What Lifestyle Measures Can Help Prevent Gout?

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What Lifestyle Measures Can Help Prevent Gout?
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What Is Gout?

Gout is a type of arthritis (inflammation of the joints) that mostly affects men age 40 and older. It is caused by chronic hyperuricemia--a long-lasting, abnormally high concentration of uric acid in the blood. Purines, nitrogen-containing compounds, are the chemical sources of uric acid and can be divided into two types, endogenous and exogenous. Endogenous purines are synthesized within the nuclei of cells in the human body itself, whereas the exogenous purines are obtained from foods. Uric acid is the end product of purine metabolism and is mostly produced in the liver. From there it enters the bloodstream. Most of uric acid eventually passes through the kidneys and is excreted in the urine; the rest is disposed of in the intestines, where it is processed and oxidized by bacteria.

Normally these processes keep the concentration of uric acid in the blood plasma (the liquid part of the blood) below 7 milligrams per deciliter (7 mg/dL). Under certain circumstances, however, the body produces too much uric acid or excretes too little, resulting in levels above 7 mg/dL--the point at which hyperuricemia develops. In the bloodstream, uric acid exists predominantly as a dissolved salt called monosodium urate (MSU). At 37 degrees C (normal body temperature) and at a uric acid concentration approaching 7 mg/dL, the blood plasma becomes supersaturated, and needlelike crystals of MSU form. Crystallization is governed by other factors as well. In joints, such as the knee and ankle, temperatures are cooler (29 degrees C to 32 degrees C), and MSU crystals are able to form at even lower uric acid concentrations, which explains why gout favors these joints. In time, MSU crystals can provoke an inflammatory response that produces the symptoms characteristic of gout. In respect to gout, humans are less fortunate than many animals, which never suffer from gout because they possess uricase, an enzyme that converts uric acid to allantoin, a substance much more easily excreted by the kidneys.


What Causes Gout?
Gout is classified as either primary (the most common type) or secondary, depending on the cause of the associated hyperuricemia. In both types of gout, between 70% to 95% of hyperuricemia cases are the result of underexcretion of uric acid, rather than uric acid overproduction.

Primary Gout.
Hyperuricemia in primary gout arises or is presumed to arise from a genetic or other inborn disorders that cause metabolic problem resulting in overproduction of uric acid or reduced excretion of uric acid. More than 99% of primary gout cases, however, are idiopathic, meaning that the cause of the hyperuricemia cannot be determined. The remaining cases are traceable to either of two rare inherited enzyme defects that affect purine synthesis in the cells.

Secondary Gout.
In secondary gout, hyperuricemia is caused by drug therapy or by medical conditions other than an inborn metabolic disorder.

Medications. Thiazide diuretics (the "water pills" used to control hypertension) cause hyperuricemia by decreasing uric acid excretion. The list of drugs that cause hyperuricemia is long and includes not only diuretics but also pyrazinamide (used to treat tuberculosis) and the immunosuppressive drug cyclosporine (given to transplant recipients to prevent organ rejection). Low doses of aspirin and other salicylates decrease uric acid excretion, whereas high doses have the opposite effect.

Kidney Disorders. Renal (meaning kidney) insufficiency is the impaired ability of the kidneys to eliminate waste products, including uric acid, which then build up in the blood. Gout is associated with three primary disorders that can cause renal insufficiency: urate nephropathy; uric acid nephropathy; and uric acid nephrolithiasis.

Urate nephropathy occurs when monosodium urate crystals form in kidney tissue is uncommon and researchers believe that it usually causes only minor kidney damage.

Uric acid nephropathy is a disorder that occurs uric acid crystals from urine forming in the structures and tubes that carry fluid from the kidney. It most often occurs during chemotherapy for lymphoma or leukemia. It can result in kidney failure by obstructing urine flow, but is preventable and reversible.

Uric acid nephrolithiasis occurs when kidney stones form from uric acid. Uric acid and other kidney stones are present in 10% to 25% of patients with primary gout--a prevalence more than 1000 times that in the general population. In secondary gout, the reported incidence reaches 42%. Uric acid stones can also form in the absence of gout or hyperuricemia. Not all of the kidney stones in patients with gout are composed of uric acid; some are composed of calcium oxalate, calcium phosphate, or those substances combined with uric acid. Kidney stones can be extraordinarily painful and can cause infection and kidney failure if untreated.

Other Medical Conditions. A number of diseases, including leukemia, lymphoma, and psoriasis, can cause gout. Over exposure to lead can cause gout.

Alcohol Use. Alcohol use increases uric acid levels in three ways: by providing an additional dietary source of purines (the compounds from which uric acid is formed); by intensifying the body's production of uric acid; and by interfering with the kidneys' ability to excrete uric acid.

Purine-Rich Diet. A purine-rich diet rarely causes hyperuricemia, although it may precipitate an attack in some people with existing gout. [For a list of purine-rich foods, see What Lifestyle Measures Can Help Prevent Gout?, below.]

What Lifestyle Measures Can Help Prevent Gout?
Avoid Purine-Rich Foods.
Because uric acid levels are only minimally affected by diet, dietary therapy does not play a large role in the prevention of gout. Still, people who have suffered an attack of gout may benefit from reducing their intake of purine-rich foods if they habitually eat unusually large quantities of such foods. They include They include beer and other alcoholic beverages, anchovies, sardines (in oil), fish roes, herring, yeast, organ meats (e.g., liver, kidneys), legumes (e.g., dried beans, peas, and soybeans), meat extracts, consommé, gravies, mushrooms, spinach, asparagus, cauliflower, and poultry.

Protein Restriction.
Diets high in protein, particularly animal protein, increase uric acid. Although few studies have been conducted and none of determined the value of reducing protein, one study of gout patients suggested that eating tofu, which is made from soy and is a source of complete protein, may be a better choice than meats.

Maintain Healthy Weight.
A supervised weight-loss program may, however, be a more effective way to reduce uric acid levels if the patient is overweight. Crash dieting, on the other hand, is counterproductive because it can increase uric acid levels and can cause an acute attack.

Maintain Fluids and Avoid Alcohol.
Drinking plenty of water and other nonalcoholic beverages helps remove MSU crystals from the body. Heavy drinking, especially binge drinking of beer or distilled spirits, should be avoided, because alcohol is a source of purines and can also cause overproduction and underexcretion of uric acid.

Avoid Joint Injury.
People with gout should also attempt to identify and avoid activities that cause repetitive joint trauma, such as the wearing of tight shoes.