Search

The diversity and dominant bacterial taxa in the vagina are reported to be influenced by multiple intrinsic and extrinsic factors, including but not limited to pregnancy, contraceptive use, pathogenic states, socioeconomic status, and ancestry. However, the extent to which host genetic factors influence variation in the vaginal microbiota is unclear. We used a biometrical genetic approach to determine whether host genetic factors contribute to inter-individual differences in taxa from a sample of 332 twins who self-identified as being of African (44 pairs) or European ancestry (122 pairs). Lactobacillus crispatus, a major determinant of vaginal health, was identified as heritable among European American women (narrow-sense heritability = 34.7%, P-value = 0.018). Heritability of L. crispatus is consistent with the reduced prevalence of adverse reproductive disorders, including bacterial vaginosis and preterm birth, among women of European ancestry. Wright et al. apply biometric genetic approach to identify the extent to which host genetic factors influence species-level variation in the vaginal microbiota. Their study suggests that Lactobacillus crispatus, a major determinant of vaginal health, is heritable among European American women, consistent with the reduced prevalence of adverse reproductive disorders in them. [ABSTRACT FROM AUTHOR]

In this article, we explore the effect of public policy on the extent to which genes influence smoking desistance. Using a sample of adult twins (n(mz) = 363, n(dz) = 233) from a large population registry, we estimate Cox proportional hazards models that describe similarity in the timing of smoking desistance among adult twin pairs. We show that identical twin pairs are significantly more likely to quit smoking within a similar time frame compared with fraternal twin pairs. Importantly, we then show that genetic factors for smoking desistance increase in importance following restrictive legislation on smoking behaviors that occurred in the early and mid-1970s. These findings support the social push perspective and make important contributions to the social demography and genetic epidemiology of smoking as well as to the gene-environment interaction literatures. [ABSTRACT FROM AUTHOR]

dult romantic attachment styles reflect ways of relating in close relationships and are associated with depression and negative emotionality. We estimated the extent to which dimensions of romantic attachment and negative emotionality share genetic or environmental risk factors in 1,237 middle-aged men in the Vietnam Era Twin Study of Aging (VETSA). A common genetic factor largely explained the covariance between attachment-related anxiety, attachment-related avoidance, depressive symptoms, and two measures of negative emotionality: Stress-Reaction (anxiety), and Alienation. Multivariate results supported genetic and environmental differences in attachment. Attachment-related anxiety and attachment-related avoidance were each influenced by additional genetic factors not shared with other measures; the genetic correlation between the attachment measure-specific genetic factors was 0.41, indicating some, but not complete overlap of genetic factors. Genetically informative longitudinal studies on attachment relationship dimensions can help to illuminate the role of relationship-based risk factors in healthy aging. [ABSTRACT FROM AUTHOR]

The causes of correlation between parental treatment and offspring behavior are ambiguous since genetic and social factors are correlated in typical family studies. The problem is complicated by the need to characterize the effects of genes and environment on both juvenile and adult behavioral outcomes. A model is developed for the resemblance between juvenile and adult twins and their parents that allows some of these effects to be resolved. Data on childhood adversity, parental anti-social behavior, and longitudinal adult and juvenile anti-social behavior were obtained from 1,412 families of adolescent and young adult twins. A structural model is fitted that allows for the effects of genetic and social transmission of information from parents to children. Environmental effects of parents may be mediated through measured features of the home environment. Parameters were estimated by diagonal weighted least squares applied to the 33 distinct polychoric correlations between relatives and between variables within and between ages. Sub-hypotheses were tested. Results confirmed that effects of genes and environment were both highly significant. Genetic effects were large in juveniles and largely age and sex-specific. Approximately 30% of the variation due to the shared environment was due to the effect of childhood adversity. The remaining shared environmental effects are unexplained. Adversity is affected significantly by maternal anti-social behavior. The correlation between paternal ASP and adversity may be explained by antisocial fathers selecting (or creating) antisocial mothers. All significant environmental effects of parental ASP are mediated through the measure of adversity. Though transmission of ASP is both genetic and social, passive genotype–environment correlation is very small. Assortative mating for ASP has barely detectable consequence for the genetic correlation between siblings. The longitudinal study of twins and their parents makes it possible to demonstrate there is a direct causal effect of childhood adversity on child conduct disorder over and above any indirect genetic correlation. [ABSTRACT FROM AUTHOR]

Cortisol is an indicator of hypothalamic–pituitary–adrenal axis responsivity to stress, but few twin studies have examined the heritability of cortisol concentrations in adults across the diurnal cycle and in different contexts. Saliva samples were provided by 783 middle-aged male twins on one laboratory and two home days as part of the Vietnam Era Twin Study of Aging. Significant cortisol heritability estimates were found for laboratory measures only: awakening (.56); 30 min after awakening (.48); 1000 h (.42); mean output across the day (.43); and mean cortisol awakening response (.64). Twin correlations at home were low. In the laboratory, they were unchanged for fraternal twins, but increased for identical twins. Greater measurement error at home did not appear to account for home-laboratory differences. The results suggest that genetic factors influence cortisol responses to specific environmental stressors. Thus, cortisol levels are correlated in identical twins only when they undergo similar experiences. [ABSTRACT FROM AUTHOR]

We examined the genetic architecture of a Tower of London test of planning and problem-solving in 690 middle-aged male twins. Phenotypic analyses revealed only one general factor, but the best-fitting genetic model indicated two correlated genetic factors: speed and efficiency. One variable—number of attempts required to mentally figure the puzzles—loaded on both factors. Shared environmental effects could be dropped with virtually no reduction in model fit. Despite significant nonshared environmental correlations across measures, there was no discernable nonshared environmental factor structure. The correlation between genetic factors ( r = 0.46) and the variable loading on both factors could reflect modulation of planning, testing alternatives, and working memory that are required to perform the test. Such coordinated activity is consistent with the notion of a supervisory attentional system, a central executive, or metacognitive ability. The different phenotypic and genetic factor results suggest that relying solely on the former could obscure genetic associations. [ABSTRACT FROM AUTHOR]

Following the publication of Purcell’s approach to the modeling of gene by environment interaction in 2002, the interest in G × E modeling in twin and family data increased dramatically. The analytic techniques described by Purcell were designed for use with continuous data. Here we explore the re-parameterization of these models for use with ordinal and binary outcome data. Analysis of binary and ordinal data within the context of a liability threshold model traditionally requires constraining the total variance to unity to ensure identification. Here, we demonstrate an alternative approach for use with ordinal data, in which the values of the first two thresholds are fixed, thus allowing the total variance to change as function of the moderator. We also demonstrate that when using binary data, constraining the total variance to unity for a given value of the moderator is sufficient to ensure identification. Simulation results indicate that analyses of ordinal and binary data can recover both the raw and standardized patterns of results. However, the scale of the results is dependent on the specification of (threshold or variance) constraints rather than the underlying distribution of liability. Example Mx scripts are provided. [ABSTRACT FROM AUTHOR]

The biological and social transmission of attitudes toward abortion and gay rights are analyzed in a large sample of adult twins, siblings, and their parents. We present a linear model for family resemblance allowing for both genetic and cultural transmission of attitudes from parents to offspring, as well as phenotypic assortative mating (the tendency to marry like) and other environmental sources of twin and sibling resemblance that do not depend on the attitudes of their parents. The model gives a close fit to the patterns of similarity between relatives for the two items. Results are consistent with a substantial role of genetic liability in the transmission of both attitudes. Contrary to the dominant paradigm of the social and political sciences, the kinship data are consistent with a relatively minor non-genetic impact of parental attitudes on the development of adult attitudes in their children. By contrast, the choice of mate is a social action that has a marked impact on the polarization of social attitudes and on the long-term influence that parents exert upon the next generation. [ABSTRACT FROM AUTHOR]

Previous research has shown that many heterosexuals hold negative attitudes toward homosexuals and homosexuality (homophobia). Although a great deal of research has focused on the profile of homophobic individuals, this research provides little theoretical insight into the aetiology of homophobia. To examine genetic and environmental influences on variation in attitudes toward homophobia, we analysed data from 4,688 twins who completed a questionnaire concerning sexual behaviour and attitudes, including attitudes toward homosexuality. Results show that, in accordance with literature, males have significantly more negative attitudes toward homosexuality than females and non-heterosexuals are less homophobic than heterosexuals. In contrast with some earlier findings, age had no significant effect on the homophobia scores in this study. Genetic modelling showed that variation in homophobia scores could be explained by additive genetic (36%), shared environmental (18%) and unique environmental factors (46%). However, corrections based on previous findings show that the shared environmental estimate may be almost entirely accounted for as extra additive genetic variance arising from assortative mating for homophobic attitudes. The results suggest that variation in attitudes toward homosexuality is substantially inherited, and that social environmental influences are relatively minor. [ABSTRACT FROM AUTHOR]

Considerable evidence from twin and adoption studies indicates that genetic and shared environmental factors play a significant role in the initiation of smoking behavior. Although twin and adoption designs are powerful to detect genetic and environmental influences, they do not provide information on the processes of assortative mating and parent–offspring transmission and their contribution to the variability explained by genetic and/or environmental factors. We examined the role of genetic and environmental factors for smoking initiation using an extended kinship design. This design allows the simultaneous testing of additive and non-additive genetic, shared and individual-specific environmental factors, as well as sex differences in the expression of genes and environment in the presence of assortative mating and combined genetic and cultural transmission. A dichotomous lifetime smoking measure was obtained from twins and relatives in the Virginia 30,000 sample. Results demonstrate that both genetic and environmental factors play a significant role in the liability to smoking initiation. Major influences on individual differences appeared to be additive genetic and unique environmental effects, with smaller contributions from assortative mating, shared sibling environment, twin environment, cultural transmission and resulting genotype–environment covariance. The finding of negative cultural transmission without dominance led us to investigate more closely two possible mechanisms for the lower parent–offspring correlations compared to the sibling and DZ twin correlations in subsets of the data: (i) age × gene interaction, and (ii) social homogamy. Neither mechanism provided a significantly better explanation of the data, although age regression was significant. This study showed significant heritability, partly due to assortment, and significant effects of primarily non-parental shared environment on smoking initiation. [ABSTRACT FROM AUTHOR]

The expression of many important behavioral outcomes is contingent on passing a developmental milestone, such as puberty, or exposure to an age-dependent risk factor, such as alcohol or drugs. Current models for genetic effects on development have not provided explicit theoretical insight about possible patterns of epistasis and genotype × environment interaction generated by genetic and environmental heterogeneity in the timing of developmental milestones that influence gene expression. We explore theoretically the effects of individual differences in the timing of a developmental milestone on the expression of genetic differences in outcome. The consequences of additive genetic variation and shared environmental variation on timing are examined. Additive genetic effects on timing generate transient epistatic effects on outcome because they modulate the expression of otherwise additive genetic differences in outcome. Epistatic effects will be greatest at ages when there is the most heterogeneity in developmental maturity. Epistasis will gradually disappear as proportionately more individuals mature. Similarly, shared environmental effects on the timing of a milestone will generate transient genotype × shared environment interaction appearing as shared environmental effects on outcome that are greatest when there is the most heterogeneity in developmental maturity. The impact of these effects on age patterns in twin correlations is examined and their relevance to current data on developmental change discussed briefly. [ABSTRACT FROM AUTHOR]

Akiake's Information Criterion (AIC) is commonly used in univariate twin modeling of a discrete trait to prune a full model into a more parsimonious submodel. It is possible that this practice could introduce bias and inaccuracy, and we could identify no prior systematic study of these issues. Thus, we used simulation to investigate the performance of AIC-guided modeling across a broad range of parameters. Our simulations indicated that the use of the AIC to determine the “best” univariate model for a discrete trait tended to yield the incorrect model rather frequently. Moreover the parameter estimates of the “best” model by AIC were biased sharply upward as were the associated 95% confidence intervals. These results suggest that the use of AIC to guide twin modeling for univariate discrete traits should either be abandoned or used with great caution. [ABSTRACT FROM AUTHOR]

We examine the hypothesis that environmental transmission is a significant factor in individual differences for Neuroticism among 45,850 members of extended twin kinships from Australia (N = 20,945) and the United States (N = 24,905). To this large data set we fitted a model estimating genetic and environmental components of variance and gene-environmental covariance to examine the causes of individual differences in Neuroticism. For the combined sample we reject models including environmental transmission, shared environment, and a special twin environment in favor of more parsimonious genetic models. The best-fitting model involved only modest assortative mating, nonshared environment, and both additive and nonadditive genetic components. We conclude, first, that there is no evidence for environmental transmission as a contribution to individual differences in Neuroticism in these replicated samples, drawn from different continents, and, second, that a simple genetic structure underlies familial resemblance for the personality trait of Neuroticism. It is interesting that, despite the opportunity provided by the elaborate design and extensive power of our study, the picture revealed for the causes of individual differences in Neuroticism is little more complex than that found from earlier, simpler designs applied to smaller samples. However, this simplicity could not have been confirmed without using a highly informative design and a very large sample. [ABSTRACT FROM AUTHOR]

We used a simulation study to evaluate six approaches for behavior genetic analyses of psychiatric symptom scores. For the selection of the correct model, the best results were obtained with approaches using transformed scores in combination with a procedure involving p-values. With normalizing transformations, the χ$^2$ test statistic gave a reasonable impression of the overall fit of the model but was less accurate when used as a difference test. The asymptotic distribution free estimation methods yielded χ$^2$s that were much too large. All data analysis techniques yielded substantially biased parameter estimates. The most biased results were obtained with normalizing transformations. The least biased results were obtained with tobit correlations, but because of its large standard errors the most precise estimates were obtained with polychoric correlations and optimal scale scores. An empirical study showed that a recognition of the role of methodological factors was helpful to understand part of the differences between assessment instruments, raters, and data analysis techniques that were found in the real data. [ABSTRACT FROM AUTHOR]

Underlying phenotypic and genetic factors involving motives for smoking were assessed using data from 1756 twins, including 390 complete pairs. Respondents were aged 50 or older and included both current and former smokers. The Motives for Smoking Questionnaire (MSQ) hypothesizes eight correlated but distinct motives for smoking, which correspond to pharmacological and nonpharmacological second-order factors. This paper concentrates on the pharmacological motives. Principal-factor analysis recovered five categories. Items constituting Sedative, Stimulative, and Addictive reasons for smoking merged into one factor, whereas Automatic smoking, also considered to have pharmacological origins, formed a separate factor. Twin analysis was used to test for genetic effects and to determine whether these factors, although combined phenotypically, were affected by distinct genetic or environmental influences. Genetic effects accounted for a significant amount of the variance in the four hypothesized pharmacological motives for smoking, as did shared environment. The separate factor for Automatic smoking in the phenotypic analysis was due to environmental effects, and shared environment was a greater influence on Automatic smoking for women than men. One common effect explained the genetic variance; no genetic influence uniquely affected any specific motive. Therefore, individual differences in the hypothesized pharmacological motives for smoking appear to originate from a common genetic pathway. [ABSTRACT FROM AUTHOR]

The magnitude of genetic and environmental factors and the influence of contrast effects on attention-deficit hyperactivity disorder (ADHD) symptomatology were examined on a sample of 900 twin pairs, aged 7–13, participating in the Virginia Twin Study of Adolescent Behavioral Development (VTSABD). In addition, the genetic and environmental correlations between ADHD and oppositional-defiant disorder/conduct disorder (ODD/CD) symptomatology were estimated. A series of structural models was applied to maternal ratings from a telephone survey, designed to screen for the three dimensions of ADHD symptomatology (hyperactivity, impulsivity, and inattention) and ODD/CD symptomatology. Model-fitting results suggested that ADHD symptomatology is highly heritable and influenced mostly by additive genetic, specific environmental, and contrast effects. However, this analysis could not exclude with statistical significance additional effects from dominance. The results of the best-fitting bivariate model suggested that the genetic correlation between the two traits is 50% and replicated previous findings of a common genetic factor influencing the comorbidity of ADHD and ODD/CD symptomatologies. [ABSTRACT FROM AUTHOR]

We review the literature on the familial resemblance of body mass index (BMI) and other adiposity measures and find strikingly convergent results for a variety of relationships. Results from twin studies suggest that genetic factors explain 50 to 90% of the variance in BMI. Family studies generally report estimates of parent–offspring and sibling correlations in agreement with heritabilities of 20 to 80%. Data from adoption studies are consistent with genetic factors accounting for 20 to 60% of the variation in BMI. Based on data from more than 25,000 twin pairs and 50,000 biological and adoptive family members, the weighted mean correlations are .74 for MZ twins, .32 for DZ twins, .25 for siblings, .19 for parent–offspring pairs, .06 for adoptive relatives, and .12 for spouses. Advantages and disadvantages of twin, family, and adoption studies are reviewed. Data from the Virginia 30,000, including twins and their parents, siblings, spouses, and children, were analyzed using a structural equation model (Stealth) which estimates additive and dominance genetic variance, cultural transmission, assortative mating, nonparental shared environment, and special twin and MZ twin environmental variance. Genetic factors explained 67% of the variance in males and females, of which half is due to dominance. A small proportion of the genetic variance was attributed to the consequences of assortative mating. The remainder of the variance is accounted for by unique environmental factors, of which 7% is correlated across twins. No evidence was found for a special MZ twin environment, thereby supporting the equal environment assumption. These results are consistent with other studies in suggesting that genetic factors play a significant role in the causes of individual differences in relative body weight and human adiposity. [ABSTRACT FROM AUTHOR]

Genetic and environmental influences in the determination of individual differences in self-reported symptoms of separation anxiety (SAD), overanxious disorder (OAD), and manifest anxiety (MANX) were evaluated in children and adolescents for three age groups (8–10, 11–13, and 14–16). Symptom counts for SAD and OAD were assessed for 1412 twin pairs using the children's version of the Child and Adolescent Psychiatric Assessment, and MANX scores were based on child report from the Revised Children's Manifest Anxiety Scales. Despite significant age and gender differences in thresholds of liability for child reports of symptoms of SAD and OAD, additive genetic and environmental effects could be set equal across age and gender for these variables. For MANX, however, the best-fitting model was a common effects sex-limitation model with estimates of heritabiliry varying dependent upon age and gender. Parameter estimates from the ACE models of OAD and SAD showed that additive genetic variation was a necessary component in the explanation of individual differences in child-reported symptoms of OAD (h [sup 2] = .37) across gender, but does not appear to be a major contributor to the explanation of individual differences in symptoms of SAD reported by children. Shared environmental effects (c [sup 2] = .40) were found to play a moderate role for SAD but could be dropped from the model for OAD and from all of the age groups for MANX, although the parameter approached significance among 11 yr to 13-year-old males. [ABSTRACT FROM AUTHOR]