A considerable number of studies in epidemiology and biomedicine investigate the etiology of complex diseases by considering (self-identified) race as a relevant variable and focusing on the differences in risk among racial groups in the United States; they extensively draw on a genetic hypothesis--viz. the hypothesis that differences in the risk of complex diseases among racial groups are largely due to genetic differences covarying with genetic ancestry--that appears highly problematic in the light of both current biological evidence and the theory of human genome evolution. Is this reason for dismissing self-identified races? No. An alternative promising use of self-identified races exists, and ironically is suggested by those studies that investigate the etiology of complex diseases without focusing on racial differences. These studies provide a large amount of empirical evidence supporting the primacy of the contribution of non-genetic as opposed to genetic factors to the risk of complex diseases. We show that differences in race--or, better, in racial self-identification--may be critically used as proxies for differences in risk-related exposomes and epigenomes in the context of the United States. Self-identified race is what we need to capture the complexity of the effects of present and past racism on people's health and investigate risk-related external and internal exposures, gene-environment interactions, and epigenetic events. In fact patterns of racial self-identifications on one side, and patterns of risk-related exposomes and epigenomes on the other side, constantly coevolve and tend to match each other. However, there is no guarantee that using self-identified races in epidemiology and biomedical research will be beneficial all things considered: special attention must be paid at balancing positive and negative consequences.
Keywords: Biomedicine; Epidemiology; Epigenome; Exposome; Genetic variation; Self-identified race.
Copyright © 2015. Published by Elsevier Ltd.