CHAPTER 10

Rheumatoid Arthritis

images A five-thousand-year-old mummy found in Egypt has been identified as the remains of a Syrian immigrant who had suffered greatly from the swollen fingers, knees, and feet typical of rheumatoid arthritis (RA). If he was seeking pain relief, he should have headed up to Greece, where the herb willow bark (an herbal predecessor of aspirin) was in favor long before Hippocrates recommended it, around 400 BC.

What’s curious—besides the fact that the ancient remedies have not been improved on all that much today—is that the father of medicine identified rheumatoid arthritis as a disease of men. Around AD 2, his follower Soranus of Ephesus noted that it occasionally occurred in women but never in eunuchs. Given the shortage of eunuchs today, statisticians can collect little data on RA incidence among them. However, they report that RA is now three times more common in women than men.

This fact, plus a paucity of rheumatoid arthritis references in the Bible, art, or literature up to the early twentieth century, leads many experts to conclude that the disease has not only increased but changed with modern civilization. The rare early evidence of rheumatoid arthritis may, in fact, represent special cases of gout combined with osteoarthritis. Although references to swollen, deformed joints make people think of RA, sure diagnostic techniques were not available until the advent of the X-ray machine in 1900 and the identification of the so-called rheumatoid factor in blood in 1948.

Today the disease is commonplace enough to affect between 1.3 and three million people in the United States alone. The numbers depend on who is counting and who is being counted. The statistical difficulty is considerable given the fact that the course of this disease is both variable and erratic. Indeed, there are so many variations of rheumatoid arthritis that some scientists wonder whether it is a single disease or a collection of discrete symptoms with features in common. The one group counted without fail are those who fall prey to a vicious form of the disease that progresses until the joints become painfully deformed and possibly dislocated and body organs harmed. The result can be complete invalidism.

Members of the public sometimes confuse osteoarthritis and rheumatoid arthritis, but there are substantial differences. RA is primarily a disease of the soft tissue, one reason the only proof of it in early humankind is found in mummified as opposed to skeletal remains. Unlike osteoarthritis, RA generally affects both sides of the body symmetrically—both hands, both knees, are affected. Also unlike OA, it tends to come on suddenly and appear as a waxing and waning condition. Although people with OA also have their ups and downs, their disease generally progresses steadily over time. Yet another difference is that RA usually first attacks between the ages of twenty and forty, although older persons and children are occasionally afflicted.

What brings on rheumatoid arthritis? Theories abound, but no one knows for sure. Some people believe the disease originates with bacteria or is triggered by bacteria or viruses. Whatever the cause, the initial infection is followed by an immunologic overreaction that perpetuates the disease. That makes it an autoimmune disease in which the body’s own immune system mistakes its very own tissues for foreign invaders and attacks them.

Synovitis—an inflamed joint lining—is the classic sign of RA. It is caused by armies of white blood cells that overreact to the triggering inflammation. They then multiply prolifically, stick around too long, and cause the normally thin, smooth inner membrane known as the synovium to become abnormally thick and swollen. The synovial fluid, which is usually transparent like raw egg whites, thickens into pus and eventually dries out. Adding injury to the insult, the renegade white blood cells also release enzymes and growth factors that cause runaway growth of the synovial membrane. Once it is built up it becomes known as a pannus and may start to invade and destroy the cartilage, bones, tendons, and ligaments. No wonder there is so much pain, swelling, and burning!

Seeking a Cure

Can broth help rheumatoid arthritis? Anecdotal evidence and clinician reports suggest it can, although we do not have much hard science. Gelatin researcher Nathan R. Gotthoffer apparently found nothing on RA, though gelatin’s effect on infectious diseases suggests the potential for prevention if RA is precipitated by either a bacterial or a viral attack as many researchers believe; or, as we’ll discuss later in this chapter, if RA is actually caused and perpetuated by pleomorphic bacteria in the cartilage as per the controversial theory of the late Thomas McPherson Brown, MD (1906–1989).

Whatever its cause, over the past fifty years, bovine tracheal cartilage, chicken sternal cartilage, and collagen hydrolysate have all been successfully employed in RA treatment. Unfortunately, the studies have been limited, and the most rigorous of them showed success through injection and at therapeutic doses far in excess of what is ever found in broth. That doesn’t mean that broth can’t help with RA—we’ve heard from many people that it does, and it’s something that every sufferer should try.

An indication that broth might work came from John F. Prudden, MD, DSci, in 1970 when he decided to test bovine tracheal cartilage on rheumatoid arthritis patients. At the time, he simply hoped its anti-inflammatory powers would stave off pain and possibly halt the self-perpetuating progression of the disease. To his complete surprise, his first case proved the soundness of his theory—and more. Injected cartilage actually healed the diseased joints of his first nine rheumatoid arthritis patients.

In a major article published in Seminars in Arthritis and Rheumatism in 1974, Dr. Prudden reported the cases of nine rheumatoid arthritis patients ages forty-three to sixty-nine. Each had been injected with 500 cc of bovine cartilage for ten to thirty-five days, followed up by booster shots at three-to four-week intervals. As most doctors will attest, RA patients respond very slowly to medications. This was the case with Dr. Prudden’s patients as well. Indeed, most became temporarily worse, perhaps experiencing what natural healers often call a “healing crisis.” This generally turns the tide of the illness, and those who manage to grin and bear it tend to eventually see dramatic improvements. Of Dr. Prudden’s nine cases, three improved from severe to excellent and the remaining six improved from severe to good.

What’s most striking about this success is that many of the patients had already experienced either the destruction or the partial destruction of some of their major joints. Several had undergone artificial joint replacements, fusions, and other serious surgical procedures. Even so, Dr. Prudden was able to report that “there was no patient who did not show what was considered by us and the patient as either an excellent or good response.” And there were no unfavorable side effects.

Because Dr. Prudden used injections, the anti-angiogenic factors in cartilage can be credited with some of the good effect. Anti-angiogenic means the inhibition of blood vessel formation and growth. Abnormal capillary growth into cartilage, after all, begins the destruction of joint cartilage. Oral cartilage supplements—bovine, chicken, shark—would not be expected to work as well or even at all because the anti-angiogenic factors are destroyed in the gut by digestive enzymes. The same, of course, would be true of broth or gelatin. This does not make Dr. Prudden’s findings irrelevant, however; rather, it suggests added benefit from the injections, especially for people with advanced cases of RA or other autoimmune diseases. In fact, oral therapies using bovine tracheal cartilage, shark cartilage, type II collagen, collagen hydrolysate, and glucosamine have all shown benefits to patients with RA.

During his lifetime, I. William Lane, PhD, of Sharks Don’t Get Cancer fame, marketed shark cartilage for RA as well as for cancer and other diseases. Although Lane’s trumped-up claims for anti-angiogenesis from oral use were roundly dismissed by Judah Folkman, MD, the scientist who founded the field of angiogenesis research, useful mucopolysaccharides and other active components are found in all cartilages. Studies on shark cartilage for RA are scant, but a 2012 study from the Institute of Pharmacy, Shandong Traffic Hospital in Jinan, China, showed benefits for rats in terms of improved joint alignment and smooth articular surface.

Not surprisingly, glucosamine has been tried on RA, not only because it can repair cartilage—as discussed in chapter 9 on osteoarthritis—but because of its track record of lowering circulating levels of TNF-α and C-reactive protein, two biomarkers used to measure the progression of RA and other inflammatory disorders. In a study published in ISRN Pharmacology in 2013, rats treated with glucosamine showed not only reduced levels of those biomarkers but also reduced histopathological changes in the joints. The researchers concluded that glucosamine suppressed the chronic inflammatory phase of RA and obtained a “rapid and significant beneficial effect.”

Overall, the studies on glucosamine are inconsistent, whether researchers are trying it on osteoarthritis, rheumatoid arthritis, or other diseases. That fact has led researchers to try all manner of doses as well as combinations with other remedies. In 2012, a team from the Juntendo University Graduate School of Medicine in Tokyo tested glucosamine, methionine, and a combination of glucosamine plus methionine on rats. They determined glucosamine and methionine each worked in minor fashion alone, but much better in combination, a result that suggests to us the need for a traditional diet balanced in methionine-rich muscle meats as well as collagen-rich skin and bones. Rat chows based on soy protein would be low in methionine unless extra has been added.

Given that glucosamine cannot be patented, it is not surprising that researchers have tried to improve on it. Accordingly, the Pharmacology Unit at the International Center for Chemical and Biological Sciences at the University of Karachi, Pakistan, “took an interest in the synthetic manipulation of amino sugars to develop some efficient pharmacophores.” Because good old glucosamine had not proved good “enough to combat severe inflammatory RA,” they came up with a “novel synthetic analogue” and tested it on rats. In Inflammation Research, they announced β-D-glucosamine had both anti-arthritis and anti-inflammatory properties and could be useful in the treatment of rheumatoid arthritis.

Oral Tolerance Therapy

In a very different approach to RA, collagen type II is used for a therapy called oral tolerance or oral tolerization. Basically patients are fed the “hair of the dog”—small amounts of collagen II. The idea is to help them tolerate their own collagen and shut down the body’s overreactive autoimmune rejection system. Study results suggest that a daily dose of broth might be just the thing for overcoming the immune reactions that occur in RA.

Oral tolerance therapy came about when researchers realized healthy people rarely mount an immune response to food. As explained by medical writer Thomas H. Maugh II in the Los Angeles Times, “If a calf’s liver is transplanted into a human, it is quickly and violently rejected because the body recognizes proteins in the liver as foreign and attacks them. But if the organ is fried and eaten, those same proteins are easily absorbed. That’s because the stomach and intestines have their own branch of the immune system, an unusual mechanism that suppresses, rather than triggers, immune responses to foreign material. Without it, we would not be able to eat meat and many other foods.”

In 1993, in the journal Science, David E. Trentham, MD, of Harvard Medical School and Beth Israel Hospital in Boston, published the results of a randomized, double-blind trial. He and his colleagues treated sixty patients with severe active rheumatoid arthritis with small doses of chicken sternal cartilage for a month and then an increased dose for the next two months. Both the treatment group and the placebo group had similar demographics and clinical and laboratory measures. Dr. Trentham measured objective improvements in the number of swollen and tender joints, morning stiffness, walking time, grip strength, Westergren erythrocyte sedimentation rate, and subjective physician and patient assessments. All these patients had been on serious immunosuppressive and anti-inflammatory drugs such as methotrexate and mercaptopurine, yet the ones in the treatment group experienced a 25 to 30 percent reduction in symptoms such as swelling. The placebo group, which had also been taken off the drugs, deteriorated. Four of the treated patients had complete remissions, an effect that Dr. Howard L. Weiner, one of the researchers from Beth Israel, said, “rarely happens on its own.”

Dr. Trentham and eleven other researchers followed up with 274 patients who were randomized to receive either a placebo or one of four doses of collagen II. The oral doses given were 20, 100, 500, or 2500 mcg per day. As reported in Arthritis and Rheumatism in 1998, only eighty-three patients completed the full twenty-four weeks of treatment, but the best results came from the low-dose, 20-mcg-per-day treatment group, suggesting that less can be more.

In 1996, Trentham and two colleagues did a pilot trial of oral type II collagen for juvenile RA and reported it, too, to be a safe and effective therapy worthy of further investigation.

Can a daily dose of collagen in the form of broth help treat RA and other autoimmune collagen diseases? Common sense and the evidence of oral tolerance therapy suggests it can. In contrast, the typical medical treatments for RA are notoriously ineffective, often with horrendous side effects. The first line of assault is typically aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) to stop the pain and reduce the inflammation, followed by steroids, methotrexate, and other highly toxic drugs with downsides such as kidney damage, lung inflammation, bone marrow suppression, and severe liver damage.

Mycobacteria Theory

In the more distant past, surgeons removed the gallbladders and other organs of rheumatoid arthritics thinking they “seeded” the diseased joints, an approach that was notoriously unsuccessful. Though it is easy to mock that approach today, what will future physicians say about the millions of prescriptions written today for high-priced drugs that rarely work well, that at best only address symptoms, and almost always carry ghastly side effects?

Fifty years ago, Dr. Prudden published research showing incontestable success with the nontoxic natural substance of cartilage. His work has never been disproven. Yet with none of the profit-minded pharmaceutical companies pushing it, few people are even aware of it today, the injections are not available, and it’s challenging to even find whole bovine cartilage products.

Likewise, there has been a marked lack of interest in the work of Thomas McPherson Brown, MD (1906–1989), a renowned rheumatologist who published more than a hundred papers in major medical journals and was former chairman of the Department of Medicine at George Washington University School of Medicine in Washington, DC. While working as a young man at the Rockefeller Institute in New York City, Dr. Brown first isolated mycobacteria from the joint fluid of a woman with rheumatoid arthritis. Albert Sabin, MD, searching for the answer to infantile paralysis, was working nearby.

Dr. Brown suspected the mycobacteria settled into connective tissue and provoked severe allergic and inflammatory reactions, and he published an important paper in 1939. Although his theory was favorably received for a time, World War II intervened, and establishment medicine moved on to cortisone therapies. Soon after, the very arthritis foundations and groups Dr. Brown had helped found turned on his ideas, calling them “disproven and dangerous.” In 1988, Joan Lunden on Good Morning America introduced him as a doctor with a bestselling book The Road Back, which was “turning the American medical establishment upside down.” Dr. Brown, who had once been at the pinnacle of his profession, joked that he was trying to “turn it right side up!”

Dr. Brown’s theory of RA has earned the respect of many health experts over the years, including Harold E. Paulus, MD, of the University of California at Los Angeles, who observed, “A well-protected infection may be at least partially responsible for rheumatoid arthritis manifestations and the treatment may suppress the infection.”

More recently scientists have come up with a theory of “molecular mimicry” that helps explain this phenomenon. The idea is that some viruses and bacteria have evolved to successfully “hide out” from immune cells by camouflaging themselves with amino acid sequences similar to those found in cellular proteins. While this initially fools the immune cells, they eventually do attack, but appear to be attacking the body itself as in an autoimmune disorder.

Many alternative practitioners, including David Brownstein, MD, and Joseph Mercola, DO, have modified Dr. Brown’s protocol to include diet and have used it to treat RA as well as other rheumatic diseases such as scleroderma, lupus, psoriatic arthritis, polymyositis, and dermatomyositis.

Thomas Cowan, MD, author of The Fourfold Path to Healing, and a founding board member of the Weston A. Price Foundation, believes Dr. Brown’s treatment can be helpful, though he qualifies that “the holistic view sees the mycoplasma merely as a symptom of a more basic cause.” In his medical practice, Dr. Cowan has successfully used small doses of tetracycline along with omega-3 oils, evening primrose oil, willow bark extract, boswellia complex, liver-strengthening formulas, and oral tolerance therapy.

Dr. Trentham’s work may have made news headlines in the early 1990s, but Royal Lee, DDS (1895–1967), actually discovered it sixty years before. Discussing Dr. Lee and oral tolerance therapy, Dr. Cowan explains, “When the body has an excessive immune or antibody reaction against a particular tissue, such as cartilage, we can ‘trick’ the body by giving it oral doses of the same tissue from an animal. For rheumatoid arthritis, Dr. Lee formulated oral Ostrophin or cartilage tissue from a bull. According to Dr. Lee, Ostrophin stimulates destructive antibodies, many of which are located in the intestines, to direct their attack against the medicine instead of the body’s own tissue. This theory may explain why chicken soup, containing an abundance of dissolved cartilage, is such a time-honored method for treating rheumatism. The use of cartilage-rich broths, along with Ostrophin from Standard Process, often provides enough relief from inflammation to permit the patient to address the more fundamental causes of his disorder.”

Though Dr. Brown recommended the antibiotic minocycline, Dr. Prudden found bovine tracheal cartilage alone could do the job. As discussed in chapter 13 on wound healing, it has pronounced antibacterial effects but without the side effects of antibiotics, and without the risk of breeding stronger, antibiotic-resistant bacteria. Cartilage supplements nourish the body’s own immune system, equipping it to dispatch all harmful microbes, bacteria included. At the same time, its built-in “watchdogs” curb any tendency of the immune system to overreact and perpetuate an autoimmune disorder. In that bovine tracheal cartilage also has distinguished itself in treating nearly every possible disorder affecting connective tissue, it seems a reasonable weapon against mycoplasma bacteria lurking in connective tissue.

Whether broth can do much the same is a theory unproven but instinctively understood. Anecdotal evidence suggests it can, and oral tolerance therapy suggests a mechanism. At the very least, ancestral wisdom supports the value of broth for nourishing good overall health, which includes joint health and a high-functioning, finely tuned immune system.