SES and Anxiety Symptoms in Emerging Adulthood: Gene-Environment Correlation (rGE) and Interaction (G x E)

Résumé fourni par la source

Anxiety is one of the most common mental health conditions and has been increasing in young adults in the UK (Dykxhoorn et al. 2025). One reason for this increase could be the challenging socio-economic climate young people are now facing. This is supported by previous research which found significant associations between SES indicators and mental health problems among emerging adults in Europe (Bacigalupe, Esnaola, & Martın, 2016; Fiori et al., 2016). There are two key theories seeking to explain the relationship between SES and mental health: social selection and social causation (Dohrenwend et al. 1992). The social selection hypothesis proposes that individuals with health conditions are more likely to drift into or remain in lower SES because of reduced employment (Marwaha & Johnson, 2004), discrimination (Ameri et al. 2015), reduced economic and educational productivity (Haas, 2006), as a result of their health conditions during the critical developmental stage. The social causation hypothesis argues that exposures to socio-economic environmental stressors associated with low SES (e.g., childhood maltreatment, lack of access to medical care/health insurance) increases the risk for developing physical and mental health conditions (Dohrenwend et al. 1992). Extensive evidence has shown that gene-environmental interplay might have contributed to the process of social selection and causation. Genetic influences on mental health conditions could shape individuals’ likelihood of exposing to certain environments (rGE) (Plomin, DeFries & Loehlin, 1977; Rutter et al. 2006). For example, previous research has found genetic correlations between education levels and anxiety (Tambs et al. 2011; Yuan et al., 2021). In the context of social selection theory, we might be able to explain the associations between anxiety and SES in emerging adults by rGE, that individuals with anxiety would often find themselves prone to SES disadvantages because they were genetically predisposed to do so (South & Krueger, 2011). Alternatively, genetic influences on mental health conditions might be amplified or attenuated corresponding to the levels of exposure to a certain environmental trait (GxE) (Plomin, DeFries & Loehlin, 1977; Jaffee & Price, 2007), explaining the social causation theory that SES stressors might increase the risk for developing anxiety symptoms (South, Hamdi & Krueger, 2017). To date, several studies have examined relationships between SES and mental health psychopathology through the approach of gene-environment interplay, but very few specifically focused on anxiety. Existing biometrical evidence indicates a potential joint mechanism of social selection and social causation underlying the association between SES and mental health conditions. Studies examine the rGE between SES and mental health conditions have found shared genetic basis (Badini et al. 2023; Garrison & Lee Rodgers, 2019; Tambs et al. 2011; Yuan et al., 2021). For anxiety specifically, one study found a significant genetic overlaps between internalizing disorders (including Generalized Anxiety Disorders) and SES, could be suggesting a form of rGE (South & Krueger, 2011). Similarly, another study found substantial genetic correlations between anxiety disorder and a range of SES indicators such as household income and educational attainment (Marees et al. 2021). Moreover, two previous studies found that individuals who are genetically predisposed to higher education levels also tend to be at greater risk of developing anxiety disorders (Tambs et al. 2011; Yuan et al., 2021). This association is explained primarily by common genetic factors rather than shared environments within twin pairs (Tambs et al. 2011). To our knowledge, no study to date has focused on gene-environment interaction between SES and anxiety symptoms specifically. Supporting a GxE interpretation, a US study found that low household income amplified non-shared environmental influences on internalizing syndromes (including GAD), while the genetic variance in internalizing syndromes increased across low to high levels of income (South & Krueger, 2011). This finding suggests that economic hardship moderates genetic effects on the aetiology of internalizing syndromes and therefore make genetic effects easier to detect in enriched environments (South & Krueger, 2011). Consistent with this, a Sri Lanka study found that individuals with lower SES exhibited greater variability depression symptoms. This association arose because depression-specific familial and nonshared environmental influences were stronger in low-SES contexts, rather than due to influences that overlap with SES (Badini et al. 2023). Previous research using the MZ differences approach found that after controlling for familial influences (i.e. shared genetics and environment), within-twin pair associations remained significant only for composite SES indicators, NEET (Not in Education, Employment or Training) and SES composite score. This finding potentially suggests that the phenotypic associations between individual SES indicators and anxiety symptoms were due to shared genetic and environmental influences. Although attenuated in magnitude, the phenotypic association between SES composite score and anxiety symptoms remained within-twin pairs, suggesting that the association was not solely confounded by genetic or environmental influences shared with anxiety. The aims of the present study therefore are: To examine the extent to which associations between individual and composite SES indicators and concurrent anxiety symptoms reflect shared genetic and environmental influences (rGE) at ages 21 and 26, and to determine whether these associations persist after accounting for such shared aetiology. To explore whether composite SES indicators associated with concurrent anxiety symptoms at age 21 and 26, moderate genetic and environmental influences on anxiety through the form of GxE.

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