Nonshared Environmental Effects Research Articles

Sources of structure: genetic, environmental, and artifactual influences on the covariation of personality traits.

The phenotypic structure of personality traits has been well described, but it has not yet been explained causally. Behavior genetic covariance analyses can identify the underlying causes of phenotypic structure; previous behavior genetic research has suggested that the effects from both genetic and nonshared environmental influences mirror the phenotype. However, nonshared environmental effects are usually estimated as a residualterm that may also include systematic bias, such as that introduced by implicit personality theory. To reduce that bias, we supplemented data from Canadian and German twin studies with cross-observer correlations on the Revised NEO Personality Inventory. The hypothesized five-factor structure was found in both the phenotypic and genetic/familial covariances. When the residual covariance was decomposed into true nonshared environmental influences and method bias, only the latter showed the five-factor structure. True nonshared environmental influences are not structured as genetic influences are, although there was some suggestion that they do affect two personality dimensions, Conscientiousness and Love. These data reaffirm the value of behavior genetic analyses for research on the underlying causes of personality traits.

Heritability and Prevalence of Specific Fears and Phobias in Childhood

Fears and phobias are relatively common in childhood. Both environmental and genetic theories have tried to explain the etiology behind these conditions. However, data supporting the different theories are sparse. To investigate the relative importance of genetic and environmental influences on specific phobias and fears, parental reports of animal, situational, and mutilation fears and phobias were completed for 1106 pairs of 8- to 9-year-old Swedish twins. The prevalence of specific phobias was 7.3% for boys and 10.0% for girls. Genetic. shared environmental, and nonshared environmental effects contributed to individual differences in fears and phobias in young children, but the magnitude of the effects differed between sexes. Shared environmental effects contributed to a general susceptibility for fearfulness. Genetic and nonshared environmental effects, on the other hand, contributed both to the general susceptibility and specific fearfulness, even though these effects primarily were fear specific. These results indicate that both heritable factors as well as environmental factors such as trauma, vicarious learning, and/or negative information are important for differences in fearfulness and phobias--at least in children.

Genetic and environmental influences on a measure of infant attachment security

A twin study of infant attachment security at age 24 months was conducted on archival data for a sample of 99 MZ pairs and 108 DZ pairs from the Louisville Twin Study. MZ concordance for attachment was 62.6%, which was significantly greater than the DZ concordance of 44.4%. Concordances were transformed into polychoric correlations, and LISREL was used to conduct a quantitative genetic analysis of the data. Results indicated that 25% of the variability in attachment was attributable to genetic factors, and the remaining 75% was attributable to non-shared environmental effects. No evidence was found for a contribution from shared environmental influences to attachment security. Possible concerns about the validity of twin methodology are addressed and various interpretations of the results are presented. Twin Research (2000) 3, 242–250.

On the application of queuing theory for analysis of twin data

A mathematical model based on queuing theory is used to study the dynamics of environmental influence on twin pairs. The model takes into consideration genetic factors and effects of nonshared environment. Histograms are exploited as base analysed characteristics, with the method of minimum chi-square yielding estimated characteristics. The proposed technique was applied to analysis of longitudinal data for MZ and DZ twins. It was shown that the same environment impact may yield different contributions to final variances of the IQ parameters under investigation. Magnitudes of these contributions depend on the genetic factor represented by distributions of an analysed parameter at the point of birth.

Genetic effects on the liability of developing pre-eclampsia and gestational hypertension

Genetic factors are known to be important in the etiology of pre-eclampsia and possibly also gestational hypertension, but the degree of genetic influence has not been quantified. To estimate the genetic and environmental effects on the liability of developing pre-eclampsia and gestational hypertension, we cross-linked the population-based Swedish Twin Register and the Swedish Medical Birth Register. We included female twin pairs with known zygosity, both of whom gave birth in Sweden from 1973 through 1993; in all 917 monozygotic and 1,199 dizygotic twin pairs. For pre-eclampsia, the estimates of heritability and nonshared environmental effect were 0.54 (95% confidence interval 0–0.71) and 0.46 (0.29–0.67), respectively; corresponding estimates for gestational hypertension were 0.24 (0–0.53) and 0.76 (0.47–1.00), respectively. When considering both diseases as a single entity (pregnancy-induced hypertensive diseases), the heritability estimate was 0.47 (0.13–0.61). These results suggest that genetic factors are important in the development of pre-eclampsia as well as gestational hypertension. The heritability estimates can be of importance when planning genetic linkage studies. In efforts to identify women with elevated risk of developing pre-eclampsia during pregnancy, a question about family history of pre-eclampsia should be included. Am. J. Med. Genet. 91:256–260, 2000. © 2000 Wiley-Liss, Inc.

Genetic effects on the liability of developing pre-eclampsia and gestational hypertension

Genetic factors are known to be important in the etiology of pre-eclampsia and possibly also gestational hypertension, but the degree of genetic influence has not been quantified. To estimate the genetic and environmental effects on the liability of developing pre-eclampsia and gestational hypertension, we cross-linked the population-based Swedish Twin Register and the Swedish Medical Birth Register. We included female twin pairs with known zygosity, both of whom gave birth in Sweden from 1973 through 1993; in all 917 monozygotic and 1,199 dizygotic twin pairs. For pre-eclampsia, the estimates of heritability and nonshared environmental effect were 0. 54 (95% confidence interval 0-0.71) and 0.46 (0.29-0.67), respectively; corresponding estimates for gestational hypertension were 0.24 (0-0.53) and 0.76 (0.47-1.00), respectively. When considering both diseases as a single entity (pregnancy-induced hypertensive diseases), the heritability estimate was 0.47 (0.13-0. 61). These results suggest that genetic factors are important in the development of pre-eclampsia as well as gestational hypertension. The heritability estimates can be of importance when planning genetic linkage studies. In efforts to identify women with elevated risk of developing pre-eclampsia during pregnancy, a question about family history of pre-eclampsia should be included.

On the application of queuing theory for analysis of twin data

A mathematical model based on queuing theory is used to study the dynamics of environmental influence on twin pairs. The model takes into consideration genetic factors and effects of non-shared environment. Histograms are exploited as base analysed characteristics, with the method of minimum chi-square yielding estimated characteristics. The proposed technique was applied to analysis of longitudinal data for MZ and DZ twins. It was shown that the same environment impact may yield different contributions to final variances of the IQ parameters under investigation. Magnitudes of these contributions depend on the genetic factor represented by distributions of an analysed parameter at the point of birth. Twin Research (2000) 3, 92–98.

OVERVIEW OF BIOLOGIC FACTORS

Exploring the biology of neurotransmitters and polymorphic genes that influence behavior most certainly will increase understanding of the complexity of personality disorders and the people who suffer with them. Continuing biologic exploration of the personality disorders will also provide new and valuable information that will inform and direct ever more sophisticated and specific psychiatric treatments. Further, it will supply knowledge that might begin to erode the strong biases and negative labels that have for too long been applied to these patients. These labels may have been applied not because these patients are bad people, but because of ignorance in understanding their complexity and limited ability to improve their condition. Nonetheless, clinicians must refrain from concluding that the answers to all problems in psychiatric treatment can be answered by the molecular geneticist or biologic researcher. As Reiss et al have written when speaking about nonshared environmental effects and its role in the development of psychopathology: "Psychiatry has been forced into the chronically uncomfortable position of straddling biomedicine and the social sciences and seems always to hunger for relief.... [Yet] the data simply do not permit a conception of the future centered on a straightforward biomedical answer to the fundamental question of the pathogenesis of major disorders. Indeed, a balanced image of the future contains a growing and equal partnership of the social sciences and molecular biology."

GENETICS OF PATIENTS WITH BORDERLINE PERSONALITY DISORDER

An overview of the existing literature suggests that traits similar to BPD are influenced by genes. It is too early to say to what extent BPD is also influenced by genes, but because personality traits generally show a strong genetic influence, this should also be true for BPD. Nonetheless, if the equal-environment assumption were to be violated for MZ and DZ pairs, twin studies may be overestimating genetic effects and hiding the effect of common family environment. The less than-ideal reliability of measurements used in this research may also reduce the effects of genes and common environment while increasing the effects of unique or nonshared environment. The effect of genes on the development of BPD is likely substantial. The effect of common family environment may be close to zero. More studies, large and small, are needed to reach firmer conclusions about the influence of genetics on BPD.

Estimation of genetic and environmental components in colorectal and lung cancer and melanoma.

Cancer has predominant environmental and somatic causes but the assessment of hereditary (genetic) causes is difficult, except for highly penetrant single-gene causes. Family studies are only partially informative in this regard because family members share diet and life-styles. Twin studies have been classically used to disentangle the effects of heredity and environment on disease etiology. We estimate the genetic and environmental components in colorectal and lung cancer and melanoma by comparing cancer risks in family members. The Swedish Family-Cancer Database, comprising more than 6 million individuals, was used as the source of family and cancer data. Tetrachoric correlations were used to describe similarity in cancer liability among family members. Structural equation modelling was used to derive estimates of the importance of genetic and environmental effects. The estimated genetic component ranged from 10% in colon and colorectal cancer to 18% in melanoma. For lung cancer, the share was 14%. If assortative mating were important for liability to cancer, these heritability estimates may be an underestimation of the true genetic effects. Non-shared environmental effect was 67-68% in colorectal cancer and melanoma, and 71% in lung cancer. Shared and childhood environments were equally important in colorectal cancer and melanoma, whereas no childhood effect was observed for lung cancer.

A study of the genetic and environmental etiology of stuttering in a selected twin sample.

Stuttering is a developmental disorder of speech production that usually emerges in childhood. In this study, a large population-based twin sample from the Australian Twin Registry (1567 pairs and 634 singles aged 17-29 years) was screened to identify twin pairs in which one or both members reported themselves to be affected by stuttering. Telephone interview-based diagnoses were obtained for 457 of these individuals (self-reported affected cases, cotwins, and controls) to determine whether the self-report was correct. To correct for ascertainment bias we carried out a bivariate analysis of the final diagnosis in the selected sample with the screening item in the full sample, using the categorical raw data option of Mx 1.47c. After correcting for ascertainment bias, approximately 70% (95% confidence interval: 39-86%) of the variance in liability to stuttering was found to be attributable to additive genetic effects, with the remainder due to nonshared environmental effects.

Genetic Disposition for Global Maturity: An Explanation for Genetic Effects on Parental Report on ADHD

Attention deficit hyperactivity disorder (ADHD) has been shown to be substantially influenced by genetic factors. However it is still not known how these effects are mediated. The aim of this study is to evaluate whether genetic disposition for global maturity could be a mediator of the well-known findings of genetic factors for ADHD symptoms. A total of 1480 pairs of twins aged 8-9 years were identified through the population-based Swedish Twin Registry. A mailed questionnaire with items from DSM-III-R for ADHD and items concerning global maturity were completed by the parents. The results showed that global maturity mediated part of genetic effects for ADHD for both boys and girls. There were also genetic, shared environmental, as well as nonshared environmental effects unique to ADHD not in common with global maturity. Thus, there are at least two pathways through which genetic effects can influence ADHD: one through predisposition for maturational lag and one unique to ADHD, possibly mediated by personality. The results indicate that maturational lag could be of importance for treatment and prognosis of ADHD.

Maximum-likelihood generalized heritability estimate for blood pressure in Nigerian families.

Elevated blood pressure (BP) is more common in relatives of hypertensives than in relatives of normotensives, indicating familial resemblance of the BP phenotypes. Most published studies have been conducted in westernized societies. To assess the ability to generalize these estimates, we examined familial patterns of BP in a population-based sample of 510 nuclear families, including 1552 individuals (320 fathers, 370 mothers, 475 sons, and 387 daughters) from Ibadan, Nigeria. The prevalence of obesity in this community is low (body mass index: fathers, 21.6; mothers, 23.6; sons, 19.2; and daughters=21.0 kg/m2). The BP phenotype used in all analyses was created from the best regression model by standardizing the age-adjusted systolic blood pressure (SBP) and diastolic blood pressure (DBP) to 0 mean and unit variance. Heritability was estimated by use of the computer program SEGPATH from the most parsimonious model of "no spouse and neither gender nor generation difference" as 45% for SBP and 43% for DBP. The lack of a significant spouse correlation is consistent with little or no influence of the common familial environment. However, the heritability estimate of <50% for both SBP and DBPs reinforces the importance of the nonshared environmental effect.

Heritability of anxiety sensitivity: a twin study.

In attempting to explain the familial predisposition to panic disorder, most studies have focused on the heritability of physiologic characteristics (e.g., CO2 sensitivity). A heretofore unexplored possibility is that a psychological characteristic that predisposes to panic-anxiety sensitivity-might be inherited. In this study, the authors examined the heritability of anxiety sensitivity through use of a twin group. Scores on the Anxiety Sensitivity Index were examined in a group of 179 monozygotic and 158 dizygotic twin pairs. Biometrical model fitting was conducted through use of standard statistical methods. Broad heritability estimate of the Anxiety Sensitivity Index as a unifactorial construct was 45%. Additive genetic effects and unique environmental effects emerged as the primary influences on anxiety sensitivity. There was no evidence of genetic discontinuity between normal and extreme scores on the Anxiety Sensitivity Index. This study suggests that one psychological risk factor for the development of panic disorder-anxiety sensitivity-may have a heritable component. As such, anxiety sensitivity should be considered in future research on the heritability of panic disorder.

Genetic and social determinants of initiation and age at onset of smoking in Australian twins.

Retrospective data on age at onset of smoking, reported by 3810 adult Australian twin pairs, were analyzed to determine the role of genetic and environmental factors in the onset of smoking. Results of nonmetric multidimensional scaling supported a two-process model in which different etiologic factors determined which individuals were at risk of becoming smokers and the age at onset of smoking in those who were at risk. Parametric model-fitting confirmed this difference. For female twins and younger male twins (aged 30 years or less), the onset of smoking was strongly influenced by genetic factors, with shared and nonshared environmental effects having a more modest impact. For older male twins, shared environmental influences on onset of smoking were very important, and the influence of genetic predisposition was slight. The age at which smoking onset occurred, however, was influenced by both genetic and nonshared environmental effects, but not by shared environmental effects, in both sexes and both cohorts.

Genetics and Child Psychiatry: I Advances in Quantitative and Molecular Genetics

Advances in quantitative psychiatric genetics as a whole are reviewed with respect to conceptual and methodological issues in relation to statistical model fitting, new genetic designs, twin and adoptee studies, definition of the phenotype, pervasiveness of genetic influences, pervasiveness of environmental influences, shared and nonshared environmental effects, and nature-nurture interplay. Advances in molecular genetics are discussed in relation to the shifts in research strategies to investigate multifactorial disorders (affected relative linkage designs, association strategies, and quantitative trait loci studies); new techniques and identified genetic mechanisms (expansion of trinucleotide repeats, genomic imprinting, mitochondrial DNA, fluorescent in-situ hybridisation, behavioural phenotypes, and animal models); and the successful localisation of genes.

Adolescents' relationships to siblings and mothers: A multivariate genetic analysis.

Research has consistently demonstrated that children's behavior toward their siblings tends to resemble interactions occurring in the parent-child relationship. This study examined the relative contributions of genetic and environmental influences to the covariation between sibling relationships and mother-adolescent relationships. Reported and observed family interactions were assessed for 719 same-sex sibling pairs of varying degrees of genetic relatedness. The covariance between mother-adolescent and sibling interactions was decomposed into genetic, shared, and nonshared environmental components. The overlapping effects of shared environment on the two relationship subsystems explained most of the covariance. Smaller but significant genetic and nonshared environmental effects were also found. The consistency of these findings with family processes, such as modeling, is discussed.

Genetic and environmental influence on asthma: a population-based study of 11,688 Danish twin pairs

The aim of this study was to estimate the relative influence of genetic and environmental factors on the aetiology of asthma. The classic twin study design was used to analyse data on self-reported asthma obtained by a questionnaire mailed to 34,076 individuals, aged 12-41 yrs and originating from the Danish Twin Register. The cumulative incidence of asthma was 6.2% in the pooled sample. The data showed a decreasing cumulative incidence with age for males, but no sex or zygosity difference was observed. Substantially higher concordance rates, odds ratios and correlations for asthma were estimated in the monozygotic than in the dizygotic twins. Using biometric modelling, a model including additive genetic and nonshared environmental effects provided the best overall fit to the data. According to this model, 73% of the variation in liability to asthma was explained by genetic factors. No sex difference or age-dependency in the magnitude of genetic effects was observed. The biometric analysis emphasized a major influence of genetic factors in the aetiology of asthma. However, a substantial part of the variation in liability to asthma is due to the impact of environmental factors specific to the individual. There is no evidence for a substantial impact of genetic dominance or the shared environment.

A comparison of power to detect a QTL in sib-pair data using multivariate phenotypes, mean phenotypes, and factor scores.

The power to detect a quantitative trait locus (QTL) in sib-pair data is investigated. We assume that we have at our disposal 3 or 4 related phenotypic measures in a sample of sib-pairs. Individual differences in these phenotypes are due to a common QTL and specific (i.e., unique to each phenotype) nonshared environmental and specific polygenic additive effects. In addition, models are considered that include common nonshared environmental effects and/or common polygenic additive effects. We calculate the power to detect the QTL in a genetic covariance structure analysis of the multivariate data, of the mean phenotypic data, and of factor scores. The use of factor scores is shown to be universally more powerful than the use of multivariate or mean phenotypic data. We also investigate the effect of using a single sample of sib-pairs to both calculate the factor score regression matrix and to carry out the QTL analysis. The use of a single sample to both these ends results in a loss of power compared to the theoretical, expected power. The gain in power attributable to the use of factor scores, however, outweighs this observed loss in power. The advantages of using factor scores in selecting sib-pairs are discussed.

Integrating nature and nurture: Implications of person–environment correlations and interactions for developmental psychopathology

The developmental interplay between nature and nurture is discussed, with particular reference to implications for research in developmental psychopathology. The general principles include individual differences in reactivity to the environment, two-way interplay between intraindividual biology and environmental influences, and the need to consider broader social contextual features. Individuals actively process their experiences; they also act on their environment to shape and select their experiences, and individual characteristics change over time. Key findings on genetic effects include their ubiquitous influence, the multifactorial origin of most psychopathology, the involvement of several genes in most mental disorders, some genetic effects operate through dimensional risk features rather than directly on disorder, some genetic effects are dependent on gene-environment correlations and interactions, and genetic effects increase with age. Key findings on environmental effects include their ubiquitous influence, the genetic mediation of some supposed environmental effects, the importance of passive gene-environment correlations, the paucity of evidence regarding environmental effects on lifetime liability to psychopathology, the lack of understanding of environmental effects on the organism, and the importance of nonshared environmental effects. Research strategies to investigate environmental risk mediation include the range of genetically sensitive designs, migration studies, secular trend investigations, studies of nonfamilial environments, and examination of intraindividual change in relation to measured environmental alterations. Proximal processes involved in person-environment interplay are discussed in relation to person-environment interactions and evocative and active person-environment correlations.