medwireNews: A meta-analysis published in The BMJ suggests that diet only explains a small proportion of variation in serum uric acid levels, with genetic variation making a much larger contribution to hyperuricemia risk.
“Hyperuricaemia is a well established risk factor for gout,” and these results counter “harmful but well established views” that gout is caused by an unhealthy lifestyle, which results in patients being reluctant to seek treatment for the condition, say the authors of an accompanying editorial.
Tony Merriman (University of Otago, Dunedin, New Zealand) and study co-authors analyzed data from five cohort studies including a total of 16,760 people of European ancestry who did not have gout or kidney disease, and identified 15 individual dietary items that were significantly associated with serum uric acid levels.
Seven food and drink types – beer, liquor, wine, potato, poultry, soft drinks, and red meat – were associated with an increase in serum uric acid levels, whereas eight – eggs, peanuts, cereal, skimmed milk, cheese, wholemeal bread, margarine, and noncitrus fruit – were linked to lower levels. However, each of these items explained less than 1% of variance in uric acid levels (range, 0.06–0.99%), and added together they accounted for just 3.28% of the variation.
In accordance with these findings, the Healthy Eating, DASH, and Mediterranean diet scores only accounted for 0.15%, 0.28%, and 0.06% of variation, respectively, indicating that “diet explains very little variation in serum urate levels in the general population,” say Merriman and team.
By contrast, they found that common inherited genetic variants had “a much greater contribution to hyperuricaemia,” accounting for 23.9% of variance in uric acid levels, and a weighted serum urate genetic risk score based on 30 variants known to be associated with serum urate levels explained 7.9% of variation.
Although the researchers emphasize that their study did not include patients with established gout, the editorialists note that “it is unlikely that the cause of hyperuricaemia in the studied populations is substantially different to those with clinically evident gout,” and the results may therefore have “broad implications for people with gout and those who care for them.”
Lorraine Watson and Edward Roddy, both from Keele University in the UK, believe that the study findings represent “important evidence that much of patients’ predisposition to hyperuricaemia and gout is non-modifiable.”
And the findings provide “an opportunity to address these serious barriers to reducing the burden of this common and easily treatable condition,” they conclude.
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