NEW YORK (Reuters Health)—Heredity plays a substantially larger role than diet in determining serum urate levels, according to new findings in BMJ.
Nearly 25% of the variation in serum urate is attributable to common genetic variants, while dietary pattern explained less than 1%, Dr. Tanya J. Major of the University of Otago in Dunedin, New Zealand, and colleagues found.
“Our results challenge widely held community perceptions that hyperuricemia is primarily caused by diet, showing that genetic variants have a much greater contribution to hyperuricemia in the general population than dietary exposure,” they write in their October 10 report.
The researchers analyzed data from the Atherosclerosis Risk in Communities, CARDIA, Cardiovascular Heart, and Framingham Heart studies, as well as the Third National Health and Nutrition Examination Survey, on 16,760 white U.S. adults without kidney disease or gout. All completed validated food frequency questionnaires, and the investigators also scored participants’ diets in relation to Harvard Healthy Eating Pyramid recommendations, the Dietary Approaches to Stop Hypertension (DASH) diet, and the Mediterranean diet.
Seven foods were associated with increased serum urate: beer, liquor, wine, potato, poultry, soft drinks and meat, including beef, pork or lamb. Beer and liquor had the largest effect, increasing serum urate by 1.38 mmol/L per serving per week.
Eight foods were linked to lower serum urate, including eggs, peanuts, cold cereal, skim milk, cheese, brown bread, margarine and non-citrus fruit.
Each food item accounted for 0.06% to 0.99% of serum urate variation, the authors found, and in total explained 4.29% of variation.
Adherence to the Harvard Healthy Eating, DASH, or Mediterranean diets was inversely associated with serum urate, with each diet pattern accounting for 0.3% of variance or less.
Thirty genetic variants linked to serum urate accounted for a total of 8.7% of variation in urate levels, Dr. Major and her team found, while genetic risk score based on a genome-wide weighted association study explained 7.9% of variation.
The findings can’t be generalized to people with gout, the authors note, or to those with non-European heritage.
“The study by Major and colleagues is an important step in trying to correct the societal misconception that gout is self-inflicted by dietary habits,” Lorraine Watson of the Arthritis Research UK Primary Care Centre at Keele University in Staffordshire, UK, who co-authored an editorial accompanying the study, told Reuters Health in an email. “This misconception causes stigma for people living with gout, can deter them from seeking help, and acts as a significant barrier to optimal management of gout.”
While the study didn’t include people with gout, Watson said, “it is unlikely that the cause of high levels of serum urate in the study population is substantially different to those in gout.” There is evidence that alcohol and purine-rich foods can trigger gout flares in some people, she added, but the current study did not address this issue and there is little research on how changing diet might affect flares.
“The study by Major and colleagues does not provide any evidence to support a change to current guidelines which advise that patients with gout should modify their diet if they consume higher risk foods (alcoholic drinks, meat, seafood, sugar- sweetened soft drinks) excessively,” she said.
Reference
- Watson L, Roddy E. The role of diet in serum urate concentration. BMJ. 2018 Oct 10;363:k4140.
