Social disadvantage accelerates aging

Social disadvantage, like advanced age, is a risk factor for a broad range of health conditions; however, whether it influences the aging process remains unclear. Here, using a multicohort approach, we investigated the associations of social disadvantage with age-related plasma proteins and age-related diseases. We found proteomic signatures of accelerated immune aging and 14 specific age-related proteins linked to social disadvantage during both early and later life. Individuals experiencing social disadvantage had an increased risk of 66 age-related diseases, with up to 39% of these associations mediated by the 14 age-related proteins (for example, DNAJB9, F2, HSPA1A, BGN). The main enriched pathway involved the upregulation of the pro-inflammatory regulator NF-κB24 and its downstream factor interleukin-8. Our findings support the hypothesis that social disadvantage throughout the life course may accelerate aging, a biological mechanism that could explain why social stratification plays such a fundamental role in determining human health.

Authors

Institutions

Publication Details

Journal
Nature Medicine
Published
2025-03-14
DOI
https://doi.org/10.1038/s41591-025-03563-4
Citations
22
Primary Topic
Tryptophan and brain disorders
Type
article
Field-Weighted Citation Impact
12.71

Funders

Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Social disadvantage accelerates aging

Philipp Frank, Joni V. Lindbohm, Jaana Pentti, Alexandre Blake et al.
22 citations
Nature Medicine
Tryptophan and brain disorders
12.71
article

Social disadvantage accelerates aging

Philipp Frank, Joni V. Lindbohm, Jaana Pentti, Alexandre Blake, Tony Wyss‐Coray, Mika Kivimaki B, Solja T. Nyberg, Jussi Vahtera, Linda Partridge, Archana Singh‐Manoux, Keenan A. Walker, Fangyu Liu
article en
22 citations

Abstract

Social disadvantage, like advanced age, is a risk factor for a broad range of health conditions; however, whether it influences the aging process remains unclear. Here, using a multicohort approach, we investigated the associations of social disadvantage with age-related plasma proteins and age-related diseases. We found proteomic signatures of accelerated immune aging and 14 specific age-related proteins linked to social disadvantage during both early and later life. Individuals experiencing social disadvantage had an increased risk of 66 age-related diseases, with up to 39% of these associations mediated by the 14 age-related proteins (for example, DNAJB9, F2, HSPA1A, BGN). The main enriched pathway involved the upregulation of the pro-inflammatory regulator NF-κB24 and its downstream factor interleukin-8. Our findings support the hypothesis that social disadvantage throughout the life course may accelerate aging, a biological mechanism that could explain why social stratification plays such a fundamental role in determining human health.

Nature MedicineVol. 31(5)
Broad Institute (US), National Institutes of Health (US), University of Helsinki (FI), Harvard University (US), Inserm (FR), University of Turku (FI), Neurosciences Institute (US), Université Paris Cité (FR), Turku University Hospital (FI), Sorbonne Paris Cité (FR), Mathematical Institute of the Slovak Academy of Sciences (SK), National Institute on Aging (US), MRC Unit for Lifelong Health and Ageing (GB), University College London (GB), Stanford University (US)
Wellcome Trust, Päivikki ja Sakari Sohlbergin Säätiö, Medical Research Council, National Institute on Aging, National Heart, Lung, and Blood Institute
Reduced inequalities
Openalex Percentile: Top 1%
Tryptophan and brain disorders
12.71
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.