Early Trauma and Inflammation: Role of Familial Factors in a Study of Twins

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 the age of 18 years, were measured retrospectively with the Early Trauma Inventory 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 and interleukin 6 were measured to determine levels of inflammation. Mixed-effects 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 C-reactive protein (p = .03) but not to interleukin 6 (p = .12). When estimating within- and between-pair effects, only the between-pair association of early trauma with the inflammatory markers remained significant. Conclusions: 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.