Epigenetics: Understanding Race through Biological Disparities

It is widely accepted that race is a social, rather than biological, construct (Laden, 2016). How, then, do biological disparities exist among socially defined races? The answer lies in the nascent field of epigenetics, which studies the environmental influences that can change gene expression and therefore biological functions. The primary mechanisms through which epigenetic changes occur are DNA methylation and histone modifications, both methylation and acetylation (Kuwaza & Sweet, 2009). DNA methylation involves the binding of a methyl group (–CH3) to a CpG site composed of adjacent cytosine and guanine nucleotide bases. CpG sites often occur in the promoter region of a gene, which signals an enzyme called RNA polymerase in the cell to

Psychosocial effects of racism involve social occurrences that have psychological effects. These psychological effects can in turn have physiological implications, primarily through chronic stress and the resulting elevated levels of stress hormones, such as cortisol. The stress associated with repeated and unrelenting discrimination as well as the anticipation and internalization of that racism has far reaching impacts on all Black Americans (Williams & Mohammed, 2013). For poor Black Americans, the stress associated with racism is compounded with that of poverty. This chronic high level of cortisol circulated in the body leads to a physiological phenomenon known as biological weathering, in which the accumulation of stressors over time leads to a gradual wearing down of the body’s systems and accelerated biological aging (Sullivan, 2013). Mechanistically, weathering is associated with chronic inflammation that can lead to tissue damage and a higher risk for chronic and age related conditions such as cardiovascular disease and Alzheimer’s (Simons et al., 2016). Although the exact mechanism of epigenetic modification is not yet known, weathering can be measured by methylation at various CpG sites across the genome (Simons et al.,

According to research done at the Tufts University Friedman School of Nutrition, through various mechanisms, vitamins such as folate, B-12, methionine, choline, and betaine function as methyl and acetyl donors, catalyze DNA methylation reactions, and act as substrates in histone modifications (Choi & Friso, 2010). Without these nutrients, epigenetic modifications cannot occur, and because epigenetic methylation and acetylation can change the expression of genes in beneficial ways, this can create lasting health ramifications, especially for the fetuses of those who are pregnant. For example, a study in which pregnant sheep were fed a folate-deficient diet during gestation correlated this nutrient poor diet with obesity, insulin resistance, and hypertension in the offspring (Sinclair et al., 2007). Interestingly, these effects were more obvious in males. This phenomenon could be one contributor to the larger difference in life expectancy between Black and White men than women. Similarly, choline deprivation during embryonic development has shown to cause hypermethylation within the calbindin 1 (calb1) gene in mice, impairing development of the hippocampus, a brain structure important in the formation and storage of memories (Choi & Friso, 2010). Thereby, nutrient deprivation can also