Dr McDougall on Arthritis




Phyllis Heaphy: Cured of Rheumatoid Arthritis on the

McDougall Program


Diet & Rheumatoid Arthritis


Jackie Swoboda: Cured her Rheumatoid Arthritis, Lost

50 Pounds on McDougall Program

Juliea is cured of Rheumatoid Arthritis I The McDougall


McDougall: Rheumatoid Arthritis, ESL Medical


Rheumatoid Arthritis Diet – Natural treatment for RA


Rheumatoid Arthritis


Commercial presentation on on RH buy the program if you like but I think you can get the same thing for free on Dr McDougall but I think it is a good presentation never the less so I have included it here for the moment

Orignal article at


Diet: Only Hope for Arthritis    Dr McDougall

A dentist writes, “In April of 1994 I met you briefly at the Michigan Dental Association Annual Meeting in Grand Rapids. During this seminar, I asked you about my 4-year-old son having juvenile rheumatoid arthritis. Bryan was on 35 mg of prednisone (a powerful steroid) and 1200 mg of Advil daily. He was in so much pain he screamed and cried day and night. In one year he lost weight and did not grow one inch. His blood work reflected a sed rate of over 40 (This is a measurement of severity of inflammation and should be below 5). The suggestions you gave me that day lead me to remove all animal products from his diet, as well as refined carbohydrates.”

“Within six months, we had Bryan off all his medication. He was free of pain, gaining weight and growing again. His last blood work was superb with a sed rate of 1 – can you believe it!”

That’s how bad it can get. But for millions arthritis is much more subtle. Marvin Burk (Louise’s husband–Louise works in the McDougall Health Center office) couldn’t hardly get out of the chair. Then he would walk straddle-legged halfway across the room until he could loosen up enough to get his joints moving. His hands were so stiff he could not use his tools and he often dropped things. He figured a man of 65 shouldn’t be so crippled and decided he’d do whatever it takes to get well. He changed his diet 8 years ago with immediate and dramatic results. Now he pops out of the chair, walks without a bit of stiffness or pain and he handles his tools with no trouble. Many of us can relate to Marvin’s troubles.

People’s Most Common Affliction

Diseases of the muscles and bones are among the most common of all human afflictions, affecting all ages, but becoming more prevalent with years. Government surveys indicate in the United States approximately 33% of adults currently suffer from troublesome arthritis with symptoms of swelling, limitation of motion, or pain. Approximately half of all people over 65 years report having arthritis. The regions of the body most affected are the neck, lower back, hip and shoulder.

Arthritis means inflammation of a joint–no more, no less. The fact that a person has arthritis tells nothing about the cause or the cure. Joints can be inflamed as a result of an injury, such as from tripping and spraining an ankle. That’s called traumatic arthritis. Joints can be infected with bacteria resulting in suppurative arthritis. Uric acid crystals can accumulate in the joints causing gouty arthritis. The causes of all three of these forms of arthritis are known and once the causes are stopped the joints heal. Unfortunately, most forms of arthritis are said by doctors to have “no known cause.” And whether or not they will admit it, there is no cure to be found in modern drug therapy either.

Degenerative and Inflammatory

Arthritis of “no known cause” can be divided into two broad categories: degenerative arthritis and inflammatory arthritis. Degenerative arthritis most commonly represents a condition known as osteoarthritis. This is the most common arthritis found in people living in Western civilizations–seen in x-rays of the hands of over 70% of people 65 years and older. However, this same disease is comparatively rare in African and Asian countries, where people physically labor to survive (Br J Rheumatol 24:321, 1985). How can that be? Osteoarthritis is said to be due to wear and tear on the joints, so why is it less common among hard working people of underdeveloped countries? Nor does it explain why with light use, the hands of women often become twisted and deformed with age.

The inflammatory forms of arthritis include juvenile rheumatoid arthritis, rheumatoid arthritis, psoriatic arthritis, lupus, and ankylosing spondylitis. These aggressive diseases affect less than 5% of the people living in the United States today. Classifying these inflammatory diseases by different names, such as rheumatoid or lupus provides no further benefits to the patient, because it does not lead to better understanding of the cause of the inflammation, or to the successful treatment of the disease.

People diagnosed with degenerative arthritis (osteoarthritis) have inflammation in their joints in addition to the long-standing damage (degeneration). This inflammation can often be stopped with a change in diet and the swelling, pain, and stiffness relieved. What won’t change in either form of arthritis is the permanent destruction left by years of disease, leaving deformity, stiffness and pain. To understand how most people with arthritis can be helped by a healthy diet, I will focus on the more aggressive inflammatory forms of arthritis.

Hope for Arthritis Sufferers

Arthritis is not a genetic disease, nor is it an inevitable part of growing older–there are causes for these joint afflictions, and they lie in our environment–our closest contact with our environment is our food. Some researchers believe rheumatoid arthritis did not exist anywhere in the world before 1800 (Arthritis Rheum 34:248, 1991). It is well documented that these forms of arthritis were once rare to nonexistent in rural populations of Asia and Africa (Chung Hua Nei Ko Tsa Chih 34:79, 1995; Arthritis Rheum 34:248, 1991). As recently as 1957, no case of rheumatoid arthritis could be found in Africa. That was a time when people in Africa followed diets based on grains and vegetables.

These once unknown joint diseases are now becoming common as people migrate to wealthier nations or move to the big cities in their native countries. With these changes they abandoned their traditional diets of grains and vegetables for meat, dairy products, and highly processed foods (J Rheumatol 19:2, 1992; Ann Rheum Dis 49:400, 1991). For example, although unknown in Africa before 1960, African-Americans lead in the incidence of lupus in the US (J Am Med Women’s Assoc 1998;53(1):9-12). The mechanisms by which an unhealthy diet causes inflammatory arthritis are complex and poorly understood, but involve our intestine and immune system.

Intestine and Immune System

Increased Intestinal Permeability

The intestine forms an effective barrier to separate and exclude intestinal contents from the interior of the body. Only a single layer separates the individual from enormous amounts of antigens (foreign proteins) both of dietary and microbial origin. The intestinal mucosa absorbs and digests nutrients, turning large complex molecules into small simple ones. Normally, only the small molecules are allowed to pass through the intestinal wall, while the large ones that can act as antigens, causing immune reactions, have a limited ability to pass through. Infections and toxins can cause gaps in this barrier and allow large molecules to pass into the blood. This condition of increased intestinal permeability is referred to as a “leaky gut.” Patients with inflammatory arthritis have been shown to have inflammation of the intestinal tract resulting in increased permeability (Baillieres Clin Rheumatol 10:147, 1996).

The largest amount of lymphoid tissue in the body is associated with the gut. This tissue protects the body from antigens that do get through the intestinal barrier. Unfortunately, an unhealthy diet–too high in fat, cholesterol, and animal protein–can compromise the capacities of the lymphoid tissue to destroy invading antigens that make it through the intestinal wall.

Fasting is known to decrease intestinal permeability, thus making the gut “less leaky.” This may be one of the reasons fasting has been shown to dramatically benefit patients with rheumatoid arthritis (Scand J Rheumatol 1982;11(1):33-38). When patients return after the fast to a diet with dairy products, the gut becomes more permeable and the arthritis returns. An unhealthy diet containing dairy and other animal products causes inflammation of the intestinal surfaces and thereby increases the passage of dietary and/or bacterial antigens (Br J Rheumatol 33:638, 1994). A vegan diet (one with no animal products) has been found to change the fecal microbial flora in rheumatoid arthritis patients, and these changes in the fecal flora are associated with improvement in the arthritis activity (Br J Rheumatol 36:64, 1997).

In addition to being devoid of animal products, the diet needs to be very low in fat for maximum benefits. Dietary fat has a toxic effect on the intestine of experimental animals, causing injury that increases the permeability of the gut allowing more antigens to enter the body (Pediatr Res 33:543, 1993). Feeding high cholesterol diets to young animals also increases their “leaky gut” (J Pediatr Gastroenterol Nutr 9:98, 1989; Pediatr Res 21:347, 1987). Those vegan diets that have failed to help arthritis patients have been high in vegetable oils, which are know to damage intestinal integrity.

One dangerous paradox in arthritis treatment is that the drugs most commonly used to treat arthritis are toxins to this intestinal barrier. All commonly used nonsteroidal antiinflammatory drugs (like Advil, Motrin, Naprosyn, etc.), apart from aspirin and nabumetone (Relafen), are associated with increased intestinal permeability in man. While reversible in the short term, it may take months to improve the barrier following prolonged use. (Baillieres Clin Rheumatol 10:165, 1996).

Foreign Protein in the Body

Through the “leaky gut” pass foreign proteins from foods and bacteria into the blood stream. The food proteins are recognized by the body as “not self,”– as something harmful, just like it recognizes the proteins of viruses, parasites, and bacteria as foreign. Then it makes antibodies against these invaders. Elevated levels of antibodies to gut bacteria and to food have been found in various forms of inflammatory arthritis (Rheumatol Int 1997;17(1):11-16; Clin Chim Acta 203:153, 1991).

Antigen-Antibody Complexes

A “leaky gut” can lead to the formation of large complexes, made up of antibodies and the foreign protein (antigens) in the blood (Curr Opin Rheumatol 10:58, 1998; Ann Prog Clin Immunol 4:63, 1980). The healthy body has mechanisms that easily remove these large complexes from the blood. In some people, however, these complexes survive–because they are formed too rapidly for complete removal and/or the removal mechanisms are insufficient to handle the load. The persistent complexes are then filtered out by the smallest capillaries of the body which are found in the joints, skin, and kidneys. Stuck in the capillaries these complexes cause an inflammatory reaction, like a sliver of wood stuck in the skin.

Molecular Mimicry

Another fate of the foreign proteins is they can cause the body to make antibodies that are not solely specific to that foreign protein, but also interact with similar human proteins. This mechanism is known as molecular mimicry. The body attacks itself and the resulting diseases are referred to as autoimmune diseases. Rheumatoid arthritis, lupus, psoriatic arthritis, ankylosing spondylitis, and the other inflammatory forms of arthritis are autoimmune diseases.

Molecular mimicry in rheumatoid arthritis has been identified with cow’s milk. One analysis showed that the amino acid residues 141-157 of bovine albumin were essentially the same as the amino acids found in human collagen in the joints (Clin Chim Acta 203:153, 1991). The antibodies synthesized to attack the foreign cow’s milk proteins, end up attacking the joint tissues because of shared sequences of amino acids between the cartilage and the milk proteins, that the antibody is directed to attack.

The Defense System

A healthy diet allows the defense systems to work to its full capacity removing antigens that enter the system and removing immune-complexes from the blood. Components of the rich American diet are known to impair its function. Vegetable oils, including those of the omega-3 and omega-6 variety, are particularly strong suppressors of the immune system. This immune suppressing quality of oils (for example, fish oil and primrose oil) has been used to suppress the pain and inflammation of arthritis, but like too many drug therapies the ultimate outcome may not be best for the patient. Suppression of the immune system prevents it from doing its work of removing invading foreign proteins. Low-fat diets have been shown to retard the development of autoimmune diseases, similar to lupus and rheumatoid arthritis, in experimental animals (Ann Rheum Dis 48:765, 1989).

A healthy diet also supplies antioxidants and other phytochemicals that keep the joints strong and repair damage (Am J Clin Nutr 53(1 Suppl):362S, 1991). Animal studies have shown that the foods consumed on the rich American diet fail to provide adequate antioxidants to destroy the damaging free radicals that form in the joint tissues (J Orthop Res 8:731, 1990).

Treatment of arthritis with diet became fashionable in the 1920s and many studies over the last 20 years have shown a healthy diet, one very different from the typical American diet, can be a very effective treatment of inflammatory arthritis for many people.

In 1979, Skoldstam fasted 16 patients with rheumatoid arthritis for 7-10 days with a fruit-and vegetable juice fast, followed by a lactovegetarian diet for 9 weeks. One-third of the patients improved during the fast, but all deteriorated when the milk products were reintroduced (a lactovegetarian diet) (Scan J Rheumatol 8:249, 1979).

In 1980, Hicklin reported clinical improvement in 24 of 72 rheumatoid patients on an exclusion diet. Food sensitivities were reported to: grains in 14, milk in 4, nuts in 8, beef in 4, cheese in 7, eggs in 5, and one each to chicken, fish, potato, and liver (Clin Allergy 10:463, 1980).

In 1980, Stroud reported on 44 patients with rheumatoid arthritis treated with the elimination of food and chemical avoidance. They were then challenged with foods. Wheat, corn, and beef were the greatest offenders (Clin Res 28:791A, 1980).

In 1981, Parke described a 38-year-old mother with 11-years of progressive erosive seronegative rheumatoid arthritis who recovered from her disease, attaining full mobility, by stopping all dairy products. She was then hospitalized and challenged with 3 pounds of cheese and seven pints of milk over 3 days. Within 24 hours there was a pronounced deterioration of the patient’s arthritis (BMJ 282:2027, 1981).

In 1981, Lucas found a fat-free diet produced complete remission in 6 patients with rheumatoid arthritis. Remission was lost within 24-72 hours of eating a high-fat meal, such as one containing chicken, cheese, safflower oil, beef, or coconut oil. The authors concluded, “…dietary fats in amounts normally eaten in the American diet cause the inflammatory joint changes seen in rheumatoid arthritis.” (Clin Res 29:754, 1981).

In 1982 Sundqvist studied the influence of fasting with 3 liters of fruit and vegetable juice daily and lactovegetarian diet on intestinal permeability in 5 patients with rheumatoid arthritis. Intestinal permeability decreased after fasting, but increased again during a subsequent lactovegetarian diet regime (dairy products and vegetables). Concomitantly it appeared that disease activity first decreased and then increased again. The authors conclude, “The results indicate that, unlike a lactovegetarian diet, fasting may ameliorate the disease activity and reduce both the intestinal and the non-intestinal permeability in rheumatoid arthritis.” (Scand J Rheumatol 11:33, 1982.)

In 1983, Lithell studied twenty patients with arthritis and various skin diseases on a metabolic ward during a 2-week period of modified fast on vegetarian broth and drinks, followed by a 3-week period of a vegan diet (no animal products). During fasting, joint pains were less intense in many subjects. In some types of skin diseases (pustulosis palmaris et plantaris and atopic eczema) an improvement could be demonstrated during the fast. During the vegan diet, both signs and symptoms returned in most patients, with the exception of some patients with psoriasis who experienced an improvement. The vegan diet was very high-fat (42% fat). (Acta Derm Venereol 63:397, 1983).

In 1984 Kroker described 43 patients from three hospital centers who underwent a 1-week water fast, and overall the group improved significantly during the fast. In 31 patients evaluated, 25 had “fair” to “excellent” responses and 6 had “poor” responses. Those with more advanced arthritis had the poor responses. (Clin Ecol 2:137, 1984).

In 1985, Ratner removed all dairy products from the diet of patients with seronegative rheumatoid arthritis, 7 out of 15 went into remission when switched to milk-free diets (Isr J Med Sci 21:532, 1985)

In 1986, Panush described a challenge of milk in a 52-year-old white woman with 11 years of active disease with exacerbations allegedly associated with meat, milk, and beans. After fasting (3 days) or taking Vivonex (2 days) there was no morning stiffness or swollen joints. Challenges with cow’s milk (blinded in a capsule) brought all of her pain, swelling and stiffness back (Arthritis Rheum 29:220, 1986).

In 1986, Darlington published a 6-week, placebo-controlled, single-blinded study on 48 patients. Forty-one patients identified foods producing symptoms. Cereal foods, such as corn and wheat gave symptoms in more than 50% of patients (Lancet 1:236, 1986).

In 1986, Hanglow performed a study of the comparison of the arthritis-inducing properties of cow’s milk, egg protein and soy milk in experimental animals. The 12-week cow’s milk feeding regimen produced the highest incidence of significant joint lesions. Egg protein was less arthritis-inducing than cow’s milk, and soy milk caused no reaction. (Int Arch Allergy Appl Immunol 80:192, 1986).

In 1987, Wojtulewski reported on 41 patients with rheumatoid arthritis treated with a 4-week elimination diet. Twenty-three improved. (Food allergy and intolerance. London: Bailliere Tindall 723, 1987).

In 1988, Beri put 14 patients with rheumatoid arthritis on a diet free from pulses, cereals, milk, and non-vegetarian protein foods. Ten (71%) showed significant clinical improvement. Only three patients (11%) adhered to the diet for a period of 10 months (Ann Rheum Dis 47:69, 1988.)

In 1988, Hafstrom fasted 14 patients with water only for one week. During fasting the duration of morning stiffness, and number and size of swollen joints decreased in all 14 patients. No adverse effects of fasting were seen except transient weakness and lightheadedness. The authors consider fasting as one possible way to induce rapid improvement in rheumatoid arthritis (Arthritis Rheum 31:585, 1988).

In 1991, Kjeldsen-Kragh put 27 patients on a modified fast with vegetable broths, followed by a vegan diet, and then a lacto-ovovegetarian diet. Significant improvement occurred in objective and subjective parameters of their disease (Lancet 2:899, 1991) A two-year follow-up examination found all diet responders but only half of the diet nonresponders still following the diet, further indicating that a group of patients with rheumatoid arthritis benefit from dietary manipulations and that the improvement can be sustained through a two-year period (Clin Rheumatol 13:475, 1994.) Patients dropping out with arthritic flares in the diet group left the study mainly when the lactovegetarian diet (dairy products) were introduced (Lancet 338:1209, 1991).

In 1991 Darlington reported on 100 patients who had undergone dietary manipulation therapy in the past decade, one-third were still well and controlled on diet alone without any medication up to 7 ½ years after starting the diet treatment. They found most patients reacted to cereals and dairy products (Lancet 338:1209, 1991).

In 1991, Skoldstam fasted 15 patients for 7 to 10 days. Almost all of the patients showed remarkable improvement. Many patients felt the return of pain and stiffness on the day after returning to their “normal” eating and all benefit was lost after a week (Rheum Dis Clin North Am 17:363, 1991).

In 1992, Sheignalet reported on 46 adults with rheumatoid arthritis who eliminated dairy products and cereals. Thirty-six patients (78%) responded favorably with 17 clearly improved, and 19 in complete remission for one to five years. Eight of those 19 stopped all medications with no relapse. Favorable benefits appeared before the end of the third month in 32 of the patients (Lancet 339:68, 1992).

In 1992, van de Laar showed benefits of a hypoallergenic, artificial diet in six rheumatoid patients. Placebo controlled rechallenges showed intolerance for specific foodstuffs in four patients. In two patients, biopsy of the joints showed specific (IgE) antibodies to certain foods (Ann Rheum Dis 51:303, 1992).

In 1992, Shigemasa reported a 16-year-old girl with lupus who changed to a pure vegetarian diet (no animal foods) and stopped her steroids without her doctor’s permission. After starting the diet her antibody titers (a reflection of disease activity) fell to normal and her kidney disease improved (Lancet 339:1177, 1992).

In 1995, Kavanaghi showed an elemental diet (which is an hypoallergenic protein-free artificial diet consisting of essential amino acids, glucose, trace elements and vitamins) when given to 24 patients with rheumatoid arthritis improved their strength and arthritic symptoms. Reintroduction of food brought the old symptoms back (Br J Rheumatol 34:270, 1995).

In 1998, Nenonen tested the effects of an uncooked vegan diet, rich in lactobacilli, in rheumatoid patients randomized into diet and control groups. The intervention group experienced subjective relief of rheumatic symptoms during intervention. A return to an omnivorous diet aggravated symptoms. The results showed that an uncooked vegan diet, rich in lactobacilli, decreased subjective symptoms of rheumatoid arthritis (Br J Rheumatol 37:274, 1998).

It’s the Whole Diet

The importance of the overall diet cannot be overemphasized. Proper foods keep the intestinal barriers strong and the immune system in a fighting condition. Those foods are whole starches, vegetable, and fruits. In addition to being free of animal products, the diet must be low in fat of all kinds — vegetable oil (even olive oil, corn, safflower, and flaxseed oil) and animal fat. When it comes to blaming individual foods, dairy products seem to be the most troublesome foods, causing the most common and severe reactions. Many reports indicate grains, such as corn and wheat can also aggravate of symptoms. The truth seems to be almost any food can cause trouble, but few people react to vegetable foods.

My experience and this research has lead me to prescribe for the past 22 years a starch-based diet with the addition of fruits, and vegetables (low-fat and devoid of all animal products). If no improvement is seen within 2 weeks, I suggest wheat and corn be eliminated. The final step is to follow an elimination diet based on the foods least likely to cause problems, such as sweet potatoes and brown rice with the addition of noncitrus fruits, and green and yellow vegetables. All thoroughly cooked. Water is the beverage. If improvement is found (usually within 1 to 2 weeks), then foods are added back one at a time to see if there is an adverse reaction. (A complete description of this diet can be found in The McDougall Program — 12 days to Dynamic Health). Nonsteroidal anti-inflammatory drugs should be stopped, and if necessary, replaced by aspirin or nabumetone (Relafen). Other medications are reduced and/or discontinued as the symptoms improve.

I have just finished a study on 28 patients with rheumatoid arthritis using the McDougall Diet (with corn and wheat included) and the results were remarkable. Full publication will appear this fall.

For Whole Body Benefits

By no small coincidence the same diet that keeps the joints healthy also keeps the rest of the body sound. Diane of Walnut Creek wrote to me last year. “I had what I can only call a miserable life until about five years ago. Nothing seemed to go right for me. In late 1991 I was diagnosed with spinal stenosis and degenerative arthritis. I was declared permanently disabled and left my job as a daily newspaper journalist. My therapist gave me a wonderful gift–she suggested I try your program. I shrugged off her suggestion at first. I swore that I ate well anyway: only dairy and shellfish and white meats. Only! She did not push the point, wisely waiting for me to think about the idea. I did wait for two years. Then two years ago she suggested your program again. I told her I didn’t believe it would work, but agreed to try it for two months. I was overweight, very overweight, by 100 pounds, most of my life — carrying all that poundage caused a lot of wear on my joints. That was two years ago, and I’m a lifelong convert.”

“Of course what you predicted happened: My migraines went away completely; I stopped swelling in my joints; I could sleep easily; I had no indigestion problems of any kind; and I began to drop weight. As you probably know, it was a lot easier than I thought it would be. Before I started the McDougall plan, I was losing weight slowly. Afterward, the weight loss was dramatic. After about six months, people started noticing and commenting. They kept saying things like ‘you look ten years younger,’ or most often, ‘You look great. What did you do?’ I no longer take the anti-inflammatory drugs and painkillers that I was taking before the McDougall way. My knee and low-back are virtually pain-free. Now, what I’ve found is that nobody believes it can be as simple as eating carefully and exercising. They all want some magic or some pill.”

John McDougall, MD



Original article here



Diet therapy for the patient with rheumatoid arthritis?

In spite of the great advances that have been made in the development of new drugs for the treatment of rheumatoid arthritis (RA), many patients are interested in alternative treatments like dietary therapy. Although relatively few studies have been carried out on the possible impact of dietary therapy on disease activity in RA, interest in this matter is growing as our understanding of disease pathology and the effect of nutrients on immunity and inflammation increases.

Most clinical dietary therapy studies undertaken so far have focused on some form of dietary elimination. Scandinavian health farms have long promoted fasting and vegetarian diets for patients with rheumatic diseases.

In 1979 and 1983, Sköldstam et al. [1, 2] carried out two studies to verify whether diet therapy could alleviate disease activity and symptoms in patients with RA. In one study, 16 RA patients fasted for 7–10 days and followed a lactovegetarian diet for the subsequent 9 weeks. There was a significant improvement in both objective and subjective disease symptoms during the fasting period, followed by rapid deterioration when the patients began on the lactovegetarian diet.

In the second study, 20 patients with RA completed a 7- to 10-day fast, followed by 3 months on a vegan diet (a diet without meat, fish or dairy products). Physician’s general assessment revealed that 11 patients had undergone subjective improvement, seven were unchanged and two were worse after the study period than before. Nineteen patients had lost weight and no improvement was seen in objective variables like erythrocyte sedimentation rate (ESR) and C-reactive protein during the dietary period. However, 5 (25%) of the patients showed both objective and subjective improvement. Several patients complained about the diet and only two patients had continued with a strict vegetarian diet after the study period. This confirms that many patients experience difficulty in implementing strict dietary changes.

In 1983, Panush et al. [3] conducted a study of the then popular Dong diet (which eliminated dairy products, red meat, citrus fruits, tomatoes, alcohol and coffee). This was an elegantly performed clinical dietary study with a double-blind, placebo-controlled design. Twenty-six patients took part, 11 on the experimental diet and 15 on a control diet. Although there was no statistical difference between the experimental and placebo diet groups, two patients in the experimental group improved noticeably. One patient experienced disease exacerbation after eating dairy products and the other after eating meat, spices and alcoholic beverages.

In 1986, Darlington et al. [4] published the results of a single-blinded, placebo-controlled study of 6 weeks of dietary manipulation in 53 patients with RA. During the first week, the patients were only allowed to eat foods they were unlikely to be intolerant to. In the article, it is not stated which food items these were. Other food items were then reintroduced one at a time to see whether any symptoms were elicited by the dietary challenge. Foods producing symptoms were then excluded from the diet. Both objective and subjective variables improved significantly, and a subgroup of 33 patients were graded as good responders. However, the patients were only observed for 6 weeks, which is a weakness in a study undertaken on patients with a chronic disease.

In 1991, we published the results of a single-blinded controlled clinical trial testing the effect on disease activity in patients with RA of dietary elimination combined with the vegetarian diet traditionally practised on Scandinavian health farms [5]. Fifty-seven patients took part in the study, 27 in the diet group and 26 in the control group. The patients were followed for 13 months, making this by far the most comprehensive study undertaken with regard to dietary therapy in RA.

We found statistically significant improvement in both objective and subjective disease variables in the diet group compared with the control group. Twelve patients (44%) in the diet group were responders, according to the Paulus criteria, compared with 2 (8%) in the control group [6]. Ten patients (37%) in the diet group reported aggravation of symptoms after reintake of one or more food items. Eight of these belonged to the responder group.

After 2 yr, we conducted a follow-up study on the same patients and found that the responders had continued with the diet and still had a significant reduction in all clinical disease variables and ESR [7]. In this study, 13 patients (59%) in the diet group reported an increase in disease symptoms after intake of meat, and 10 patients (45%) after intake of sugar and coffee. Of the 10 responders examined in the follow-up study, eight reported an increase in disease symptoms after intake of different kinds of meat, and six after intake of coffee, sweets and refined sugar.

Fasting has been documented to have beneficial effects on both clinical and laboratory variables reflecting disease activity in RA [1, 5, 8]. It thus serves as a useful model for studying the biological changes associated with simultaneous improvement in disease activity. Previous studies in healthy subjects have revealed that fasting decreases mitogen- and antigen-induced lymphocyte proliferative responses [9], and suppresses interleukin-2 (IL-2) production [10]. We have recently shown that a 7 day fast in RA patients also decreases CD4+ lymphocyte activation and numbers, suggesting transient immunosuppression [11]. We also found an increase in IL-4 production from mitogen-stimulated peripheral blood cells. Thus, further studies should be carried out to clarify the immunomodulatory mechanism behind fasting.

Evidence suggesting that food allergy, defined as an immunological response to food antigens or to intestinal bacterial flora, might be involved in disease pathology in most patients with RA is weak. However, it is possible that an exogenous agent like a food antigen can initiate a pathological immune process in a genetically susceptible individual [12].

Food antigens, food antibodies and their complexes have been detected in the systemic circulation of healthy subjects [13, 14]. Animal models indicate that the gut is an important trigger of and pathway for the immune response. Encounters with complex proteins, like gluten and milk proteins, lead to either oral tolerance or sensitization and possible loss of self-tolerance to cross-reacting epitopes [15].

An association between a special food item and disease activity has been reported by patients with a variety of rheumatic diseases, such as palindromic rheumatism [16, 17], systemic lupus erythematosus [18, 19], Sjögren’s syndrome [20] and juvenile RA (JRA) [21, 22]. Case reports describing an association between diet and disease activity in RA include both seropositive and seronegative disease [2325]. Although the extent of food allergy involvement is still not known, it has been suggested that between 5 and 30% of patients with RA may be affected [26, 27].

We found an increase in humoral response in all patients with RA, with a general increase in IgG, IgA and IgM antibodies to various food antigens, like gluten and milk proteins. However, the elevated concentrations of specific immunoglobolins could not be used to predict which food items would aggravate the disease symptoms [28].

Wheat and other rough grain products can elicit an allergic T-cell response through their lectin structures. Lectins are glycoprotein molecules that bind to carbohydrate-specific receptors on lymphocytes with high affinity and thus elicit a significant immune response. Lentils and grain products have a particularly high lectin content. Lectins are fairly heat resistant; for example, lentils have to be cooked for a long time to inactivate the lectins.

While the results of a questionnaire-based survey revealed that 37–43% of patients with rheumatic diseases experienced an increase in disease symptoms after intake of certain food items, no difference could be found between the various diseases [29]. This suggests that diet may influence the inflammatory process in general and is not a specific feature of RA.

One of the mechanisms involved may be the release or secretion of vasoactive amines (bioactive amines) like histamine and serotonin [30]. Several of the food items reported to cause disease aggravation have a high histamine content, like pork and beef sausage, meat, tomato and spinach. Since no immunological response to pork and other meat has been demonstrated, a pharmacological response would explain the often reported increase in symptoms resulting from these foods [31]. Other foods like shellfish, strawberries, chocolate and fish can cause a release of histamine.

Citrus fruits, which contain other vasoactive amines (octopamine and phenylephrine), are often said to aggravate symptoms [30]. Consumption of both coffee and alcohol has been shown to liberate adrenaline and/or noradrenaline, which suggests that they have a pharmacological effect [30, 32]. Consumption of alcohol can also result in the release of histamine, and certain red wines have in addition a high concentration of histamine, which may explain the frequently reported intolerance.

A pharmacological reaction would also explain why the patients reported immediate reactions to these food items, as opposed to the more delayed reactions to dairy products and gluten. This may mean that a different mechanism is involved in symptom aggravation. The reported aggravation of symptoms after intake of refined sugar and sweets in patients with RA may have a metabolic explanation, such as an increased concentration of blood glucose due to impaired glucose handling [3335].

Gut involvement in the pathogenesis of rheumatic diseases was proposed by Rea Smith [36], who reported that surgical removal of intestinal segments with focal infection had a beneficial effect on disease activity. Monroe and Hall [37] reported differences in the stools of 142 patients with chronic arthritis as compared with controls. Månsson and Olhagen [38] found not only an abnormal faecal flora, with an increase in Clostridium perfringens in patients with RA, systemic lupus erythematosus and psoriatic arthropathies compared with healthy controls, but also a higher level of alpha-antitoxin in the serum of these patients. Alpha-toxin (phospholipase-C) is produced by a special strain of C. perfringens often found in RA patients. Månsson and Olhagen [38] found a rise in alpha-antitoxin titre in 75% of the patients with RA in the study, but in none of the controls.

A significantly higher carriage rate of C. perfringens in patients with RA than in healthy controls has also been documented by Shinebaum et al. [39]. An altered intestinal bacterial flora has been reported in patients with seropositive erosive RA compared with patients with seronegative RA and controls [40]. An increased concentration of antibodies to Proteus has been described in patients with active RA [41, 42] and to Klebsiella in patients with ankylosing spondylitis [43]. Several of these reports have suggested that RA and ankylosing spondylitis could be mediated by cross-reactivity between self and bacterial antigens.

The intestinal bacterial flora is known to be affected by diet [4446], and it has been suggested that a diet which could alter the intestinal flora might have an effect on disease activity. This theory was supported by the finding that changes in disease activity correlated with alterations in the intestinal flora measured in patients who switched from an omnivorous to a vegetarian diet [47]. The effects of the intake of functional foods (i.e. food as medicine; in this case, food which promotes the growth of health-promoting bacteria in the intestine or food items that contain natural healthy intestinal bacteria) should be an interesting field for further research.

Much interest has been taken in recent years in the immunomodulatory effects of polyunsaturated fatty acids (PUFAs) and their therapeutic potential as anti-inflammatory agents [48]. Both clinical and in vitro studies have established that long-chain n-3 and n-6 fatty acids inhibit T-lymphocyte function [4952].

Research suggests that manipulating the balance of dietary fatty acids in favour of increased n-3 fatty acids and decreased n-6 fatty acids may have a beneficial effect on disease activity in RA [49, 5356]. These studies have shown that long-chain n-3 fatty acids can diminish peripheral blood mononuclear cell proliferation and reduce the production of IL-1, IL-2, IL-6, tumour necrosis factor alpha (TNF-α) and interferon gamma (IFN-γ). However, clinical studies on supplementation of ω-3 fatty acids have not supported the expectations raised by the laboratory findings [5357].

The balance between unsaturated and saturated fatty acids may also affect lymphocyte proliferation (in vitro) [58]. The practical implications of these observations for the in vivo situation are currently unclear, but suggest that a diet which is high in unsaturated fatty acids and very low in saturated fatty acids may have a stronger immunosuppressive effect than that obtained by only n-3 fatty acid supplementation.

In this respect, the Mediterranean diet, with a low content of red meat and a high content of olive oil, is of interest. Olive oil has been shown to reduce lymphocyte proliferation, natural killer cell activity, adhesion molecule expression on lymphocytes and the production of pro-inflammatory cytokines in animal models [59]. In an intervention study in which dietary saturated fatty acids were partly replaced by olive oil, mononuclear cell expression of ICAM-1 was found to be significantly reduced [60].

It has also been reported that a very low intake of saturated fats is beneficial in multiple sclerosis, where, as in RA, CD4+ lymphocytes are thought to play a pathogenic role [61]. It is thus worth investigating whether a diet low in saturated fats, with a high content of olive oil and with n-3 supplementation, could have immunosuppressive effects in vivo and could thus be of benefit in the treatment of RA.

The pathological hallmark of RA is persistent destructive inflammation in the synovial membranes of joints, which leads to a gradual destruction of the supporting structures of the joints, such as bone and cartilage. Although the aetiology is still unknown, the inflammation resulting from the immunological reaction is quite well described. It is known that neutrophil granulocytes, macrophages and lymphocytes are activated, and that oxygen free radicals are produced [62]. Hence, a low concentration of antioxidants may perpetuate tissue destruction in RA. Free oxygen radicals and oxidative stress may also be of importance for the aetiology and chronicity of the inflammatory rheumatic diseases [63, 64]. Two epidemiological studies have recently suggested that antioxidants may play a protective role [65, 66].

The most important antioxidants known today are vitamin A, vitamin E, vitamin C, beta-carotene, the bioflavonoids, zinc and selenium. The antioxidant properties of vitamin A and vitamin E lead to a reduction in the oxidation catalysed by free radicals [67]. Vitamin E functions as a physiological antioxidant for the cell membrane and is the most important fat-soluble antioxidant in the cell membrane lipids [64, 68]. Zinc plays a significant role in antioxidant protection and immunity because it is a constituent of the cytoplasmic enzyme superoxide dismutase [69]. Selenium, on the other hand, is part of the glutathione peroxidase enzyme, which can react with peroxides formed during inflammation. Beta-carotene is a fat-soluble, chain-breaking antioxidant and a quencher of singlet oxygen, and is known, along with alpha-tocopherol, to be the most important element of the non-enzymatic antioxidant defence in biological systems [70, 71].

Low serum concentrations of selenium and zinc in RA patients were reported as early as 1978 [72] and were further investigated by Tarp et al. [7375]. Mezes and Bartosiewicz [63] found reduced plasma vitamin A content in patients with RA. Honkanen et al. [76] found lower serum levels of vitamin A and E in patients than in healthy controls. Sklodowska et al. [64] found lower vitamin E concentrations in plasma in children with JRA than in controls. Studies have also shown reduced concentrations of zinc and selenium in children with JRA [77, 78].

The reduced serum concentrations of antioxidants found in patients with inflammatory rheumatic diseases do not appear to be a consequence of reduced dietary intake in these patient groups compared with healthy controls [7880]. They may, therefore, indicate a high turnover of antioxidants and an increased antioxidant requirement in these patients which is necessary in order to balance the higher production of free radicals.

Although studies of supplementation with a single antioxidant have not shown disease reduction in RA patients, it is still possible that patients with an inflammatory rheumatic disease will benefit from supplementation with a combination of several antioxidants or from a dietary intake that exceeds the recommended dietary allowances.

Studies of immunomodulation have revealed that nutrients other than food proteins and fats also have an impact. The effects of fatty acids, antioxidants and food proteins on immunomodulation need to be investigated further, and so should the question of the involvement of the gut in the aetiology and pathology of rheumatic diseases. More knowledge on the effects of dietary components upon immunological function is necessary if the potential use of dietary therapy as a tool in the treatment of RA is to be adequately assessed.

  1. M. Haugen,
  2. D. Fraser and
  3. Ø. Førre

+ Author Affiliations

  1. Centre for Rheumatic Diseases, The National Hospital, Oslo, Norway
  1. M. Haugen, Centre for Rheumatic Diseases, The National Hospital, Akersbakken 27, 0172 Oslo, Norway.


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