Diet, nutrition and osteoarthritis
© Rayman 2015
Published: 1 December 2015
Osteoarthritis (OA) is the fastest growing cause of disability worldwide. In the absence of effective therapies, patients may wish to take some control of their own condition by making dietary changes that have the potential to ameliorate symptoms or reduce disease progression.
A number of dietary factors have been associated with OA symptoms or progression. Most notably, in those overweight, weight reduction of ≥10% has the potential to lead to important changes in pain and function. Losing weight also reduces pain-associated inflammation. Weight loss combined with physical activity has an even greater capacity to improve pain and function.
It has been suggested that OA is a metabolic disease in which lipids essentially contribute to the pathophysiology of cartilage degradation. Dietary long-chain ω-3 PUFA may affect articular cartilage composition and appear to have beneficial effects in OA. In a US cohort of individuals with, or at high risk of, knee OA, there was a significant inverse relationship between total n-3 PUFAs and patella-femoral cartilage loss.
A positive association has been shown between elevated serum cholesterol and OA; hypercholesterolemia (OR 1.61; 95% CI 1.06-2.47) and high serum cholesterol (3rd vs. 1st tertile: OR 1.73; 95% CI 1.02-2.92) were independently associated with generalized OA in the Ulm study. Hence there may be a potential benefit in adopting dietary cholesterol-lowering strategies (such as consumption of sterol/stanol spreads/drinks).
Vitamin D affects the state of multiple articular structures. The evidence for association between the vitamin D biomarker, serum 25(OH)D, and OA was assessed in a systematic review. For knee radiographic OA progression and cartilage loss, there was strong evidence for an association with low 25(OH)D.
Vitamin K is important in cartilage metabolism as an inhibitor of extracellular matrix calcification and a promoter of cell survival/proliferation. In the US MOST study, vitamin K deficiency was associated with incident radiographic knee OA and MRI-based cartilage lesions (RR 2.39; 95% CI, 1.05-5.40) compared with no deficiency.
▪ lose weight, if overweight, preferably combined with exercise;
▪ reduce plasma cholesterol by dietary means;
▪ at least for a trial period, increase intake of long-chain n-3 fatty acids preferably by eating oily fish twice a week;
▪ aim for a safe level of sun exposure, eat rich vitamin-D dietary sources or take vitamin D supplements, ≤ 25 µg/d;
▪ increase vitamin K intake by eating green leafy vegetables.
- Conaghan PG, Porcheret M, Kingsbury SR, Gammon A, Soni A, Hurley M, Rayman MP, Barlow J, Hull RG, Cumming J, Llewelyn K, Moscogiuri F, Lyons J, Birrell F: Impact and therapy of osteoarthritis: the Arthritis Care OA Nation 2012 survey. Clin Rheumatol. 2014, Jun 3. [Epub ahead of print]Google Scholar
- Riddle DL, Stratford PW: Body weight changes and corresponding changes in pain and function in persons with symptomatic knee osteoarthritis: a cohort study. Arthritis Care Res (Hoboken). 2013, 65: 15-22. 10.1002/acr.21692View ArticleGoogle Scholar
- Hauner H: Secretory factors from human adipose tissue and their functional role. Proc Nutr Soc. 2005, 64: 163-9. 15960861, 1:CAS:528:DC%2BD2MXlvFKlurk%3D, 10.1079/PNS2005428View ArticlePubMedGoogle Scholar
- Brosseau L, Wells GA, Tugwell P, Egan M, Dubouloz CJ, Casimiro L, Bugnariu N, Welch VA, De Angelis G, Francoeur L, Milne S, Loew L, McEwan J, Messier SP, Doucet E, Kenny GP, Prud'homme D, Lineker S, Bell M, Poitras S, Li JX, Finestone HM, Laferrière L, Haines-Wangda A, Russell-Doreleyers M, Lambert K, Marshall AD, Cartizzone M, Teav A: Ottawa Panel. Ottawa Panel evidence-based clinical practice guidelines for the management of osteoarthritis in adults who are obese or overweight. Phys Ther. 2011, 91: 843-61. 21493746, 10.2522/ptj.20100104View ArticlePubMedGoogle Scholar
- Masuko K, Murata M, Suematsu N, Okamoto K, Yudoh K, Nakamura H, Kato T: A metabolic aspect of osteoarthritis: lipid as a possible contributor to the pathogenesis of cartilage degradation. Clin Exp Rheumatol. 2009, 27: 347-53. 19473582, 1:STN:280:DC%2BD1MznsVequw%3D%3DPubMedGoogle Scholar
- Baker KR, Matthan NR, Lichtenstein AH, Niu J, Guermazi A, Roemer F, Grainger A, Nevitt MC, Clancy M, Lewis CE, Torner JC, Felson DT: Association of plasma n-6 and n-3 polyunsaturated fatty acids with synovitis in the knee: the MOST study. Osteoarthritis Cartilage. 2012, 20: 382-7. 22353693, 1:STN:280:DC%2BC38vjsl2jtg%3D%3D, 3471561, 10.1016/j.joca.2012.01.021View ArticlePubMedPubMed CentralGoogle Scholar
- Stürmer T, Sun Y, Sauerland S, Zeissig I, Günther KP, Puhl W, Brenner H: Serum cholesterol and osteoarthritis. The baseline examination of the Ulm Osteoarthritis Study. J Rheumatol. 1998, 25: 1827-32. 9733467PubMedGoogle Scholar
- Cao Y, Winzenberg T, Nguo K, Lin J, Jones G, Ding C: Association between serum levels of 25-hydroxyvitamin D and osteoarthritis: a systematic review. Rheumatology (Oxford). 2013, 52: 1323-34. 1:CAS:528:DC%2BC3sXhtVeiu7bF, 10.1093/rheumatology/ket132View ArticleGoogle Scholar
- Misra D, Booth SL, Tolstykh I, Felson DT, Nevitt MC, Lewis CE, Torner J, Neogi T: Vitamin K deficiency is associated with incident knee osteoarthritis. Am J Med. 2013, 126 (3): 243-8. 23410565, 1:CAS:528:DC%2BC3sXisVaqtr4%3D, 3641753, 10.1016/j.amjmed.2012.10.011View ArticlePubMedPubMed CentralGoogle Scholar
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.