Review of \u3ci\u3eTheir Own Frontier: Women Intellectuals Re-Visioning the American West\u3c/i\u3e Edited and with an introduction by Shirley A. Leckie and Nancy J. Parezo

Pioneering women ethnohistorians and anthropologists who studied American Indians and the trans-Mississippi West deserve greater recognition, not only for the important information they gathered but also for their theoretical insights and methodological advances. As we learn about these women\u27s lives and scholarly contributions, we also come to understand the barriers and prejudices they dealt with in order to pursue the work they valued. This is the argument of Shirley Leckie and Nancy Parezo\u27s collection of intellectual biographies of ten women, born between 1873 and 1910, whose active research careers spanned most of the twentieth century. Their Own Frontier extends the scope of cultural anthropologist Parezo\u27s earlier Hidden Scholars: Women Anthropologists and the Native American Southwest (1993) into the Great Plains and the discipline of history (coeditor Leckie is a historian), although anthropologists remain in the majority

The Association Between the MAOA 2R Genotype and Delinquency Over Time Among Men: The Interactive Role of Parental Closeness and Parental Incarceration

Using a panel of 6,001 males from the National Longitudinal Study of Adolescent and Adult Health, we examine potential moderation by paternal incarceration and parent-child closeness altering the relationship between the rare 2R MAOA genotype and delinquency. By jointly examining moderation patterns for both the mother and father with the transmission of the MAOA genotype from mother to son, we are able to make inferences about the specific genetic model that best explains these outcomes. In line with prior research, we find a direct relationship between the MAOA 2R genotype and delinquency, independent of parental incarceration and closeness. Examining moderation patterns, we find that delinquency risk for the 2R allele is buffered for males close to their biological or social father, but not their biological mother. We conclude that the 2R delinquency association is not due to passive gene-environment correlation but is best characterized as a social control gene-environment interaction

Does Crime Trigger Genetic Risk for Type 2 Diabetes in Young Adults? A G x E Interaction Study Using National Data

Background Living in neighborhoods perceived as disordered exacerbates genetic risk for type 2 diabetes (T2D) among older adults. It is unknown whether this gene-neighborhood interaction extends to younger adults. The present study aims to investigate whether crime, an objectively measured indicator of neighborhood disorder, triggers genetic risk for T2D among younger adults, and whether this hypothesized triggering occurs through exposure to obesity. Methods Data were from the Wave I (2008) National Longitudinal Study of Adolescent to Adult Health. A standardized T2D polygenic score was created using 2014 GWAS meta-analysis results. Weighted mediation analyses using generalized structural equation models were conducted in a final sample of 7606 adults (age range: 25–34) to test the overall association of T2D polygenic scores with T2D, and the mediating path through obesity exposure in low, moderate, and high county crime-rate groups. Age, sex, ancestry, educational degree, household income, five genetic principal components, and county-level concentrated advantage and population density were adjusted. Results The overall association between T2D polygenic score and T2D was not significant in low-crime areas (p = 0.453), marginally significant in moderate-crime areas (p = 0.064), and statistically significant in high-crime areas (p = 0.007). The mediating path through obesity was not significant in low or moderate crime areas (ps = 0.560 and 0.261, respectively), but was statistically significant in high-crime areas (p = 0.023). The indirect path through obesity accounted for 12% of the overall association in high-crime area. Conclusion A gene-crime interaction in T2D was observed among younger adults, and this association was partially explained by exposure to obesity

Genetic Sensitivity to Peer Behaviors: 5HTTLPR, Smoking, and Alcohol Consumption

We investigate whether the serotonin transporter-linked polymorphic region (5HTTLPR), a gene associated with environmental sensitivity, moderates the association between smoking and drinking patterns at adolescents' schools and their corresponding risk for smoking and drinking themselves. Drawing on the school-based design of the National Longitudinal Study of Adolescent Health in conjunction with molecular genetic data for roughly 15,000 respondents (including over 2,000 sibling pairs), we show that adolescents smoke more cigarettes and consume more alcohol when attending schools with elevated rates of tobacco and alcohol use. More important, an individual's susceptibility to school-level patterns of smoking or drinking is conditional on the number of short alleles he or she has in 5HTTLPR. Overall, the findings demonstrate the utility of the differential susceptibility framework for medical sociology by suggesting that health behaviors reflect interactions between genetic factors and the prevalence of these behaviors in a person's context

The social genome of friends and schoolmates in the National Longitudinal Study of Adolescent to Adult Health

Our study reported significant findings of a “social genome” that can be quantified and studied to understand human health and behavior. In a national sample of more than 5,000 American adolescents, we found evidence of social forces that act to make friends and schoolmates more genetically similar to one another compared with random pairs of unrelated individuals. This subtle genetic similarity was observed across the entire genome and at sets of genomic locations linked with specific traits—educational attainment and body mass index—a phenomenon we term “social–genetic correlation.” We also find evidence of a “social–genetic effect” such that the genetics of a person’s friends and schoolmates influenced their own education, even after accounting for the person’s own genetics

The National Longitudinal Study of Adolescent to Adult Health (Add Health) Sibling Pairs Genome-Wide Data

Here we provide a detailed description of the genome-wide information available on the National Longitudinal Study of Adolescent to Adult Health (Add Health) sibling pair subsample (Harris et al., 2012). A total of 2020 samples were genotyped (including duplicates) arising from 1946 Add Health individuals from the sibling pairs subsample. After various steps for quality control (QC) and quality assurance (QA), we have high quality genome-wide data available on 1,888 individuals. In this report, we first highlight theQC and QA steps that were taken to prune the data of poorly performing samples and genetic markers. We further estimate the pairwise biological relationships using genome-wide data and compare those estimates to the assumed relationships in Add Health. Additionally, using genome-wide data from knownregional reference populations from Europe, West Africa, North and South America, Japan and China, weestimate the relative genetic ancestry of the respondents. Finally, rather than conducting a traditional cross-sectional genome-wide association study (GWAS) of body mass index (BMI), we opted to utilize the extensivepublicly available genome-wide information to conduct a weighted genome-wide association study (GWAS) of longitudinal BMI while accounting for both family and ethnic variation

Erratum: Testing the key assumption of heritability estimates based on genome-wide genetic relatedness

Comparing genetic and phenotypic similarity among unrelated individuals seems a promising way to quantify the genetic component of traits while avoiding the problematic assumptions plaguing twin- and other kin-based estimates of heritability. One approach uses a Genetic Relatedness Estimation through Maximum Likelihood (GREML) model for individuals who are related at less than .025 to predict their phenotypic similarity by their genetic similarity. Here we test the key underlying assumption of this approach: that genetic relatedness is orthogonal to environmental similarity. Using data from the Health and Retirement Study (and two other surveys), we show two unrelated individuals may be more likely to have been reared in a similar environment (urban versus non-urban setting) if they are genetically similar. This effect is not eliminated by controls for population structure. However, when we include this environmental confound in GREML models, heritabilities do not change substantially and thus potential bias in estimates of most biological phenotypes is probably minimal

Genome‑wide stress sensitivity moderates the stress‑depression relationship in a nationally representative sample of adults

We re-evaluate the findings of one of the most cited and disputed papers in gene-environment interaction (GxE) literature. In 2003, a paper was published in Science in which the authors demonstrated that the relationship between stress and depression is moderated by a polymorphism in the promoter region (5-HTTLPR) of the gene SLC6A4. Replication has been weak and led many to challenge the overall significance of GxE research. Here, we utilize data from Add Health, a large, nationally representative, and well-powered longitudinal study to re-examine the genetic determinants of stress sensitivity. We characterize environmental sensitivity using a genome-wide polygenic indicator rather than relying on one polymorphism in a single candidate gene. Our results provide support for the stress-diathesis perspective and validate the scientific contributions of the original paper. </div

Is the Gene-Environment Interaction Paradigm Relevant to Genome-Wide Studies? The Case of Education and Body Mass Index

This 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

Gene–environment interactions related to body mass: School policies and social context as environmental moderators

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