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Socioeconomic disadvantage and inflammatory processes across the lifecourse: mega- and meta-analytic approaches

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In the United States, those who have lower income, education level, and occupational prestige, are more likely to develop, have worse symptoms of, and die from a wide range of chronic diseases. This phenomenon prompted much research trying to delineate the underlying pathways, and inflammation has been highlighted as a key factor for it is predictive of the very chronic diseases disadvantage is linked. Indeed, accumulating evidence suggests that greater socioeconomic disadvantage is linked to higher levels of inflammation. However, three major gaps in the literature limit our understanding of the theoretical basis of this association. First, most extant studies have focused on circulating markers of inflammation, which precluded mechanistic understanding of how the body comes to sustain a level of inflammation. Second, while conceptual models have postulated a broad array of underlying mechanisms, few studies have formally tested these indirect effects. Third, despite consensus that pathogenesis processes begin early in life and can vary across the lifecourse, empirical research has not tested these propositions. Accordingly, we sought to (a) examine whether disadvantage exposed during childhood and adolescence was associated with both functional inflammatory processes and circulating inflammation, (b) evaluate psychological stress and adiposity as underlying pathways, and (c) delineate whether the disadvantage-inflammation link vary across the lifecourse. To address these aims, we leveraged the fact that extant data or literature has utilized children, adolescent, and adult samples to build our own large lifecourse samples using mega- and meta-analytical techniques. Across three studies, we found that socioeconomic disadvantage was associated with both functional inflammatory processes (i.e., exaggerated response to challenges that was less able to shut down) as well as low-grade inflammation (i.e., higher levels of circulating inflammation markers). In addition, these associations were mediated by heightened psychological stress and excess adiposity respectively, and that these pathways varied across the lifecourse. Specifically, when targeting functional inflammatory processes, effects of disadvantage were stronger during earlier periods of life and dissipated across the lifecourse; whereas when targeting low-grade inflammation, effects of disadvantage were weaker during earlier periods of life and strengthened across the lifecourse. Together, these findings advanced mechanistic understanding of socioeconomic disparities with an emphasis of developmental timing, which has broader implications for theory-building and clinical practice.

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