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There is recognized comorbidity of obesity and depression, and research suggests chronic low-grade inflammation as a potential shared mechanism for these two health conditions (Milaneschi et al., 2018). However, this hypothesis is mainly based on cross-sectional studies with adult clinical populations, which limits our understanding of the developmental nature of these processes. Furthermore, there is a debate on whether adiposity and inflammation are causes or consequences of depression (Byrne et al., 2013). Recent research also suggests that there are sex differences not only in the individual processes of depression, obesity and inflammation, but also in the associations among them (Derry et al., 2015). Examining these processes in adolescence is particularly important given the high prevalence of first onset depression during adolescence. Biological mechanisms are critical to consider because obesity and inflammation are associated with endocrine processes which are salient during puberty, and sex differences may be especially apparent during this period. However, few studies have examined these questions in a prospective longitudinal manner throughout adolescent development.
Thus, the current study aimed to examine both concurrent and transactional associations between obesity, inflammation and depressive symptoms in the period from pre-adolescence (age 9) to late adolescence (ages 15.5-16 and 17.5), and to test the moderating role of sex. These questions were explored in a subset of data from the Avon Longitudinal Studies of Parents and Children (ALSPAC; N=6,558). Body Mass Index and Fat Mass Index were aggregated to create an obesity score which reflects both general and central adiposity. C-reactive protein (CRP) was used as a marker of systemic inflammation. Depressive symptoms were assessed by the Short Mood and Feelings Questionnaire (Angold et al., 1995), which was completed by the mother when the child was 9 years-old and by the teen at ages 16 and 17.5 years.
Findings from a 3-level, 3-wave cross-lagged analysis revealed both concurrent and transactional positive associations between obesity and CRP across all waves (all ßs > .15, all ps < .001), demonstrating that adiposity is a robust predictor of CRP during adolescent development.
A subsequent multiple groups comparison analysis revealed significant sex differences, such that lower CRP at age 9 years predicted elevated depressive symptoms in 16 years-old boys (ß = -.08, p < .01; Figure 1), suggesting that hypo-activity of the inflammatory branch may contribute to the development of depressive symptoms in boys. A different significant pattern was observed for girls, such that increased obesity at age 9 years predicted elevated depressive symptoms at age 16 years (ß = .06, p < .05; Figure 2).
These findings provide evidence for the existence of concurrent and predictive relations among obesity, inflammation and depressive symptoms across adolescent development, however, sex-specific mechanisms are observed. Additionally, our results support the hypothesis that adiposity and inflammation are causes rather than consequences of depression. Future research on this topic would benefit from including data on sex hormones and pubertal development in order to further elucidate the biological mechanisms involved in the development of these processes during adolescence.