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Original Research |

Impact of Obesity and Knee Osteoarthritis on Morbidity and Mortality in Older Americans

Elena Losina, PhD; Rochelle P. Walensky, MD, MPH; William M. Reichmann, MA; Holly L. Holt, BA; Hanna Gerlovin, BA; Daniel H. Solomon, MD, MPH; Joanne M. Jordan, MD, MPH; David J. Hunter, MD, PhD; Lisa G. Suter, MD; Alexander M. Weinstein, BA; A. David Paltiel, PhD; and Jeffrey N. Katz, MD, MSc
[+] Article, Author, and Disclosure Information

From Brigham and Women's Hospital, Boston University School of Public Health, Massachusetts General Hospital, and Harvard School of Public Health, Boston, Massachusetts; University of North Carolina, Chapel Hill, North Carolina; University of Sydney, Sydney, New South Wales, Australia; and Yale University School of Medicine, New Haven, Connecticut.

Note: Dr. Losina had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Acknowledgment: The authors thank Sara Burbine for her expert editorial assistance.

Grant Support: By the National Institutes of Health, National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01 AR053112, K24 AR057827, K23 AR054095, P60 AR47782, T32 AR 055885, and K24 AR 02123); an Arthritis Foundation Innovative Research grant (Dr. Losina); and an Arthritis Investigator Award (Dr. Suter).

Potential Conflicts of Interest: Disclosures can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M10-2150.

Reproducible Research Statement:Study protocol, statistical code, and data set: Available from Dr. Losina (e-mail, Elosina@partners.org).

Requests for Single Reprints: Elena Losina, PhD, Department of Orthopaedic Surgery, Orthopaedic and Arthritis Center for Outcomes Research, Brigham and Women's Hospital, 75 Francis Street, BC-4, Boston, MA 02115; e-mail, Elosina@partners.org.

Current Author Addresses: Drs. Losina and Katz: Department of Orthopaedic Surgery, Orthopaedic and Arthritis Center for Outcomes Research, Brigham and Women's Hospital, 75 Francis Street, BC-4, Boston, MA 02115.

Dr. Walensky: Division of General Medicine, Massachusetts General Hospital, 50 Staniford Street, 9th Floor, Boston, MA 02114.

Mr. Reichmann, Ms. Holt, Ms. Gerlovin, and Mr. Weinstein: Orthopaedic and Arthritis Center for Outcomes Research, Brigham and Women's Hospital, 75 Francis Street, BC-4, Boston, MA 02115.

Dr. Solomon: Division of Rheumatology, Brigham and Women's Hospital, 75 Francis Street, PBB-B3, Boston, MA 02115.

Dr. Jordan: Thurston Arthritis Research Center, University of North Carolina, 3300 Doc J. Thurston Jr. Building, CB #7280, Chapel Hill, NC 27599-7280.

Dr. Hunter: Rheumatology Department, Royal North Shore Hospital and Northern Clinical School, University of Sydney, Sydney, New South Wales, Australia.

Dr. Suter: Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, 300 Cedar Street, Room TAC S541, PO Box 208031, New Haven, CT 06520-8031.

Dr. Paltiel: Department of Epidemiology and Public Health, Yale School of Medicine, 60 College Street, New Haven, CT 06520-8034.

Author Contributions: Conception and design: E. Losina, R.P. Walensky, W.M. Reichmann, D.H. Solomon, J.M. Jordan, D.J. Hunter, J.N. Katz.

Analysis and interpretation of the data: E. Losina, R.P. Walensky, H.L. Holt, H. Gerlovin, L.G. Suter, A.M. Weinstein, J.N. Katz.

Drafting of the article: E. Losina, R.P. Walensky, H.L. Holt, H. Gerlovin, L.G. Suter, A.M. Weinstein, J.N. Katz.

Critical revision of the article for important intellectual content: E. Losina, R.P. Walensky, W.M. Reichmann, D.H. Solomon, J.M. Jordan, D.J. Hunter, L.G. Suter, A.D. Paltiel, J.N. Katz.

Final approval of the article: E. Losina, R.P. Walensky, W.M. Reichmann, H. Gerlovin, J.M. Jordan, D.J. Hunter, L.G. Suter, A.M. Weinstein, A.D. Paltiel, J.N. Katz.

Provision of study materials or patients: J.M. Jordan.

Statistical expertise: E. Losina, W.M. Reichmann.

Obtaining of funding: E. Losina.

Administrative, technical, or logistic support: H.L. Holt, H. Gerlovin, D.H. Solomon, A.M. Weinstein, J.N. Katz.

Collection and assembly of data: E. Losina, W.M. Reichmann, H.L. Holt, A.M. Weinstein, J.N. Katz.

Ann Intern Med. 2011;154(4):217-226. doi:10.7326/0003-4819-154-4-201102150-00001
Text Size: A A A

Background: Obesity and knee osteoarthritis are among the most frequent chronic conditions affecting Americans aged 50 to 84 years.

Objective: To estimate quality-adjusted life-years lost due to obesity and knee osteoarthritis and health benefits of reducing obesity prevalence to levels observed a decade ago.

Design: The U.S. Census and obesity data from national data sources were combined with estimated prevalence of symptomatic knee osteoarthritis to assign persons aged 50 to 84 years to 4 subpopulations: nonobese without knee osteoarthritis (reference group), nonobese with knee osteoarthritis, obese without knee osteoarthritis, and obese with knee osteoarthritis. The Osteoarthritis Policy Model, a computer simulation model of knee osteoarthritis and obesity, was used to estimate quality-adjusted life-year losses due to knee osteoarthritis and obesity in comparison with the reference group.

Setting: United States.

Participants: U.S. population aged 50 to 84 years.

Measurements: Quality-adjusted life-years lost owing to knee osteoarthritis and obesity.

Results: Estimated total losses of per-person quality-adjusted life-years ranged from 1.857 in nonobese persons with knee osteoarthritis to 3.501 for persons affected by both conditions, resulting in a total of 86.0 million quality-adjusted life-years lost due to obesity, knee osteoarthritis, or both. Quality-adjusted life-years lost due to knee osteoarthritis and/or obesity represent 10% to 25% of the remaining quality-adjusted survival of persons aged 50 to 84 years. Hispanic and black women had disproportionately high losses. Model findings suggested that reversing obesity prevalence to levels seen 10 years ago would avert 178 071 cases of coronary heart disease, 889 872 cases of diabetes, and 111 206 total knee replacements. Such a reduction in obesity would increase the quantity of life by 6 318 030 years and improve life expectancy by 7 812 120 quality-adjusted years in U.S. adults aged 50 to 84 years.

Limitations: Comorbidity incidences were derived from prevalence estimates on the basis of life expectancy of the general population, potentially resulting in conservative underestimates. Calibration analyses were conducted to ensure comparability of model-based projections and data from external sources.

Conclusion: The number of quality-adjusted life-years lost owing to knee osteoarthritis and obesity seems to be substantial, with black and Hispanic women experiencing disproportionate losses. Reducing mean body mass index to the levels observed a decade ago in this population would yield substantial health benefits.

Primary Funding Source: The National Institutes of Health and the Arthritis Foundation.


Grahic Jump Location
Figure 1.
Transitions among health states in the OAPol Model.

The circles represent the 4 major health states in the OAPol Model. Persons may spend several cycles in the same health state or transition to another health state. Arrows specify transitions between health states, defined by transition probabilities (the OAPol Model input parameters). Comorbid conditions may occur in each state and lead to increased mortality. Incidence of comorbid conditions increases with age and obesity. In particular, comorbid conditions are considered in combination with obesity and knee osteoarthritis. Patients may have 0 to 5 comorbid conditions, for a total of 32 combinations. Therefore, the total number of states is equal to the product of 4 knee osteoarthritis states (no osteoarthritis, Kellgren–Lawrence grade 2, Kellgren–Lawrence grade 3, and Kellgren–Lawrence grade 4), 3 obesity states (normal, obese, and morbidly obese), 32 comorbidity states, and 1 absorbing state (death), for a total of 385 states. Each health state is associated with quality-of-life utilities (i.e., coefficients applied to each cycle [year] spent in a corresponding health state). Death can occur in any health state. OAPol = Osteoarthritis Policy.

Grahic Jump Location
Grahic Jump Location
Figure 2.
Excess of quality-adjusted life-years lost owing to obesity and knee osteoarthritis, as a ratio relative to population size.

The height of each bar represents the ratio of the proportion of total quality-adjusted life-years lost attributable to each sex and race or ethnic group to each group's size relative to the total U.S. population.

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Submit a Comment/Letter
Growth hormone against osteoarthritis
Posted on February 20, 2011
Hernando Rafael
Universidad Nacional Autonoma de M?xico
Conflict of Interest: None Declared

TO THE EDITOR.With great interest I read the article by Losina et al(1)about the impact of obesity on knee osteoarthritis(OA).The authors concluded that a reduction of mean BMI would yield substantial health benefits.However,there are many nonobese patients with knee OA.Up to date,in early stages,the diagnosis and therapeutic management of the lumbar and peripheral(interphalangeal,wrist,ankle,knee,shoulder and hip joints)OA is a challenge to clinicians due to the unclear etiology. For this reason,I wish to comment some data which should be analysed:FIRST,OA occurs at the same time as the people aged.SEC0ND,between 25 to 30 years of age,the producing hypothalamic nuclei of growth hormone-releasing hormone(GHRH) are the first one in to suffer ischemic injury(2,3).Thus,virtually all people who are 30 years old or more there is a direct correlation between decreasing growth hormone(GH) levels and the effects of aging.THIRD,the accumulation of adipose tissue is the result of,at least,four key factors involved in the pathogenesis of obesity: 1)a caloric intake bigger than the energy requirement of the body;2)a decreased physical activity;3) a decline of GH levels in our bodies,and 4)elevated levels of circulating cortisol.Thus,in adults,the obesity is related with the four factors.FOURTH,in children and adolescents,GH favours the:1)transformation of aminoacids in proteins;2)conversion of prolin in hydroxiporlin for the collagen synthetized by fibroblasts and chondrocytes,and 3)incorporation of sulfates in the cartilage in form of chondroitin-4-sulfate and chondroitin -6-sulfate.In other words,GH favours the regeneration of the hyaline cartilage(2).FIFTH,an omental transplantation on the optic chiasma,carotid bifurcation and anterior perforated space can cause rejuvenation,weight loss and to normalize essential arterial hypertension(EAH)due to hypothalmic revascularization,especially in the arcuate nucleus, and ventromedial and posterior nuclei(3,4).SIXTH,up to now,chondroprotective agents(hyaluronan, polysulphated glycosaminoglycan and among others)have not much effect in the intervertebral discs and/or peripheral joints (2,5). Thereby,I believe that GH replacement therapy must be associated for treatment of the OA.Although by means of an omental transplantation we could to fight against aging,obesity,EAH and OA.


1-Losina E,Walensky RP,Reichmann WM,Holt HL,Gerlovin H,Solomon DH,et al.Impact of obesity and knee osteoarthritis on morbility and mortality in older Americans.Ann Intern Med 2011;154:217-26.

2-Rafael H.Degenerative spondylolisthesis and joint disease in adult people.Rev Hosp Jua Mex 2008;75(3):218-22. www.medigraphic.com

3-Rafael H.Therapeutic methods against aging. Turk J Geriatri 2010;13(2):138-44. www.geriatri.dergisi.org

4-Rafael H,Fernandez E,Ayulo V,D?vila L.Weight loss following omental transplantation on the anterior perforated space.Case Rep Clin Pract Rev 2003;4(3):160-2. www.amjcaserep.com

5-Wilkens P,Scheel IB,Grundnes O,Hellum C,Storheim K. Effect of glucosamine on pain-related disability in patients with chronic low back pain and degenerative lumbar osteoarthritis:A randomized controlled trial. JAMA 2010;304:45-52.

Conflict of Interest:

None declared

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