Rheumatology 2004;43:12081209 doi:10.

1093/rheumatology/keh315
Advance Access publication 20 July 2004
Editorial
Gout and alcohol
The title of this editorial is focused on alcohol. However, at least
in the venal West, food and drink are inseparable. There has
recently been a surge of interest in gout, diet and alcohol. Around
Christmas 2003, several pieces appeared in the print and broadcast
media. These appeared to be precipitated in part by the various
public murmurings about binge-drinking and its threats to law
and order. A common question from journalists was: Since young
women are increasingly indulging in binge-drinking, is there an
epidemic of gout in young women?. I could personally answer this
with neither anecdote nor evidence. I would be interested to know
if other rheumatologists are seeing any such trend. Yet it seemed a
perfectly reasonable question, predicated upon the hallowed belief
in there being a strong relationship between how much alcohol
one drinks and ones risk of developing gout. A second question
commonly expressed by journalists around the same time con-
cerned the Atkins diet. Here we are on rmer ground. The relation-
ships between weight loss, urate metabolism and gout are complex.
The matter has been the subject of considerable clinical research,
much of it predating the electronic databases. For instance, long
before Dr Atkins popularized his diet it was known that crash-
dieting could provoke acute gout. Provided one does not become
ketotic, plasma and urinary urate fall with decreasing body weight
[1, 2]. The Atkins breath reects the ketosis induced by this
protein-rich, carbohydrate-poor diet. The metabolic explanation
is that the increased levels of circulating lactate and hydroxybuty-
rate compete with urate for renal tubular excretion. This results in
reduced urinary urate, increased plasma urate and an increased
risk of precipitating gout in the previously hyperuricaemic.
However, things are never simple. Alcoholic gouty patients
appear to develop acute episodes at lower blood urate levels than
non-alcoholic gouty patients. To put it another way, during attacks
of gout alcoholics have lower plasma urate levels than non-
alcoholics [3]. Acutely intoxicated alcoholic patients have higher
plasma urate levels than after they have sobered up. They are,
not surprisingly, very likely not to have been eating whilst drink-
ing heavily. Experimentally high levels (over 200 mg per 100 ml) of
plasma ethanol in non-gouty, non-alcoholic normal subjects were
associated with reduced urinary urate excretion [4] and increased
plasma levels of urate [5].
Authors from Hippocrates to Sydenham, and many in between,
asserted that gout affected more rich men than poor. Hence
aldermanic gout of the 18th and 19th centuries [4, 6], and
quotations from such as Lord Chestereld: gout is the distemper
of a gentlemanwhereas the rheumatism is the distemper of a
hackney coachman [6, p. 50]. In more recent times, either the
prole of sufferers from the disease has changed or its observers
have altered their opinions. Talbott [7] maintained in his excellent
monograph of 1967 that the indigent and the well-to-do suffer
alike from gout. The author of Gout in primary care in a recent
Drugs and Therapeutics Bulletin [8] was perhaps a little perfec-
tionist in tone, but did have a point when indicating that there
is a relative paucity of recent evidence to guide treatment or pro-
phylaxis for gout. However, the US Health Professionals Follow-
up Study has provided useful data that illuminate, equally for
the present-day consumer and doctor, the topics of gout, diet and
alcohol. Fifty-one thousand male dentists, optometrists, osteo-
paths, pharmacists, podiatrists and veterinarians were followed up
over 12 yr. Forty-seven thousand, one hundred and fty partici-
pants, who had not had gout at the outset and who provided
complete dietary information, were available for study. The
New England Journal of Medicine report by Choi et al. [9], with
its attendant publicity, conrmed the conventional wisdom that
seafood and meat carry more risk than dairy products. The Lancet
paper by the same authors, soon afterwards, went some way to
correct the alcohol stereotype [10, 11]. Beer was more likely to be
associated with gout than spirits, and spirits in turn more than
wine. The large size of the study naturally makes it likely that
there were many exceptions obscured by the numbers. However, it
was probably useful for the public to be informed that beer is
at least as likely to cause gout as the stereotyped port wine.
Whether this will form any inuential plank of the Downing
Street platform on a public health strategy to reduce harm from
alcohol is a different matter.
There are a number of ways in which gout, alcohol and plasma
and urinary urate may be inter-related. In the days of lead-lined
chambers for moonshine whisk(e)y, tubular nephropathy may
have underlined saturnine gout [12]. In addition to the inuence
of lactate discussed above, there is the question of the contribution
to plasma urate of purines, such as guanosine, in alcoholic drinks
[13, 14]. The effects of other constituents may be less straight-
forward. For example, isohumulones derived from hops and
responsible for the bitter taste of beer, have been found to reduce
the development of body fat in mice [15]. Chronic alcohol intake
is a bad idea for gouty patients in at least two ways. The produc-
tion of oxypurinol, the active metabolite of allopurinol, may be
impaired by high alcohol intake; and urate production is
stimulated by it [16, 17].
I am not aware of any epidemiological studies on the fre-
quency of gout in vegetarian, teetotal non-obese individuals, or
on the prevalence in populations where alcohol intake is minimal.
However, for Western populations of gout-prone people, I suppose
our medical advice must include the following: Dont drink to
excess, especially if your father had gout. If you must drink to
excess, dont stop eating. If you do eat, rethink your diet [18, 19].
If you are on allopurinol or benzbromarone, watch your urate
level if you drink [20].
The author has declared no conicts of interest.
M. SNAITH
Fircliffe, Whitworth Road, Darley Dale, Near Matlock,
Derbyshire, UK
E-mail: michael@mikesnaith.demon.co.uk
References
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serum uric acid and acute attacks of gout. Am J Med 1967;42:3857.
2. Nicholls A, Scott JT. Effect of weight-loss on plasma and urinary
levels of uric acid. Lancet 1972;2:12234.
3. Vandenberg MK, Moxley G, Breitbach SA, Roberts WN. Gout
attacks in chronic alcoholics occur at lower serum urate levels than
in non-alcoholic. J Rheumatol 1994;21:7004.
Rheumatology Vol. 43 No. 10 British Society for Rheumatology 2004; all rights reserved
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4. Rodnan GP. The pathogenesis of aldermanic gout: procatarctic role
of uctuations in serum urate concentration in gouty arthritis
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8. Gout in primary care. Drugs Ther Bull 2004;42:3740.
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and its effect on uric acid. Br J Rheumatol 1984;23:2039.
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15. ProBrewer.com. Beer news. http://www.probrewer.com/news/
news-001985.php, accessed 5 June 2004.
16. Ralston SH, Capell HA, Sturrock RD. Alcohol and response to
treatment of gout. BMJ 1988;296:16412.
17. Faller J, Fox IH. Ethanol-induced hyperuricemia: evidence for
increased urate production by activation of adenine nucleotide
turnover. N Engl J Med 1982;307:1598602.
18. Yamashita S, Matsuzawa Y, Tokunaga K, Fujioka S, Tarui S.
Studies on the impaired metabolism of uric acid in obese subjects:
marked reduction of renal urate excretion and its improvement by a
low-calorie diet. Int J Obesity 1986;10:25564.
19. Dessein PH, Shipton EA, Stanwix AE et al. Benecial effects of
weight loss associated with moderate calorie/carbohydrate restric-
tion, and increased proportional intake of protein and unsaturated
fat on serum urate and lipoprotein levels in gout: a pilot study. Ann
Rheum Dis 2000;59:53943.
20. Kaneko K, Fujimori S, Akaoka I. Changes caused by ethanol intake
on metabolism of hypouricemic agents (combination of allopurinol
and benzbromarone). Adv Exp Med Biol 1991;309A:13942.
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