Shared Environmental Influences Research Articles

The nature of the self: Neural analyses and heritability estimates of self-evaluations in middle childhood.

How neural correlates of self‐concept are influenced by environmental versus genetic factors is currently not fully understood. We investigated heritability estimates of behavioral and neural correlates of self‐concept in middle childhood since this phase is an important time window for taking on new social roles in academic and social contexts. To do so, a validated self‐concept fMRI task was applied in a twin sample of 345 participants aged between 7 and 9 years. In the self‐concept condition, participants were asked to indicate whether academic and social traits applied to them whereas the control condition required trait categorization. The self‐processing activation analyses (n = 234) revealed stronger medial prefrontal cortex (mPFC) activation for self than for control conditions. This effect was more pronounced for social‐self than academic self‐traits, whereas stronger dorsolateral prefrontal cortex (DLPFC) activation was observed for academic versus social self‐evaluations. Behavioral genetic modeling (166 complete twin pairs) revealed that 25–52% of the variation in academic self‐evaluations was explained by genetic factors, whereas 16–49% of the variation in social self‐evaluations was explained by shared environmental factors. Neural genetic modeling (91 complete twin pairs) for variation in mPFC and anterior prefrontal cortex (PFC) activation for academic self‐evaluations confirmed genetic and unique environmental influences, whereas anterior PFC activation for social self‐evaluations was additionally influenced by shared environmental influences. This indicates that environmental context possibly has a larger impact on the behavioral and neural correlates of social self‐concept at a young age. This is the first study demonstrating in a young twin sample that self‐concept depends on both genetic and environmental factors, depending on the specific domain.

Socioeconomic Background and Gene–Environment Interplay in Social Stratification across the Early Life Course

AbstractTo what extent are differences in education, occupational standing, and income attributable to genes, and do genetic influences differ by parents’ socioeconomic standing? When in a children’s life course does parents’ socioeconomic standing matter for genetic influences, and for which of the outcomes, fixed at the different stages of the attainment process, do they matter most? We studied these research questions using Finnish register-based data on 6,529 pairs of twins born between 1975 and 1986. We applied genetically sensitive variance decompositions and took gene–environment interactions into account. Since zygosity was unknown, we compared same-sex and opposite-sex twins to estimate the proportion of genetic variation. Genetic influences were strongest in education and weakest in income, and always strongest among those with the most advantaged socioeconomic background, independent of the socioeconomic indicator used. We found that the shared environment influences were negligible for all outcomes. Parental social background measured early during childhood was associated with weaker interactions with genetic influences. Genetic influences on children’s occupation were largely mediated through their education, whereas for genetic influences on income, mediation through education and occupational standing made little difference. Interestingly, we found that non-shared environment influences were greater among the advantaged families and that this pattern was consistent across outcomes. Stratification scholars should therefore emphasize the importance of the non-shared environment as one of the drivers of the intergenerational transmission of social inequalities.

Genetically informative analysis of the association between intimate relationship adjustment and health.

Prior research has found a positive association between the quality or adjustment of an individual's intimate relationship, such as marriage, and their physical health. However, it is possible that this association may be due, at least in part, to confounding variables (i.e., variables that are causally associated both with relationship adjustment and health and could account for their covariation), including genetically influenced confounds. This study was conducted using a genetically informative sample of twins to examine the association between intimate relationship adjustment and self-rated health, accounting for unmeasured genetic and environmental confounds. A Swedish sample of 539 monozygotic and dizygotic twins (321 male twin pairs and 218 female twin pairs) and their spouse or long-term partner completed self-report measures of relationship adjustment and health. Relationship adjustment was positively associated with self-rated health in male and female twins. For male twins, nonshared environmental influences largely accounted for the association between relationship adjustment and health; for female twins, this association was generally explained by shared and nonshared environmental influences. For male twins, results obtained from partners' reports of relationship adjustment were largely consistent with those obtained from twins' reports. Results suggest that the association between relationship adjustment and self-rated health remains after accounting for shared genetic influences, and that nonshared environmental influences, such as partners' characteristics, account for the association between relationship adjustment and self-rated health in men. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

Maternal Parenting Behaviors Amplify Environmental Influences on Developmental Trajectories of Alcohol Use During Adolescence.

Compared to peer alcohol use, less is known on how parenting practices may modify genetic and environmental contributions to alcohol use longitudinally across adolescence. This study examined whether two maternal parenting behaviors, supervision and harsh parenting, may suppress or amplify genetic and environmental influences on three distinct developmental trajectories of adolescent alcohol use: normative increasing, early-onset, and low trajectories. Participants were drawn from a longitudinal study of a population-based twin sample (N = 842, 84% European descent, 52.7% female). Adolescents self-reported their past year alcohol use at ages 13, 14, 15, and 17years, and their mothers reported their supervision and harsh parenting when twins were 13, 15, and 17years old. Maternal supervision amplified non-shared environmental influence on the normative increasing and early-onset trajectories, whereas maternal harsh parenting amplified shared environmental influence on the early-onset trajectory and non-shared environmental influence on the low trajectory, respectively. The findings suggest maternal parenting practices as a potent developmental context that modulates the environmental influences of other proximal processes on adolescent alcohol use, and suggest that family-based parenting-focused intervention could be especially beneficial for adolescents following the early-onset trajectory.

Creative expressiveness in childhood writing predicts educational achievement beyond motivation and intelligence: A longitudinal, genetically informed study.

Creativity is linked with educationally relevant constructs such as achievement, intelligence, and motivation. However, very few studies have explored longitudinal links between the constructs or the aetiology of individual differences in childhood creativity. The study addresses the gap in the literature of developmental studies on the relationship of creativity with other educationally relevant measures. Additionally, the present study is the first adequately powered genetically informative analysis of childhood creativity. The present study utilized data from 1,306 twins, a subsample from a longitudinal, representative twin sample in the UK. Creativity was operationalised as a Creative Expressiveness score, using the Consensual Assessment Technique on stories written by 9-year-olds. Intelligence and writing motivation were assessed at age 9. Academic achievement was collected at ages 9, 12, and 16. Creative Expressiveness was associated with intelligence and motivation, all measured at age 9. It also predicted variance in English grades at ages 9 and 16. The associations were weak, but significant, over and above intelligence, motivation, and earlier English grades. The variance in Creative Expressiveness was explained by genetic (35%), shared environmental (21%), and non-shared environmental (45%) influences. The phenotypic correlations with other study variables were mainly mediated genetically. The results provide information that can be used for planning educational content. First, creativity can be detected in childhood writing. Second, childhood creativity may be overlooked in early educational assessments. Third, the results from the genetic analyses are important indications on the role of environments in the development of creativity.

Shared Genetic and Environmental Influences on Altered Functional Connectivity and Schizophrenia Liability

Schizophrenia liability and functional connectivity are associated, and both are influenced by genetic and environmental factors. It currently remains unclear to what extent a shared genetic or environmental association exists.

P.321 Shared genetic and environmental influences on altered functional connectivity and schizophrenia liability

P.321 Shared genetic and environmental influences on altered functional connectivity and schizophrenia liability

Genetic Correlates of Psychological Responses to the COVID-19 Crisis in Young Adult Twins in Great Britain

We investigated how the COVID-19 crisis and the extraordinary experience of lockdown affected young adults in England and Wales psychologically. One month after lockdown commenced (T2), we assessed 30 psychological and behavioural traits in more than 4000 twins in their mid-twenties and compared their responses to the same traits assessed in 2018 (T1). Mean changes from T1 to T2 were modest and inconsistent. Contrary to the hypothesis that major environmental changes related to COVID-19 would result in increased variance in psychological and behavioural traits, we found that the magnitude of individual differences did not change from T1 to T2. Twin analyses revealed that while genetic factors accounted for about half of the reliable variance at T1 and T2, they only accounted for ~ 15% of individual differences in change from T1 to T2, and that nonshared environmental factors played a major role in psychological and behavioural changes. Shared environmental influences had negligible impact on T1, T2 or T2 change. Genetic factors correlated on average .86 between T1 and T2 and accounted for over half of the phenotypic stability, as would be expected for a 2-year interval even without the major disruption of lockdown. We conclude that the first month of lockdown has not resulted in major psychological or attitudinal shifts in young adults, nor in major changes in the genetic and environmental origins of these traits. Genetic influences on the modest psychological and behavioural changes are likely to be the result of gene–environment correlation not interaction.

On Naevi and Melanomas: Two Sides of the Same Coin?

Benign naevi are closely linked to melanoma, as risk factors, simulators, or sites of melanoma formation. There is a heavy genetic overlap between the two lesions, a shared environmental influence of ultraviolet radiation, and many similar cellular features, yet naevi remain locally situated while melanomas spread from their primary site and may progress systemically to distal organs. Untangling the overlapping contributors and predictors of naevi and melanoma is an ongoing area of research and should eventually lead to more personalized prevention and treatment strategies, through the development of melanoma risk stratification tools and early detection of evolving melanomas. This will be achieved through a range of complementary strategies: risk-adjusted primary prevention counseling; the use of lesion imaging technologies such as sequential 3D total body photography and consumer-performed lesion imaging; artificial intelligence deep phenotyping and clinical assistance; a better understanding of genetic drivers of malignancy, risk variants, clinical genetics, and polygenic effects; and the interplay between genetics, phenotype and the environment.

Genetic and environmental architecture of conscientiousness in adolescence

Using a genetically informative design (about 2000 twin pairs), we investigated the phenotypic and genetic and environmental architecture of a broad construct of conscientiousness (including conscientiousness per se, effortful control, self-control, and grit). These four different measures were substantially correlated; the coefficients ranged from 0.74 (0.72–0.76) to 0.79 (0.76–0.80). Univariate genetic analyses revealed that individual differences in conscientiousness measures were moderately attributable to additive genetic factors, to an extent ranging from 62 (58–65) to 64% (61–67%); we obtained no evidence that shared environmental influences were observed. Multivariate genetic analyses showed that for the four measures used to assess conscientiousness, genetic correlations were stronger than the corresponding non-shared environmental correlations, and that a latent common factor accounted for over 84% of the genetic variance. Our findings suggest that individual differences in the four measures of conscientiousness are not distinguishable at both the phenotypic and behavioural genetic levels, and that the overlap was substantially attributable to genetic factors.

Shared Environmental Influences on Electronic Cigarette Use Among Adolescent and Young Adult Females.

Electronic cigarettes are now the most commonly used form of tobacco product among youth in the United States. Current evidence suggests that although e-cigarettes are perceived as less harmful and preferred over combustible cigarettes by adolescents, adolescents who try e-cigarettes are at greater risk of transitioning to combustible cigarettes. The genetic and environmental contributions to liability for e-cigarette use have not yet been examined using a behavioral genetic design. Behavioral genetic models of lifetime and current e-cigarette use and friends who use e-cigarettes were examined among female monozygotic and dizygotic twins. A total of 41 female twin pairs (65.9% monozygotic twins; age = 19.7, SD = 1.6) with complete data on the study variables were included in the present analyses. The majority of the sample (68.1%) had at least some friends who use e-cigarettes. Additive genetic effects on e-cigarette use were not present, but the shared environment explained 98.7% of the variance in lifetime e-cigarette use, 96.6% in current e-cigarette use, and 94.9% in affiliation with friends who use e-cigarettes. This first study on the behavioral genetics of e-cigarette use among adolescents and young adults suggest that environmental factors shared by twins within a family seem to play a predominant role in the initial stages of e-cigarette use, a finding that is consistent with what has been found for tobacco. The findings emphasize the importance of continuing population-based tobacco control interventions to reduce the burden of e-cigarette use among adolescents. The shared environment significantly influences the initiation and regular use of electronic cigarettes and affiliation with friends who use electronic cigarettes among adolescent and young adult females. These findings underscore the importance of formulating preventive interventions that mitigate the social effects of familial influences on e-cigarette use through social skills training, education on harms of e-cigarettes for young people, or altering social norms regarding initiation of novel tobacco products.

Co‐development of alcohol use problems and antisocial peer affiliation from ages 11 to 34: selection, socialization and genetic and environmental influences

Social context is an important factor in determining the developmental trajectory of alcohol use. We examined the co-development between alcohol use problems and antisocial peer affiliation. We also estimated the genetic and environmental influences on alcohol use problems, antisocial peer affiliation and their co-development over time. Longitudinal study using bivariate latent basis models with structured residuals (LBM-SR). A biometric model was then fitted to estimate the genetic and environmental influences on the growth factors and their covariances. The United States mid-west region. Members of the Minnesota Twin Family Study (MTFS), an ongoing, longitudinal study of 3762 (52% female) twins (1881 pairs). Alcohol use problems were assessed using a composite measure of average number of drinks per occasion in the past 12months, maximum number of drinks in 24hours and DSM-III-R symptoms of alcohol abuse and dependence. Antisocial peer affiliation was measured by self-report of the proportion of one's friends who exhibited types of antisocial behaviors. The LBM-SR model revealed that there was a large correlation between the growth factors for alcohol use problems and antisocial peer affiliation [r=0.78, 95% confidence interval (CI)=0.76, 0.80] and cross-lagged effects consistent with both selection and socialization effects. Additionally, antisocial peer affiliation in adolescence was associated with greater increases in alcohol use problems over time (r=0.57, 95% CI=0.54, 0.60). Genetic influences largely accounted for the association between antisocial peer affiliation in pre-adolescence and growth in alcohol use problems, while shared environmental influences accounted for the correlation between antisocial peer affiliation and alcohol use problems growth factors. Antisocial peer affiliation in adolescence appears to be a salient, genetically influenced risk factor for early alcohol use and increase in alcohol use from adolescence to young adulthood.

Are prescription misuse and illicit drug use etiologically distinct? A genetically-informed analysis of opioids and stimulants.

Drug classes are grouped based on their chemical and pharmacological properties, but prescription and illicit drugs differ in other important ways. Potential differences in genetic and environmental influences on the (mis)use of prescription and illicit drugs that are subsumed under the same class should be examined. Opioid and stimulant classes contain prescription and illicit forms differentially associated with salient risk factors (common route of administration, legality), making them useful comparators for addressing this etiological issue. A total of 2410 individual Australian twins [Mage = 31.77 (s.d. = 2.48); 67% women] were interviewed about prescription misuse and illicit use of opioids and stimulants. Univariate and bivariate biometric models partitioned variances and covariances into additive genetic, shared environmental, and unique environmental influences across drug types. Variation in the propensity to misuse prescription opioids was attributable to genes (41%) and unique environment (59%). Illicit opioid use was attributable to shared (71%) and unique (29%) environment. Prescription stimulant misuse was attributable to genes (79%) and unique environment (21%). Illicit stimulant use was attributable to genes (48%), shared environment (29%), and unique environment (23%). There was evidence for genetic influence common to both stimulant types, but limited evidence for genetic influence common to both opioid types. Bivariate correlations suggested that prescription opioid use may be more genetically similar to prescription stimulant use than to illicit opioid use. Prescription opioid misuse may share little genetic influence with illicit opioid use. Future research may consider avoiding unitary drug classifications, particularly when examining genetic influences.

Generalist genes and specialist environments for adolescent internalizing and externalizing problems: A test of severity and directionality.

The generalist genes specialist environment model, when applied to developmental psychopathology, predicts that genetic influences should explain variance that is shared across internalizing and externalizing problems, whereas environmental influences should explain variance that distinguishes the two overarching problem types. The present study is a direct test of this hypothesis, leveraging a sample of 708 twins and siblings (aged 10-18 years, 93% White) from the United States. Measures of severity of symptoms, regardless of type, and of directionality of symptoms - whether the adolescent tended to exhibit more externalizing or internalizing problems - were subjected to genetic (A), shared environmental (C), and nonshared environmental (E) (ACE) variance decompositions. As expected, severity of problems was under substantial genetic influence, but there were also significant shared and nonshared environmental influences. Contrary to the generalist genes specialist environment model, directionality of problem type was also under considerable genetic influence, with modest nonshared environmental influence. Findings corroborate existing evidence from other designs highlighting the role of familial influences (including generalist genes) in comorbidity of adolescent internalizing and externalizing problems, but suggest that the specialist environments hypothesis may not be the key factor in distinguishing problem type.

Twins and Causal Inference: Leveraging Nature's Experiment.

In this review, we discuss how samples comprising monozygotic and dizygotic twin pairs can be used for the purpose of strengthening causal inference by controlling for shared influences on exposure and outcome. We begin by briefly introducing how twin data can be used to inform the biometric decomposition of population variance into genetic, shared environmental, and nonshared environmental influences. We then discuss how extensions to this model can be used to explore whether associations between exposure and outcome survive correction for shared etiology (common causes). We review several analytical approaches that can be applied to twin data for this purpose. These include multivariate structural equation models, cotwin control methods, direction of causation models (cross-sectional and longitudinal), and extended family designs used to assess intergenerational associations. We conclude by highlighting some of the limitations and considerations that researchers should be aware of when using twin data for the purposes of interrogating causal hypotheses.

Longitudinal effects of family psychopathology and stress on pubertal maturation and hormone coupling in adolescent twins.

Adolescents experience profound neuroendocrine changes, including hormone "coupling" between cortisol, testosterone, and dehydroepiandrosterone. Emerging research has only begun to elucidate the role of hormone coupling, its genetic and environmental etiology, and the extent to which coupling is impacted by gender, puberty, and family context. We included measures on parent and child mental health, parenting stress, and family conflict of 444 twin pairs and their parents across two timepoints, when youth were on average 8 and 13years old, respectively. Structural equation models examined the impact of family context effects on coupling during adolescence. Biometric twin models were then used to probe additive genetic, shared, and non-shared environmental effects on hormone coupling. Hormones were more tightly coupled for females than males, and coupling was sensitive to parental depression and co-twin psychopathology symptoms and stress exposure in females. The association between family context and coupling varied across specific neuroendocrine measures and was largely distinct from pubertal maturation. Biometric models revealed robust shared and non-shared environmental influences on coupling. We found that family antecedents modify the strength of coupling. Environmental influences account for much of the variation on coupling during puberty. Gender differences were found in genetic influences on coupling.

Glenoid version: the role of genetic and environmental factors on its variability. An MRI study on asymptomatic elderly twins.

Glenoid version is the most variable parameter of the shoulder joint. No authors investigated if intrinsic genetic factors or influences from extrinsic sources are responsible for its variability. We compared glenoid version between elderly monozygotic and dizygotic twins intending to separate the contributions of genetics from shared and unique environments. Glenoid version of the dominant shoulder was assessed by MRI using Friedman's method in 30 pairs of elderly twins (16 monozygotic-14 dizygotic; mean age ± SD: 63.72 ± 3.37, 53-72). Heritability was estimated as twice the difference between the intraclass correlation coefficients for monozygotic and dizygotic pairs. The influence of shared environment was calculated as the difference between monozygotic correlation coefficient and the heritability index. According to job category, one way analysis of variance was used to estimate the differences between groups in the total sample and within zygosity groups. Glenoid version angle in monozygotic and dizygotic twins was -2° (SD: 2°) and -3° (SD: 3°), respectively (p = 0.334). Heritability index was 0.98, while the contributions of shared and unique environment were 0 and 0.02, respectively. According to working classes, no significant differences were found between the groups (p = 0.732, F = 0.31). Glenoid version is mainly genetically determined and only marginally influenced by environments.Level of evidence: III.

Decomposition of Mean Sex Differences in Alcohol Use Within a Genetic Factor Model.

A wealth of literature suggests that normative and heavy alcohol consumption continue to follow a historical pattern of greater prevalenceamong males as compared to females. Some prior research suggested that sex-specific factors might explain some of this gender gap. Generally speaking, though, more recent studies have indicated that the sources of differences for most complex traits, both genetic and environmental, are similar for males and females. To the best of our knowledge, however, no studies have tested whether genetic and environmental factors common to both sexes are more often expressed in males, on average, thereby accounting for some of the mean sex difference in alcohol use. The current study used nationally representative data from American twin respondents and a multiple group genetic factor model with a mean structure to address this gap in the literature. Results provide no evidence of sex differences in covariance structure and suggest that genetic and nonshared environmental influences common to both sexes largely explain why male alcohol use is more frequent and severe, on average, than is female use. In contrast, shared environmental influences seem to play a less important role. We discuss our findings in the context of the existing literature and chart out directions for future research.

A Twin Study of Sex Differences in Genetic Risk for All Dementia, Alzheimer's Disease (AD), and Non-AD Dementia.

While sex differences in incidence of Alzheimer's disease (AD) and potential explanations have received considerable attention, less attention has been paid to possible sex differences in genetic risk for AD. We examined sex differences in genetic and environmental influences on disease risk and age at onset for All Dementia, AD Only, and Non-AD Dementia. Twin pairs were drawn from the Swedish Twin Registry. All Dementia analysis included 9,467 pairs; AD only, 8,696 pairs; and non-AD dementia, 8,195 pairs. APOE analyses included 1,740 individual twins with measured ɛ4 alleles. Dementia diagnoses were based on clinical workup and national health registry linkage. Although within-pair correlations for All Dementia and AD Only were higher for women than for men, sex differences did not statistically differ for genetic or environmental etiology of All Dementia, AD Only, and Non-AD dementia. Similar results were observed when looking at specific genetic effects (APOEɛ4). Co-twin control analyses indicated that among twin pairs discordant for dementia, female twins without dementia had approximately 40% greater risk of developing dementia, compared with their male counterparts, in the 2-5 years following the first twin's diagnosis. For All Dementia, AD Only, and Non-AD Dementia, genetic influences could be equated across sex. Co-twin analyses, however, suggest greater risk to female than to male co-twins of dementia cases even though sex differences in either genetic or shared environmental influences on the risk of dementia could not be differentiated.

Genetics and Not Shared Environment Explains Familial Resemblance in Adult Metabolomics Data.

Metabolites are small molecules involved in cellular metabolism where they act as reaction substrates or products. The term 'metabolomics' refers to the comprehensive study of these molecules. The concentrations of metabolites in biological tissues are under genetic control, but this is limited by environmental factors such as diet. In adult mono- and dizygotic twin pairs, we estimated the contribution of genetic and shared environmental influences on metabolite levels by structural equation modeling and tested whether the familial resemblance for metabolite levels is mainly explained by genetic or by environmental factors that are shared by family members. Metabolites were measured across three platforms: two based on proton nuclear magnetic resonance techniques and one employing mass spectrometry. These three platforms comprised 237 single metabolic traits of several chemical classes. For the three platforms, metabolites were assessed in 1407, 1037 and 1116 twin pairs, respectively. We carried out power calculations to establish what percentage of shared environmental variance could be detected given these sample sizes. Our study did not find evidence for a systematic contribution of shared environment, defined as the influence of growing up together in the same household, on metabolites assessed in adulthood. Significant heritability was observed for nearly all 237 metabolites; significant contribution of the shared environment was limited to 6 metabolites. The top quartile of the heritability distribution was populated by 5 of the 11 investigated chemical classes. In this quartile, metabolites of the class lipoprotein were significantly overrepresented, whereas metabolites of classes glycerophospholipids and glycerolipids were significantly underrepresented.