A diet rich in fruits, vegetables, and low-fat dairy, and reduced in fats and saturated fats (the DASH diet), designed decades ago to reduce high blood pressure, also appears to significantly lower uric acid, the causative agent of gout. Further, the effect was so strong in some participants that it was nearly comparable to that achieved with drugs specifically prescribed to treat gout, a new study led by Johns Hopkins researchers shows.
The findings—derived from a randomized clinical trial—could offer an effective, safe, and sustainable dietary approach to lower uric acid and possibly prevent gout flare-ups in those with mild to moderate disease and who can’t or don’t want to take gout drugs.
Dietary excesses, such as consuming a lot of red meat and alcohol, have long been associated with gout, a disease marked by high levels of uric acid in the blood and whose causes remain somewhat of an enigma despite centuries of investigation. The Hopkins researchers noted that while symptoms of gout outbreaks—severe inflammation and sharp pain in the joints, particularly the base of the big toe—have been linked to elevated uric acid, it’s been unclear exactly what type of diet might lower uric acid and decrease the risk of flare-ups.
In an effort to find out, Stephen P. Juraschek, MD, PhD, research and clinical fellow in general internal medicine at the Johns Hopkins University School of Medicine, and his colleagues used data from the DASH (Dietary Approaches to Stop Hypertension) clinical trial, a widely popular and often-cited study whose results were first published in 1997. These results showed that the DASH diet—which emphasizes reduced salt, whole grains, fruits, vegetables, and low-fat dairy products, and reduced intake of red meats, sweets, and saturated fats—had a marked positive improvement on blood pressure and cholesterol.
In the original DASH-sodium trial, 412 participants ate either the DASH diet or a typical American diet for three months. For each month of the study, the participants’ diets provided a different level of sodium in a random order, including low (1.2 grams per day or about half a teaspoon), medium (2.3 grams per day or about one teaspoon), and a high level (3.4 grams per day or about 1.5 teaspoons). The high sodium level was comparable to the average daily intake in a typical American diet.
At baseline and at the end of each sodium intake period, the researchers conducting the original study also took blood samples, which were analyzed for a variety of blood markers, including uric acid.
In this new study, Juraschek and his colleagues examined these data to determine whether and how each intervention affected uric acid blood concentrations. They found that the DASH diet led to a modest 0.35 milligrams per deciliter decrease in uric acid concentrations overall. However, the higher participants’ baseline uric acid levels, the more dramatic the decrease. For those with the highest baseline uric acid levels—more than 7 milligrams per deciliter—for example, the decrease was as high as 1.3 milligrams per deciliter.
In the context of what is known about levels of uric acid linked to gout flare-up risk, “That’s a large reduction in uric acid,” explains Juraschek. Gout-treating medications, such as allopurinol, often reduce patients’ blood uric acid concentrations about 2 milligrams per deciliter. “When you get as high as the reduction we believe occurred with the original DASH diet in this study, the effect starts being comparable with gout medications.”
Juraschek noted that the effect of sodium on uric acid concentrations was small, but significant and quite the opposite of what the researchers expected. Specifically, during the part of the DASH trial in which participants were given the least sodium, their uric acid concentrations were the highest, with slight decreases achieved during the medium and high sodium portions of the trial.
Although high sodium levels appear to slightly decrease uric acid concentrations, Juraschek cautions against jumping to the conclusion that to reduce blood uric acid it’s a good idea to purposely consume lots of sodium. “More than 70 percent of people with gout have high blood pressure,” Juraschek says. “If one was to consume more sodium to improve uric acid, it could worsen blood pressure.”
The researchers caution that further research is needed to more clearly establish the link between the DASH diet and uric acid in patients with gout and to directly explore whether the DASH diet might reduce or prevent gout flare-ups. But, they conclude, the new study, described in the August 15 issue of Arthritis and Rheumatology, could offer patients a viable way to control uric acid concentrations—and presumably gout flare-ups—through a diet already shown to have positive effects on blood pressure, a well-established risk factor for cardiovascular disease.
There are about 8.3 million people in the United States with gout, costing the health care system an estimated $7.7 billion.
“Results of this trial are good news to patients with high blood levels of uric acid or those at risk for gout. A dietary approach to prevent gout should be considered first line therapy. This study suggests that standard dietary advice for uric acid reduction which is to reduce alcohol and protein intake, should now include advice to adopt the DASH diet,” says senior author Edgar R. Miller III, MD, PhD, professor of medicine at the Johns Hopkins University School of Medicine.
Other researchers who participated in this study include Allan C. Gelber, MD, PhD, Lawrence J. Appel, MD, MPH, and Edgar R. Miller III, MD, PhD, all from Johns Hopkins, and Hyon K. Choi, MD, DrPH, of Harvard Medical School.
Funding for this study was provided by the National Heart Lung and Blood Institute under grant/contract numbers U01-HL57173, U01-HL57114, U01-HL57190, U01-HL57139, K08 HL03857-01 and U01-HL57156 and by the General Clinical Research Program of the National Center for Research Resources under grant/contract number M01-RR02635 and M01-RR00722. Juraschek receives support from The National Institute of Diabetes and Digestive and Kidney Diseases under grant number T32DK007732-20.
SOURCE Johns Hopkins Medicine