Osteoarthritis (OA) is one of the more challenging diagnoses to successfully treat as a physical therapist. In trying to find a more effective way to educate and treat patients, I went to Pub Med to find complimentary approaches to OA.
Guest Blog from Grant Glass, PT, CIMT, OCS, CAFS, GPS
Some recent articles have posited biochemical relationships between metabolic syndromes and osteoarthritis.,,, Metabolic syndromes have many definitions and have changed over time. Overall metabolic syndrome is generally the combination of abnormal blood glucose control/diabetes, hypertension, obesity/waist circumference, and/or abnormal lipoprotein/triglyceride findings.
In Is osteoarthritis a metabolic disease?, a paper compiling knowledge from other primary and meta-analysis research papers published in Dec. 2013 and included research references from 2013, included research that correlated metabolic syndrome with OA with proposed mechanisms. The single factors of hyperglycemia, lipids, and hypertension and their individual contributions to biochemical pathways resulted in OA. The discussion offered, suggests that the same exercise and dietary approach to counter metabolic syndrome may also decrease OA risk even in the absence of obesity.
Another study, Association of metabolic risk factors with cartilage degradation assessed by T2 relaxation time at the knee: data from the osteoarthritis initiative, used epidemiological data and estimated those with metabolic syndrome.2 This study correlated a combination of individual factors comprising metabolic syndrome and individually diabetes, with MRI T2 relaxation times. MRI T2 signal from tissue is compared to pure water to estimate the amount of water in tissue. Early onset presymptomatic OA has been correlated to this T2 signal mapping, as sited in the paper., This T2 mapping showed subchondral bone and cartilage baseline changes were increased in those with metabolic syndrome markers compared to those without metabolic syndrome markers. This was a longitudinal study lasting two years. There was no statistically significant difference in progression of T2 signal mapping indicating worsening degeneration between the metabolic syndrome group and those that didn’t have evidence of metabolic syndrome.
The two other studies use obesity as a primary criterion for study.3,4 Leptin - a link between obesity and osteoarthritis. applications for prevention and treatment reviews the link between obesity and OA through impaired leptin signaling. Leptin is a hormone released by fat cells that was first identified in 1994. According to the article leptin blood concentration levels signal the hypothalamus to regulate energy consumption and increase energy expenditure. What blocks the leptin signal was not offered in this article. In obese individuals this signaling falters resulting in an excess of blood leptin. The review also sites evidence that the joints also secrete their own leptin and that the excess leptin in the blood leads to an increase in leptin in the joints. This leptin excess in the joint fluid signals the biochemical deterioration pathways of the cartilage.
Another article, Using diet-induced obesity to understand a metabolic subtype of osteoarthritis in rats, was a direct animal model study of obesity and OA. In this study the researchers found that surgically induced joint dysfunction leading to OA showed similar results to OA induced by obesity.
Leptin resistance was reviewed in the article, Role of the blood-brain barrier in the evolution of feeding and cognition. The author reports that leptin protein transport across the blood brain barrier can reach a saturation point where by the amount of leptin in the blood can increase above a point where no higher transports rates can be achieved despite higher blood leptin levels. There is also a table that lists the up-regulators and down-regulators of leptin passage across the blood brain barrier. Up-regulators are starvation, epinephrine, insulin, glucose, and alcohol. Down-regulators are obesity, fasting, triglycerides, ovarectomy, lack of leptin receptors, and defects in leptin receptors. One of the author’s conclusions was that leptin stimulates energy consumption during times of starvation but is poor at signaling cessation of overconsumption.
An article, Nutraceuticals: Potential for Chondroprotection and Molecular Targeting of Osteoarthritis, on foods or supplements that inhibited the inflammatory pathways of OA, was informative. This article offered curcumin (turmeric), ginger, pomegranate, EGCG (found in greatest concentrations in green tea), glucosamine/chondroitin sulfate, resveratrol (as a supplement), and rosehips as disruptors at multiple sites along the metabolic pathway from pro-inflammatory cytokines to OA. (http://www.renosoar.com/holistic-health-tips/reno-physical-therapy-inflammation-and-osteoarthritis)
As for the leptin metabolic subset of OA, returning the metabolic syndrome parameters to normal seems key. As a physical therapist, I’m forbidden from recommending any medications, but there do seem to be dietary approaches that work. They utilize traditional diets devoid of processed foods, comprised entirely of constituents raised, harvested or hunted and kept in their whole forms, traditionally prepared. Individuals may have to modify any particular traditional approach if they are not fully achieving their goals. They can do this by using an elimination-style approach of any group of foods to self-test their reaction (grain, dairy, beans, nightshades can be some of those groups).
Remove. Replace. Restore.
Remove refined and processed foods, refined grains, and refined sugars (this is a must for metabolic syndrome and may need to be close to 0 grams for a while). All of these components contribute to developing metabolic syndrome by abnormally increasing blood glucose and insulin levels.
Replace whole nutrient rich foods in the form of organic fruits, vegetables and sustainably harvested meats or wild game if you have access to it. Include spices like turmeric and ginger to cooking. Consider drinking green tea and eating pomegranate and other produce high in resveratrol (purple grapes, bilberries, blueberries, cranberries, cocao, dark chocolate, and pistachio). Making homemade bone broth is a natural source of glucosamine. See http://www.renosoar.com/holistic-health-tips/fix-it-and-forget-it-rotisserie-chicken-that-turns-into-3-meals1. Be sure to include healthy movement and exercise as well.
Restore healthy metabolism and healthy movement. Maintain the new eating for a minimum of 30-60 days. More time is often needed when recovering from metabolic diseases. If you are NOT achieving your goals related to OA, then trial an elimination type diet to look for specific food reactions. And contact a licensed professional for further testing or evaluation.
Eat Well. Move Well. Thrive On.
 Joint Bone Spine. 2013 Dec;80(6):568-73. doi: 10.1016/j.jbspin.2013.09.007. Epub 2013 Oct 29. Is osteoarthritis a metabolic disease? Sellam J1, Berenbaum F.
 Arthritis Care Res (Hoboken). 2013 Dec;65(12):1942-50. doi: 10.1002/acr.22093. Association of metabolic risk factors with cartilage degradation assessed by T2 relaxation time at the knee: data from the osteoarthritis initiative. Jungmann PM1, Kraus MS, Alizai H, Nardo L, Baum T, Nevitt MC, McCulloch CE, Joseph GB, Lynch JA, Link TM.
 Basic Clin Pharmacol Toxicol. 2014 Jan;114(1):103-8. doi: 10.1111/bcpt.12160. Epub 2013 Nov 20. Leptin - a link between obesity and osteoarthritis. applications for prevention and treatment. Vuolteenaho K1, Koskinen A, Moilanen E.
 Osteoarthritis Cartilage. 2015 Feb 3. pii: S1063-4584(15)00028-X. doi: 10.1016/j.joca.2015.01.015. Using diet-induced obesity to understand a metabolic subtype of osteoarthritis in rats. Collins KH1, Reimer RA2, Seerattan RA3, Leonard TR4, Herzog W5.
 Diab Vasc Dis Res. 2007 Mar;4(1):32-8. Metabolic syndrome, or What you will: definitions and epidemiology. Day C
 Radiology. 2003 Feb;226(2):373-81. Osteoarthritis: MR imaging findings in different stages of disease and correlation with clinical findings. Link TM, Steinbach LS, Ghosh S, Ries M, Lu Y, Lane N, Majumdar S.
 Arthritis Rheum. 2011 Aug;63(8):2248-56. doi: 10.1002/art.30419 Physical activity is associated with magnetic resonance imaging-based knee cartilage T2 measurements in asymptomatic subjects with and those without osteoarthritis risk factors. Hovis KK1, Stehling C, Souza RB, Haughom BD, Baum T, Nevitt M, McCulloch C, Lynch JA, Link TM.
 Ann N Y Acad Sci. 2012 Aug;1264:13-9. doi: 10.1111/j.1749-6632.2012.06568.x. Epub 2012 May 21. Role of the blood-brain barrier in the evolution of feeding and cognition. Banks WA
 Int J Mol Sci. 2013 Nov 21;14(11):23063-85. doi: 10.3390/ijms141123063. Nutraceuticals: potential for chondroprotection and molecular targeting of osteoarthritis. Leong DJ1, Choudhury M, Hirsh DM, Hardin JA, Cobelli NJ, Sun HB.
 Nutr Res. 2014 Jul;34(7):559-68. doi: 10.1016/j.nutres.2014.06.012. Epub 2014 Jun 26. Certain dietary patterns are beneficial for the metabolic syndrome: reviewing the evidence. Calton EK1, James AP1, Pannu PK1, Soares MJ2.
Dr Carolyn Dolan DPT, Cert MDT, MSHN
Where physical therapy, nutrition and lifestyle meet, because how you live your life determines whether or not you soar. Inspiring action with information so you can reduce pain, optimize healing and improve function naturally during recovery from injury, surgery or painful condition. This is a website for the open-minded; obstinate need not apply.