Epigenetics: An Emerging Tool for Health Equity SciencePosted on by
A recent review provides recommendations to improve the scientific investigation of the associations between epigenetic markers, socioeconomic status, and adverse health outcomes.
Health equity means that everyone has the opportunity to be as healthy as possible. Health equity science studies the association between social determinants of health (SDOH) and adverse health outcomes. SDOH refer to environmental and social conditions in which people live their daily lives. SDOH have been associated with adverse health outcomes such as cardiovascular disease and diabetes. CDC is transforming its public health research, surveillance, and implementation science efforts to enhance the study of markers of health inequities and to identify and address the drivers of disparities in health outcomes.
The Promise of Epigenetics: Interface Between Biology and SDOH
The biological connections between SDOH and adverse health outcomes are not fully understood. Could the field of epigenetics help us gain better insight into these connections? Epigenetics involves biological processes such as DNA methylation or histone modification that do not change the genome sequence but alter gene expression. Epigenetic markers have been shown to be affected by natural, built, and social environmental exposures such as nutrition, stress, and air pollution. Epigenetic markers may shed light on potential causal links between SDOH and adverse health outcomes and are potentially modifiable, providing new approaches to therapeutics (e.g., cancer).
Many types of measurements are used to describe SDOH, including socioeconomic status (SES), discrimination, neighborhood exposures, etc. In a recent systematic review, Evans et al. found that SES was used most often in epigenetic studies of SDOH. While epigenetics provides an exciting approach for studying the health effects of SES, both the SES and epigenetic components of such studies face substantial methodological challenges.
The Challenges of Epigenetics: Methodologic Issues in Measurement and Interpretation
SES is not a straightforward concept. It comprises many different factors, including education, occupation, household status, neighborhood income, etc. Researchers use these factors, alone or in various combinations, to measure SES, with education used most often. Each factor has both advantages and disadvantages; for example, education is usually stable after adulthood but has varying social meanings and effects in different cultures and time periods. While income provides information about access to goods and services, it varies over time and has a higher nonresponse rate on questionnaires. Research has also provided evidence that some individual markers of SES may be associated with health outcomes while other SES markers are not. In addition, SES can be measured at the individual or the community level. For example, the Centers for Disease Control/Agency for Toxic Substances and Disease Registry use a social vulnerability index (a composite of 15 United States census variables) to identify communities impacted by external and social stresses on human health. Nevertheless, misclassifying the SES and other SDOH of individuals in epigenetic studies—for example, by classifying all residents as moderate-income based on the average income in their neighborhood—could obscure an epigenetic association.
Epigenetic markers can change over time and can also be inherited. As a result, it can be difficult to determine if an epigenetic marker is the result of SES, the health outcome of interest, an indirect exposure from a previous generation, or another factor. Consider for example a study that collects epigenetic data from adults to investigate the effects of low SES in childhood. The cross-sectional study design makes it difficult to determine whether observed epigenetic differences are due to low SES in childhood or to the development of a health outcome associated with low SES.
Epigenetic markers also differ among various tissues. Blood is commonly used to measure global DNA methylation patterns. However, differences in blood methylation patterns may not reflect differences in brain cells or liver cells. For example, environmental exposures could impact epigenetic markers in liver cells while having little or no impact on cells in the blood.
Improving Studies of SES, Epigenetics, and Health Outcomes
A recent review by Cerutti J et al. provides recommendations to improve investigations of epigenetic links between SES and health outcomes. The authors recommended developing more precise measures of SES by using consistent terminology, collecting a variety of measurements across individual and community levels, and choosing appropriate measurements for each population. For example, the authors prioritize the use of wealth as a more accurate SES indicator in elderly populations. They also suggest designing epigenetic studies in lower SES countries or across broader SES gradients to increase the probability of finding true associations. Another important recommendation is to analyze longitudinal data containing both multiple SES and epigenetic measurements over time.
These recommendations provide a springboard for designing better epidemiologic studies of SES and health outcomes and help disentangle the role of epigenetics in moderating or mediating health effects of social and economic exposures. New insights gained from epigenetic studies in more diverse populations may help mitigate the adverse health effects associated with SES.
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