What should I know about Gout?

Gout has been defined as one of the most painful rheumatic diseases. It results when crystals of uric acid are deposited in connective tissue, joint spaces, or both, and is due to a disorder of uric acid metabolism. It is caused by either an overproduction, or under excretion of uric acid and is manifested by hyperuricemia, acute or chronic recurrent arthritis, and deposits of monosodium urates.

Uric acid serves no bodily purpose and is the end product of purine metabolism. Purines are the end product of the digestion of protein. Gout occurs only in humans where there is a pool of uric acid. Under normal conditions, uric acid is dissolved in the blood and passes through the kidney and into the urine for elimination. The amount of cumulated uric acid in men is about 1,200mg and in women, about 600mg. These values are increased several-fold in individuals with gout.

Population studies have shown that serum urate concentrations (and consequently risk of gout) correlates with age, male gender, blood pressure, body weight, and alcohol intake. Prevalence increases with age, especially in men. (1) In fact, men are affected by gout approximately 10 times more often than women. Although no genetic marker has been isolated for gout, the familial nature of gout strongly suggests an interaction between genetic and environmental factors. (2)

This abnormally high level of uric acid in the blood, called hyperuricemia, may result when a person eats too many high-purine foods such as liver, dried beans and peas, anchovies, and gravies. Hyperuricemia is not a disease and by itself is not dangerous.

The purines, from which uric acid is produced, come from three sources: diet, conversion of tissue nucleic acids, and synthesis of purine bases. The purines derived from these three sources enter a common metabolic pathway, leading to either the production of nucleic acid or uric acid. Uric acid may accumulate excessively if more is produce than is excreted. (3) Several enzyme systems regulate the metabolism of purines, and a partial deficiency of one or more enzymes may be responsible for the increase in uric acid in otherwise normal individuals. Uric acid may also be overproduced as a consequence of certain metabolic disorders.

About two thirds of uric acid is eliminated through the kidneys. The remaining one third is eliminated through the GI tract as a result of the digestive process. There are a number of conditions that affect either uric acid clearance or increase its production. Therefore, a person with these conditions has a greater risk of developing gout.

In the absence of pre-existing conditions or drugs that may affect uric acid levels, the physician needs to determine whether the patient is over-producing or under excreting uric acid. This may be accomplished by placing the patient on a purine-free diet for three to five days, then measuring the amount of uric acid excreted in the urine in 24 hours.


New Zealand Rheumatology Association, 2002.

  • Gout is very common in New Zealand and it is particularly common in Maoris and Pacific Islanders. Some surveys have shown it to be present in up to 10% of adult males.

Mayo Foundation for Medical Education and Research, 1999.

    Gout is a painful problem for over two million Americans. Gout is more common in men than women and is associated with being overweight, overeating, and drinking alcohol excessively.

National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institute of Health, 1999.

  • Gout occurs in approximately 275 out of 100,000 people.
  • Men aged 40 to 50 years are most commonly affected.
  • Gout accounts for about 5% of all arthritis cases.

Signs and Symptoms

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The attacks of acute gouty arthritis most often affect joints in the toes and then the insteps, ankles, heels, knees, wrists, fingers, and elbows. Attacks most often occur at night, with a patient awakening in excruciating pain. The National Institute of Arthritis and Musculoskeletal and Skin Disorders division of the National Institute of Health (NIH) describes the following four stages of disease progression: (4)

    The first stage is known as asymptomatic hyperuricemia—In this stage, a person has high levels of uric acid in the blood but no other symptoms. The tendency to develop gout is present. A person at this stage does usually not require treatment. The second stage is acute gout or gouty arthritis—In this stage, the high levels of uric acid in the blood has caused the deposit of crystals in joint spaces known as tophi. This leads to sudden onset of intense pain and swelling in the joints, which may also be warm and tender. An acute attack commonly occurs at night and can be triggered by stressful events, alcohol or drugs, or other acute illness. Early attacks usually last 3-10 days, even without treatment, and the next attack may not occur for months or even years. Over time, however, attacks can last longer and occur more frequently. Third is the interval or intercritical gout—This is the period between acute attacks. In this stage, a person does not have any symptoms and has normal joint function. Finally, chronic tophaceous gout—This is the most disabling stage of gout and usually develops over a log period, such as 10 years. In this stage, the disease has caused permanent damage to the affected joints and sometimes to the kidneys. With proper treatment, most people do not progress to this advanced stage.


  • The primary symptom of gout is severe pain that strikes suddenly in a single joint (most often the big toe)
  • Swelling, warmth, and redness of the joint
  • Attacks often occur at night
  • Develops quickly, usually in one day, rather than hurting gradually, over time
  • Deposits under the skin (called tophi) cause a lumpy appearance, occurring most often in the cartilage of the ear
  • Blood tests may show a high level of uric acid in the blood Early attacks may last 3-10 days
  • Long periods of time may elapse (months to years) between attacks
  • Between attacks, there are no symptoms, and joints act normally

Treatment Options


Treatment goals are to ease the pain of an acute attack, prevent recurrent attacks, and avoid formation of new deposits and kidney stones.

Acute attacks of gouty arthritis can be treated by a variety of non-steroidal anti-inflammatory agents or colchicine. About 75 to 95 percent of patients with acute gouty arthritis respond favorably to colchicine when ingestion of the drug is begun within 24 to 48 hours of the onset of joint symptoms. (5) The probability of success with the drug diminishes substantially if initiation is delayed longer than 48 hours after the onset of symptoms.

The greatest problem with colchicine is that it causes GI side effects in 50-80 percent of patients before the relief of the attack. Giving the drug intravenously can circumvent the GI side effects. Colchicine should be diluted with 20ml of normal saline prior to administration to reduce sclerosis of the vein. Indomethacin is also used to treat acute gouty arthritis. It has been shown to be as effective as colchicine and has fewer GI side effects; thus, it is generally chosen as the preferred treatment. Indomethacin may produce headache and dizziness as a side effect, and, as with all NSAIDs, there is the possibility of gastric ulceration and bleeding; but with short-term therapy, this is unlikely. A number of other NSAIDs are also effective in treating the inflammation of acute gout. Some patients may never have a second attack, or attacks may not occur for as many as 5-10 years.

Nutritional Suplementation

This category contains no therapies clinically applicable to this disease state.

Herbal Suplementation


Bromelain is a general name for a family of sulfhydryl proteolytic enzymes obtained from Ananas comosus, the pineapple plant. It is usually classified as either fruit bromelain or stem bromelain depending on its source, with all commercially available bromelain being derived from the stem. These enzymes act on a wide variety of proteins, including food proteins, other enzymes, fibrin and plasminogen, and have been used for years in the food industry as meat tenderizers. (6)

In Europe, a patented tape has been developed containing bromelain that is used clinically for debriding wound eschar. (7) The German Commission E approves the use of bromelain in surgical swelling, particularly of the nasal sinuses. (8) Bromelain is used clinically in conditions such as soft tissue inflammation and arthritis, dyspepsia, and dysmenorrhea, as well as a digestive aid. (9)

Bromelain is used as an anti-inflammatory and analgesic agent in treating the symptoms of arthritis. (10) , (11)

Devil's Claw

Historically, devil’s claw tuber has been used as an adjunct therapy for a variety of conditions related to the liver and kidneys. It has also been used to treat lymph toxicity, diabetes, respiratory ailments, and arthritic complaints. (12) It reportedly helps with joint mobility and reduces pain and swelling. (13) , (14) The current use of devil’s claw focuses around its anti-inflammatory properties.

Diet & Lifestyle

Increase fluids:

Eliminate homogenized milk; it may be a source of xanthine oxidase, which can increase levels of uric acid (15) , (16) potentially leading to an attack of gouty arthritis. Though not specifically related to gout, the activity in the body of xanthine oxidase absorbed from homogenized milk in the diet has been reported to be too weak to be responsible for any changes in the body, (17) , (18) thus questioning the elimination of homogenized milk from the diet.

Eliminate alcohol, as studies have found an increased risk of gout with alcohol consumption. (19) , (20)


  1. Kelley WN, Worthman RL. Gout and hyperuricemia. In: Kelley WN, Harris EP, Ruddy S, Sledge CB, eds. Textbook of Rheumatology. Philadelphia: Saunders; 1997:1313-1351.
  2. Hawkins DW, Rahn DW. Gout and Hyperuricemia. In: DiPiro JT, et al, eds. Pharmacotherapy, A Pathophysiologic Approach, 4th ed. Stamford, CT: Appleton & Lange; 1999.
  3. Hawkins DW, Rahn DW. Gout and Hyperuricemia. In: DiPiro JT, et al, eds. Pharmacotherapy, A Pathophysiologic Approach, 4th ed. Stamford, CT: Appleton & Lange; 1999.
  4. National Institute of Arthritis and Musculoskeletal and Skin Diseases fact sheet: Questions and Answers about Gout. Jan1999.
  5. View Abstract: Tan N, Lertratanalcul Y, Barr WG. Acute gouty arthritis. Postgrad Med. 1993;94:73-78.
  6. View Abstract: Monograph: Bromelain. Altern Med Rev. Aug1998;3(4):302-5.
  7. View Abstract: Houck JC, et al. Isolation of an effective debriding agent from the stems of pineapple plants. Int J Tissue React. 1983;5(2):125-34.
  8. Blumenthal M, et al, eds. Herbal Medicine: Expanded Commission E Monographs. MA: Integrative Medicine Communications Newton; 2000:33-35.
  9. View Abstract: Monograph: Bromelain. Altern Med Rev. Aug1998;3(4):302-5.
  10. View Abstract: Taussig SJ, et al. Bromelain, the enzyme complex of pineapple (Ananas comosus) and its clinical application. An update. J Ethnopharmacol. Feb1988;22(2):191-203.
  11. View Abstract: Rovenska E, et al. Enzyme and combination therapy with cyclosporin A in the rat developing adjuvant arthritis. Int J Tissue React. 1999;21(4):105-11.
  12. Bradley P, ed. British Herbal Compendium. Bournemouth: British Herbal Medicine Association; 1992:78-80.
  13. Newall CA, et al. Herbal Medicines: A Guide for Health Care Professionals. London: The Pharmaceutical Press; 1996:98-100.
  14. View Abstract: Baghdikian B, et al. An Analytical Study, Anti-inflammatory and Analgesic Effects of Harpagophytum procumbens and Harpagophytum zeyheri. Planta Med. 1997;63(2):171-76.
  15. View Abstract: Bhavadasan MK. Free and membrane-bound xanthine oxidase in bovine milk during cooling and heating. J Dairy Sci. Mar1980;63(3):362-7.
  16. View Abstract: Eger BT, Okamoto K, Enroth C, Sato M, Nishino T, Pai EF, Nishino T. Purification, crystallization and preliminary X-ray diffraction studies of xanthine dehydrogenase and xanthine oxidase isolated from bovine milk. Acta Crystallogr D Biol Crystallogr. Dec2000;56(Pt12):1656-8.
  17. View Abstract: McCarthy RD, Long CA. Bovine milk intake and xanthine oxidase activity in blood serum. J Dairy Sci. Jun1976;59(6):1059-62.
  18. View Abstract: Mangino ME, Brunner JR. Homogenized milk: is it really the culprit in dietary-induced atherosclerosis? J Dairy Sci. Aug1976;59(8):1511-2.
  19. View Abstract: Sharpe CR. A case-control study of alcohol consumption and drinking behavior in patients with acute gout. Can Med Assoc J. Sep1984;131(6):563-7.
  20. View Abstract: Choi HK, et al. Alcohol intake and incidence of gout in men; a prospective study. Lancet. Apr 2004;363:1277-81.