scholarly journals Genetic and Environmental Influences on Cognitive Abilities in Extreme Poverty

2019 ◽  
Vol 22 (5) ◽  
pp. 297-301 ◽  
Author(s):  
Yoon-Mi Hur ◽  
Timothy Bates

AbstractTo improve global human capital, an understanding of the interplay of endowment across the full range of socioeconomic status (SES) is needed. Relevant data, however, are absent in the nations with the most abject poverty (Tucker-Drob & Bates, 2016), where the lowest heritability and strong effects of SES are predicted. Here we report the first study of biopsychosocial gene–environment interaction in extreme poverty. In a sub-Saharan sample of early teenage twins (N = 3192), we observed substantial (~30–40%) genetic influence on cognitive abilities. Surprisingly, shared environmental influences were similar to those found in adolescents growing in Western affluent countries (25–28%). G × SES moderation was estimated at aˋ = .06 (p = .355). Family chaos did not moderate genetic effects but did moderate shared environment influence. Heritability of cognitive abilities in extreme poverty appears comparable to Western data. Reduced family chaos may be a modifiable factor promoting cognitive development.

2007 ◽  
Vol 38 (9) ◽  
pp. 1287-1297 ◽  
Author(s):  
J. M. McCaffery ◽  
G. D. Papandonatos ◽  
M. J. Lyons ◽  
K. C. Koenen ◽  
M. T. Tsuang ◽  
...  

BackgroundSmoking initiation and persistence are clearly associated with factors commonly thought to be environmental in origin, including socio-economic status. However, twin models that incorporate gene–environment correlation and gene×environment interaction have not been applied to elucidate the genetic or environmental role that socio-economic status plays in smoking initiation and nicotine dependence.MethodTwin structural equation modelling was used to examine gene–environment correlation and gene×environment interaction of one index of socio-economic status, educational attainment, with smoking initiation and nicotine dependence among 5119 monozygotic and 4295 dizygotic male–male Vietnam-era twins from the Vietnam Era Twin Registry, a national registry of twin pairs who served in the military during the Vietnam era.ResultsEducational attainment correlated significantly with smoking initiation (r=−0.27, p<0.001). Additive genetic (p=0.011), shared environment (p=0.002) and unique environment (p=0.027) components contributed to the correlation between educational attainment and smoking initiation. Educational attainment also significantly moderated the variance in smoking initiation (p<0.001), suggestive of gene×environment interaction, although the interaction with the additive genetic, shared environmental and unique environmental components could not be resolved due to multicollinearity. In contrast, educational attainment neither correlated with nor moderated nicotine dependence, once smokers had initiated.ConclusionsOur study suggests that educational attainment is associated with smoking initiation, in part due to gene–environment correlation and gene×environment interaction. However, once smoking initiation is taken into account, there are no effects – be they gene–environment correlation or gene×environmental interaction – of educational attainment on nicotine dependence.


2013 ◽  
Vol 25 (1) ◽  
pp. 93-104 ◽  
Author(s):  
Paul O. Wilkinson ◽  
Maciej Trzaskowski ◽  
Claire M. A. Haworth ◽  
Thalia C. Eley

AbstractDepression is known to be associated with a wide array of environmental factors. Such associations are due at least in part to genetic influences on both. This issue has been little explored with preadolescent children. Measures of family chaos and parenting style at age 9 and child depressive symptoms at age 12 were completed by 3,258 twin pairs from the Twins Early Development Study and their parents. Quantitative genetic modeling was used to explore common and unique genetic and environmental influences on both family environment and later depressive symptoms. Depressive symptoms at age 12 were significantly heritable. Moderate genetic effects influenced parenting style and family chaos at the age of 9, indicating gene–environment correlation. There were significant genetic correlations between family environment and depressive symptoms. There was some evidence of a Gene × Environment interaction, with stronger genetic effects on depressive symptoms for children with more suboptimal family environment. There was an Environment × Environment interaction, with effects of nonshared environment on depressive symptoms stronger for twins with more adverse parenting experiences. There is some evidence for gene–environment correlation between aspects of family environment in middle childhood and subsequent depressive symptoms. This suggests that one of the mechanisms by which genes lead to depressive symptoms may be by themselves influencing depressogenic environments.


2013 ◽  
Vol 44 (5) ◽  
pp. 1065-1076 ◽  
Author(s):  
S. A. Burt ◽  
K. L. Klump

BackgroundPrior research has suggested that, consistent with the diathesis–stress model of gene–environment interaction (G × E), parent–child conflict activates genetic influences on antisocial/externalizing behaviors during adolescence. It remains unclear, however, whether this model is also important during childhood, or whether the moderation of child conduct problems by negative/conflictive parenting is better characterized as a bioecological interaction, in which environmental influences are enhanced in the presence of environmental risk whereas genetic influences are expressed most strongly in their absence. The current study sought to distinguish between these possibilities, evaluating how the parent–child relationship moderates the etiology of childhood-onset conduct problems.MethodWe conducted a series of ‘latent G by measured E’ interaction analyses, in which a measured environmental variable was allowed to moderate both genetic and environmental influences on child conduct problems. Participants included 500 child twin pairs from the Michigan State University Twin Registry (MSUTR).ResultsShared environmental influences on conduct problems were found to be several-fold larger in those with high levels of parent–child conflict as compared with those with low levels. Genetic influences, by contrast, were proportionally more influential at lower levels of conflict than at higher levels.ConclusionsOur findings suggest that, although the diathesis–stress form of G × E appears to underlie the relationship between parenting and conduct problems during adolescence, this pattern of moderation does not extend to childhood. Instead, results were more consistent with the bioecological form of G × E which postulates that, in some cases, genetic influences may be most fully manifested in the absence of environmental risk.


2017 ◽  
Vol 210 (5) ◽  
pp. 350-355 ◽  
Author(s):  
A. Kate Fairweather-Schmidt ◽  
Tracey D. Wade

BackgroundWeight-related peer-teasing is considered a potent prospective risk factor for development of disordered eating and clinical eating disorders. Currently, the interplay between genetic and environmental influences has yet to be elucidated.AimsTo determine whether peer-teasing moderates latent genetic and/or environmental risk for disordered eating among female adolescent twins.MethodFull quantitative gene–environment interplay modelling of longitudinal trajectory of disordered eating in 685 female twins from the Australian Twin Registry.ResultsA model permitting moderation of disordered eating by peer-teasing involving genetic and non-shared environment effects fit these data best. As levels of peer-teasing increased, both genetic and environmental influences on disordered eating strengthened; however, genetic sources increased proportionally more than environmental sources.ConclusionsWeight-related peer-teasing represents a particularly powerful trigger for disordered eating. Nevertheless, it is amenable to intervention/prevention activities spanning individual to universal levels of endeavour.


1997 ◽  
Vol 78 (01) ◽  
pp. 457-461 ◽  
Author(s):  
S E Humphries ◽  
A Panahloo ◽  
H E Montgomery ◽  
F Green ◽  
J Yudkin

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