A developmental pathway from early life stress to inflammation: The role of negative health behaviors

• Type of Material: Article
• Authors: Elizabeth B. Raposa, University of California, Los Angeles; Julienne E. Bower, University of California, Los Angeles; Constance L. Hammen, University of California, Los Angeles; Jake M. Najman, University of Queensland; Patricia Brennan, Emory University
• Language: English
• Date: 2014-01-01
• Publisher: SAGE Publications (UK and US)
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © The Author(s) 2014.
• Final Published Version (URL): http://dx.doi.org/10.1177/0956797614530570
• Title of Journal or Parent Work: Psychological Science in the Public Interest
• ISSN: 1529-1006
• Volume: 25
• Issue: 6
• Start Page: 1268
• End Page: 1274
• Grant/Funding Information: This work was supported by the National Health and Medical Research Council; Mater Misericordiae Mother’s Hospital; NIMH Grant R01 MH52239; NIMH training grant MH15750; the UCLA Norman Cousins Center for Psychoneuroimmunology; and the UCLA OAIC, NIH/NIA Grant P30-AG028748.
• Keywords: Depression; Surveys and Questionnaires; Inflammation; Stress, Psychological; depression; Longitudinal Studies; inflammation; Female; smoking; Humans; Body Mass Index; Inflammation Mediators; early adversity; body mass index; Health Behavior; Young Adult; C-Reactive Protein; Male
• Research Categories: Health Sciences, Mental Health; Psychology, Psychobiology

Abstract

Early life stressors are associated with elevated inflammation, a key physiological risk factor for disease. However, the mechanisms by which early stress leads to inflammation remain largely unknown. Using a longitudinal data set, we examined smoking, alcohol consumption, and body mass index (BMI) as health-behavior pathways by which early adversity might lead to inflammation during young adulthood. Contemporaneously measured early adversity predicted increased BMI and smoking but not alcohol consumption, and these effects were partially accounted for by chronic stress in young adulthood. Higher BMI in turn predicted higher levels of soluble tumor necrosis factor receptor type II (sTNF-RII) and C-reactive protein (CRP), and smoking predicted elevated sTNF-RII. These findings establish that early adversity contributes to inflammation in part through ongoing stress and maladaptive health behavior. Given that maladaptive health behaviors portend inflammation in young adulthood, they serve as promising targets for interventions designed to prevent the negative consequences of early adversity.