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A Cross-Lagged Study of Emotional Symptoms, Social Isolation, and Victimisation from Adolescence to Young Adulthood

Sat, March 25, 8:15 to 9:45am, Salt Palace Convention Center, Floor: 1, Meeting Room 151 G

Abstract

Introduction. Emotional symptoms such as anxiety and depression often emerge in adolescence and can later escalate into full-syndrome disorders (Johnson et al., 2018; Wolitzky-Taylor et al., 2014). Therefore, understanding the mechanisms underlying their development is essential to inform early intervention strategies. One such mechanism may be through reciprocal associations with peer victimisation, which may create a negative feedback loop between emotional symptoms and victimisation and lead to persisting emotional symptoms (Cook et al., 2010; Reijntjes et al., 2010). In addition, other types of peer problems, such as social isolation, may play a role in explaining both ends of this feedback loop (Boivin, Petitclerc, Feng, & Barker, 2010, Bowker et al., 2013). To identify the factors driving these associations, twin studies provide useful insight into the contributions of genetic and environmental factors. They show that genetic risk for emotional symptoms may increase the likelihood of experiencing victimisation and social isolation via gene-environment correlations (Boivin et al., 2013). In turn, victimisation and social isolation may increase emotional symptoms via environmental exposure (Arseneault et al., 2008). Therefore, genetic and environmental factors may be differentially involved in the pathways leading to emotional symptoms.

Objectives. The present study aimed to examine 1) the reciprocal associations between emotional symptoms and peer victimisation from 12 to 21 years old, 2) the role of social isolation in explaining these bidirectional relationships, and 3) the genetic and environmental contributions to these associations.

Hypotheses. We expected that 1) emotional symptoms and peer victimisation would mutually predict each other over time, 2) social isolation would explain these bidirectional associations, 3) genetic and environmental factors would play different roles in these pathways.

Methods. Participants were 8262 twin pairs from the Twins Early Development Study (Rimfeld et al., 2019). We used child reports of the Strength and Difficulties Questionnaire (Goodman, 1997) for emotional symptoms, social isolation, and peer victimisation at 12, 16, and 21 years old. We conducted phenotypic and genetic cross-lagged panel models to examine the bidirectional associations between variables and the genetic and environmental factors underlying these associations.

Results. Most cross-lagged paths were modest but significant, suggesting that emotional symptoms, social isolation, and victimisation mutually reinforce each other, thereby creating a negative feedback loop leading to the persistence of emotional symptoms across adolescence. A genetic risk for social isolation at 12 years old accounted for the prediction of higher victimisation at 16 years old, indicating that a genetic vulnerability specific to social isolation in early adolescence may partially explain why social isolation leads to more victimisation over time. Non-shared environmental factors associated with emotional symptoms at 12 years old predicted higher social isolation and victimisation at 16 years old, and those associated with emotional symptoms at 16 years old predicted higher victimisation at 21 years old. This supports the possibility of causal pathways from emotional symptoms to social isolation and victimisation and therefore suggests that reducing anxiety and depressive symptoms may be one way of disrupting the negative cycle of reciprocal influences between emotional symptoms, social isolation, and victimisation.

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