Early adversity predicts greater disease risk later in life across numerous outcomes; however, biological pathways are incompletely understood. Previous studies have implicated altered immune function in these relationships, specifically chronic inflammation, which is associated with both adversity and multiple health outcomes, including cardiovascular disease (CVD) and all-cause mortality. While these studies have been informative, inflammation is only one component of the immune system, and there is suggestive evidence that adversity might have broader effects besides heightened inflammation that impact later life health. The immune system consists of two subsystems, non-specific innate immunity and specific acquired immunity. Chronic inflammation represents up-regulation of innate immunity, while studies linking adversity to acquired immunity tend to report suppressive effects. Research in evolutionary biology and ecological immunity has suggested that an up-regulation of innate immunity and down-regulation of acquired immunity could be an adaptive “future-discounting” strategy in harsh and unpredictable environments, as innate immune activation can provide short term benefits but comes with long-term costs to health and longevity, while acquired immunity provides less immediate benefits but enhances future defense.

Consistent with the above model, we have recently found evidence that early adversity (e.g., low SES) in the Cebu Longitudinal Health and Nutrition Survey (CLHNS) predicts a lower percentage of circulating acquired immune cells and higher percentage of innate inflammatory cells in young adulthood. Here we propose to expand on this work by testing whether similar associations are found in the ALSPAC cohort, using immune cell composition data derived from both flow cytometry and DNA methylation (DNAm) at multiple ages.