Offer sound nutritional advice for your rheumatoid arthritic patients

The clinical realities of rheumatoid arthritis (RA) are quite profound. Approximately 1% of the population suffers from RA. It most commonly develops in the fourth to fifth decades of life; approximately 80% of total cases occur between the ages of 35 and 50, and it is associated with substantial morbidity and accelerated mortality. The prevalence is two to three times greater among women than men.¹

Experts think that RA may actually be a disease of modern man, such that there is little persuasive historical evidence suggesting that RA compromised early man. Indeed, skeletal remains of early man do not show signs of RA, and it is not depicted in the art or literature of antiquity.¹

In short, RA is a disease characterized by chronic immune-driven inflammation in synovial joints. This sometimes seems confusing to health care practitioners as our physiology books inform us that inflammation leads to healing, and this is true; however, we also know that chronic inflammation is responsible for driving most, if not all, degenerative diseases. Consider Type 2 diabetes. Most think it is a sugar-handling disorder that people get as they age, gain weight, and stop exercising, which is true. Aging, fat gain, and lack of exercise is expressed physiologically as inflammation.

Insulin resistance precedes Type 2 diabetes, and it is known that inflammatory mediators inhibit the insulin receptor, which leads to hyperinsulinemia, hyperglycemia, insulin resistance, and a prediabetic state.² The conclusion is that “evidence favors chronic inflammation as a trigger for chronic insulin insensitivity, rather than the reverse situation.”² However, once Type 2 diabetes develops, it then exerts a proinflammatory influence.²

Modern Man’s Disease?
As with most chronic degenerative diseases, the etiology of RA remains obscure. Intriguingly, as mentioned above, it appears that RA is a disease of modern man. With that in mind, we might be led to believe that texts would look at lifestyle factors that would lead to RA expression. It does not typically appear until after the fourth decade, so we must be doing some things wrong during the first 30 years of life that would act as a trigger. Regretfully, pathology texts do not closely examine potential causes of RA.

For example, in a text titled Inflammation, the RA chapter focuses solely on bacterial and viral causes.² At first glance, this may not seem that surprising, as we blame bugs for so many conditions. The experts, however, have already established that RA is a disease of modern man, who has a far more sanitary environment in which to live. So, why would we blame the germs? The focus on germs as an important cause of RA seems misplaced.

Pathology-type texts do mention lifestyle issues, but the depth of discussion is very superficial. The lifestyle factor that most directly and dramatically influences our tissue biochemistry is nutrition, so a nutritional etiology is a most likely culprit.

Studies have, in fact, demonstrated that there is a high prevalence of insulin resistance in rheumatoid arthritis,^3,4 such that researchers state, “The biochemical disturbances clustering in the metabolic syndrome (insulin-resistance syndrome) may participate in the onset and persistence of inflammatory arthritis.”⁴ It is quite possible that inflammation causes insulin resistance, which then exerts a proinflammatory effect. Collectively, the original and secondary inflammatory states contribute to the expression of rheumatoid arthritis.

If diet-driven inflammation promotes RA, then it should follow that antiinflammatory nutritional interventions would reduce RA expression. In fact, research has demonstrated this to be the case.

Fight RA With Nutrition
In 1991, an article was published in Lancet that described a study in which 27 RA patients stayed at a health farm for 4 weeks, wherein they adopted an entirely different dietary program. After a 7- to 10-day subtotal fast, which consisted of herbal teas, garlic, vegetable broth, decotion of potatoes and parsley, and juice extracts from carrots, beets, and celery, each subject was placed on an individually adjusted gluten-free vegan diet for 3 to 5 months.

During the first 3 to 5 months, patients were asked not to eat gluten, meat, fish, eggs, dairy products, refined sugar, or citrus fruits. Salt, strong spices, and preservatives were avoided, as were alcoholic beverages, teas, and coffee. After the 3- to 5-month period, patients reintroduced milk, other dairy products and gluten foods. Every 2 days, a new food was tested. If pain, stiffness, or joint swelling occurred during the 2- to 48-hour postconsumption period, the food was removed for 7 days. If a second introduction caused symptoms, the food was removed completely during the study period.⁵ This approach represents an attempt to determine if food allergies may be promoting RA.

At the end of the 4-week stay, there was a significant improvement in the number of tender and swollen joints, Ritchie’s articular index, pain score, duration of morning stiffness, grip strength, C-reactive protein, and white blood cell count. There was also a significant improvement in a health assessment questionnaire, and all the benefits were present after 1 year. The authors explained that food allergy was suspected in only 10 of 27 subjects, such that food allergy is an unlikely explanation for improvements in all patients on the diet.⁴ It is likely that the benefits were derived from the heavy increase in consumption of antiinflammatory fruits and vegetables.

From a supplemental perspective, ingestion of dietary supplements of omega-3 (n-3) fatty acids (eicosapentaenoic [EPA] and docosahexaenoic [DHA] acids) has been consistently shown to reduce both the number of tender joints on physical examination and the amount of morning stiffness in patients with rheumatoid arthritis. In these cases, supplements were consumed daily in addition to background medications, and the clinical benefits of the n-3 fatty acids were not apparent until they were consumed for 12 weeks or longer. A minimum daily dose of 3 grams of EPA/DHA is necessary to derive the expected benefits. Several investigators have reported that rheumatoid arthritis patients consuming n-3 dietary supplements were able to lower or discontinue their background doses of nonsteroidal antiinflammatory drugs or disease-modifying antirheumatic drugs. Omega-3 fatty acids have virtually no reported serious toxicity in the dose range used in rheumatoid arthritis and are generally very well-tolerated.⁶

It is likely that RA patients eat themselves into a deficient state. One study compared the dietary intake of 48 RA patients (13 men, 35 women; mean age of 64.5 years) as measured by a 5-day dietary survey with recommended dietary intake (RDI) guidelines. The percentage of patients who achieved the RDI was 23% for calcium, 46% for folic acid, 29% for vitamin E, 10% for zinc, and only 6% for selenium. The authors suggested that patients with RA should receive dietary education or supplementation to bring their intake of calcium, folic acid, vitamin E, zinc, and selenium up to the RDI.⁷

Patients with RA are likely to be helped by dietary modifications, and these need not be complicated and involve an elimination diet. Simply have your RA patients dramatically increase their fruit and vegetable intake. Supplement their diets with a multivitamin, EPA/DHA, magnesium, CoQ10, and antiinflammatory botanicals, such as ginger and turmeric. Your RA patients will feel the benefits within a month, and you will be the one they thank and whom they tell their friends about. CP

David R. Seaman, DC, MS, DABCN, DACBN, FACC, is an assistant professor at Palmer College of Chiropractic, Port Orange, Fla, and is on the postgraduate faculties of several chiropractic colleges. He presents postgraduate seminars for chiropractic colleges and associations, is a clinical nutrition consultant, has written a textbook on nutrition, and published several articles in JMPT. Seaman can be reached via email: docseaman@mac.com.

References
1. Kavanaugh AF, Lipsky PE. Rheumatoid arthritis. In: Gallin JI, Synderman R, eds. Inflammation: Basic Principles and Clinical Correlates. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 1999:1017-1037.
2. Grimble RF. Inflammatory status and insulin resistance. Curr Opin Clin Nutr Metab Care. 2002;5:551–559.
3. Dessein PH, Joffe BI, Stanwix AE. Effects of disease modifying agents and dietary intervention on insulin resistance and dyslipidemia in inflammatory arthritis: a pilot study. Arthritis Res. 2002;4(6):R12.
4. Dessein PH, Stanwix AE, Joffe BI. Cardiovascular risk in rheumatoid arthritis versus osteoarthritis: acute phase response related decreased insulin sensitivity and high-density lipoprotein cholesterol as well as clustering of metabolic syndrome features in rheumatoid arthritis. Arthritis Res. 2002;4(5):R5.
5. Kjeldsen-Kragh J, Haugen M, Borchgrevink CF, et al. Controlled trial of fasting and one-year vegetarian diet in rheumatoid arthritis. Lancet. 1991;338:899–902.
6. Kremer JM. n-3 fatty acid supplements in rheumatoid arthritis. Am J Clin Nutr. 2000;71(1 Suppl):S349–S351.
7. Stone J, Doube A, Dudson D, Wallace J. Inadequate calcium, folic acid, vitamin E, zinc, and selenium in rheumatoid arthritis patients: results of a dietary survey. Semin Arthritis Rheum. 1997;27:180–185.