摘要：Advances in stress physiology and molecular dynamics can illuminate population health inequality. The “weathering” hypothesis posits that socially structured, repeated stress process activation can accumulate and increase disease vulnerability across the life course in marginalized groups. The developmental origins of health and disease (DOHaD) hypothesis focuses on youthful programming for later life disease via epigenetic modifications to limiting uterine or early environments. Weathering and DOHaD are overlapping biopsychosocial models; yet, their emphases and implications vary. Evidence for the primacy of early development over experiences in young through middle adulthood for explaining population health inequality is lacking. By considering weathering and DOHaD together, we call for biomedical researchers to be more cautious in their claims about the social world and for a broader range of social researchers—including qualitative ones—to collaborate with them. Recent progress in theorizing and researching stress physiology’s role in chronic disease onset, epigenetics, oxidative stress, and telomere dynamics promises new understanding of the mechanistic pathways through which the social experience of race affects the health of individuals and populations. Studies find differences in epigenetic modifications among monozygotic twins that enlarge with age and lifestyle or residential differences, illustrating the continuing role of environment in translating a common genotype into different phenotypes. 1 Telomere length differences between twins become more pronounced with age, and are associated with adult social class and stress, suggesting that life experiences in adulthood have molecular impacts that affect cellular aging. 2,3 Ultimately, such findings offer new hope of identifying means to short circuit the processes—both social and biological—whereby membership in a racialized, gendered, and economically stratified society may lead to health inequalities.
