Discussion
Despite strong evidence that internalizing symptoms that manifest during adolescence have long-term implications for mental and physical health across the lifespan, little is known about the individual specific and contextual risk factors that impact risk for internalizing problems, particularly among Black adolescents who show rising rates and carry a disproportionate burden of internalizing symptoms. Addressing this gap is critical to reduce health disparities and inform an understanding of environmental exposures that influence the epigenetic landscape and internalizing psychopathology. Leveraging a novel Bayesian statistical method, joint contributions of potentially malleable factors, including indices of biological aging (i.e., telomere length) and the social environment, were examined with internalizing symptoms during adolescence, a crucial developmental window characterized by increased susceptibility to contextual factors.
The results of this study revealed several novel interactive effects linking telomere length, the social environment, and anxiety and depressive symptoms in adolescence. In the best fitting (Bayesian) regression model, the results demonstrated that the association of TL and anxiety symptoms was moderated by perceived stress, such that the telomere length—anxiety symptom association was more pronounced among youth with higher perceived stress. In other words, telomere length and anxiety symptoms were more tightly coupled under conditions of higher perceived stress. Although adolescence is marked by normative increases in perceived stress (Spear,
2009), it is possible that adolescents who report higher levels of perceived stress may be exposed to more frequent and severe contextual stressors (Heinze et al.,
2017), low self-esteem or self-efficacy (Piekarska,
2020), or may experience higher levels of negative affective and behavioral states (Felton et al.,
2017; Cook et al.,
2012) that make them more likely to interpret situations as stressful. It is also possible that cognitive appraisals of situations as more stressful may activate stress-related neurobiological systems including the hypothalamic-pituitary adrenal axis (HPA), autonomic nervous system (ANS), and promote inflammation (O’Donovan et al.,
2013). Higher perceived stress may contribute to dysregulation of neural stress response systems and changes in immune cell receptor functioning, both of which may contribute to telomere shortening and increased risk for anxiety symptoms (O’Donovan et al.,
2013), leading to a stronger coupling of these two markers of health.
School belongingness also moderated the association of telomere length with anxiety symptoms such that greater school belongingness attenuated the association between shorter telomere length and anxiety symptoms. In line with social ecological frameworks and the integrative model of development (Bronfenbrenner,
1977; Garcia Coll et al.,
1996), promotive school environments may serve as sources of resilience for adolescents by providing them with the opportunity to form supportive social networks with peers and teachers alike, which may increase positive affect, self-efficacy, and self-esteem. Similarly, youth who report greater school affiliation may be more likely to employ healthy coping strategies and may be more adept at self-regulating negative emotions in response to stressors (Arslan,
2021). Concurrently, shorter telomere length may reflect the accumulation of prior risk from the lens of the diathesis-stress model, such that shorter telomere length under conditions of low school belongingness as a social stressor is linked with higher anxiety symptoms. In this study, shorter telomere length and higher anxiety symptoms was more strongly coupled under conditions of low school belongingness than higher school belongingness. Given that feelings of belonginess have been previously identified as a positive social determinant of mental (Santamaría-García et al.,
2020) and physical health outcomes (Michalski et al.,
2020) across the life span, the present results provide suggestive evidence for the potential benefit of school connection in decoupling cellular aging and anxiety symptoms.
A significant interaction was also observed for parent inter-partner psychological aggression and telomere length with depressive symptoms. Inter-partner psychological aggression reflected the degree to which caregivers in the household yell, shout, insult, swear, destroy belongings, or threaten to hit their partner. In the context of greater parent inter-partner psychological aggression, shorter telomere length was associated with higher depressive symptoms. Although numerous studies have documented the effects of witnessing inter-partner psychological aggression during the early childhood years (Artz et al.,
2014; Caldeira & Woodin,
2012), exposure to these behaviors may also have impacts during adolescence, a developmental period characterized by increased vulnerability to context and rapid changes in brain maturation (Schiff et al.,
2014), along with a developmentally different understanding of inter-partner relationships than children. This study did not assess the history of inter-partner aggression prior to study enrollment. Thus, it is not possible to fully disentangle whether the effect of inter-partner aggression is due to longer-term or recent exposure to this type of interaction in adolescence only. In either case, it is plausible that adolescents with exposure to the chronic stress of inter-partner psychological aggression may evidence prolonged activation of physiological response systems (even when the stressor has dissipated) (Howell et al.,
2016) which may be associated with telomere length erosion and exacerbate risk for depression symptoms (Jiang et al.,
2019).
In addition to the novel interaction effects that were the focus of the study, several main effects of the social environment on anxiety and depressive symptoms were observed in this study. Lower family support, higher perceived stress, and higher loneliness were associated with higher levels of youth anxiety and depressive symptoms, whereas lower school belongingness was uniquely associated with greater anxiety symptoms. Prior research using GLM based models have linked lower family support (Guberman & Manassis,
2011), higher levels of loneliness (Danneel et al.,
2019; Ebesutani et al.,
2015), and perceived stress (Felton et al.,
2017) to heightened risk for internalizing symptoms, and greater school connection to school during the high school years with lower internalizing symptoms (Arslan,
2021; Pittman & Richmond,
2007). The present findings are in line with both the risk and resilience model of developmental psychopathology (Cicchetti & Rogosch,
2002; Andreotti et al.,
2013) and integrative model of development (Garcia Coll et al.,
1996) as they highlight the association of environmental stressors with psychopathological symptoms during racial minority youth development. Taken together, the present findings using a Bayesian modeling approach highlight that support within the family system, school belongingness, perceived stress, and loneliness are among the most robust individual-specific and environmental correlates that are associated with the manifestation of internalizing problems among Black adolescents, enhancing an understanding of factors linked to anxiety and depressive symptoms in this population.
The results of this study should be interpreted in light of the population, study design, and analytic strategy, which affords both strengths and limitations. First, the study population were Black adolescent youth in the U.S., which may limit generalizability to other demographic groups. The focus on a historically marginalized population, both in terms of social and economic opportunity as well as biobehavioral research, was a deliberate choice to address the broader goal of improving the understanding of minority health. No a priori assumptions were made that findings from prior studies conducted in primarily White or mixed-race adolescents inherently generalize to Black youth; in contrast, this study adopted a minority youth development approach that centers on the experiences of marginalized youth.
Second, this study utilized Bayesian modeling approach to identify the strongest set of predictors of a target outcome, estimate predictor strength, and assign each a probability that quantifies how important it is to include in the regression model. Whereas Bayesian model results are not directly comparable to “significance” testing conducted under GLM-based models, the Bayesian approach had notable advantages: first, it enabled us to reject the inclusion of certain variables (accept the null); second, it permitted us to include important demographic and seasonal differences across participants by default (setting priors to 1); and third, it allowed us to identify the strongest set of predictors given the totality of data in a complex, real-world dataset, allowing it to more cleanly estimate the credible effects in absence of non-credible effects.
Finally, a limitation of the present study is the cross-sectional study design. Longitudinal methods would be needed to clearly parse apart directionality between mental health, biological aging, and social context. In all likelihood, bi- or multi-directional effects may occur, whereby the emergence of internalizing symptoms may put additional strain on both social relations and health behaviors that impact stress-sensitive neurobiological systems, inflammatory responses and oxidative stress, further eroding telomere integrity. At present, interpretation of directionality effects even in longitudinal samples is limited by technological challenges to accurately comparing telomere length for samples collected over the span of several years (Nettle et al.,
2021). Nevertheless, the present findings conducted with a population of over 400 Black youth primarily from low- to middle- income neighborhoods offer an important step forward towards understanding biological aging in a population that is historically marginalized and under-represented in research, among whom biological aging occurs more rapidly than their White counterparts, and who are disproportionately burdened by mental and physical health disorders.
Conclusion
With depression and anxiety symptoms are on the rise among adolescents and growing evidence that cellular aging may be associated with depressive and anxiety symptoms, there is an urgent need to identify the social environment context that modulates this link. This study addressed this research gap by investigating the moderating role of the social environment on the relation between telomere length and emotional health in youth. Using a Bayesian modeling approach to identify the most robust interaction effects, the results of the study demonstrated that the social environment moderated the association of telomere length with internalizing problems among Black youth. Specifically, the association of shorter telomere length and higher anxiety symptoms was stronger under conditions of low school belongingness than higher school belongingness, and high perceived stress compared to lower perceived stress. In addition, adolescents with shorter telomeres were more likely to exhibit depressive symptoms under conditions of living with high parent inter-partner psychological aggression. Stated differently, adolescents with shorter telomeres were more prone to depressive symptoms if they had parents with high inter-partner aggression, and more prone to anxiety symptoms if they had higher perceived stress or low school belongingness. Notably, among children with higher levels of school belongingness or lower perceived stress, associations between telomere length and anxiety symptoms were comparatively mild. There are several implications of these findings. First, from a preventive intervention lens, perceived stress and school belongingness may be potentially modifiable targets for preventive intervention to reduce the burden of anxiety among Black youth, and that intervention efforts focused on depressive symptoms among Black youth may need to carefully consider adverse experiences within the home when tailoring intervention efforts. Second, from an empirical and conceptual lens, the results speak to the need to model social context in understanding the relation of biological aging and mental health and more broadly, the interaction of biological factors such as telomere length that reflect the accumulation of early life experiences with the present social environment. Third, from a methodological lens, given the “distance” between the social environment and chromosomes—including cognitive, emotional, and physiological systems, observed association between variation in the social environment and telomere length is expected to be small and difficult to detect statistically. Associations detected with a robust analytic strategy such as Bayesian modeling—which affords the ability to assign confidence to credible effects—are noteworthy and indicate strong confidence that social context moderates the association of biological aging and internalizing problems. Overall, this study adds novel information to the literature on telomere length with mental health by highlighting ways in which the social environment matters for understanding the link between biological aging and mental health.
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