The study is published in the 9 March online issue of Nature Genetics and is the work of researchers based at the MRC Human Genetics Unit, Western General Hospital, Edinburgh, and colleagues from other research centres in the UK and also in Croatia and Germany.
Gout (also called metabolic arthritis) is a painful condition caused when uric acid, a waste product of purine metabolism that in humans and great apes is mostly excreted via the kidneys into urine, deposits in the joints.
In some people the kidneys don't clear all the uric acid from the bloodstream, a condition that is called hyperuricemia.
Some 10 per cent of people with hyperuricemia go on to develop gout, where uric acid is deposited in the joints as monosodium urate crystals, resulting in inflammation and often considerable pain. The condition usually affects the joint of the big toe, but it can also affect fingers, elbows, ankles, knees and other joints.
Causes of gout have often been attributed to diet and lifestyle, with overconsumption of protein, refined sugar and alcohol being the main culprits, but the mystery that has remained is why thousands of people with these lifestyles don't develop gout.
The answer, according to this study, could be genetic. The researchers studied the genes of more than 12,000 people and found that a gene variant may increase or lower the risk of a person developing gout.
The gene variant in question is called SLC2A9, already known to scientists as a transporter of fructose, but in this new study, the researchers, led by Professor Alan Wright of the MRC Human Genetics Unit, found the variant also plays a key role in transporting uric acid.
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