Prolonged psychosocial stress is associated with accelerated biological ageing, visible through epigenetic clocks, telomere shortening and cellular senescence. The relationship is likely causal, but the exact magnitude differs between studies and direct causality in humans has not yet been fully demonstrated for some mechanisms.
Multiple studies show that prolonged psychosocial stress accelerates biological ageing. This can be measured using so-called 'epigenetic clocks': mathematical models that estimate how old your cells are biologically, based on DNA methylation (a chemical marking on the DNA). Early-childhood adversity, an accumulation of stressful experiences and a low socioeconomic status are associated, across various studies, with a higher biological age than your calendar age would predict. Findings do differ between studies and measurement methods, however, so the exact size of the effect has not been established conclusively (PMID 32204828).
Beyond epigenetic ageing, prolonged stress also accelerates other measurable ageing processes. Telomeres, the protective 'caps' at the ends of chromosomes, shorten more quickly. Cells enter a state of 'cellular senescence' earlier: they stop dividing but continue to secrete pro-inflammatory substances. Both animal experiments and large population studies in humans support the link between persistent stress and an increased risk of diabetes and fatty liver disease. Less stress was associated in those studies with fewer new cases of these conditions (PMID 36224493).
In population groups that face a combination of biological, psychosocial, socioeconomic and environmental stressors, such as poverty or structural inequality, age-related disease occurs earlier and more severely. Researchers at the National Institute on Aging call this 'weathering': the body ages faster, as it were, under the cumulative burden of stress. Measurable signs include elevated oxidative stress (cell damage caused by reactive oxygen compounds), earlier DNA damage and higher inflammatory markers. This represents an association; full proof of direct causality is still lacking (PMID 34883202).
At the cellular level, the protein SIRT7 also plays a role. This protein acts as a guardian of cells' genetic integrity and helps cells cope with stress. Prolonged exposure to stress can undermine the functioning of SIRT7, which appears to accelerate ageing and increases the risk of age-related conditions. This evidence comes primarily from laboratory and animal research, however; whether the same applies in humans has not yet been sufficiently demonstrated (PMID 37676263).
There is good news as well: a large American study involving nearly 24,000 participants shows that people with better cardiovascular health are biologically younger than their calendar age. Every 10-point increase in a cardiovascular health score corresponds to an average of 1.14 years lower biological age. Oxidative stress turned out to be an intermediate step in this relationship: less chronic physical burden, partly through healthy lifestyle habits, appears to measurably slow biological ageing (PMID 37813096).
Five studies were used: two epidemiological reviews/meta-analyses on epigenetic ageing and metabolic diseases, an NIA review on 'weathering', a cell/animal-model study on SIRT7, and a large cross-sectional population study (n~24,000). The evidence is predominantly associational or based on animal models; randomised controlled trials in humans on stress reduction and biological ageing were not provided.