DAVID WELLS BSc. (Hons) Ost., cert. ICAK

 

Understanding ARTHRITIS, part 2

 

The previous article focused on Osteoarthritis (OA), in this article we look at how Rheumatoid Arthritis (RA) is distinct from OA. There are similarities and RA may lead to OA, but not the other way around.

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​Rheumatism is classed as a connective tissue disorder; its primary target is connective tissue such as joint capsules and ligaments. The joint capsule seals the joint and ligaments prevent them bending beyond their normal range of movement. If you ever twisted your ankle badly and found it swollen and blue the following day, that's because the ligaments or joint capsule were damaged in the injury. It's worse than muscle damage because the tissues don't repair so quickly.

 

RA is a systemic condition, meaning it is the product of some underlying health issue. It is believed there is an inherited factor predicting why some develop the condition, usually in later life, affecting women more than men. A blood test looks for the presence of the Rheumatoid Factor (RF), although curiously it is not always present in cases where RA has been diagnosed, and conversely its confirmed presence does not always produce symptoms. One has to wonder, if RF is not a certainty in the condition, what else is going on. In addition, a raised ESR level, always seen in RA, indicates the undeniable presence of inflammation, and inflammation is only present when there is damaged tissue. So, if ESR goes up, we know somewhere in the body tissues are damaged (not just in the fingers, it could be anywhere).

 

As seen in the x-ray below, RA produces a characteristic 'mole' hands distortion of the fingers, the most commonly affected joints. Damage to the joint capsules and ligaments causes this distortion, leaving the joints a bit lax, and therefore at risk or cartilage damage and osteoarthritis as well, in advanced cases.

 

So what causes this connective tissue disruption?

There has been a lot of research into answering this question, which I am not going to delve into here. I will just note that to date the standard clinical response to RA is still, long-term non-steroidal anti-inflammatory drugs (NSAIDS) like neurofen, and in more advanced cases, steroids; powerful natural anti-inflammatory chemicals. To my mind if the real cause had been identified clinically, sufferers would not be expected to use long-term anti-inflammatory drugs, which deal only with the symptoms. There are also drugs which aim to suppress immunity, recognizing there is immune system involvement in RA, but that seems to overlook an obvious clue. If the immune system is involved it must have been triggered by something. Immune system chemistry is outrageously complicated so I am over-simplifying this here just to make a point. The immune system is triggered by special receptors in the blood recognizing, or not recognizing, other things floating around in there. It is said, even in some clinical books, that it's as if the immune system is attacking itself. But is that really logical?

 

Here's another perspective.

Again, think 'broad brush' here, don't get bogged down by electron-microscopic analysis. The immune system identifies entities in the blood it doesn't like the look of, and rather than stopping to carry out an investigation, it shoots first and asks questions later. Once the immune system is triggered, a chemical barrage is released to deal with the foreign invaders and any damage they may cause. This includes pain inducing inflammatory chemicals and, as we noted in the previous article, sticky red blood cells blocking capillaries and starving their target tissues of nutrition.

 

Let's suppose blood test results show your white blood cell (WBC) count is within parameters. WBCs are the cells which gobble up foreign invaders in the blood and tissues. So if their number is about normal we might conclude there are no obvious infections going on. Hence another trigger must be identified. In my experience from years of testing sufferers of RA, that trigger comes primarily from the food. If you consume and digest something your body doesn't like it may be identified as 'foreign' by the immune system producing an immune response just as if you had an infection. If this process happens repeatedly and frequently for years, and you happen to have genes which predispose you to connective tissue disorders, your body releases a different set of inflammatory chemicals; chemicals far more potent than those which deal with a simple cut finger. Those chemicals are very destructive to connective tissues.

 

To give credence to this idea, again in my experience, sufferers of RA get significant relief by identifying and cutting out the problematic foods. This prevents the immune system triggers and slowly allows long-standing inflammatory conditions to subside. This is what we mean by food intolerances. They are not true allergies, but share similar responses. There are other factors to consider with intolerance however, because certain underlying health problems may increase the risk of these allergy-like symptoms. Parasitic infections cause all manner of complications and often remain undetected by blood or stool tests. Gut dis-biosis and therefore liver toxicity also elevate the chance of immune system flare-ups.

 

Looking at RA from this perspective should give you hope that you can halt its progress. All you need to do is find well hidden parasites or other toxins and clear them out. Then identify the wrong foods and stop eating them. This gives bowel function a chance to return to normal. Follow this with a proper gut cleanse so you don't re-absorb years old waste back into the bloodstream, and enjoy a life without anti-inflammatory drugs!

 

Article by David Wells 2021

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The perspective shared in this article comes not just from medical training but from symptoms and treatment protocols observed over more than 20 years of clinical experience.

 

If you found this article interesting, this topic and many more are explained in depth in the book, 'Finding Awesome: Proven Steps to Extraordinary Health'. Read more about it here.