DMSO (Dimethylsulfoxide) Treatments in Arthritis

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The Arthritis Trust of America.

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The Arthritis Trust of America

DMSO (Dimethylsulfoxide) Treatments in Arthritis
Supplement to The Art of Getting Well

Sources are given in references.

Authors of contributions\quotations are alphabetically arranged; major author, if any, is underlined.

Jack Blount, M.D., Ronald M. Davis, M.D., Ray Evers, M.D., Stanley Wallace Jacob, M.D., Pat McGrady, Sr., Efrain Olszewer, M.D., Gus J. Prosch, Jr., M.D., Dr. Paul K. Pybus, Fuad C. Sabbag, M.D., Roger Wyburn-Mason, M.D., Ph.D., Alan Rory Zapata, M.D./Responsible editor/writer Anthony di Fabio.

AKA The Arthritis Trust of America
7111 Sweetgum Road, Suite A, Fairview, TN 37062-9384

Several years ago Ronald M. Davis, M.D. demonstrated, in our publication A Treatment for Scleroderma & Lupus Erythematosus, the strategic use of DMSO (Dimethylsulfoxide). We've also reported on the good results of DMSO used with and without EDTA (Ethylene Diamine Tetracetic Acid) in our Chelation Therapy.

DMSO is a prolific, and inexpensive byproduct of the pulp paper industry, and its medical uses has been reported many times, by many people, but especially in the works of chemist Robert J. Herschler and surgeon Stanley Wallace Jacob, M.D., and also as popularized by Pat McGrady, Sr. in The Persecuted Drug: The Story of DMSO¹³.

The external and internal use of DMSO by veterinarians for pain in animals has long been accepted. Those humans who've managed to obtain a sufficiently pure variety of DMSO have also benefited from its pain-relieving qualities. Apparently, as Ronald M. Davis, M.D. has learned, when used in an IV over a number of months, even the most hopeless cases of Scleroderma and Lupus Erythematosus can be drastically reversed; while its use (as developed by Ray Evers, M.D. (deceased) in EDTA/DMSO IV's has long been accepted by many holistic physicians for peripheral circulation problems, as well as many other problems all of which are related -- as is Scleroderma and Lupus Erythematosus -- to free radical excess in the human physiological systems.

Those of us who've suffered from Rheumatoid Diseases of one or the other of the 75 to 100 differently named collagen tissue diseases know the nature of free radical pathology first hand. We could not, on the best of days, dispute that collagen tissue diseases (Rheumatoid Diseases) generate as a by-product many free radicals which create hob with every working apparatus of our human bodies.

The message to be learned from the pioneer physicians Stanley Jacobs, Roger Wyburn-Mason, M.D., Ph.D., Dr. Paul K. Pybus, Jack Blount, M.D., Gus Prosch, Jr., M.D., Ray Evers, M.D., Ronald Davis, M.D., Efrain Olszewer, M.D., Fuad C. Sabbag, M.D., Alan Rory Zapata, M.D. and others is that (1) collagen tissue diseases can be licked; (2) the pain of these diseases do not need to be endured; (3) one does not need to destroy self with the use of cytotoxic drugs, gold, penicillamine or long-term corticosteroids to rid oneself of the disease and its effects. Indeed, we have now learned that all of these traditional rheumatic treatments generate more dangerous free-radicals than the disease itself, thus over-burdening the body even further.

It is clear, in the reports that follow, that Doctors Olszewer, Sabbag and Zapata, along with Jacobs, Evers and Davis, have added new and important knowledge to our persistent search for wellness.

Anthony di Fabio

Control of Free Radicals in Rheumatoid Arthritis and Osteoarthritis Efrain Olszewer, M.D., Fuad C. Sabbag, M.D., Alan Rory Zapata, M.D.

Copyright Townsend letter for Doctors, June 1922, #107, p.495; re- produced by permission of the authors and the publication.

Rheumatoid diseases are some of the most crippling pathologies on earth1. Statistically one-third of individuals more than 35 years old suffer from Osteoarthritis, and also a large number of patients with Rheumatoid Arthritis, two of the most common diseases of this group of pathologies.

Rheumatoid Arthritis (RA) is an autoimmune disease, and Osteoarthritis (OA) is a degenerative disease, but both have something in common. They are closely related to Free Radical (FR) synthesis, as an inflammatory disease in RA in the prostaglandin metabolism and synthesis of leukotrienes, and in the destruction of cartilage in patients with OA².

Considering that these two pathologies are the most frequently seen in rheumatoid diseases we decided to study a correlation between FR synthesis before therapy, attempting to measure the decrease of FR production using antioxidant therapy with the following objectives:

1. Confirming that there is a relationship between FR synthesis with both diseases;

2. If the antioxidant therapy works not only with clinical improvement but also with an important reduction in the FR production;

3. How we can keep, if possible, the low levels of FR in these patients -- helping to keep the patient asymptomatic for long periods of time.

Methods and Materials

Thirty patients were included, 15 of them with RA, and 15 with OA, with a follow-up of 18 months.

The antioxidant used was DMSO (Dimethylsulfoxide in doses of 5 cc for each therapy together with B complex, Vitamin C, and Magnesium Sulphate) in a five-week, twice-weekly for the first period, and a followup of one bottle monthly for 18 months. As we know DMSO³ is one of the most powerful antioxidants known, that also blocks the CH-(hydroxyl) FR (It is well known that the human body does not have any antioxidant enzyme to block its formation.)⁴. DMSO is also an important anti-inflammatory substance, and as we showed in another study, is extremely useful in patients with inflammatory and degenerative diseases.

In order to measure the FR production we used the method HLB (Heitan-La Garde-Bradford)⁵ that determines the presence of ROTS (reactive oxygen toxic species), mostly formed by FR, that plays a role in virtually all disease states and metabolic dysfunctions. The production of ROTS affects the basic cellular structures and metabolic pathways and also reacts with blood constituents to form various by-products which can be seen as morphological changes in the blood. The specific morphological changes in the blood vary as a function of the pathological condition; in this case on Rheumatoid pathologies, strength of the immune system, specific ROTS as well as level of ROTS being generated. The study includes the extracellular matrix formed by: proteoglycan (as chondroitin sulphate, dermatan sulphate), hyaluronic acid, collagen and elastin.Each of these substances may be degraded by enzymes specific for each substance. The degradation enzymes are as follows: chondrotinase (degrades condroitin sulphate), hyaluronidase (degrades hyaluronic acid), collagenase (degrades collagen) and elastase (degrades elastin).

In patients with Rheumatoid pathologies, we can find, as seen in induced-experimental arthritis studies in rats, the activity of collagenase increase in skin, bone, liver, kidney, and spleen, while that of hyaluronidase decreased significantly in liver, kidney and spleen⁶. When traumatized normal pig synovia was cultured with normal pig cartilage for 14 days the breakdown of cartilage collagen and proteoglycan was accompanied by the appearance of both collagenase and proteoglycanase⁷. Studies in patients with inflammatory Rheumatoid Arthritis indicated an increase of prolyl hydroxylase in 70% of those with active disease⁸.

The measuring of ROTS was done in the first visit of the patient to the office, a second measure was done after any one of the infusions of DMSO, and the third evaluation after 18 months in order to measure its antioxidant effect in long-term therapy in maintenance doses.

Results

In a recent study^9,10 we showed that antioxidants are extremely important in order to control the synthesis of FR, as well as the symptoms of patients with Osteoarthritis. As we know FR are closely related to degeneration in OA, and also in the inflammatory response in patients with RA.

From the beginning we have used in patients with rheumatoid diseases the antioxidant DMSO (Dimethylsulfoxide) that has an important role over the OH-FR, instead of the popular antioxidant EDTA, that we use in patients with cardiovascular diseases as we show in our other studies^11,12

Our protocol in the last 5 years includes: one infusion twice weekly for 5 weeks, followed by one weekly or each 15 days, followed by one infusion monthly for as long as 1 or 2 years. With this protocol we have been successful in over 85% of patients with OA, and over 77% in patients with RA, with long-lasting effects, without using any other oral or parenteral non-steroidal or steroidal anti-inflammatory.

The 30 patients included in this study were regular patients in our clinic and were evaluated three times in order to see if it was possible to use the HLB test as a measuring method of FR, as well as DMSO as an optimum antioxidant. The results obtained are represented in Figure 1, where we find an initial average FR measuring 30.6% of the patients included, with an important and significant decrease of FR production after DMSO administration, obtaining lower levels with an average of 10.6%. That represents a 66% decrease in patients before beginning the DMSO therapy, and keeping the patients in monthly applications we obtained an average of 13.3% of FR synthesis. That represents 52% decrease than the patients had in the beginning, and 12% higher than patients after any DMSO infusion.

It is important to verify that the higher values were obtained in patients with RA, and the lowest in patients with OA.

This study was done by: Centro Internacional de Medicina Preventiva, Rua Compevas 211 Perdizes, Sao Paulo 1501. Brazil; Tel: (011) 623000.

References

1. Beary J. III. Ed. Manual of Rheumatology and outpatient orthopedic disorders. A Little Brown 1981.
2. Decker J., Scott T. Eds. Perspectives in Rheumatology. Curr Med Lit Ltd. 1984.
3. Wood D. and J. and JU., Pharmacology and Biochemical considerations of DMSO. Annals of the NY Acad of Sci. 1982.
4. Gorog P, Kovacs I. Antiarthritic and antithrombotic effects of topically applied DMSO. Annals of the NY Acad of Sci. 1982.
5. Bradford, Allen, Cullen: Oxidology. The R. Bradford Fdtn. Los Altos, CA 1985.
6. Kuberampata T. et al. Effect of Adjuvant Arthritis on collangenase and certain lysosomal enzymes in relation to the catabolism of collagen. Agents Actions 10 78 1980.
7. Crossley M. et al. Biochemical and Pharamcological Studies on Synovium Cartilage Interactions in Organic Culture. European Journal of Rheumatology and Inflammation 5 15 1982.
8. Acta Univ. Ouluensis, Series A, 85(1979). Savulainen E.R. Enzymes of Collagen biosynthesis in diseases of the liver and connective tissues. Chyem Abst 9 1. 1729 lit. 1979.
9. Olszewer et al. Evaluacion clinica de pacientes con artrosis, sometidos a tratamento com DMSO, mesoterapia y mucopolisacaridios. Vol. 15, pp 14-17. Junio de 1991.
10. Olszewer E. A new approach to Rheumatoid diseases Townsend Letter for Doctors. October 1991. Letter.
11. Olszewer E. Carter J. EDTA Chelation Therapy in Chronic Degenerative Disease. Med. Hyp. 27, 41-49. 1988.
12. Olszewer E., Carter J., Sabbag F. A pilot double blind study of Na-Mg EDTA in peripheral vascular disease, JNMA Vol. 82, N 3, March 1990.
13. Pat McGrady, Sr., The Persecuted Drug: The Story of DMSO, The Nutri-Books Corp., Box 5793, Denver, CO 80217, 1979.

A New Approach to Rheumatic Diseases
by Efrain Olszewer, M.D.

Copyright Townsend letter for Doctors, October1991, #99, p.778; reproduced by permission of the author and the publication.

No matter how many nonsteroidal antiinflammatory, immunosuppressive, and cortisone-related drugs were introduced in the past year as first option for rheumatic diseases, the improvement obtained was poor because most of the time we only control the pain and the inflammatory symptoms, but the disease continues to destroy the tissues.

Because of this situation, four years ago we proposed a triple approach for sero-negative and sero-positive rheumatic diseases with clinical and laboratory results above what we originally expected.

The triple approach includes:

1. DMSO (Dimethylsulfoxide) one of the most powerful antioxidants known, and has a strong antiinflammatory effect. It has been used since 1940 as an industrial solvent, and after the studies of Jacobs was included in 1960, for osteomuscular diseases.

In 1978 the FDA approved the use of DMSO for interstitial cystitis, but there are multiple studies showing an improvement in different pathologies with the use of DMSO.

In degenerative diseases like Osteoarthritis free radicals (FR) attach and degenerate the cartilage, decreasing the space in between the bones of the joint, and this contact will produce pain with movement.

In inflammatory diseases, FR are closely related to leukotrines synthesis as described in pathologies like rheumatic arthritis. In both cases DMSO will decrease the synthesis of FR, inhibiting its deleterious effect on the bone structures.

Experimental studies in animals confirmed that DMSO dissolves the collagen of the fundamental matrix, improving elastic tissue and increasing the elimination of hydroxyproline, only in patients with collagenopathies, but not in normal individuals.

2. Enzymo-Injection-Pressure (EIP) consists in using a complex formula in order to create pressure points in the ailing joints; this approach has antipain, antiinflammatory and fibrinolitic effects.

It works by a pressure mechanism that will stimulate the amyelinated fibers that measure from 5 to 15 microns in diameter, and send to the brain the pressure stimuli with a speed of 30 to100 meters per second. By this method the pressure stimuli will always arrive first at the brain regulatory center over the pain stimuli.

The formula (called F3) included in each 30cc multiple vial dose the following:

Papain    0.005 grams
hyaluronidase    0.001grams
trypsin    0.005 grams
UTP    0.001 grams
novocaine chloride    0.100 grams
saline solution 0.9%    30 cc

3. Mucopolysaccharides, also called glycoaminoglycans, formed by the hyaluronic acid, chondroitan and dermatan sulphate, that are components of the fundamental matrix, and are used to stimulate the mitotic activity of the condrocytes to keep the cartilage integrity.

After a follow-up of three years in 36 eligible patients with Osteoarthritis, we prepared a retrospective analysis that soon will be published, where we obtained the following results:

a. From the 36 patients included in the follow up, 33 (91.66%) had a complete recovery of the general signs and symptoms as: joint swelling, joint pain, limitation of movements, morning rigidity, crippling, partial social inactivity.

The other 3 (8.45%) had a partial recovery but much better than obtained with traditional therapy, and without side effects.

b. The important aspect of thus study was that it included only patients that had been using three or more different kinds of antirheumatic drugs as follows:

1.) 100% use nonsteroidal drugs
2.) 89% use or used cortisone
3.) 66.6% use or used oral gold salts
4.) 22.7% use or used IM gold salts
5.) 18% use or used different kinds of immunosuppressive drugs
6.) 0% plasmapheresis

c. Thirty two (89%) of the patients were women and 4 (11%) men. Our protocol included an intensive course of treatments for 5 weeks and a maintenance therapy monthly.

d. Nine patients (25%) had a partial recurrence.

e. Multiple joint diseases were included: coxo-femoral, knee, shoulder, hand (interphalangeal distal) cervical and lumbar backbone, etc.

In the last two years we included patients with Rheumatoid Arthritis and sero-negative rheumatic diseases. After more than 500 patients were treated we are extremely positive of this triple approach for rheumatic disease and we present the following conclusions:

1. The triple approach therapy is highly successful in patients with Rheumatoid Arthritis but it takes more treatments in the first part of the therapy; however in our opinion this therapy modality keeps the patients antisymptomatic for longer periods of time.

2. Patients with Ankylosing Spondylitis represent a small number of our patients, but the improvement seen in these patients is sometimes astonishing compared to the usual approach (antiinflammatories and physiotherapy).

3. Other sero-negative rheumatic patients have variable results that suggest more intensive studies in each particular disease.

4. Finally, patients with Rheumatoid Arthritis and Psoriasis, Lupus Erythematosis and other autoimmune diseases complicated with joint pathology need more attention, but it seems that we can get an outstanding therapeutic result in a long term therapy. But we still need longer follow-up studies in these specific diseases.

As we know, one third of the population over 35 suffer from Osteoarthritis and millions of others suffer from Rheumatoid Arthritis and other rheumatic diseases, so we should consider this group of pathologies the most crippling diseases in the world.

Most of the drugs used for rheumatic disease are associated with heavy side effects, a situation not observed with the triple approach therapy.

Conclusions

Rheumatic diseases represent one of the most crippling of all diseases and deserves special attention because most of the control is done by drugs associated with side effects, which only control pain and inflammation no matter how fast the disease develops.

Simultaneously using DMSO plus Mucopolysaccharides and enzymo-pressure-injection, seems to be an important way to control the disease evolution, and at the same time, gets the patient back to normal activities. In this kind of therapy we did not find any complications and no side effects. Instead we find extremely important improvements in the patients treated.

As much as we know of the implication of the free radicals (FR) with degenerative and inflammatory pathologies, more important seems to be the relationship with antioxidants like DMSO.

Regrowing damaged but not dead cells, is possible when we can offer the tissues that which is necessary material for autoregeneration. The homeostasis of the body is a result of the equilibrium between tissues. That is the mechanism of action of our triple conjugate therapy for rheumatic diseases.

References

1. Stein H. Jay. Medicina Interna. Tomo II. Slvat Editors. 1989.
2. Hughes R. Graham. Connective Tissue Diseases. Blackwell Scientific Publ. 1977.
3. Jacobs S. Herschler R. Editors. Biological Actions of DMSO. Annals of the New York Academy of Sciences. 1975.
4. Jacobs et al. American Journal of Surgery. 114:114. 1967.
5. Handler S. The Complete Guide to Anti-aging Nutrients. Simon & Schuster. 1984.
6. Scherbel A. McCormack M. Alternation of collagen in generalized scleroderma after treatment of DMSO. Cleveland Clin.Quart. 32:47. 1965.
7. Gries B. Bublitz and lindner. The effects of DMSO on the components of connective tissue. Ann. N.Y. Acad. Sci. 141:630. 1967.
8. Melzack R. Wall P. The Challenge of Pain. Penguin Books. 1988.
9. Harper H. Review of Physiological Chemistry. 17th Ed. Lange Med. Publ. 1979.
10. McGrady P. The Persecuted Drug: The Story of DMSO. Doubleday Co. 1973.