Early Life Obesity and Social Stratification in Adulthood

Add Health Users Conference Abstracts July 22-23, 2010 Thursday, July 22, 2010 Plenary Session: Early Life Origins of Adult Health and Well-Being Moderator: Michael Spittel, Eunice Kennedy Shriver National Institute of Child Health and Human Development Genetic Interactions with Prenatal Social Environment: Effects on Academic and Behavioral Outcomes Dalton Conley, New York University Emily Rauscher, coauthor Caspi et al. (2002, 2003), Guo et al. (2008), and Pescosolido et al. (2008) all claim to have demonstrated allele-by-environment interactions, but in all cases environmental influences are endogenous to the unmeasured genetic characteristics of the subjects and their families. Thus, gene-gene interactions cannot be ruled out as an alternative explanation. Second, these studies have not deployed adjustments for multiple hypothesis testing—always an issue, but particularly so for GE studies with multiple alleles and outcomes. We address these limitations of previous studies by taking advantage of a natural experiment that randomizes a particular environmental influence – fetal position that results in birth weight discordance within monozygotic twin pairs (validated with dizygotic twins as well). Whether or not we use a Bonferroni correction for multiple statistical tests, we find no support for any of the past research (including main effects of genes and birth weight) and, in fact, the only significant allele-birth weight interaction we find works in the opposite direction of Caspi et al.’s classic finding on 5-HTTP and maltreatment. Impact of Early Life Health on Educational Attainment: Racial/Ethnic and SES Differentials Jon M. Hussey, University of North Carolina at Chapel Hill Liana J. Richardson and Narayan Sastry, coauthors The association between socioeconomic status (SES) and health is one of the most widely studied relationships in the social and health sciences. While support for the social causation hypothesis (i.e., that SES affects subsequent health) is consistently found, evidence for the social selection hypothesis (i.e., that health affects subsequent SES) is mixed. The combination of these findings has led to the dominant assumption that selection mechanisms have a minor influence on relationships between SES and health. However, a growing number of studies challenge this assumption. Our research seeks to extend these studies in a number of important ways. Drawing on multiple waves of Add Health data, we examine the impact of early life health on educational attainment. Specifically, we model the relationship between multiple indicators of adolescent physical and mental health (including self-rated health, depressive symptoms, BMI, and drug use) and three measures of educational attainment: high school completion, college enrollment, and college completion. We also evaluate whether these associations differ by sex, race/ethnicity, and parental SES. In all analyses, we adjust for potential confounders and, when appropriate, we explicitly account for errors in measured variables. Add Health Users Conference Abstracts July 22-23, 2010 Early Life Obesity and Social Stratification in Adulthood Hedwig Lee, University of Michigan Kathleen Mullan Harris, coauthor This paper examines the social and economic consequences of obesity trajectories in early life— from adolescence through the transition to adulthood. We use data from all waves (Wave I to Wave IV) of Add Health. With data on measured height and weight, we track BMI and obesity trajectories from adolescence (Wave II) through the transition to adulthood (Wave III) and classify young people according to the following trajectories of obesity experience: i) persistent obesity—those who were obese in adolescence and through the transition to adulthood; ii) become obese—those who were not obese in adolescence and become obese in early adulthood; and iii) not obese—those who were never obese, or only obese in adolescence and then not obese by early adulthood. We then examine the social and economic consequences in adulthood (Wave IV) associated with different trajectories of obesity, controlling for various important family background and demographic measures in childhood/adolescence (Wave I). We will examine the relationship between obesity trajectories in early life and multiple measures of social stratification in adulthood when the Add Health cohort is aged 24-32. The outcomes we plan to examine include impacts on education (finishing high school, attending college, finishing college), employment, idle status (not in school or at work), personal earnings, welfare usage, poverty status, household income, assets, debts, home ownership, family formation, and marriage. We anticipate that greater exposure to obesity in early life, especially persistent obesity, will place individuals at the bottom of the social stratification system on these outcomes, relative to no exposure to obesity. How Do Genes, Environmental Stressors and Their Interactions Get Inside the Body to Increase Disease Risk in Add Health Participants at Wave IV (and Thereafter)? Redford Williams, Duke University Beverly Brummett and Ilene Siegler, coauthors Genes, environmental stressors, and their interactions can only influence the development of medical disorders via effects on psychosocial, behavioral and biological characteristics (endophenotypes) that are directly involved in ethiology and pathogenesis. Lower socioeconomic status (SES) is one environmental factor that has been shown to have profound effects on risk of cardiovascular disease (CVD). Using Wave IV biomarker data, we have been able to replicate (p < 0.0001) an earlier finding in a French cohort that one’s educational level is inversely associated with systolic blood pressure (SBM). This association was largely accounted for by BMI, race/ethnicity,gender, marital status and lifestyle characteristics (physical activity, alcohol consumption and smoking). Our prior research has identified several genetic variants that are also associated with pre-disease endophenotypes. The more active allele (L) of a serotonin transporter promoter polymorphism (5HTTLPR) is associated with increased SBP reactivity to acute stress in both men and women, blacks and whites. In comparison to women carrying the 5HTTLPR L allele and exposed to high or low stress life situations, women who are homozygous for the less active allele (SS) and exposed to high stress have higher levels of depressive symptoms (a risk factor for CVD), but those in low stress situations have lower depressive symptom levels. Among men, it is those with the 5HTTLPR L allele who have high depressive symptom levels in stressful life situations. A single nucleotide polymorphism (SNP) on the APOE gene is associated with an adverse lipid profile in persons exposed to a high live stress situation, but with a more positive profile in those not so exposed. A functional SNP on the 5HT2C serotonin receptor gene is robustly associated in men with larger cortisol responses to acute mental stress. It will be possible, in our ongoing investigations using Add Health Wave IV data, to both replicate these associations and determine whether these same genetic variants influence the development of major medical disorders. Is, for example, the incidence of hypertension significantly higher among those with low education levels who also carry the 5HTTLPR L allele? Is the 5HTTLPR SS genotype associated with increased depression among women exposed to stressful life situations, but with decreased Add Health Users Conference Abstracts July 22-23, 2010 depressive symptoms in those not so exposed? Is the LL genotype associated with increased depression in men exposed to chronic stress? Is the APOE SNP we find associated with bad and good lipid profiles in persons exposed to high vs normal stress life situations also associated with similar profiles in Wave IV participants, depending on stress exposure? And is the 5HTR2C SNP we find associated with larger cortisol responses to acute mental stress in men also associated with disorders like type 2 diabetes, central obesity and hypertension whose pathogenesis is increased by chronic cortisol excess?