Natural gout medication

by Nathan Wei, MD, FACP, FACR

Nathan Wei is a nationally known board-certified rheumatologist and author of the Second Opinion Arthritis Treatment Kit. It's available exclusively at this website... not available in stores.

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Gout is due to an inability to process uric acid.

Uric acid levels can become elevated by eating purine-rich foods such as meats, by the overproduction of uric acid by the body, or inability of the kidneys to eliminate excess uric acid.

When uric acid reaches a critical level in the blood it precipitates out in the form of monosodium urate crystals. In gout, the crystals are deposited in connective tissue and joint spaces leading to inflammation.

People with high levels of uric acid in the blood (hyperuricemia) do not always develop gout. Therefore, it is not necessarily the high level of uric acid causing gout but perhaps a shift in its distribution or other factors. Gout attacks can occur as a result of dehydration, injury, fever, heavy eating, heavy drinking of alcohol, and recent surgery. Other contributory factors include obesity, weight gain, high blood pressure, abnormal kidney function, and drugs.

Gout usually attacks a single joint suddenly. An initial attack of gout may last several days and disappear even if untreated. Subsequent attacks may not occur for weeks, months, years, or never. In severe cases, repeated attacks occurring over a long period cause damage to joints and internal organs.

A definitive diagnosis of gout can be made by examination of aspirated joint fluid with a polarizing light microscope for evidence of crystals. Approximately one million people in the United States suffer from gout. The incidence is rising dramatically. It is nine times more common in men than women, predominantly after puberty with a peak age of 75. Gout attacks in women usually occur after menopause.

Prevention of acute gout involves:

• maintaining adequate fluid intake
• weight reduction
• dietary changes
• reduction in alcohol consumption
• medications to reduce hyperuricemia

Medication treatment of gout:

1. Tylenol or other analgesics - for pain
2. NSAIDS, colchicine, or corticosteroids - for anti-inflammatory response for acute attacks
3. Probenecid and Anturane - to decrease uric acid blood levels by increasing the excretion of uric acid into the urine.
4. Allopurinol - to lower blood uric acid by preventing uric acid production. Zyloprim blocks the conversion of purine in foods to uric acid.
5. Uloric- to lower uric acid levels through a mechanism similar to that of allopurinol.
6. Krystexxa- converts uric acid to allantoin, an inert ingredient that is then excreted by the kidneys.

Results of a preliminary study by Agricultureal Research Service Scientists and their university colleagues suggest that some natural compounds in bing cherries may reduce painful arthritic inflammation. Eating cherries may also help lessen the severity of other inflammatory conditions, such as cardiovascular disease or cancer.

Cherries already have a reputation for fighting inflammation. So what's new about the ARS study?

"Our test is among the first to track anti-inflammatory effects of fresh bing cherries in a controlled experiment with healthy volunteers," says chemist Robert A. Jacob, who led the investigation. Jacob is now retired from the ARS Western Human Nutrition Research Center in Davis, California.

In previous studies at other laboratories, scientists analyzed extracts from sweet or tart cherries in vitro to learn more about the fruit's potential health-promoting properties. In contrast to these test-tube experiments, the California study is apparently the first to test key inflammatory disease indicators, or markers, in blood samples from healthy volunteers who were fed precise amounts of fresh bing cherries. Reported in a 2003 issue of the Journal of Nutrition, the California investigation paved the way for a recent followup study at the Davis center.

Ten healthy women, aged 22 to 40, agreed to do that for the California scientists' preliminary study. Volunteers were instructed not to eat strawberries or other fruits and vegetables, or to drink tea or red wine, for the 2 days before the cherry breakfast. These foods are high in antioxidants, thought to fight inflammation. "They could have interfered with our ability to determine the specific effects of the Bing cherry antioxidants," explains Jacob.

"Our main focus in this study was gout, a very painful form of arthritis," says co-investigator Darshan S. Kelley, a chemist at the nutrition center. "During gout attacks, crystals of a naturally occurring chemical, uric acid, accumulate in joints—commonly in the toes—and cause pain. Urate in blood plasma is a precursor of these uric acid crystals. So, we closely measured volunteers' levels of plasma urate.

"We also indirectly measured the amount of urate that was moved out of the body in urine. We took blood plasma and urine samples before the volunteers ate the cherry breakfast and at intervals of 1-1/2, 3, and 5 hours afterward."

Volunteers' plasma urate levels decreased significantly over the 5 hours after their meal of cherries. Levels of urate removed from the body in urine increased over those 5 hours.

These urate results strongly suggest that cherries can play an important role in fighting gout. So do the results from the scientists' assays of some other indicators of inflammation. Significant changes in the levels of markers are an indication of a healthy immune system at work, attacking inflammation. Markers monitored included C-reactive protein, nitric oxide, and tumor necrosis factor alpha.

C-reactive protein, produced by the liver, increases rapidly during inflammation, such as during a gout atta

Another reliable sign of inflammation: the unwanted increase in nitric oxide. This biochemical is thought to play a role in damaging arthritic joints. The third marker, tumor necrosis factor alpha, is secreted in greater quantities when the body is fighting tumors that may induce inflammation. As is true for C-reactive protein, a healthy body that isn't fighting an inflammation has very little of this marker.

At the 3-hour monitoring interval, C-reactive protein and nitric oxide were somewhat lower than at the start of the study. "Even though these levels were not significantly lower, the trend was in the right direction and so is of interest," notes Kelley.

Unexpectedly, the scientists found no change in levels of tumor necrosis factor alpha. That's in contrast to a previous study, conducted elsewhere, in which natural compounds in fruits and vegetables were found to decrease levels of this marker. But the trends toward decreases in the other two markers do agree with results of other scientists' earlier, in vitro studies of cherry extracts.

Jacob and Kelley collaborated with chemists Giovanna M. Spinozzi and Vicky A. Simon of the nutrition center; chemist Ronald L. Prior, who is with ARS at Little Rock, Arkansas; and research associate Betty Hess-Pierce and professor Adel A. Kader, of the University of California, Davis.

The follow-up study, conducted in 2003, involved more people, more cherries, and a greater array of inflammatory-response markers. Eighteen women and two men—aged 22 to 40—participated in the 64-day investigation.

Many of the new volunteers began the study with elevated C-reactive protein levels. "That made it easier to detect any decline in C-reactive protein levels as the study progressed," says Kelley. "We're particularly interested in this protein because a recent major study indicated that it's more reliable than cholesterol as a predictor of cardiovascular disease.

"This group ate the same daily amount of fresh bing cherries as our earlier volunteers. But we asked them to eat the cherries throughout the day instead of just at breakfast." The volunteers did that for 28 consecutive days. The researchers are now analyzing blood samples.

Another study published in Arthritis and Rheumatism (2012) by Zhang and colleagues confirmed that cherry intake is associated with a lower risk of gout.

Other potentially helpful natural items to consider are:

• Vitamin C—8 g per day can lead to decreased blood uric acid levels. Note that there is a small subset of people with gout who will actually get worse with this level of vitamin C.
• Folic acid—10 to 75 mg per day inhibits xanthine oxidase, which is required for uric acid production.
• EPA (eicosapentaenoic acid) inhibits pro-inflammatory leukotrienes. Dose is 1,500 mg per day.

• Devil's claw (Harpagophytum procumbens) reduces pain and inflammation. Dose is 1 to 2 g three times per day of dried powdered root, 4 to 5 ml three times per day of tincture, or 400 mg three times per day of dry solid extract during attacks.
• Bromelain (Ananas comosus)—proteolytic enzyme found in pineapples (anti-inflammatory) when taken on an empty stomach. Dose is 125 to 250 mg three times per day during attacks.

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