Page last updated: Tuesday, November 18, 2008
Drinking Alcohol, and Gout
Gout is one of the oldest diseases in medical literature. The condition is not uncommon; it accounts for at least 5 percent of all significant problems in the field of systemic arthritis. It is uncommon, however, in women; the male-female ratio is 20:1.

In nearly three-quarters of the total number of cases the first attack of gout is confined to the large joint of one of the great toes; hence the Greek term Podagra, or gout of the foot. Podagra was also the name of a lesser goddess born of the seduction of Aphrodite by Dionysus, the deities, respectively, of love and the grape. Down through the ages gout has had a mixed reputation. It is slightly scandalous, through association with excessive food, drink, and sex. Gout was widespread during the Roman Empire and running through the ancient annals on gout is the relation between this disease and the consumption of dainty dishes and alcoholic beverages. Gout stood out as a disease you bring on yourself.

Gout - The Thorn in the Rose of Gastronomy

The Roman gourmands found their equals in the gluttonous and bibulous English gentry of the 18th and 19th centuries. The notion that acute attacks of gout are often provoked by the consumption of large quantities of food and drink enjoyed a popularity that is perhaps best illustrated in the works of the English caricaturists of the early 19th century. The punch-bowl or the wine bottle was usually a close companion to the gouty patient. George H. Ellwanger made the following observation in his book “Meditations on Gout with a consideration of its cure through the use of wine” (New York: Dodd Mead & Co., 1897): “In England, as compared with other countries, the malady was much more common during the three and four bottle days when port was the stable liquid and great quantities of heavy viands were consumed.” Ellwanger regarded gout as the sequence of high-living and thorn in the rose of gastronomy, with many years of savoury dinners and fragrant vintages as its genesis and means of evolution. He was aware, however, that over indulgence was not the only cause of the malady. “It must be remembered that before gout can appear, goitiness must be present, and that uric acid, the toxic property of gout, already exists even in the normal condition of the blood. Man therefore, is born with a distinct gouty tendency, aggravated through the dietetic misdeeds of his ancestors, and furthered by his own voluntary or involuntary lapses.”

From Historical Evidence to Controlled Studies

A multitude of observations of patients with a history of gout provide circumstantial evidence that dietary over indulgence contributes to the development of hyperuricaemia in susceptible individuals. A relationship between excessive alcohol intake and hyperuricaemia was also well established by historical evidence. Alfred Garrod declared in 1859: “There is no truth in medicine better established than that the use of fermented or alcoholic liquors is the most powerful of all the predisposing causes of gout; nay, so potent, that it may be a question whether the malady would ever have been known to mankind had such beverages not been indulged in”.

These days scientific data from controlled studies enable us a better understanding of the complex interaction between heredity and lifestyle. Concerning the role of alcohol George H. Ellwanger already knew most of the story: “Alcohol is almost universally considered injurious in the diathesis, both by increasing the production of uric acid, and by lessening the excretory power of the kidneys through its continued use.” Only today we know the biochemical mechanism:

Increased production of urate: Ethanol administration has been shown to increase uric acid production by increasing adenosine triphosphate degradation to adenosine monophosphate, a uric acid precursor. This process involves acetate conversion to acetyl CoA in the metabolism of ethanol.

Decreased urate excretion: Via conversion of ethanol to lactic acid, which reduces renal uric acid excretion by competitively inhibiting uric acid excretion by the proximal tubule.

The Proscribed Fluids

Uric acid is the metabolic end-product of purines and normally is steadily excreted into the urine. Gout is a hereditary disorder of purine metabolism resulting in deposition, in and about the joints, of salts of uric acid, which is present in marked excess throughout the body in persons with the disorder. Diet plays a role in gout, and the usual advice is to go easy on high-purine foods, particularly kidney, liver and other innards. The purine content of alcoholic drinks is negligible - except for beers. In a group of English patients with gout, beer was the most popular beverage, and 40% of the gouty men consumed more than 2.5 litres of beer daily. The heavy drinkers had a significantly higher intake of purine nitrogen, half of which was derived from beer (Annals of Rheumatic Diseases 1983;42:123-27).

These findings have been echoed by a recent study. Systematic prospective research on the effect of different alcoholic beverages on gout remained lacking until the report in the April 17 2004 issue of The Lancet by Hyon Choi and colleagues. These researchers did a prospective study on 47150 male medical professionals with a follow-up as long as 12 years. 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 four or five drinks daily, and even those who consumed as little as one drink had a 30 percent increase in risk.

The risk varied substantially according to the type of alcoholic beverage. Intake of two or more beers daily increased risk 2.5 fold, while consuming two drinks that each contained a shot of liquor increased risk 1.6 times. Moderate drinking of wine did not increase the risk of gout. “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.” As to why beer confers a larger risk than spirits and wine, Choi and colleagues think that the high purine content of beer has a role. However, special ingredients of hops, such as isohumolones, could have a role in uric-acid metabolism and excretion. As to why wine does not increase the risk of gout, the researchers say that some unknown factor might be present in wine which mitigates alcohol’s effect on the risk of gout.

Erik Skovenborg is a General Practitioner, founder member of the Scandanavian Medical Alcohol Board and a member of AIM’s Council.

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