Psychoneuroendocrinology
Volume 33, Issue 8 , Pages 1102-1110, September 2008

Higher body mass index (BMI) is associated with reduced glucocorticoid inhibition of inflammatory cytokine production following acute psychosocial stress in men

  • Petra H. Wirtz

      Affiliations

    • Department of Clinical Psychology and Psychotherapy, University of Zurich, Switzerland
    • Corresponding Author InformationCorresponding author. Department of Clinical Psychology and Psychotherapy, University of Zurich, Binzmühlestrasse 14/Box 26, CH-8050 Zurich, Switzerland. Tel.: +41 44 635 7367; fax: +41 44 635 7359.
    • ,
  • Ulrike Ehlert

      Affiliations

    • Department of Clinical Psychology and Psychotherapy, University of Zurich, Switzerland
    • ,
  • Luljeta Emini

      Affiliations

    • Department of Clinical Psychology and Psychotherapy, University of Zurich, Switzerland
    • ,
  • Tobias Suter

      Affiliations

    • Clinical Immunology, Department of Internal Medicine, University Hospital, Zurich, Switzerland

Received 11 January 2008; received in revised form 21 April 2008; accepted 23 May 2008.

Summary 

Background

Body mass index (BMI) and mental stress seem to exert part of their cardiovascular risk by eliciting inflammation. However, the adverse effects of stress on inflammatory activity with BMI are not fully understood. We investigated whether higher BMI is associated with reduced glucocorticoid inhibition of inflammatory cytokine production following stress in men while controlling for age and blood pressure. We measured glucorticoid inhibition of lipopolysaccharide (LPS)-stimulated release of the proinflammatory cytokine tumor necrosis factor (TNF)-α.

Methods

Forty-two men (age range 21–65 years; BMI range 21–34kg/m2) underwent the Trier Social Stress Test (combination of mock job interview and mental arithmetic task). Whole blood samples were taken immediately before and after stress, and during recovery up to 60min post-stress. Glucocorticoid sensitivity of LPS-stimulated TNF-α expression was assessed in vitro with and without coincubating increasing doses of dexamethasone. Moreover, salivary cortisol was measured during the experiment and on a normal day for assessment of baseline circadian cortisol.

Results

Higher BMI was associated with lower glucocorticoid sensitivity of monocyte TNF-α production after stress (main effect of BMI: p<0.001) and with more pronounced decreases of glucocorticoid sensitivity following stress (interaction of stress-by-BMI: p=0.002). Neither LPS-stimulated TNF-α release nor baseline glucocorticoid sensitivity were associated with BMI. Similarly, BMI was not associated with salivary cortisol, either in reaction to stress or in circadian cortisol secretion.

Conclusions

Our data suggest that with increasing BMI, glucocorticoids are less able to inhibit TNF-α production following stress. This might suggest a new mechanism linking BMI with elevated risk for adverse cardiovascular outcomes following stress.

Keywords: BMI, Atherosclerosis, Stress, Glucocorticoid sensitivity, TNF-α

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PII: S0306-4530(08)00134-0

doi:10.1016/j.psyneuen.2008.05.002

Psychoneuroendocrinology
Volume 33, Issue 8 , Pages 1102-1110, September 2008

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