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Dietary and Drug Management of Gout

Posted on: 11/30/1999
If you have gout (or are at risk for developing gout) do you have to restrict your diet? Is it okay to eat meat? Dairy products? Is protein helpful or harmful? If meat isn't okay, what about seafood? Can alcohol and leafy green vegetables bring on an attack of gout?

These and other questions about the prevention and treatment of gout are discussed in this update on the condition. For years, dietary restrictions and advice have been at the forefront of managing gout. Studies over the last 30 years are starting to shed some light on the true evidence behind some of these recommendations.

Gout is a disease that involves the build-up of uric acid in the body. Uric acid is a normal chemical in the blood that comes from the breakdown of other chemicals in the body tissues. About 95 percent of gout patients are men. Most men are over 50 when gout first appears. Women generally don't develop gout until after menopause. But some people develop gout at a young age.

Everyone has some uric acid in his blood. Excess uric acid causes needle-shaped crystals to form in the synovial fluid. As your immune system tries to get rid of the crystals, inflammation develops. For the person with too much uric acid, this inflammation can cause painful arthritis. Gout was the first disease in which researchers recognized that crystals in the synovial fluid could be the cause of joint pain. Synovial fluid is the fluid that the body produces to lubricate the joints.

We know that eating too much meat (especially organ meat) and seafoods high in protein and purine content increases the risk of a gouty attack. But is it the protein or the purine that causes the problem? Studies have confirmed it's the purine content (not the protein) that's causing the elevated urate levels in the blood.

On the other hand, dairy products seem to help reduce levels of urate in the blood. In fact, it looks like the combination of high protein and low purine levels in dairy products is what functions as a natural anti-gout diet. And although leafy, green vegetables are high in purine, eating them doesn't seem to really be linked with an increased risk of gout.

And now for the beverages (alcoholic and nonalcoholic). Beer and hard liquor definitely increase blood levels of uric acid. The more alcohol is consumed, the higher the levels of serum urate, and the greater risk of gout. But there's been a surprising finding about wine. Wine seems to lower serum urate levels. Whether or not red versus white wine works better and in what amounts remains a mystery for now.

Sugar may also be a key factor in the development of gout. Data supports a rising number of obese patients are developing gout these days. The introduction of high-fructose corn syrup in the 1960s has escalated these findings even faster. Sugar consumption in many and varied forms has increased dramatically in the last 50 years.

Sweeteneners are used now more than ever and in products previously sold without such sweeteners. Scientists have been able to pinpoint the complex mechanism by which fructose stimulates uric acid production. Once again, men seem more susceptible to the effects of beverages containing fructose (e.g., soda pop, sports drinks) as a potential cause of gout.

And finally, the link between caffeine (and especially caffeinated coffee) and gout has been investigated. It appears that coffee actually lowers serum urate levels -- but not because it has caffeine in it. Some other chemical or factor is involved. Scientists aren't sure what that is just yet.

There are drugs to prevent and/or treat painful gouty attacks. But they don't work for everyone and they often have nasty side effects. And many patients have other health problems (e.g., diabetes, hypertension, kidney disease) that make it impossible to take the current drugs for gout.

So there's a call for safer, more effective therapy for gout. What's on the horizon right now? Well, the European Commission (like the U.S. Food and Drug Administration) has approved a new therapy called febuxostat. It lowers uric acid slowly enough to avoid flaring up the gout. It isn't processed by the kidney, so it's possible patients with kidney disease may be able to take it. But it is metabolized by the liver. Anyone with a liver problem or who abuses alcohol may not be able to take this drug.

When all else fails, there is a rather expensive ($8,000 per dose), but effective enzyme treatment (pegylated uricase) that may be helpful for rescue therapy. Rescue therapy refers to the patient with extreme, uncontrolled, and very painful gout for whom nothing else has worked. Once the worst of the problem has been treated, the patient can be switched to something else (one of the more standard treatments available).

Scientists continue to explore all avenues of possibility in seeking a way to prevent, treat, and/or manage gout. As new biologic agents are developed for other inflammatory conditions, these will be tried with patients who have gout. The hope is to find something that works quickly in order to offset the high cost of most new drugs.

References:
Michael H. Pillinger, MD, and Robert T. Keenan, MD. Update on the Management of Hyperuricemia and Gout. In Bulletin of the NYU Hospital for Joint Diseases. 2008. Vol. 66. No. 3. Pp. 231-239.

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