Nutritional Influences on Illness: Gout


Observational Study: The major dietary difference of 61 men with gout versus healthy controls was that 41% of the afflicted men drank more than seven 12-ounce cans of beer daily compared to 17% of the healthy men. This difference was associated with a significantly higher intake of purine nitrogen, half of which was derived from beer (Gibson T et al., A controlled study of diet in patents with gout. Ann Rheum Dis 42( 2):123-27, 1983).


It is well known that dietary sources of purines (such as organ meats, seafood, lentils, beans and peas) may increase uric acid and thereby precipitate gout in people with impaired uric acid metabolism. The above study is interesting because it found that beer, rather than the foods just mentioned, was the major dietary feature that distinguished a group of patients from normals. Since beer has a higher purine content than wine or spirits, it is particularly important to avoid it as part of the dietary treatment of gout -- which, by the way, is said to decrease serum uric acid by as much as 1 milligram per 100 milliliters.

The other dietary manipulation is to minimize the consumption of fructose. Fructose has been found to increase urate production, and thus may foster hyperuricemia.( 1)

The literature on nutritional treatments for gout is rather sparse. In 1976, researchers found that 8 grams of vitamin C daily decreased serum uric acid levels by 1.2 to 3.1 mg% as a result of a sustained increase in urinary excretion of uric acid.( 2) Rather than viewing this as a possible therapeutic effect, the investigators simply warned their readers that ascorbic acid could invalidate uric acid measurements and thus obscure the diagnosis of gout. A study published the following year confirmed that vitamin C had a uricosuric effect at higher levels of intake, and suggested that this effect may be due to competition with uric acid for renal tubular reabsorptive transport.( 3)

In 1981, however, a group of investigators, using different laboratory procedures, was unable to demonstrate any effect of 12 grams of vitamin C on serum uric acid concentration or uric acid excretion and clearance by the kidney. They suggested that the earlier findings were merely due to interference by ascorbic acid with the measurement of uric acid.( 4) While subsequent studies -- performed on normal subjects -- also failed to find much of a uricosuric effect, the question of how effective high-dose ascorbate supplementation may be for the treatment of hyperuricemia seems to remain unanswered.

Folic acid supplementation has met a similar fate. Folate inhibits xanthine oxidase, an enzyme needed for uric acid production, and Kurt Oster had suggested that, at high dosages, it could reduce elevated uric acid levels more safely than drugs.( 5) However, a 1980 study found that massive dosages, while well absorbed, failed to affect uric acid levels in hyperuricemic subjects.( 6) Since then nobody has been interested in replicating that study -- or in studying the combined effect of folic acid and ascorbic acid in hyperuricemic patients.

Niacin competes with uric acid for renal excretion.( 7) As it could precipitate an attack of gout in these patients, its use as a supplement should be avoided. Caution is also advised with vitamin A supplementation, as the same enzyme that converts xanthine to uric acid (xanthine oxidase) also converts retinol to its more toxic metabolite, retinoic acid.( 8)

Dr. Werbach cautions that the nutritional treatment of illness should be supervised by physicians or practitioners whose training prepares them to recognize serious illness and to integrate nutritional interventions safely into the treatment plan.

(1.) Henry RR, Crapo PA, Thorburn AW. Current issues in fructose metabolism. Annu Rev Nutr 11:21-39, 1991.

(2.) Stein HB, Hasan A, FoxIH. Ascorbic acid-induced uricosuria. A consequence of megavitamin therapy. Ann Intern Med 84(4):385-8, 1976.

(3.) Berger L, Gerson DC, Yü TF. The effect of ascorbic acid on uric acid excretion with a commentary on the renal handling of ascorbic acid. Am J Med 62(1):71-6, 1977.

(4.) Mitch WE, Johnson MW, Kirshenbaum JM, Lopex RE. Effect of large oral doses of ascorbic acid on uric acid excretion in normal subjects. Clin Pharmacol Ther 29(3):318-21, 1981.

(5.) Oster KO. Evaluation of serum cholesterol reduction and xanthine oxidase inhibition in the treatment of atherosclerosis. Recent Adv Stud Cardiac Struct Metab 3:73-80, 1973.

(6.) Boss GR et al. Failure of folic acid (pteroylglutamic acid) to affect hyperuricemia. J Lab Clin Med 96:783, 1980.

(7.) Pfeiffer CC. Mental and Elemental Nutrients. New Cannaan, CT, Keats Publishing, 1975: 121.

(8.) Mawson AR, Onor GI. Gout and vitamin A intoxication: is there a connection? Semin Arthritis Rheum 20(5):297-304, 1991.

Reprinted with permission from the Journal of Alternative and Complementary Medicine, Green Library, Homewood NHS Trust (DHQ), Guildford Road, Chertsey, Surrey KT16 0QA, United Kingdom.

Article copyright Townsend Letter for Doctors & Patients.


By Melvyn R. Werbach

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