The Gout FAQ.
Newsgroups: alt.folklore.herbs
Subject: Re: Gout
From: smills1138.aol.com (SMills1138)
Date: 11 Aug 1995 23:59:58 -0400
> Does anyone know of an effective herbal remedy for gout (or the prevention of)?
Best treatment is decrease protein intake--no red meat whatsoever, some fish maybe. There are several herbs that help with decreasing uric acid but I don't have that info at hand. Later.
From: vonbrundz.aol.com (VON BRUNDZ)
Hi I have a friend who had a bad attack and got rid of it with juniper berries. He is taking the capsuals 2 a day at first then 1 a day. Juniper can be hard on the kidneys and bladder for some people. we did a test and he stopped taking them and in two days the gout returned. Once he got back on the juniper the problem once again dissappeared. He hasn't had any side effects or problems with his kidney or bladder function and its been about 2 months now.
From: chaugen.Direct.CA (Colleen Haugen)
>Does anyone know of an effective herbal remedy for gout (or the prevention of)?
June 6, 1995
Gout (crystal arthritis)
What is it:
GOUT, n. A physician's name for the rheumatism of a rich patient. <VVBG> From "The Devil's Dictionary" 1911, by Ambrose Bierce.
Gout is a relatively common disease, which has been recognized from antiquity. An estimated 500,000 Americans suffer from this disorder, which affects primarily middle-aged men over 40, but it can occur anytime after puberty. It is a disease of rich and poor alike.
Only five out of a hundred patients are women a ratio of 20:1. In women, gout seldom occurs before menopause suggesting a hormonal involvement in the disorder. (See note about prostaglandin's under indocin.)
Gout or crystal arthritis is caused by a metabolic dysfunction of body chemistry causing an increased concentration of uric acid which precipitates out of solution causing monosodium urate crystals to be deposited in the joints, tendons, kidneys, and other tissues, where they cause considerable inflammation and damage.
Attacks of gout may be caused by the over-production (due to inherited enzyme deficiencies) or under-secretion of uric acid (do to drugs or possible kidney insufficiency).
Uric acid is the final breakdown product of purine metabolism. Purine is made in the body and ingested in foods, and its byproduct, uric acid is normally, excreted steadily into the urine. The biochemical defect associated with gout that leads to abnormal concentration of the substance in the body is not yet known. Both increased uric acid production and decreased excretion may be responsible. Gout is probably an inborn metabolic defect, but the initial attack of acute joint inflammation, or gouty arthritis, does not usually appear until middle age.
If untreated, the pain and swelling caused by the very sharp, star-burst shaped crystals can be crippling. Most references indicate that gout seldom causes permanent deformation of the joints, but others suggest that it can cause destruction of bone in the hands and feet. It is often associated with kidney stones and may ultimately lead to kidney failure in about 10% of afflicted patients.
Gout (crystal arthritis) reportedly causes at least 5% of significant problems in the field of systemic arthritis. It tends to run in families.
Gout may be acute, intercritical, or tophaceous.
An acute, initial attack is usually sudden in an otherwise healthy person. It may be triggered by a rich, heavy meal or by an alcoholic spree, but such circumstances do not cause the disorder. Factors that may precipitate an attack include acute infection, emotional upset, diuresis, surgery, trauma, and the administration of certain drugs. Thiazide diuretics or low dose salicylates (aspirin) may contribute to an attack of gout.
Attacks are often preceded by the heavy passage of urine during the day and night, a general feeling of malaise and nausea, and some soreness in the joints and muscles. If these symptoms are recognized and treated for what they are, an acute and severely painful attack may be avoided. Gout sometimes develops following a chronic blood disease.
During an attack, any peripheral joint may be affected, but, nine times out of ten the attack occurs in the joint of the big toe, although it can occur on the wrist, ankle, and thumb joints. The toe may become shiny, red to purplish red, swollen, and excruciating to the touch so that even the weight of the lightest clothes cannot be tolerated. (Ordinary arthritis produces pain that is deep and aching; in gout the pain that is sharp and agonizing.)
There may be fever and chills, with a rapid pulse. The first attack can last from one to four days; later attacks may not be as intense but will last longer. As the disease progresses, the attacks tend to become more frequent. The arthritis is due to the deposits of uric acid crystals in the joint.
The sharp pain usually occurs in a single joint, especially the base of the big toe, but it can also affect other joints such as the feet, ankles, knees, wrists, and fingers. The intensity of the pain usually reaches its peak in 24-36 hours. It can be so painful that affected joints may not be able to support body weight and even the weight of a blanket can be intolerable. The first attack frequently may last from a few days to several weeks. An affected joint is red, swollen, and excruciatingly tender. If it spreads, it is easily confused with cellulitis which is an inflammation of the connective tissue.
The time between acute attacks is known as the intercritical period. Second attacks most often occur 6-24 months after the first. After the second attack, more and more joints are often involved and the damage to the joint from chronic inflammation may cause constant pain. Some patients experience only a single attack or a few attacks, while others have repeated, recurring attacks. Joints are seldom deformed permanently if the condition is treated.
Gout is often associated with other diseases such as diabetes, alcoholism, obesity, high blood pressure, kidney stones, albumin in the urine, hardening of the arteries, and occasionally fever.
Chronic: Ongoing inflammation of the joints caused by accumulation of crystals in the tissues.
Chronic tophaceous gout occurs when the high uric acid levels are left untreated and results in masses of uric acid crystals, called tophi being deposited in the joints, especially of the fingers, and in the cartilage of various parts of the body, including of the outer ear. The lumpy deformities signal an irreversible degeneration of the joints, but this usually occurs about 10 years after the initial clinical symptoms of untreated gout.
High uric acid levels is a chronic condition, but it can be reversed if the patient follows the daily regimen recommended by his physician. The silent, symptomless period between attacks (the inter-critical period) may lull a patient into ignoring diet and medication. It is during this quiet period that much of the damage of gout takes place. Over 50% of patients will have a second acute attack within a year. Over time, the attacks become more frequent, longer lasting and often involve several or many joints. This may lead to the disease process being constant with no painfree periods inbetween acute attacks. It is usually during this intercritical period that bony erosions may occur. The prognosis (outlook) is mostly up to the patient.
A secondary type of gout, sometimes called saturnine gout, can result from lead toxicity. Historically, saturnine gout was due to consuming alcoholic beverages stored in containers containing lead (for example, leaded crystal). Use of such containers for storage of foods should be avoided.
In such conditions as leukemia, lymphoma, and polycythemia, increased production of uric acid sometimes results in secondary gout.
Prevention:
Middle-aged men who come from gout susceptible families and who want to prevent the development of chronic gout symptoms should alert their doctors of their family histories and any early signs of the disease.
If the first attack can be traced to a particular irritant or causal agent, continued exposure to it should be avoided. There is no positive evidence that so-called "anti-gout" diets affect the course of the disease. Preventive medications are more effective in the management of this disorder than following a purine-free diet.
How is it diagnosed:
Patient history. If an extremely painful attack of arthritis suddenly affects a single joint, it is usually classified as gout particularly if other members of the family are afflicted.
The diagnosis is made when six of the following are present:
(1) more than one attack of acute joint pain;
(2) pain reaches maximum within one day;
(3) pain involving only one joint;
(4) redness of the joint;
(5) painful, swollen base of a big toe;
(6) involvement of one big toe;
(7) involvement on one joint on the top of the foot close to the ankle;
(8) bump under the skin on the elbow (called a tophus);
(9) elevated uric acid levels in the blood;
(10) abnormal x-rays of involved joint(s);
(11) negative culture of joint fluid during attack.
Diagnosis can be confirmed by microscopically examining fluid removed from a swollen joint to determine if uric acid crystals are present. A blood test with high levels of uric acid suggests gout, but blood levels may be high without gout.
The blood level of uric acid is of limited helpfulness in diagnosing gout. In up to 25% of cases of acute gout attacks, blood levels of uric acid are within the normal range. Those initially normal results may be useful in following response to long-term treatment, even though the results may not help with a diagnosis.
High blood levels of uric acid do not automatically result in gout, in fact fewer than 20% of patients with high uric acid will develop gout. However, if blood levels exceed 12.8 mg/dL (760 (moles/1)) for men and 10 mg per dL (600 (moles/l)) in women, the patient should be considered for treatment even in the absence of symptomatic gout due to the increased risk of kidney complications.
A 24 hour urine uric acid should be obtained to help determine whether the patient is a uric acid overproducer or an undersecreter. This can guide in the selection of the proper urate-lowering treatment. Patients who should not be put on a uricosuric agents (drugs to lower uric acid) include the 10% of patients who are uric acid overproducers with high uric acid output, those with a history of kidney disease, poor renal function, or patients over 60 years of age.
What Causes Gout?
High levels of purine (a product of DNA) can raise the blood levels of uric acid which precipitates out of solution and forms crystals in the space between the bones of joints and in soft tissue. Crystals may also be deposited in soft tissues around joints, in the ears especially the earlobes, and around the tendons often producing hard, painless tumors called tophi. Uric acid is the main excretory product of protein metabolism and nucleic acids.
When uric acid crystals are deposited in the kidneys, serious kidney damage can follow. In addition, and excess spillage of uric acid into the urine may produce kidney stones (in 10 to 20 % of the patients). Gout is readily recognized when tophi are present or when typical attacks of arthritis occur. Demonstration of uric acid crystals in the joint fluid or urine confirms the diagnosis. A high uric acid level in the blood is presumptive evidence of gout.
Previously injured joints are most prone to attacks of gout.
Drugs (such as diuretics) taken for high blood pressure may initiate an attack of gout.
Treatment Goals:
Treatment should safely provide relief from acute attacks and prevent future attacks. It should also prevent destruction of the joints and formation of tophi and kidney stones.
Non drug Treatments:
Regular, daily, consistent exercise apparently helps decrease uric acid in the blood.
The site of an acute attack should be cradled, wrapped in cotton, and kept immobile. Ice may help reduce joint inflammation, help numb the pain and reduce the heat in the joint.
Diet:
Gout was once treated with modifications of diet that involved following these guidelines. Although a strict diet is no longer the primary course of treatment, this information may help patients identify factors which may precipitate attacks.
1. Introduction of a low-purine diet.
2. Elimination of alcohol intake.
3. Achievement of ideal body weight.
4. Liberal consumption of complex carbohydrates.
5. Low fat intake.
6. Low protein intake.
7. Liberal fluid intake.
Low-purine Diet: For many years, a low-purine diet was the mainstay of the dietary therapy for gout. However, with the advent of potent drugs that lower uric acid levels, many physicians lower the serum urate levels without subjecting the patient to the inconvenience and deprivation people may associate with a purine-free diet. Dietary restriction of purines is, however, recommended to reduce metabolic stress.
Foods with the highest purine levels include:
Organ meats such as liver, kidney, sweetbreads
Fish, such as herring, sardines, mackerel, and anchovies.
Yeast, both brewer's and baker's
Meat extracts such as bullion
Legumes, all kinds of peas and beans
Poultry, especially chicken
Other high-purine foods include:
whole grain cereals
refined carbohydrates,
all fish and shellfish.
Alcohol:
Beer is higher in purine than wine or other spirits, and may precipitate an attack in susceptible individuals. Alcohol increases uric acid production and reduces uric acid excretion by increasing lactate production (as a result of the breakdown of alcohol), which impairs kidney function. The net effect is a significant increase in serum uric acid levels. This explains why alcohol consumption is often a precipitating factor in acute attacks of gout. In many individuals, elimination of alcohol is all that is needed to reduce uric acid levels and prevent gout. If alcohol is consumed, it seems to be less harmful if taken with food rather than on an empty stomach. Other references indicate that alcohol is tolerated by many gout patients.
Weight reduction:
Individuals with gout are typically obese, prone to high blood pressure and diabetes, and at relatively high risk for cardiovascular disease. Weight reduction in obese individuals significantly reduces serum uric acid levels. For these people, achieving ideal body weight may be the most important dietary goal. Overweight patients tend to have high uric acid levels and excess weight causes additional strain on the joints. However, affected individuals should lose weight gradually, because fad diets and fasting cause cellular break down causing a release of uric acid.
Carbohydrates, Fats, and Protein:
One reference recommended that refined carbohydrates and saturated fats be kept to a minimum as refined carbohydrates increase uric acid production, while saturated fats decrease uric acid excretion. For dietary control, protein intake should not exceed 0.8 g/kg of body weight per day. It has been shown that uric acid synthesis may be accelerated in both normal and gouty patients by a high protein intake. Adequate protein (0.8 g/kg of body weight) is necessary, however, since amino acids decrease the reabsorption of uric acid in the kidney, thus increasing uric acid excretion and reducing serum uric acid concentrations.
Fluid Intake:
Liberal fluid intake dilutes uric acid concentrations in the urine, thereby reducing the individual's risk of having it crystallize in the body or developing kidney stones to which some patients are prone. In a recent study, large dosages of niacin (especially the slow release form) precipitated attack of hyperurimea gout. Some evidence exists to suggest that vitamin A may also cause gout to flare. Other references indicate that an excessive intake of Vitamin D may cause a flare.
Blood pressure should be controlled by reducing salt intake, exercising, and weight reduction. It is important to keep blood pressure low since the diuretics used to lower blood pressure raise uric acid levels resulting in attacks of gout, creating a catch-22 situation.
Drugs:
The frequency of attacks may be reduced by lowering uric acid blood levels with drugs that either inhibit the formation of uric acid (such as Allpurinol) or increase the elimination of uric acid by the kidneys with uricosuric drugs (such as Probenecid and Sulfinpyrazone). If uric acid blood levels are very high, these drugs may need to be taken for life because if untreated, hyperuricemia may lead to high blood pressure or kidney disease.
Treatment should begin at the first sign of an attack, and patients with recurring attacks should carry their gout medication with them.
Large doses of Ibuprofen may be used to reduce inflammation. This NSAID (Non-Steroidal Anti-Inflammatory Drug) apparently has one of the higher anti-inflammatory properties of over-the-counter NSAIDs. It also eases pain. Although sold without prescription, Ibuprofen (like other NSAIDS) can cause stomach irritation and other complications which may occur after long-term use. It should always be taken with food to reduce stomach irritation. Dosages as high as 800 mg 4 x a day may be needed, so Indomethacin is often prescribed. Ibuprofen should not be used by anyone with a prior history of hypersensitivity to aspirin.
If NSAID's cannot be used for some reason or are ineffective, then colchicine may be prescribed.
Once treatment starts, an inflammation may subside within 2-3 days or it may last for several weeks.
If neither NSAID anti-inflammatories nor colchicine reduce the inflammation, then corticosteroid drugs may be injected into the affected joint/s.
Prescription Drug Information: In alphabetical order by generic name.
Allpurinol: (Allopurinol)
(Brand names that include allpurinol include Lopurin, Zyloprim). This drug inhibits the formation of uric acid stones in patients excreting large amounts of uric acid. Uric acid is soluble in an alkaline environment, and the alkalization of urine is induced using sodium bicarbonate. Allopurinol should never be used in the treatment of an acute attack because it can make it worse. When used to treat intercritical gout, Allopurinol will decrease levels of uric acid, but it also may trigger acute attacks during the early stages of treatment. Consequently, low dosages of colchicine is sometimes used in conjunction with Allopurinol during the initial period to help prevent the possibility of triggering an attack (called mobilization gout).
Allpurinol is currently the drug of choice with most physicians and 200-300 mg is a common dosage level, but it may range from 100-800 mg.
Side effects: skin rashes, vomiting, diarrhea, and abdominal pain. The drug should be discontinued at the first sign of skin rash or other adverse reaction. An extremely potent drug, it should be monitored regularly by the prescribing physician.
Colchicine:
Colchicine, which comes from the autumn crocus, was discovered by an unknown Egyptian genius in 500 B.C. and has been in steady use ever since. No one knows why or how it works, but it does bring relief within a comparatively short time. Since colchicine has no effect on any other disease, it provides confirmation of the diagnosis. It is thought to reduce uric acid, but the precise pharmacological activity of colchicine in gout is not known. If used, it needs to be started immediately since delay of even a few hours reduces its effectiveness.
Colchicine Side effects: This extremely powerful drug usually needs to be given in doses high enough to cause vomiting and diarrhea before backing off. Other side effects may include weakness, abdominal cramps, and anorexia. Prolonged usage may cause bone marrow depression and several other serious complications.
Colchicine should be used with caution if the patient has a history of renal problems, gastrointestinal disorder, or heart disease.
Colchicine overdoses cause severe problems and can be fatal.
Corticosteroids: (prednisone)
Used to treat inflammation in acute attacks, corticosteroids may be given orally, injected into the joints, or given systematically by injection. A typical oral dose is 20-40 mg for the first 2-4 days tapering down over a period of 2 weeks. Injection into affected joints is feasible if only 1 or 2 joints are involved.
Indomethacin: (Indocin)
This NSAID may be prescribed in doses as high as 150 mg/day in divided doses. It should always be taken with food or antacids. Indocin, if tolerated, is the preferred NSAID. It's effect in treatment of acute gout (50 mg 3-4 times a day with food) is pretty spectacular, often giving quite dramatic relief by reducing fever, swelling, redness, and tenderness. Beneficial effects often start to occur within a few hours. Dosages should never exceed 200 mg/day and dosages should be reduced as quickly as possible. Treatment may be continued at lower dosages for 10-14 days. Indocin suppresses prostaglandin. Some speculate that it may be this action that makes it so effective for gout.
Side effects: It has the same side effects as the other NSAID's. It should be used with caution since it can cause other, more serious side effects in some individuals.
Other useful NSAIDs include Naproxen (Naprosyn), Ketoprofen (Orudis),
Diclofenac (Voltaren), and Tolmetin (Tolectin).
Probenecid:
(Brand names that include probenecid: Benermide, CoBenemid, Polycillim-PRB, Principen with Probenecid, Probenecid & Colchicine, Wycillin and Probenecid.) Probenecid increases elimination of uric acid by reducing reabsorption of urate, retards urate deposits, and promotes reabsorption of urate deposits. It is used primarily for patients with prominent tophi.
Side effects: headache, gastrointestinal symptoms (which may indicate that dosage is too high), urinary frequency, and dermatitis pruritus (itchy skin). This drug may increase gout attacks when first started which may be temporarily controlled with other drugs. The manufacturers recommend drinking large amounts of water and keeping the urine alkaline with bicarbonate of soda.
Probenecid increases the blood levels of many other compounds, particularly penicillin. It increases blood levels of penicillin 2-4 times above normal. It does not have the same effect with other antibiotics. It does increase blood levels of salicylates (aspirin) which tends to nullify the effectiveness of probenecid. Probenecid should be used cautiously by diabetics as it can increase the hypoglycemic effect of some oral diabetic medications. It also affects blood levels of methotrexate. Therapy with this drug is not usually started until an acute attack subsides.
Sulfinpyrazone:
(Anturane/Ciba) increases elimination of uric acid This drug is used for both chronic and intermittent gouty arthritis, but it has few anti-inflammatory properties and is not recommended for relief of initial symptoms.
The PDR suggests that Sulfinpyrazone should be used with caution for pregnant women, patients with a history of peptic ulcers, and diabetics. It reportedly increases the effectiveness of certain sulfonamides (including sulfa drugs and hypoglycemic agents) and insulin. Periodic blood tests for several blood abnormalities that may occur, and kidney function tests are recommended.
Side effects: The most common side effects include upper GI disturbances
so it should always be taken with meals.
Unproved treatments:
(Treatments based on anecdotal accounts that are not confirmed by scientific double-blind studies.)
Flavonoids: Reports from a number of sources suggest that cherries help prevent the crystallization of uric acid that causes attacks of gout. Advocates indicate that both sweet and sour cherries are effective and that fresh, canned, frozen, or juiced are equally effective. Advocates indicate that results are frequently obtained within a few days, and that attacks resume if the consumption of cherries is stopped. Anecdotal reports indicate that a large initial quantity can bring almost immediate relief and that about 6 cherries twice a day will prevent future, severe attacks. Other reports indicate that consuming the equivalent of ½ pound of fresh cherries per day has been shown to be very effective in lowering uric acid levels and preventing attacks of gout.
Cherries, hawthorn berries, blueberries, and other dark red-blue berries are rich sources of anthocyanidins and proanthocyanidins. These flavonoid molecules give the fruits their deep red-blue color and help prevent collagen destruction.
Cherries apparently have no impact on Rheumatoid arthritis, but a number of patients who had both rheumatoid and crystal arthritis also reported reduced pain.
Other flavonoids may benefit individuals with gout as well. For example, the flavonoid quercetin has demonstrated several effects in experimental studies that indicate its possible benefit to individuals with gout. Quercetin may offer significant protection by inhibiting uric acid production in a similar fashion to the drug allopurinol, as well as by inhibiting the manufacture and release of inflammatory compounds. Quercetin is widely found in fruits and vegetables.
Strawberries:
The botanist Linneaus reported that after eating almost nothing but strawberries his gout was dramatically relieved.
The French herbalist Messegue recommended a strawberry regime lasting several days for individuals suffering from gout or kidney stones.
Laser treatments:
Some chiropractors and physiotherapists have tried Laser (low level) on some gout patients and report that this treatment seems to reduce their patients discomfort. They indicate that an infrared laser at 830 nm can penetrate soft tissue from 2-8 cm and that it may be the heat that causes crystals to dissolve suggesting that similar results might occur from the use of a heating pad.
Gout Weed:
An old herbalist remedy involves drinking a tea brewed from the flowers of the broom plant or crushing the leaves and roots of gout weed (Aegopodium podagraria) and using it as a poultice to reduce swelling and inflammation in affected joints.
Charcoal:
Activated charcoal taken in ½- 1 teaspoon doses 4 times per day may help reduce uric acid levels in the blood. Charcoal capsules may be taken upon rising, at midmorning, mid afternoon, and at bedtime.
Some sources also recommend using a charcoal poultice on the affected joint.
This FAQ compiled by Margaret Baker <cmbaker.teleport.com> and Colleen Haugen <chaugen.direct.ca> in an internet collaboration. We would like to thank Drs. Kam Shojania and Sjanna Johnston for their input and critique.
