Diet is much less important than genes in the development of hyperuricaemia – according to meta-analysis from New Zealand.
Although the study population excluded people with a diagnosis of gout, the findings suggest that less emphasis on diet and lifestyle and more on urate-lowering drugs might improve management of the condition.
The meta-analysis of five US cohort studies comprising more than 16,000 men and women found seven foods – beer, liquor, wine, potato, poultry, soft drinks and meat – were associated with raised urate levels.
However, individually these and other foods explained less than 1% of the variation in urate levels. Collectively, 14 food items explained 3.28% of the variation.
“In contrast, 30 genetic variants previously associated with serum urate levels at a genome wide level of significance in Europeans additively explained 8.7% of the variance in serum urate levels in the full cohort,” the study said.
The study also found that various diet scores such as the Healthy Eating score, the Dietary Approaches to Stop Hypertension (DASH) diet score and the Mediterranean diet score explained very little variance in serum urate levels (0.15%, 0.28% and 0.06% respectively).
“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,” the researchers said.
An editorial in the BMJ, said the study did not provide evidence to support a change in guideline recommendations that patients with gout should modify their diet to avoid high risk foods such as alcohol.
However the findings did have broader implications, the authors said.
“Gout is often poorly managed; only a third of patients are prescribed definitive urate-lowering drugs. Only a minority of patients taking drugs increase the dose to achieve the target serum urate level required to rid the body of causative crystals, prevent flares, and shrink tophi.”
And valuable opportunities to initiate treatment were missed because patients were frequently given ‘inaccurate or conflicting information which trivialises gout and misrepresents its causes and treatment’.
“The study … provides important evidence that much of patients’ predisposition to hyperuricaemia and gout is non-modifiable, 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,” the editorial authors concluded.