Despite accumulating evidence that gout isn’t all about diet, the condition retains its reputation as the “rich man’s disease”—or the disease that afflicts those who eat richly, regardless of their fortunes. Back in 2008, a study appeared suggesting that about 12% of gout cases could be attributed to dietary causes. A little later, additional studies identified genes that were associated with gout or gout’s chief risk factor, hyperuricemia, or elevated uric acid levels. And now, a new study that has revisited the causes of hyperuricemia has concluded that in contrast with genetic contributions, diet explains very little of the variation in uric acid levels.
In the new study, scientists based in New Zealand found that diet scores explained less than 0.3% of variance in serum urate. In contrast, they determined that common, genome-wide single nucleotide variation explained 23.9% of the variance.
Additional details appeared recently in BMJ, in an article titled, “Evaluation of the diet wide contribution to serum urate levels: meta-analysis of population-based cohorts.” The article described how the scientists analyzed dietary survey data for 8,414 men and 8,346 women of European ancestry from five U.S. cohort studies. Participants were aged over 18 without kidney disease or gout, and were not taking urate-lowering or diuretic drugs.
Blood urate measurements and genetic profiles were recorded. Factors that could have affected the results, such as sex, age, body mass index, daily calorie intake, education, exercise levels, and smoking status, were also considered.
Elevated serum urate levels were associated with seven foods: beer, liquor, wine, potato, poultry, soft drinks, and meat (beef, pork, or lamb). Reduced serum urate levels were associated with eight foods: eggs, peanuts, cold cereal, skim milk, cheese, brown bread, margarine, and noncitrus fruits. Each of these foods, however, explained less than 1% of the variation in urate levels.
Similarly, three diet scores, based on healthy diet guidelines, were also associated with lowered urate levels, while a fourth, based on a diet high in unhealthy foods, was associated with increased urate levels. Again, however, each of these diet scores explained very little (less than 0.3%) variance in urate levels. In contrast, genetic analysis revealed that common genetic factors explained almost a quarter of the variation in urate levels.
“Our data are important in showing the relative contributions of overall diet and inherited genetic factors to the population variance of serum urate levels,” the authors of the BMJ research article indicated. “Our results challenge widely held community perceptions that hyperuricaemia is primarily caused by diet, showing that genetic variants have a much greater contribution to hyperuricaemia in the general population than dietary exposure.”
In an accompanying editorial (“The role of diet in serum urate concentration“), researchers at Keel University pointed out that people with gout often experience stigma from the misconception that it is a self-inflicted condition caused by unhealthy lifestyle habits and, as a result, are often reluctant to seek medical help.
This study, the Keel scientists wrote, “provides important evidence that much of patients' preponderance to hyperuricaemia and gout is nonmodifiable, countering these harmful but well-established views and practices and providing an opportunity to address these serious barriers to reducing the burden of this common and easily treatable condition.”