How Gout Works

Humans lack the specific enzyme that can transform uric acid to a compound that the human body can easily absorb.

Thus, when there is an excess of uric acid due to kidney impairment, diet, or other factors, concentrated uric acid can crystallize, becoming monosodium urate. An excess of monosodium urate crystals in the body’s fluids will affect the functioning and health of various joints, bones, organs and tissue (called hyperuricemia), resulting in joint inflammation, pain, and further kidney impairment.

The general course of the disease is as follows:

  • Inflammation of the joints and surrounding areas begins
  • Crystalline uric acid deposits form around bones, joints and other tissue
  • Inflammation begins to affect the kidneys and impair functions
  • Uric acid stones (similar to kidney stones) develop in the urinary tract

It is estimated that 90% of gout cases are due to under-excretion (though it can also occur with over-production as well). Certain compounds can decrease the body’s ability to excrete uric acid, including:

  • Alcohol
  • Low doses of aspirin
  • Vitamin B3 / Niacin / Nicotinic acid
  • Thiazide-based diuretics
  • Loop diuretics (such as furosemide)
  • Tuberculosis drugs ethambutol and pyrazinamide

Although excessive consumption of foods with high levels of purine can also contribute to uric acid over-production and hyperuricemia, this tends not to be the primary or sole cause.