Modern Medicine's Approach to Gout
The goal of modern medical treatment is to stop the pain and inflammation associated with initial attacks of gout and pseudogout, and to prevent future attacks. This is approached in several different ways, including joint aspiration, in which fluid is withdrawn from the affected joint with a needle and syringe to relieve the swelling and to analyze the fluid found in the joint. Modern medical doctors may also use x-ray technology as a diagnostic tool to locate the crystals associated with pseudogout. However, this tool does not always properly diagnose the pain source. Another problem with this approach is that it does nothing to strengthen the weakened ligaments caused by the inflammation and degeneration associated with these two conditions and, thus, does not alleviate the chronic pain that afflicted individual’s experience.
Another
standard practice of modern medicine is the use of medications. For
example, colchicine is used to reduce the pain, swelling and
inflammation associated with acute gout and pseudogout attacks. It works
by decreasing the inflammation caused by uric acid crystals within the
joint. However, it does not decrease the uric acid levels in the
bloodstream. Steroids and anti-inflammatory medications are also used.
However, in the long run, these treatments do more damage than good.
Although cortisone shots and anti-inflammatory drugs have been shown to
produce short-term pain benefit, both result in long-term loss of
function and even more chronic pain by actually inhibiting the healing
process of soft tissues and accelerating cartilage degeneration. Plus,
long-term use of these drugs can lead to other sources of chronic pain,
allergies and leaky gut syndrome. Codeine or other analgesics may also
be prescribed for pain relief. In addition, a diet low in purines may
also be prescribed.
The Natural Approach to Gout and Pseudogout
Chronic
pain is most commonly due to tendon weakness, ligament weakness or
cartilage deterioration. The safest and most effective natural medicine
treatment for repairing tendon, ligament and cartilage damage is
Chiropractic. In simple terms, Chiropractic stimulates the body to
repair painful areas.
Diet and supplements to manage uric acid metabolism:
A
swollen big toe and a hobbled gait—finally, excruciating pain sends most patients to fill a prescription for allopurinol, the standard drug
for treating gout. Are there natural remedies one can recommend to ease a patient's suffering in addition to or instead of the pharmaceutical?
While
gout cannot be cured, it can be controlled with medication, herbs, diet
and nutritional supplements. Gout certainly isn't a new condition and,
in fact, usually is associated with the gluttony of the rich in the
1700s and 1800s. Since ancient times people have suffered from the pain
and swelling caused by a precipitation of uric acid crystals (monosodium
urate) in joints, tendons, kidneys and other tissues. Diet was always
blamed—particularly rich foods such as gravies, organ meats and other
proteins—but we now know gout can result from a number of genetic
disorders that cause overproduction or impaired excretion of uric acid.
Gout
affects between three and five adults per thousand in the general
population, but more than 95 percent of cases occur in males older than
30. [ 1 ] This means roughly one in 100 adult men have gout. Some 70
percent of gout patients have an overproduction of uric acid, while
about 30 percent have problems eliminating it from their bodies. The
result of either situation is excess uric acid (sodium urate) that
crystallizes in joints and causes painful inflammation and severe
arthritic symptoms. It is not clear what makes the uric acid precipitate
in the joints, but it is not simply because there is too much present.
Some patients can have chronically elevated uric acid levels with no
other gout symptoms.
Interestingly, the first joint of the big
toe is affected in almost half of all first attacks, and there is a 90
percent chance that gout patients will have an attack in their toe at
some time. Why the toe? Uric acid has a lower saturation point at lower
temperatures, which may explain why deposits tend to form in the cooler
extremities including the toe, or the top of the ear.
Uric acid
is the normal form in which biochemicals called purines are excreted
after they are digested and metabolized. Purines are components of the
nucleic acids DNA and RNA. Randolph Nesse, M.D., of the University of
Michigan Medical School, Ann Arbor, says uric acid is not all bad. In
fact, it has antioxidant activity nearly equivalent to vitamin C,
prompting some researchers to speculate that genes causing high levels
of uric acid were not selected against because the uric acid helps
protect against oxidative damage to cells. [ 2 ]
Dietary Management of Uric Acid:
It
is impossible for anyone to completely eliminate purine metabolism, nor
would anyone want to, because a large percentage of purines are
generated as the body recycles its own tissue proteins. But dietary
recommendations for gout management limit purine intake, and eliminate
nearly all protein, especially meat. The high-purine foods to limit or
avoid are organ meats, which are rich in nucleic acids, as well as
anchovies, baker's and brewer's yeast, herring, mackerel, red meat,
sardines and shellfish. Poultry and white fish—which also contain
purines but have less dense muscle fibers, a different protein
composition and more water per unit weight than red meat and dark
fish—are better choices but should not be eaten in excess either.
Legumes, especially peanuts, should also be limited or avoided because
of their purine content. Nutritional yeast, supplements with DNA, RNA or
organ tissue extracts such as thyroid or thymus can also pose a risk if
taken regularly.
Alcohol consumption exacerbates gout by
reducing uric acid elimination from the body and slightly increasing
uric acid production. Beer and wine are higher in purines than other
alcoholic beverages because of their yeast residues. Heavy drinkers are
more likely to have gout than those who drink less. [ 3 ]
Very
high intakes of fructose—25 to 30 percent of calories—can also elevate
uric acid, so those with gout should minimize fructose intake, namely
high fructose corn syrup, which is present in many processed foods and
beverages. [ 4 ]
A gout-prevention diet should emphasize complex
carbohydrates and plenty of water. Adequate fluid intake dilutes the
urine and promotes excretion of uric acid. The more diluted the urine,
the less risk there is for developing kidney stones, which can be a
problem for gout patients.
Herbal Options:
The
enzyme xanthine oxidase catalyzes the last step in the conversion of
purines to uric acid. Allopurinol, the medication prescribed for gout
prevention, is a xanthine oxidase inhibitor. In vitro, xanthine oxidase
is inhibited by the flavonoids luteolin and apigenin nearly as well as
it is by allopurinol. [ 5 ] The flavonoids chrysin, baicalein,
isorhamnetin, and several caffeic acid esters are also effective. [ 6 ]
Flavonoids, which are water-soluble plant pigments, are part of a large
group of antioxidant phytochemicals. Chamomile (Matricaria recutita),
chiso (Perilla frutescens), many mints (Mentha spp.) and yarrow
(Achillea millefolium) are rich in luteolin, apigenin and caffeic acids.
[ 7 ] Those flavonoids can also be found in carrots. There are no
clinical studies proving these herbs can prevent gout recurrence, but
they are safe and worth a try.
Baikal skullcap (Scutellaria
baicalensis) and Taiwanese skullcap (S. rivularis) contain baicalein as
well as several other anti-inflammatory flavonoids. Both the isolated
flavonoids and herbal extracts from skullcap have shown effectiveness
against paw inflammation in mice and are used traditionally for chronic
inflammatory conditions and liver disorders. [ 8,9 ]I recommend a
combination of the herbs daily as a preventive measure: three capsules
each of standard dose baikal skullcap, chamomile and yarrow.
Incorporating chiso leaf and peppermint tea is also a good idea. Keep in
mind that a customer would need quite high doses of these herbs to make
an impact, but they can be supportive when taken in conjunction with
diet modification.
Other xanthine oxidase inhibitors, albeit weak
ones, are anthocyanidins and proanthocyanidins. [ 7 ] Cherries, grapes,
blueberries and bilberries contain both these antioxidants. Eating
cherries has been shown to lower uric acid levels and prevent gout
attacks. [ 10 ] Gout sufferers should try to incorporate one-half pound
of fresh cherries (weighed with pits) into their daily diet. In addition
to berries, extracts of bilberry (Vaccinium myrtillus), grape seed
(Vitis vinifera) or pine bark (Pinus maritima) are rich sources of
anthocyanidins and proanthocyanidins.
James Duke, Ph.D., botanist
and medicinal plant authority in Fulton, Md., treats his gout with
celery (Apium graveolens) seed extract instead of allopurinol. Though
there is no research to support this medicinal use, Duke says celery has
at least 26 anti-inflammatory compounds. These anti-inflammatory
qualities explain at least part of celery's beneficial effects. The
celery plant has apigenin, but it is not concentrated in the seeds, so
if the seeds do inhibit xanthine oxidase, the mechanism is currently
unknown. Duke takes four capsules of celery seed extract daily—a 450-mg
dose—and has not had an attack since he began the treatment.
Colchicine,
an anti-inflammatory drug originally derived from the autumn crocus,
also called meadow saffron (Colchicum autumnale) bulb, is often
prescribed to alleviate acute gout. Colchicine does not affect uric acid
levels; rather it stops the inflammatory process. A typical dose of
colchicine is 1 mg orally every two hours or up to 7 mg in 24 hours for
acute attacks. Many patients cannot tolerate the therapeutic dose, which
can cause gastrointestinal side effects. Autumn crocus and related lily
bulbs such as daylilies may have colchicine and are sometimes available
in herbal products. These plants have poisonous alkaloids, so advise
customers not to self-medicate with crocus or lily bulbs.
During
acute gout attacks, herbal anti-inflammatories including boswellia
(Boswellia serrata), curcumin (Curcuma longa), devil's claw
(Harpagophytum procumbens) and yucca (Yucca spp.) can be tried instead
of aspirin or arthritis drugs. [ 11 ]The British Pharmacopoeia
recommends guaiacum resin extract (Guaiacum officinale; G. sanctum), an
anti-inflammatory, for gout. Commercial preparations are available in
the United Kingdom. [ 12 ] Boswellia is similar to guaiacum in terms of
the types of phytochemicals present and is more readily available in
North America. [ 13 ] Whichever herb is selected, the dosage should be
at least two 500-mg caspsules of the dried herb three times daily for
two to seven days. While the herbs mentioned here do not work as quickly
as colchicine, they should help within 24 to 48 hours.
Nutrients to Keep Gout at Bay:
Though not as useful as some of the herbal remedies for easing pain, supplements can be an important part of a preventive plan.
Omega-3
fatty acids can be useful in the treatment of gout. Eicosapentaenoic
acid (EPA) inhibits production of the inflammatory leukotrienes, which
are responsible for much of the inflammation and tissue damage that
occurs with gout. [ 14 ]
Folic acid has been shown to inhibit
xanthine oxidase. [ 15 ]While research isn't totally conclusive,
positive results have been reported by gout sufferers. The recommended
daily dose is 10 to 40 mg. Folic acid should only be supplemented under a
health care provider's supervision.
Other anti-inflammatory
supplements, including the amino acids alanine, aspartic acid, glutamic
acid and glycine; the flavonoid quercetin; and vitamin E, can be useful
but do not have research specifically supporting their application for
gout.
High doses of niacin, greater than 50 mg daily, are not
recommended for people with gout because niacin competes with uric acid
for bodily excretion. Vitamin C in doses greater than 3,000 mg is also
contraindicated for gout sufferers because it may increase uric acid in
some people. [ 16 ]
Gout should not be left untreated! Over
time, microscopic crystals of sodium urate can damage organs,
particularly the heart and kidneys. Increased uric acid levels can also
increase the risk of kidney stones. Luckily, modest dietary
modifications and a carefully planned supplements program can obviate
prescriptions and lessen the suffering from gout attacks.
References:
1. Strohecker J. Editor. Alternative medicine: the definitive guide. Puyallup (WA): Future Medicine Publishing; 1994.
2. Nesse RM, Williams GC. Why we get sick—the new science of Darwinian medicine. New York: Random House; 1994.
3. Gibson T, et al. A controlled study of diet in patients with gout. Ann Rheum Dis 1983;42:123-7.
4. Henry RR, et al. Current issues in fructose metabolism. Ann Rev Nutr 1991;11:21-39.
5.
Cos P, et al. Structure-activity relationship and classification of
flavonoids as inhibitors of xanthine oxidase and superoxide scavengers. J
Nat Prod 1998;61:71-6.
6. Nakanishi T, et al. Two new potent
inhibitors of xanthine oxidase from leaves of Perilla frutescens Britton
var. acuta Kudo. Chem Pharm Bull 1990;38:1772-4.
7. Duke JA, et
al. U.S. Department of Agriculture Phytochemical and Ethnobotanical Data
Base (http://www.ars-grin.gov/duke/) 1999.
8. Lin CC, Shieh DE.
In vivo hepatoprotective effect of baicalein, baicalin, and wogonin from
Scutellaria rivularis. Phytother Res 1996;10:651-4.
9. Chung CP,
et al. Pharmacological effects of methanolic extract from the root of
Scutellaria baicalensis and its flavonoids on human gingival
fibroblasts. Planta Med 1995;61:150-3.
10. Blau LW. Cherry diet control for gout and arthritis. Texas Rep Biol Med 1950;8:309-11.
11. Handa SS, et al. Plants with anti-inflammatory activity. Fitoterapia 1992;63:3-12.
12. Evans WC. Trease and Evans' pharmacognosy. London: W.B. Saunders; 1998.
13. Ammon HPT, et al. Mechanism of anti-inflammatory actions of curcumine and boswellic acids. J Ethnopharm 1993;38:113-9.
14.
Terano T, et al. Eicosapentaenoic acid as a modulator of inflammation,
effect on prostaglandin and leukotriene and leukotriene synthesis.
Biochem Pharmacol 1986;35:779-85.
15. Lewis AS, et al. Inhibition of mammalian xanthine oxidase by folate compounds and amethopterin. J Biol Chem 1984;259:12-5.
16. Stein HB, et al. Ascorbic acid-induced uricosuria: a consequence of megavitamin therapy. Ann Int Med 1976;84:385-8
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