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Hypothesis

Adipose Tissue as a Modulator of Clinical Inflammation: Does Obesity Reduce the Prevalence of Rheumatoid Arthritis?

TAMAS BARTFAI, JILL WAALEN, and JOEL N. BUXBAUM

ABSTRACT.

Objective. Obese individuals display circulating proinflammatory cytokine elevations similar to those in patients with rheumatoid arthritis (RA). We wished to determine if extremely obese individuals were overrepresented among a group of patients with RA.

Methods. We performed both multi- and univariate analyses of data from a large, community-based population attending the "wellness" clinic of a large health maintenance organization in Southern California. We also examined the data from 5 other studies that examined the relationship between various environmental factors and the incidence and prevalence of RA.

Results. We found no relationship between the prevalence of RA and body mass index (BMI) in our own data or in the preponderance of previously published studies examining the same question.

Conclusion. Although both RA and obesity have been reported to be characterized by high serum levels of inflammatory cytokines, the frequency of one disorder was not increased in the other. We propose that the lack of association in prevalence between the 2 inflammatory states, rather than reflecting a post-hoc effect of the disease on BMI, is a function of the relative amounts of pro- and antiinflammatory mediators produced in adipose tissue, which under many circumstances leads to an overall systemic antiinflammatory tone. (First Release Feb 15 2007; J Rheumatol 2007;34:488-92)

Key Indexing Terms:

OBESITY
RHEUMATOID ARTHRITIS
CYTOKINES
INFLAMMATORY TONE


From the Department of Molecular and Integrative Neurosciences and Department of Molecular Medicine, The Scripps Research Institute, La Jolla, California, USA.

T. Bartfai, PhD, Department of Molecular and Integrative Neurosciences; J. Waalen, MD, MPH; J.N. Buxbaum, MD, Department of Molecular Medicine, The Scripps Research Institute.

Address reprint requests to Dr. J.N. Buxbaum, The Scripps Research Institute, Molecular and Experimental Medicine, 10550 N. Torrey Pines Road, La Jolla, CA 92037, USA. E-mail: jbux@scripps.edu

Accepted for publication November 16, 2006.




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