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 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.