Sunday, December 5, 2010

Weight Loss Reduces the Risk for Symptomatic Knee

Osteoarthritis in Women

The Framingham Study


Objective: To evaluate the effect of weight loss in preventing symptomatic knee osteoarthritis in women.

Design: Cohort analytic study.

Setting: The Framingham Study, based on a sample of a defined population.

Patients: Women who participated in the Framingham Knee Osteoarthritis Study (1983 to 1985): Sixty-four out of 796 women studied had recent-onset symptomatic knee osteoarthritis (knee symptoms plus radiographically confirmed osteoarthritis) were compared with women without disease.

Measurements: Recalled date of symptom onset was used as the incident date of disease. Historical weight was defined as baseline body mass index up to 12 years before symptom onset. Change in body mass index was assessed at several intervals before the current examination. Odds ratios assessing the association between weight change and knee osteoarthritis were adjusted for age, baseline body mass index, history of previous knee injury, habitual physical activity level, occupational physical labor, smoking status, and attained education.

Results: Weight change significantly affected the risk for the development of knee osteoarthritis. For example, a decrease in body mass index of 2 units or more (weight loss, approximately 5.1 kg) over the 10 years before the current examination decreased the odds for developing osteoarthritis by over 50% (odds ratio, 0.46; 95% Cl, 0.24 to 0.86; P = 0.02). Among those women with a high risk for osteoarthritis due to elevated baseline body mass index (> 25), weight loss also decreased the risk (for 2 units of body mass index, odds ratio, 0.41 ; P = 0.02). Weight gain was associated with a slightly increased risk for osteoarthritis, which was not statistically significant.

Conclusion: Weight loss reduces the risk for symptomatic knee osteoarthritis in women.

Article and Author Information

  • From the Boston University Arthritis Center, Boston City Hospital; and University Hospital, Boston, Massachusetts. For current author addresses, see end of text.

  • Grant Support: By NIH Arthritis Center Grant AR20613, and by a Clinical Sciences Grant from the Arthritis Foundation.

  • Requests for Reprints: David Felson, MD, MPH, A203, 80 East Concord Street, Boston, MA 02118.

  • Current Author Addresses: Drs. Felson, Zhang, and Anderson and Mr. Anthony: A203, 80 East Concord Street, Boston, MA 02118.

    Dr. Naimark: Dept. of Radiology, University Hospital, 71 East Newton Street, Boston, MA 02118.

Weight Reduction Increases Plasma Levels of an Adipose-Derived Anti-Inflammatory Protein, Adiponectin

Wei-Shiung Yang, Wei-Jei Lee, Tohru Funahashi, Sachiyo Tanaka, Yuji Matsuzawa, Chia-Ling Chao, Chi-Ling Chen, Tong-Yuan Tai and Lee-Ming Chuang

Department of Internal Medicine (W.-S.Y., C.-L.C., T.-Y.T., L.-M.C.), Graduate Institute of Clinical Medicine (W.-S.Y., L.-M.C.), College of Medicine, and Institute of Epidemiology (C.-L.C.), College of Public Health, National Taiwan University, Taipei 100; Department of Surgery (W.-J.L.), En Chu Kong Hospital, Taipei Hsien 237, Taiwan; and Department of Internal Medicine and Molecular Science (T.F., S.T., Y.M.), Graduate School of Medicine, Osaka University, 565-0871, Osaka, Japan

Address all correspondence and requests for reprints to: Lee-Ming Chuang, M.D., Ph.D., Department of Internal Medicine, National Taiwan University Hospital, 7 Chung-Shan South Road, Taipei 100, Taiwan. E-mail:


Adiponectin, an adipose tissue-specific plasma protein, was recently revealed to have anti-inflammatory effects on the cellular components of vascular wall. Its plasma levels were significantly lower in men than in women and lower in human subjects with obesity, type 2 diabetes mellitus, or coronary artery disease. Therefore, it may provide a biological link between obesity and obesity-related disorders such as atherosclerosis, against which it may confer protection. In this study, we observed the changes of plasma adiponectin levels with body weight reduction among 22 obese patients who received gastric partition surgery. A 46% increase of mean plasma adiponectin level was accompanied by a 21% reduction in mean body mass index. The change in plasma adiponectin levelswas significantly correlated with the changes in body mass index (r = -0.5, P = 0.01), waist (r = -0.4, P = 0.04) and hip (r = -0.6, P = 0.0007) circumferences, and steady state plasma glucose levels (r = -0.5, P = 0.04). In multivariate linear regression models, the increase in adiponectin as a dependent variable was significantly related to the decrease in hip circumference (ß = -0.16, P = 0.028), after adjusting body mass index and waist circumference. The change in steady state plasma glucose levels as a dependent variable was related to the increase of adiponectin with a marginal significance (ß = -0.92, P = 0.053), after adjusting body mass index and waist and hip circumferences. In conclusion, body weight reduction increased the plasma levels of a protective adipocytokine, adiponectin. In addition, the increase in plasma adiponectin despite the reduction of the only tissue of its own synthesis suggests that the expression of adiponectin is under feedback inhibition in obesity.