Objective: Systemic inflammation can induce somatic symptoms (e.g., pain, nausea, fatigue) through neuroimmune signaling pathways. Previous research suggests that early-life adversity amplifies signaling between peripheral inflammation and the brain. We therefore hypothesized that greater lifetime trauma exposure at baseline would predict stronger associations between systemic inflammation and somatic symptoms at 2.5-year follow-up in a cohort study of sexual and gender minority youth assigned male at birth ( n = 694).
Methods: We measured prior trauma exposure (lifetime count of traumatic event types reported at baseline), somatic symptoms (Brief Symptom Inventory somatization score), and systemic inflammation (C-reactive protein, interleukin 6, interleukin 1β, and tumor necrosis factor α). All models included age, gender, education, recent trauma exposure, substance use, body mass index, and HIV status as covariates.
Results: Higher C-reactive protein concentrations were associated with greater somatic symptoms in the main effects model ( β = 0.019, 95% confidence interval [CI] = 0.006 to 0.031). Contrary to our hypothesis, we observed a negative interaction between prior trauma exposure and C-reactive protein levels in predicting somatic symptoms ( β = -0.017, 95% CI = -0.030 to -0.004). Higher C-reactive protein was associated with greater somatic symptoms only in participants without prior trauma exposure at baseline ( β = 0.044, 95% CI = 0.026 to 0.062). Specificity analyses revealed similar patterns when nonsomatic depressive symptoms were used as the outcome variable.
Conclusions: These results suggest that sexual and gender minority youth assigned male at birth who have a history of prior trauma exposure may experience decoupling of systemic inflammation and somatic symptoms. The absence of inflammation-related symptoms may prevent individuals from seeking necessary medical care by reducing interoceptive awareness of pathological states.
Copyright © 2023 by the American Psychosomatic Society.