Denna studie understryker den sociala miljöns betydelse för enäggstvillingars identitetsskapande. Hur utvecklas identiteten hos två genetiskt identiska individer som växer upp i samma miljö? Undersökningen bygger på kvalitativa intervjuer med tio enäggstvillingar, som även vill ge en inblick i hur enäggstvillingar upplever sin relation till sin tvilling och hur de upplever att de uppfattas av den sociala omgivningen. I vår teoretiska referensram har vi använt oss av diverse identitetsteorier som betonar interpersonella- och grupprocesser, Cooleys teori om spegeljaget samt den sociala jämförelseteorin som presenteras av Festinger. I resultatet framgick det hur enäggstvillingars identitet uppfattas i förhållande till sin tvilling, där omgivningen hade en betydande roll i enäggstvillingarnas identitetsskapande men även hur jämförelser direkt påverkade den egna självkänslan. Vi vill även konstatera att samtliga enäggstvillingar delade upplevelsen av trygghet och gemenskap i relationen till sin tvilling. / This study emphasizes the social environment to identical twins identity. How does the identity of two genetically identical individuals who grow up in the same environment develop? The study is based on qualitative interviews with ten identical twins, who also want to give a glimpse of how identical twins experience their relationship with their twin and how they experience they are perceived by the social environment. We have been using various identity theories that emphasize interpersonal and group processes in our theoretical framework, also Cooley's theory of the looking glass self and the social comparison theory presented by Festinger. The result showed how identical twins identity was perceived in relation to its twin, where the social environment had a significant role for identical twins identity but also how comparisons directly affected their self-esteem. We would also note that all identical twins shared the experience of safety and fellowship in relation to its twin.

Background: Androgens are important in prostate cancer development but how circulating levels of androgens affect risk of prostate cancer of different aggressiveness is not clear. Being childless has been associated with a lower risk of prostate cancer, but it is not clear if this association is causal or a result of residual confounding. Fathering of dizygotic twins, a marker of high fertility, has not been studied in relation to risk of prostate cancer. Another marker of life-long hormonal exposure is height, which has been associated with increased risk of cancer and cancer death. However, the association to separate cancer sites has not been consistent. The aims of this thesis were to study hormonal factors (paper I), and proxies of hormonal factors (paper II and III), and risk of prostate cancer; as well as height and risk of cancer and cancer death by separate sites (paper IV). Methods: Study designs were i) case-control studies, nested within the Västerbotten Intervention Project (paper I), and in Prostate Cancer database Sweden 2.0 (PCBaSe 2.0) (paper II and III), and ii) cohort study, in the Metabolic Syndrome and Cancer project (Me-Can) (paper IV). Results, prostate cancer: In paper I, increasing levels of serum androgens were not associated with risk of prostate cancer overall or in tumor risk categories. In paper II, childless men had a lower risk of prostate cancer, overall and in all risk categories, compared to fathers, an association which was in part explained by differences in marital status and educational level.  In paper III, fathers of dizygotic twins did not have an increased risk of prostate cancer, either overall or in risk categories, when compared to fathers of singletons. Results, cancer overall: In paper IV, height was associated with an increased risk of cancer and cancer death overall in both women and men. The strongest association for cancer was to malignant melanoma in both women and men, and for cancer death to post-menopausal breast cancer in women and renal cell carcinoma in men. Conclusions: These studies indicate that hormonal factors, when studied as serum levels or when studied using proxies of fertility, do not have a major impact on the risk of prostate cancer. The association between height and an increased risk of cancer appears robust for total cancer and cancer death, as well as for several separate cancer sites.

Darbo tikslas. Įvertinti gyvensenos ir genetinių veiksnių sąsajas su dvynių antropometriniais rodikliais. Uždaviniai. 1. Nustatyti monozigotinių ir dizigotinių dvynių antropometrinius rodiklius; 2. Įvertinti antropometrinių rodiklių ir gyvensenos sąsajas su genetiniais veiksniais; 3. Nustatyti normalaus svorio ir antsvorio turinčių dvynių gyvensenos skirtumus; 4. Nustatyti gyvensenos veiksnių ryšį su antropometriniais rodikliais, atsižvelgiant į genetinius veiksnius. Tyrimo metodika. Tirti Lietuvoje gyvenantys 18–54 metų dvyniai, kurie yra įtraukti į Dvynių centro registrą ir kurių buvo žinomas elektroninio pašto adresas. Vykdyta apklausa paštu. Anketą sudarė 51 klausimas apie dvynių socialinius rodiklius, sveikatos būklę, jų ūgį ir svorį bei gyvensenos įpročius. Anketos buvo išsiųstos 146 dvynių poroms. Jas grąžino 159 asmenys (atsako dažnis 54,5 proc.). Analizuoti 70 (40 monozigotinių ir 30 dizigotinių) dvynių porų duomenys. Antsvorio paplitimas skaičiuotas pagal kūno masės indeksą (KMI>25 kg/m2). Rezultatai. Antsvorio paplitimas tarp vyrų buvo 31,3 proc., tarp moterų – 19,4 proc. Jis dažniau nustatytas 35 metų ir vyresniems bei turintiems kolegijos išsilavinimą dvyniams. Nustatyti stiprūs ryšiai tarp visų MZ dvynių porų antropometrinių rodiklių. Labiausiai susijęs buvo monozigotinių dvynių ūgis (koreliacijos koeficientas – 0,941). Monozigotiniai dvyniai dažniau turėjo vienodus fizinio aktyvumo, mitybos ir žalingus įpročius nei dizigotiniai. Antsvorio paplitimas buvo... [toliau žr. visą tekstą] / Aim of the study. To evaluate the associations of behavioural and genetic factors with anthropometrical measurements of twins. Objectives. 1. To assess the antropometric indicators of monozigotic and dizigotic twins; 2. To evaluate the relationship between genetical factors and anthropometric indicators; 3. To identify the differences in health behaviour of twins with normal weight and overweight; 4. To evaluate the aoosiations the behavioural factors with antropometric indicators, taking into account genetic factors. Methods. Study population was 18–54 years old twins living in Lithuania, which were registered in the Twin Center and have e-mail addresses. For this study, the original questionnaire was developed which included 51 questions on sociodemographic characteristics, health status, weight and height, and behavioural habits of twins. The questionnaires were sent by email to 146 twin pairs; 159 individuals returned the filled in questionnaires (response rate 54.5%). The data of 70 twin pairs (40 monozigotic ir 30 dizigotic) were analyzed. Overweight was defined when body mass index (BMI) was >25 kg/m2. The statistical analysis was performed using SPSS 13.0 software package for Windows Results. 31,3 percent of men and 19,4 percent of women had overweight. It is more common for twins over 35 years old, with college degree. A strong correlation among all monozigotic twin couples was found. The height of monozigotic twins was found to be the most related (correlation... [to full text]

The thesis sets out to discuss the Bronze Age cosmology in Scandinavia, based on the results from the investigations at Nibble outside Enköping in Uppland. The excavations were carried out in 2007 and revealed extensive remains of a ritual place with burials, cult houses and food preparation areas. In addition, hundreds of cupmarks and two ship rock carvings were found. The cult place was constructed by moving stones around, gathering them into stone settings, stone walls and heaps of fire-cracked stones. The importance of the stones as cosmological entities is established through this special and deliberate treatment. Nature is transformed into culture. The cult place was established in connection with the construction of a large stone setting at the top of a hillock. Cremated and crushed bones of a man had been placed centrally in the construction, and close by, several cult houses had been erected, complemented by a food preparation area, where sacrificial meals were prepared and eaten.   In many cases, stone settings and heaps of fire-cracked stones are used in similar manners. At a settlement site close to the cult place, there was a heap of fire-cracked stones that contained the cremated bones of a young woman. It had been specially constructed for her burial and contained layers of coal and fire-cracked stones from several cremation pyres. The border between what is a burial and what is not is hard to define. The burnt bones of the dead were handled in much the same way as the burnt stone. They were burnt and crushed, ground to a powder, and restored to the earth. The use of stones in connection with fire and water (and smoke) suggests the existence of a system built on the four elements: stone (earth), fire, water and air. In addition, the existence of a tripartite universe is suggested. Stone settings (and some of the heaps of fire-cracked stones) were constructed as portals to the underground, and the smoke from the funeral pyres was the means of transport to the heaven above.  During the Early Bronze Age, the functions of the warrior and the shaman were often carried out by the same individual. During the Late Bronze Age, however, the functions of the warrior and the shaman seem to have been separated.   The separation of the ritual functions show that a change in ritual practice and cosmology occurred some time in the middle of the Bronze Age. A complete cosmological change was probably not involved, and many older rituals were still carried out in the Late Bronze Age. The relationship between the four elements remained the same, and the treatment of stone in particular remained unchanged. The connection between stone and bone still prevailed, as did the crushing and grinding.

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.

Thesis (M.A.)--Bowling Green State University, 2007. / Document formatted into pages; contains viii, 71 p. Includes bibliographical references.

Diss. (sammanfattning) Stockholm : Karol. inst., 2004. / Härtill 4 uppsatser.