Self-criticism and affective spectrum symptoms during adolescence: The role of the parenting environment, genetic vulnerability, and their interaction

Studies have shown that depression and functional somatic disorders (e.g., chronic pain and fatigue conditions) are highly comorbid and tend to co-aggregate within families. Hence, researchers argue that depression and functional somatic disorders belong to an "affective spectrum" of disorders that possibly share etiological mechanisms. A growing body of research suggests that self-criticism (i.e., a personality dimension marked by high personal standards in combination with intense negative self-scrutiny) may be a key vulnerability factor in affective spectrum disorders and symptoms. This PhD study addresses a number of central areas in research on self-criticism in relation to affective spectrum symptoms that are currently insufficiently understood, specifically with regard to the role of both environmental and genetic factors. First, with regard to environmental factors, studies have reported an intergenerational similarity in self-criticism between parents and adolescents, which may explain in part why affective spectrum disorders tend to run in families. This similarity in self-criticism across generations may be explained by observational learning or, indirectly, through the parental use of achievement-oriented psychological control (demanding perfectionism and high levels of achievement from children through the use of intrusive and manipulating parenting). However, only a limited number of studies have investigated these assumptions and it is unclear what the relative contribution is of maternal versus paternal self-criticism in this regard. Furthermore, while studies suggest that self-criticism may play an intervening role in the relationship between psychologically controlling parenting and adolescent affective spectrum symptoms, no study to date has investigated longitudinally dynamic changes across time in this relationship. Second, only few studies have investigated the influence of both genetic and environmental factors in the development of self-criticism. Moreover, no study has investigated whether there is a relationship between the genetic and environmental factors implicated in self-criticism and affective spectrum symptoms. In this regard, recent research has suggested that parental psychological control may interact with genetic vulnerability in the development of affective spectrum symptoms. Yet, it is currently unknown to what extent similar gene-environment interactions are also implicated in self-criticism. To address these gaps in our knowledge, we designed five studies. Study 1 presents a cross-sectional study in 284 adolescents and their parents, investigating (a) whether the development of self-criticism in adolescents is influenced by self-criticism of both parents and (b) whether achievement-oriented psychological control may explain the intergenerational similarity in self-criticism. Results showed that achievement-oriented psychological control played an important intervening role between both parents' self-criticism and adolescent's self-criticism. When self-critical parents used more psychologically controlling parenting, this was in turn related to higher levels of adolescent self-criticism. Study 2 investigated the associations between parental achievement-oriented psychological control, adolescent self-criticism, and adolescent depressive symptoms across a one-year interval. Results showed that self-criticism played an intervening role in the relationship between parents' achievement-oriented psychological control and adolescent depressive symptoms. These effects were found both at the level of between-person differences and within-person changes across time. An increase in achievement-oriented psychological control led to an increase in self-criticism, which in turn led to higher levels of depressive symptoms. Study 3 presents a behavioral genetic study using data from a sample of parents and their biological children (266 adolescents and their biological parents) and an adoption sample (73 internationally adopted adolescents and their adoptive parents). This study investigated the relative influence of genetic and environmental factors in self-criticism and affective spectrum symptoms (i.e., depressive and functional somatic symptoms) and whether there was evidence for shared environmental and genetic factors. We found that the variance in both self-criticism and functional somatic symptoms was explained by separate genetic and environmental factors, while the variance in depressive symptoms was mostly due to an environmental factor. Furthermore, we found strong associations between the environmental factors of the affective spectrum symptoms and self-criticism, yet no relationship was found between their respective genetic factors. Study 4 presents a meta-analysis of gene-environment interaction research focusing on the relationship between the serotonin-transporter-linked polymorphic region (i.e., 5-HTTLPR), stressful life-events, and depression. This study also investigated the robustness of the effect size in relation to key methodological issues in measuring stress and depression (i.e., categorically versus dimensionally, with an interview versus self-report assessment, or early- vs. late-life stress). A significant yet small effect size was found (OR = 1.18) and this effect size was consistent across the different methodological approaches. Finally, Study 5 presents a molecular genetic study which investigated gene-environment interaction effects in the prediction of adolescent self-criticism and affective spectrum symptoms, with the environmental factor being achievement-oriented psychological control. Participants were 257 community adolescents. We found no significant gene-environment interactions for self-criticism. However, we did find significant results in the prediction of depressive and functional somatic symptoms, more specifically, with genes involved in the regulation of stress and reward systems. This suggests that affective spectrum symptoms do have associated genetic risks, but this relationship is situated at the level of gene systems and not at the level of individual polymorphisms or genes.status: publishe