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Psychological adversities are associated with accelerated epigenetic aging: systematisk översikt and metaanalys
Loneliness, depression, and stress were each associated with faster epigenetic aging across 22 studies.
Guo and colleagues reviewed 22 studies of psychological adversity and DNA-methylation age acceleration from midlife onward. Fifteen studies met the review’s high-quality classification. The pooled associations were consistent for second-generation clocks, especially PhenoAge and GrimAge. Loneliness was associated with higher age acceleration, with β=0.07 and 95% CI 0.06 to 0.08. Depression showed β=0.08 and 95% CI 0.04 to 0.13. Stress showed β=0.10 and 95% CI 0.03 to 0.16. Heterogeneity was low for loneliness, moderate for depression, and substantial for stress. The paper addresses a longevity-relevant biomarker, not lifespan or disease incidence. It does not show that distress causes faster aging. It also does not show that therapy or stress reduction reverses a clock. The authors identify limited evidence for anxiety and underrepresentation of non-Western populations. The useful result is the consistency across different adversities and second-generation clocks. The practical limit is that the underlying studies are observational and the effect sizes are small. This supports psychosocial health as a plausible aging correlate, not as a validated anti-aging treatment target.
Psychosocial stress, depression, and loneliness are each associated with accelerated aging from midlife onward. Notable gaps include the lack of studies examining anxiety and underrepresentation of non-Western population. Whether alleviating psychological adversities translates into decelerated aging trajectories requests future intervention studies.
The 22 included studies are observational. Associations do not establish causality, and epigenetic clocks are not validated surrogate endpoints for lifespan. The analysis found substantial heterogeneity for stress and limited evidence for anxiety and non-Western populations.
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