CHAPTER 11

Scleroderma

Orthodox medicine considers scleroderma incurable. Over the years, much has been tried, but nothing has put so much as a dent in its tough hide.

Scleroderma comes from the Greek words skleros, for hardening, and derma, for skin. Also known as “hidebound” disease, it makes victims want to hide, though “hidebound” refers to a leathery thickness that can bind so tightly that victims feel like prisoners in their own skin. About 300,000 people in the United States have been diagnosed with scleroderma.

Scleroderma results from a runaway growth process created when the body produces too much collagen and connective tissue. The thick overgrowth tightens over the fascia of the muscles, causing rigidity. Typically scleroderma begins with taut, shiny, discolored skin on the face and fingers and sometimes stops there. If it progresses, it takes over the arms and legs, then advances toward the middle of the body until the entire body surface is involved.

In severe cases, the connective tissues of the colon, lungs, kidneys, and heart are affected and scleroderma lives up to its other medical name, progressive systemic sclerosis. When the lungs are involved, breathing becomes difficult, because inhaling and exhaling depend on flexibility. If the GI tract becomes stiff, peristalsis stops and the victim becomes chronically constipated. Cardiac disturbances, kidney malfunction, and cirrhosis of the liver and other organ breakdowns may occur in the course of what can be an agonizing, unpredictable disease.

Scleroderma is an autoimmune disease related to rheumatoid arthritis, and blood tests on scleroderma patients usually show a positive latex fixation test, a test used to detect antigens. Hemolytic anemia, an autoimmune disorder characterized by chronic premature destruction of red blood cells, is also often part of the scleroderma clinical picture. As of yet, no drug has significantly influenced the outcome, though all manner of pharmaceutical formulas have been enlisted to attack the symptoms.

During the early 1970s, Dr. John F. Prudden successfully treated a number of severe cases of scleroderma with injections of bovine tracheal cartilage and reported them in Seminars in Arthritis and Rheumatism. “It was a phenomenal thing,” he remembered. “Very dramatic. We’d give it a depot injection and see a wide area totally turn soft, within about five minutes.” This skin change occurred so rapidly “that it must necessarily have been due to quick depolymerization of the excess collagen deposition.” The skin would then stay soft for about two days before beginning to harden again. In severe cases, the injections had to be repeated weekly in order to achieve and maintain the improvement.

Almost forty years later, in 2013, an interesting treatment for the first stage of scleroderma turned up in the Journal of Wound Care. A woman with a painful calcinosis cutis lesion on her buttocks was surgically treated with excision followed by the application of a regeneration template made of bovine collagen types I, II, and V coated with elastin. The patient’s wound healed quickly without complication, without needing a skin graft, and with no recurrence as of the ten-month follow-up. Calcinosis cutis is the first stage in the clinical pattern of scleroderma known as CREST, an acronym for calcinosis cutis, Raynaud’s phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia. Dr. Prudden would have been pleased though hardly surprised. As we discuss in chapter 13, he was applying cartilage to wounds with good effect back in the 1950s.

Over the years, Dr. Prudden also proved that bovine tracheal cartilage has strong antimicrobial powers. This fact is relevant if we believe scleroderma—like rheumatoid arthritis and other autoimmune diseases—is caused by infection from pleomorphic bacteria. This controversial theory holds that elusive bacteria hide in connective tissue, inciting the body’s immune system to attack it over and over. Because these bacteria are extremely good at eluding their attackers, the body ends up destroying its own collagen and cartilage-rich tissues.

In 1946, Virginia Wuerthele-Caspe, MD (1906–1990), found teeming crowds of pleomorphic bacteria in the skin of a nurse afflicted with severe scleroderma. The bacteria were acid-fast, indicating that they stained in a way similar to the mycobacteria that cause tuberculosis and leprosy. In laboratory culture, the scleroderma microbe was highly pleomorphic, meaning it appeared in multiple forms. When she injected these bugs into guinea pigs, the guinea pigs promptly developed scleroderma. The doctor then named the microbe Sclerobaccillus Wuerthele-Caspe after herself, published a paper naming them as the probable cause of scleroderma, and proposed treatment with antibacterials.

Dr. Wuerthele-Caspe then noticed that some of the sclerodermic guinea pigs developed cancer, a rare occurrence among guinea pigs. That revelation led, in turn, to her identification of a microbial cause and a possible cure for cancer. In 1977, Dr. Wuerthele-Caspe—later known as Dr. Livingston-Wheeler and finally simply Dr. Livingston—wrote that “the disease entities of tuberculosis, leprosy, generalized sclerosis and cancer have certain features in common. All four are characterized by a simultaneous process of production and destruction of tissue and by a progressive systemic involvement of the host.” Her discovery was then confirmed in 1953 by researchers at the Pasteur Institute of Brussels, who found the bacteria in nine additional cases.

Thomas McPherson Brown, MD (1906–1989), also staked his career on mycobacteria. As a young man at the Rockefeller Institute in New York City, Brown identified them as the probable cause of rheumatoid arthritis and for more than fifty years successfully used antibiotics to treat patients with RA, scleroderma, lupus, juvenile rheumatoid arthritis, fibromyalgia, and other rheumatic diseases. A respected “doctor’s doctor” in the field of rheumatology prior to World War II, he fell out of favor afterward when cortisone became all the rage. Although neither cortisone nor subsequent drugs have softened scleroderma’s thick hide, Dr. Brown’s treatment is dismissed by mainstream arthritis organizations as “disproven and dangerous.” The popular book Scleroderma: The Proven Therapy that Can Save Your Life by Henry Scammell, coauthor of Dr. Brown’s book The Road Back, has kept the idea in the public eye.

Similarly, Alan R. Cantwell Jr., MD, born in 1934, was a respected dermatologist at Kaiser-Permanente in Hollywood, California, who wrote or coauthored more than thirty articles published in major, peer-reviewed medical journals. At least thirteen of these, published between 1966 and 1984, reported the presence of acid-fast pleomorphic bacteria (the type of bacteria that causes TB) in cases of scleroderma, pseudoscleroderma, diabetic sclerodermatitis, lupus erythematosus, and related diseases.

Dr. Cantwell writes, “I naturally thought all these reports in the medical journals would be recognized by other dermatologists and scientists, and that scleroderma would be recognized as an infectious disease caused by acid-fast bacteria. But after more than a half-century, I’m sad to say that scleroderma is still considered a disease ‘of unknown etiology’ and the bacteria we found are simply ignored… As a result, physicians cling to the belief that the body is attacking itself through ‘autoimmune’ mechanisms; and doctors persist in advocating conventional therapies for systemic scleroderma, which are widely regarded as ineffective. We believe the body is not attacking itself, but is desperately trying to rid itself of disease-producing microbes that are not recognized by the scientific community.” Now that theories of “molecular mimicry” are capturing the interest of scientists, Dr. Cantwell may yet live to see a wider acceptance of his infectious cause of scleroderma and other auto-immune disorders.

“ Warts

About ten years ago I started to learn about the health benefits of broth, so I decided to create a batch. Being a novice in the kitchen, I had no idea what to do with it once it was made, so it sat in the fridge for a while. Then I decided to drink a cup a day. Within one week the wart I had on my finger was gone. Gone. I’m a chiropractor and have been able to convince only three other people to try this, but it worked for them, too, and one of them had dozens of warts all over.

—Jon Peterson, DC, Hilbert, Wisconsin”

In recent years, Dr. Cantwell has stepped up to full-blown medical heretic status. His work with Kaposi’s sarcoma, an AIDS-related skin cancer, led him to investigate the origin of HIV, and publish his findings in the books AIDS and the Doctors of Death (1992) and Queer Blood: Secret AIDS Genocide Plot (1993). His writings also include “Virginia Livingston, MD: Cancer Quack or Medical Genius?” and he has called the controversial Dr. Livingston “the greatest physician of the twentieth century.”

So what do mutating bacteria, medical heretics, and conspiracy theories have to do with broth? Nathan R. Gotthoffer, in Gelatin in Nutrition and Medicine, reported cases from the late nineteenth and early twentieth centuries in which gelatin helped heal tuberculosis, a disease caused by the acid-fast pleomorphic bacterium Mycobacterium tuberculosis. Earlier, Avicenna, a tenth-century philosopher and scientist during Islam’s Golden Age, claimed the very best cure for leprosy (caused by the same type of bacterium) was the broth made from a “young fat hen.” Moses Maimonides, the twelfth-century codifier of Jewish law, also recommended it for leprosy. In the twentieth century, TB and leprosy were researched by Dr. Livingston early in her career and more recently by Dr. Cantwell, who was exploring the possible role of Mycobacterium tuberculosis as a primary agent in HIV.

Gotthoffer also reported gelatin to be effective with many other infectious diseases and helpful for the prevention of infections during wound healing. Although the gelatin studies are inconsistent, benefits from gelatin go well beyond providing nourishment during convalescence. Of course, that’s not surprising given chicken soup’s long-standing reputation as “Jewish penicillin.” Furthermore, from the early 1950s to his death in 1998, Dr. Prudden found bovine cartilage surprisingly capable of killing dangerous microbes.

Obviously, Dr. Prudden’s doses were higher than would be expected from daily broth drinking or gelatin supplementation, but as discussed in chapter 10, sometimes “less is more.” As research on oral tolerance therapy has established, autoimmune disorders can sometimes be turned around with tiny doses of collagen—comparable to what could be consumed in broth.

Clearly, collagen, cartilage, and broth itself deserve further research as treatments for any and all rheumatic diseases. And broth should also be widely recommended as part of a nourishing diet that could prevent scleroderma to begin with. Instead, mainstream doctors continue to attack scleroderma with pharmaceuticals that suppress the immune system and inhibit cell proliferation, drugs that show limited benefits at best and horrendous side effects at worst.

In the early 1970s, Dr. Prudden visited a colleague who was a renowned scleroderma expert at Columbia-Presbyterian Hospital to share his findings. Although the specialist was “staggered” to see the hardened areas on a chronically ill scleroderma patient turn soft, he politely declined to test cartilage injections on his own patients. As Dr. Prudden put it, “I thought for sure he would want to start a project, but he did not. I was moving on to cancer research and hoped he would take over, but he apparently wanted to continue what he was doing already, though that was ineffectual at best and of no value at all at worst. I expect that the skin of his patients still looks like corpses prepared by the embalmer.”