Osteoarthritis and Obesity: more than just load through the joints

Causes of osteoarthritis (OA) can be from mechanical causes (a previous injury or trauma to the joint), metabolic and inflammatory factors.

We have all heard the old adage “running is bad for you knees”, and it has been repeated many times to me. Yet if I look at a cross section of my patients there are a few runners. Yes we do have the runners and the sporty people having knee and hip replacements, and many attribute their surgery to the years of sport etc. However unless a history of trauma or injury there may be more to the story. More and more research is out there showing us that running is not bad for our knees (Alenthorn-Gell et al 2017). We also know that being overweight is bad for you knees- yes I agree with this, but I think agreeing with is not as simple as it seems. Most knee patients will complain of more pain going up and down stairs as opposed to walking on a flat surface. This makes sense as the force through the knees going up and down stairs is 3-4x body weight and walking on a flat surface is 0.5x body weight. When we understand this we can understand that by losing weight this will decrease the force through the knees. Losing 10kg will decrease the force through the knee 30-40 N on the stairs. This can significantly decrease load through the knees, and as a result the pain. Looking at physical activity we may see that over time people with OA might have changed their sports from running to cycling. Again this has to do with loads through the knee- running is 4.5-7.6x body weight and cycling is 1.5x body weight. The simple explanation for losing weight or for changing sport would be to decrease the load through the knees, however there is another side to this story too- the metabolic effect of being overweight seems to have a further role to play.

The prevalence of overweight and obese individuals is increasing worldwide. As of 2014, the US National Center for Health Statistics reported that ~70% of Americans are overweight with almost half further defined as obese. Other regions of the world reported to have an increase of excessive weight and obesity in adults, as of 2008, include Southern and Central Latin America (~63% overweight, ~25% obese), Western and Eastern Europe (~48% overweight, ~23% obese), South Africa (~48% overweight, ~28% obese) and North Africa and Middle East (~60% overweight, ~28% obese)(Santangelo et al 2016). Obesity can be measured with BMI, waist circumference and waist to hip circumference. A BMI from 25-29.9 is considered overweight and a BMI of 30+ is considered obese. Looking at waist circumference, a waist more than 80cm in females and 90cm in men is considered indicative of abdominal obesity. Obese and overweight individuals are 3x more likely to develop OA than lean individuals. OA affects both load bearing (hips, knees, ankles and lumbar spine), and non load bearing joints (shoulders, thumbs and hands). It is the effect on non load bearing joints that suggests a link between obesity and OA which may be due to systemic factors and has implicated the biological role of adipose inflammation and metabolic abnormalities of OA, rather than just extra load through the joints i.e. “the wear and tear” argument.

Much like BMI, type-2-diabetes is also associated with progression of knee OA. As measured via joint space narrowing, type-2-diabetes is associated with disease progression of OA (Santangelo et al 2016). Consistent with this, high hemoglobin A1c (HBA1C) is associated with a greater risk for OA disease progression. In addition, insulin resistance is also associated with OA prevalence. Zhen et al (2015) concluded from their review that the risk of knee OA increases by 35% with a 5 kg/m2 increase in BMI. Subgroup analysis showed that obesity was an independent predictor of knee OA. Weight reduction from the point of view of decreasing the load through the joint is helpful, but also considering the potential metabolic reaction, there is also a benefit. An expanding waist line is a sign of abdominal obesity and is often an sign of carbohydrate intolerance and insulin resistance. Phil Maffetone in his blog, Carbohydrate intolerance and the two week test describes the stages of carbohydrate intolerance.

Many of our patients present with hypercholestrolaemia (high cholesterol), hypertension (high blood pressure), carbohydrate intolerance or insulin resistance and an increased BMI. A blog from Arthrits.org explains how Osteoarthritis and obesity are linked.

Su et al (2016) in a Korean study found that in women, high fat mass and low lower extremity muscle mass were associated with presence and severity of knee OA. Lower extremity muscle mass was more closely correlated with knee OA than obesity in women.

Urban et al (2018) looked at obesity as being a key risk factor in the OA incidence, progression and symptom severity. The identification of inflammatory mediators such as adipokines in OA has further incriminated the role of adiposity. Urban et al looked at adiose-derived inflammation in OA.

Local factors in joints have also been shown to play a role in OA (Santangelo et al 2016). Santangelo et al looked at the infrapatellar fat pad (IFP), which serves as a source of local inflammatory factors. Overall, studies support the concept that metabolic effects associated with systemic obesity also extend to the IFP, which promotes inflammation, pain, and cartilage destruction within the local knee joint environment, thus contributing to development and progression of OA.

The problem with weight loss is where to start. I have learnt that there is no one size fits all. Understanding food and its relation to your health is a journey, sometimes you can start the journey alone, and sometimes you need support. If you have specific health issues e.g. diabetes, on medication you need to discuss this with your GP so they can help you with the journey and adjust medication as needed. You may also need to use the help of a dietician who would be a partner in the journey.

I hope I have provided some food for thought, and that weight loss in osteoarthritis is more than just decreasing load though your joints. It is about looking at your overall health. I will end with a quote from the real meal revolution website:

“Eat vegetables, meat, nuts, seeds, little fruit and minimal starch. Eat real fats. Avoid sugar, grains, seed oils and processed food. Taste new dishes. Protect your gut. Eat when hungry. Drink when thirsty. Fast occasionally. Sleep well. Exercise. Relax. Socialise. Listen to your body. Escape routine. Seek adventure. Keep improving.”

Useful resources

References:

Alentorn-Gell E, Samuelsson K, Musahl V, Green C, Bhandari M, Karlsson J (2017) “The association of recreational and competitive running with hip and knee osteoarthritis: a systematic review and meta-analysis” Journal of orthopaedic and sports physical therapy, volume 47 (6) p 373-390 doi:10.2519/jospt.2017.0505
Santangelo K, Radakovich L, Fouts J, Foster M (2016) “Pathophysiology of obesity on knee joint homeostasis: contributions of the infrapatellar fat pad” Published Online: 2016-01-22 | DOI: https://doi.org/10.1515/hmbci-2015-0067 Pathophysiology of obesity on knee joint homeostasis: contributions of the infrapatellar fat pad
Suh DH, Han KD, Hong JY, Park JH, Bae JH, Moon YW, Kim JG. 2016 “Body composition is more closely related to the development of knee osteoarthritis in women than men: a cross-sectional study using the Fifth Korea National Health and Nutrition Examination Survey (KNHANES V-1, 2). Osteoarthritis Cartilage” Apr;24(4):605-11. doi: 10.1016/j.joca.2015.10.011. Epub 2015 Oct 27
Zheng H, Chen C (2015) “Body mass index and risk of knee osteoarthritis: systematic review and meta-analysis of prospective studies.” BMJ Open. 2015 Dec 11;5(12):e007568. doi: 10.1136/bmjopen-2014-007568.
Urban H, Little CB. (2018) “The role of fat and inflammation in the pathogenesis and management of osteoarthritis” Rheumatology (Oxford)Feb 9. doi: 10.1093/rheumatology/kex399.