LAUSR

The consistent relationship between socioeconomic status (SES) and health has been widely covered in both the popularmedia and scientific journals. These articles argue that physical health inequalities are caused by material disadvantage directly (e.g., access tomedical care) or indirectly (e.g., chronic environmental stress). Such explanations account for differences between those who have resources and those who do not, but they do not account for the finely stratified health differences that exist across the entire range of SES. Recent theories to explain the SES–health gradient have grappled with limitations and contradictions of early models and have implicated very different pathways to explain the gradient. For example, articles in differential epidemiology have argued that individual differences are the “fundamental cause” of the gradient, acting through genetic sources. Other perspectives such as the risky family model implicate the early home environment. Little research has applied behavior genetic modeling to understanding the sources of the SES–health gradient. The purpose of this article is to narrow the scope of fundamental causes by untangling the sources of variance associated with the gradient. Specifically, we decompose the gradient into genetic (a2), shared environmental (c2), and nonshared environmental (e2) pathways (ACE), using data from the National Longitudinal Survey of Youth. Monozygotic-twin, dizygotic-twin, full-sibling, half-sibling, and cousin pairs from validated kinship links are used in the current study (4,018 pairs; Rodgers et al., 2016). Three stages of analyses were conducted: (a) univariate ACE models, (b) bivariate correlated factors ACE models, and (c) trivariate correlated factors ACE models. Only the final trivariate model is reported here (see Figure 1). The estimates of a2, c2, and e2 were similar across analysis stages. The genetic correlation between SES and physical health (PCS) was .66 (95% CI [.41, .98]),