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The Physicians Committee




Section Eight: Nutrition and Arthritis

Arthritis is painful for patients and frustrating for doctors. Typical anti-inflammatory treatments help, but they often fail to ease all symptoms and do nothing to stop the progressive joint damage that leads to surgery or loss of function.

Nutrition can help, either with medicines or, in some cases, instead of them. Foods affect the joints in two major ways. First, certain foods trigger the symptoms of rheumatoid arthritis, and eliminating these foods sometimes causes even long-standing symptoms to improve or even remit entirely. Second, certain fatty acids have an anti-inflammatory action that can reduce joint pain, stiffness, and swelling.

The role of nutrition in arthritis was controversial until the early 1990s when research studies established its role beyond any reasonable doubt. Prior to that time, intriguing individual case reports were published in the medical literature showing the dramatic effects of avoiding certain foods, but left unanswered the question of how widespread such sensitivities were.

In 1981, the British Medical Journal reported the case of a woman whose battle with rheumatoid arthritis suddenly ended when doctors discovered that her symptoms were triggered by corn products. Corn was eliminated from her diet and, after 25 years of joint pains, her symptoms were gone. Her doctors reported, however, that six weeks after her remarkable recovery her joint pain returned. They began to suspect that her improvement had been nothing more than a placebo effect until they discovered that the cook preparing her food had started using corn starch as a thickening agent. After eliminating the corn starch, her symptoms again disappeared.1

Such case reports led to open and placebo-controlled food challenge experiments. In 1991, researchers in Oslo, Norway, reported in The Lancet a study in which they eliminated foods believed to be common arthritis triggers in a group of 26 arthritis patients. The average pain score fell from over five, on a scale from zero to ten, to under three. Joint stiffness, swelling, and tenderness diminished, and grip strength also improved. Most importantly, the benefits were sustained on reexamination a year later.2

Numerous studies have shown that, if testing is done with sufficient care, dietary sensitivities can be identified in 20-60 percent of subjects. Pure vegetarian (vegan) diets appear to benefit about half of arthritis patients, including some who have not identified a specific diet trigger.2-6

Clinical Use of Nutrition with Arthritis Patients

Patients can be assessed individually for the presence or absence of dietary sensitivities. Normally this is done with both the patient and doctor aware of which foods are being tested, but it can also be done using placebo controls, with the patient’s consent, as will be discussed in more detail below.

The first step is for the patient to base the diet on generous amounts of foods that are known to virtually never cause symptoms (Table 1) and, at the same time, omit those that commonly trigger symptoms (Table 2). It is important to avoid the problem foods completely, as even a small amount can cause symptoms. Foods that are on neither list can be consumed. A four-week period will be enough to gauge the effects.

Such tests are not difficult if the patient and whoever prepares his/her food receive instruction and recipes from a cooking instructor, who should meet with them at least weekly. This is best done in groups, as patients support each other through the dietary transition.

After four weeks, if the patient’s symptoms have diminished or disappeared, the next step is to identify which of the trigger foods has been responsible for the symptoms. This is done by reintroducing the eliminated foods back into the diet one at a time, every two days. The patient should have a generous amount of each newly returned food to see whether joint pains recur. If so, it should again be eliminated for at least two weeks. Many patients have more than one food trigger.

There is no clinical value in returning meats, dairy products, or eggs to the diet, since they tend to have substantial amounts of cholesterol and fat and other disadvantages. Patients who continue a vegetarian diet should be sure to include a source of vitamin B12 in their routine, such as a common multivitamin tablet.

Patients whose symptoms do not improve with the diet change may be sensitive to foods other than the common triggers. An elimination diet allows the doctor and patient to identify these culprits. For one week, the diet consists only of the foods that virtually never trigger joint pains (Table 1). Then, if symptoms have abated, the omitted foods are reintroduced one at a time, as described below.

TABLE 1: FOODS THAT VIRTUALLY NEVER TRIGGER JOINT PAINS1,3,4,7-11

Brown rice
Cooked or dried fruits: cherries, cranberries, pears, prunes (but not citrus fruits, bananas, peaches, or tomatoes)
Cooked green, yellow, and orange vegetables: artichokes, asparagus, broccoli, chard, collards, lettuce, spinach, string beans, summer or winter squash, sweet potatoes, tapioca, and taro (poi)
Water: plain water or carbonated forms
Condiments: modest amounts of salt, maple syrup, and vanilla extract

TABLE 2: COMMON ARTHRITIS TRIGGERS1,3,4,7-11

Dairy products* Citrus fruits
Corn Potatoes
Meats** Tomatoes
Wheat, oats, rye Nuts
Eggs Coffee

* All dairy products should be avoided: skim or whole cow’s milk, goat’s milk, cheese, yogurt, cream, etc.

** All meats should be avoided: beef, pork, chicken, turkey, fish, etc.

Additional foods have sparked symptoms in individuals, but are not known to do so in large numbers of people. These include alcoholic beverages, bananas, chocolate, malt, nitrates, onions, soy products, cane sugar, and spices (cardamom, coriander, and mint).

Natural Anti-Inflammatories in Foods

Common nonsteroidal anti-inflammatory pain-killers, such as aspirin or ibuprofen, work by blocking the prostaglandins that spark inflammation. Two natural plant fatty acids do much the same thing, albeit less strongly.

The first, called alpha-linolenic acid (ALA), is an omega-3 fatty acid found in many common vegetables, beans, and fruits, and in a more concentrated form in flax, canola, wheat germ, and walnut oils. The second, called gamma-linolenic acid (GLA), is an omega-6 fatty acid found in some unusual seed oils: borage oil, evening primrose oil, blackcurrant oil, and hemp oil.*

At the University of Pennsylvania in 1993, patients with rheumatoid arthritis were given four capsules of borage oil each day, while a control group took placebo capsules made of cottonseed oil. On examination six months later, joint swelling and tenderness were reduced by about 40 percent, morning stiffness was down by 33 percent, and pain was 15 percent less, compared to baseline in the borage oil group, in contrast to the gradual worsening of the placebo group over the same period.12

Similar results have been demonstrated with evening primrose, blackcurrant, and flax oil.13,14 Typical kitchen oils and fats, such olive oil, corn oil, sunflower oil, safflower oil, lard, or butter have no anti-inflammatory action.15

* Fats are named by the location of their first double bond. Omega-3 (or n-3) fatty acids have their first double bond at the third carbon atom from the methyl end of the molecule. Omega-6 (or n-6) fatty acids have their first double bond at the sixth carbon atom.

ALA CONTENT OF NATURAL OILS16-17

Canola oil

11%

Flaxseed oil

53-62%

Linseed oil

53%

Soybean oil

7%

Walnut oil

10%

Wheat germ oil

7%

GLA CONTENT OF NATURAL OILS

Blackcurrant oil

17-18%

Borage oil

24%

Evening primrose oil

8-10%

Hemp oil

19%

The Anti-Inflammatory Mechanism of Natural Oils

Inflammation is controlled by prostaglandins and other compounds produced by the cells. Prostaglandin E-2 has an inflammatory action that can damage the body’s tissues. It is produced from traces of fat stored within cell membranes. Specifically, it is made from arachidonic acid, which is found in meats (the average omnivore ingests between 200-1,000 milligrams of arachidonic acid each day) or (indirectly) from linoleic acid, which comes from cooking oils, particularly corn, sunflower, safflower, and cottonseed oils.18 Plants contain no arachidonic acid, because they do not have the enzymes that make it.

The GLA in borage, evening primrose, blackcurrant, or hemp oil is converted to prostaglandin E-1, and the ALA in many plant foods is converted to prostaglandin E-3. Both of these prostaglandins have an anti-inflammatory effect.

The fats in the diet determine the composition of the fats in the cell membranes. In turn, these membrane lipids influence which type of prostaglandin actions will predominate. Typical Western diets include 20 times as much linoleic acid as ALA, or even more. A rebalancing of the diet toward ALA is believed to reduce the tendency toward inflammation.

Patients can purchase GLA at health food stores without a prescription. It is most concentrated in borage oil. A quarter-teaspoon supplies 300 milligrams of GLA.

A typical arthritis regimen includes each of the following daily, usually with the evening meal:

  1. Borage, blackcurrant, or evening primrose oil, containing 1.4 grams of GLA
  2. Flax oil, one tablespoon (or 4 capsules)
  3. Vitamin E, 400 IU, or 100 IU for people with high blood pressure (vitamin E protects against oxidation of the oils)

It can take several weeks for these oils to work, and up to six months to see their full effect. Side effects, such as loose stools, are usually mild and transitory. GLA may increase the possibility of miscarriage.

Some people use fish oils for their omega-3s. However, plant-derived omegas-3s have none of the fish odor that can be apparent in the perspiration of people using fish oil. They also tend to be more chemically stable, and are lower in saturated fats. Between 15-30 percent of fish oil is saturated fat, which is about double that of plant oils. Fish oils are in no way unique. Fish make their omega-3 oils from ALA in plankton, just as mammals, including humans, synthesize omega-3s from land plants.

The New Science of Omega-3s

Omega-3 oils were not known to be needed in the diet until a six-year old girl demonstrated their importance in 1982. She had lost most of her intestinal tract in a gunshot accident and had to be fed intravenously. She gradually developed symptoms of nerve abnormalities, including numbness and blurred vision, and eventually became unable to walk. Her doctors suspected that the problem might be a lack of ALA in her feeding solution. They added it, and her symptoms soon disappeared.21

Natural ALA in Foods

ALA is found in green leafy vegetables, beans and other legumes, and fruits. These plants have little oil of any kind, and what they have is heavily balanced toward ALA, as opposed to other kinds of fats. Nuts are an exception in that they are quite high in oils. In 100 grams (about four ounces) of walnuts, there are 57 grams of fat, of which 7 grams are ALA.

Diets rich in animal fats, shortenings, and cooking oils (e.g., corn oil or cottonseed oil) encourage the incorporation of unhelpful fats into the cell membranes, rather than ALA. These fats tie up the enzymes that would otherwise use ALA, and, in the process, encourage inflammation.17-20 However, a change in the diet causes a gradual change in the fats within the cell membranes.

The body’s requirement for essential fatty acids is very low, only about 3-4 percent of calories. Most Americans get approximately ten times that amount, and Western diets, unfortunately, are heavily weighted toward linoleic acid and saturated fats.

PLANT FOODS RICH IN ALA

Vegetables purslane, lettuce, broccoli, spinach, etc.
Legumes navy, pinto, or lima beans; peas, spolit peas, etc.
Oils Flax, linseed, canola, and walnut oils are richest, followed by wheat germ and soy oils. Typical oils, such as corn, safflower, sunflower, or cottonseed oil are low in ALA.
Fruits Citrus fruits are rich in ALA, and can be used if you have established that they are not a pain trigger.

Ginger

The common cooking spice ginger has been used in Indian ayurvedic medicine for centuries as an arthritis treatment. In vitro studies show that it does indeed have anti-inflammatory effects, blocking enzymes that produce inflammatory prostaglandins. The same action has been demonstrated in blood tests with human volunteers.22

While ginger’s cellular effects have been well characterized, its effect on symptoms has been studied only anecdotally. A natural experiment was triggered accidentally by a team of researchers in Denmark, who had been studying ginger’s biochemical properties since the late 1980s. One of the researchers mentioned to a newspaper reporter that ginger blocks inflammation in the test tube and that it might prove useful for arthritis or other inflammatory diseases. Many readers decided to try it and began to call the research lab to report their results.23

In all, 28 patients with rheumatoid arthritis and 18 with osteoarthritis reported on their experiences. The vast majority had substantial reductions in pain and swelling. The most interesting report came from a person who had eaten a generous serving of Crabtree and Evelyn Ginger with Grapefruit Marmalade, which is 15 percent ginger. An anti-inflammatory effect persisted for several days.

The amount of ginger usually used is 1/2-1 teaspoon (1-2 grams) of powdered ginger each day, although some people have used up to four times this amount. Allow 4 to 12 weeks for benefits to appear. No adverse effects of ginger have been reported, and the U.S. government includes it on its Generally Recognized as Safe (GRAS) list.23

Other spices, including clove oil, garlic, turmeric, and cumin show similar effects in the test tube.22,24,25 In India, turmeric is applied to the skin or taken orally in doses up to five grams per day as an anti-inflammatory agent. None of these spices has been subjected to controlled tests, however, and may well never be, since they offer no profit opportunity to manufacturers.

However, clinicians can conduct well-controlled tests of diet hypotheses in what are called “n of 1” studies, referring to the fact that one patient is studied at a time. In an “n of 1” study, the doctor and patient agree that the doctor will provide the active compound or an identical placebo at different times, and the patient will carefully note the effects. If, say, three months on the active compound produce a noticeable change in the joints which disappears when the placebo is used, the result can be confirmed with repeat testing. If done carefully, such tests provide statistically meaningful results.

Stopping the Damage

On a molecular level, joint damage is caused by the actions of free radicals, unstable and destructive molecules produced during normal cellular metabolism. Free radicals are also made by white blood cells for use as weapons against bacteria.

Free radicals are an especially serious problem in joints that are already inflamed. In a swollen knee joint, for example, the blood flow is cut off momentarily with every pounding step. As the joint relaxes again, blood rushes in, and this ebb and flow of blood encourages the production of extra free radicals that assault the joint.

The cells protect themselves with antioxidants positioned within the cell membrane. Common antioxidants include beta-carotene, which gives carrots and sweet potatoes their orange color; vitamin E, found in grains, beans, and vegetables; and the mineral selenium, found in many grains and other plant foods.

Vitamin C, from fruits and vegetables, acts as an antioxidant in the blood and between cells. Vitamin C also repairs vitamin E that has been damaged in the battle against free radicals.

ANTIOXIDANTS IN FOODS

Source Vitamin C (mg) ß-carotene (mg) Vitamin E (mg)
Apple (1)

8

0.04

0.8

Broccoli

116

1.3

1.3

Brussels sprouts

96

0.67

2.0

Carrot (1)

7

12.0

3.0

Cauliflower

68

0.01

0.1

Chick peas

2

0.02

5.1

Grapefruit (1)

94

0.38

0.64

Navy beans

2

0

4.1

Pineapple

24

0.02

0.16

Rice (brown)

0

0

4.0

Soybeans

3

0.01

35.0

Spinach (fresh)

16

2.3

1.1

Strawberries

85

0.02

0.18

Sweet potato (1)

28

15.0

5.9

Serving sizes are one cup, except as otherwise noted.

Sources: Pennington JAT. Bowes and Church’s Food Values of Portions Commonly Used. 16th Edition, Philadelphia, J.B. Lippincott, 1994, and McLaughlin PJ, Weihrauch JL. Vitamin E content of foods. J Am Dietetic Asso 1979;75:647-65.

The Dangers of Iron

Iron aggravates free radical attacks. It catalyzes free radical production and also increases the damage they do.26 Although a small amount of iron is needed in order for red blood cells to carry oxygen, even modest excesses of iron can encourage free radical action.

Most American men and postmenopausal women have more stored iron than their bodies need, as a result of the overuse of supplements and meat-based diets. The following tests allow you to check your patients’ iron status:

  • Serum ferritin (normal values are 12-200 micrograms per liter)
  • Serum iron
  • Total iron binding capacity (TIBC)

Serum iron should be checked after an overnight fast. The serum iron measurement is divided by TIBC. The result should be 16-50 percent for women and 16-62 percent for men.

Results above these norms indicate excess iron. Results below these norms indicate too little iron. If the result suggests iron deficiency, you may request an additional test, called a red cell protoporphyrin test, for confirmation. A result higher than 70 micrograms per deciliter of red blood cells suggests insufficient iron. To diagnose iron deficiency, at least of two these three values (serum ferritin, serum iron/TIBC, or red cell protoporphyrin) should be abnormal.

If blood tests show excess iron, iron levels can be safely reduced with regular exercise and by donating blood. To help your patients keep iron in balance, encourage them to get their nutrition from grains, beans, vegetables, and fruits. They contain plenty of iron, but it is in a form that the body can more easily regulate. In contrast, meats contain a type of iron, called heme iron, that the body cannot regulate. Even if the body is already iron-overloaded, heme iron passes from the digestive tract into the bloodstream.

Fighting Arthritis with Antibiotics

Some forms of arthritis are caused by bacteria and are treated with antibiotics. Salmonella, campylobacter, and yersinia can cause arthritis symptoms that can linger for months or even years.27,28 About one in seven salmonella infections is accompanied by joint symptoms, typically affecting the knees, fingers, and shoulders.

The bacteria do not necessarily invade the joints. In some cases, the problem is an antibody reaction to the bacteria in the digestive tract.

Antibiotics are emerging as a potentially important, albeit controversial, treatment for arthritis, even when the responsible organism has not been identified. Bacterial infections have been suspected of playing a role in arthritis for decades, and the question now is not whether they cause joint symptoms, but how often.

Osteoarthritis

Osteoarthritis, also called degenerative joint disease, can be thought of as an effect of wear and tear on the body, causing bony spurs and damaged cartilage in the hands, wrists, hips, knees, feet, shoulders, or spine. Injuries and repetitive motions at work contribute to osteoarthritis, although running does not seem to.29-33

The most important preventive measure in osteoarthritis is weight control. Every ten pounds of excess weight increases the risk of osteoarthritis in the knees by 30 percent.29,34

The contribution of excess weight to arthritis is not simply the stress it puts on the knee joints. Overweight is also associated with a higher risk of osteoarthritis in the hands.34,35 While the reasons for this are unclear, one possible contributor is fat cells’ ability to produce estrogen. Some evidence suggests that excess estrogen contributes to joint problems, which may be why women have more osteoarthritis than men, especially if they have had symptoms of estrogen excess, such as uterine fibroids.36,37

Fortunately, the same diet changes that promote weight loss also reduce estrogen levels. Diets that are low in fat and high in fiber promote weight loss and also reduce blood estrogen concentrations.

Vitamin E has been shown to reduce pain and improve mobility in patients with osteoarthritis.38 A typical dosage regimen is 400 IU each day, or 100 IU for people with high blood pressure.

Gout

Gout is an excruciatingly painful condition that begins in the big toe, and eventually pain spreads to other joints. An examination of the joint fluid reveals uric acid crystals, and hospital treatment is usually necessary.

Uric acid is produced from the breakdown of proteins. Most animal species have enzymes in their bodies to eliminate uric acid. However, humans, insects, birds, and reptiles conserve uric acid, apparently because it is an antioxidant, rather like vitamin C. In gout, uric acid can build up in the joints, or in chalky deposits in the skin of the ear, the forearm, the elbow, or the Achilles tendon. White blood cells attempt to engulf it, triggering inflammation, pain, and joint damage.

Two parts of the diet—animal products and alcohol—increase the risk of gout. High-protein diets in general tend to encourage gout, although the worst contributors are shellfish, sardines, anchovies, organ meats (e.g., liver and kidneys), and beer.39,40

People with a tendency toward gout are particularly vulnerable to attacks during times of dietary change, so medications should be continued through any dietary transition.

A New Treatment from an Old Vine?

A surprising experimental treatment has emerged from an entirely unexpected source. The thunder god vine is a woody, rambling shrub that grows in southern China. Its leaves, flowers, and even the skins of the roots are poisonous. In fact, they are so poisonous that they have been used as an agricultural insecticide. Even ingesting honey that contains pollen from the plant can be fatal.

However, someone in the distant past somehow managed to discover that the interior of the roots of this toxic plant make an effective arthritis treatment, and it has been widely used in rural China.41

The modern history of the thunder god vine begins in the Chinese Cultural Revolution of the late 1960s, when Chairman Mao ordered China’s increasingly westernized doctors to leave the cities and become “barefoot doctors,” learning about traditional Chinese medicine in rural areas. Many of them were intrigued with the vine’s efficacy against inflammatory diseases, including arthritis. Many started to study extracts of the vine, and in the late 1980s, controlled research studies found that it effectively reduced joint stiffness, swelling, and tenderness, compared to a placebo. In fact, it worked better than typical non-steroidal anti-inflammatory drugs.42 That brought the vine to the other side of the Pacific, where University of Texas researchers are testing it in arthritis patients.41

It is a natural plant product, but it does have potential side-effects. It can cause a rash, gastrointestinal symptoms, temporary loss of menstrual periods, and reductions in blood counts. These effects will not rule it out as an arthritis treatment, however, because drugs typically used for arthritis pain also have significant side-effects. Stay tuned.

Topical Capsaicin for Osteoarthritis Pain

An unusual osteoarthritis treatment comes from hot chili peppers. Their “hot” ingredient, capsaicin (pronounced cap say’ a sin), is mixed into a cream which is applied to the skin over the painful joint. A brief stinging sensation stimulates the pain nerves and then gradually depletes a chemical called substance P, that nerves use to transmit pain signals.

In controlled studies, capsaicin reduces osteoarthritis pain by more than 70 percent.43 Because it is used topically, it has no drug interactions and no serious toxicity. The main side effect is a mild to moderate burning sensation on the skin which lasts about two hours after application during the first ten days or so of use. Capsaicin is sold in drug stores under the brand names Dolorac and Zostrix. The easiest and most effective regimen uses Dolorac (0.25 percent) cream twice a day directly on the affected joint. Zostrix is a more dilute cream that is usually used on a more frequent regimen.

Take Two Asps and Call Me in the Morning

The traditional Chinese arthritis treatment called “snake wine” was made by soaking 100 dead snakes in five liters of red wine with various herbs for three months, and adjusting the alcohol content to 40 percent. The arthritis sufferer drinks it three times per day. It is intoxicating, but it does nothing for your joints

Nutrition and Arthritis Study Questions

  1. Which foods do not commonly trigger joint pain?
  2. Which foods commonly trigger arthritis?
  3. What steps should you use to assess the presence or absence of dietary sensitivities in a patient?
  4. What two natural plant fatty acids work to block prostaglandins? What are good food sources of these fatty acids?
  5. Which spices have been found to exhibit anti-inflammatory effects?
  6. What roles do antioxidants play in patients with arthritis?
  7. What can you recommend to patients to reduce the risk of osteoarthritis?
  8. What factors influence the risk of gout?

References
1. Williams R. Rheumatoid arthritis and food: a case study. Br Med J 1981;283:563.
2. 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.
3. Hicklin JA, McEwen LM, Morgan JE. The effect of diet in rheumatoid arthritis. Clin Allergy 1980;10:463.
4. Panush RS, Carter RL, Katz P, Kowsari B, Longley S, Finnie S. Diet therapy for rheumatoid arthritis. Arth Rheum 1983;26:462-71.
5. Skoldstam L. Fasting and vegan diet in rheumatoid arthritis. Scand J Rheum 1986;15:219-23.
6. Kjeldsen-Kragh J, Haugen M, Borchgrevink CF, Forre O. Vegetarian diet for patients with rheumatoid arthritis—status: two years after introduction of the diet. Clin Rheum 1994;13:475-82.
7. Parke AC, Hughes GRV. Rheumatoid arthritis and food. A case study. Br Med J 1981;282:2027-9.
8. Ratner D, Eshel E, Vigder K. Juvenile rheumatoid arthritis and milk allergy. J Royal Soc Med 1985;78:410-3.
9. van de Laar MAFJ, van der Korst JK. Food intolerance in rheumatoid arthritis. I. A double blind, controlled trial of the clinical effects of elimination of milk allergens and azo dyes. Ann Rheum Dis 1992;51:298-302.
10. van de Laar MAFJ, Aalbers M, Bruins FG, van Dinther-Janssen ACHM, van der Korst JK, Meijer CJLM. Food intolerance in rheumatoid arthritis. I. Clinical and histological aspects. Ann Rheum Dis 1992;51:303-6.
11. Darlington LG, Ramsey NW. Review of dietary therapy for rheumatoid arthritis. Br J Rheum 1993;32:507-14.
12. Leventhal LJ, Boyce EG, Zurier RB. Treatment of rheumatoid arthritis with gammalinolenic acid. Ann Int Med 1993;119:867-73.
13. Pullman-Moor S, Laposata M, Lem D, et al. Alteration of the cellular fatty acid profile and the production of eicosanoids in human monocytes by gamma linolenic acid. Arthritis Rheum 1990;33:1526-33.
14. Belch JJF, Ansell D, Madho KAR, O’Dowd A, Sturrock RD. Effects of altering dietary essential fatty acids on requirements for non-steroidal anti-inflammatory drugs in patients with rheumatoid arthritis: a double blind placebo controled study. Ann Rheum Dis 1988;47:96-104.
15. Watson J, Madhok R, Wijelath E, et al. Mechanism of action of polyunsaturated fatty acids in rheumatoid arthritis. Biochem Soc Trans 1990;18:284-5.
16. Hunter JE. n-3 Fatty acids from vegetable oils. Am J Clin Nutr 1990;51:809-14.
17. Mantzioris E, James MJ, Gibson RA, Cleland LG. Dietary substitution with an alpha-linolenic acid-rich vegetable oil increases eicosapentaenoic acid concentrations in tissues. Am J Clin Nutr 1994;59:1304-9.
18. Phinney SD, Odin RS, Johnson SB, Holman RT. Reduced arachidonate in serum phospholipids and cholesteryl esters associated with vegetarian diets in humans. Am J Clin Nutr 1990;51:385-92.
19. Siguel EN, Maclure M. Relative activity of unsaturated fatty acid metabolic pathways in humans. Metabolism 1987;36:664-9.
20. Okuyama H. Minimum requirements of n-3 and n-6 essential fatty acids for the function of the central nervous system and for the prevention of chronic disease. Proc Exp Biol Med 1992;200:174-6.
21. Holman RT, Johnson SB, Hatch TF. A case of human linolenic acid deficiency involving neurological abnormalities. Am J Clin Nutr 1982;35:617-23.
22. Srivastava KC. Effect of onion and ginger consumption on platelet thromboxane production in humans. Prostaglandins Leukot Essent Fatty Acids 1989;35:183-5.
23. Srivastava KC, Mustafa T. Ginger (Zingiber officinale) in rheumatism and musculoskeletal disorders. Med Hypoth 1992;39:342-8.
24. Srivastava KC. Antiplatelet principles from a food spice clove (Syzgium aromaticum L). Prostglandins Leukot Essent Fatty Acids 1993;48:363-72.
25. Srivastava KC, Tyagi OD. Effects of a garlic-derived principle (ajoene) on aggregation and arachidonic acid metabolism in human blood platelets. Prostglandins Leukot Essent Fatty Acids 1993;49:587-95.
26. Merry P, Grootveld M, Lunec J, Blake DR. Oxidative damage to lipids within the inflamed human joint provides evidence of radical-medicated hypoxic-reperfusion injury. Am J Clin Nutr 1991;53:362S-9S.
27. Inman RD. Antigens, the gastrointestinal tract, and arthritis. Rheum Dis Clin N Am 1991;17:309-21.
28. Aoki S, Yoshikawa K, Yokoyama T, et al. Role of enteric bacteria in the pathogenesis of rheumatoid arthritis: evidence for antibodies to enterobacterial common antigens in rheumatoid sera and synovial fluids. Ann Rheum Dis 1996;55:363-9.
29. Hochberg MC. Epidemiologic considerations in the primary prevention of osteoarthritis. J Rheum 1991;18:1438-40.
30. Peyron JG. Is osteoarthritis a preventable disease? J Rheum 1991;18(suppl 27):2-3.
31. Felson DT, Hannan MT, Naimark A, et al. Occupational physical demands, knee bending, and knee osteoarthritis, results from the Framingham study. J Rheum 1991;18:1587-92.
32. Cooper C, McAlindon T, Coggon D, Egger P, Dieppe P. Occupational activity and osteoarthritis of the knee. Ann Rheum Dis 1994;53:90-3.
33. Lane NE, Michel B, Bjorkengren A, et al. The risk of osteoarthritis with running and aging: a 5-year longitudinal study. J Rheum 1993;20:461-8.
34. Hart DJ, Spector TD. The relationship of obesity, fat distribution and osteoarthritis in women in the general population: the Chingford Study. J Rheum 1993;20:331-5.
35. Carman WJ, Sowers MF, Hawthorne VM, Weissfeld LA. Obesity as a risk factor for osteoarthritis of the hand and wrist: a prospective study. Am J Epidemiol 1994;139:119-29.
36. Cauley JA, Kwoh CK, Egeland G, et al. Serum sex hormones and severity of osteoarthritis of the hand. J Rheum 1993;20:1170-5.
37. Spector TD, Hart DJ, Brown P, et al. Frequency of osteoarthritis in hysterectomized women. J Rheum 1991;18:1877-83.
38. Packer L. Interactions among antioxidants in health and disease: vitamin E and its redox cycle. Proc Soc Exp Biol Med 1992;200:271-6.
39. Gibson T, Rodgers AV, Simmonds HA, Court-Brown F, Todd E, Meilton V. A controlled study of diet in patients with gout. Ann Rheum Dis 1983;42:123-7.
40. Cleland LG, Hill CL, James MJ. Diet and arthritis. Ballière’s Clin Rheum 1995;9:771-85.
41. Lipsky PE, Tao XL. A potential new treatment for rheumatoid arthritis: thunder god vine. Semin Arth Rheum 1997;26:713-23.
42. Xue-Lian T, Ying S, Yi D, et al. A prospective, controlled, double-blind, cross-over study of tripterygium wilfodii hook F in the treatment of rheumatoid arthritis. Chin Med J 1989;102:327-32.
43. Schnitzer TJ, Posner M, Lawrence ID. High strength capsaicin cream for osteoarthritis pain: rapid onset of action and improved efficacy with twice daily dosing. J Clin Rheum 1995;268-73.



 

Table of Contents

Study questions included at the end of each section

Introduction

Section One:
Preventing and Reversing Heart Disease

Section Two:
Cancer Prevention

Section Three:
Cancer Survival

Section Four:
Diabetes

Section Five:
Foods and Blood Pressure

Section Six:
Nutrition and Renal Disease

Section Seven:
Preventing and Reversing Osteoporosis

Section Eight:
Nutrition and Arthritis

 
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