Research & Education

Gout: Meat or Metabolic Syndrome?


We know we know – we’re starting to sound like a broken record. We’ve made connections between chronically elevated insulin and several disorders that have reached epidemic levels in modern times. Chronic hyperinsulinemia might be at the root of disorders we would never expect it to be connected to such as vertigo tinnitus and Ménière's disease and perhaps even male-pattern baldness. Where else might hyperinsulinemia be lurking in the shadows as a contributor to pathology? How about in the big toe? That’s right: gout is looking to be yet another “hyperinsulinemic disease of civilization.”  

Incidence of gout has risen in concert with other disorders attributed to “Western” diets and lifestyles such as type 2 diabetes and heart disease. Gout involves abnormal buildup of uric acid in the blood leading to its precipitation into urate crystals which accumulate in soft tissues. This condition has long been blamed on a high intake of animal protein owing to the breakdown of purines into uric acid. For this reason diets lower in animal protein—red meat in particular—are often recommended for those who suffer from gout. However evidence suggests higher protein intakes (including from animals) may not be associated with increased risk of gout. According to a paper from The New England Journal of Medicine “High-protein diets are associated with increased urinary uric acid excretion and may reduce the blood uric acid level. In a recent open-label study involving 13 patients a dietary intervention was used that included an increased proportional intake of protein; the study showed a significant reduction in the rate of recurrent attacks of gout.” (Emphasis added.)

While a reduction of dietary animal protein may offer relief for some individuals many will not experience symptomatic improvement from going this route which suggests there may be something else driving this condition. 

If a high intake of animal protein caused gout—or was the primary cause anyway—then our hunter (and gatherer) ancestors might have had too much pain in their big toes to go chasing after yet more prey. So is there another plausible dietary explanation for why so many people are afflicted with gout in the 21st Century? And what’s really the problem in this condition anyway: do people with gout produce more uric acid or is the problem with clearance of uric acid? 

More and more research indicates that gout may be related to chronic hyperinsulinemia and also to fructose intake. Fructose was long believed to be a “safe” sugar for diabetics because it doesn’t raise blood glucose or stimulate insulin to the same degree that glucose and sucrose do. Decades ago certain candies and snack foods that were formulated to contain more fructose than glucose were even marketed as being helpful for diabetics for this reason. However “Although fructose does not appear to acutely increase insulin levels chronic exposure seems to indirectly cause hyperinsulinemia and obesity through other mechanisms.” And “Although fructose does not stimulate insulin secretion in the short term the insulin resistance and obesity induced by long-term fructose feeding in experimental animals induces compensatory hyperinsulinemia.” So while fructose may not have the same acute effect on insulin secretion that glucose does over time—decades say of consuming fruit juice sugar-sweetened soft drinks and high-sugar snack foods—fructose could well play a role in the etiology of insulin resistance largely via effects on the liver.

Regarding the clearance of uric acid high insulin levels impair the body’s capacity to excrete uric acid—an observation that has been made in healthy people as well as hypertensive individuals. Insulin has powerful effects on kidney function most notably antinatriuresis (inhibition of sodium excretion) which accounts for the role of hyperinsulinemia in hypertension. But insulin also influences the retention—or more accurately impairs the clearance—of uric acid. “Insulin antinatriuresis is accompanied by a reduction in the urinary excretion of uric acid.” Chronically high insulin is the most likely unifying factor behind several comorbidities that cluster together such as abdominal obesity hypertension dyslipidemia and type 2 diabetes. Obesity typically gets the blame for the other issues but what are we to make of the development of these conditions in individuals who are at a “normal” weight? Obesity is “associated with” these other issues but that doesn’t mean it’s the driving factor. More likely something else—elevated insulin perhaps—is the underlying cause of all of these conditions of which obesity is only one. (Cardiometabolic abnormalities suggestive of metabolic syndrome/insulin resistance also tag along with elevated uric acid in obese children and adolescents. But again is obesity driving the uric acid accumulation or is chronic hyperinsulinemia driving both?)

So what to do about gout then? 

Gout sufferers may experience relief upon reducing their consumption of animal protein so this time-honored intervention need not be disregarded. Beyond that however reduction of dietary fructose and other simple sugars should be of utmost importance along with recommendations for increased physical activity good quality and quantity of sleep and other diet and lifestyle measures that improve insulin sensitivity.