How Fat Affects RD

Just when I think I’m safe, it happens again.

Here I am, happily munching chips and allowing myself to wallow in the Internet rabbit-hole when out of the blue, I’m staring at another article about why I ought to put the chips and the laptop down, step away slowly, and start exercising.

It’s fat. Yes, fat, the same substance that makes those potato chips, this bag of French fries, cheese of all kinds, and that perfectly cooked, fried chicken leg taste so sinfully good. Fat, the bane of my existence, second only to rheumatoid disease.

With a sigh, I started reading. It’s what I do. And what is it about fat this time? “What Fat Does to Arthritis,” an article from the medical journal The Rheumatologist, addresses the fact of fat from an entirely different angle. A molecular angle, in fact.

It’s not about fat as a food substance to avoid or even about the harms of excess body weight. It’s about what goes on inside the fat cells themselves. It’s about the substances they produce and how those substances affect other cells and substances which, in turn, affect rheumatoid disease.

The gist:  Fat cells—adipocytes—release molecules called adipokines. These can secrete substances (factors) that are “operative” in the disordered physiological processes associated with inflamed joints. These factors “include tumor necrosis factor (TNF), interleukin (IL)-6, components of the complement system, growth factors, and adhesion molecules,” states the article. “The key prototype molecule … is adiponectin, a member of the complement-TNF superfamily that exerts properties remarkably similar to that of TNF, a central mediator of inflammation with well-known deleterious effects in arthritis.

It goes on to describe how these adipokines, released by fat cells, target other cells that work in chronic rheumatic diseases in a “proinflammatory and matrix-degrading direction.”

Have I lost you yet?

Rheumatoid disease is an autoimmune disorder that causes the body’s immune system to mistakenly attack and destroy its own synovial joints and their surrounding tissues, just as it does malicious foreign invaders like bacteria and viral infections. The autoimmune response causes both widespread and targeted inflammation and, over time, tissue and joint destruction.

Note that RD doesn’t always limit itself to the joints. It may also affect other synovial tissues like the linings of the heart, lungs, vascular system, skin, kidneys, and even the eyes.

How do the adipokines released by fat cells influence RD? Scientists have known for some time that TNF and the other factors above play a big part in the disease process. Per the article, levels of adiponectin are high in the synovial fluid and serum (the fluids within the rubbery synovial capsule that cushion the bones of the joints as they move). Scientists have related these high levels of adiponectin to joint destruction and long-term disease.

The good news is that these discoveries are opening the possibility of new, better, and more targeted treatments for RD as scientists learn more. Already they’ve developed anti-TNF biologic drugs that have, in some RD patients, relieved symptoms and slowed or halted the progress of the disease. Other such biologic drugs, which are unique in that they contain living molecules that target other molecules in the body, either available or under research and development.

In the end, this article didn’t mention fat at all in terms of overweight or obesity, though both can affect RD symptoms. Might those of us with more fat cells have even higher levels of inflammation because of the adipokines they produce? Maybe, but this article didn’t address or suggest that.

Nor did it address the most obvious problem with fat, at least to patients: being overweight or obese strains and stresses the weight-bearing joints of the hips, knees, ankles, and feet. That stress can worsen inflammation and joint destruction, and cause disability.

That alone is a good reason to work on maintaining a healthy weight for your height and build.

I’m endlessly curious about rheumatoid disease, and I like getting into the scientific weeds surrounding it. I’m passing it along to you just in case you’re like me. There’s a lot in the article to absorb—and it sent me, delighted, right down the Internet rabbit hole as I looked up the scientific terms, etc.—but it was worth it.

I’m so encouraged to know that medical science hasn’t forgotten or abandoned us. One day, they’re going to find a cure.

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This article represents the opinions, thoughts, and experiences of the author; none of this content has been paid for by any advertiser. The team does not recommend or endorse any products or treatments discussed herein. Learn more about how we maintain editorial integrity here.

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