![]() ![]() These data were collected through interviewer-administered questionnaires during the first trimester of pregnancy. Individual-level SES metrics included maternal education level, marital status, self-reported income at enrollment and receipt of public assistance. We created an SES index based on individual- and neighborhood-level metrics that are either associated with health outcomes of the child in Project Viva (e.g., maternal education, marital status, annual household income), or have been implicated as determinants of health in the literature (e.g., neighborhood-level income, use of welfare programs ). The exposure of interest in this study was SES during the prenatal period. At last, we examined associations of prenatal SES with global DNA methylation, hydroxymethylation and the ratio of the two during all three life stages, to complement EWAS findings. Then, we investigated whether associations of prenatal SES with the CpG sites of interest remained apparent during early and mid-childhood. Next, we carried out an epigenome-wide association study (EWAS) to identify differentially methylated CpG sites in cord blood associated with prenatal SES. ![]() First, we created an SES status index based on individual- and neighborhood-level characteristics during the prenatal period. Third, while a few small-scale (i.e., N 600 participants in Project Viva, a large multi-ethnic prebirth cohort in the greater Boston area. Second, many analyses are limited by relatively small sample size and restricted markers of DNA methylation (e.g., candidate gene approaches and proxies of global DNA methylation). First, the majority of published human studies have focused on individual socioeconomic metrics (i.e., household income, maternal education level), which may not reflect the real-life experience of social status. However, the existing evidence base is not without shortcomings. In humans, maternal education level (a proxy for socioeconomic position) has been associated with methylation of specific genes involved in growth and stress physiology in placentae, cord blood and infant blood, as well as with global DNA methylation in cord blood. ![]() Evidence for this notion has been documented in nonhuman primates for example, where researchers have detected differential DNA methylation at >25,000 genomic locations in placenta of low versus high ranking female baboons. The process of remethylation is sensitive to environmental disturbances, thereby earmarking the in utero period as a sensitive developmental time frame during which environmental factors – including the mother’s social environment – can impact the fetus’ long-term health. For instance, shortly after fertilization, a genome-wide demethylation event occurs, followed by systematic re-establishment of DNA methylation marks. ![]() The relevance of epigenetics in DOHaD stems from the fact that sensitive windows of development coincide with higher lability of the epigenome. Both lines of inquiry have placed a spotlight on epigenetic processes, with DNA methylation being the most widely studied, as a mechanism underlying DOHaD phenomena. Growing awareness of the Developmental Origins of Health and Disease (DOHaD) paradigm over the last two decades has forged interest in: the relevance of timing of exposures – namely, the importance of exposures during sensitive periods of development (typically, early in the life course), and biological mechanisms linking social exposures to disease risks. A longstanding and extensively-reviewed social sciences literature, in conjunction with mechanistic studies in animal models link lower social status – for example, lower socioeconomic position in humans or lower social rank in baboons – to a range of adverse physiological and psychological phenotypes. In hierarchical societies of both humans and animals, social status is a pervasive determinant of health and fitness. ![]()
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