For hundreds of years the painful joint malady gout has been associated with overindulgence in rich food and drink. In the April 17 issue of The Lancet, researchers report the first study to conclusively show that certain alcoholic beverages can significantly increase the risk of gout. But although greater risk was associated with intake of beer and liquor, consumption of wine did not appear to increase risk. Last month the same research team reported in The New England Journal of Medicine that consumption of certain meats and seafood – but not vegetables and overall protein – also increase the risk of gout, while dairy foods may reduce the risk.
"It is well known that alcohol can raise levels of uric acid in the blood, but its role in actually increasing the risk of gout had never been confirmed," says Hyon Choi, MD, DrPH, a staff rheumatologist at the Massachusetts General Hospital (MGH) who led the study. "This is the first study to confirm what we have long suspected." The report is part of the Health Professionals Follow-up Study, which is based at the Harvard School of Public Health (HSPH).
A painful condition affecting more than 5 million adults in the U.S., gout is caused by deposits of uric acid in connective tissue, often in joints of the feet or ankles, that lead to inflammatory arthritis. Symptoms include swelling, redness, stiffness, and severe pain. Although attacks of gout can subside in a few days, repeated attacks can cause permanent joint damage, and the disease often results in substantial disability, occupational limitations and frequent medical care. Treatment includes the pain-relieving drugs called NSAIDs (non-steroidal anti-inflammatories) and for more serious outbreaks, corticosteroid drugs like prednisone. Most patients with gout eventually require long-term treatment with medications that lower blood uric acid levels.
Initiated in 1986, the Health Professionals Follow-up Study has gathered information regarding the relationship between dietary factors and several illnesses from more than 50,000 men employed in the health professions. Every two years participants complete questionnaires regarding their diseases and health-related topics like smoking and exercise, and every four years the questionnaires also collect comprehensive dietary information, including alcohol consumption.
The current investigation began with 47,000 men who did not report a history of gout at the study's outset. Participants who subsequently reported developing gout were surveyed to verify that they met standard criteria for the disorder, confirming a diagnosis of gout in 730 men by 1998. The researchers then analyzed dietary information that all study participants provided in 1986, 1990 and 1994 to determine whether alcohol consumption had an effect on their risk for gout.
The results confirmed that alcohol intake in general was associated with increased risk for gout. Overall the risk was 2.5 times higher among men who consumed more than 50 grams of alcohol daily (the equivalent of four or five drinks), and even those who consumed as little as 10 to 15 grams a day (about one drink) had a 30 percent increase in risk.
When the type of beverage consumed was analyzed, it was found that intake of two or more 12-ounce beers daily increased risk 2.5-fold, while consuming two drinks that each contained a shot of liquor increased risk 1.6 times. No increase was seen with consumption of two 4-ounce glasses of wine.
"While there had been some suggestion that beer might have a greater contribution to risk, we were surprised to see such a strong difference," Choi says. "It certainly suggests that individuals with gout should try to limit or even cut out their beer consumption, whereas wine may be allowed, given other health benefits associated with moderate alcohol consumption" An instructor in Medicine at Harvard Medical School, Choi adds that the lack of risk associated with wine also suggests a potential direction for future research into possibly protective components of that beverage.
Choi's co-authors include senior author Gary Curhan, MD, ScD, of HSPH and the Channing Laboratory at Brigham and Women's Hospital (BWH), Karen Atkinson, MD, MPH, of the MGH Rheumatology Unit; and Elizabeth Karlson, MD, and Walter Willett, MD, DrPH, of BWH and HSPH. The study was supported by grants from the National Institutes of Health and TAP Pharmaceuticals.
Materials provided by Massachusetts General Hospital. Note: Content may be edited for style and length.
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