Posttraumatic stress disorder and physical illness: results from clinical and epidemiologic studies.
Research indicates that exposure to traumatic stressors and psychological trauma is widespread. The association of such exposures with posttraumatic stress disorder (PTSD) and other mental health conditions is well known. However, epidemiologic research increasingly suggests that exposure to these events is related to increased health care utilization, adverse health outcomes, the onset of specific diseases, and premature death. To date, studies have linked traumatic stress exposures and PTSD to such conditions as cardiovascular disease, diabetes, gastrointestinal disease, fibromyalgia, chronic fatigue syndrome, musculoskeletal disorders, and other diseases. Evidence linking cardiovascular disease and exposure to psychological trauma is particularly strong and has been found consistently across different populations and stressor events. In addition, clinical studies have suggested the biological pathways through which stressor-induced diseases may be pathologically expressed. In particular, recent studies have implicated the hypothalamic-pituitary-adrenal (HPA) and the sympathetic-adrenal-medullary (SAM) stress axes as key in this pathogenic process, although genetic and behavioral/psychological risk factors cannot be ruled out. Recent findings, indicating that victims of PTSD have higher circulating T-cell lymphocytes and lower cortisol levels, are intriguing and suggest that chronic sufferers of PTSD may be at risk for autoimmune diseases. To test this hypothesis, we assessed the association between chronic PTSD in a national sample of 2,490 Vietnam veterans and the prevalence of common autoimmune diseases, including rheumatoid arthritis, psoriasis, insulin-dependent diabetes, and thyroid disease. Our analyses suggest that chronic PTSD, particularly comorbid PTSD or complex PTSD, is associated with all of these conditions. In addition, veterans with comorbid PTSD were more likely to have clinically higher T-cell counts, hyperreactive immune responses on standardized delayed cutaneous hypersensitivity tests, clinically higher immunoglobulin-M levels, and clinically lower dehydroepiandrosterone levels. The latter clinical evidence confirms the presence of biological markers consistent with a broad range of inflammatory disorders, including both cardiovascular and autoimmune diseases.
Boscarino
Joseph A
JA
Division of Health and Science Policy, Room 552, The New York Academy of Medicine, 1216 Fifth Avenue, New York, NY 10029-5293, USA. jboscarino@nyam.org
D001172:Arthritis, Rheumatoid / Q000453:epidemiology; D001327:Autoimmune Diseases / Q000453:epidemiology; D003687:Dehydroepiandrosterone / Q000378:metabolism; D003922:Diabetes Mellitus, Type 1 / Q000453:epidemiology; D005260:Female; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology; D007075:Immunoglobulin M / Q000378:metabolism; D016015:Logistic Models; D018655:Lymphocyte Count; D008297:Male; D008875:Middle Aged; D013313:Stress Disorders, Post-Traumatic / Q000150:complications* / Q000453:epidemiology*; D013601:T-Lymphocytes / Q000276:immunology; D013959:Thyroid Diseases / Q000453:epidemiology; D014728:Veterans
D007075:Immunoglobulin M; D003687:Dehydroepiandrosterone