Osteoarthritis should be viewed as “heart disease” of the joints

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At first glance, the title of this blog may seem like a preposterous notion; however, it is a fact. Years ago, osteoarthritis (OA) was misperceived to be a wear-and-tear condition of joints, a myth that is still perpetuated today…however, we now know that OA is actually a chronic inflammatory state within joint tissues. Years ago, we also misperceived that heart disease was simply a buildup of cholesterol and other substances on top of the wall of an artery…now we know that heart disease is actually a chronic inflammatory state in the within the artery wall. Consider the title of this article:

Conaghan P et al. Is progressive osteoarthritis an atheromatous vascular disease? Ann Rheum Dis. 2005;64:1539-41.

The answer to the title of this article is “yes.” For all practical purposes, the chemistry of osteoarthritis and atherosclerotic heart disease is identical. The view we should take is as follows: osteoarthritis is “heart disease” of the joints and heart disease is “osteoarthritis” of arteries.

The difficulty that most have when considering this fact is that, to the naked eye, joints and arteries are very different structures. While that is true, it should not detract one from focusing on the chemistry of each condition, which is a shared state of chronic inflammation that is essentially identical.

It is generally known by many people that type 2 diabetes is a risk factor for heart disease. The reason for this is that diabetes is an inflammatory state, which predisposes one to develop related inflammatory diseases, such as heart disease. It is not well known, but equally factual, that people with diabetes are also more likely to develop osteoarthritis (1).

This relationship between diabetes and OA is obvious and becoming more well known, yet it is still difficult for many to conceptualize that OA is heart disease of joints. The fact that must be embraced is that if the inflammatory state of diabetes promotes both heart disease and OA, it means that they have similar causes and similar pro-inflammatory chemistry changes.

As stated earlier, osteoarthritis is misperceived to be a “wear-and-tear” condition that is mostly caused by direct joint injury. Superficially this appears true and is most obvious in athletes with knee injuries. What is lost in this superficial perception is that most people also develop aches and pains in joints that they did NOT injure. So in this case, an ex-running back may have painful OA of the knee due to injury, but also has pain in other joints that were never injured.

The reason OA expresses in non-injured joints as we age involves a “wear and lack of repair” state and has nothing to do with wear-and-tear of joint tissues. How do we know this for sure? Because, in the research setting it was determined that before joints develop OA, their fatty acid profile changes from one that is anti-inflammatory and healing to one that is pro-inflammatory and thus, non-healing and non-repairing (2,3). The outcome is a joint that does not heal over time as a consequence of normal “wear” and can slowly take on the appearance of being “torn” when the joint becomes painful and subsequently viewed at surgery or with radiological imaging (4).

Basic nutritional factors that have been implicated in the expression of osteoarthritis over time include omega-6 fatty acids (2), a lack of vitamin D (5), and a lack of magnesium (6). All of these and more nutritional factors that create chronic inflammation are outlined in The DeFlame Diet. In other words, if you read and understand The DeFlame Diet, you will understand how osteoarthritis, heart disease, and other chronic diseases develop as we age.


  1. Piva SR et al. Links between osteoarthritis and diabetes: implications for management from a physical activity perspective. Clin Geriatr Med. 2015;31:67-87.
  2. Bonner WM et al. Changes in the lipids of human articular cartilage with age. Arthritis Rheum. 1975;18:461-73.
  3. Gkretsi V et al. Lipid metabolism and osteoarthritis: lessons from atherosclerosis. Prog Lipid Res. 2011;50:133-40.
  4. Robinson WH et al. Low-grade inflammation as a key mediator of the pathogenesis of osteoarthritis. Nature Rev Rheumatol. 2016;12:580-92.
  5. Ding C et al. Serum levels of vitamin D, sunlight exposure, and new cartilage loss in older adults. Arth Rheum. 2009;60:1381-89.
  6. Zhang F et al. Magnesium and osteoarthritis: from a new perspective. Ann Joint. 2016;1:29.