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AbstractWe evaluate the hypothesis that genetic factors influence the use of health services and prevention behaviors in a national sample of adult twins in the United States. The analysis compares the correlation of these outcomes between identical twins, who share all their genes, to the correlation between nonidentical twins, who share, on average, only one‐half of their genes. Because the environmental similarities of twins are assumed to be the same for identical and nonidentical twin pairs, researchers can partition the variance in behavioral outcomes that are due to genetic and environmental factors. Using established methods in this field, we find evidence of significant genetic influences on preferences toward prevention, overall prevention effort, routine checkups, and prescription drug use. Use of curative services does not appear to be influenced by genes. Our findings offer several implications for policymakers and researchers and suggest that genetics could be informative for health services and policy research.

Children raised in neighborhoods with low socio-economic status (SES) are at risk for low academic achievement. Identifying factors that help children from disadvantaged neighborhoods thrive is critical for reducing inequalities. We investigated whether children's prosocial behavior buffers concurrent and subsequent academic risk in disadvantaged neighborhoods in Bradford, UK. Diverse children (N = 1,175) were followed until age seven, with measurements taken at four times. We used governmental indices of neighborhood-level SES, teacher observations of prosocial behaviors, and direct assessments of academic achievement. Neighborhood SES was positively associated with academic achievement among children with low levels of prosocial behavior, but not among children with high levels of prosocial behavior. Prosocial behavior may mitigate academic risk across early childhood.

AbstractThis study uses data from the Framingham Heart Study to examine the relevance of the gene-environment interaction paradigm for genome-wide association studies (GWAS). We use completed college education as our environmental measure and estimate the interactive effect of genotype and education on body mass index (BMI) using 260,402 single-nucleotide polymorphisms (SNPs). Our results highlight the sensitivity of parameter estimates obtained from GWAS models and the difficulty of framing genome-wide results using the existing gene-environment interaction typology. We argue that SNP-environment interactions across the human genome are not likely to provide consistent evidence regarding genetic influences on health that differ by environment. Nevertheless, genome-wide data contain rich information about individual respondents, and we demonstrate the utility of this type of data. We highlight the fact that GWAS is just one use of genome-wide data, and we encourage demographers to develop methods that incorporate this vast amount of information from respondents into their analyses.

This paper highlights the role of institutional resources and policies, whose origins lie in political processes, in shaping the genetic etiology of body mass among a national sample of adolescents. Using data from Waves I and II of the National Longitudinal Study of Adolescent Health, we decompose the variance of body mass into environmental and genetic components. We then examine the extent to which the genetic influences on body mass are different across the 134 schools in the study. Taking advantage of school differences in both health-related policies and social norms regarding body size, we examine how institutional resources and policies alter the relative impact of genetic influences on body mass. For the entire sample, we estimate a heritability of .82, with the remaining .18 due to unique environmental factors. However, we also show variation about this estimate and provide evidence suggesting that social norms and institutional policies often mask genetic vulnerabilities to increased weight. Empirically, we demonstrate that more restrictive school policies and policies designed to curb weight gain are also associated with decreases in the proportion of variance in body mass that is due to additive genetic influences.

This paper highlights the role of institutional resources and policies, whose origins lie in political processes, in shaping the genetic etiology of body mass among a national sample of adolescents. Using data from Waves I and II of the National Longitudinal Study of Adolescent Health, we decompose the variance of body mass into environmental and genetic components. We then examine the extent to which the genetic influences on body mass are different across the 134 schools in the study. Taking advantage of school differences in both health-related policies and social norms regarding body size, we examine how institutional resources and policies alter the relative impact of genetic influences on body mass. For the entire sample, we estimate a heritability of .82, with the remaining .18 due to unique environmental factors. However, we also show variation about this estimate and provide evidence suggesting that social norms and institutional policies often mask genetic vulnerabilities to increased weight. Empirically, we demonstrate that more-restrictive school policies and policies designed to curb weight gain are also associated with decreases the proportion of variance in body mass that is due to additive genetic influences.

This paper highlights the role of institutional resources and policies, whose origins lie in political processes, in shaping the genetic etiology of body mass among a national sample of adolescents. Using data from Waves I and II of the National Longitudinal Study of Adolescent Health, we decompose the variance of body mass into environmental and genetic components. We then examine the extent to which the genetic influences on body mass are different across the 134 schools in the study. Taking advantage of school differences in both health-related policies and social norms regarding body size, we examine how institutional resources and policies alter the relative impact of genetic influences on body mass. For the entire sample, we estimate a heritability of .82, with the remaining .18 due to unique environmental factors. However, we also show variation about this estimate and provide evidence suggesting that social norms and institutional policies often mask genetic vulnerabilities to increased weight. Empirically, we demonstrate that more restrictive school policies and policies designed to curb weight gain are also associated with decreases in the proportion of variance in body mass that is due to additive genetic influences. [Reprinted by permission of Sage Publications Ltd., copyright holder.]

Abstract
Lower socioeconomic status is associated with faster biological aging, the gradual and progressive decline in system integrity that accumulates with advancing age. Efforts to promote upward social mobility may, therefore, extend healthy lifespan. However, recent studies suggest that upward mobility may also have biological costs related to the stresses of crossing social boundaries. We tested associations of life-course social mobility with biological aging using data from participants in the 2016 Health and Retirement Study (HRS) Venous Blood Study who provided blood-chemistry (n = 9,255) and/or DNA methylation (DNAm) data (n = 3,976). We quantified social mobility from childhood to later-life using data on childhood family characteristics, educational attainment, and wealth accumulation. We quantified biological aging using 3 DNAm "clocks" and 3 blood-chemistry algorithms. We observed substantial social mobility among study participants. Those who achieved upward mobility exhibited less-advanced and slower biological aging. Associations of upward mobility with less-advanced and slower aging were consistent for blood-chemistry and DNAm measures of biological aging, and were similar for men and women and for Black and White Americans (Pearson-r effect-sizes ∼0.2 for blood-chemistry measures and the DNAm GrimAge clock and DunedinPoAm pace-of-aging measures; effect-sizes were smaller for the DNAm PhenoAge clock). Analysis restricted to educational mobility suggested differential effects by racial identity; mediating links between educational mobility and healthy aging may be disrupted by structural racism. In contrast, mobility producing accumulation of wealth appeared to benefit White and Black Americans equally, suggesting economic intervention to reduce wealth inequality may have potential to heal disparities in healthy aging.