(PS5-83) The Interplay Between Rumination and Inflammatory Biomarkers on Concurrent and Prospective Depression Severity During Adolescence

Background: Depression is a common and debilitating disorder that often presents and worsens during adolescence (Liu et al., 2020; Avenevoli et al., 2015). A dysregulation of the innate immune system has been implicated in the etiology and pathogenesis of depression (e.g., Mac Giollabhui et al., 2021). Given that not all individuals with elevated inflammatory activity develop depression (Udina et al., 2012), it is likely that other psychological and physiological factors are involved. Rumination, broadly defined as perseverative negative thinking about personal problems and feelings (Watkins & Roberts, 2020), may amplify the association between inflammatory biomarkers and depressive symptoms. This hypothesis stems from the view that rumination maintains physiological arousal following stressful life events by keeping them present in the mind (Brosschot et al., 2006), thereby potentiating and extending symptom severity. However, relatively little research has systematically examined the interplay between these risk factors on depression symptom severity. We addressed this gap by investigating the interaction of rumination and peripheral levels of three inflammatory proteins on current and future depressive symptom severity among adolescents. 

Method: Community adolescents (N = 217, M_age = 16.58 years, SD = 1.60, 46% Female, 54% Black) completed self-report measures of trait rumination (CRSQ-rumination subscale; Abela et al., 2004) and depressive symptoms (CDI; Kovacs, 1985) at baseline. They also provided blood samples to determine interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor-alpha (TNF-α). Six months later, participants completed the CDI to reassess symptom severity.

Results: Controlling for adolescents’ body mass index, sex assigned at birth, medication use, and history of major illness, hierarchical regression modeling did not detect a rumination-by-inflammatory protein interaction on concurrent symptom severity for either IL-6 (ß = -.03, t = -.08, p = .938, ΔR² < .001), CRP (ß = -.35, t = -.84, p = .402, ΔR² = .002), or TNF-α (ß = -.29, t = -.79, p = .430, ΔR² = .001). However, there was a significant interaction between rumination and CRP that was predictive of future depressive symptom severity (ß = .88, t = 2.57, p < .05, ΔR² =.015), above and beyond baseline symptom severity. That is, only at high levels of trait rumination, CRP significantly predicted depressive symptom severity at follow-up (ß = 1.62, t = 2.98, p < .01). We did not find a rumination-by-inflammatory protein interaction for IL-6 (ß = .44, t = 1.44, p = .153, ΔR² = .004) or TNF-α (ß = .19, t = .61, p = .540, ΔR² < .001) that was predictive of future depressive symptom severity.

Conclusion: Rumination interacted with CRP levels, but not two inflammatory cytokines, to predict future depressive symptom severity among adolescents. Our results indicated that high levels of trait rumination and CRP – a clinical marker of chronic, low-grade inflammation – are predictive of future depressive symptom severity among adolescents. However, this conclusion did not hold for IL-6 and TNF-α, two commonly assessed markers of inflammation. The implications for research and practice will be discussed.