We found that men had higher levels

We found that men had higher levels of AL scores than women across every age category, a novel finding among US Hispanics/Latinos of diverse backgrounds. In analyses of specific AL components, metabolic markers were generally higher in men and inflammatory markers were higher in women. Sex differences in components of AL have been previously reported in other cohorts. For instance, results from the Social Environment and Biomarkers of Aging Study in Taiwan, the Wisconsin Longitudinal Survey, and the MacArthur studies of successful aging demonstrated that men had higher cardiovascular/ metabolic markers whereas women had a disadvantage in markers of sympathetic nervous system (SNS) and HPA axis functioning (Goldman et al., 2004). Findings from NHANES (1998–2006) showed a higher overall cumulative burden of carboxypeptidase a in women than in men, which tended to decline with age (Yang & Kozloski, 2011). Similarly, in the Boston Puerto Rican Study, women exhibited higher levels of inflammatory markers than men (Mattei et al., 2010). It\'s unclear to what extent sex differences in AL and its components are driven by genetic, hormonal, or contextual influences. There is, however, some empirical evidence from the Texas City Stress and Health Study to show that sex modifies the relationship between duration of residence in a stressful environment and AL (Mair, Cutchin, & Kristen Peek, 2011), suggesting that men and women may manifest stressors differently. Additional work is necessary to further understand the complex inter-relationships between sex, stressors, AL and its components in Hispanics/Latinos. Our study had several limitations. The cross-sectional design precludes any inferences of a causal effect. Related to this is the possibility that the differences in AL across groups might be influenced, in part, by age and period effects such as shifts in immigration policies. For instance, a rise in late-age immigration due to US admission policies since 1981 (Carr & Tienda, 2013) may create imbalances in the cohort related to family reunification/cohesion and lead to health consequences. Disentangling age, period, and cohort effects on AL and subsequent health outcomes is a target of future study in HCHS/SOL when longitudinal data are made available. Secondly, we did not have neuroendocrine markers available for analyses, which have been previously included in studies of AL. This reduces the ability to compare our findings with some prior studies that included a different set of markers of AL.
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Introduction Stratification scholars widely acknowledge that social status dimensions, such as race/ethnicity, gender, and socioeconomic status (SES), structure lived experience by constraining or bolstering resources, opportunities, and life chances. If we view health as a life chance (Haas, 2006), then it becomes clear that these dimensions also structure susceptibility and resilience to illness. As a result, racial/ethnic, gender, and socioeconomic disparities in health have been increasingly recognized as both consequences of and contributors to social stratification processes across the life course (Haas, 2006; House et al., 1994). What is less well acknowledged is the need for a multidimensional—or intersectional—approach to understanding social stratification generally and the social stratification of health in particular. Instead, it is more common for race/ethnicity, gender, and other dimensions of inequality to be treated as separate categories of analysis or, when examined together, viewed as additive rather than mutually reinforcing and inseparable. Likewise, considering the inextricable linkages among social status dimensions is an uncommonly pursued approach to health disparities research. This neglect may obscure the social processes underlying these disparities. To demonstrate the utility and importance of an intersectional approach to longitudinal research on health disparities, we use the exemplar of hypertension. In the U.S., hypertension is the leading cause of cardiovascular disease and a major contributor to high medical and work productivity loss costs, home productivity loss, and consequent family financial and caregiving burdens (Druss et al., 2001; Heidenreich et al., 2011; Kessler, Ormel, Demier, & Stang, 2003; Merikangas et al., 2007). Racial/ethnic and gender disparities in hypertension prevalence have been well-documented, suggesting that it is a key contributor to inequalities in life chances. Although many studies have been conducted to identify determinants of hypertension, our understanding of the determinants of hypertension disparities remains incomplete (Flack, Ferdinand, & Nasser, 2003; Minor, Wofford, & Jones, 2008; Rieker, Bird, & Lang, 2010). Not only have previous studies frequently considered race/ethnicity and gender as separate (rather than intersecting) categories of analysis (see the Canadian study by Veenstra (2013) for an exception), but they also have focused primarily on contemporaneous risk factors rather than risk histories. Moreover, much of what we know about gender and racial/ethnic differences in hypertension—and their age patterns—comes from cross-sectional data (e.g., Cutler et al., 2008; Geronimus, Bound, Keene, & Hicken, 2007), which are not well-suited for testing hypotheses about group differences in intra-individual change with age.