Early Trauma and Inflammation

Abstract

Objective Although early trauma (trauma in childhood) has been linked to adult inflammation and adult disease of inflammatory origin, it remains unknown whether this relationship is due to long-term consequences of early life stress or other familial factors. Methods We examined 482 male middle aged twins (241 pairs) born between 1946 and 1956 from the Vietnam Era Twin Registry. Childhood traumatic experiences, before age 18, were measured retrospectively with the Early Trauma Inventory (ETI) and included physical, sexual, emotional abuse, and general trauma. Lifetime major depressive disorder and posttraumatic stress disorder were assessed with the Structured Clinical Interview for DSM IV. Traditional risk factors for cardiovascular disease were also assessed. Plasma C-reactive protein (CRP) and interleukin-6 (IL-6) were measured to determine levels of inflammation. Mixed-effect regression models with a random intercept for pair were used to separate between and within twin pair effects. Results When twins were analyzed as individuals, increasing levels of early trauma were positively related to CRP (p=0.03) but not IL-6 (p=0.12). When estimating within and between pair effects, only the between pair association of early trauma with the inflammatory markers remained significant. Conclusion The link between early trauma and inflammation is largely explained by familial factors shared by the twins, because levels of inflammation were highest when both twins were exposed to trauma. Exposure to early trauma may be a marker for an unhealthy familial environment. Clarification of familial factors associated with early stress and adult inflammation will be important to uncover correlates of stress and disease.

Maternal Exposure to Childhood Trauma Is Associated During Pregnancy With Placental-Fetal Stress Physiology

“…CRH, in turn, has been shown to have a pro-inflammatory effect in the periphery (85, 86), and increased levels of p CRH have been associated with intra-amniotic infection (72, 87). Moreover, previous studies of non-pregnant CT+ women have reported they exhibit an increased inflammatory status (88–90). Thus, the maternal environment also may modulate p CRH production via changes in the inflammatory milieu.…”

Childhood sexual abuse and posttraumatic stress disorder among pregnant and postpartum women: review of the literature

“…Other investigations of the biological link between early life stress and PTSD have implicated irregularities in inflammatory response and highlighted some novel biochemical and molecular markers that may prove useful for quantifying PTSD risk. Studies have shown shorter lengths of telomeres (the regions of repetitive nucleotide sequences located at the end of chromosomes) with early life stress history (Tyrka et al 2010; Shalev et al 2013) and with PTSD (O'Donovan et al 2011; Ladwig et al 2013; Zhang et al 2013); increased global DNA methylation with PTSD (Smith et al 2011); increased glucocorticoid receptor gene (NR3C1) methylation with CSA history (Perroud et al 2011); increased pathway activity of NF-κB (a protein complex that controls expression of genes that code for inflammatory cytokines) in individuals with childhood-abuse related PTSD (Pace et al 2012); as well as higher C-reactive protein (CRP) and Interleukin-6 (IL-6) levels in individuals with a history of early life stress (Rooks et al 2012). However, since most studies of biological pathways have been cross-sectional, the chronology of early life stress, PTSD and biological changes remain unclear.…”

Genetic and environmental determinants of population variation in interleukin-6, its soluble receptor and C-reactive protein: Insights from identical and fraternal twins

“…For example, it has been reported previously that both CRP and IL-6 levels are similar in twins, a finding that will emerge when the influence of adiposity is not taken into account, nor statistically considered as a contributing factor (Rooks et al, 2012; Wörns et al, 2006). In addition, there is a substantial literature reporting that allele polymorphisms affect IL-6 release, but that effect is most apparent in the context of inflammatory disorders, or when cells are activated in vitro by a proinflammatory stimulant (Bennermo et al, 2004; Brull et al, 2001; Burzotta et al, 2001; Shah et al, 2013).…”