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. Gout 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.
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natural treatment of gout, and their practical interpretation by Ray Sahelian, M.D.
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 for gout
It appears that diet has a lot to do with gout. I would recommend
increasing the intake of vegetables, particularly those with apigenin and other
flavonoids. Apigenin is
one of the Flavonoids,
and is 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.
The supplement propolis
has been found to inhibit xanthine oxidase.
Diets high in purine-rich
beef, pork, lamb, organ meats, and seafood 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 gout. Wine does not appear to cause gout. Perhaps a high fructose
diet is also a factor in gout.
Vitamin C supplementation decreases
uric acid levels.
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
Cause of
gout
There are many causes for gout, including genetics.
Obesity,
hypertension,
diabetes,
leukemia,
psoriasis, and chronic
renal disease are known causes of gout. A rare condition known as Lesch-Nyhan
syndrome can also increase the risk for gout.
Drugs can cause gout. Diuretics such as thiazides are
common causes, so are high dose aspirin,
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 of
gout.
Most people who have gout are
middle-aged men, but gout can occur at any age. Only 5 to 10% of cases of
gout occur in women, most often after menopause.
Reducing Risk for Gout - the role
of food and gout
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.
Gout Tophi
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.
Gout Symptom
Gout usually develops after a number of years of buildup of uric
acid crystals in the joints and surrounding tissues. Symptoms of gout
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.
Gout Treatment
- Gout medication
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.
Treatment of 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.
Gout and Xanthine
Oxidase inhibition
Propolis has xanthine oxidase
inhibitory activity.
Stages of Gout
Asymptomatic hyperuricemia, acute flares, intercritical segments,
and advanced gout. 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 Blood
Uric Acid
High uric acid levels in the bloodstream is called hyperuricemia.
Hyperuricemia is a serum urate concentration above 6.8 mg per deciliter.
Gout Research Update
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.
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 39 percent 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. SOURCE: Archives of Internal Medicine, April 11, 2005.
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.
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, December 15, 2004.
Molecular modeling of flavonoids that inhibits xanthine
oxidase.
Biochem Biophys Res Commun. 2002 May 31;294(1):167-72.
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 flavonoids.
Biosci Biotechnol Biochem. 1999 Oct;63(10):1787-90.
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 (IC50
values from 0.40 to 5.02 microM) 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.
Inhibition of xanthine oxidase by some Chinese
medicinal plants used to treat gout.
J Ethnopharmacol. 2000 Nov;73(1-2):199-207.
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, selected according to the clinical
efficacy and prescription frequency for the treatment of gout and other
hyperuricemia-related disorders, have been evaluated for the enzyme inhibitory
activity. The most active was the methanol extract of the twig of Cinnamomum
cassia (Lauraceae) (IC(50), 18 microg/ml), which was followed immediately by
those of the flower of
Chrysanthemum
indicum (Asteraceae) (IC(50), 22 microg/ml) and the leaves of Lycopus
europaeus (Lamiatae) (IC(50), 26 microg/ml). Among the water extracts, the
strongest inhibition of the enzyme was observed with that of the rhizome of
Polygonum cuspidatum (Polygonaceae) (IC(50), 38 microg/ml). The IC(50) value of
allopurinol used as a positive control was 1.06 microg/ml. 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.
Gout is the result of either increased synthesis of uric acid; reduced
ability to excrete uric acid; or both over production and under excretion of
uric acid.
Gout emails
Q. "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."
In regards to these comments on your web site I have
just been told after a re-check of blood that I need to increase the dosage from
200m to 300m as my uric acid level is still 6.9 after 3 months on pills. Was
told to check back in another year? This sound like good advice?
A. We can't give specific advice as to whether to
increase your medicines, that is for your doctor to decide, however, the
research should be interpreted cautiously. It is possible that the overall
dietary or other factors causing the high uric acid may be associated with the
complications.
Q. 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.