Effects of obesity on neuroendocrine, cardiovascular, and immune cell responses to acute psychosocial stress in premenopausal women

• Published in: Psychoneuroendocrinology 2009-02, Vol.34 (2), p.181-189
• Main Authors: Benson, S, Arck, P.C, Tan, S, Mann, K, Hahn, S, Janssen, O.E, Schedlowski, M, Elsenbruch, S
• Format: Article
• Language: English
• Subjects: Adrenocorticotropic Hormone - blood; Adult; Behavioral psychophysiology; Biological and medical sciences; Blood Pressure; C-Reactive Protein - metabolism; Case-Control Studies; Cortisol; Endocrinology & Metabolism; Female; Fundamental and applied biological sciences. Psychology; Heart Rate; Hemodynamics; Hormones and behavior; Humans; Hydrocortisone - blood; IL-6; Immune system; Immunity, Cellular; Interleukin-6 - blood; Leukocytes; Medical sciences; Metabolic diseases; Obesity; Obesity - complications; Obesity - physiopathology; Premenopause; Psychiatry; Psychological stress; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Speech; Stress, Psychological - complications; Stress, Psychological - physiopathology
• ISSN: 0306-4530; 1873-3360
• DOI: 10.1016/j.psyneuen.2008.08.019

Summary Objective To analyze the neuroendocrine and immune cell responses to acute psychosocial stress in obese compared to non-obese premenopausal women. Methods N = 15 obese (BMI ≥ 30) and N = 24 (BMI < 30) non-obese premenopausal women underwent public speaking stress. State anxiety, ACTH, cortisol, and the redistribution of immune cells were measured before, during, and 10 and 45 min after public speaking. Serum hsCRP and serum IL-6 levels were analyzed before, and IL-6 additionally 45 min after stress. Results In response to public speaking stress, both groups showed significant but comparable increases in state anxiety, plasma ACTH, and blood pressure (all p < 0.01; time effects). The cortisol stress response was significantly enhanced in obese women ( p < 0.05; interaction effect). In addition, heart rate and diastolic blood pressure were significantly higher in obese women 10 min following stress ( p < 0.05, t -tests). Public speaking stress led to a significant increase in IL-6 concentrations ( p < 0.001; time effect), and obese women displayed higher IL-6 levels both pre- and post-stress ( p < 0.05; group effect; between-group t -tests: pre-stress p < 0.05; post-stress p < 0.01). Baseline numbers of circulating leukocytes, granulocytes, CD3+ cells and hsCRP concentration were significantly higher in obese women (between-group t -tests: all p < 0.05, but the groups did not differ in the stress-induced redistribution of circulating leukocyte subpopulations. Conclusions Our data reveal a strong association of obesity with chronic low-grade inflammation in premenopausal women. This pro-inflammatory state, together with altered neuroendocrine and cardiovascular stress responsiveness, may conceivably constitute one of the mechanisms linking psychological stress and the long-term health risks associated with obesity.