CMAJ • April 26, 2005; 172 (9). doi:10.1503/cmaj.1040769.
© 2005 CMA Media Inc. or its licensors
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Behavioural treatments for chronic systemic inflammation: effects of dietary weight loss and exercise training

Barbara J. Nicklas, Tongjian You and Marco Pahor

From the Sticht Center on Aging, Section on Gerontology and Geriatric Medicine, Department of Internal Medicine, Wake Forest University School of Medicine, Winston-Salem, NC (Nicklas, You); the Department of Aging and Geriatric Research and the University of Florida Institute on Aging, University of Florida, Gainesville, Fla. (Pahor)



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  		Fig. 1: Reported behavioural factors associated with chronic subclinical inflammation, and diseases and adverse health conditions for which inflammation is a risk factor. {downarrow} = decreased; BMI = body mass index.

 

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  		Table 1.

 


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  		Fig. 2: Effects of 18 months of weight loss, exercise, or both upon mean CRP concentrations, adjusted for baseline BMI, baseline CRP level, sex and race. The treatment effect of dietary weight loss was significant compared with the control and exercise-only groups (p = 0.01). Modified from Nicklas et al (Am J Clin Nutr 2004;79:544-51), with permission.

 


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  		Fig. 3: Schematic of possible mechanisms by which weight loss and exercise training reduce sources of inflammation that lead to chronic activation of a pro-inflammatory state. Weight loss and increased activity affect the immune system by reducing the number of mononuclear cells in the peripheral blood, which are a source of pro-inflammatory cytokines (such as interleukins IL-6, IL-1ß and IL-8; tumour necrosis factor-{alpha} and its receptors TNFR1 and TNFR2; and transforming growth factor TGFß). A reduction in adipose tissue would not only reduce the volume of adipocytes and pre-adipocytes, but also decrease the number of endothelial cells and macrophages that reside there. These cells produce many pro-inflammatory mediators such as C-reactive protein (CRP), serum amyloid protein A (SAA) and cytokines. Weight loss and exercise may also increase the expression of anti-inflammatory mediators such as IL-10 and IL-1 receptor antagonist (IL-1ra) in these cells. The resulting circulatory changes could, in turn, cause the liver to contribute by decreasing its production of fibrinogen and other pro-inflammatory mediators. Photo: Lianne Friesen and Nicholas Woolridge

 

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  		Table 2.

 


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  		Fig. 4: Median changes in high-sensitivity (HS) C-reactive protein concentrations in patients with coronary heart disease after 19 weeks of follow-up (standard deviation 3 weeks) in cardiac rehabilitation compared with control patients with coronary artery disease. Reprinted with permission from Milani et al (J Am Coll Cardiol 2004;43:1056–61).