Depression and anxiety have been linked to elevated inflammation in cross-sectional and longitudinal studies. Yet, in terms of longitudinal studies, findings are inconsistent regarding whether depression predicts worsening inflammation or vice versa, and anxiety has been infrequently examined. Further, we know little about longitudinal relationships between inflammation and specific symptom profiles of depression and anxiety. The current study examined longitudinal associations between depression and anxiety symptoms and inflammation in 13,775 people (59% women, average age = 67) participating in the Health and Retirement Study - a population-based study focused on older adults. High sensitivity C-reactive protein and depression and anxiety symptoms were measured at two time-points separated by four years. We used cross-lagged panel models to examine bidirectional relationships, and tested interactions with gender. We found that depressive symptoms predicted increasing inflammation for men, but not for women, and inflammation predicted worsening depression for women, but not for men. These gender differences were driven by somatic symptoms. Specifically, somatic symptoms predicted increasing inflammation for men only and were predicted by inflammation for women only. Regardless of gender, inflammation predicted worsening dysphoric symptoms of depression, and lack of positive affect predicted increasing inflammation over time. Anxiety was not associated with inflammation longitudinally. These findings indicate bidirectional relationships between depressive symptoms and inflammation, but not between anxiety symptoms and inflammation, and that the direction of these effects may differ by gender and type of depressive symptom.

Mounting evidence highlights specific forms of psychological stress as risk factors for ill health. Particularly strong evidence indicates that childhood adversity and adulthood trauma exposure increase risk for physical and psychiatric disorders, and there is emerging evidence that inflammation may play a key role in these relationships. In a population-based sample from the Health and Retirement Study (n = 11,198, mean age 69 ± 10), we examine whether childhood adversity, adulthood trauma, and the interaction between them are associated with elevated levels of the systemic inflammatory marker high sensitivity C-reactive protein (hsCRP). All models were adjusted for age, gender, race, education, and year of data collection, as well as other possible confounds in follow-up sensitivity analyses. In our sample, 67% of individuals had experienced at least one traumatic event during adulthood, and those with childhood adversity were almost three times as likely to have experienced trauma as an adult. Childhood adversities and adulthood traumas were independently associated with elevated levels of hsCRP (β = 0.03, p = 0.01 and β = 0.05, p < 0.001, respectively). Those who had experienced both types of stress had higher levels of hsCRP than those with adulthood trauma alone, Estimate = −0.06, 95% CI [−0.003, −0.12], p = 0.04, but not compared to those with childhood adversity alone, Estimate = −0.06, 95% CI [0.03, −0.16], p = 0.19. There was no interaction between childhood and adulthood trauma exposure. To our knowledge, this is the first study to examine adulthood trauma exposure and inflammation in a large population-based sample, and the first to explore the interaction of childhood adversity and adulthood trauma with inflammation. Our study demonstrates the prevalence of trauma-related inflammation in the general population and suggests that childhood adversity and adulthood trauma are independently associated with elevated inflammation.

Background: Posttraumatic stress disorder (PTSD) is associated with increased risk for morbidity and mortality, which may be mediated through elevated inflammation. In contrast, social support appears to protect against morbidity and mortality, reduce levels of inflammation, and improve PTSD outcomes. Methods:We examined relationships among social isolation, perceived social support, and inflammation in Veterans Affairs (VA) patients with and without PTSD. Our sample included 735 (35% PTSD+) participants from the Mind Your Heart Study (mean age = 58 ± 11; 94% male). Social isolation was assessed with the Berkman Syme Social Network Index; perceived social support with the Multidimensional Scale of Perceived Social Support; and PTSD with the Clinician Administered PTSD Scale. Inflammation was indexed by high sensitivity C-reactive protein, white blood cell count, and fibrinogen. Hierarchical linear regression was used to examine associations between social measures and inflammation. PROCESS was used to examine the interactive effects of social relationships and PTSD on inflammation.Results: Social isolation, but not low perceived social support, trended towards an association with elevated inflammation in the full sample. However, considering groups with and without