Gout is a disease usually caused by having too much uric acid in the body and and the deposition of monosodium urate crystals in tissues. It is more common in men. Too much uric acid may not cause gout symptoms for years, but after a time it can cause painful joint inflammation. The problem is often not with the amount of uric acid produced by the body, but the fact that the body cannot excrete it well. Gout is more common in those who overeat. The risk is lower in those who are more physically active, maintain ideal body weight, and consume diets enriched in fruits and vegetables and limited in meat and alcohol. Basically, gout is the result of either increased synthesis of uric acid; reduced ability to excrete uric acid; or both over production and under excretion.
Gout is the most common cause of inflammatory arthritis
in men over 40 years old; it is a debilitating disease and, if
untreated, can result in a chronic progressive disease, including
tophaceous gout. In the elderly it represents a special issue, with
notable clinical and therapeutic differences from the classical form
with a systemic involvement. The burden of the disease increases
particularly in the very old people, in whom arthritis, impaired gait
and eyesight problems may enhance the related disability. Chronic gout
moreover could aggravate heart and kidney disease and increase overall
mortality and organ-related damage.
Which joints are involved?
The most common site of inflammation is the joint between the foot and the big toe. Later attacks often affect other joints of the foot and leg. Less often, the arms and hands are affected. Uric acid crystals are deposited in joints, tendons, kidneys, and other tissues, where they cause considerable inflammation and damage. The reason that the joints of the extremities are more effected is probably because they are colder and uric acid crystals are more likely to deposit at lower temperatures.
Gout diet - natural remedy
It appears that diet has a lot to do with gout prevention or reduction in occurrence. I would recommend increasing the intake of vegetables, particularly those with apigenin and other flavonoids. Apigenin is a flavonoid found in high amounts in parsley, thyme, and peppermint. The enzyme xanthine oxidase catalyses the oxidation of hypoxanthine to xanthine and then to uric acid, which plays a crucial role in gout. Apigenin is a potent inhibitor of xanthine oxidase. Chrysin, luteolin, quercetin, kaempferol, myricetin, and isorhamnetin are other flavonoids that also inhibit xanthine oxidase activity. It is possible that curcumin or turmeric could be of benefit.
Diets high in purine-rich beef, pork, lamb, organ meats, liver, and seafood (anchovies) increase the risk of gout. Beer is more likely to be associated with gout than spirits. Moderate wine consumption does not appear to raise the risk. Of all the dietary factors listed above, shellfish and beer are the most likely to cause this condition. Perhaps a high fructose diet is also a factor in gout.
It is possible that drinking coffee could reduce gout occurrence. Lower levels of uric acid are found in the blood of those who consume a lot of coffee.
A higher intake of added sugars or sugar-sweetened drinks leads to higher blood levels of uric acid.
Milk does not seem to make it worse, perhaps it can help. Ann Rheum Dis. 2010. Acute effect of milk on serum urate concentrations: a randomised controlled crossover trial. Department of Medicine, Faculty of Medical and Health Sciences, University of Auckland, Grafton, Auckland, New Zealand.
Vitamin C supplements and gout
Vitamin C intake of at least 1500 milligrams per day reduces uric acid levels and the odds of gout by half compared with an intake of less than 250 milligrams per day. Dr. Hyon K. Choi, from the University of British Columbia, Vancouver, Canada, has found that high vitamin C levels are strongly associated with a lower risk of gout, and dietary increases in this vitamin may prevent the development of gout. Archives of Internal Medicine, March 9, 2009.
Comments: One has to consider the possible side effects of long term use of high dosages of vitamin C versus the potential benefits of gout symptom reduction.
Consumption of cherries lowers plasma urate in healthy women.
J Nutr. 2003.
We measured plasma urate, antioxidant and inflammatory markers in 10 healthy women who consumed Bing sweet cherries. The women, age 22-40 y, consumed two servings (280 g) of cherries after an overnight fast. The decrease in plasma urate after cherry consumption supports the reputed anti-gout efficacy of cherries. The trend toward decreased inflammatory indices (CRP and NO) adds to the in vitro evidence that compounds in cherries may inhibit inflammatory pathways.
Comments: Perhaps the use of cherry extract may be a better option in order to avoid the fructose in the fruit.
Inhibition of xanthine oxidase by flavonoids.
Biosci Biotechnol Biochem. 1999.
Various dietary flavonoids were evaluated in vitro for their inhibitory effect on xanthine oxidase, which has been implicated in oxidative injury to tissue by ischemia-reperfusion. Xanthine oxidase activity was determined by directly measuring uric acid formation by HPLC. The structure-activity relationship revealed that the planar flavones and flavonols with a 7-hydroxyl group such as chrysin, luteolin, kaempferol, quercetin, myricetin, and isorhamnetin inhibited xanthine oxidase activity at low concentrations in a mixed-type mode, while the nonplanar flavonoids, isoflavones and anthocyanidins were less inhibitory. These results suggest that certain flavonoids might suppress in vivo the formation of active oxygen species and urate by xanthine oxidase.
Gout and xanthine oxidase inhibition
Propolis has xanthine oxidase inhibitory activity.
There are many causes, including genetics, obesity with excessive weight around the abdomen, hypertension also known as high blood pressure, diabetes or high blood sugar, leukemia, psoriasis which is a skin condition, and chronic renal disease. A rare condition known as Lesch-Nyhan syndrome can also increase the risk.
Drugs that can cause gout include diuretics such as thiazides, so can high dose aspirinuse, L Dopa, and cyclosporine. You may be surprised to learn that perhaps excess ingestion of a certain vitamin, nicotinic acid, has been associated with a higher incidence.
Most people who have gout are middle-aged men, but this joint inflammation can occur at any age. Only 5 to 10% of cases occur in women, most often after menopause.
Being obese, gaining weight since young adulthood, high blood pressure and taking a diuretic "water pill' are all linked to an increased likelihood of developing gout, but losing weight decreases the risk. Dr. Hyon K. Choi, at Massachusetts General Hospital in Boston, and his colleagues evaluated risk factors and the occurrence of gout among 47,150 men in the Health Professionals Follow-up Study. They were interviewed first in 1986, at ages ranging from 40 to 75 years. By 1998, there were 730 newly diagnosed cases of gout. After adjusting for starting weight and other risk factors, men who lost 10 pounds or more since 1986 had a lower risk of gout compared with those who had maintained their weight. Compared with subjects with a low-normal weight, the risk of gout increased in step with increasing weight. In subjects considered obese, the risk of gout was 4.41 times higher. The researchers estimated that the risk of developing gout was 2.31 among men with high blood pressure compared to those with normal blood pressure, and 1.77 higher among those taking a diuretic. Archives of Internal Medicine, 2005.
Cause in women
High uric acid levels, obesity, hypertension, alcohol use and diuretics all increase the risk of gout. Arthritis Rheumatism 2010.
Reducing risk for gout - the role
of food by Ray Sahelian, M.D.
Try a low-purine diet, for instance avoiding or minimizing shellfish.
Reduce alcohol intake, particularly beer - Drinking alcohol, even a small amount, may trigger recurrent painful bouts of gout. The gout-triggering effect of alcohol "occurs within a short period of time, perhaps less than 24 hours
Reduce body weight, eliminate junk foods such as simple carbohydrates and fructose. Although not a gout cure, eating healthy reduces the risk for developing gout.
Consume plenty of fresh fruits and vegetables.
Drink plenty of fluids, especially water.
Eliminate intake of sugar-sweetened soft drinks. Drinking sodas with sugar or consuming lots of high fructose corn syrup is strongly tied to an elevated risk of gout. Fructose rich fruits and fruit juices may also increase the risk for gout. Diet soft drinks are not associated with the risk of gout.
A 12-year study has largely confirmed the conventional wisdom about the dietary causes of gout. Diets high in purine-rich beef, pork, lamb, and seafood were found to increase the risk of gout. Diets high in dairy foods that are rich with casein and lactalbumin, which reduce serum uric acid levels, were found to decrease the risk of gout. Surprisingly, intake of purine rich vegetables did not affect gout risk.
This joint inflammation usually develops after a number of years of buildup of uric acid crystals in the joints and surrounding tissues. Symptoms include: warmth, pain, swelling, and extreme tenderness in a joint, usually a big toe joint. Pain that starts during the night and is so intense that even light pressure from a sheet is intolerable. Rapid increase in discomfort, lasting for some hours of the night and then easing during the next 2 to 7 days. In addition to the arthritis, gout causes the formation of tophi. Tophi are lumpy deposits of uric acid crystals just under the skin. Common places for tophi to develop are in the outer edge of the ear, on or near the elbow, over the fingers and toes, and around the Achilles tendon in the ankle. Gout can also cause kidney stones made of uric acid.
Acute gout attacks occur more often during the night and early morning than during the day.
Gout's is associated with a host of vascular events including coronary artery disease, peripheral vascular disease, and cerebrovascular events.
with medication, drugs
While some medications are used to treat the hot, swollen joint, other medications are used to prevent further attacks of gout. Medicines used to treat acute gout and/or prevent further attacks include: Nonsteroidal anti-inflammatory drugs (NSAIDs) such as indomethacin (Indocin), ibuprofen (Advil), and naproxen (Aleve). High doses are needed to control the inflammation but can be tapered off within a week or two. The primary complications of these medications include upset stomach, bleeding ulcers, and decreased kidney function.
Colchicine is given in two different ways: To treat the hot, swollen joint, colchicine is given rapidly (up to once an hour until symptoms improve, side effects develop, or a maximum of 8 doses is reached). While this approach is often effective, most people develop nausea, vomiting, or diarrhea. There is little need to use colchicine in this way any longer. To help prevent an attack from coming back, colchicine can be given once or twice a day. At this frequency, diarrhea is much less likely to occur. While the chronic use of colchicine can reduce the attacks of gout, it does not prevent the accumulation of uric acid that can lead to joint damage even without attacks of hot, swollen joints. Hence, a gout diet is crucial to minimize gout recurrence or severity.
After a 5-year monopoly on the sale of colchicine put the gout medication out of reach for many patients, a federal judge in January 2015 denied an injunction request by Takeda Pharmaceuticals U.S.A. to halt the distribution of colchicine products by Hikma Pharmaceuticals PLC. Thus, the price of colchicine will drop back down to a more reasonable cost.
There is probably no important difference
between benzbromarone and allopurinol at achieving serum urate normalisation,
but that benzbromarone is probably more successful than probenecid at achieving
serum urate normalisation in people with gout. Cochrane Database Syst Rev. 2014
Nov 14. Uricosuric medications for chronic gout.
Drugs are used to help the kidneys excrete more uric acid. These are called uricosuric drugs. These drugs include allopurinol, probenecid, and sulfinpyrazone. Allopurinol blocks the conversion of hypoxanthine to xanthine to uric acid. Allopurinol is appropriate for gout patients who are overproducers of uric acid. Allopurinol is taken once daily. Rare and life-threatening hypersensitivity reactions are possible with allopurinol use. Other agents include uricase enzymes that catabolize uric acid to a more soluble form which is readily excreted by the kidneys. One such drug is Rasburicase which became available in 2002, however serious side effects such as anaphylaxis, hemolysis, and methemoglobinemia can occur.
Treating acute gout attacks alone is not sufficient to prevent the disease from progressing. When treating gout one needs to treat acute attacks, and lower excess stores of uric acid to achieve dissolution of monosodium urate crystals through a long-term reduction of SU concentrations far beyond the threshold for saturation of urate and provide prophylaxis to prevent acute flares. The options available for the treatment of acute gout are NSAIDs, colchicine, corticosteroids, adrenocorticotropic hormone (ACTH) and intra-articular corticosteroids. The most important determinant of therapeutic success is not which anti-inflammatory agent is chosen, but rather how soon therapy is initiated and that the dose be appropriate. Prophylaxis should be considered an adjunct, rather than an alternative, to long-term urate-lowering therapy. The optimal agent, dose and duration for gout prophylaxis are unknown and require further investigation. The importance of long-term management of gout is the reduction and maintenance of SU in a goal range, usually defined as less than 6.0 mg/dL. Allopurinol and benzbromarone remain the cornerstone drugs for reducing SU levels lower than the saturation threshold to dissolve urate deposits effectively. Febuxostat and pegloticase help to optimize control of SU levels, especially in those patients with the most severe gout. Other agents, such as fenofibrate and losartan may be helpful as adjuvant drugs. Treatment for gout has advanced little in the last 40 years, until recently.
Asymptomatic hyperuricemia, acute flares, intercritical segments, and advanced gout are the stages that patient may go through. For quite a number of years, high uric acid levels deposit uric acid in tissues and during this time there are no gout symptoms. Then, an acute gout attack occurs, followed by periods of remission and more acute gout attacks, eventually leading to advanced gout. High uric acid levels in the bloodstream is called hyperuricemia. Hyperuricemia is a serum urate concentration above 6.8 mg per deciliter.
In middle-aged men, high blood levels of uric acid are a strong predictor of death, from both cardiovascular disease and all causes. Uric acid is a product of the breakdown of nitrogen compounds, and is normally excreted in urine. It has been recognized for decades that uric acid is found at high levels in the joints of people with gout. More recently, it has been suggested that uric acid may be a "danger signal" released by damaged cells that triggers inflammation and a strong immune response. A research team followed 1423 middle-aged Finnish men, initially free of heart disease, cancer and diabetes, for about 12 years. During that period, 157 men died -- 55 from cardiovascular causes. Analyzing the data, the researchers found that men with uric acid in the upper third level had a more than 2.5-fold increased risk of death from cardiovascular disease, and a 1.7-fold higher risk of death from any cause, than men with uric acid levels in the lower third.
There is substantial difference between alcoholic drinks in their effect on blood levels of uric acid -- and this could affect the likelihood of developing gout -- Harvard investigators have found. Beer confers a larger increase than liquor, whereas moderate wine drinking does not increase serum uric acid levels." Because of this, and because gout is caused by the deposition of uric acid crystals in joints, different drinks may result in "variation in the risk of incident gout," Drs. Hyon K. Choi and Gary Curhan, from Harvard School of Public Health, Boston, conclude. The researchers examined the association between consumption of beer, liquor, and wine in relation to blood levels of uric acid in a nationally representative sample of subjects -- that is, 14,809 participants at least 20 years of age enrolled in the Third National Health and Nutrition Examination Survey. Uric acid levels were greatest for high beer consumers, followed by those with the highest intake of liquor, the team reports. No association was found between wine intake and uric acid levels. This pattern held true for men and women, and for all categories of body weight. "No association was found with wine intake in any of the subgroups," the investigators report. SOURCE: Arthritis and Rheumatism, 2004.
Molecular modeling of flavonoids that inhibits xanthine
Biochem Biophys Res Commun. 2002.
The inhibition of xanthine oxidase activity by various flavonoids was assessed. All of the tested flavonoids were competitive inhibitors, and from the kinetic analysis suggested that flavonoids bind to the reactive site. To further understand the stereochemistry between these flavonoids and xanthine oxidase, structure-based molecular modeling was performed. Apigenin was the most potent inhibitor which showed the most favorable interaction in the reactive site. The bicyclic benzopyranone ring of apigenin stacked with phenyl of Phe 914, and the phenolic group stretched to the space surrounding with several hydrophobic residues. Quercetin and myricetin composed a 3-hydroxyl group on benzopyranone which resulting in reduction of binding affinity. The phenolic group of genistein positioned in opposite orientation comparison with apigenin, and resulted in a weaker interaction with xanthine oxidase. Isovitexin showed the weakest inhibitory effect among the compounds tested. The bulky group of sugar in isovitexin may hamper its interaction with xanthine oxidase.
Inhibition of xanthine oxidase by some Chinese
medicinal plants used to treat gout.
J Ethnopharmacol. 2000.
The enzyme xanthine oxidase catalyses the oxidation of hypoxanthine to xanthine and then to uric acid, which plays a crucial role in gout. A total of 122 traditional Chinese medicinal plants have been evaluated for the enzyme inhibitory activity. The most active was the methanol extract of the twig of Cinnamomum cassia, which was followed immediately by those of the flower of Chrysanthemum indicum and the leaves of Lycopus europaeus. Among the water extracts, the strongest inhibition of the enzyme was observed with that of the rhizome of Polygonum cuspidatum. The study demonstrated that the effects for these medicinal plants used for the gout treatment were based, at least in part, on the xanthine oxidase inhibitory action.
Having read somewhere that cat's claw is helpful in cases of food sensitivity, and having a husband with regular bad bouts of gout I suggested he try it, since everyone always mentions various foods as being the cause of gout. He takes one capsule per day and hasn't had a trace of gout for two years.
I read your recent article on n acetyl cysteine. I wanted to share my experience. I've had recurrent gout attacks for 15 years and it was getting progressively worse. I took several doctor prescribed drugs to prevent, but frankly some of the drug side effects were very bad for me. Then I was advised to take 600 mg NAC per day by a nearby health foods owner and haven't had a problems for over a year.