Hyperuricemia (high blood uric acid) a health issue apart from gout. Gout is the best known result of high uric acid blood levels in humans, causing painful, swollen joints. Gout symptoms come from deposits of uric acid crystals in joints of colder parts of the body. Hyperuricemia is from excess uric acid production or insufficient urinary loss of uric acid.
In this article, we discuss the metabolic syndrome, urinary stones, arterial pulmonary hypertension, and lead toxicity, all of which show elevated uric acid levels. Natural treatments are sought because of the side effects from the medications used. Phyllanthus niguri (Stonebreaker) is discussed for lowering uric acid, as is the Asian herb, kudzu, and others. Lead toxicity can cause high uric acid levels and can be treated with homeopathy and herbs. Diet suggestions are made for hyperuricemia.
The metabolic syndrome, with high uric acid, is a combination of high triglycerides, abdominal obesity, insulin resistance, low HDL and hypertension. These are risk factors for cardiovascular disease. The diagnosis of metabolic syndrome triples a person’s cardiovascular risk and is seen in 27% of the U.S. population. Lowering the uric acid levels reduces the severity of the symptoms.
Patients with gout must reduce their uric acid levels to relieve their symptoms. Hyperuricemia patients should not use fructose. There is a marked recent increase in fructose intake in the United States. Fructose is eaten as table sugar and high fructose corn syrup (HFCS.) Table sugar is 50% fructose and corn syrup is 55% fructose. Soft drinks and fruit juices commonly contain fructose.
Fructose increases blood uric acid levels. (Glucose does not.) High blood uric acid reduces the availability of nitric oxide (NO) in the body needed for normal circulation. Insulin requires NO for glucose absorption. It is demonstrated that fructose is a likely cause of the metabolic syndrome by causing hyperuricemia. Lowering uric acid by eliminating fructose or with xanthine oxidase (XOD) enzyme inhibitors reduces the severity of the metabolic syndrome.
There is a relationship between gout and cancer risk. Uric acid, as an antioxidant, should be protective of cancer, but, it is not. The slight increase of cancer in people with high uric acid levels from gout is interpreted as showing that the uric acid was associated with, but, not causative of cancer. Cancer causes hyperuricemia because of rapid cell growth and increased purine production. Increased purine levels raise uric acid levels.
Hyperuricemia contributes to urinary stone formation. Dr. Pak created a list of risks for stone formation, including hypercalciuria, hypocitraturia, hyperuricosuria, low urine pH, high urine pH and cystinuria. He studied the links between gouty urinary stones, obesity and insulin resistance.
Idiopathic pulmonary arterial hypertension (IPAH) is a serious disease of the lungs with increased uric acid levels. High uric acid levels in IPAH are the result of increased xanthine oxidase (XOD) enzyme activity. The results were that XOD activity was found to be increased in patients with IPAH.
Lead in the body can elevate uric acid. Gout patients should be tested for lead. Lead toxicity reduces the kidney’s ability to remove uric acid from the body. The elevated uric acid can appear as gout when it is, actually, a sign of lead toxicity. Lead stores in the body for many years. (We had lead in our gasoline that we breathed for many years.) Lead workers have an increased incidence of “gout.”
Plumbum metallicum homeopathic can remove lead from the body. Chelation therapy removes the lead from the body faster. Lead chelation is a good alternative treatment for hyperuricemia and gout.
Treatment of hyperuricemia means increasing the urinary release of uric acid or inhibition of XOD enzyme to reduce the production of uric acid. Allopurinal is a medication which reduces uric acid, but, has some serious side effects.
Lifestyle changes needed for treatment of hyperuricemia include weight loss, reduced use of alcohol and reduced consumption of purines. Low purine diets are suggested for people with hyperuricemia. Low purine foods include asparagus, cauliflower, mushrooms, peas, spinach, whole grain breads and cereals, poultry like chicken, duck and turkey, kidney beans and lima beans.
High purines are found in the following: beef, pork, bacon, lamb, liver, kidney, sweetbreads, meat extracts, game meats, anchovies, sardines, herring, mackerel, scallops, alcoholic beverages and high yeast foods like beer and bread.
Flavonoids are XOD inhibitors. Flavonoids were studied for their uric acid lowering actions in mice. Quercitin, morin, kaempferol, apigenin and puerarin were all found to lower uric acid levels of the blood, even at the low 50 mg/kg dose, with fewer side effects than Allopurinol. Flavonoids, figs, black tea, astragulus, cocoa polyphenols and white mulberry twigs have been shown to have XOD inhibitor activity, reducing uric acid to prevent gout.
Kudzu (Pueraria montana or lobata) contains the flavonoid, puerarin, which blocks XOD enzyme and reduces uric acid in gout. It is an Asian herb. It is a traditional medicine for alcohol abuse. Kudzu has many health benefits. It is our best source of puerarin.
Morin is a flavonoid from Morus alba (White mulberry) tree and figs. Morin lowers uric acid levels at micromolar concentrations. Morin is an antioxidant. Morin was demonstrated to have both XOD inhibitor and uric reabsorption inhibitor effects and is of benefit in hyperuricemia.
Phyllanthus niruri herbal extract has been shown to be of benefit, without side effects, causing urinary stones to become smaller and softer, especially calcium oxylate stones. Phyllanthus niruri is a plant from South America. Phyllanthus niruri extract and the lignans in it can be used to treat hyperuricemia in animals. It increases uric acid excretion and inhibits the XOD enzyme.
Phyllanthus niruri is “quebra pedra” or “stone breaker.” It has been previously shown to cause smooth muscle relaxation for easier passing of kidney stones. It has a pain relieving effect. Phyllanthus has been shown to reduce calcium levels in patients who are stone formers and has been found to reduce the uric acid in people with elevated uric acid levels.
Uric acid reduces the production of blood vessel relaxing nitric oxide (NO) in cultured cells. Hypertension and vascular disease caused by hyperuricemia can be reversed by supplementing with arginine, a building block for NO. The authors say that uric acid damages blood vessels by inhibition of NO production and arginine corrects NO deficiency to improve circulation.
Niacin increases blood uric acid levels and should be used with caution in gout. Niacin supplementation is a lifestyle change that can improve the triglyceride blood levels and increase HDL cholesterol. Side effects of niacin include flushing, impaired glucose tolerance and increased uric acid levels due to prostaglandin release.
Alkaline citrate therapy can treat kidney stones. Potassium citrate 30-60 meq./day is given to increase urinary alkalinization to a pH of 6.0 to 6.5 to dissolve uric acid. It works for both uric acid and calcium stones. Citrate juice levels are highest in grapefruit juice, and, then, in lemon and orange juices, next.
ASK YOUR DOCTOR FOR:
Urine citrate 24 hour citrate analysis.
Urinary pH test. (You can buy pH paper.)
Uric acid blood level.
Hair analysis for lead.
A prescription for a higher dose of potassium citrate.
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