Sexuality is central to our individual lives, our society, and our evolution, but its etiology is not thoroughly understood. Using data from 4904 Australian twins who completed a questionnaire on sexual attitudes and behaviours, I investigated the genetic and environmental influences underlying variation in and covariation between psychological and behavioural aspects of sexuality. Moreover, I explored the role of sexuality traits in several different contexts: evolution, mental health, public health, personality, and problematic behaviour. Before presenting reports of the four main empirical studies in this thesis, I make the case for the importance of studying human sexuality, outline previous findings on the etiology of individual differences in sexuality, and describe the behavioural genetic principles and techniques that were used in the investigations. I also present an additional fifth paper reporting a behavioural genetic analysis of EEG power, which I undertook in order to learn twin data modelling and complex multivariate techniques. In the first empirical paper I investigated sexual orientation from an evolutionary perspective. As sexual orientation is genetically influenced, it is not known how homosexuality, which tends to lower reproductive success, is maintained in the population at a relatively high frequency. I tested the hypothesis that while genes predisposing to homosexuality reduce homosexuals’ reproductive success, they may confer some advantage for heterosexuals who carry them. Results showed that psychologically masculine females and feminine men are 1) more likely to be nonheterosexual, but 2) when they are heterosexual have more opposite-sex sexual partners. Genetic modelling revealed that both these relationships are partly due to pleiotropic genetic influences common to each trait. Further, heterosexuals with a nonheterosexual twin had more opposite-sex partners than do heterosexual twin pairs. Taken together, these results suggest that genes predisposing to homosexuality may confer a mating advantage in heterosexuals, which could contribute to the evolution and maintenance of homosexuality in the population. In the second empirical paper I investigated sexual orientation from the perspective of mental health risk. Large epidemiological studies have shown that homosexuals are at much greater risk of psychiatric disorder than the general population. This has been assumed, with some supporting evidence, to be because of the prejudice and discrimination experienced by homosexuals in a heterosexist society. Here I tested the viability of alternative explanations, using Eysenck’s Neuroticism and Psychoticism scales as markers for psychiatric vulnerability. Firstly, I tested whether apparent sexual orientation differences in psychiatric vulnerability simply mirror sex differences – for our traits, this would predict nonheterosexual males having elevated Neuroticism scores as females do, and nonheterosexual females having elevated Psychoticism scores as males do. The results contradicted this idea, with nonheterosexual men and women scoring significantly higher on both Neuroticism and Psychoticism than their heterosexual counterparts, suggesting an overall elevation of psychiatric risk in nonheterosexuals. Secondly, I used the genetically informative sample to assess the viability of explanations invoking a common cause of both nonheterosexuality and psychiatric vulnerability. We found significant genetic correlations between sexual orientation and both Neuroticism and Psychoticism, but no corresponding environmental correlations, suggesting that if there is a common cause of both nonheterosexuality and psychiatric vulnerability it is likely to have a genetic basis rather than an environmental basis. The third empirical paper investigated the etiology of risky sexual behaviour, which is relevant to public health and welfare through its role in STD transmission and unwanted pregnancies. Results showed that variation in risky sexual behaviour is due to genetic, shared environmental, and unshared environmental influences to approximately equal degrees. The genetic influences partly overlapped with genetic influences on dispositional factors, with significant genetic correlations between risky sexual behaviour and Eysenck’s Impulsivity, Extraversion, Psychoticism, and Neuroticism. This suggests that the genetic influences that shape our personality may also predispose us to risky sexual behaviour. The fourth empirical paper investigated the etiology of a strong association (r = .50) between risky sexual behaviour and adolescent misconduct. Results indicated that the association is due to overlapping genetic and environmental influences, but that in males genes are the primary source of the association whereas in females shared environment plays the greater role. These findings suggest that a general predisposition to risky behaviour may manifest in different potentially harmful ways in adolescence (misconduct) and adulthood (risky sexual behaviour), and that different processes are involved in male and female etiology. Following the empirical reports, I provide a general discussion of my research findings and the study of human sexuality more generally. After summarising the findings and their implications, I then provide a detailed description of potential limitations of the research and to what extent they qualify the conclusions drawn. I also critically discuss the absence of sexuality traits from the major models of personality, and why this and other shortcomings make the personality models inadequate from an evolutionary perspective. Finally, I suggest directions for future research in light of the research and discussion presented in this thesis.

Sexuality is central to our individual lives, our society, and our evolution, but its etiology is not thoroughly understood. Using data from 4904 Australian twins who completed a questionnaire on sexual attitudes and behaviours, I investigated the genetic and environmental influences underlying variation in and covariation between psychological and behavioural aspects of sexuality. Moreover, I explored the role of sexuality traits in several different contexts: evolution, mental health, public health, personality, and problematic behaviour. Before presenting reports of the four main empirical studies in this thesis, I make the case for the importance of studying human sexuality, outline previous findings on the etiology of individual differences in sexuality, and describe the behavioural genetic principles and techniques that were used in the investigations. I also present an additional fifth paper reporting a behavioural genetic analysis of EEG power, which I undertook in order to learn twin data modelling and complex multivariate techniques. In the first empirical paper I investigated sexual orientation from an evolutionary perspective. As sexual orientation is genetically influenced, it is not known how homosexuality, which tends to lower reproductive success, is maintained in the population at a relatively high frequency. I tested the hypothesis that while genes predisposing to homosexuality reduce homosexuals’ reproductive success, they may confer some advantage for heterosexuals who carry them. Results showed that psychologically masculine females and feminine men are 1) more likely to be nonheterosexual, but 2) when they are heterosexual have more opposite-sex sexual partners. Genetic modelling revealed that both these relationships are partly due to pleiotropic genetic influences common to each trait. Further, heterosexuals with a nonheterosexual twin had more opposite-sex partners than do heterosexual twin pairs. Taken together, these results suggest that genes predisposing to homosexuality may confer a mating advantage in heterosexuals, which could contribute to the evolution and maintenance of homosexuality in the population. In the second empirical paper I investigated sexual orientation from the perspective of mental health risk. Large epidemiological studies have shown that homosexuals are at much greater risk of psychiatric disorder than the general population. This has been assumed, with some supporting evidence, to be because of the prejudice and discrimination experienced by homosexuals in a heterosexist society. Here I tested the viability of alternative explanations, using Eysenck’s Neuroticism and Psychoticism scales as markers for psychiatric vulnerability. Firstly, I tested whether apparent sexual orientation differences in psychiatric vulnerability simply mirror sex differences – for our traits, this would predict nonheterosexual males having elevated Neuroticism scores as females do, and nonheterosexual females having elevated Psychoticism scores as males do. The results contradicted this idea, with nonheterosexual men and women scoring significantly higher on both Neuroticism and Psychoticism than their heterosexual counterparts, suggesting an overall elevation of psychiatric risk in nonheterosexuals. Secondly, I used the genetically informative sample to assess the viability of explanations invoking a common cause of both nonheterosexuality and psychiatric vulnerability. We found significant genetic correlations between sexual orientation and both Neuroticism and Psychoticism, but no corresponding environmental correlations, suggesting that if there is a common cause of both nonheterosexuality and psychiatric vulnerability it is likely to have a genetic basis rather than an environmental basis. The third empirical paper investigated the etiology of risky sexual behaviour, which is relevant to public health and welfare through its role in STD transmission and unwanted pregnancies. Results showed that variation in risky sexual behaviour is due to genetic, shared environmental, and unshared environmental influences to approximately equal degrees. The genetic influences partly overlapped with genetic influences on dispositional factors, with significant genetic correlations between risky sexual behaviour and Eysenck’s Impulsivity, Extraversion, Psychoticism, and Neuroticism. This suggests that the genetic influences that shape our personality may also predispose us to risky sexual behaviour. The fourth empirical paper investigated the etiology of a strong association (r = .50) between risky sexual behaviour and adolescent misconduct. Results indicated that the association is due to overlapping genetic and environmental influences, but that in males genes are the primary source of the association whereas in females shared environment plays the greater role. These findings suggest that a general predisposition to risky behaviour may manifest in different potentially harmful ways in adolescence (misconduct) and adulthood (risky sexual behaviour), and that different processes are involved in male and female etiology. Following the empirical reports, I provide a general discussion of my research findings and the study of human sexuality more generally. After summarising the findings and their implications, I then provide a detailed description of potential limitations of the research and to what extent they qualify the conclusions drawn. I also critically discuss the absence of sexuality traits from the major models of personality, and why this and other shortcomings make the personality models inadequate from an evolutionary perspective. Finally, I suggest directions for future research in light of the research and discussion presented in this thesis.

The experiences of lesbian, gay, bisexual and transgender (LGB)(T) secondary school students are often problematic. The literature documents that LGB(T) students often experience harassment in secondary school settings. The participants in this study identify that issues around subject content, the need to address bullying and strategies around support are three key issues that might be targeted if LGB(T) school experiences are to improve. This thesis responds to participant perspectives by outlining a broad approach that is anchored by their concerns.

Sexuality is central to our individual lives, our society, and our evolution, but its etiology is not thoroughly understood. Using data from 4904 Australian twins who completed a questionnaire on sexual attitudes and behaviours, I investigated the genetic and environmental influences underlying variation in and covariation between psychological and behavioural aspects of sexuality. Moreover, I explored the role of sexuality traits in several different contexts: evolution, mental health, public health, personality, and problematic behaviour. Before presenting reports of the four main empirical studies in this thesis, I make the case for the importance of studying human sexuality, outline previous findings on the etiology of individual differences in sexuality, and describe the behavioural genetic principles and techniques that were used in the investigations. I also present an additional fifth paper reporting a behavioural genetic analysis of EEG power, which I undertook in order to learn twin data modelling and complex multivariate techniques. In the first empirical paper I investigated sexual orientation from an evolutionary perspective. As sexual orientation is genetically influenced, it is not known how homosexuality, which tends to lower reproductive success, is maintained in the population at a relatively high frequency. I tested the hypothesis that while genes predisposing to homosexuality reduce homosexuals’ reproductive success, they may confer some advantage for heterosexuals who carry them. Results showed that psychologically masculine females and feminine men are 1) more likely to be nonheterosexual, but 2) when they are heterosexual have more opposite-sex sexual partners. Genetic modelling revealed that both these relationships are partly due to pleiotropic genetic influences common to each trait. Further, heterosexuals with a nonheterosexual twin had more opposite-sex partners than do heterosexual twin pairs. Taken together, these results suggest that genes predisposing to homosexuality may confer a mating advantage in heterosexuals, which could contribute to the evolution and maintenance of homosexuality in the population. In the second empirical paper I investigated sexual orientation from the perspective of mental health risk. Large epidemiological studies have shown that homosexuals are at much greater risk of psychiatric disorder than the general population. This has been assumed, with some supporting evidence, to be because of the prejudice and discrimination experienced by homosexuals in a heterosexist society. Here I tested the viability of alternative explanations, using Eysenck’s Neuroticism and Psychoticism scales as markers for psychiatric vulnerability. Firstly, I tested whether apparent sexual orientation differences in psychiatric vulnerability simply mirror sex differences – for our traits, this would predict nonheterosexual males having elevated Neuroticism scores as females do, and nonheterosexual females having elevated Psychoticism scores as males do. The results contradicted this idea, with nonheterosexual men and women scoring significantly higher on both Neuroticism and Psychoticism than their heterosexual counterparts, suggesting an overall elevation of psychiatric risk in nonheterosexuals. Secondly, I used the genetically informative sample to assess the viability of explanations invoking a common cause of both nonheterosexuality and psychiatric vulnerability. We found significant genetic correlations between sexual orientation and both Neuroticism and Psychoticism, but no corresponding environmental correlations, suggesting that if there is a common cause of both nonheterosexuality and psychiatric vulnerability it is likely to have a genetic basis rather than an environmental basis. The third empirical paper investigated the etiology of risky sexual behaviour, which is relevant to public health and welfare through its role in STD transmission and unwanted pregnancies. Results showed that variation in risky sexual behaviour is due to genetic, shared environmental, and unshared environmental influences to approximately equal degrees. The genetic influences partly overlapped with genetic influences on dispositional factors, with significant genetic correlations between risky sexual behaviour and Eysenck’s Impulsivity, Extraversion, Psychoticism, and Neuroticism. This suggests that the genetic influences that shape our personality may also predispose us to risky sexual behaviour. The fourth empirical paper investigated the etiology of a strong association (r = .50) between risky sexual behaviour and adolescent misconduct. Results indicated that the association is due to overlapping genetic and environmental influences, but that in males genes are the primary source of the association whereas in females shared environment plays the greater role. These findings suggest that a general predisposition to risky behaviour may manifest in different potentially harmful ways in adolescence (misconduct) and adulthood (risky sexual behaviour), and that different processes are involved in male and female etiology. Following the empirical reports, I provide a general discussion of my research findings and the study of human sexuality more generally. After summarising the findings and their implications, I then provide a detailed description of potential limitations of the research and to what extent they qualify the conclusions drawn. I also critically discuss the absence of sexuality traits from the major models of personality, and why this and other shortcomings make the personality models inadequate from an evolutionary perspective. Finally, I suggest directions for future research in light of the research and discussion presented in this thesis.

Thesis (doctoral)--Universität, Freiburg (Breisgau), 2007. / Includes bibliographical references and sources (p. 332-390).

Thesis (Ph. D.)--University of Auckland, 1990. / Includes bibliographical references (leaves 149-159).

Diss. Linköping : Linköpings universitet, 2007. / Bilaga innehållande engelsk sammanfattning med titeln: We don't dance on the table : lesbian immigrant women in Sweden : stigmatization & pride. S. 265-284: Bibliografi.

Thesis (Ph.D.)--University of Wollongong, 2004. / Typescript. Includes bibliographical references: p. 299-323.

Thesis (M.A.)--Texas State University-San Marcos, 2008. / Vita. Includes bibliographical references (leaves 109-112). Also available on microfilm.

Thesis (Ph. D.)--Ohio State University, 2008. / Title from first page of PDF file. Includes bibliographical references (p. 71-73).