Gout is a metabolic disorder that causes an extremely uncomfortable arthritic pain in the joints and synovial fluids. It is due to an increased amount of uric acid (the final end product of purine metabolism), also known as hyperuricemia, in biological fluids.
Gout causes extreme discomfort because of the deposited amounts of uric acid crystals that become lodged in joints and other small spaces in the body. All mammals except humans possess an enzyme called uricase, which assists in the breakdown of purines for excretion from the body. Tophi (deposits of uric acid) can accumulate and cause inflammation and the destruction of the joint spaces, bones, and cartilage.  In some cases, tophi can break through the skin and appear as white chalky nodules that look like crab eyes.
Uric acid is produced from purines that are manufactured in human cells (usually DNA and RNA), from the breakdown in energy substrates, and are also obtained from foods. Uric acid is excreted through the kidneys into urine. A small amount passes through the intestines where it is broken down by specialized bacteria. Men typically excrete 1200 mg and women approximately 600 mg of uric acid daily. In the past, gout was considered a “rich man’s disease”, suffered by kings and other lordly men, who were overweight, inactive, and consumed a diet rich in meat and wine. This theory may have some legitimacy, as organ meats are particularly high in purines and were a significant source of protein in earlier years. Alcohol also slows down uric acid excretion by interfering with the kidney and liver’s normal functioning and was readily consumed during this time period as well.
Gout is classified as either primary or secondary depending on the cause of the hyperuricemia. More than 99% of primary gout cases are considered idiopathic, meaning that there is no clear cause. It is most likely due to a combination of genetic and hormonal factors that cause either an overproduction, or reduced excretion of uric acid. Secondary gout is usually caused by drug therapy or by other medical conditions. Medications such as diuretics and low doses of aspirin can reduce uric acid excretion and increase the chance of hyperuricemia. Alcohol use and renal (kidney) insufficiency can also cause gout, especially in older patients. Exposure to lead is also associated with build up of uric acid and should be ruled out in all suspected cases. 
The initial gout symptom experienced is a severe, nearly debilitating pain in one joint, most often in the lower limbs. About 60% of cases occur in the big toe. In the elderly, symptoms are more likely to occur in the upper extremities, especially in the fingers. If the attack continues, fever and chills can occur. The pain usually peaks in the late evening and will often awaken the patient.
Gout is often divided into four symptomatic stages:
- Asymptomatic- the patient is unaware of the high uric acid levels and has no symptoms at present
- Acute gouty arthritis- the patient has developed high levels and is experiencing pain and discomfort from the formation of tophi under the skin and in joint spaces. The attacks come on quickly, can last for days, and may reoccur sporadically. The condition usually worsens and the attacks become more frequent.
- Intercritical gout- this is the period between attacks when there are no clinical symptoms present.
- Chronic tophaceous gout- this is when the condition has become chronic and has caused lasting damage to the joints and the kidneys. It is unusual for patients to reach this stage in today’s medical system.
Diagnosing gout is often based on clinical signs and symptoms. Infections should always be ruled out as the cause of symptoms. A serum uric acid test should be run, as well as an aspiration of fluid, to culture and evaluate for crystal formation. 
- Gout affects over 2 million Americans a year
- Over 95% of sufferers of gout are men over the age of 30
- Gout is responsible for approximately 5% of all arthritic cases in the country
- Some degree of kidney dysfunction occurs in nearly 90% of patients with gout and they will at an elevated risk for the development of kidney stones
Standard conventional gout treatments rely upon the use of non-steroidal anti-inflammatory (NSAIDs) drugs or the use of colchicines. Colchicine is derived from the autumn crocus plant and certain constituents in this plant can help with the inflammatory process. Over 75% of patients show major improvement in symptoms within 12 hours of ingesting these medications. However, colchicines tend to cause major gastrointestinal side-effects such as nausea, vomiting, diarrhea, and abdominal pain. [5, 6] Colchicines may also cause bone marrow depression, hair loss, liver damage, seizures and even death.
NSAIDs, such as indomethacin, are also used to treat acute gouty arthritis. It is generally the preferred treatment in causes of standard diagnosed gout, and is prescribed at the typical dosage of 25 mg/day. NSAIDs are often the cause of gastrointestinal bleeding and ulceration. These type of prescriptions should be used with medical supervision and extreme precaution because of the likelihood of adverse side effects.
A healthy diet and body weight is one of the most important factors in preventing and treating gout. Obesity is probably the most important factor that contributes to the onset of this condition.  Healthy weight loss should be a goal for every patient with gout.  Foods with high purine levels should be avoided, such as organ meats, shellfish, and certain types of fish, like sardines and anchovies. Homogenized milk should also be avoided due to its tendency to increase uric acid levels.  Adequate amounts of protein should be ingested, but should not be excessive. Foods that should be added to one’s diet may include; black cherries, purple grapes, raspberries, blackberries and strawberries.  Certain fats, such as those found in fish, flax or olive oil, may also have some anti-inflammatory effects and should also be consumed. Adequate hydration is also important. In addition, there should be an avoidance of beverages that contain both alcohol and caffeine.
Vitamins and Nutrients:
800 IUs of Vitamin E per day inhibits some of the inflammatory pathways associated with gout and also acts as a potent antioxidant. Selenium, another antioxidant, acts synergistically with vitamin E, and these nutrients should be taken together.
High levels, up to 10-40 mg/day, of folic acid may be used to help diminish the enzyme responsible for producing uric acid.  These high doses may interfere with some drugs that are used for epilepsy. Caution should be used.
This essential fatty acid helps to decrease the inflammation and joint damage that may occur in gout sufferers. Flax seed oil and fish oil are extremely important to help with inflammation. Levels of eicosapentaenoic acid (EPA) should be approximately 1.8 gm/day.
Avoidance of high levels of vitamin C and niacin- may increase uric acid in some patients.  Niacin competes with uric acid in excretion and may contribute to levels which are higher than normal.
Bromelain is an enzyme derived from the pineapple and is a potent anti-inflammatory agent and analgesic. It should be taken between meals on an empty stomach. 
This bioflavanoid may inhibit the enzyme xanthine oxidase, as well as the drug allopurinol. It should be taken with Bromelain between meals, since the Bromelain will help enhance absorption.
Harpagophytum procumbens has been used for many sorts of arthritis in the past.  Research has shown it to be a potential treatment for gout by reducing serum uric acid levels. It also lowers serum cholesterol levels.
 Wortman RL. Gout and other disorders of purine metabolism. Harrison’s Principles of Internal Medicine, 14th ed. New York, McGraw Hill, 1998, pp 2158-2165.
 Hawkins DW, Rahn DW. Gout and Hyperuricemia. Pharmacotherapy: A Pathophysiologic Approach, 4th ed. Stamford, CT, Appleton and Lange, 1999.
 Lin JL. Environmental lead exposure and urate excretion in the general population. Am J Med. Nov 2002; 113(7): 563-8.
 Siva, C. Diagnosing acute monoarthritis in adults: a practical approach for the family physician. Jul 2003; 68(1); 83-90.
 Conaghan RG, Day RO. Risks and benefits of drugs used in the management and prevention of gout. Drug Safety. 1994; 11:252-258.
 Van Doornum S, Ryan PF. Clinical manifestations of gout and their management. Med J Aust 2000 172: 493-497.
 Scott JT. Obesity and hyperuricaemia. Clin Rheum Dis 1977; 3: 25-35.
 Dessein PH, et al. Beneficial effects of weight loss associated with moderate calorie/carbohydrate restriction, and increased proportional intake of protein and unsaturated fat on serum urate and lipoprotein levels in gout: A pilot study. Ann Rheum Dis. 2000; 59: 539-543.
 Egar BT et al. Purification, crystallization and preliminary X-ray diffraction studies of xanthine dehydrogenase and xanthine oxidase isolated from bovine milk. Acta Crystallogr D Biol Crystallogr. Dec 2000; 56: 1056-62.
 Blau LW. Cherry diet control for gout and arthritis. Texas Rep Bio Med 1950; 8: 309-11.
 Spector T, Ferone R. Folic acid does not activate xanthine oxidase. J Biol Chem 259 (1984): 10784-6.
 Wortman RL. Gout and other disorders of purine metabolism. Harrison’s Principles of Internal Medicine, 14th ed. New York, McGraw Hill 1998, pp 2158-2165.
 Dombeck C. Pineapple. In The Lawrence Review of Natural Products. St. Louis, MO, Wolters Kluwer, July 1993: 1-2.
 Baghidikian B, et al. An Analytical Study, Anti-inflammatory and Analgesic Effects of Harpagophytum procumbens and Harpagophytum zeyheri. Planta Med. 1997; 63(2): 171-76.
 Kong LD, et al. Inhibition of xanthine oxidase by some Chinese medical plants used to treat gout. J Ethnopharmacol 2000; 73: 199-207.