We work from a life course perspective and identify several reasons to expect age and gender differences in the link between marital quality and health. We present growth curve evidence from a national longitudinal survey to show that marital strain accelerates the typical decline in self-rated health that occurs over time and that this adverse effect is greater at older ages. These findings fit with recent theoretical work on cumulative adversity in that marital strain seems to have a cumulative effect on health over time-an effect that produces increasing vulnerability to marital strain with age. Contrary to expectations, marital quality seems to affect the health of men and women in similar ways across the life course.

The purpose of this study was to examine the association between socioeconomic status (SES) and leukocyte telomere length (LTL) – a marker of cell aging that has been linked to stressful life circumstances – in a nationally representative, socioeconomically and ethnically diverse sample of US adults aged 20–84. Using data from the National Health and Nutrition Examination Survey (NHANES), 1999–2002, we found that respondents who completed less than a high school education had significantly shorter telomeres than those who graduated from college. Income was not associated with LTL. African-Americans had significantly longer telomeres than whites, but there were no significant racial/ethnic differences in the association between education and telomere length. Finally, we found that the association between education and LTL was partially mediated by smoking and body mass index but not by drinking or sedentary behavior.

Some recent studies suggest that sexual minorities may have worse health-related outcomes during adolescence because they report lower levels of family connectedness, a key protective resource. Using data from wave 3 of the National Longitudinal Study of Adolescent Health (n = 11,153; 50.6% female; mean age = 21.8 years), this study extends prior research on adolescents to young adults. We examine whether lesbian, gay, and bisexual (LGB) young adults report lower levels of parental support than their heterosexual peers and whether differences in parental support help explain why LGB young adults tend to have worse health-related outcomes. We find that lesbian and bisexual women report lower levels of parental support than heterosexual women and that gay men report lower levels of parental support than bisexual and heterosexual men. Compared to heterosexual women, lesbian and bisexual women have higher odds of suicidal thoughts and recent drug use; bisexual women also have higher odds of elevated depressive symptomatology and heavy drinking. Gay men have higher odds of suicidal thoughts than heterosexual men. With the exception of heavy drinking, parental support either partially or fully mediates each of the observed associations. Even though the transition from adolescence to young adulthood is characterized by increased independence from parents, parental support remains an important correlate of health-related outcomes during this stage of life. Sexual minorities report lower levels of parental support during young adulthood, which helps explain why they have worse health-related outcomes. Interventions designed to strengthen relationships between LGB young adults and their parents could lead to a reduction in health disparities related to sexual orientation.

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y Co-first authors. Keywords: DNA methylation, gene expression, inflammation, socioeconomic status, stress reactivityEpigenetic changes, such as DNA methylation, have been hypothesized to provide a link between the social environment and disease development. The purpose of this study was to examine associations between life course measures of socioeconomic status (SES) and DNA methylation (DNAm) in 18 genes related to stress reactivity and inflammation using a multi-level modeling approach that treats DNAm measurements as repeat measures within an individual. DNAm and gene expression were assessed in purified monocytes for a random subsample of 1,264 nonHispanic white, African-American, and Hispanic participants aged 55-94 from the Multi-Ethnic Study of Atherosclerosis (MESA). After correction for multiple testing, we found that low childhood SES was associated with DNAm in 3 stressrelated genes (AVP, FKBP5, OXTR) and 2 inflammation-related genes (CCL1, CD1D), low adult SES was associated with DNAm in one stress-related gene (AVP) and 5 inflammation-related genes (CD1D, F8, KLRG1, NLRP12, TLR3), and social mobility was associated with DNAm in 3 stress-related genes (AVP, FKBP5, OXTR) and 7 inflammation-related genes (CCL1, CD1D, F8, KLRG1, NLRP12, PYDC1, TLR3). In general, low SES was associated with increased DNAm. Expression data was available for 7 genes that showed a significant relationship between SES and DNAm. In 5 of these 7 genes (CD1D, F8, FKBP5, KLRG1, NLRP12), DNAm was associated with gene expression for at least one transcript, providing evidence of the potential functional consequences of alterations in DNAm related to SES. The results of this study reflect the biological complexity of epigenetic data and underscore the need for multi-disciplinary approaches to study how DNAm may contribute to the social patterning of disease.

This study explores whether the interplay of health problems and school environment predicts academic failure, an individual event with consequences for the life course, as well as for society at large. This exploration proceeds in three steps: 1) we examine whether physical and mental health problems are an academic risk factor during secondary school; 2) we investigate the academic mechanisms underlying this risk status; and 3) we explore whether this risk status varies by school context. A series of logistic regressions reveals that self-rated health and emotional distress are both associated with greater likelihood of failing one or more classes in the next year and that absenteeism, trouble with homework, and student-teacher bonding account for much of these associations. Associations of physical and mental health problems with academic failure vary only slightly across schools, however. We discuss the implications of these findings for both research and policy and argue that the examination of overlap among different domains of adolescent functioning can advance the sociological understanding of health, education, and social problems in general.Academic performance, including academic failure, is often viewed in narrow terms, as an individual behavior limited to the early life course. However, academic performance has implications that play out across life stages and on multiple levels. On the individual level, academic struggles predict short-term problem behavior and dropout, and can derail educational and occupational trajectories well into adulthood (Crosnoe 2002b;Miller 1998;Rosenbaum, DeLuca, and Miller 1999). On the institutional level, academic problems among students can create disorder and undermine the general mission of schools (Steinberg, Brown, and Dornbusch 1996). On the population level, widespread academic failure influences rates of fertility, mortality, marriage, and unemployment through its relation to educational attainment and the development of human capital (Becker 1962;Mirowsky and Ross 2003b;Wilson 1978). Thus, what appears merely to be an aspect of the adolescent experience actually has far-reaching consequences across a variety of social phenomena.Educational research has identified numerous family, peer, and economic factors that contribute to academic failure (Schneider and Coleman 1993;Steinberg et al. 1996). Often lost in this inquiry, however, is consideration of physical and mental health problems for academic performance in secondary school. The relative lack of attention to health is unfortunate given that related literatures strongly suggest the possibility that health problems disrupt academic functioning. For example, research on adult populations has shown that mental and physical health problems negatively affect work performance (Dewa and Lin 2000). This study suggests that performance in the educational system-the social institution most directly equivalent to the labor force for adolescents-is also likely affected by health problems. Moreover, small- NIH...

Living in a disadvantaged neighborhood is associated with poor health outcomes even after accounting for individual-level socioeconomic factors. The chronic stress of unfavorable neighborhood conditions may lead to dysregulation of the stress reactivity and inflammatory pathways, potentially mediated through epigenetic mechanisms such as DNA methylation. We used multi-level models to examine the relationship between 2 neighborhood conditions and methylation levels of 18 genes related to stress reactivity and inflammation in purified monocytes from 1,226 participants of the Multi-Ethnic Study of Atherosclerosis (MESA), a population-based sample of US adults. Neighborhood socioeconomic disadvantage, a summary of 16 census-based metrics, was associated with DNA methylation [False discovery rate (FDR) q-value ≤ 0.1] in 2 out of 7 stress-related genes evaluated (CRF, SLC6A4) and 2 out of 11 inflammation-related genes (F8, TLR1). Neighborhood social environment, a summary measure of aesthetic quality, safety, and social cohesion, was associated with methylation in 4 of the 7 stress-related genes (AVP, BDNF, FKBP5, SLC6A4) and 7 of the 11 inflammation-related genes (CCL1, CD1D, F8, KLRG1, NLRP12, SLAMF7, TLR1). High socioeconomic disadvantage and worse social environment were primarily associated with increased methylation. In 5 genes with significant associations between neighborhood and methylation (FKBP5, CD1D, F8, KLRG1, NLRP12), methylation was associated with gene expression of at least one transcript. These results demonstrate that multiple dimensions of neighborhood context may influence methylation levels and subsequent gene expression of stress- and inflammation-related genes, even after accounting for individual socioeconomic factors. Further elucidating the molecular mechanisms underlying these relationships will be important for understanding the etiology of health disparities.

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