scholarly journals Perceived Family Cohesion Moderates Environmental Influences on Prosocial Behavior in Nigerian Adolescent Twins

2017 ◽  
Vol 20 (3) ◽  
pp. 226-235 ◽  
Author(s):  
Yoon-Mi Hur ◽  
Jeanette Taylor ◽  
Hoe-Uk Jeong ◽  
Min-Seo Park ◽  
Brett C. Haberstick

Research shows that perceived family cohesion is positively related to prosocial behavior in adolescents. In this study, we investigated heritability of prosocial behavior (PB) and perceived family cohesion (FC) among Nigerian twins attending public schools in Lagos State, Nigeria (mean age = 14.7 years, SD = 1.7 years), and explored the issue of whether children's perception of cohesive family environment moderated genetic and environmental influences on (PB). The PB scale of the Strengths and Difficulties Questionnaire and the FC scale of the Family Adaptability and Cohesion Evaluation Scale III were completed by 2,376 twins (241 monozygotic (MZ) male, 354 MZ female, 440 dizygotic (DZ) male, 553 DZ female, and 788 opposite-sex DZ twins). A general sex-limitation and the bivariate genotype by environment interaction (G×E) models were applied to the data. The general sex-limitation model showed no significant sex differences, indicating that additive genetic and non-shared environmental influences were, 38% (95% CI = 31, 46) and 62% (95% CI = 54, 69) for PB and 33% (95% CI = 24, 40) and 67% (95% CI = 60, 76) for FC in both sexes. These estimates were similar to those found in Western and Asian twin studies to date. The correlation between PB and FC was 0.36. The best-fitting bivariate G×E model indicated that FC significantly moderated non-shared environmental influence unique to PB (E×E interaction). Specifically, non-shared environmental contributions to PB were highest when FC was lowest, and decreased as the levels of FC increased. However, genetic variances in PB were stable across all levels of FC. These findings suggest that FC reduces individual differences in PB by changing non-shared environmental experiences rather than genetic factors in PB.

Collabra ◽  
2016 ◽  
Vol 2 (1) ◽  
Author(s):  
David A. Sbarra

Objective: Low levels of perceived social integration, or loneliness, are associated with increased risk for a range of poor health outcomes. Sleep disturbance plays a central role in the evolutionary theory of loneliness, which provides a mechanistic account of how low levels of social integration may negatively impact health. No studies, however, have examined whether the association between social integration and sleep disturbance is consistent with a causal effect after accounting for genes that are common to both variables. Method: Using twin data (N = 905 twin pairs) from the nationally-representative Midlife in the United States (MIDUS) survey, I evaluated a series of bivariate twin models exploring whether the phenotypic association between low social integration and sleep disturbance can be explained by shared genetics. In addition, the current study specified a series of quantitative models for studying gene x environment (G X E) interactions to determine whether the genetic and environmental influences on sleep disturbance differ as a function of social integration. Results: The phenotypic association between social integration and sleep disturbance was fully accounted for by genes that are common between the two variables, suggesting that within-twin pair differences in social integration do not exert a causal influence on sleep disturbance. Social integration, however, moderated the non-shared environmental influence on sleep disturbances, with the greatest environmental influences observed at the lowest levels of social integration. Conclusions: The results of this study suggest that an essential feature of the evolutionary model of loneliness may need refinement or elaboration. The moderation findings are discussed in terms of the fit with a stress-buffering model of social support in which environmental influences on sleep disturbance are strongest when social resources are low.


2017 ◽  
Vol 20 (7) ◽  
pp. 836-842 ◽  
Author(s):  
Jorien L Treur ◽  
Karin J H Verweij ◽  
Abdel Abdellaoui ◽  
Iryna O Fedko ◽  
Eveline L de Zeeuw ◽  
...  

Abstract Introduction Classical twin studies show that smoking is heritable. To determine if shared family environment plays a role in addition to genetic factors, and if they interact (G×E), we use a children-of-twins design. In a second sample, we measure genetic influence with polygenic risk scores (PRS) and environmental influence with a question on exposure to smoking during childhood. Methods Data on smoking initiation were available for 723 children of 712 twins from the Netherlands Twin Register (64.9% female, median birth year 1985). Children were grouped in ascending order of risk, based on smoking status and zygosity of their twin-parent and his/her co-twin: never smoking twin-parent with a never smoking co-twin; never smoking twin-parent with a smoking dizygotic co-twin; never smoking twin-parent with a smoking monozygotic co-twin; and smoking twin-parent with a smoking or never smoking co-twin. For 4072 participants from the Netherlands Twin Register (67.3% female, median birth year 1973), PRS for smoking were computed and smoking initiation, smoking heaviness, and exposure to smoking during childhood were available. Results Patterns of smoking initiation in the four group children-of-twins design suggested shared familial influences in addition to genetic factors. PRS for ever smoking were associated with smoking initiation in all individuals. PRS for smoking heaviness were associated with smoking heaviness in individuals exposed to smoking during childhood, but not in non-exposed individuals. Conclusions Shared family environment influences smoking, over and above genetic factors. Genetic risk of smoking heaviness was only important for individuals exposed to smoking during childhood, versus those not exposed (G×E). Implications This study adds to the very few existing children-of-twins (CoT) studies on smoking and combines a CoT design with a second research design that utilizes polygenic risk scores and data on exposure to smoking during childhood. The results show that shared family environment affects smoking behavior over and above genetic factors. There was also evidence for gene–environment interaction (G×E) such that genetic risk of heavy versus light smoking was only important for individuals who were also exposed to (second-hand) smoking during childhood. Together, these findings give additional incentive to recommending parents not to expose their children to cigarette smoking.


2017 ◽  
Vol 41 (S1) ◽  
pp. S102-S102
Author(s):  
K.-W. Nilsson ◽  
C. Åslund

IntroductionThe candidate gene-environment interaction (cG × E) research field in psychiatry has traditionally been dominated by the diathesis–stress framework, where certain genotypes are assumed to confer increased risk for adverse outcomes in a stressful environment. In later years, theories of differential susceptibility or biological sensitivity have been presented, suggesting that cGs that interact with environmental events do not exclusively confer a risk for behavioural or psychiatric disorders but rather seem to alter the sensitivity to both positive and negative environmental influences.AimsThe present study investigates the susceptibility properties of the 5HTTLPR gene in relation to depressive symptoms and delinquency in two separate adolescent community samples: n = 1457, collected in 2006; and n = 191, collected in 2001.ResultsTwo-, three- and four-way interactions between the 5HTTLPR, positive family environment, negative family environment, and sex were found in relation to both depressive symptoms and delinquency. However, the susceptibility properties of the 5HTTLPR gene were distinctly less pronounced in relation to depressive symptoms.ConclusionsIf the assumption that the 5HTTLPR gene induces differential susceptibility to both positive and negative environmental influences is correct, the previous failures to measure and control for positive environmental factors might be a possible explanation for former inconsistent findings within the research field.Disclosure of interestThe authors have not supplied their declaration of competing interest.


2007 ◽  
Vol 10 (2) ◽  
pp. 315-326 ◽  
Author(s):  
Danielle M. Dick ◽  
Jason L. Pagan ◽  
Richard Viken ◽  
Shaun Purcell ◽  
Jaakko Kaprio ◽  
...  

AbstractIn contrast to many phenotypes that have been studied using twin designs, substance use shows considerable evidence of environmental influence. Accordingly, specifying the relevant environments and understanding the nature of their effects is an important research priority. Twin studies also have demonstrated that the importance of genetic and environmental influences varies across development for a variety of behavioral outcomes, including substance use. Here, we report analyses exploring moderating effects associated with parenting and peer characteristics on adolescent smoking and drinking, measured at ages 14 and 17. We find significant evidence of moderating effects associated with two dimensions of parenting (parental monitoring and time spent in activities with parents) on adolescent smoking, measured at two time points across development, but no moderating effects on adolescent drinking. Genetic influences on smoking increased, and common environmental effects decreased, as adolescents reported less parental monitoring and spending more time with their parents. Conversely, we find evidence that adolescent drinking is more strongly influenced by peer characteristics. The importance of genetic predispositions was increased among adolescents who reported more friends who used alcohol. These analyses illustrate the importance of incorporating measured aspects of the environment into genetically informative twin models to begin to understand how specific environments are related to various outcomes. Furthermore, they illustrate the importance of using a developmental perspective to understand how specific influences may vary across different ages, and across different phenotypes.


2021 ◽  
pp. 1-11
Author(s):  
Hailey L. Dotterer ◽  
Alexandra Y. Vazquez ◽  
Luke W. Hyde ◽  
Craig S. Neumann ◽  
Pekka Santtila ◽  
...  

Abstract Background Psychopathic traits involve interpersonal manipulation, callous affect, erratic lifestyle, and antisocial behavior. Though adult psychopathic traits emerge from both genetic and environmental risk, no studies have examined etiologic associations between adult psychopathic traits and experiences of parenting in childhood, or the extent to which parenting practices may impact the heritability of adult psychopathic traits using a genetically-informed design. Methods In total, 1842 adult twins from the community reported their current psychopathic traits and experiences of negative parenting during childhood. We fit bivariate genetic models to the data, decomposing the variance within, and the covariance between, psychopathic traits and perceived negative parenting into their genetic and environmental components. We then fit a genotype × environment interaction model to evaluate whether negative parenting moderated the etiology of psychopathic traits. Results Psychopathic traits were moderately heritable with substantial non-shared environmental influences. There were significant associations between perceived negative parenting and three of four psychopathy facets (interpersonal manipulation, erratic lifestyle, antisocial tendencies, but not callous affect). These associations were attributable to a common non-shared environmental pathway and not to overlapping genetic effects. Additionally, we found that primarily shared environmental influences were stronger on psychopathic traits for individuals with a history of greater negative parenting. Conclusions Utilizing a genetically-informed design, we found that both genetic and non-shared environmental factors contribute to the emergence of psychopathic traits. Moreover, perceptions of negative parenting emerged as a clear environmental influence on the development of interpersonal, lifestyle, and antisocial features of psychopathy.


1999 ◽  
Vol 31 (1) ◽  
pp. 29-41 ◽  
Author(s):  
JOSEPH LEE RODGERS ◽  
DAVID C. ROWE ◽  
MAURY BUSTER

Fisher (1930) presented both theoretical and empirical results concerning genetic influences on fertility. Since then, only sparse research has been done on the genetics of fertility, although more sophisticated methodogy and data now exist than were available to Fisher. This paper presents a behavioural genetic analysis of age at first intercourse, accounting for genetic, shared environmental, and selected non-shared environmental influences. The data came from the nationally representative National Longitudinal Survey of Youth (NLSY). A newly developed kinship linking procedure was used that identifies links for cousins, half-siblings, full-siblings and twins in the NLSY. The results suggest a genetic influence in the overall dataset, and also among whites and in male–male and opposite-sex pairs. Genetic influences were extremely small or non-existent for blacks and for female–female pairs. Shared environmental influences were small for most subsets of the data, but moderate for female–female pairs. Two specific non-shared environmental influences – self-esteem and locus of control – were ruled out as accounting for any meaningful variance, although other general sources of non-shared environmental influence appear potentially important. Analysis of selected samples from upper and lower tails suggested that genetic influences are important in accounting for both early and late non-virginity. These findings are consistent with work reported by Miller et al. (1999), who used molecular genetic methods. Generally, these findings support the existence of genetic influences and implicate non-shared environmental influences as being important determinants of the timing of loss of virginity among US adolescents and young adults.


2020 ◽  
Author(s):  
Samantha M Freis ◽  
Claire Morrison ◽  
Jeffrey M. Lessem ◽  
John K. Hewitt ◽  
Naomi P. Friedman

Executive functions (EFs) and intelligence (IQ) are phenotypically correlated and heritable; however, they show variable genetic correlations in twin studies spanning childhood to middle age. We analyzed data from over 11,000 children (9-10-year-olds, including 749 twin pairs) in the Adolescent Brain Cognitive Development (ABCD) Study to examine the phenotypic and genetic relations between EFs and IQ in childhood. We identified two EF factors – Common EF and Updating-Specific, which were both related to IQ (rs = .64-.81). Common EF and IQ were heritable (53-67%), and their genetic correlation (rG = .86) was not significantly different than 1. These results suggest that EFs and IQ are phenotypically but not genetically separable in middle childhood.


2021 ◽  
pp. 194855062199297
Author(s):  
Nickola C. Overall ◽  
Valerie T. Chang ◽  
Paula R. Pietromonaco ◽  
Rachel S. T. Low ◽  
Annette M. E. Henderson

The COVID-19 pandemic presents acute, ongoing relationship challenges. The current research tested how (1) preexisting vulnerabilities assessed prior to the pandemic (attachment insecurity) and (2) stress as couples endured a mandated quarantine predicted residual changes in relationship functioning. Controlling for prequarantine problems, relationship quality, and family environment, greater partners’ attachment anxiety predicted greater relationship problems, lower relationship quality, and a less stable and cohesive family environment when people were experiencing more stress. Greater partners’ attachment avoidance predicted lower problem-solving efficacy and family cohesion. The effects of partners’ preexisting vulnerabilities and pandemic-related stress demonstrate the utility of key models in relationship science in identifying who is at most risk of relationship problems in the unprecedented context of a mandated quarantine. The results emphasize that the effects of the COVID-19 pandemic on relationship functioning will be shaped by the characteristics of partners with whom people are confined with during the pandemic.


2008 ◽  
Vol 99 (S1) ◽  
pp. S15-S21 ◽  
Author(s):  
Jane Wardle ◽  
Lucy Cooke

Omnivores have the advantage of a variety of food options but face a challenge in identifying foods that are safe to eat. Not surprisingly, therefore, children show a relative aversion to new foods (neophobia) and a relative preference for familiar, bland, sweet foods. While this may in the past have promoted survival, in the modern food environment it could have an adverse effect on dietary quality. This review examines the evidence for genetic and environmental factors underlying individual differences in children's food preferences and neophobia. Twin studies indicate that neophobia is a strongly heritable characteristic, while specific food preferences show some genetic influence and are also influenced by the family environment. The advantage of the malleability of human food preferences is that dislike of a food can be reduced or even reversed by a combination of modelling and taste exposure. The need for effective guidance for parents who may be seeking to improve the range or nutritional value of foods accepted by their children is highlighted.


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