Romantic relationships are one of the most important relationships a woman will develop in her life. Women are often socialized to be compliant within their relationships, and are reminded of how a thin body type is ideal. The implications of this socialization can affect the way a woman feels about her body. The current study included 207 women who ranged in age from 18-30, were in a relationship (neither married nor engaged) for 6 months or longer, and identified as either being attracted to the same or opposite sex. Results of the study indicated a significant effect of higher levels of body dissatisfaction between both negative relationship quality, and increased engagement in unhealthy dietary behaviours. In addition, self-silencing was found to be a significant mediator in the relationship between relationship quality and both body dissatisfaction and unhealthy dietary behaviours. Limitations of the study and directions for future research are discussed.

Romantic relationships are one of the most important relationships a woman will develop in her life. Women are often socialized to be compliant within their relationships, and are reminded of how a thin body type is ideal. The implications of this socialization can affect the way a woman feels about her body. The current study included 207 women who ranged in age from 18-30, were in a relationship (neither married nor engaged) for 6 months or longer, and identified as either being attracted to the same or opposite sex. Results of the study indicated a significant effect of higher levels of body dissatisfaction between both negative relationship quality, and increased engagement in unhealthy dietary behaviours. In addition, self-silencing was found to be a significant mediator in the relationship between relationship quality and both body dissatisfaction and unhealthy dietary behaviours. Limitations of the study and directions for future research are discussed.

A narrative inquiry methodology was utilized to investigate experiences of fluidity of sexuality and the broader processes of sexuality and sexual identity development. Five adult co-researchers, all members of various sexual and gender minority groups, participated in semi-structured, in-depth interviews centering on their experiences of changes in sexuality over time. The stories told were presented in the research text. Only one experience of a significant and lasting shift in sexual desire during adulthood was reported, occurring in the context of a transition from a male to a female gender identity. A thematic analysis of the co-researchers’ narratives was undertaken, and 3 common and 14 important themes were identified. The co-researchers’ stories and the common and important themes were brought together to form a partial model of sexuality and sexual identity development. Implications for counselling and for further research in this area were also considered. / Counselling Psychology

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.

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.

Patient-doctor relationships between same-sex attracted women and general practitioners (GPs) have been presented as problematic in the literature. The problems arise from women’s concerns about the potential for negative attitudes amongst GPs. They also relate to GPs’ concerns about offending patients if they ask about sexual orientation due to the stigmatised nature of minority sexual orientation. As a result, disclosure of sexual orientation can be difficult and the patient-doctor relationship can be compromised. The aim of this study was to explore the nature of patient-doctor relationships in this context and how optimal relationships can be achieved. / Using a critical hermeneutic approach, I conducted in-depth interviews with 33 same-sex attracted women and 28 doctors. This included 24 pairs of people in a current patient-doctor relationship. I found that women commonly experienced silencing of their minority sexual orientation within general practice settings, but that this was occasionally desired and not problematic for some women and most GPs. For other women and for many GPs, the silence resulting from a lack of disclosure was a response to perceived risks to women’s personal identity and GPs’ professional identity. Few GPs asked directly about sexual orientation, placing the burden of responsibility for disclosure on same-sex attracted women. Building reciprocal trust could overcome the perceived risks inherent in revealing minority sexual orientation. I initially defined optimal patient-doctor relationships in terms of existing models of cultural competence and patient-centredness; however I found that such relationships were built on cultural sensitivity rather than cultural competence, and relationship-centredness rather than patient-centredness. / I developed a new model of sexual identity disclosure that demonstrated the key influences on disclosure of sexual orientation to GPs for same-sex attracted women. These influences were women’s sexual identity experience, risk perceptions, and the level of knowing within the patient-doctor relationship. The model depicts women’s range and fluidity of sexual identity experiences and challenges current assumptions that disclosure is essential for effective health care. The model has transformative potential for general practice education and research. It could assist GPs to understand that not all women desire disclosure, but that the majority of women are happy to disclose if asked. GPs would be encouraged to take note of the socio-political environment in which women live and its influence on women’s fears and actual experiences of discrimination. Finally, understanding the role of trust and reciprocal knowing in mitigating perceived risks would encourage GPs to focus more on relationship building. This could also assist GPs to overcome their own perceptions of risk and encourage them to broach the subject of sexual orientation, ultimately enhancing the patient-doctor relationship.

Thesis (Ph. D.)--Texas State University-San Marcos, 2007. / Vita. Appendices: leaves 316-341. Includes bibliographical references (leaves 293-315).

Thesis PlanB (M.S.)--University of Wisconsin--Stout, 2007. / Includes bibliographical references.