The purpose of this study was to explore the relation between anxiety symptoms and victimization experiences. It was expected that anxiety (both at age 5 and follow-up) and victimization (both overt and relational subtypes) would be heritable. It was also expected that early anxiety would predict future victimization experiences and that these experiences would be correlated with concurrent anxiety. Finally, it was predicted that early anxiety and high risk genotypes of the 5-HTTLPR serotonin transporter and DRD2 dopamine receptor genes would serve as diatheses, which upon experiencing the stressor of victimization, would put an individual at a multiplicatively greater risk for experiencing anxiety symptoms. Sixty-five children from the Southern Illinois Twins and Siblings Study (SITSS) were examined longitudinally. Parent-reported anxiety was obtained at age 5. Then during a follow-up study when the children were aged 6-16 years, parent- and self-report measures of anxiety and a self-report measure of victimization experiences were collected. Results indicated that the genetic influences on parent-reported anxiety at age 5 and total victimization were significant, with practically no influence of the shared environment. However, self-reported anxiety appeared to be largely due to the non-shared environment. A diathesis stress framework was not supported in this study, as early anxiety and high-risk genotype did not put an individual at greater risk for developing subsequent anxiety after being victimized. Although significant heritability was demonstrated for early anxiety and victimization, high risk alleles for both of the genes examined in this study (5-HTTLPR and DRD2) were not significant contributors to the demonstrated genetic underpinnings. Likewise, early anxiety did not serve as a diathesis for subsequent anxiety. However, age 5 and follow-up measures were positively correlated when both were reported by a parent, a result that did not remain true when measures were taken from different informants. The relation between anxiety symptoms and victimization also varied by informant and time. Early anxiety, as reported by a parent, was predictive of overt victimization specifically, whereas youth reports of anxiety were significantly related to both subtypes of victimization (both of which were measured at follow-up). However, parent-reported anxiety at follow-up was not significantly associated with any form of victimization. These results indicate that the relation between anxiety symptoms and victimization is complex and dependent on the type of victimization and reporter of anxiety symptoms. Understanding the maladaptive consequences of experiencing peer victimization as well as the psychological factors that put children at risk for being bullied will inform teachers, parents, and counselors how to effectively prevent and handle these maladaptive interactions. Given that peer victimization is a very common phenomenon, research in this field will generalize to a large portion of the population.

People differ, often strikingly, in their views on desired social structures and processes. For example, while some value ethnic diversity in their society, others believe non-indigenous individuals (whatever that might mean) should be repatriated to their land of origin. Similarly, whereas some believe religion should play no role in determining social policy, others strongly advocate the importance of living according to religious scripture, including at a social level. This variation in attitudes, and its implication for societal cohesion, has made research on the origins of social and political attitudes of enduring interest to psychologists, sociologists, political scientists, among many others. The goal of the current thesis was to extend work in this literature in two key ways: Firstly, I examined whether political attitudes can be understood within a personality system model. This work addresses previous mixed results on the links of basic personality traits to political conservatism. In Chapter 3, I test predictions from this model; namely, that direct influences on political behaviour flow from moral values, with personality mostly acting indirectly via these moral values, rather than directly affecting political attitudes. Findings from two studies (published as Lewis & Bates, 2011a) supported these predictions suggesting that the new model helps explain inconsistencies in previous research attempting to link personality to political orientation that have not included the intermediary level of values. Secondly, I examined the genetic architecture of social attitudes constructs in three separate studies. Chapter 4 addressed whether in-group favouritism reflects heritable effects, and, secondly, whether race-favouritism was accounted for broad or specific genetic effects. Results indicated that a common biological mechanism exists facilitating generalised favouritism, with evidence for additional genetic effects specific to each form of group favouritism. These findings(published as Lewis & Bates, 2010) suggest that (at least) at the genetic level, race favouritism is multiply determined. In Chapter 5, I examined whether prosocial obligations across the domains of welfare, work, and civic obligation share a common genetic basis, or reflect specific heritable components (published as Lewis & Bates, 2011b). In females, results indicated the existence of a common heritable factor underlying each of these prosocial obligations. In males, a prosocial factor was also observed; familial effects (genetic and shared-environment effects were indistinguishable) influenced this general mechanism. At the domain-specific level, modest genetic effects were observed in females for civic and work obligations, with shared environment effects influencing welfare obligations. In males, genetic influences were observed for welfare obligation, with unique-environments affecting work and civic duty. Finally, in Chapter 6, I present work examining the genetic architecture of religious belief. Although genetic factors are known to influence strength of religious belief, the psychological mechanism(s) through which this biological influence is manifest are presently unknown. Two non-theological constructs – 1) need for community integration and 2) need for existential certainty – were hypothesised to account for the genetic effects on religiosity. The results supported this hypothesis, with genetic influences on these traits wholly accounting for the heritable basis of religiosity, suggesting that religion “re-uses” systems involved in meeting both social and existential needs.

This thesis investigated the etiology of individual differences in Chinese language and literacy skills with a two-wave longitudinal design using a sample of 312 Chinese twin pairs aged 3 to 11 in Hong Kong. Children were individually given tasks of Chinese word reading, receptive vocabulary, phonological memory, tone awareness, syllable and rhyme awareness, rapid automatized naming, morphological awareness, and orthographic skills, as well as nonverbal reasoning and audiometric screening tests. They were tested again on the same tasks, except nonverbal reasoning, one year after the initial testing. Children’s saliva was collected to perform SNP testing for zygosity determination. Also, their demographic information, home literacy environment profile, and motivation for learning text, were obtained from parent-rated questionnaires. Overall, there were four major findings on Chinese language and literacy abilities with the effects of age and nonverbal reasoning controlled for. First, genes and environments had differential influences on various skills, and there was a possibility of different etiology in language and reading development. Second, socioeconomic status and home literacy environment were plausible mediators but not moderators of general language and reading abilities. Third, the stability of various skills across a one-year time period was mainly mediated by genetic influences, but shared environmental factors also influenced syllable and rhyme awareness. Also, new genetic and environmental factors came into play at Time 2 for word reading, and results suggested new genetic influences and new shared environmental influences emerged at Time 2 for tone awareness and morphological awareness respectively. Fourth, both genes and environments contributed to parent-rated communicative ability and motivation for learning text. Furthermore, the link between word reading and parent-rated motivation was mediated by genetic processes. The universality of the genetic and environmental origins across languages and their specificity to Chinese, as well as the implications of these findings, were discussed.

This thesis investigated reading and related skills in Chinese children learning English as a second language (ESL) in 279 Chinese twin pairs aged from 3 to 11 years. Children were tested twice, a year apart, with measures of visual word recognition, receptive vocabulary, phonological awareness, phonological memory and speech perception in both Chinese and English and Chinese tone awareness. The thesis was divided into two sections with the first section exploring the phenotypic relationships and the second section estimating the genetic and environmental influences. In the first section, the causal relationships among the five ESL skills were modelled (chapter 4) and the relationships between Chinese and ESL skills were sought (chapter 4). In section two, the univariate heritability (chapter 6), the cross-linguistic genetic overlap (chapter 7) and the stability and instability of heritability estimates (chapter 8) for all skills were examined. Findings have shown that ESL speech perception is important to the development of ESL phonological awareness, phonological memory and receptive vocabulary, in turn, has an impact on ESL reading development. Genes play an important role in ESL and Chinese reading development. The differential environmental effects may be due to the differences in the ESL and Chinese acquisition ecologies.

Although previous research has shown a significant association between bulimia nervosa (BN) and drug use disorders (DUD), our knowledge of the underlying causes for this comorbidity remains limited. The purpose of the present study was to investigate possible influences on the comorbidity between BN and DUD. Subjects included 490 monozygotic and 354 dizygotic female twin pairs from the Virginia Adult Twin Study of Psychiatric and Substance Use Disorders. Multiple logistic regression analyses were used to test where putative shared correlates mediated the comorbidity between BN and DUD. Bivariate twin analyses were used to investigate the contribution of genes and environment to the correlation between BN and DUD. Regression analyses indicated a lifetime history of major depression, the personality trait of neuroticism, and childhood sexual abuse significantly mediated the associated between BN and DUD (using BN as the independent variable), while major depression, conduct disorder diagnosis, and childhood sexual abuse most significantly impacted the association when DUD was used as the independent variable. Bivariate twin analyses indicated there is additive genetic and nonshared environmental overlap between BN and DUD with genetic and unique environmental correlations of 0.39 and 0.10, respectively. Results show the reason for the association between BN and DUD is due mostly to overlapping genes with a smaller contribution from nonshared environmental influences. Major depression, the personality trait of neuroticism, and childhood sexual abuse are likely important shared correlates between BN and DUD.

The etiological connection between internalizing and externalizing disorders is poorly understood. This manuscript aims to investigate the roles of genes and then environment in the development of Major Depressive Disorder (MDD) and Antisocial Personality Disorder (ASPD) and the nature of their comorbidity in young adults. Data from a sample of 2,291 young adult male and female twins from the Young Adult Follow Up Study (YAFU) of the Virginia Twin Study of Adolescent Behavioral Development (VTSABD) were used to estimate the proportion of variation in these traits that can be accounted for by additive genetic, shared environmental, and unique environmental factors. In addition to traditional methods of measurement of psychiatric disorders (symptom sum scores), a more novel approach to measurement through item response theory (IRT) was employed. Through both measurement methods, variation in depression was found to be influenced almost entirely by environmental factors, however IRT analysis revealed genetic influences related to specific symptoms that cannot be gleaned from a traditional univariate analysis. While the symptoms of MDD appear to work well together to define the latent construct, symptoms of ASPD are less cohesive. ASPD item loadings are more disparate and the item response models are somewhat unstable compared with the MDD item analyses. Consistent with the literature, results using traditional sum score data indicated that ASPD was influenced by additive genetic and unique environmental effects. IRT analysis, however, did indicate a role for the shared environment in ASPD variation.ASPD/MDD comorbidity analyses suggest that more than one mechanism may reasonably explain the relationship between the disorders. It appears to be more likely that common genetic factors account for some of the observed comorbidity in females than in males. Conversely, the shared environment is that the most likely link between the two disorders in males. The etiological nature of these disorders is complex and analysis may be further complicated in a population spanning a critical developmental period, such as young adulthood. The item response approach has the potential to provide new insight into how these disorders develop and differ between the sexes and different age groups.

Sweden and Norway have the worldwide highest incidence of osteoporotic fractures. As these fractures constitute a tremendous and growing problem, primary prevention is of great importance. The principal causes of an osteoporotic fracture are a fall and a fragile skeleton. The aim of the studies reported in these papers was therefore to determine the genetic and environmental influences on fractures and the genetic influence on the two main reasons to the emergence of osteoporotic fractures; bone mineral density and propensity to fall. In the present thesis, we display that the heritability of fractures is dependent on fracture site and age. With increasing age, lifestyle becomes the dominant explanatory factor. These results indicate that focus should be on lifestyle interventions for the prevention of fractures in the elderly. Although the genetic liability to impaired balance is modest, twins with self-reported impaired balance have a substantially increased risk of osteoporotic fractures compared to their co-twin without impaired balance. Asking a patient about his or her balance might be a simple tool for future risk assessment. The genetic influence on bone phenotypes is under strong genetic influence in Swedish adult twins. These findings are in agreement with the results from previous studies in other countries, with a lower incidence of osteoporotic fractures compared to Sweden. The high heritability of bone phenotypes together with the low heritability of fractures at old age, indicates that bone mineral density has a modest influence on fracture risk at old age. In summary, based on the results in this thesis, more emphasis should be targeted to the prevention of falls, by strength and balance training in order to prevent the occurrence of  low energy fractures in the elderly.

To understand the etiology of psychopathic personality traits and thus in the long run to be able to develop successful prevention, a first step is to find out what role genetic and environmental effects play. A meta-review of 15 twin studies (N=26, 981), was conducted to estimate the magnitude of genetic and environmental influences on psychopathic personality traits. The results show that additive genetic (heritable) factors and non-shared environmental factors each explain 50% of the variance in psychopathic personality traits, while shared environmental factors were of no importance. Measure, informant, age, and sex were investigated as potential moderators showing that informant had an impact on the findings. This meta-analysis provides a structured synthesis of the relative genetic and environmental contributions in psychopathic personality traits through various stages of development and across sex. / För att förstå etiologin av psykopatiska personlighetsdrag och därmed i det långa loppet kunna utveckla framgångsrik prevention, är ett första steg att klargöra vilken roll genetiska och miljömässiga effekter spelar. En meta-översikt på 15 tvillingstudier (N=26,981), genomfördes för att uppskatta i vilken grad genetiska och miljömässiga faktorer påverkar psykopatiska personlighetsdrag. Resultaten visade att additiva genetiska (ärftliga) och unika miljömässiga faktorer förklarar 50% var av variansen i psykopatiska personlighetsdrag, medan delade miljömässiga faktorer inte var av betydelse. Mått, informant, ålder och kön undersöktes som potentiella moderatorer och visade att informant påverkade resultaten. Denna meta-analys ger en strukturerad syntes av de relativa genetiska och miljömässiga bidrag som påverkar psykopatiska personlighetsdrag genom olika utvecklingsstadier och mellan könen.

Childhood sexual abuse (CSA) is a stressful life experience with lasting/far-reaching health and psychopathological consequences. Our laboratory recently identified a significantly increased frequency of acquired chromosomal anomalies (assessed using the cytokinesis-blocked micronucleus assay) in adult female twins exposed to CSA when compared to their unexposed co-twin. The primary aim of this study was to evaluate potential mechanism(s) underlying the observed increases in levels of micronuclei in an expanded group of 90 female identical twins (61 CSA+ females and 29 CSA- females [including a total of 27 MZ co-twin pairs]) using fluorescence in situ hybridization (FISH) methodologies, with PNA probes specific for the centromeric and telomeric regions of all chromosomes coupled with the standard CBMN assay, we were able to characterize the chromosomal contents of MN and, thus, gain insight into the mechanisms underlying MN formation. By scoring 100 MN per study participant for the number of centromeric signal(s) and/or telomeric signal(s) present, we categorized the MN as harboring either: (1) terminal fragments (only a telomeric signal); (2) acentric interstitial fragments (no telomeric or centromeric signal); (3) centric interstitial fragments (only a centromeric signal); or (4) an intact chromosome(s) or chromatid(s). We identified elevated frequencies of intact chromosome-derived MN in CSA+ women as compared to CSA- women (P=0.014), implicating chromosome loss as a mechanism potentially underlying the increased frequencies of MN identified in adult females with a history of CSA. MN containing fragmented chromosomes were also observed in all of the study participants evaluated; however MN containing terminal fragments and MN containing acentric interstitial fragments were seen less frequently in CSA+ women compared to CSA- women. This study represents the first time that the chromosomal contents of MN have been evaluated in individuals in the context of a psychosocial factor. As chromosomal loss and breakage contributes to the development of age-related health problems, these observations provide important insight into the biological mechanisms that may underlie the latent morbidity and psychopathology associated with childhood adversity. Future studies aimed at understanding the biological impact of early-life trauma could determine if the observed increase in acquired chromosomal abnormalities results in detectable somatic clonal mosaicism. This knowledge could ultimately be used to develop screening tools to identify individuals “at risk” for negative health outcomes in adulthood.

Decades of work has led researchers to believe that risk for complex behavioral phenotypes, such as alcohol use disorders, is likely influenced by multiple genes of small effect acting in conjunction with each other and the environment. Currently, the field of psychiatric genetics is developing methodologies for the identification of genetic risk variants that predispose individuals to the development of complex behavioral disorders. Several challenges related to the complex and polygenic nature of these phenotypes, must be considered. This dissertation study attempts to address these important challenges in the context of alcohol use disorders and related phenotypes. A rich twin and family study literature has indicated that 40-70% of the variance in alcohol use disorders (AUDs) is influenced by genetics. Recent attempts to identify specific x genetic risk variants associated with AUDs have been met with limited success. Meanwhile, evidence of the moderating effects of the environment on AUDs has been mounting, providing a strong rationale for examining gene-environment interaction. In the following chapters several studies will be described that integrate established twin methodologies into gene identification projects in an effort to reduce heterogeneity (both phenotypic and genotypic), elucidate environmental constructs that moderate genetic influences, and to enhance statistical power to detect the subtle genetic influences on alcohol related phenotypes.