How fat cells can worsen arthritis

Fat cells secrete leptin, which activates NF-kappaB, resulting in inflammation

Osteoarthritis has been called “wear and tear” arthritis. But that’s somewhat misleading. Osteoarthritis results not from years of use, but from years of chronic, low grade inflammation.

Yes, mechanical stress (the pounding your knee joint takes every time you walk or run) does cause mild inflammation. But that inflammation would normally resolve quickly and entirely. When it doesn’t – when your body can’t entirely turn off the inflammation – chronic inflammation results.

Chronic, mild inflammation eventually progresses to chronic severe inflammation. Osteoarthritis results when that inflammation begins causing pain.

One reason your body might have trouble turning off the inflammation is “leptin.”

Leptin is produced by fat cells. It stimulates NF-kB, resulting in inflammation. And, with high levels of leptin constantly in circulation, it keeps NF-kB, and inflammation, from ever fully turning off.

That’s why excess weight results in a higher incidence of osteoarthritis not only in the knees, but in the hands, shoulders, and every other joint in your body.

Basically, the inflammation stimulants (leptin is only one of many) have overwhelmed the inflammation inhibitors – which is why most of us are walking around with chronic, low grade inflammation – leading to a higher incidence of osteoarthritis, Alzheimer’s, cancer, autoimmune disease, and a nearly endless list of inflammation related ailments.

The solution is simple. Reduce inflammation stimulants (through weight loss and lifestyle changes) and add inflammation inhibitors (e.g. eat more fruits and vegetables.)

The publication:

August, 2009

Leptin enhances synthesis of proinflammatory mediators in human osteoarthritic cartilage–mediator role of NO in leptin-induced PGE2, IL-6, and IL-8 production.

Obesity is an important risk factor for osteoarthritis in weight-bearing joints, but also in hand joints, pointing to an obesity-related metabolic factor that influences on the pathogenesis of OA.

Leptin is an adipokine regulating energy balance, and it has recently been related also to arthritis and inflammation as a proinflammatory factor. In the present paper, the effects of leptin on human osteoarthritis cartilage were studied.

Leptin resulted in the production of pro-inflammatory mediators.

The effects of leptin are mediated through activation of transcription factor nuclear factor kappaB (NF-kB.)

These findings support the idea of leptin as a factor enhancing the production of pro-inflammatory factors in osteoarthritis and as an agent contributing to the obesity-associated increased risk for osteoarthritis.


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