Same-Sex Partner Preference in Zebra Finches: Pairing Flexibility and Choice

This study examined flexibility and choice in same-sex pair-bonding behavior in adult zebra finches (Taeniopygia guttata). Zebra finches form life-long monogamous relationships and extra pair behavior is very low, making them an ideal species in which to study same-sex pairing. We examined same-sex behaviors using both semi-naturalistic choice paradigms and skewed sex ratios. In the first experiment, we allowed zebra finches to pair in aviaries with equal sex ratios as part of multiple experiments. On average, 6.4 % (N = 78) of unmanipulated pairs were same-sex: all but one was female–female. In a second experiment, we identified pairs from same-sex cages and selected 20 total same-sex pairs (10 of each sex). We then gave pairs a chance to court and pair with members of the opposite sex and observed their behavior for three days. Females did not retain their partner, but most paired with males. In contrast, some males did retain their partner. Similarly, females were more likely to engage in pairing behaviors with males than with their partners or other females whereas males were equally likely to engage in same-sex and opposite-sex pairing behaviors. These findings suggest that same-sex partnerships in zebra finches can be facultative, based on the sex ratio of the group in which they live, but can also be a choice, when opportunities to pair with opposite-sex individuals are possible. Furthermore, it is possible that females are more flexible in this choice of same-sex partnerships than are males.     

Bivariate genetic analysis of fasting insulin and glucose levels

The main aim of this study was to estimate the relative influence of genes and environment on fasting insulin levels, which were considered a proxy of insulin resistance. Possible sex differences in genetic and environmental influences, and the origin of the covariance between fasting insulin and glucose were investigated. Subjects were 209 pairs of middle-aged twins, divided into 5 sex-by-zygosity groups. A general bivariate model and a reciprocal causation model including fasting insulin and glucose were used in the analyses. For both quantitative genetic models, a model specifying additive genetic and unique environmental factors, which were the same in males and females, showed the best fit to the data. Heritability estimates were modest and highly similar in both models: 20-25% of the variance in fasting insulin, and around 50% of the variance in fasting glucose levels could be attributed to genetic factors. The two models could not be discriminated on the basis of their fit to the data. A submodel of the general bivariate model suggested that the covariance between glucose and insulin has a unique environmental basis, whereas for the reciprocal causation model both causal paths were needed to explain the phenotypic correlation between insulin and glucose and estimates of the reciprocal paths were of opposite sign, an indication for the expected negative feedback loop.     

汉族儿童青少年体型遗传的双生子研究

目的分析遗传与环境因素对儿童青少年体型的影响,并探讨其中年龄和性别的作用。方法采用Heath-Carter法对376对6～18岁同性别汉族双生子（同卵双生子245对,异卵双生子131对）的体型三因子进行计算。调整另外两项体型因子后,用Mx软件拟合最佳模型,计算各体型因子的遗传与环境方差组分,分析年龄和性别的作用,并按体格突增分期估算不同发育期各因子的遗传度。结果校正年龄后,男生内、中、外三因子的遗传度分别为0．45,0．80,0．44;女生内、中、外三因子的遗传度分别为0．82,0．79,0．81;男生内因子的遗传度在青春期晚期明显高于前期（t=4．99,P〈0．01）和早期（t=6．16,P〈0．01）,外因子的遗传度在青春期晚期明显低于前期（t=3．35,P〈0．01）和早期（t=4．12,P〈0．01）;女生内因子（t=2．77,P〈0．01）、中因子（t=2．08,P〈0．05）的遗传度均为青春期前期明显高于早期。结论遗传因素对女生体型的影响明显高于男生,尤以内因子和外因子最为明显,男生中因子主要受遗传因素影响,内、外因子受环境因素影响较大。不同发育阶段对体型各因子遗传度的影响应引起重视。     

Genetic and environmental effects on blood pressure in a Norwegian sample.

Systolic (SBP) and diastolic (DBP) blood pressures were measured in a health screening of the adult population in Nord-Trøndelag, Norway. Correlations were computed for 23,936 pairs of spouses, 43,586 pairs of parent and offspring, 19, 151 pairs of siblings, 1,251 pairs of grandparents-grandchildren, 1,146 pairs of biological uncles/aunts-nephews/nieces (avuncular), 801 non-biological avuncular pairs, 169 pairs of same-sex twins, and smaller groups of other types of relationships. Spouse correlations of 0.08 and 0.09 were approximately constant or slightly decreasing with marital duration. The correlation values for SBP and DBP were approximately 0.16 for parents-offspring, 0.19 to 0.23 for same-sex siblings with similar values for DZ twins, 0.19 and 0.16 for opposite-sex siblings, 0.52 and 0.43 for MZ twins, and close to zero for most of the second-order relationships. Genetic additive variance was estimated at 0.29 and genetic dominance variance at 0.18 with the best model for SBP. The corresponding estimates from the best models for DBP were 0.29 or lower and 0.22 or lower, the sum not exceeding 0.35. There was evidence of a moderate effect of environmental factors shared by same-sex siblings and twins (for DBP), but no cultural transmission, and whether or not adult relatives live together does not affect familial resemblance for BP. The data did not permit a very precise resolution of the relative magnitude of genetic dominance and sibling effects. The correlation structure did not show sex-specific genetic effects. © 1992 Wiley-Liss, Inc.     

Genetic and environmental influences on binge eating in the absence of compensatory behaviors: a population-based twin study

OBJECTIVE: The current study explores the extent to which genetic and environmental factors influence liability to binge eating in the absence of compensatory behaviors (BE) in a population-based sample of twins. METHOD: Questionnaire data on 8,045 same-sex and opposite-sex twins, aged 18-31 years, from a Norwegian twin registry were used to assess BE during the last 6 months. RESULTS: The best-fitting biometrical model suggested that the heritability of BE was 41% (95% confidence interval [CI]: 0.31-0.50). Individual environmental factors accounted for the rest of the variance (59%; 95% CI: 0.50-0.69). No significant sex differences were found, but the statistical power to detect such effects was low. Shared environmental influences on the liability to BE in males could not be ruled out. DISCUSSION: The findings indicate significant additive genetic influences on BE, supporting the validity of the core features of binge eating disorder as a diagnostic category.     

A comparison of genetic and environmental variance structures for asthma, hay fever and eczema with symptoms of the same diseases: a study of Norwegian twins

BACKGROUND: We compared patterns of genetic and environmental influences on variation in liability for asthma, hay fever and eczema with those for symptoms of the same diseases, and determined how common sets of genes and environmental factors contribute to the relationship between diseases and symptoms among Norwegian twins. METHODS: Analyses were based on self-reported asthma, hay fever and eczema and symptoms of the same diseases among 3334 pairs of Norwegian twins aged 18-35 years. Structural equation modelling was conducted to estimate the genetic and environmental variance structures. RESULTS: For all diseases the concordances and the twin correlations were higher among monozygotic than among dizygotic twins. The results of the modelling confirmed that genetic effects were substantial for the diseases, and were more moderate for symptoms. The phenotypic correlation between disease and symptom was 0.67 for asthma and wheeze (a/w), 0.64 for hay fever and sneeze (hf/s), and 0.54 for eczema and itch (e/i). Decomposition of these correlations into genetic (G) and environmental (E) pathways revealed that G = 0.48 and E = 0.19 for a/w, G = 0.40 and E = 0.24 for hf/s, and G = 0.34 and E = 0.20 for e/i. For the diseases, the specific sources of genetic variance accounted for more variation than the specific environmental variance. Variance decomposition revealed that specific sources of variance were primarily explained by genetic effects for diseases and by environmental influences for symptoms. CONCLUSIONS: Genetic effects account for greater variation in reported diseases than symptoms. Co-occurrence of diseases and symptoms is mainly explained by genetic effects common to both phenotypes, but non-shared environment is also important.     

Sexual Orientation and Psychiatric Vulnerability: A Twin Study of Neuroticism and Psychoticism

Recent evidence indicates that homosexuals and bisexuals are, on average, at greater risk for psychiatric problems than heterosexuals. It is assumed with some supporting evidence that prejudice often experienced by nonheterosexuals makes them more vulnerable to psychiatric disorder, but there has been no investigation of alternative explanations. Here we used Eysenck’s Neuroticism and Psychoticism scales as markers for psychiatric vulnerability and compared heterosexuals with nonheterosexuals in a community-based sample of identical and nonidentical twins aged between 19 and 52 years (N = 4904). Firstly, we tested whether apparent sexual orientation differences in psychiatric vulnerability simply mirrored 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. Our results contradicted this idea, with nonheterosexual men and women scoring significantly higher on Neuroticism and Psychoticism than their heterosexual counterparts, suggesting an overall elevation of psychiatric risk in nonheterosexuals. Secondly, we used our genetically informative sample to assess the viability of explanations invoking a common cause of both nonheterosexuality and psychiatric vulnerability. We found significant genetic correlation 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.     

Prevalence and Stability of Sexual Orientation Components During Adolescence and Young Adulthood

Analyses of three waves (6 years) of the National Longitudinal Survey of Adolescent Health data explored the prevalence and stability of sexual orientation and whether these two parameters varied by biologic sex, sexual orientation component (romantic attraction, sexual behavior, sexual identity), and degree of component. Prevalence rates for nonheterosexuality varied between 1 and 15% and depended on biologic sex (higher among females), sexual orientation component (highest for romantic attraction), degree of component (highest if “mostly heterosexual” was included with identity), and the interaction of these (highest for nonheterosexual identity among females). Although kappa statistics testing for temporal stability across waves were significant, they failed to reach acceptable levels of agreement and could be largely attributable to the stability of opposite-sex rather than same-sex attraction and behavior. Migration over time among sexual orientation components was in both directions, from opposite-sex attraction and behavior to same-sex attraction and behavior and vice versa. To assess sexual orientation, investigators should measure multiple components over time or abandon the general notion of sexual orientation and measure only those components relevant for the research question.     

Habitual physical activity in children: the role of genes and the environment

BACKGROUND: Understanding the factors that contribute to physical inactivity in children is important because sedentary behavior strongly relates to metabolic disorders such as obesity and diabetes. OBJECTIVE: We aimed to quantify the genetic and environmental influences on physical activity energy expenditure (PAEE) in 100 sex-concordant dizygotic (n = 38) and monozygotic (n = 62) twin pairs aged 4-10 y. DESIGN: Resting metabolic rate (RMR) was assessed by using respiratory gas exchange, total energy expenditure (TEE) by using doubly labeled water, and body composition by using dual-energy X-ray absorptiometry. Structural equation modeling was used to partition the phenotypic variance into additive genetic (a2) and common (c2) and unshared (e2) environmental components. RESULTS: Because PAEE [TEE - (RMR + 0.1 x TEE)] depends on body weight, which is highly heritable, we tested several models: 1) after adjustment for age, sex, ethnicity, study date, season, and weight, a2 explained none of the phenotypic variance in PAEE (95% CI: 0%, 38%), whereas c2 and e2 accounted for 69% (33%, 77%; P = 0.001) and 31% (23%, 39%; P < 0.001) of the variance, respectively; 2) after adjustment for the cofactors in model 1, a2 explained 19% of the phenotypic variance in TEE (0%, 60%; P = 0.13), whereas c2 and e2 accounted for 59% (16%, 79%; P = 0.007) and 23% (17%, 31%; P < 0.0001) of the variance, respectively; 3) in models adjusted as above (excluding weight), a2 explained no variance in physical activity level (TEE/RMR) (0%, 32%; P = 0.50), whereas c2 and e2 explained 65% (34%, 60%; P = 0.001) and 35% (28%, 45%; P < 0.0001) of the variance, respectively. CONCLUSIONS: Our data suggest that the familial resemblance in physical activity in these children is explained predominantly by shared environmental factors and not by genetic variability.     

Sex,stressful life events,and adult onset depression and alcohol dependence: Are men and women equally vulnerable?

Higher rates of major depression (MD) among females, and of alcohol dependence (AD) among males, are among the most routinely reported findings in psychiatric epidemiology. One of the most often pursued explanations for sex differences in both disorders suggests that males and females have a differential vulnerability to stressors, which is manifested in sex-specific ways (MD for females, AD for males). However, existing evidence in support of this explanation is mixed. In the present study, we investigated sex differences in the association between stressful life events and MD and AD in a large national sample of adults in the United States (n = 32,744) using a prospective design. Logistic regression was used to estimate associations between stressful life events and both MD and AD; sex-specific effects of stress on MD and AD were evaluated by testing interaction terms between sex and stressors in the prediction of both outcomes. The number of stressful life events was predictive of first onset MD and AD. This was true for both males and females, and sex-by-stress interaction terms did not support the hypothesis that sex-specific responses to stressful life events lead to sex differences in first onset of MD and AD among adults. These results indicate the resistance of sex differences in MD and AD to simple explanations, and suggest the need for more nuanced models that incorporate both physiological and social aspects of vulnerability.     

Sex-specific QTL effects on variation in paraoxonase 1 (PON1) activity in Mexican Americans

Paraoxonase 1 (PON1), a high-density lipoprotein-associated enzyme known to protect against cellular damage from toxic agents, may also have antioxidant properties. PON1 activity levels have been reported to differ by sex in human and animal studies with females exhibiting higher basal levels. We measured PON1 activity frozen serum for 1,406 individuals in over 40 extended pedigrees from the San Antonio Family Heart Study (SAFHS). We used a maximum likelihood-based, variance decomposition approach implemented in SOLAR to test for genotype-by-sex (G x S) interaction on variation in PON1 activity and to determine if any of the four PON1 quantitative trait loci (QTL) previously reported by us for this population might account for sex differences in PON1 activity levels. The residual additive genetic correlation (rho(G) = 0.82) between males and females is significantly different from 1 (P = 0.009), suggesting that some of the genes that influence PON1 activity act differently in females and males or, possibly, that a different combination of genes influences this trait in each sex. In addition to the QTL at or near the PON structural locus on 7q21-22, three other potential QTLs were evaluated for sex-specific effects: one each on chromosomes 12, 17 and 19. The QTL on chromosome 17 (LOD = 2.32, P = 0.0003; flanked by microsatellite marker loci D17S974 and D17S969) shows a significant (P = 0.005) sex-specific effect on PON1 activity; accounting for 6% of the additive genetic variance in males and 20% in females. This study represents the first formal statistical genetic test for G x S interactions on normal quantitative variation in PON1 activity in humans.     

The correlation of fecundability among twins: evidence of a genetic effect on fertility?

BACKGROUND: Numerous rare genetic conditions are known to influence fecundability in both males and females. It is less clear to what extent more subtle genetic differences influence fecundability on a population level. METHODS: In 1994 a population-based survey was conducted among Danish twins born 1953-1982. Fecundability was assessed as the waiting time to pregnancy at the first attempt to achieve a pregnancy. RESULTS: The reported time to pregnancy for males was slightly shorter than for females but there were no sex differences in intrapair similarity. We found an intrapair correlation in time to pregnancy for 645 monozygotic twin pairs (r = 0.22; 95% confidence interval = 0.12 to 0.32), but no intrapair correlation for 826 like-sex dizygotic twin pairs (r = 0.00; 95% confidence interval = -0.09 to 0.10). CONCLUSIONS: The correlation in time to pregnancy for monozygotic twins suggests genetic factors, although similarities in reporting behaviors could also be contributing to the correlation. The lack of correlation in time to pregnancy for dizygotic twins indicates that possible genetic factors of importance for fecundabililty are acting nonadditively. Hence, it may prove difficult to identify specific gene variants that influence fecundability on a population level if their effects depend on gene-gene interactions.     

Sex differences in human mortality: the role of genetic factors

This paper reviews evidence concerning genetic factors that influence sex differences in human mortality, with attention to the interactions between genetic and environmental factors. Some widely quoted earlier conclusions, for example, that males have consistently higher fetal mortality than females, are not supported by current evidence. For example, for late fetal mortality, males had higher rates than females in earlier historical data, but not in recent data for several advanced industrial countries. This reflects a changing balance between an inherently greater female vulnerability for one major type of late fetal mortality and inherently greater male vulnerability for several other types of late fetal mortality that have declined in importance as health care has improved. Males appear to be inherently more vulnerable than females to infant mortality, although the causes of this vulnerability are poorly understood. X-linked immunoregulatory genes appear to contribute to greater female resistance to infectious diseases. Despite these apparent inherent advantages for females, in some situations females have had higher infant mortality and higher infectious disease mortality than males, apparently due to environmental disadvantages for females, such as less adequate diet and health care. Inherent sex differences in reproductive physiology and anatomy contribute to higher female mortality for breast cancer and maternal mortality. For these causes of death, as for the other categories discussed, the death rates and thus the contributions to sex differences in total mortality vary considerably depending on environmental conditions. Several hypothesized contributions of sex hormones to sex differences in mortality are at present controversial due to contradictions and limitations in the available data. There may be effects of male sex hormones on sex differences in behavior which contribute to males' higher death rates for accidents and other violent causes. Women's endogenous sex hormones may reduce women's risk of ischemic heart disease. For both violent deaths and ischemic heart disease it appears that any genetic contributions to sex differences in mortality are strongly reinforced by the cultural influences that foster more risky behavior in males, including more use of weapons, employment in hazardous occupations, heavy alcohol consumption and cigarette smoking. It appears that these cultural influences on sex differences in behavior are widespread cross-culturally in part because of the effects of inherent sex differences in reproductive functions on the cultural evolution of sex roles. These examples illustrate the complexity and importance of interactions between genetic and environmental factors in determining sex differences in human mortality.     

Body dissatisfaction and drive for thinness in young adult twins

OBJECTIVE: We explored correlates of the Eating Disorder Inventory subscales Body Dissatisfaction (BD) and Drive for Thinness (DT) and genetic and environmental influences on these traits. METHOD: In a population-based sample of 4,667 Finnish twins aged 22-27 years, we conducted twin modeling to explore genetic and environmental contributions to body dissatisfaction and drive for thinness. Logistic regression was used for the correlational analysis. RESULTS: Various eating and body size-related factors and psychosomatic symptoms were significantly associated with high body dissatisfaction and drive for thinness in both genders. In women, early puberty onset, early initiation of sexual activity, and multiple sex partners were statistically significant risk factors of body dissatisfaction. In gender-specific univariate twin models, additive genes accounted for 59.4% (95% confidence interval [CI] = 53.2-64.7%) of the variance in body dissatisfaction and for 51.0% (95% CI = 43.7-57.5%) of the variance in drive for thinness among females, but for none of the variance among males. DISCUSSION: There are very distinct gender differences in the heritability patterns of body dissatisfaction and drive for thinness in young adults.     

Sex-specific effects for body mass index in the new Norwegian twin panel

Sex-specific effects for body mass index (BMI) were explored in a newly established, population-based Norwegian twin panel. The sample includes 5,864 individuals, aged 18–25 years, who responded to a questionnaire containing items for zygosity classification, height, weight, health, health-related behaviors, well-being, and demographic information. Among the 2,570 intact pairs who returned the questionnaire there were 416 identical (MZ) male pairs, 387 fraternal (DZ) male pairs, 528 MZ female pairs, 443 DZ female pairs, and 796 unlike-sexed pairs. Alternate sets of models testing for either sex-specific genetic or environmental parameters were evaluated using structural equation analysis. Results from the most parsimonious model indicated that the genes contributing to variation in BMI are not identical for men and women; rather, some genetic effects were shared by the sexes and some were unique to each sex. Total variation in BMI could be explained by sex-specific additive genetic effects, as well as genetic and non-shared environmental effects common to men and women. Estimates of heritability were .708 for men and .789 for women, and the male-female genetic correlation was 0.622. The series of models specifying sex-specific shared environment also fit the data and suggests that shared environmental factors may be important for males but not for females. The findings raise questions concerning the relationship between sex-specific effects for BMI and sex differences in health outcomes. ©1995 Wiley-Liss, Inc.     

Pedigree analysis of blood pressure in subjects from rural Greece and relatives who migrated to Melbourne, Australia.

Diastolic blood pressure readings taken in 1983-1984 on 1,474 Greek individuals (628 living on the island of Levkada, 846 relatives having migrated to Melbourne, Australia) from 204 two generational pedigrees were analysed. Blood pressure was regressed as a quadratic in age by sex and migrant status, and on temperature. Variance increased with age and was greater in migrant males. The covariance between relatives in different countries was significant. Variation was modeled by a multivariate normal model for pedigree analysis in terms of genetic effects, a common environment effect, and effects particular to an individual. The genetic component was 25.9 mm Hg2, independent of sex and migrant status. Importantly, the common environment component was not significant. The third component was greatest in migrant males. Spouse correlation was -0.09 (SE = 0.03). Exclusion of 86 individuals who reported currently receiving medication for elevated blood pressure stabilised the variance and decreased the genetic component. The data suggest that familial aggregation of diastolic blood pressure is due to genetic factors which produce the same variation in males and females, living on Levkada or in Melbourne. Nongenetic factors explain the greater variation in blood pressure of migrant males living in Melbourne.     

Genetic contribution to variation in larval development time, adult size, and longevity of starved adults of Anopheles gambiae.

The variation in mosquito life-history traits such as adult size has been studied with respect to environmental factors, but the genetic contribution to such variation has received almost no consideration. Using a full-sib design of F1s produced by wild caught Anopheles gambiae (M molecular form) females, we estimated broad-sense heritability of larval developmental time, adult size (based on dry weight and wing length), and longevity of starved adults. These traits were correlated (at the phenotypic level) with each other in females and males (|r(p)|>0.5, P<0.001). Longevity of starved adults increased with adult size, and both traits (adult longevity and size) decreased with longer larval development. Genetic correlations were lower (|r(g)|>0.45, P<0.05) but provided consistent evidence against a trade off between adult size and larval development time predicting that a mosquito can develop faster into a smaller adult or be a larger adult by a longer development. Estimates of heritability of the three traits were moderate to high (range: 0.05-0.48) and statistically significant (P<0.05), indicating substantial genetic contribution to the phenotypic variation in these traits. These results suggest that adaptive differences are likely to be found in these traits between A. gambiae populations.     

The heritability of cause-specific mortality: a correlated gamma-frailty model applied to mortality due to respiratory diseases in Danish twins born 1870-1930

The genetic influence on susceptibility to diseases of the respiratory system and all-cause mortality was studied using data for identical (MZ) and fraternal (DZ) twins. Data from the Danish Twin Register include 1344 MZ and 2411 DZ male twin pairs and 1470 MZ and 2730 DZ female twin pairs born between 1870 and 1930, where both individuals were alive on 1 011943. We used the correlated gamma-frailty model. Proportions of variance in frailty attributable to genetic and environmental factors were assessed using the structural equation model approach. For all-cause mortality the correlation coefficients of frailty for MZ twins tend to be higher than for DZ twins. For mortality with respect to respiratory diseases this effect was only seen in females, whereas males showed the opposite effect. Five standard biometric models are fitted to the data to evaluate the magnitude and nature of genetic and environmental factors on mortality. Using the best fitting biometric model heritability for cause of death was found to be 0.58 (0.07) for all-cause mortality (AE-model) and zero for diseases of the respiratory system for males. Heritability was 0.63 (0.11) for all-cause mortality (DE-model) and 0.18 (0.09) for diseases of the respiratory system (DE-model) for females. The analysis confirms the presence of a strong genetic influence on individual frailty associated with all-cause mortality. For respiratory diseases, no genetic influence was found in males and only weak genetic influence in females. The nature of genetic influences on frailty with respect to all-cause mortality is probably additive in males and dominant in females, whereas for frailty with respect to deaths caused by respiratory diseases in females, there are genetic factors present which are caused by dominance. Environmental influences are non-shared with exception of frailty with respect to respiratory diseases in males, where the shared environment plays an important role.     

儿童青少年双生子瘦素遗传度估计及影响因素分析

目的 分析影响儿童青少年瘦素的遗传因素和环境因素,探讨性别、年龄和体质量指数(BMI)的作用,为儿童肥胖早期预防提供依据.方法 选择6～18岁同性别双生子337对,平均年龄(12.3±3.5)岁,其中同卵双生子257对,异卵双生子80对.采用DNA微卫星多态性鉴定卵性.应用Mx结构方程模型分别计算年龄和BMI调整前后瘦素的遗传度,并检验性别、年龄和BMI对于模型的作用.结果 不同性别间身高、体重和瘦素水平差异均有统计学意义(P值均＜0.05).相关分析显示,瘦素水平与性别、年龄和BMI相关(P值均＜0.0l).遗传分析发现,调整前年龄方差在女生中影响较大,而男生则受共同环境方差影响较大.调整后男生特异性性别方差降低,最适模型为ACE(scale)模型.男、女生瘦素遗传模型一致,遗传度为20％.结论 儿童青少年人群中瘦素水平与性别、年龄和BMI相关.瘦素受遗传和环境因素共同影响.调整年龄及BMI后,瘦素遗传度不受性别影响.     

Major genetic susceptibility for venous thromboembolism in men: a study of Danish twins

BACKGROUND: Although several genetic determinants (mutations or polymorphisms) have been associated with increased risk of venous thromboembolism, the overall influence of genetic factors on this disease is unknown. METHODS: We linked the Danish Twin Registry, which includes twins born 1870-1953, with the Danish National Registry of Patients, comprising all hospitalizations in Denmark since 1977. We then determined the risk of venous thromboembolism as determined from discharge diagnosis. RESULTS: We identified 26,982 twins who were alive on 1 January 1977, and computed measures of familial and genetic association of venous thrombotic disorders. Individuals were classified according to zygosity and hospitalization with venous thromboembolism. Since 1977, 678 twins were hospitalized with an episode of venous thromboembolism. Of these, only 545 pairs (281 male pairs and 264 female pairs) were alive in 1977. For men, the concordance rates for mono- and dizygotic twin pairs, respectively, were 0.22 (95% confidence interval = 0.14 to 0.30) and 0.08 (0.04-0.12). The odds ratio (interpreted as the relative risk of venous thromboembolism for one twin, given venous thromboembolism in the partner twin) was 13.5 (7.3-24.8) among monozygotic twins and 3.8 (1.8-8.3) among dizygotic twins. The respective correlations for venous thromboembolism were 0.55 (0.38-0.70) and 0.26 (0.09-0.42). The proportion of the variance attributable to genetic effects on venous thromboembolism in males was 55% (39%-68%). The remaining variation could be attributed to men's nonfamilial environments. In contrast, for women there was no intra-twin pair similarity for venous thromboembolism. CONCLUSIONS: We found differences in genetic susceptibility to venous thromboembolism between the sexes, with genetic factors playing a substantially stronger role in males than in females.