4.3 Article

Cumulative Childhood Stress and Autoimmune Diseases in Adults

期刊

PSYCHOSOMATIC MEDICINE
卷 71, 期 2, 页码 243-250

出版社

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/PSY.0b013e3181907888

关键词

childhood abuse; traumatic stress; autoimmune diseases; stress; inflammatory response

资金

  1. Garfield Memorial Fund [TS44 to 10/11]
  2. Kaiser Foundation Research Institute [200-2005-M-13275]
  3. National Heart, Lung and Blood Institute [R01 FIL087033]

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Objective: To examine whether childhood traumatic stress increased the risk of developing autoimmune diseases as an adult. Methods: Retrospective cohort study of 15,357 adult health maintenance organization members enrolled in the Adverse Childhood Experiences (ACEs) Study from 1995 to 1997 in San Diego, California, and eligible for follow-up through 2005. ACEs included childhood physical, emotional, or sexual abuse; witnessing domestic violence; growing up with household substance abuse, mental illness, parental divorce, and/or an incarcerated household member. The total number of ACEs (ACE Score range = 0-8) was used as a measure of cumulative childhood stress. The Outcome was hospitalizations for any of 21 selected autoimmune diseases and 4 immunopathology groupings: T- helper 1 (Th1) (e.g., idiopathic myocarditis); T-helper 2 (Th2) (e.g., myasthenia gravis); Th2 rheumatic (e.g., rheumatoid arthritis); and mixed Th1/Th2 (e.g., autoimmune hemolytic anemia). Results: Sixty-four percent reported at least one ACE. The event rate (per 10,000 person-years) for a first hospitalization with any autoimmune disease was 31.4 in women and 34.4 in trien. First hospitalizations for any autoimmune disease increased with increasing number of ACEs (p < .05). Compared with persons with no ACEs, persons with :2 ACEs were at a 70% increased risk for hospitalizations with Th1, 80% increased risk for Th2, and 100% increased risk for rheumatic diseases (p < .05). Conclusions: Childhood traumatic stress increased the likelihood of hospitalization with a diagnosed autoimmune disease decades into adulthood. These findings are consistent with recent biological studies on the impact of early life stress on subsequent inflammatory responses.

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