running population studies of ageing in the world. In 2014 to 2016, researchers comprehensively examined 70-year-olds born in 1944 who were living in Gothenburg, achieving a 72 percent response rate. Participants underwent extensive interviews and clinical assessments covering education, income, childhood family economic circumstances, mental health, cardiovascular disease, anthropometry, and laboratory measures, and they provided blood samples for genotyping. A follow-up examination was conducted five to eight years later, with a mean follow-up of roughly six years and a response rate of 77.6 percent among survivors. After excluding participants with missing parental data and those whose parents died before age 41, likely from causes unrelated to biological ageing such as accidents, the final baseline sample comprised 1,126 individuals, 523 men and 603 women.

The researchers classified parental longevity, or PL, into three groups. Participants were considered to have high parental longevity if both parents survived to age 85, which applied to 17.2 percent of the sample; medium parental longevity if one parent reached 85, applying to 43.3 percent; and low parental longevity if neither parent did, applying to 39.4 percent. The age-85 threshold was chosen deliberately: the participants’ parents were born around 1920, when cohort life expectancy was only about 74 years, so reaching 85 represented genuinely exceptional survival for that generation. Alongside this family-history measure, the team constructed two polygenic longevity scores, or PGLSs, using genome-wide association summary statistics from a large international meta-analysis of longevity genes, combined with a Bayesian shrinkage method and a European ancestry reference panel. One score included variants in the APOE locus, a gene region strongly tied to age-related disease and mortality, while the other excluded it.

At baseline, both higher parental longevity and higher polygenic scores were associated with more favourable social circumstances. People with long-lived parents, and people with higher genetic longevity scores, had spent longer in education, reported better childhood family economic conditions, and enjoyed higher current household income. Both measures were also linked to vascular health: high parental longevity and higher scores on the APOE-inclusive polygenic score were associated with less hypertension, and higher polygenic scores were inversely related to myocardial infarction, a finding the authors report as novel. But the two measures diverged sharply beyond that point, and the divergence is where the study becomes genuinely provocative.

Parental longevity, unlike the genetic scores, was associated with a broad constellation of biological advantages. Participants with high parental longevity had better scores on the Mini-Mental State Examination, higher levels of total cholesterol, HDL cholesterol and LDL cholesterol, lower body mass index, lower homocysteine, and lower levels of the inflammatory markers interleukin-6 and C-reactive protein. They were also less likely to be current smokers. Participants with even one long-lived parent showed better cognition, higher cholesterol, lower homocysteine and less smoking than those with two short-lived parents. The polygenic scores, by contrast, captured mainly the socioeconomic and cardiovascular factors and little else. Strikingly, the two measures showed no statistical association with each other at all, whether parental longevity was analysed as groups, as the mean of both parents’ ages, or as mothers’ and fathers’ ages separately.

Some of these findings challenge conventional assumptions. The higher total cholesterol and LDL cholesterol among offspring of long-lived parents may seem paradoxical, but they echo previous research, including studies suggesting that rising cholesterol in late life is associated with reduced dementia risk and lower mortality in older adults. Cholesterol is a precursor to steroid hormones essential for metabolism and immune function, and the authors caution that the so-called cholesterol paradox in late life should be interpreted carefully, noting that lipid-lowering therapy did not appear to explain the association and that frailty was rare in this relatively young-old population. Lower homocysteine among those with long-lived parents is also notable, since elevated homocysteine is linked to folate and vitamin B deficiency, endothelial dysfunction, atherosclerosis, cardiovascular events, and dementia.

Perhaps the most forward-looking result emerged at follow-up. Plasma phosphorylated-tau 217, or pTau217, is one of the most accurate blood biomarkers currently available for Alzheimer’s disease pathology, and its levels are known to rise steeply with age. In the longitudinal analyses, participants with high parental longevity showed significantly less increase in pTau217 over the six years than those whose parents had both died before 85. This suggests that Alzheimer’s pathology may establish itself later, or accumulate more slowly, in people with long-lived parents, potentially delaying the onset of dementia. Consistent with this, the high-parental-longevity group also had higher baseline MMSE scores. No such longitudinal associations were observed for the polygenic scores, and neither measure was associated with plasma neurofilament light, another age-sensitive neurodegeneration marker.

The authors are careful about causality. Lower interleukin-6 and C-reactive protein in offspring of long-lived parents may reflect healthier lifestyles and better overall health rather than a direct determinant of longevity, although low-grade inflammation, sometimes called inflammaging, is considered a central driver of accelerated ageing, dementia, cardiovascular disease and mortality. Sex also mattered: several associations, including those involving C-reactive protein, neurofilament light, creatinine and triglycerides, were significant only in women. The team also acknowledges limitations, including self-reported parental ages, possible selective survival bias, a predominantly white and age-homogeneous sample, and the smaller follow-up cohort, and they report both uncorrected and false-discovery-rate-corrected statistics, noting that some findings, including those on inflammatory markers and pTau217, did not survive multiple-comparison correction.

Nevertheless, the overall pattern is coherent and biologically plausible. Polygenic longevity scores, in their current form, appear to capture only a narrow slice of the biology of ageing, likely because longevity’s genetic architecture is highly heterogeneous and heavily environment-dependent. Parental longevity, by contrast, seems to summarise everything at once: inherited genetics, shared early environment, transgenerational social advantage, and accumulated lifestyle influences. The authors conclude that asking about parental lifespan could serve as a simple, inexpensive proxy for biological ageing, suitable for routine health assessments of older adults to flag individuals who might benefit from preventive screening for hypertension, cognitive decline, inflammation and emerging Alzheimer’s pathology. In an era of billion-dollar biomarker pipelines, the humble family history may still be one of medicine’s most underrated diagnostic instruments.

Subject of Research: Parental longevity and polygenic longevity scores in relation to ageing-related social, cardiovascular, inflammatory and neurodegenerative factors in 70-year-olds

Article Title: Parental longevity and polygenic longevity scores in relation to ageing-related factors in a population of 70-year-olds followed over six years: The Gothenburg H70 Birth Cohort Study

Article References: Seidu, N. M., Rydén, L., Skoog, J., Samuelsson, J., Kern, S., Waern, M., Zetterberg, H., Holstege, H., Erhag, H. F., Westman, E., & Skoog, I. (2026). Parental longevity and polygenic longevity scores in relation to ageing-related factors in a population of 70-year-olds followed over six years: The Gothenburg H70 Birth Cohort Study. GeroScience. https://doi.org/10.1007/s11357-026-02501-7

Image Credits: AI Generated

DOI: 10.1007/s11357-026-02501-7

Keywords: parental longevity, polygenic longevity score, ageing, GeroScience, APOE, pTau217, Alzheimer's disease, inflammation, cholesterol, cardiovascular risk, socioeconomic status, H70 cohort