Journal
MOLECULAR PSYCHIATRY
Volume 21, Issue 5, Pages 642-649Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/mp.2015.67
Keywords
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Funding
- grant 'Persistent Fatigue Induced by Interferon-alpha: A New Immunological Model for Chronic Fatigue Syndrome' from the Medical Research Council (UK) [MR/J002739/1]
- National Institute for Health Research Mental Health Biomedical Research Centre in Mental Health at South London
- National Institute for Health Research Mental Health Biomedical Research Centre in Mental Health at South London and Maudsley NHS Foundation Trust and King's College London
- MRC [G108/603, MR/J002739/1, MR/N029488/1] Funding Source: UKRI
- Academy of Medical Sciences (AMS) [AMS-SGCL5-Mondelli] Funding Source: researchfish
- Medical Research Council [MR/J002739/1, MR/N029488/1, G108/603] Funding Source: researchfish
- National Institute for Health Research [CL-2008-17-005] Funding Source: researchfish
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Childhood trauma confers higher risk of adulthood physical and mental illness; however, the biological mechanism mediating this association remains largely unknown. Recent research has suggested dysregulation of the immune system as a possible biological mediator. The present paper conducted a meta-analysis to establish whether early-life adversity contributes to potentially pathogenic pro-inflammatory phenotypes in adult individuals. A systematic search of Pubmed, PsycINFO, EMBASE, Scopus and Medline identified 25 articles for the meta-analysis, including 18 studies encompassing a sample of 16 870 individuals for C-reactive protein (CRP), 15 studies including 3751 individuals for interleukin-6 (IL-6) and 10 studies including 881 individuals for tumour necrosis factor-alpha (TNF-alpha). Random-effects meta-analysis showed that individuals exposed to childhood trauma had significantly elevated baseline peripheral levels of CRP (Fisher's z = 0.10, 95% confidence interval (CI) = 0.05-0.14), IL-6 (z = 0.08, 95% CI = 0.03-0.14) and TNF-alpha (z = 0.23, 95% CI = 0.14-0.32). Subgroup analyses for specific types of trauma (sexual, physical or emotional abuse) revealed that these impact differentially the single inflammatory markers. Moreover, meta-regression revealed greater effect sizes in clinical samples for the association between childhood trauma and CRP but not for IL-6 or TNF-alpha. Age, body mass index (BMI) and gender had no moderating effects. The analysis demonstrates that childhood trauma contributes to a pro-inflammatory state in adulthood, with specific inflammatory profiles depending on the specific type of trauma.
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