Gout and Hyperuricemia
Gout is one of the oldest known and most common forms of arthritis; it is a crystal deposition disease in which crystals of monosodium urate form in joints and other tissues. Gout attacks cause a characteristic painful inflammation of one or more joints of the extremities, or nodules in soft tissues called tophi. An acute attack of gout, although brief and usually subsiding spontaneously, can be temporarily debilitating, and predisposes an individual to subsequent attacks.
Once a disease of only the affluent (who could afford the purine-rich foods and drink linked to gout risk), this "disease of kings" has rapidly become a disease of everyman. The prevalence of gout among US adults, according to the National Health and Nutrition Examination Survey (2007‒2008) is estimated at 3.9% (8.3 million people), favoring men over women by almost 3:1.1 This represents a significant 44% increase in gout frequency from previous estimates just a decade earlier.2
The primary risk factor for gout is elevated levels of a metabolic byproduct called uric acid in the blood; this condition is known as hyperuricemia. Hyperuricemia is estimated to affect over 21% of the US population, and doubles in frequency between ages 20 and 80 years.1
Hyperuricemia increases the risk of not only gout, but other diseases as well, including hypertension, kidney disease, and metabolic syndrome. Even during the asymptomatic periods between gout attacks, the body is exposed to periods of low-grade, chronic inflammation. The propensity for excessive blood uric acid and gout is also increased by other disease states; therefore, a gout or hyperuricemic patient should consider Life Extension's recommendations and protocols for inflammation, cardiovascular disease, hypertension, kidney health, and weight loss as well.