Gout and alcohol

M. Snaith

‘Fircliffe’, Whitworth Road, Darley Dale, Near Matlock, Derbyshire, UK

E-mail: michael{at}mikesnaith.demon.co.uk

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 one's risk of developing gout. A second question commonly expressed by journalists around the same time concerned the Atkins diet. Here we are on firmer ground. The relationships 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’ reflects the ketosis induced by this protein-rich, carbohydrate-poor diet. The metabolic explanation is that the increased levels of circulating lactate and hydroxybutyrate 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 drinking 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 Chesterfield: ‘gout is the distemper of a gentleman—whereas the rheumatism is the distemper of a hackney coachman’ [6, p. 50]. In more recent times, either the profile 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 perfectionist in tone, but did have a point when indicating that there is a relative paucity of recent evidence to guide treatment or prophylaxis 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, osteopaths, pharmacists, podiatrists and veterinarians were followed up over 12 yr. Forty-seven thousand, one hundred and fifty participants, 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, confirmed 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 influential 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 influence 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 straightforward. 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 production 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 frequency 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: Don’t drink to excess, especially if your father had gout. If you must drink to excess, don’t 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 conflicts of interest.

References

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  4. Rodnan GP. The pathogenesis of aldermanic gout: procatarctic role of fluctuations in serum urate concentration in gouty arthritis provoked by feast and alcohol [abstract]. Arthritis Rheum 1980;23(Suppl.):737.
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  15. ProBrewer.com. Beer news. http://www.probrewer.com/news/news-001985.php, accessed 5 June 2004.
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  19. Dessein PH, Shipton EA, Stanwix AE et al. Beneficial effects of weight loss associated with moderate calorie/carbohydrate restriction, and increased proportional intake of protein and unsaturated fat on serum urate and lipoprotein levels in gout: a pilot study. Ann Rheum Dis 2000;59:539–43.[Abstract/Free Full Text]
  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:139–42.[Medline]




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