The FDA's Approach To The Treatment Of Arthritis
Mainstream medicine, which works through the U.S. Food & Drug Administration (FDA), treats arthritis patients with corticosteroids and non-steroidal anti-inflammatory drugs (NSAIDs), such as Motrin (Upjohn), Clinioril (Merck, Sharp & Dohme), and Indomethacin (Lederle). While these drugs can be of benefit in the short-term, they produce serious side effects such as gastric ulceration along with liver and kidney damage. Estimates are that conventional arthritis drugs kill over 7,000 Americans and cause 70,000 hospitalizations a year! Worst of all, long term use of many of these drugs results in complete joint immobilization, as these drugs fail to treat the underlying cause of most forms of arthritis. FDA-approved drugs exacerbate catabolic cartilage breakdown and prevent the expression of natural anabolic repair.
NSAIDS block the production of certain prostaglandins that contribute to the destructive arthritis process. Prostaglandins are the products of the breakdown of polyunsaturated fatty acids to arachidonic acid. Although prostaglandins can promote inflammation, they can also inhibit it, and are necessary for many life processes. The problem with NSAIDs is that they inhibit prostaglandins throughout the body. This can be a problem in the gut, where prostaglandins are necessary for the integrity of the mucous; hence, ulcerative conditions can develop. They can also have liver and renal toxicity.
Scientists have observed that, the higher the dose of FDA-approved anti-inflammatory drugs, the faster the loss of joint function!
In many cases, conventional arthritis drugs provide very little relief, as patients are switched from one expensive prescription drug to another in a desperate attempt to relieve their pain and inflammation, or to alleviate an adverse side effect that a particular drug may have caused.
European doctors have been using non toxic, natural therapies to treat arthritis with great success for many years. These natural therapies work because they treat the underlying degenerative process affecting the linings of the joints and/or improve the autoimmune disorder that is destroying the joint linings.
The Causes Of Arthritis
The cartilage in our joints is vulnerable to a wide range of insults that can result in cartilage degeneration, including bacterial infection, free radical damage, and autoimmune attack. The attack on the cartilage in our joints intensifies as we grow older. First our immune system becomes so dysfunctional that it turns on the body it has been designed to protect. Next we have the age-related breakdown of our antioxidant enzyme systems, which permits uncontrolled free radical activity to attack the cartilage in our joints. Then there is our increasing susceptibility to bacterial (and viral) infection, and the subsequent diminishment of our ability to fight off these infections. Finally, there is our age-related decline in our ability to repair the cartilage in our joints.
Among the common reasons for the arthritic breakdown of bone, cartilage and synovial fluid are:
- Dysregulation of proinflammatory cytokines (autoimmune phenomena).
- Free radicals generated by cytokines and the breakdown of antioxidant defense systems.
- Bacterial and viral infections.
- Anatomical misalignment of joints.
- Traumatic injury from accidents.
- Atherosclerosis in cartilage blood vessels.
- Long-term use of FDA-approved anti-inflammatory drugs.
A cause and a result of joint injury is the formation of free radicals generated by pro-inflammatory cytokines that physically attack and degrade the cartilage and lubricating synovial fluid within the joint. These free radicals stimulate osteoclasts, cells which break down bone. They can trigger a cascade of autoimmune events that contributes to the chronic loss of cartilage structure and function, which conventional doctors usually accept as the normal, irreversible aging-related progression of arthritis. Newly published research indicates that a deficiency of antioxidant enzymes and other compounds often is a factor in the development of arthritis. While dietary antioxidants can be of help to some early-stage arthritis patients, more direct anti-arthritis therapies are required for those whose joint degeneration has progressed significantly further.
Protecting Yourself From Arthritis
In order for osteoarthritis to be treated effectively, the cartilage and synovial fluid in the joint must be protected against further destruction. At the same time, it is desirable to stimulate anabolic restoration of joint cartilage and synovial fluid.
Chondroprotective agents protect and restore joint cartilage by:
- Supporting and enhancing anabolic chondrocyte synthesis.
- Supporting or enhancing the synthesis of synovial fluid, which is required to lubricate the joint.
- Inhibiting free radical enzymes and autoimmune processes that degrade joint cartilage.
- Removing blockages in blood vessels leading to the joint.
Chondroprotective agents are compounds the body manufactures naturally in order to regenerate cartilage and healthy joint function. Aging and trauma disrupt the body's ability to use its own chondroprotective agents, which has led to an epidemic of arthritis throughout the world.
Chondro-protective agent number one
Glucosamine is used extensively in Europe to treat osteoarthritis. Numerous published studies document glucosamine's ability to function as a chondroprotective agent.
Glucosamine provides the raw material needed for chondrocytes to regenerate cartilage. A glucosamine deficiency caused by aging and/or trauma leads to osteoarthritis. The oral consumption of glucosamine salts provides the raw material needed for joint cartilage synthesis and repair.
In nine European studies, the oral administration of glucosamine produced major reductions in joint pain, joint tenderness and joint swelling. Improvements in joint function and overall physical performance were noted in these studies compared to placebo and/or the drug ibuprofen. While ibuprofen worked faster than glucosamine in relieving pain, glucosamine imtributed in the joint cartilage matrix.
While the studies show that glucosamine takes 4-10 weeks to produce noticeable results, the new arthritis formula discussed in this article has been producing noticeable reductions in inflammation and pain in most arthritis patients in less than two weeks! This new formula (patent pending) includes two forms of glucosamine, along with EPA, DHA and GLA essential fatty acids.
Chondro-protective agent number two
The Chondroitin Sulfates
The chondroitin sulfates provide the structural components of the cartilage found in the joint. Chondroitin sulfate is a constituent of shark cartilage, which helps to explain the beneficial effects that shark cartilage produces in arthritis patients.
The chondroitin sulfates have been tested extensively in humans with outstanding success as anti-atherosclerotic agents. The FDA has ruled, however, that, since each chondroitin sulfate molecule is different than all other molecules, which makes it impossible to produce a precisely standardized product, it cannot be approved as a therapy. Nevertheless, research studies have provided much useful data on the safety and effectiveness of chrondroitin sulfates in arthritis patients.
When intramuscular injections of chondroitin sulfates were given to arthritis patients, there were major reductions in joint pain and increases in joint function. Chondroitin sulfates inhibit free radicals that degrade joint cartilage and collagen. Chondroitin sulfates also improve blood circulation to joints, which enables antioxidants and glucosamine to enter inflamed joints to stimulate the repair process required for the regression of osteoarthritis.
Protecting Against Cartilage Destruction From Inflammation And Autoimmunity
There is now solid evidence of the value of treating rheumatoid arthritis patients with omega-6 essential fatty acids derived from plants, such as the GLA (Gamma Linolenic Acid) found in evening primrose oil, borage oil, and blackcurrant seed oil and oils rich in the omega-3 fatty acids, EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid). These essential fatty acids are precursors of prostaglandins such as PG1, which have known anti-inflammatory and anti-autoimmune effects, and decrease the activity of pro-inflammatory prostaglandins such as PG2. Here are findings from some of the new studies documenting the benefits of essential fatty acids in treating arthritis:
In the Annuals of Internal Medicine (1993 119/9), the findings of a 24-week, double-blind, placebo-controlled trial with GLA derived from borage oil have been reported. The patients receiving the borage oil experienced a 36% reduction in the number of tender joints, a 45% reduction in the tender joint score, a 41% reduction in the swollen joint score, and a 28% reduction in the swollen joint count. The placebo group showed no benefits.
A paper in the British Journal of Rheumatology (1994 33/9) reports the findings of a 24-week double-blind, placebo-controlled trial in rheumatoid arthritis patients using blackcurrant seed oil rich in gamma linolenic acid (GLA) and alphalinolenic acid. Patients receiving blackcurrant seed oil showed reductions in the signs and symptoms of the disease. The placebo group showed no change in disease status. The researchers concluded that their study showed that blackcurrant seed oil is a potentially effective treatment for active rheumatoid arthritis. No adverse reactions were observed, although some people dropped out of the trial because of size and number of capsules they were required to take.
In Seminars in Arthritis and Rheumatism (1995 25/2), there was a review of all the published literature on the use of gamma linolenic acid (GLA) for the treatment of rheumatoid arthritis. GLA was shown to reduce the effects of autoimmune disease on joint linings, though more research was said to be needed to determine the ideal dose of GLA for arthritis.
A study in the Journal of Clinical Epidemiology (1995 48/11), reviewed all the published studies on the use of fish oil to treat rheumatoid arthritis. They revealed that, in general, after three months of use, there was a significant reduction in tender joint count and morning stiffness in patients receiving fish oils. The placebo groups experienced no relief from pain.
In a study inArthritis and Rheumatism (1995 38/8), rheumatoid arthritis patients stopped taking non-steroidal anti-inflammatory drugs and switched to fish oil. This placebo-controlled, double-blind study showed that the group receiving the fish oil experienced significant decreases in the number of tender joints, duration of morning stiffness, improvements in the physicians' and patients' evaluation of global arthritis activity, and the physicians' evaluation of pain. Patients receiving fish oil exhibited improvement in clinical functions compared to patients receiving placebo. Some patients were able to stop taking conventional arthritis drugs altogether.
These new studies confirm numerous previous reports showing broad-spectrum benefits when arthritis patients take EPA/DHA from fish oil and GLA from borage or blackcurrant seed oil.