Emily Rauscher

Heritability and the Equal Environments Assumption: Evidence from Multiple Samples of Misclassified Twins

Classically derived estimates of heritability from twin models have been plagued by the possibility of genetic-environmental covariance. Survey questions that attempt to measure directly the extent to which more genetically similar kin (such as monozygotic twins) also share more similar environmental conditions represent poor attempts to gauge a complex underlying phenomenon of GE-covariance. The present study exploits a natural experiment to address this issue: Self-misperception of twin zygosity in the National Longitudinal Survey of Adolescent Health (Add Health). Such twins were reared under one “environmental regime of similarity” while genetically belonging to another group, reversing the typical GE-covariance and allowing bounded estimates of heritability for a range of outcomes. In addition, we examine twins who were initially misclassified by survey assignment—a stricter standard—in three datasets: Add Health, the Minnesota Twin Family Study and the Child and Adolescent Twin Study in Sweden. Results are similar across approaches and datasets and largely support the validity of the equal environments assumption.

Genetic Interactions with Prenatal Social Environment Effects on Academic and Behavioral Outcomes

Numerous studies report gene-environment interactions, suggesting that specific alleles have different effects on social outcomes depending on environment. In all these studies, however, environmental conditions are potentially endogenous to unmeasured genetic characteristics. That is, it could be that the observed interaction effects actually reflect underlying genetic tendencies that lead individuals into certain environments. What is critical to move this literature forward is random environmental variation that we know is not correlated with innate characteristics of subjects. We exploit a natural experiment that randomizes a particular stressor—birth weight discordance within twin pairs—to address this challenge and ask: Do random differences in early environment (prenatal nutrition) moderate genetic effects on depression, delinquency, or GPA? Using Add Health data, the only consistently significant allele–birth weight interaction we reveal works in the opposite direction of Caspi et al.’s classic finding regarding the interaction of maltreatment with genetic variation in the serotonin transporter promoter. Less robust interactions found for DRD2 and MAOA are consistent with this pattern that reverses prior findings. These results do not necessarily overturn existing research but support our methodological point that gene-environment research must address endogeneity.

Beyond Orchids and Dandelions: Testing the 5-HTT "Risky" Allele for Evidence of Phenotypic Capacitance and Frequency-Dependent Selection

The persistence of behaviorally deleterious genes in the human population poses an interesting question for population genetics: If certain alleles at these loci are deleterious, why have they survived in the population? We consider evidence for phenotypic capacitance and/or frequency-dependent selection for an allele that has been putatively shown to have negative associations with human behaviors (the “short” 5-HTT promoter region allele) yet has persisted in human and nonhuman primate populations. Using data from the National Longitudinal Study of Adolescent Health, we compare sibling and twin variation in depression by 5-HTT genotype (specified in several ways) and investigate sibship-level cross-person gene-gene interactions. In support of the “orchid/dandelion” hypothesis, we find evidence that the short allele increases variation in phenotypes in response to environmental (or genetic) differences (i.e., acts as a perturbation of a phenotypic capacitor). Further, we also find some evidence that the effects of allelic variation at this locus are moderated by the genetic environment of the sibship unit (i.e., effects may be susceptible to frequency-dependent selection). We discuss implications of these findings for genetic models in general, specifically with respect to stable unit treatment value assumption violations (i.e., nonindependence of units of analysis).

Genetic Interactions with Prenatal Social Environment: Effects on Academic and Behavioral Outcomes

Numerous studies report gene-environment interactions, suggesting that specific alleles have different effects on social outcomes depending on environment. In all these studies, however, environmental conditions are potentially endogenous to unmeasured genetic characteristics. That is, it could be that the observed interaction effects actually reflect underlying genetic tendencies that lead individuals into certain environments. What is critical to move this literature forward is random environmental variation that we know is not correlated with innate characteristics of subjects. We exploit a natural experiment that randomizes a particular stressor—birth weight discordance within twin pairs—to address this challenge and ask: Do random differences in early environment (prenatal nutrition) moderate genetic effects on depression, delinquency, or GPA? Using Add Health data, the only consistently significant allele–birth weight interaction we reveal works in the opposite direction of Caspi et al.’s classic finding regarding the interaction of maltreatment with genetic variation in the serotonin transporter promoter. Less robust interactions found for DRD2 and MAOA are consistent with this pattern that reverses prior findings. These results do not necessarily overturn existing research but support our methodological point that gene-environment research must address endogeneity.

Youth Early Employment and Behavior Problems Human Capital and Social Network Pathways to Adulthood

We examine the relationship between early youth employment and behavior problems and ask whether this relationship differs by race, job quality, or work intensity. Drawing on Panel Study of Income Dynamics data, we depict the employment patterns of American youth aged 12 through 18 and test conflicting hypotheses about mediating mechanisms through which youth employment shapes children’s behavior. Results show that employment is associated with fewer behavior problems but only when the jobs offer opportunities for human capital development and only when working moderate hours. We find significant differences in employment rates and job characteristics between black and white youth. High-quality employment has a stronger impact on black than on white youth, and the positive effect of work is mediated by positive peer influence. Findings support social and human capital theories and, more broadly, the social network/role model explanation for adolescent behavior.

Hidden Gains Effects of Early U.S. Compulsory Schooling Laws on Attendance and Attainment by Social Background

Research on early compulsory schooling laws finds minimal effects on attendance but fails to investigate heterogeneous effects. Similarly, research proposes limited contexts in which expansion policies can increase equality but has difficulty separating policy and cohort effects. Capitalizing on within-country variation in timing of early compulsory laws, passed 1852 to 1918, I ask whether they improved equality of school attendance or educational attainment by class, nativity, and race. Based on census data, compulsory laws increased equality of attendance and attainment, particularly among young men in the North, where the laws reduced class and race gaps by over 20%. Early compulsory schooling laws provided “hidden gains,” missed in previous analyses, suggesting policies that raise minimum schooling can increase educational equality in certain contexts.

Does Educational Equality Increase Mobility? Exploiting Nineteenth-Century U.S. Compulsory Schooling Laws

Existing evidence of educational effects on intergenerational mobility is associational. This study employs early compulsory schooling laws to approach a causal estimate of the relationship between education and mobility in the context of a large-scale policy change. Using IPUMS Linked Representative Samples (linked census data), regression discontinuity models exploit state differences in the timing of compulsory schooling laws to estimate an intent-to-treat effect on intergenerational occupational mobility among white males. Despite increasing equality of attendance, results reveal that compulsory laws initially reduced relative mobility for the first few cohorts affected by the laws. Among later cohorts, who were required to attend the maximum years of school, mobility was similar to prelaw levels. School funding and other data suggest that structural lag could explain this nonlinear relationship. It seems, therefore, that educational expansion inadvertently reduced mobility through institutional inertia rather than elite efforts to maintain advantage.

Genetic Interactions with Prenatal Social Environment

Numerous studies report gene-environment interactions, suggesting that specific alleles have different effects on social outcomes depending on environment. In all these studies, however, environmental conditions are potentially endogenous to unmeasured genetic characteristics. That is, it could be that the observed interaction effects actually reflect underlying genetic tendencies that lead individuals into certain environments. What is critical to move this literature forward is random environmental variation that we know is not correlated with innate characteristics of subjects. We exploit a natural experiment that randomizes a particular stressor—birth weight discordance within twin pairs—to address this challenge and ask: Do random differences in early environment (prenatal nutrition) moderate genetic effects on depression, delinquency, or GPA? Using Add Health data, the only consistently significant allele–birth weight interaction we reveal works in the opposite direction of Caspi et al.’s classic finding regarding the interaction of maltreatment with genetic variation in the serotonin transporter promoter. Less robust interactions found for DRD2 and MAOA are consistent with this pattern that reverses prior findings. These results do not necessarily overturn existing research but support our methodological point that gene-environment research must address endogeneity.

The Relationship between Income and Net Worth in the United States: A Virtuous Cycle for High- but Not Low-Income Households

ABSTRACT Is there a reciprocal relationship between household income and net worth and does that relationship depend on initial income? Using cross-lagged panel models of household income and net worth data from the Panel Study of Income Dynamics, the authors compare the income-wealth relationships of high- and low-income households from 1989 to 2011. Adjusting for demographic differences, the authors find a reciprocal relationship between income and wealth for high-, but not low-, income households. Results suggest intragenerational mobility works differently by initial income, which could partially explain the difficulty of escaping poverty and low U.S. support for liberal social welfare policy.

Sibling genes as environment: Sibling dopamine genotypes and adolescent health support frequency dependent selection

While research consistently suggests siblings matter for individual outcomes, it remains unclear why. At the same time, studies of genetic effects on health typically correlate variants of a gene with the average level of behavioral or health measures, ignoring more complicated genetic dynamics. Using National Longitudinal Study of Adolescent Health data, we investigate whether sibling genes moderate individual genetic expression. We compare twin variation in health-related absences and self-rated health by genetic differences at three locations related to dopamine regulation and transport to test sibship-level cross-person gene-gene interactions. Results suggest effects of variation at these genetic locations are moderated by sibling genes. Although the mechanism remains unclear, this evidence is consistent with frequency dependent selection and suggests much genetic research may violate the stable unit treatment value assumption.