From The July 1999 issue of Nutrition Science News
Ease Gout Pain
By C. Leigh Broadhurst. Ph.D.
Diet and supplements to manage uric acid metabolism
A swollen big toe and a hobbled gait–finally, excruciating pain sends your customer to fill a prescription for allopurinol, the standard drug for treating gout. Are there natural remedies you can recommend to ease his suffering in addition to or instead of the pharmaceutical?
While gout cannot be cured, it can be controlled with medication, herbs, diet and nutritional supplements. Gout certainly isn’t a new condition and, in fact, usually is associated with the gluttony of the rich in the 1700s and 1800s. Since ancient times people have suffered from the pain and swelling caused by a precipitation of uric acid crystals (monosodium urate) in joints, tendons, kidneys and other tissues. Diet was always blamed–particularly rich foods such as gravies, organ meats and other proteins–but we now know gout can result from a number of genetic disorders that cause overproduction or impaired excretion of uric acid.
Gout affects between three and five adults per thousand in the general population, but more than 95 percent of cases occur in males older than 30. This means roughly one in 100 adult men have gout. Some 70 percent of gout patients have an overproduction of uric acid, while about 30 percent have problems eliminating it from their bodies. The result of either situation is excess uric acid (sodium urate) that crystallizes in joints and causes painful inflammation and severe arthritic symptoms. It is not clear what makes the uric acid precipitate in the joints, but it is not simply because there is too much present. Some patients can have chronically elevated uric acid levels with no other gout symptoms. Interestingly, the first joint of the big toe is affected in almost half of all first attacks, and there is a 90 percent chance that gout patients will have an attack in their toe at some time. Why the toe? Uric acid has a lower saturation point at lower temperatures, which may explain why deposits tend to form in the cooler extremities including the toe, or the top of the ear.
Uric acid is the normal form in which biochemicals called purines are excreted after they are digested and metabolized. Purines are components of the nucleic acids DNA and RNA. Randolph Nesse, M.D., of the University of Michigan Medical School, Ann Arbor, says uric acid is not all bad. In fact, it has antioxidant activity nearly equivalent to vitamin C, prompting some researchers to speculate that genes causing high levels of uric acid were not selected against because the uric acid helps protect against oxidative damage to cells.
Dietary Management of Uric Acid
It is impossible for anyone to completely eliminate purine metabolism, nor would anyone want to, because a large percentage of purines are generated as the body recycles its own tissue proteins. But dietary recommendations for gout management limit purine intake, and eliminate nearly all protein, especially meat. The high-purine foods to limit or avoid are organ meats, which are rich in nucleic acids, as well as anchovies, baker’s and brewer’s yeast, herring, mackerel, red meat, sardines and shellfish. Poultry and white fish–which also contain purines but have less dense muscle fibers, a different protein composition and more water per unit weight than red meat and dark fish–are better choices but should not be eaten in excess either. Legumes, especially peanuts, should also be limited or avoided because of their purine content. Nutritional yeast, supplements with DNA, RNA or organ tissue extracts such as thyroid or thymus can also pose a risk if taken regularly.
Get the Lead Out
Several hundred years ago, gout was attributed solely to overindulging in rich, fatty foods and alcohol, and the consequent obesity. While the implications of rich foods and alcohol for gout sufferers is well understood, the issue is slightly more complex.
For instance, saturnine gout, an uncommon and secondary type of gout, can result from lead toxicity. Historically, alcoholic beverages were often stored or served in vessels that contained lead. For example, lead crystal and ceramic glazes were used in drinking vessels. Even worse were pewter tankards–pewter is a metal alloy that traditionally contained lead.
When wine and fruit juices, which are quite acidic, are placed in lead-containing vessels, they react with the material and leach lead. Water and beer are less acidic and more neutral, but to a lesser extent also leach lead. It is now believed that long-term, subacute lead poisoning damaged the kidneys of heavy wine drinkers, greatly reducing their ability to excrete uric acid.
Today, lead-free ceramic glazes are used and pewter tankards are less prevalent. However, anyone with gout should still make an effort to remove sources of heavy-metal contamination from their drinking water, food and home environment. Drinking-water filtration systems that remove lead are inexpensive and readily available.
Alcohol consumption exacerbates gout by reducing uric acid elimination from the body and slightly increasing uric acid production. Beer and wine are higher in purines than other alcoholic beverages because of their yeast residues. Heavy drinkers are more likely to have gout than those who drink less.
Very high intakes of fructose–25 to 30 percent of calories–can also elevate uric acid, so those with gout should minimize fructose intake, namely high fructose corn syrup, which is present in many processed foods and beverages.
A gout-prevention diet should emphasize complex carbohydrates and plenty of water. Adequate fluid intake dilutes the urine and promotes excretion of uric acid. The more diluted the urine, the less risk there is for developing kidney stones, which can be a problem for gout patients.
The enzyme xanthine oxidase catalyzes the last step in the conversion of purines to uric acid. Allopurinol, the medication prescribed for gout prevention, is a xanthine oxidase inhibitor. In vitro, xanthine oxidase is inhibited by the flavonoids luteolin and apigenin nearly as well as it is by allopurinol. The flavonoids chrysin, baicalein, isorhamnetin, and several caffeic acid esters are also effective. Flavonoids, which are water-soluble plant pigments, are part of a large group of antioxidant phytochemicals. Chamomile (Matricaria recutita), chiso (Perilla frutescens), many mints (Mentha spp.) and yarrow (Achillea millefolium) are rich in luteolin, apigenin and caffeic acids. Those flavonoids can also be found in carrots. There are no clinical studies proving these herbs can prevent gout recurrence, but they are safe and worth a try.
Baikal skullcap (Scutellaria baicalensis) and Taiwanese skullcap (S. rivularis) contain baicalein as well as several other anti-inflammatory flavonoids. Both the isolated flavonoids and herbal extracts from skullcap have shown effectiveness against paw inflammation in mice and are used traditionally for chronic inflammatory conditions and liver disorders. I recommend a combination of the herbs daily as a preventive measure: three capsules each of standard dose baikal skullcap, chamomile and yarrow. Incorporating chiso leaf and peppermint tea is also a good idea. Keep in mind that a customer would need quite high doses of these herbs to make an impact, but they can be supportive when taken in conjunction with diet modification.
Other xanthine oxidase inhibitors, albeit weak ones, are anthocyanidins and proanthocyanidins. Cherries, grapes, blueberries and bilberries contain both these antioxidants. Eating cherries has been shown to lower uric acid levels and prevent gout attacks. Gout sufferers should try to incorporate one-half pound of fresh cherries (weighed with pits) into their daily diet. In addition to berries, extracts of bilberry (Vaccinium myrtillus), grape seed (Vitis vinifera) or pine bark (Pinus maritima) are rich sources of anthocyanidins and proanthocyanidins.
James Duke, Ph.D., botanist and medicinal plant authority in Fulton, Md., treats his gout with celery (Apium graveolens) seed extract instead of allopurinol. Though there is no research to support this medicinal use, Duke says celery has at least 26 anti-inflammatory compounds. These anti-inflammatory qualities explain at least part of celery’s beneficial effects. The celery plant has apigenin, but it is not concentrated in the seeds, so if the seeds do inhibit xanthine oxidase, the mechanism is currently unknown. Duke takes four capsules of celery seed extract daily–a 450-mg dose–and has not had an attack since he began the treatment.
Colchicine, an anti-inflammatory drug originally derived from the autumn crocus, also called meadow saffron (Colchicum autumnale) bulb, is often prescribed to alleviate acute gout. Colchicine does not affect uric acid levels; rather it stops the inflammatory process. A typical dose of colchicine is 1 mg orally every two hours or up to 7 mg in 24 hours for acute attacks. Many patients cannot tolerate the therapeutic dose, which can cause gastrointestinal side effects. Autumn crocus and related lily bulbs such as daylilies may have colchicine and are sometimes available in herbal products. These plants have poisonous alkaloids, so advise customers not to self-medicate with crocus or lily bulbs.
During acute gout attacks, herbal anti-inflammatories including boswellia (Boswellia serrata), curcumin (Curcuma longa), devil’s claw (Harpagophytum procumbens) and yucca (Yucca spp.) can be tried instead of aspirin or arthritis drugs. The British Pharmacopoeia recommends guaiacum resin extract (Guaiacum officinale; G. sanctum), an anti-inflammatory, for gout. Commercial preparations are available in the United Kingdom. Boswellia is similar to guaiacum in terms of the types of phytochemicals present and is more readily available in North America. Whichever herb is selected, the dosage should be at least two 500-mg caspsules of the dried herb three times daily for two to seven days. While the herbs mentioned here do not work as quickly as colchicine, they should help within 24 to 48 hours.
Nutrients to Keep Gout at Bay
Though not as useful as some of the herbal remedies for easing pain, supplements can be an important part of a preventive plan.
Omega-3 fatty acids can be useful in the treatment of gout. Eicosapentaenoic acid (EPA) inhibits production of the inflammatory leukotrienes, which are responsible for much of the inflammation and tissue damage that occurs with gout.
Folic acid has been shown to inhibit xanthine oxidase. While research isn’t totally conclusive, positive results have been reported by gout sufferers. The recommended daily dose is 10 to 40 mg. Folic acid should only be supplemented under a health care provider’s supervision.
Other anti-inflammatory supplements, including the amino acids alanine, aspartic acid, glutamic acid and glycine; the flavonoid quercetin; and vitamin E, can be useful but do not have research specifically supporting their application for gout.
High doses of niacin, greater than 50 mg daily, are not recommended for people with gout because niacin competes with uric acid for bodily excretion. Vitamin C in doses greater than 3,000 mg is also contraindicated for gout sufferers because it may increase uric acid in some people.
Gout should not be left untreated. Over time, microscopic crystals of sodium urate can damage organs, particularly the heart and kidneys. Increased uric acid levels can also increase the risk of kidney stones. Luckily, modest dietary modifications and a carefully planned supplements program can obviate prescriptions and lessen the suffering from gout attacks.
1. Strohecker J. Editor. Alternative medicine: the definitive guide. Puyallup (WA): Future Medicine Publishing; 1994.
2. Nesse RM, Williams GC. Why we get sick–the new science of Darwinian medicine. New York: Random House; 1994.
3. Gibson T, et al. A controlled study of diet in patients with gout. Ann Rheum Dis 1983;42:123-7.
4. Henry RR, et al. Current issues in fructose metabolism. Ann Rev Nutr 1991;11:21-39.
5. Cos P, et al. Structure-activity relationship and classification of flavonoids as inhibitors of xanthine oxidase and superoxide scavengers. J Nat Prod 1998;61:71-6.
6. Nakanishi T, et al. Two new potent inhibitors of xanthine oxidase from leaves of Perilla frutescens Britton var. acuta Kudo. Chem Pharm Bull 1990;38:1772-4.
7. Duke JA, et al. U.S. Department of Agriculture Phytochemical and Ethnobotanical Data Base (http://www.ars-grin.gov/duke/) 1999.
8. Lin CC, Shieh DE. In vivo hepatoprotective effect of baicalein, baicalin, and wogonin from Scutellaria rivularis. Phytother Res 1996;10:651-4.
9. Chung CP, et al. Pharmacological effects of methanolic extract from the root of Scutellaria baicalensis and its flavonoids on human gingival fibroblasts. Planta Med 1995;61:150-3.
10. Blau LW. Cherry diet control for gout and arthritis. Texas Rep Biol Med 1950;8:309-11.
11. Handa SS, et al. Plants with anti-inflammatory activity. Fitoterapia 1992;63:3-12.
12. Evans WC. Trease and Evans’ pharmacognosy. London: W.B. Saunders; 1998.
13. Ammon HPT, et al. Mechanism of anti-inflammatory actions of curcumine and boswellic acids. J Ethnopharm 1993;38:113-9.
14. Terano T, et al. Eicosapentaenoic acid as a modulator of inflammation, effect on prostaglandin and leukotriene and leukotriene synthesis. Biochem Pharmacol 1986;35:779-85.
15. Lewis AS, et al. Inhibition of mammalian xanthine oxidase by folate compounds and amethopterin. J Biol Chem 1984;259:12-5.
16. Stein HB, et al. Ascorbic acid-induced uricosuria: a consequence of megavitamin therapy. Ann Int Med 1976;84:385-8.
C. Leigh Broadhurst, Ph.D., is a visiting scientist for a government nutrition research laboratory and heads 22nd Century Nutrition, a nutrition and scientific consulting firm in Silver Spring, Md.