Evidence for the Scarr–Rowe Effect on Genetic Expressivity in the Health and Retirement Study

2021 ◽  
pp. 1-6
Author(s):  
Michael A. Woodley of Menie ◽  
Mateo Peñaherrera-Aguirre ◽  
Curtis S. Dunkel ◽  
Matthew A. Sarraf
Keyword(s):  
Educational Attainment ◽  
Cognitive Ability ◽  
Low Socioeconomic Status ◽  
Environment Interaction ◽  
Low Socioeconomic ◽  
Gene Environment Interaction ◽  
Interaction Terms ◽  
Gene Environment ◽  
Parental Educational Attainment ◽  
Retirement Study

Abstract The Scarr–Rowe effect is a gene × environment interaction, which is characterized by a negative association between exposure to low socioeconomic status (SES) environments and the additive heritability of cognitive ability. Utilizing a polygenic score for educational attainment (EA3), it was found that the two-way interaction between EA3 and parental educational attainment (EA; used as a proxy for parental SES) was a significant positive predictor of participants’ composite cognitive ability (IQ) score (β = .018, SE = .008, p = .028) after controlling hierarchically for the direct effects of (population-stratification-controlled) EA3, parental EA, and 20 distinct interaction terms (10 involving the interactions between the principal components [PCs] and EA3, and 10 involving the interaction between the PCs and parental EA). The presence of this interaction is consistent with the Scarr–Rowe effect, as the expressivity of EA3 on cognitive ability increases with increasing parental EA. No statistically significant sex differences in the effect magnitudes were found, although the effect was significantly present in the female but not male sample.

The Effect of Prenatal Valproate Exposure in Serotonin Transporter Knockout Rats On Anxiety and Cognition: A Gene*Environment Interaction Model of Autism Spectrum Disorder

2021 ◽  
Author(s):  
◽  
Caren L. August
Keyword(s):  
Autism Spectrum Disorder ◽  
Cognitive Ability ◽  
Serotonin Transporter ◽  
Neurodevelopmental Disorder ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Starting Point

<p>Autism Spectrum Disorder is a complex neurodevelopmental disorder which is often associated with increased anxiety and deficits in cognitive ability. The present research investigated a potential gene*environment interaction between two factors previously implicated in ASD in a rat model; prenatal exposure to valproate (VPA) and genetic reduction of the serotonin transporter (SERT). Wildtype and heterozygous SERT knockout rats prenatally exposed to VPA or saline on gestational day12.5 (G12.5) were assessed on measures of anxiety: elevated plus-maze and novelty suppressed-feeding and cognitive ability: prepulse inhibition and latent inhibition. A significant main effect was found for VPA exposure in all paradigms, showing increased anxiety-typical behaviour and abnormal cognitive ability. However, no significant effect of genotype or interaction was observed. Results from the present study do not confirm gene*environment interaction between prenatal VPA and heterozygous SERT knockout but this may be due to several factors that are discussed within the thesis. In any case, this study represents a starting point for further studies investigating other combinations of genetic and environmental factors as models of ASD pathogenesis.</p>

scholarly journals Educational attainment, smoking initiation and lifetime nicotine dependence among male Vietnam-era twins

2007 ◽  
Vol 38 (9) ◽  
pp. 1287-1297 ◽  
Author(s):  
J. M. McCaffery ◽  
G. D. Papandonatos ◽  
M. J. Lyons ◽  
K. C. Koenen ◽  
M. T. Tsuang ◽  
...  
Keyword(s):  
Educational Attainment ◽  
Nicotine Dependence ◽  
Economic Status ◽  
Smoking Initiation ◽  
Shared Environment ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Socio Economic Status ◽  
Gene Environment ◽  
Vietnam Era

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.

scholarly journals Alcohol consumption and lifetime change in cognitive ability: a gene × environment interaction study

AGE ◽  
2014 ◽  
Vol 36 (3) ◽  
Author(s):  
Stuart J. Ritchie ◽  
Timothy C. Bates ◽  
Janie Corley ◽  
Geraldine McNeill ◽  
Gail Davies ◽  
...  
Keyword(s):  
Alcohol Consumption ◽  
Cognitive Ability ◽  
Environment Interaction ◽  
Interaction Study ◽  
Gene Environment Interaction ◽  
Gene Environment

The Effect of Prenatal Valproate Exposure in Serotonin Transporter Knockout Rats On Anxiety and Cognition: A Gene*Environment Interaction Model of Autism Spectrum Disorder

2021 ◽  
Author(s):  
◽  
Caren L. August
Keyword(s):  
Autism Spectrum Disorder ◽  
Cognitive Ability ◽  
Serotonin Transporter ◽  
Neurodevelopmental Disorder ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Starting Point

<p>Autism Spectrum Disorder is a complex neurodevelopmental disorder which is often associated with increased anxiety and deficits in cognitive ability. The present research investigated a potential gene*environment interaction between two factors previously implicated in ASD in a rat model; prenatal exposure to valproate (VPA) and genetic reduction of the serotonin transporter (SERT). Wildtype and heterozygous SERT knockout rats prenatally exposed to VPA or saline on gestational day12.5 (G12.5) were assessed on measures of anxiety: elevated plus-maze and novelty suppressed-feeding and cognitive ability: prepulse inhibition and latent inhibition. A significant main effect was found for VPA exposure in all paradigms, showing increased anxiety-typical behaviour and abnormal cognitive ability. However, no significant effect of genotype or interaction was observed. Results from the present study do not confirm gene*environment interaction between prenatal VPA and heterozygous SERT knockout but this may be due to several factors that are discussed within the thesis. In any case, this study represents a starting point for further studies investigating other combinations of genetic and environmental factors as models of ASD pathogenesis.</p>

scholarly journals Replicated evidence that endophenotypic expression of schizophrenia polygenic risk is greater in healthy siblings of patients compared to controls, suggesting gene–environment interaction. The EUGEI study

2019 ◽  
Vol 50 (11) ◽  
pp. 1884-1897 ◽  
Author(s):  
Jim van Os ◽  
Lotta-Katrin Pries ◽  
Philippe Delespaul ◽  
Gunter Kenis ◽  
Jurjen J. Luykx ◽  
...  
Keyword(s):  
Cognitive Ability ◽  
Psychotic Disorder ◽  
Genetic Risk ◽  
Environment Interaction ◽  
Replication Sample ◽  
Polygenic Risk ◽  
Gene Environment Interaction ◽  
Intermediate Phenotypes ◽  
Gene Environment ◽  
Healthy Siblings

AbstractBackgroundFirst-degree relatives of patients with psychotic disorder have higher levels of polygenic risk (PRS) for schizophrenia and higher levels of intermediate phenotypes.MethodsWe conducted, using two different samples for discovery (n = 336 controls and 649 siblings of patients with psychotic disorder) and replication (n = 1208 controls and 1106 siblings), an analysis of association between PRS on the one hand and psychopathological and cognitive intermediate phenotypes of schizophrenia on the other in a sample at average genetic risk (healthy controls) and a sample at higher than average risk (healthy siblings of patients). Two subthreshold psychosis phenotypes, as well as a standardised measure of cognitive ability, based on a short version of the WAIS-III short form, were used. In addition, a measure of jumping to conclusion bias (replication sample only) was tested for association with PRS.ResultsIn both discovery and replication sample, evidence for an association between PRS and subthreshold psychosis phenotypes was observed in the relatives of patients, whereas in the controls no association was observed. Jumping to conclusion bias was similarly only associated with PRS in the sibling group. Cognitive ability was weakly negatively and non-significantly associated with PRS in both the sibling and the control group.ConclusionsThe degree of endophenotypic expression of schizophrenia polygenic risk depends on having a sibling with psychotic disorder, suggestive of underlying gene–environment interaction. Cognitive biases may better index genetic risk of disorder than traditional measures of neurocognition, which instead may reflect the population distribution of cognitive ability impacting the prognosis of psychotic disorder.

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