The unwalkable diseaseby Ruth Nichol
Long dismissed as the price of overindulgence, gout is now known to be genetically determined.
First-time gout sufferers may not know what gout is but they certainly know something is wrong: one day they feel fine; the next they’re in agony.
“The classic first presentation is in the big toe,” says Christchurch rheumatologist Lisa Stamp. “It’s red-hot and swollen and extremely painful. Many people think they’ve broken a bone, because they can’t walk.”
Gout attacks typically come on overnight, but they are the result of a much longer process. Gout, a type of arthritis, is caused by high levels of uric acid in the blood. The acid turns into crystals in the joints – not only the big toe, but also the knees, elbows, wrists and fingers – and can produce excruciating pain.
Most gout attacks settle down quickly. However, unless it is treated with drugs to lower uric acid levels, it can become chronic and may cause permanent joint damage. It’s also associated with other diseases, such as diabetes, heart disease and kidney problems.
Known for centuries as the “disease of kings”, because it can be triggered by consuming red meat, seafood and alcohol, gout is poorly understood. But it’s now clear that rather than being a symptom of overindulgence, gout is caused by a complex interaction between genetic and environmental factors.
“There is a lot of stigma around gout, but we now think the biggest reason some people don’t excrete uric acid properly is genetic,” says Stamp.
Men are three times more likely than women to suffer from gout, and some ethnic groups – notably Maori and Pacific people – are particularly susceptible. Up to 15% of Maori and Pasifika men have gout, compared with fewer than 5% of Pakeha men.
Given our high rates of gout, it’s not surprising that New Zealand researchers are now trying to unravel the mysteries of the condition described by the ancient Greek physician Hippocrates as “the unwalkable disease”.
Among them are a group at the University of Otago, where a study is comparing the DNA of thousands of people – some with gout, some without – in a bid to identify the predisposing genetic factors. The study has already found that a variation on one particular gene doubles the risk of developing gout for Pakeha, but increases it more than five times for Maori and Pasifika.
Traditionally gout has been portrayed as a disease of fat old men with a fondness for rich food and port. But you don’t have to be fat or old to get gout. Former All Black Neemia Tialata was just 20 and in great shape when he was diagnosed.
In any case, the rich-food hypothesis is a myth. University of Otago PhD student Tanya Flynn hit the headlines in August when she published a paper suggesting that tomatoes raise uric acid levels in the blood and may be a trigger for gout. Flynn emphasises that you’ll only develop gout if you are genetically predisposed to it. “It doesn’t matter what you eat,” she says. “You’re not at risk unless you have that background genetic thing going on.”
Even the well-established triggers, red meat, seafood and alcohol, as well as the more recent additions to the watch list – tomatoes and sugary drinks – don’t affect all gout sufferers in the same way. Some people can eat seafood, for example, but not drink beer.
Flynn says that, anecdotally, tomatoes seem to be a particular problem for Maori and Pacific people.
“Someone from the Cook Islands told me that if you went there and asked if tomatoes trigger their gout, 100% of people would say yes.”
If foods that raise uric acid levels can exacerbate gout, it seems logical that foods that do the opposite (possibilities include vitamin C and tart cherry juice) could help treat it.
But Stamp published research in 2013 suggesting that taking vitamin C does not have a clinically significant effect on uric acid levels. She’s about to turn her attention to tart cherry juice with a preliminary study involving 50 people.
She’s open-minded about using complementary therapies to treat gout, but says they’re more likely to work in combination with conventional drug treatment.
“I don’t think we’re going to get to the point where we use a totally dietary intervention.”
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