Environment Flashcards
(30 cards)
What are sources of non-shared enviro? Cite
Sources of non-shared environmental effects include parental treatment, sibling interactions and peers in addition to non-systematic factors. The important point here is that any environmental factor can be viewed in terms of its contribution to non-shared environmental effects, as long as it can be assessed separately for each child (child-specific).
plomin 2011
what is non-shared enviro? - use as intro
NSE influences are nongenetic influences that are unique and independent to an individual, and not shared by children growing up in the same family. Any differences between MZ twins cannot be caused by genes, because MZ twins share their genes. Nor, by definition, can MZ differences be the result of shared environmental influence and so must reflect non-shared environmental influences and measurement error.
how are non-shared and shared estimated?
Shared environment is estimated as family resemblance not explained by genetics, and non- shared environment is the rest of the variance: variance not explained by genetics or shared environment.
Non-shared enviro effects can only be measured using child-specific measurs and are implied if MZ differences in experience correlate with MZ differences in outcome.
The contribution of the shared environment is estimated as the difference between the identical twin correlation and heritability. Non-shared environments are estimated by the difference between the identical twin correlation and 1, because they are the only source of variance making identical twins different.
what is passive rGE? give example
Passive rGE is a result of parents providing their children with both genes and with environments that are correlated with genetically-influenced characteristics of parents
For example, parents with internalizing problems may express their anxiety by becoming emotionally overinvolved towards their children. Thus, the children will not only inherit a propensity for internalizing problems, but also experience an environment that enhances their likelihood of developing such problems
what is evocative rGE?
Evocative rGE appears when a child’s inherited characteristics evoke a response from their environment
what is active rGE?
Active rGE refers to children actively selecting their environments for genetically influenced reasons.
Plomin and Bergeman 1991 -
GE correlation is responsible for one of the most extraordinary findings in behavioral genetics: environmental measures used widely in the behavioral sciences show nearly as much genetic influence as behavioral measures
There is little evidence of shared environmental influences beyond childhood and adolescence - CITE
Plomin, 2011
longitdudinal twin res has shown heritability for intelligence to increase across the lifespan - CITE .. from .. to .. CITE
Davis, Haworth & Plomin, 2009
41% to 66% - Haworth et al., 2010 - childhood to young adulthood
Shared enviro becomes less important for g across lifespan, decreasing from.. to … CITE
early childhood 74% to middle childhood 33% - Davis, Haworth & Plomin, 2009
shared enviro for science performance shows opposite trend to g … CITE and give figures
Haworth et al., 2009
at age 9, heritability = 64% SE = 16%
at age 12, heritability = 47% SE = 32%
who to cite for ‘dwindling enthusaism for science?
Jenkins and Nelson 2005
In early adolescence as well as moving to secondary schools, students start making decisions about their own education and their future, searching for more autonomy in their learning, as well as for positive and supportive relationships with peers and nonparental adults (CITE)
Ryan & Patrick, 2001)
Asbury (2008) study
found that MZ twins did experience their classrooms differently. In a multiple regression analysis, MZ differences in positivity about school significantly predicted MZ differences in Mathematics achievement, and MZ differences in ‘flow’ in Science significantly predicted MZ differences in Science achievement. Peer relationships emerged as a potential NSE influence on achievement to be explored in a larger study with more power to detect small effects. No significant predictors of differential achievement in English emerged. It is interesting that Science and Mathematics outcomes appear to be more strongly linked to the school environment than English
=At this early stage the research simply indicates that children who enjoy school more do better at school, particularly in Science and Mathematics. We cannot disentangle cause from effect but the implication is that making the classroom a happy and engaging place to be, perhaps by focusing on personalized learning given our evidence that the classroom is experienced differently even by very similar children, will pay off in terms of children’s achievement levels.
who to cite when discussing rGE?
Plomin and Bergeman 1991
role of genes in shaping environments accepted in evolutionary biologoy - CITE
Darwin, 1999
discuss life events in relation to rGE
Specific life events such as smoking, divorce and diet are all found to have modest to moderate heritability [McGue et al., 1992]. To understand the apparent genetic influence on life events, we need to identify the pathway from genes to experience. Life events are not randomly distributed amongst the population; they are more likely to occur to people in certain environments. This indicates a gene–environment correlation between behaviours and life events such that genetic predispositions make individuals more likely to encounter environments (McAdams et al., 2013).
Wootton et al., 2017 wellbeing example
why is finding rGE sig?
Findings of gene-environment correlations are significant because they emphasise that individuals are not passive to the environment (Asbury et al., 2008) and that heritability does not equate to genetic deterministic (Haworth & Davies, 2014).
Plomin 2014 suggests that GE correlation will in the end be more enlightening about the developmental interplay between genes and environment.
Wootton et al., 2017 - discuss study
used the twin design to investigate if heritability of subjective wellbeing could account for the heritability of positive and negative life events.
Bivariate twin models were conducted between positive and negative life events and subjective wellbeing and positive psychological traits including subjective happiness, life satisfaction, optimism, hopefulness and gratitude measured at 16 years.
Life events have an estimated heritability of 28% (Kendler & Baker, 2007).
= observed a trend of positive genetic correlation between the wellbeing traits and positive life events. This supports our hypothesis that wellbeing traits are part of the gene–environment correlation that makes life events heritable. Inheriting propensity for positive traits might cause you to seek environments that lead to positive life events.
=Secondly, there was a trend of negative genetic correlation between negative life events and wellbeing. This suggests that the inherited wellbeing traits that drive us towards positive experiences also make us less driven towards negative ones.
=Roughly, half of the phenotypic correlation was accounted for by genetics and half by shared- environments.
Wootton et al., 2017 evaluate study
However, the confidence intervals on these estimates are large due to the small phenotypic correlations. Correlations with life events were generally weak, being stronger between positive life events than negative life events. The findings should therefore be interpreted in light of this. Finding a genetic correlation between life events and wellbeing could also indicate the presence of pleiotropy, where the same genes are having different effects on wellbeing compared with life events. This is further suggested by the small phenotypic correlation despite a moderate genetic correlation
=The strength of genetic correlations observed is not as large as seen between negative life events and conduct behaviours or depression and anxiety (McAdams et al., 2013). McAdams et al (2013) found the highest correlation to be .99 for delinquency and negative life events. However, the negative life events items are quite similar to behaviours we might class as delinquent. For example, suspension from school, being arrested, and being involved in drugs. We would, therefore, expect the correlations to be higher for these more phenotypically similar traits. In the current study, the average
We cannot rule out the possibility that the correlation between wellbeing and life events is the result of reporting bias: individuals with a positive appraisal bias are more likely to rate their subjective wellbeing as high and more likely to remember positive things happening to them. However, if this were the case we might expect to see higher genetic correlations for positive psychological traits more associated with reflective appraisal, for example, gratitude. The low genetic correlation for gratitude and high genetic correlations for grit and ambition suggest that gene–environment correlation is a more likely explanation
Heritability itself changes with age.
BUT GOOD - focuses on pos as well as neg
Belsky et al., 2016
‘genetics of success’ study
A previous genome-wide association study (GWAS) identified molecular-genetic predictors of educational attainment (Rietvald et al., 2013). Data were prospectively collected from a population-representative birth cohort followed through midlife, the Dunedin Study. Belsky et al., (2016) undertook in-depth life-course investigation of the polygenic score derived from this GWAS.
Measurement of life-course phenotypes included social origin, educational attainment, aspirations, SES (including income), life satisfaction, geographic mobility, and cognitive abilities etc.
There were several main findings.
1) First, polygenic scores predicted adult economic outcomes even after accounting for educational attainments and social-class origins
2) Genes and environments were correlated: Children with higher polygenic scores were born into better-off homes.
3) Polygenic scores predicted behavior across the life course, from early acquisition of speech and reading skills through geographic mobility and mate choice and on to financial planning for retirement.
Our findings point to a gene-environment correlation: The polygenic score for educational attainment was stratified by childhood SES such that children with higher polygenic scores tended to have grown up in families with higher SES, whereas children with lower polygenic scores tended to have grown up in families with lower SES
Studies that compare siblings within the same family (who share identical ancestries) find that the sibling with the higher polygenic score tends to complete more years of schooling (Rietveld et al., 2014), thereby suggesting a mechanism to explain the gene-environment correlation in which children of socially advantaged families tend to have higher polygenic scores.
The current findings lend weight to earlier twin study observations that genes shape not just behavior, but also the environment that contextualizes and constrains behavioral choices (Plomin & Bergeman, 1991)
limitations of Belsky et al 2016 (x2)
- The study concerned a single birth cohort from New Zealand. The extent to which findings generalize to other birth cohorts growing up under other circumstances needs to be tested.
- follow-up of social and economic outcomes in our study is right censored, extending through the fourth decade of life, but not beyond. Extension of findings into longitudinal cohort studies of older adults is needed to clarify the extent of genetic associations into the second half of the life course
who orginally said that the heritability of IQ is moderated by SES..
and why is this appealing?
and who found no support
Turkheimer et al., 2003 - lower SES predicted to have lower heritability of IQ.
Whilst this hypothesis is appealing because of its environmental implications: If heritability is lower in lower-SES families, it suggests that environmental interventions might be more effective in boosting cognitive development for children in lower-SES families.
Hanscombe et al., 2012 found no support
Hanscombe et al 2012 study
Within their large population-based United Kingdom (UK) twin sample, TEDS, they used longitudinal data on IQ from infancy to adolescence, to investigate the main effects of SES on intelligence, as well as a moderating effect of SES on the genetic and environmental components of intelligence.
They also used the basic continuous GxE model to estimate the moderating effect of SES on IQ. This model allows the putative moderator to have a main effect on the trait, as well as a moderating effect on any or all of the residual A, C, and E components of the trait.
One limitation of the basic GxE model is that it cannot detect potential moderation of any genetic variation in common between the measured environment and the trait, and SES is phenotypically correlated with IQ. It is well established that ‘environmental’ measures are to some extent heritable – a phenomenon known as genotype-environment correlation
= the source for low SES is C rather than A –
= The genetic effect does not differ for low- and high-SES groups using unstandardized estimates (A, C, and E) that take into account the greater total variance in the low-SES group, but the relative contribution of genes – heritability or h2 = A/(A+C+E)) – is lower in low-SES families because the shared environmental effect increases.
=thus the emerging pattern appears to be one of environment-environment interaction rather than gene-environment interaction: shared experiences explain more of the variance in children’s performance on IQ tests in more disadvantaged backgrounds, suggesting that family-based environmental interventions might be more effective in these families.