Gout, a common form of joint disorder, is one of the most controllable metabolic disorders. Gout occurs when uric acid such as monosodium urate accumulates in the blood. This accumulation is due to the inability of kidneys to process this normal waste product. The dysfunction may be due to excess uric acid in the blood, a disorder of purine metabolism or decreased kidney efficiency.
In either case, uric acid crystals form and then accumulate in body areas where blood flow is too slow or sluggish to remove the crystals. The knuckles, elbows, knees, and toes are common places of accumulation. If found between the joints, the surrounding tissue becomes inflamed. Nerve endings then become irritated and this causes extreme pain.
There may only be one attack, or several. If the crystals lodge in the kidneys themselves, they can cause partial or complete kidney damage. Furthermore, gout can be a symptom of a more serious underlying disorder.
Males contract the disorder after puberty, females after menopause. It is at these times uric acid levels increase.
If not treated, gout may cause joint deformity. Death may occur from kidney disease, hypertension, atherosclerosis, or stroke.
Treatments include a change in dietary habits, a decrease in ethanol consumption, and the use of diuretics and antibiotics. Aspirin should not be taken since, like ethanol, it inhibits uric acid excretion.
Gout is primarily due to more serum uric acid than the kidney can process, such that elevated levels cause crystals to form.
Lead poisoning, diuretic therapy, especially mercurial diuretics, medications including penicillin and insulin, temporary over-indulgence in food, temporary over-indulgence in ethanol, surgical procedures, fatigue, arthritis, alcoholism, obesity, infection, myxedema, psoriasis, hypertension, emotional disturbances, hypo- or hyperparathyroidism; proliferative hemopoietic diseases such as: leukemia, polycythemia, chronic hemolytic anemia, pernicious anemia; myocardial infarction, advanced primary renal disease; and hereditary diseases such as: Down Syndrome, glycogen storage diseases.
Signs & Symptoms
Severe throbbing, crushing, or excruciating pain, usually in the elbows, hands, knees or feet; pain usually appears without warning and even may appear while sleeping
Red, purple, shiny, and/or dry skin
Symptoms of kidney stones
Structure & Function:
Joint Support &
Adult Folic acid 1,000 - 10,000 mcg Quercetin* Vitamin C 4,000 - 6,000 mg Vitamin E 400 - 800 mg
* Please refer to the respective topic for specific nutrient amounts.
Note: All amounts are in addition to those supplements having a Recommended Dietary Allowance (RDA). Due to individual needs, one must always be aware of a possible undetermined effect when taking nutritional supplements. If any disturbances from the use of a particular supplement should occur, stop its use immediately and seek the care of a qualified health care professional.
Most cases of gout are managed by drugs alone. However, an individual may be advised to follow a Low Purine Diet (see below) to eliminate any needless increase in uric acid levels, and to increase the efficacy of antigout medication. Uric acid is the end product of purine metabolism. The increased uric acid levels found in gout are caused by increased ingestion of purines, or the kidney's inability to excrete the metabolic waste product. Sodium urates then collect in the joints and tissue, creating inflammation and inducing great pain which resemble arthritis.
Low purine diet is designed to restrict the intake of purine-rich foods, thereby decreasing uric acid levels and joint inflammation.
Foods to be restricted in a Low Purine Diet:
Meat Soybean Fish Asparagus Poultry, especially goose Anchovies Mackerel Sardines* Mussels Brains Fish roe Veal sweetbread Scallops* Beef liver Dried beans Heart Green peas Kidney* Lentils Mincemeat* Mushrooms Gravy* Spinach Baker's yeast Celery Brewer's yeast*
*Foods extremely high in purines are never to be consumed by individuals with gout.
Care should be taken to include one serving per day in the following category: meat, fish, milk, cheese, eggs or poultry; otherwise the diet will be deficient in iron, niacin and thiamine. The individual is encouraged to drink plenty of fluids to help the kidney flush uric acid from the body. The individual would benefit by incorporating elements of the Alkaline Ash Diet into the Low Purine Diet.
Alkaline ash diet is composed primarily of fruits and vegetables, increases the alkalinity of the urine. Cranberries, plums, prunes and corn are excluded from this recommendation because they are acid-forming. Milk and milk products, olives, molasses, chestnuts, almonds and coconut are all considered alkaline-forming foods.
The serum levels of vitamin B-12, fat, carotene, sodium, potassium, lactose, nitrogen and cholesterol should be monitored periodically. Supplements should be prescribed if deficiencies arise. In general, antigout drugs decrease the absorption of fat-soluble vitamins; therefore, supplements should be prescribed for the user.
1.* Colchicum autumnale - 30X to 15C
2. Cinchona officinalis tinct. - 30C or 30X long term
Doses cited are to be administered on a 3X daily schedule, unless otherwise indicated. Dose usually continued for 2 weeks. Liquid preparations usually use 8-10 drops per dose. Solid preps are usually 3 pellets per dose. Children use 1/2 dose.
X = 1 to 10 dilution - weak (triturition)
C = 1 to 100 dilution - weak (potency)
M = 1 to 1 million dilution (very strong)
X or C underlined means it is most useful potency
Asterisk (*) = Primary remedy. Means most necessary remedy. There may be more than one remedy - if so, use all of them.
Boericke, D.E., 1988. Homeopathic Materia Medica.
Coulter, C.R., 1986. Portraits of Homeopathic Medicines.
Kent, J.T., 1989. Repertory of the Homeopathic Materia Medica.
Koehler, G., 1989. Handbook of Homeopathy.
Shingale, J.N., 1992. Bedside Prescriber.
Smith, Trevor, 1989. Homeopathic Medicine.
Ullman, Dana, 1991. The One Minute (or so) Healer.
Ferr. Phos. fever and inflammatory symptoms; Nat. Phos. chronic gout, cream-coated tongue, sour-smelling sweat; Nat. Sulf. primary remedy, especially with biliousness, acute attacks;
Cornsilk (Stigmata maydis)
Dandelion Root (Taraxacum officinale)
Licorice Root (Glycyrrhiza glabra)
Note: The misdirected use of an herb can produce severely adverse effects, especially in combination with prescription drugs. This Herbal information is for educational purposes and is not intended as a replacement for medical advice.
The gout patient must make some permanent changes in their diet and lifestyle (i.e. no alcohol, low fat, low calorie, low purine diet etc.).
Detoxification may relieve symptoms and speed the transition.
Diuretic herbs may be taken for the edema due to gout: ranging from the common-place: Cornsilk (Stigmata maydis), Dandelion Root, or Parsley; to more exotic choices e.g. Buchu Leaves or Uva Ursi (Bearberry) Leaves. Buchu is credited with dissolving and flushing the crystal sediment (i.e. uric acid crystals).
Devil's Claw may also be useful in reducing uric acid levels and cholesterol, as well as having anti-inflammatory properties.
Laxative herbs may also be useful: Licorice Root (also anti-inflammatory) or Cascara Sagrada Bark.
Extracts which are rich in flavonoids can lower uric acid levels, thereby removing the threat of a gout attack. (Bilberry and cherry fruits may be available in season, while grape seed and Hawthorn extracts may be more convenient.) [Blau, 1950]
Blau, LW: Cherry diet control for gout and arthritis. Texas. Rep. Biol. Med. 1950, 8:309-311.
Aromatherapy - Essential Oils
Cajeput Essence, Frankincense Essence, Juniper Essence, Pine Essence, Rosemary Essence, Tea Tree Essence, Wintergreen Essence.
Related Health Conditions
Alcoholism Arthritis Coronary heart disease Fatigue Fever Hereditary disorders Hypertension Infection Inflammation Menopause Myocardial infarction Obesity Pain Parathyroid disorders Proliferative hemapoietic disease Psoriasis Renal disorders (Kidney disease) Stroke
Alpers, D.H., R.E. Clouse & W.F. Stenson. 1983. Manual of Nutritional Therapeutics. Little, Brown, and Company, Boston. 457 pp.
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Berkow, R. 1977. The Merck Manual. Merck Sharp and Dohme Research Laboratories Pub., Rahway, New Jersey. 2165 pp.
Berman EL: Clues in the eye: ocular signs of metabolic and nutritional disorders. Geriatrics, 1995 Jul, 50:7, 34-6, 43-4.
Bland, Jeffrey. Medical Applications of Clinical Nutrition. New Canaan, Conn.: Keats, 1983.
Chicago Dietetic Association and the South Suburban Dietetic Association of Cook and Will Counties. 1981. Manual of Clinical Dietetics. W.B. Saunders Co., Philadephia.
Gelber AC et al., Gout and risk for subsequent coronary heart disease. The Meharry-Hopkins Study. Arch Intern Med, 1997 Jul 14, 157:13, 1436-40.
Gregoline PE et al., Gout and hypothyroidism. J Am Podiatr Med Assoc, 1997 Aug, 87:8, 394-6.
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Hunt, S.M., J.L. Groff & J.M. Holbrook. 1980. Nutrition: Principles and Clinical Practice John Wileyand Sons, N.Y. 506 pp.
Iowa Dietetics Association. 1984. Simplified Diet Manual: with Meal Patterns. 5th ed. Iowa State Univ Press; Ames, Iowa. 108 pp.
Jancin, B.: Sports Nutrition: What Works and What Doesn't. Family Practice News, September 15, 1993;5. Migraine Headache and Diet.
Kirschmann, J.D. 1990. Nutrition Almanac: Nutrition Search. McGrew-Hill: New York.
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Pauri, A. Therapy of Gout and Hypercericemia. Clin. Ter., 107 1981.
Pennington, J. 1978. Nutritional Diet Therapy. Bull Publ. Palo Alto, Ca. Petersdorf, R.G. & R.D. Adams. 1983. Harrison's Principles Of Internal Medicine. 10th ed. McGraw Hill Pub Co., New York. 2212 pp.
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Simmonds HA et al., When to investigate for purine and pyrimidine disorders. Introduction and review of clinical and laboratory indications. J Inherit Metab Dis, 1997 Jun, 20:2, 214-26.
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Wang, Y.M. & J. Van Eys. Nutritional Significance of Fructose and Sugar Alcohols. Ann. Rev. Nutrition, 1. 1981.
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