This study looked at the gender roles of individuals in the LGBT community, who hold gender-inverting and gender-conforming queer identities. The specific identities looked at were twinks (gender-inverted) and bears (gender-conforming) for men, and lipsticks (gender-conforming) and butches (gender-inverting) for women. The hypothesis was that individuals with gender-inverting identities would react effectively to a masculine gender role selecting prime, as well as a feminine gender role selecting prime.

Anti-Semitism is a recurrent phenomenon in modern history, but has garnered relatively little focus among research psychologists compared to prejudice toward other groups. The present work frames anti-Semitism as a strategy for managing the implications of Jews’ extraordinary achievements compared to other groups. Anti-Semitic beliefs are sorted into two types: stereotypes that undercut the merit of Jews’ achievements by attributing them to unfair advantages such as power behind the scenes; and stereotypes that offset Jews’ achievements by attaching unfavorable traits or defects to Jews, which are unrelated to the achievement domains, e.g. irritating personalities or genetically-specific health problems. The salience of Jews’ disproportionate achievements was hypothesized as driving greater endorsement of anti-Semitic stereotypes, and envy was hypothesized as mediating this effect. Individual differences in narcissistic self-esteem and moral intuitions around in-group loyalty and equity-based fairness were hypothesized as moderating the effect of Jewish achievement on anti-Semitic beliefs. The results showed greater endorsement of undercutting – but not offsetting – stereotypes after reading about Jewish achievements, compared to Jewish culture or general American achievement conditions. Envy did not significantly mediate this effect. The moral foundation of in-group loyalty predicted greater endorsement of anti-Semitic stereotypes in the Jewish Achievement condition, and lesser endorsement in the Jewish Culture condition. Fairness intuitions did not significantly predict stereotype endorsement. Limitations of the sample and next steps are discussed.

A variety of studies have shown that the tendency toward nicotine dependence has a genetic component. The work described in this thesis addresses three separate questions: i) are there unidentified SNPs in the nicotinic receptors or other genes that contribute to the risk for nicotine dependence; ii) is there evidence of ongoing selection at nicotinic receptor loci; and, iii) since nicotine dependence is unlikely to be the phenotype undergoing selection, is a positive effect on memory or cognition the selected phenotype. I first undertook a genome –wide association scan of imputed data using samples from the Collaborative Study of the Genetics of Nicotine Dependence (COGEND). A novel association was found between nicotine dependence and SNPs at 13q31. The genes at this newly associated locus on chromosome 13 encode a group of micro-RNAs and a member of the glypican gene family. These are among the first findings to implicate a non-candidate gene in risk for nicotine dependence. I applied several complimentary methods to sequence data from the 1000 Genomes Project to test for evidence of selection at the nicotinic receptor loci. I found strong evidence for selection for alleles in the nicotinic receptor cluster on chromosome 8 that confer risk of nicotine dependence. I then used the dataset from the Collaborative Studies on the Genetics of Alcoholism (COGA) and looked for an association between neuropsychological phenotypes and SNPs conferring risk of nicotine dependence. One SNP passed multiple test correction for association with WAIS digit symbol score. This SNP is not itself associated with nicotine dependence but is in reasonable (r 2 = 0.75) LD with SNPs that are associated with nicotine dependence. These data suggest at best, a weak correlation between nicotine dependence and any of the tested cognitive phenotypes. Given the reproducible finding of an inverse relationship between SNPs associated with risk for nicotine dependence and cocaine dependence, I hypothesize that the apparently detrimental phenotype of nicotine dependence may confer decreased risk for cocaine dependence. As cocaine use impairs the positive rewards associated with social interactions, reducing the risk of cocaine addiction may be beneficial to both the individual and the group.

Externalizing behaviors are pervasive, widespread, and disruptive across a multitude of settings and developmental contexts. While the conventional diathesis-stress model typically measures the disordered end of the spectrum, studies that span the range of behavior, from externalizing to competence behaviors, are necessary to see the full picture. To that end, this study examined the additive and nonadditive relations of a dimension of parenting (ranging from warm to rejecting), and variants in dopamine, vasopressin, and neuropeptide-y receptor genes on externalizing/competence in a large sample of predominantly Caucasian twin children in toddlerhood, middle childhood, and early adolescence. Variants within each gene were hypothesized to increase biological susceptibility to both negative and positive environments. Consistent with prediction, warmth related to lower externalizing/higher competence at all ages. Earlier levels of externalizing/competence washed out the effect of parental warmth on future externalizing/competence with the exception of father warmth in toddlerhood marginally predicting change in externalizing/competence from toddlerhood to middle childhood. Warmth was a significant moderator of the heritability of behavior in middle childhood and early adolescence such that behavior was less heritable (mother report) and more heritable (father report) in low warmth environments. Interactions with warmth and the dopamine and vasopressin genes in middle childhood and early adolescence emphasize the moderational role gene variants play in relations between the rearing environment and child behavior. For dopamine, the long variant related to increased sensitivity to parent warmth such that the children displayed more externalizing behaviors when exposed to rejection but they also displayed more competence behaviors when exposed to high warmth. Vasopressin moderation was only present under conditions of parental warmth, not rejection. Interactions with neuropeptide-y and warmth were not significant. The picture that emerges is one of gene-environment interplay, wherein the influence of both parenting and child genotype each depend on the level of the other. As genetic research moves forward, gene variants previously implicated as conferring risk for disorder should be reexamined in conjunction with salient aspects of the environment on the full range of the behavioral outcome of interest.

The interplay of genes and environment on children's development is a complex dynamic process. As behavior geneticists begin to model protective as well as risk factors, and interactive as well as main effect influences, development is elucidated. It was hypothesized that positive parenting, a quality home environment, and high family cohesion would moderate the heritability of three components of temperament: Effortful Control, Negative Affectivity, and Extraversion/Surgency. Participants were drawn from the Wisconsin Twin Project and consisted of 1573 twins (51% boys), 88.5% Caucasian, M=7.93 years (SD=0.87). Higher order composites for the parenting and family environment moderators were formed from mother and father reports of Behavior Management Self-Assessment, Child Rearing Practices Report, Family Assessment Device, and Family Conflict Scale. Measures of the home environment (LEOS Living Environment Observation Scale and CHAOS Confusion, Hubbub, and Order Scale) were not composited due to the nature of the variables. Correlational analyses showed a majority of the temperament and environmental measures to be correlated (rs = -.49-.57). For Effortful Control, Negative Affectivity, and Extraversion/Surgency, estimates for the heritability and nonshared environment were 0.60 and 0.40, 0.80 and 0.20, and 0.59 and 0.41, respectively, with no significant main effects of the shared environment. Models incorporating environmental moderation of these estimates yielded parenting as a significant moderator for Negative Affectivity, LEOS for Effortful Control and Extraversion/Surgency, and CHAOS for Effortful Control and Extraversion/Surgency. Results suggest that the quality of the family environment may act as a permissive or determinative influence on the heritability and expression of temperament. Future analyses include the examination of interactive genetic influences. These findings underscore the importance of shared environment, and support the recent literature on the benefits of positive influences on children's development.