Genetic and environmental influences on coping styles: a twin study.

OBJECTIVE: Coping styles are generally considered to be environmentally driven, primarily by family influences. However, because personality traits are commonly influenced by genetic effects, we hypothesized that heredity is also important for coping. METHODS: We tested this hypothesis by assessing 19 coping styles, as well as four secondary coping factors, by questionnaire in 212 pairs of monozygotic and dizygotic twins. We then examined heredity by structural equation modeling. RESULTS: All coping styles showed evidence of genetic influences. The coping styles shared one common genetic factor. In addition, each coping style was also influenced by other separate genetic factors. Shared environment had no significant influence on coping styles. Three of 19 more specific coping styles showed shared environmental effects as well as genetic influences, 14 were solely under genetic influences, and two showed only shared environment effects. CONCLUSIONS: We suggest that hereditary effects on certain coping style preferences cannot be explained solely by genetic influences on major personality traits and temperament. An analysis of the relationships between coping and personality in twin subjects may elucidate the distinction between genetic and environmental effects.     

Genetic and environmental influences on frontal EEG asymmetry: a twin study

Research suggests that frontal EEG asymmetry (FA) is a relatively stable trait associated with individual differences in dispositional affect (affective style) and liability to mood disorders. If FA is genetically determined, it can potentially serve as an endophenotype in genetic studies of temperament and mood disorders. The purpose of this study was to assess heritability of FA as well as alpha band EEG power measured at different frontal recording sites. Resting EEG data from a population-based sample of 246 young adult female twins including 73 monozygotic (MZ) and 50 dizygotic (DZ) pairs were analyzed using linear structural equation modeling. FA measured at mid-frontal locations (F3 and F4) showed low but significant heritability, suggesting that 27% of the observed variance can be accounted for by genetic factors. There was no evidence for genetic influences on FA measured at lateral-frontal (F7 and F8) locations. In contrast, alpha band power was highly heritable at all four frontal sites (85-87%). These findings suggest that: (1) genetic influences on FA are very modest and therefore FA has a limited utility as an endophenotype for genetic studies of mood disorders and (2) prefrontal neural circuitry underlying individual differences in affective style is characterized by high developmental plasticity.     

Genetic and environmental influences on emotion-modulated startle reflex: a twin study

Emotion-modulated startle reflex is an important indicator of traitlike differences in affective processing implicated in the biological basis of personality and psychopathology. This study examined heritability of startle modulation by affective pictures in 66 pairs of monozygotic and 57 pairs of dizygotic female twins. Consistent with previous studies, startle magnitude was significantly influenced by emotional valence of the picture (positive < neutral < negative). Absolute response magnitude showed high heritability in all three valence conditions (59-61%); however, there were no significant genetic influences on the amount of startle modulation. Thus, our data do not support the hypothesis that emotion-modulated startle can serve as an indicator of genetically transmitted individual differences in affective processing.     

Type A behavior: a longitudinal study from childhood to adulthood

In a longitudinal study of a sample of Swedish males and females (n = 170), Type A-related behavior at age 13 was related to the scores on an abbreviated Type A scale based on JAS which was administered when the same subjects were 27 years old. Aggression, Motor Hyperactivity, Overambition, and Overachievement measured at age 13 were used as predictors in a multiple regression analysis, with Type A score at age 27 as the dependent variable. The following results were obtained: 1) for men the multiple correlation was 0.41 (p less than 0.01), with Aggression and Overambition accounting for most of the prediction, and b) for women the multiple correlation was 0.36 (p less than 0.05), with Motor Hyperactivity accounting for most of the prediction. It was concluded that Type A-related behavior could be identified rather early and that it shows an unexpected degree of stability over a period of 14 years.     

Genetic and environmental factors affecting self-esteem from age 14 to 17: a longitudinal study of Finnish twins

BACKGROUND: We analysed genetic and environmental influences on self-esteem and its stability in adolescence. METHOD: Finnish twins born in 1983-1987 were assessed by questionnaire at ages 14 (n = 4132 twin individuals) and 17 years (n = 3841 twin individuals). Self-esteem was measured using the Rosenberg global self-esteem scale and analyzed using quantitative genetic methods for twin data in the Mx statistical package. RESULTS: The heritability of self-esteem was 0.62 [95% confidence interval (CI) 0.56-0.68] in 14-year-old boys and 0.40 (95% CI 0.26-0.54) in 14-year-old girls, while the corresponding estimates at age 17 were 0.48 (95% CI 0.39-0.56) and 0.29 (95% CI 0.11-0.45). Rosenberg self-esteem scores at ages 14 and 17 were modestly correlated (r = 0.44 in boys, r = 0.46 in girls). In boys, the correlation was mainly (82%) due to genetic factors, with residual co-variation due to unique environment. In girls, genetic (31%) and common environmental (61%) factors largely explained the correlation. CONCLUSIONS: In adolescence, self-esteem seems to be differently regulated in boys versus girls. A key challenge for future research is to identify environmental influences contributing to self-esteem during adolescence and determine how these factors interact with genetic influences.     

Genetic and environmental influences on antisocial behavior and alcohol dependence from adolescence to early adulthood

Genetic and environmental influences on symptoms of adult antisocial behavior (AAB) and alcohol dependence at ages 17, 20, and 24 were examined cross-sectionally and longitudinally in 188 monozygotic and 101 dizygotic male twin pairs. A moderate genetic influence on both AAB and alcohol dependence was found at each age, with a substantial proportion of this influence common to the two disorders, suggesting they share susceptibility genes. Biometrical models showed that continuity effects accounted for most of the stable variance in symptoms of both AAB and alcohol dependence, indicating that genetic and environmental effects associated with each of these disorders were similar at each age. Significant cross-lag effects (effects of alcohol dependence contributing to variance in AAB and vice versa) were observed at ages 20 and 24 for both disorders. The largest and theoretically most interesting of these effects indicated that one sixth of the genetic influence on AAB at age 20 was due to genetic effects associated with alcohol dependence at age 17. Thus, alcohol dependence symptoms at age 17 in particular had an effect on antisocial behavior symptoms at age 20, suggesting that alcohol involvement in adolescence may ensnare otherwise desisting youth in persistent antisocial behavior.     

Genetic and environmental influences on early childhood behavior

The Child Behavior Checklist for Ages 2–3 (Adelbachet al., J. Abnorm. Child Psychol. 15;629–650; 1987) was completed by mothers of 229 pairs of twins (mean age=33 months). Using the two broad-band groupings of Internalizing and Externalizing described by Achenbachet al. (1987), various models to estimate genetic and environmental parameters were fitted using LISREL 7. Model-fitting results showed that the genetic components to the observed phenotypical variation were small and not necessary in the model. Influences from the shared environment, howerver, could not be dropped from the model without a deterioration in fit. Parameter estimates were not significantly different in boys and girls.     

Genetic and environmental influences on sleep quality in middle‐aged men: a twin study

Poor sleep quality is a risk factor for a number of cognitive and physiological age‐related disorders. Identifying factors underlying sleep quality are important in understanding the etiology of these age‐related health disorders. We investigated the extent to which genes and the environment contribute to subjective sleep quality in middle‐aged male twins using the classical twin design. We used the Pittsburgh Sleep Quality Index to measure sleep quality in 1218 middle‐aged twin men from the Vietnam Era Twin Study of Aging (mean age = 55.4 years; range 51–60; 339 monozygotic twin pairs, 257 dizygotic twin pairs, 26 unpaired twins). The mean PSQI global score was 5.6 [SD = 3.6; range 0–20]. Based on univariate twin models, 34% of variability in the global PSQI score was due to additive genetic effects (heritability) and 66% was attributed to individual‐specific environmental factors. Common environment did not contribute to the variability. Similarly, the heritability of poor sleep—a dichotomous measure based on the cut‐off of global PSQI>5—was 31%, with no contribution of the common environment. Heritability of six of the seven PSQI component scores (subjective sleep quality, sleep latency, sleep duration, habitual sleep efficiency, sleep disturbances, and daytime dysfunction) ranged from 0.15 to 0.31, whereas no genetic influences contributed to the use of sleeping medication. Additive genetic influences contribute to approximately one‐third of the variability of global subjective sleep quality. Our results in middle‐aged men constitute a first step towards examination of the genetic relationship between sleep and other facets of aging.     

Genetic and environmental influences on anorexia nervosa syndromes in a population-based twin sample

BACKGROUND: Genetic and environmental influences on broadly-defined anorexia nervosa (AN) syndrome were examined in a population-based twin sample. METHODS: AN syndrome was assessed in 672 female 17 year-old twins using structured interviews and a self-report questionnaire. RESULTS: Twenty-six probands with AN syndrome were identified. Biometrical model-fitting analyses indicated that genetic and non-shared environmental factors accounted for 74% and 26% of the variance in AN syndrome, respectively. CONCLUSIONS: Findings support previous research indicating significant genetic and non-shared environmental influences on AN syndromes.     

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.     

Genetic and environmental influences on dimensional representations of DSM-IV cluster C personality disorders: a population-based multivariate twin study

BACKGROUND: The DSM-IV cluster C Axis II disorders include avoidant (AVPD), dependent (DEPD) and obsessive-compulsive (OCPD) personality disorders. We aimed to estimate the genetic and environmental influences on dimensional representations of these disorders and examine the validity of the cluster C construct by determining to what extent common familial factors influence the individual PDs. METHOD: PDs were assessed using the Structured Interview for DSM-IV Personality (SIDP-IV) in a sample of 1386 young adult twin pairs from the Norwegian Institute of Public Health Twin Panel (NIPHTP). A single-factor independent pathway multivariate model was applied to the number of endorsed criteria for the three cluster C disorders, using the statistical modeling program Mx. RESULTS: The best-fitting model included genetic and unique environmental factors only, and equated parameters for males and females. Heritability ranged from 27% to 35%. The proportion of genetic variance explained by a common factor was 83, 48 and 15% respectively for AVPD, DEPD and OCPD. Common genetic and environmental factors accounted for 54% and 64% respectively of the variance in AVPD and DEPD but only 11% of the variance in OCPD. CONCLUSION: Cluster C PDs are moderately heritable. No evidence was found for shared environmental or sex effects. Common genetic and individual environmental factors account for a substantial proportion of the variance in AVPD and DEPD. However, OCPD appears to be largely etiologically distinct from the other two PDs. The results do not support the validity of the DSM-IV cluster C construct in its present form.     

Genetic and environmental influences on impulsivity: a meta-analysis of twin, family and adoption studies

A meta-analysis of twin, family and adoption studies was conducted to estimate the magnitude of genetic and environmental influences on impulsivity. The best fitting model for 41 key studies (58 independent samples from 14 month old infants to adults; N = 27,147) included equal proportions of variance due to genetic (0.50) and non-shared environmental (0.50) influences, with genetic effects being both additive (0.38) and non-additive (0.12). Shared environmental effects were unimportant in explaining individual differences in impulsivity. Age, sex, and study design (twin vs. adoption) were all significant moderators of the magnitude of genetic and environmental influences on impulsivity. The relative contribution of genetic effects (broad sense heritability) and unique environmental effects were also found to be important throughout development from childhood to adulthood. Total genetic effects were found to be important for all ages, but appeared to be strongest in children. Analyses also demonstrated that genetic effects appeared to be stronger in males than in females. Method of assessment (laboratory tasks vs. questionnaires), however, was not a significant moderator of the genetic and environmental influences on impulsivity. These results provide a structured synthesis of existing behavior genetic studies on impulsivity by providing a clearer understanding of the relative genetic and environmental contributions in impulsive traits through various stages of development.     

Genetic factors in evolution of sleep length – a longitudinal twin study in Finnish adults

Genetic factors affect many aspects of sleep, such as sleep length. We investigated the contribution of genetic factors to stability and change of sleep length among adults over a 15‐year period. In this representative follow‐up study we used the Finnish Twin Cohort as the study population. Questionnaire surveys were performed in 1975 (response rate 89%, 11 041 twin pairs; age ≥18 years), 1981 (84%, 9323; ≥24 years) and 1990 (77%, 4507; 33–60 years). Sleep was categorized as short (<7 h), average or long (>8 h). Pairwise similarity in monozygotic and dizygotic pairs was examined at each survey by age group and sex. Quantitative genetic modelling was used to estimate cross‐sectional and longitudinal genetic effects. The proportion of variance in sleep length at one point in time that was accounted for by genetic effects was very stable over the study period, being 0.31 in 1975, 0.32 in 1981 and 0.30 in 1990. Longitudinal genetic modelling indicated that the correlations of genetic effects between the three measurement points were high: 0.85 between 1975 and 1981; 0.93 between 1981 and 1990; and 0.76 between 1975 and 1990. Despite a high contribution of environmental effects, their correlations over time were modest: 0.31 between 1975 and 1981; 0.33 between 1981 and 1990; and 0.18 between 1975 and 1990. In conclusion, genetic factors have a modest but stable effect on the evolution of sleep length over a long time span in adults. Multiple measures are a more robust basis for genetic analyses than a single cross‐sectional measure.     

Heritability of somatotype components from early adolescence into young adulthood: a multivariate analysis on a longitudinal twin study

Background : Several studies with different designs have attempted to estimate the heritability of somatotype components. However they often ignore the covariation between the three components as well as possible sex and age effects. Shared environmental factors are not always controlled for. Aim : This study explores the pattern of genetic and environmental determination of the variation in Heath-Carter somatotype components from early adolescence into young adulthood. Subjects and methods : Data from the Leuven Longitudinal Twin Study, a longitudinal sample of Belgian same-aged twins followed from 10 to 18 years ( n = 105 pairs, equally divided over five zygosity groups), is entered into a multivariate path analysis. Thus the covariation between the somatotype components is taken into account, gender heterogeneity can be tested, common environmental influences can be distinguished from genetic effects and age effects are controlled for. Results : Heritability estimates from 10 to 18 years range from 0.21 to 0.88, 0.46 to 0.76 and 0.16 to 0.73 for endomorphy, mesomorphy and ectomorphy in boys. In girls, heritability estimates range from 0.76 to 0.89, 0.36 to 0.57 and 0.57 to 0.76 for the respective somatotype components. Sex differences are significant from 14 years onwards. More than half of the variance in all somatotype components for both sexes at all time points is explained by factors the three components have in common. Conclusions : The finding of substantial genetic influence on the variability of somatotype components is further supported. The need to consider somatotype as a whole is stressed as well as the need for sex- and perhaps age-specific analyses. Further multivariate analyses are needed to confirm the present findings.     

Heritability of somatotype components from early adolescence into young adulthood: a multivariate analysis on a longitudinal twin study

BACKGROUND: Several studies with different designs have attempted to estimate the heritability of somatotype components. However they often ignore the covariation between the three components as well as possible sex and age effects. Shared environmental factors are not always controlled for. AIM: This study explores the pattern of genetic and environmental determination of the variation in Heath-Carter somatotype components from early adolescence into young adulthood. SUBJECTS AND METHODS: Data from the Leuven Longitudinal Twin Study, a longitudinal sample of Belgian same-aged twins followed from 10 to 18 years (n = 105 pairs, equally divided over five zygosity groups), is entered into a multivariate path analysis. Thus the covariation between the somatotype components is taken into account, gender heterogeneity can be tested, common environmental influences can be distinguished from genetic effects and age effects are controlled for. RESULTS: Heritability estimates from 10 to 18 years range from 0.21 to 0.88, 0.46 to 0.76 and 0.16 to 0.73 for endomorphy, mesomorphy and ectomorphy in boys. In girls, heritability estimates range from 0.76 to 0.89, 0.36 to 0.57 and 0.57 to 0.76 for the respective somatotype components. Sex differences are significant from 14 years onwards. More than half of the variance in all somatotype components for both sexes at all time points is explained by factors the three components have in common. CONCLUSIONS: The finding of substantial genetic influence on the variability of somatotype components is further supported. The need to consider somatotype as a whole is stressed as well as the need for sex- and perhaps age-specific analyses. Further multivariate analyses are needed to confirm the present findings.     

Risk factors for hospital admission for asthma from childhood to young adulthood: a longitudinal population study

BACKGROUND: Predictors of hospital admissions for asthma in children and young adults in a general population are not well defined, because most studies have used selected subpopulations. OBJECTIVE: The purpose of this investigation was to determine risk factors for single and multiple hospital admissions for asthma. METHODS: The members of a population-based, unselected birth cohort of 1037 New Zealanders answered questionnaires and underwent lung function, airway responsiveness, and allergy testing on 7 occasions to the age of 26 years. RESULTS: Among the 766 study members (74% of the cohort) who reported wheezing symptoms ever by the age of 26 years, 136 hospitalizations were reported by 62 individuals (8.3% of those at risk, 6.2% of the total cohort). Only 55 of these 136 admissions involved children less than 9 years of age; admissions continued to occur between the ages of 9 and 18 years (40 admissions) and at >18 years (41 admissions). Those admitted were predominantly male, had earlier ages of onset of symptoms, were more atopic, and had more airway hyperresponsiveness to methacholine than those not admitted. Frequent symptoms and low lung function were evident among the 45 study members with single admissions and even more evident among the 17 study members with multiple (2-10) admissions. CONCLUSIONS: A surprisingly large fraction of this unselected population experienced hospitalization for asthma during the 26-year follow-up, many being admitted in later childhood, adolescence, and early adulthood. Clinical characteristics and markers of severity, including frequent respiratory symptoms, airway hyperresponsiveness, atopy, and low lung function, identify those at high risk for hospitalization for asthma, particularly with respect to multiple admissions.     

Genetic and environmental influences on premenstrual symptoms in an Australian twin sample

BACKGROUND: We aimed to explore the prevalence and factor structure of premenstrual symptoms in a sample of Australian twins; to investigate phenotypic associations between reported premenstrual symptoms, personality and reproductive dimensions; and to identify the relative contributions of genes and environment to premenstrual symptoms and the extent of genetic and environmental covariation with the personality trait Neuroticism and lifetime major depression. METHOD: Seven hundred and twenty female twin pairs (454 monozygotic and 266 dizygotic) from the Australian National Health and Medical Research Council Twin Register reported on experience of 17 premenstrual symptoms during the previous 12 months. In the same questionnaire twins also responded to questions on symptom states, and personality dimensions including neuroticism. Interview data enabling diagnosis of lifetime history of DSM-IV major depression were also available. We fitted univariate and multivariate genetic models to the data. RESULTS: Most frequently reported symptoms were breast tenderness/pain and bloating/weight gain, followed by affective symptoms. Twelve-month prevalence was 24% for the combination of symptoms and functional interference meeting a very rough approximation of DSM-III-R criteria for late luteal dysphoric disorder. Principal factor analysis identified a single premenstrual (PMS) factor. Additive genetic influences (44% of total variance) were identified for PMS. Although we found genetic correlations of 0.62 between reported PMS and neuroticism, and 0 70 with lifetime major depression, 39 % of the genetic variance of PMS was not explained by these factors. CONCLUSIONS: Our findings support the existence of genetic influences on premenstrual symptoms, but we were unable to distinguish between liability to symptom experience and symptom reporting. Retrospective reporting may have contributed to our finding that PMS genes were shared in part with neuroticism and liability to lifetime major depression.     

Genetic and environmental influences on illicit drug use and tobacco use across birth cohorts

BACKGROUND: The prevalence of use of many psychoactive substances has changed considerably in recent years. While genetic factors impact on overall risk for substance use, we know little about whether the etiological importance of these factors differs across birth cohorts. One theory, which postulates that heritability of deviant traits increases in permissive environments, predicts a positive relationship across cohorts between prevalence and heritability of substance use. METHOD: The lifetime history of use of tobacco, cannabis, cocaine, sedatives and stimulants were assessed in 4826 twins from male-male and female-female pairs born in Virginia from 1934 to 1974. Using empirical methods based on prevalence by birth year, these twins were divided into three cohorts for each substance (e.g. for cannabis 1934-1953, 1954-1968 and 1969-1974). Structural equation modeling was performed using the Mx software package. RESULTS: Prevalence rates for psychoactive substance use differed substantially across cohorts, most markedly for cocaine, sedatives and stimulants, which were highest in the 1958-1963 cohort. However, for all substances, the best-fit model constrained estimates of the etiological role of genetic and environmental risk factors to be equal across both sex and cohort. CONCLUSIONS: We found no evidence in this sample for any systematic relationship between heritability and prevalence of psychoactive substance use--which should be a rough index of drug availability and/or acceptability. This sample had reasonable power to detect large changes in heritability across cohorts and at least moderate power to detect relatively small changes.     

Genetic and environmental contributions to allergen sensitization in a Chinese twin study

Background Allergic disease is on the rise worldwide. Effective prevention of allergic disease requires comprehensive understanding of the factors that contribute to its intermediate phenotypes, such as sensitization to common allergens. Objective To estimate the degree of genetic and environmental contributions to sensitization to food and aeroallergens. Methods Sensitization was defined as a positive skin prick test to an allergen. We calculated the zygosity‐specific concordance rates and odds ratios (ORs) for sensitization to food and aeroallergens in 826 Chinese twin pairs [472 monozygotic (MZ) and 354 dizygotic (DZ)] aged 12–28 years. We also applied structural equation modelling procedures to estimate genetic and environmental influences on sensitization. Results The concordance rates and risk of sensitization in one twin given the presence vs. the absence of sensitization in the other twin were higher in MZ twins than those in DZ twins. However, a large number of MZ twins were discordant in sensitization to common allergens. These observations suggest both genetic and environmental factors influence sensitization. Consistently, the estimated heritability and individual environmental components of the liability to sensitization ranged from 0.51 to 0.68 and 0.32 to 0.49, respectively, based on the best‐fitted structural equation model. We also observed high phenotypic correlations between sensitization to two aeroallergens (cockroach and dust mite: 0.83) and two food allergens (peanut and shellfish: 0.58), but only moderate correlations for the pairs between sensitization to a food and an aeroallergen (0.31–0.46). The shared genetic and environmental factors between paired sensitizations contribute to the observed correlations. Conclusion We demonstrated that sensitization to common food and aeroallergens were influenced by both genetic and environmental factors. Moreover, we found that paired allergen sensitizations might share some common sets of genes and environmental factors. This study underscores the need to further delineate unique and/or pleiotropic genetic and environmental factors for allergen sensitization.