Social disadvantage accelerates aging
Mika Kivimäki, Jaana Pentti, Philipp Frank, Fangyu Liu, Acer Blake, Solja T. Nyberg, Jussi Vahtera, Archana Singh‐Manoux, Tony Wyss‐Coray, Keenan A. Walker, Linda Partridge, Joni V. Lindbohm
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.