~Arthritis, part 2 - Beyond Drugs

~Arthritis, part 2 - Beyond Drugs
When Conventional Drugs Are Not Enough

A problem identified by LEF is that high levels of TNF-alpha may persist even in people receiving Enbrel drug therapy. Even if Enbrel brings TNF-alpha down to a safe range, other inflammatory cytokines (such as IL-6 and IL-1b) may continue to wreak havoc throughout the body.

High levels of TNF-alpha are destructive to many vital tissues such as joint cartilage (e.g., RA) and heart muscle (e.g., congestive heart failure). Excess IL-6 and other inflammatory cytokines attack bone and cartilage and promote the formation of fibrinogen that can induce a heart attack or stroke via several established mechanisms (di Minno et al. 1992).

In order to prevent and treat the multiple diseases of aging, it is critical to keep these destructive immune chemicals (cytokines) in safe ranges. The chart found in the Summary section of this protocol relates the currently determined safe ranges of inflammatory factors as measured by blood levels.

Supplements such as DHA fish oil, nettle leaf extract, vitamin K, and DHEA have been shown to suppress the dangerous cytokines, TNF-alpha, IL-6, IL1b, and the proinflammatory eicosanoid LTB4. We discuss these supplements in detail later in this protocol. For those whose blood tests reveal persistently high inflammatory cytokine levels despite taking these supplements, a low-cost prescription drug may be of enormous benefit.

The generic name of this drug is pentoxifylline (PTX); the brand name is Trental. It was first used in Europe in 1972 and long ago came off patent (meaning it is not cost-prohibitive). PTX is prescribed to improve the flow properties of blood by decreasing its viscosity. It works by improving red blood cell flexibility, decreasing platelet aggregation, and reducing fibrinogen levels (Manrique et al. 1987; di Minno et al. 1992; de la Cruz et al. 1993; Gara 1993; Gaur et al. 1993). PTX has fallen out of favor because no drug company has the economic incentive to market it to physicians. PTX is primarily prescribed to patients with peripheral artery disease, although we believe it has potential efficacy in treating a wide range of diseases relating to chronic inflammation.

Numerous studies show that PTX is a potent inhibitor of TNF-alpha, IL-1b, IL-6, and other proinflammatory cytokines (Neuner et al. 1994; Blam et al. 2001; Pollice et al. 2001). A similar number of studies show that DHA fish oil suppresses these same cytokines (De Caterina et al. 1998, 1999; Das et al. 2000; James et al. 2000; Kelley et al. 1999; Kremer 2000; Watanabe et al. 2000). In people suffering from the effects of a chronic disease involving elevated levels of the inflammatory cytokines, the daily administration of 800 mg of PTX or 1000-2000 mg of DHA fish oil could be of enormous benefit.

The first line of defense in protecting against excess proinflammatory cytokine activity is proper diet and use of appropriate cartilage-protecting supplements. We will discuss antiarthritic diets next. For arthritic patients who are unable to obtain relief via dietary modification and supplements, we suggest that PTX be considered as a cytokine-suppression therapy.

Why does your physician not tell you about PTX? The reason is that the FDA prohibits the companies that manufacture PTX from distributing off-label information about its potential antiarthritic benefits. Life Extension can provide this information because we do not sell PTX. Before taking PTX, refer to the precautions that we list at the end of this protocol.

Convincing a physician to prescribe PTX as an adjuvant therapy for arthritis can be difficult. That is why most people first choose to try natural therapies that have a proven track record of safety and efficacy.

Diet and Inflammation

Dietary modification can help block common inflammatory pathways involved in cartilage destruction. One such pathway involves overproduction of proinflammatory hormone-like messengers (such as PE2) and underproduction of anti-inflammatory messengers (such as PE1 and PE3).

Omega-3 fatty acids found in fish oil help to suppress the formation of undesirable PE2 and promote synthesis of beneficial PE3 (Kelley et al. 1985; Wanatabe et al. 2000). GLA induces the production of the anti-inflammatory PE1 (Das et al. 1989; Fan et al. 1997). Diet can significantly affect whether you have more of the beneficial prostaglandins (E1 and E3) as opposed to the proinflammatory PE2.

Since PE2 is a culprit in inflammation, reducing the consumption of foods that are high in omega-6 fatty acids (such as meat and egg yolks) and increasing omega-3 rich foods, such as salmon and other fish, can be beneficial. Limiting foods that convert to arachidonic acid can help reduce inflammation. Arachidonic acid is a precursor to both PE2 and the proinflammatory eicosanoid LTB4 (Brock et al. 1999). Another dietary factor that can lead to high levels of arachidonic acid is overconsumption of high-glycemic index carbohydrates that causes an excessive production of insulin (Kreisberg et al. 1983)

Foods that may contribute to chronic inflammation are foods with a high glycemic index (foods that digest quickly), such as fruit juices or rice cakes, foods heavy in polyunsaturated or saturated fats, and foods high in arachidonic acid. Some specific foods to avoid are:

  • Fatty cuts of red meat (high in saturated fats)
  • Organ meats: liver, kidney, and so forth (high in arachidonic acid)
  • Egg yolks (high in arachidonic acid)
  • Pasta (high glycemic index)
  • Juices (high glycemic index)
  • Rice, especially rice cakes (high glycemic index)
  • White bread (substitute whole grain breads such as rye or whole wheat)

Better choices are foods with a low glycemic index and foods that are heavy in monounsaturated fats. Some specific good foods are:

  • Salmon and other fish
  • Oatmeal
  • Fresh fruits and vegetables
  • Olives and olive oil
  • Peanuts and other nuts
  • Whey proteins

Food and arthritis have long been connected in the field of alternative medicine. Many nonconventional practitioners think that fasting and attention to diet could cure arthritis. For some persons with arthritis, these relatively simple dietary changes may have a beneficial impact.

For those who do not find effective relief from simple dietary changes, the addendum at the end of this protocol entitled Food and Arthritis discusses radical changes that can be made in the way one eats. We understand that many people will not be able to follow these kinds of aggressive changes in eating patterns. For persons with arthritis who are unable to substantially alter their diet, we next discuss specific natural approaches that have shown significant improvements in human clinical studies.

Osteoarthritis and Rheumatoid Arthritis

While OA and RA are medically classified as different diseases, for the purposes of this protocol, the therapies for each are similar. Our primary treatment objective for either OA or RA is to suppress the known proinflammatory factors (PGE2, TNF-alpha, IL-1b, LTB4, and IL-6) through a combination of diet, dietary supplements, and, if necessary, certain prescription drugs.

OA is a disease mainly characterized by degeneration of the articular cartilage but these changes also involve the synovial membrane and the bone next to the cartilage. It is a gradual decay that most often affects the weight-bearing joints (knees, hips, and spinal joints) and the joints of the hand. A breakdown of the cartilage matrix leads to cracks and ulcers and a thinning of the cartilage with a loss of shock absorption. The underlying bone starts to thicken as a response to the increasing stress, and bone spurs are formed. In the advanced phases of OA, an inflammatory reaction in the synovial membrane can be seen. This severe degeneration causes pain, swelling, deformation, and reduced range of motion. Because the joints of the hand and the large joints of the spine, hips, knees, and ankles are frequently involved, disability is significant. OA comes with the normal processes of aging and affects approximately 70-80% of the population over age 50. The onset is marked by stiffness, crackling joints, and pain. As it worsens, more pain and disability occur causing an enormous consumption of painkillers and anti-inflammatory drugs that many times have undesirable long-term effects.

RA is considered an autoimmune disease, characterized by chronic inflammation and thickening of the synovial lining in addition to cartilage destruction. In autoimmune diseases, the immune system attacks body tissues as if they were foreign invaders. The etiology and pathogenesis of RA is considered directly related to a chronic inflammatory syndrome. Contributing factors are thought to include food allergies, leaky gut syndrome, hereditary factors, and microbes.

RA strikes women 3 times as often as men. The clinical picture varies from mild chronic joint inflammation with occasional flareups to painfully deformed joints. Involvement of the small joints of the hands and feet are often the key to the diagnosis. Low-grade fever, weight loss, and a general feeling of sickness, fatigue, and joint deformities and pain often accompany the disease. There can be anemia and other health problems that are a result of the underlying chronic inflammatory syndrome. Most sufferers (90%) have a positive rheumatoid factor in the serum.

Scientists have identified underlying factors involved in the pathology of both OA and RA. This published research has enabled novel natural therapies to be developed that work along multiple pathways. These natural agents have an extraordinary safety profile and a long track record of clinical success.

Continued . . .

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