Childhood Sexual Abuse Moderates Genetic Influences on Age at First Consensual Sexual Intercourse in Women

We examine interactive effects of childhood sexual abuse (CSA) on heritable variation in age at first consensual sexual intercourse in a young cohort of 3,350 female and 2,724 male Australian twins. Consistent with hypotheses, genetic influences explained little if any variation in age at first consensual sexual intercourse for female twins reporting CSA (CSA(+)), with shared environment explaining 73%. For female twins reporting no history of CSA (CSA(-)), 39% of variation in age at first consensual sexual intercourse was explained by genetic effects, with shared environment accounting for 30%. For male twins, significant interactive effects of CSA on genetic and environmental variation in age at first consensual sexual intercourse were not observed. Overall genetic influences explained 51% of variation in age at first consensual sexual intercourse for male twins, with shared environment accounting for 8%. For both female and male twins, results from models that included conduct disorder as a covariate were near identical to results from models without conduct disorder.     

Genetic and Environmental Sources of Individual Religiousness: The Roles of Individual Personality Traits and Perceived Environmental Religiousness

In the current study, we examined the genetic and environmental sources of the links between individual religiousness and individual personality traits, perceived parental religiousness, and perceived peer religiousness. Data from 870 individuals (incl. 394 twin pairs) were analyzed. Variance in individual religiousness was significantly influenced by genetic effects, environmental influences shared by twins reared together, and individual-specific environmental influences. Individual religiousness showed significant associations with age, sex, specific personality traits (e.g., agreeableness, openness to values), and perceived religiousness of important social interaction partners, such as parents, best friends, and spouses. The links to personality traits were relatively small and primarily genetically mediated. The associations between individual religiousness and parental religiousness were substantial and mediated by shared environmental effects. These links significantly decreased across age accompanying a significant decrease of shared environmental influences on individual religiousness. The correlations between individual religiousness and perceived religiousness of spouses and best friends were relatively moderate but increased with age. These associations were mediated by genetic as well as nonshared environmental sources accompanying an increase of nonshared environmental influences on individual religiousness with age. The results suggest that inter-individual differences in religiousness are due to multiple sources.     

A Twin Study of Drinking and Smoking Onset and Latencies from First Use to Regular Use

The early onset of alcohol and tobacco use has been associated with increased risk for later substance abuse and dependence problems. This study investigated genetic and environmental influences on age at onset of alcohol and tobacco use by examining twin resemblance for several retrospectively reported onset milestones including age at first use, age at first alcohol intoxication experience, and age at regular use. In addition, we also examined the latency between age at first use and age at regular use of tobacco and alcohol. The subjects were a volunteer sample of older adult twins 50 to 96 years of age. MZ twin correlations for age at first alcohol use and age at first tobacco use were .57 and .44, respectively, compared to .45 and .37 for DZ same-sex twins. MZ twins correlated .30 and .26 for the latencies between first use and regular use of alcohol and of tobacco, while DZ correlations were –.01 and .05, respectively. Biometrical model-fitting results confirmed that familial resemblance for age at first use for both alcohol and tobacco was largely the result of shared environmental factors, while the latencies between first use and regular patterns of use were more genetically influenced. These findings add to a growing body of literature suggesting that initiation of substance use is influenced primarily by environmental rather than genetic factors.     

Genetic and environmental influences on birthweight in a sample of Korean twins

This study is the first report of genetic and environmental influences on birthweight using Korean twins. The sample consisted of 255 monozygotic (MZ) and 178 dizygotic (DZ) twin pairs drawn from the Seoul Twin Family Study. Intraclass twin correlations were computed for the twins' birthweights obtained from parents (typically mothers) of the twins. To estimate genetic and shared and nonshared environmental influences on birthweight, standard univariate model-fitting analyses were performed using a software, Mx. For each gender, MZ twin correlations were higher than DZ twin correlations, suggesting existence of genetic influences on birthweight; however, DZ twin correlations were higher than half the MZ twin correlations, indicating that shared environmental factors are also important. For each zygosity, twin correlations were not significantly different between males and females, implicating that genes and environments that cause individual differences in birthweight may not vary between males and females. Model-fitting analyses based on the data pooled across gender yielded estimates of 17% for genetic, 60% for shared environmental, and 23% for nonshared environmental influences on birthweight.     

Genetic and Environmental Influences on Gambling and Substance Use in Early Adolescence

This study examined the genetic and environmental architecture of early gambling involvement and substance use to determine whether genetic or environmental factors that contribute to substance use also put young adolescents at risk for early involvement in gambling. Self-reports of substance use and gambling involvement were collected at age 13 years from 279 Monozygotic and Dizygotic twin pairs. Univariate ACE modeling revealed that genetic and nonshared environmental factors almost equally accounted for gambling involvement, with no contribution from shared environmental factors. In contrast, both shared and nonshared environmental factors played important roles in substance use; the contribution of genetic factors was also substantial. Bivariate analyses identified a significant, albeit modest, overlap between the genetic influence on gambling involvement and the genetic influence on substance use. The results shed light on the etiology of early gambling involvement and substance use, suggesting that preventive interventions targeting common risk factors may also need to be complemented by modules that are specific to each behavior.     

Covariation of psychosocial characteristics associated with cardiovascular disease: genetic and environmental influences

OBJECTIVE: Three psychosocial characteristics associated with cardiovascular disease (CVD)-depression, hostility, and social support-tend to correlate with one another. However, the causes of each characteristic and why they tend to co-occur are not completely understood. Therefore, the current study used a twin design to examine the relative contributions of genetic and environmental influences to the variation and covariation of these three psychosocial characteristics. METHODS: The sources of variation and covariation among the Beck Depression Inventory, the Cook-Medley Hostility Scale, and the Interpersonal Support Evaluation List were examined in a young adult community sample of 157 monozygotic and 75 dizygotic twin pairs. RESULTS: Phenotypic confirmatory factor analysis indicated that a single latent factor could account for their moderate intercorrelations. Twin analyses indicated that the Beck Depression Inventory and Interpersonal Support Evaluation List were each influenced by genetic and nonshared environmental factors, whereas the Cook-Medley Hostility Scale was influenced by familial (genetic and/or shared environmental) and nonshared environmental factors. Bivariate associations between these scales were largely determined by common genetic effects and, to a lesser degree, common nonshared environmental effects. Covariation among the three scales could be explained by a single common genetic factor and a common nonshared environmental factor. Environmental factors shared within families did not contribute to covariation among the psychosocial characteristics. CONCLUSIONS: The results challenge the conventional approach of examining these psychosocial variables as independent risk factors for cardiovascular disease and argue for the importance of investigating specific causes for their covariation.     

The Implications of Simultaneous Smoking Initiation for Inferences about the Genetics of Smoking Behavior from Twin Data

We examined early social influences across stages of smoking within the context of a twin study using an environmental exposure specific to smoking: whether twins started smoking at the same time (“simultaneous smoking initiation”: SSI). We expected that SSI would be a good index of shared social influences on smoking initiation. Rates of SSI were indeed significantly higher in MZ twins and in twins who shared peers and classes, as well as in male twins. With the exception of regular smoking in females, we found no significant difference in estimates of genetic and environmental parameters between SSI and non-SSI pairs for any of the smoking measures that we examined (DSM-IV and Fagerstrom HSI measures of nicotine dependence; DSM-IV nicotine withdrawal; heavy smoking; and in males, regular smoking). For regular smoking in females, allowing for additional shared environmental influences associated with SSI only modestly reduced our estimates of additive genetic variance (56% vs. 68%). These results indicate the important social influences that may occur for smoking initiation do not appear to seriously bias estimates of genetic effects on later stages of smoking.     

Genetic and Environmental Risk Factors for Illicit Substance Use and Use Disorders: Joint Analysis of Self and Co-twin Ratings

The specificity of genetic and environmental risk factors for illicit substance use and substance use disorders (SUD) was investigated by utilizing self and co-twin reports in 1,791 male twins. There was a high rate of comorbidity between both use of, and SUD from, different classes of illicit substances. For substance use, the model that included one common genetic, one shared environmental, and one individual-specific (i.e., unique) environmental factor, along with substance-specific effects that were attributed entirely to genetic factors fit the data best. For illicit SUD, one common genetic and one common unique environmental risk factor, and substance specific shared environmental and unique environmental risk factors were identified. Risk factors for illicit substance use and SUD are mainly non-specific to substance class. Co-twin rating of illicit substance use and SUD was a reliable source of information, and by taking account of random and systematic measurement error, environmental exposures unique to the individual were of lesser importance than found in earlier studies.     

Genetic influences on DSM-III-R drug abuse and dependence: A study of 3,372 twin pairs

Research and clinical experience indicate that drug use disorders tend to run in families. The objective of this study was to distinguish between the family environment and genetic factors as the source of this observed family resemblance. Data were collected by telephone interview from members of the Vietnam Era Twin Registry, comprising male twin pairs who served in the U.S. military between 1965 and 1975. There were 3,372 pairs in which both twins participated. Drug use disorder was defined as receiving a diagnosis of drug abuse or dependence according to DSM-III-R; 10.1% of the sample had abused or been dependent on at least one illicit drug. A significant difference between concordance rates for monozygotic (26.2%) vs. dizygotic (16.5%) twins indicated a genetic influence on drug use disorder. Biometrical modeling indicated that genetic factors (34% of the variance), the environment shared by twins (28% of the variance), and the nonshared environment (38% of the variance) had significant influences of similar magnitudes on the individual's risk of developing a drug use disorder. These results support the application of molecular genetic approaches to elucidate the genetic influence on drug use disorder, as well as the potential efficacy of environmental intervention to reduce risk. © 1996 Wiley-Liss, Inc.     

The Etiology of Stability and Change in Religious Values and Religious Attendance

Studies have demonstrated little to no heritability for adolescent religiosity but moderate genetic, shared environmental, and nonshared environmental influences on adult religiosity. Only one longitudinal study of religiosity in female twins has been conducted (Koenig et al., Dev Psychol 44:532?C543, 2008), and reported that persistence from mid to late adolescence is due to shared environmental factors, but persistence from late adolescence to early adulthood was due to genetic and shared environmental factors. We examined the etiology of stability and change in religious values and religious attendance in males and females during adolescence and early adulthood. The heritability of both religious values and religious attendance increased from adolescence to early adulthood, although the increase was greater for religious attendance. Both genetic and shared environmental influences contributed to the stability of religious values and religious attendance across adolescence and young adulthood. Change in religious values was due to both genetic and nonshared environmental influences specific to early adulthood, whereas change in religious attendance was due in similar proportions to genetic, shared environmental, and non-shared environmental influences.     

Genetic and Cultural Transmission of Smoking Initiation: An Extended Twin Kinship Model

BACKGROUND: 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. METHODS: 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: 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 x gene interaction, and (ii) social homogamy. Neither mechanism provided a significantly better explanation of the data, although age regression was significant. CONCLUSIONS: This study showed significant heritability, partly due to assortment, and significant effects of primarily non-parental shared environment on smoking initiation.     

Parent- and Observer-Rated Positive Affect in Early Childhood: Genetic Overlap and Environmental Specificity

The sources of individual differences in both observed and parent-rated positive affect (PA) were examined in a sample of 304 3-year-old twin pairs (140 MZ, 164 DZ). Based on model-fitting analyses, individual differences in observed PA were attributed to moderate genetic and high nonshared environmental factors, but not shared environmental factors. In contrast, shared environmental effects accounted for over half of the variance in parent-rated PA and genetic and nonshared environmental effects were more modest. The genetic correlation across the two measures was high, indicating substantial overlap between genetic factors influencing the two. It was these overlapping genetic effects that fully explained the phenotypic correlation between both measures. There was no significant covariance between the environmental influences on parent rated and observed PA. Thus, the two measures of PA in early childhood have common genetic underpinnings, whereas environmental influences are measure-specific. Measurement implications are discussed.     

The Genetics of Smoking Persistence in Men and Women: A Multicultural Study

Using a correlated liability dimensions model, we examined the extent to which the same genetic and environmental factors influence both initiation of regular cigarette smoking and maintenance of the smoking habit in men and women. We analyzed questionnaire survey data obtained from large samples of male and female like-sexed twins from three countries, Australia (N = 1535 pairs), Sweden (N = 5916 pairs), and Finland (N = 4438 pairs), subdivided into three age bands (18–25, 26–35, and 36–46 years of age). We found that familial influences on risk for persistence in smoking cannot be entirely explained by the same factors responsible for risk of smoking initiation. Total genetic variance for smoking persistence varied little by age band and sex (range, 39–49% in women and 42–45% in men); however, even among twins in the youngest group (18–25 years of age), who on average have the fewest years of cigarette use, less than 40% of the total genetic variance in smoking persistence was accounted for by the same genetic factors that increased risk of smoking initiation, and this percentage decreased to less than 10% in the 36–46 year olds.     

Phenotypic and Genetic Factors in Motives for Smoking

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.     

Genetic and environmental influences on the association between smoking and panic attacks in females: a population-based twin study

BACKGROUND: Clinical and epidemiological studies have reported an association between lifetime cigarette-smoking and panic attacks. Several explanations for this relationship have been proposed, mostly focusing on direct causal pathways. The objective of this study was to investigate a hypothesis of shared vulnerability by examining whether panic attacks and cigarette-smoking share genetic or environmental liability factors. METHOD: Questionnaire data on 3172 female-female twins (1409 complete pairs), aged 18-31 years, from a population-based Norwegian twin registry, were used to calculate the correlation between genetic factors and the correlation between environmental factors that influence lifetime measures of panic attacks and daily smoking. RESULTS: The best-fitting biometrical twin model suggested that genetic factors influencing panic and smoking were uncorrelated. Shared or familial environmental factors were perfectly correlated, and accounted for 75 % of the association between the phenotypes. The correlation between individual environmental factors influencing the phenotypes was 0.25 (0.07-0.44). In the full model, the genetic correlation was 0.17 (0.00-1.00), and genetic and shared environmental factors respectively accounted for 18 % and 61 % of the co-variance between panic and smoking. CONCLUSION: The results suggest that panic attacks and lifetime smoking have few or no genetic liability factors in common. The shared environmental factors that influence the two phenotypes are identical. Liability to panic attacks in females appears to be more influenced by shared environmental factors than previously indicated by univariate studies.     

Effects of Social Attitude Change on Smoking Heritability

Societal attitudes and norms to female smoking changed in Spain in the mid-twentieth century from a restrictive to a tolerant, and an even pro-smoking, posture, while social attitudes remained stable for males. We explored whether this difference in gender-related social norms influenced the heritability of two tobacco use measures: lifetime smoking and number of years smoking. We used a population-based sample of 2285 twins (mean age?=?55.78; SD?=?7.45; 58% females) whose adolescence began between the mid-1950s and the early 1980s. After modeling the effect of sex and year of birth on the variance components, we observed that the impact of the genetic and shared environmental factors varied differently by birth cohort between males and females. For females, shared environment explained a higher proportion of variance than the genetic factors in older cohorts. However, this situation was inverted in the younger female cohorts. In contrast, no birth cohort effect was observed for males, where the impact of the genetic and environmental factors remained constant throughout the study period. These results suggest that heritability is larger in a permissive social environment, whereas shared-environmental factors are more relevant in a society that is less tolerant to smoking.     

Neonatal DNA methylation profile in human twins is specified by a complex interplay between intrauterine environmental and genetic factors, subject to tissue-specific influence

Comparison between groups of monozygotic (MZ) and dizygotic (DZ) twins enables an estimation of the relative contribution of genetic and shared and nonshared environmental factors to phenotypic variability. Using DNA methylation profiling of ～20,000 CpG sites as a phenotype, we have examined discordance levels in three neonatal tissues from 22 MZ and 12 DZ twin pairs. MZ twins exhibit a wide range of within-pair differences at birth, but show discordance levels generally lower than DZ pairs. Within-pair methylation discordance was lowest in CpG islands in all twins and increased as a function of distance from islands. Variance component decomposition analysis of DNA methylation in MZ and DZ pairs revealed a low mean heritability across all tissues, although a wide range of heritabilities was detected for specific genomic CpG sites. The largest component of variation was attributed to the combined effects of nonshared intrauterine environment and stochastic factors. Regression analysis of methylation on birth weight revealed a general association between methylation of genes involved in metabolism and biosynthesis, providing further support for epigenetic change in the previously described link between low birth weight and increasing risk for cardiovascular, metabolic, and other complex diseases. Finally, comparison of our data with that of several older twins revealed little evidence for genome-wide epigenetic drift with increasing age. This is the first study to analyze DNA methylation on a genome scale in twins at birth, further highlighting the importance of the intrauterine environment on shaping the neonatal epigenome.     

A Twin Study of Competence and Behavioral/Emotional Problems Among Adolescents in Taiwan

This work reports on a study to evaluate the relative contributions of genetic and environmental factors to both competence scales and behavioral/emotional syndromes as assessed by the Child Behavior Checklist (CBCL). A total of 279 pairs of twins and same-sex sib-pairs aged 12-16 years were recruited from 51 junior high schools in Taipei City, Taiwan. Twins' zygosity was determined by a combination of DNA typing and physical similarity. The Mx program was used to estimate parameters for a full model that contains effects from sex-specific additive genes, shared environment, and nonshared environment for the majority of the scales. The shared environment in the full model was replaced with nonadditive genetic factors for some scales when indicated. All girls' competence and behavioral/emotional syndromes exhibited a substantial heritability (h2 > 0.4), except for Social Competence and Withdrawn. For boys, though the heritability was also >0.4 for some scales (Social and School Competence, Thought Problems, Attention Problems, Delinquent Behavior, and Total Behavior Problems), environmental influences, especially shared environment, were predominant for most of the scales (10 out of 15 scales). Genetic factors are important for explaining adolescent behavioral problems, especially for girls, while shared environmental influences cannot be ignored for boys. Gender differences in heritability exist for various CBCL-based competence and behavioral/emotional problems.     

Genetic and Environmental Influences on Autistic-Like Behaviors in 2-Year-Old Twins

This study aims to explore the genetic and environmental contributions to autistic-like behaviors in a general population sample of toddlers. In a classic twin study of 313 same-sex, 2-year-old twin pairs, autistic-like behaviors were assessed via parent ratings on the pervasive developmental problems subscale of the Child Behavior Checklist and observationally using tester ratings on the orientation/engagement subscale of the Behavior Rating Scale. Analyses show moderate, significant heritabilities for both measures of autistic-like behaviors, as well as modest, but significant shared environmental effects. These genetic and environmental influences overlap greatly between the two measures. Autistic-like behaviors in 2-year-old twins are largely genetic in etiology, but are also influenced by a shared environmental component at this age. This is the first study to examine the etiology of such behaviors in a sample of toddlers, thus providing novel information which could guide future research on genetic and environmental factors that affect these behaviors. Handling Editor: Michael Joseph Lyons.     

Heritability of Smoking Initiation and Nicotine Dependence

In contrast to other aspects of smoking behavior, little attention has been paid to the genetics of nicotine dependence. In this paper, three models (single liability dimension, independent liability dimension and combined model) have been applied to data on smoking initiation and nicotine dependence (n = 1572 Dutch twin pairs, mean age 30.5). A combined model best described the data. This model postulates a smoking initiation dimension and a nicotine dependence dimension, which are not independent. For both males and females, individual differences in smoking initiation were explained by genetic (44%), shared environmental (51%) and unique environmental (5%) influences. The nicotine dependence dimension was influenced only by genetic (75%) and unique environmental (25%) factors. The substantial impact of genetic factors on nicotine dependence emphasizes the need for further research to localize and identify specific genes and pathways involved in nicotine dependence.