Uric acid is the waste product left over from the metabolism of chemical compounds called purines. The increased uric acid levels found in gout may be caused by increased ingestion of purines. Sodium urates then collect in the joints and tissue, creating inflammation and inducing pain.
Gout is caused by deposition of urate crystals in the joints. Purines are the source of urates and originate from body synthesis and diet. Uric acid levels are elevated and the kidneys may not be able to eliminate the excess effectively, causing crystals to form. Therefore, a condition known as hyperuricaemia is either due to overproduction or renal underexcretion of urate, or a combination of the two.
Uric crystals form and accumulate in body areas where blood flow is too slow to remove them. The knuckles, elbows, knees, and toes are common places of accumulation. If found between the joints, the surrounding tissue becomes inflamed. Then a nerve ending may become irritated, and extreme pain may result. If the crystals remain in the kidneys, partial or complete kidney damage may occur.
Lesch-Nyhan syndrome (LNS) is caused by a lack of the enzyme HPRT, which causes a buildup of uric acid in all body fluids leading to symptoms such as severe gout, poor muscle control, and moderate retardation, which appear in the first year of life. A prominent feature of LNS is characterized by lip and finger biting that begin in the second year of life. Abnormally high uric acid levels may cause sodium urate crystals to form in the joints, kidneys, central nervous system, and other tissues of the body. Neurological symptoms include facial grimacing, involuntary writhing, and repetitive movements of the arms and legs.
Pexioto et al. evaluated the effects of diet and medication on serum levels of uric acid in patients with hyperuricemia in hypertensive patients. Patients were divided into three groups, low purine diet, low purine diet plus allopurinol, and allopurinol only. Patients were evaluated with regards to their lifestyles (diet, smoking, physical, activity, alcohol consumption), uric acid, blood pressure, use of medication, body mass index, cholesterol, and triglyceride. The authors concluded that the low purine diet should be the first option for controlling hyperuricemia in patients with similar characteristics to the ones presented in this study because of the cost-benefit relationship.
High-quality, long-term human studies are still lacking. Many available reports describe the difficulty of committing to such a restrictive eating plan.
A low purine diet should not be used instead of medical therapy for gout or Lesch-Nyhan syndrome unless under the supervision of a qualified medical professional.
Gout may be a symptom of a more serious underlying disorder (e.g. Lesch-Nyhan syndrome). Consult a qualified healthcare provider before making any decisions about therapies and/or health conditions.
Gout may cause joint deformity if not treated. Death may occur from kidney disease, hypertension, coronary artery disease, stroke, and other complications.
This information has been edited and peer-reviewed by contributors to the Natural Standard Research Collaboration (www.naturalstandard.com).