Peripheral Neuropathy – Nutritional Support
By Ward Dean M.D.
Peripheral neuropathy is a condition that has many causes. The symptoms are numbness, irritation and pain, usually in the extremities. Its most likely causes are diabetes (most common), nutritional deficiencies, excess alcohol intake, cancer, heavy metal accumulation (lead, mercury), or even a reaction to various medications. One key to treatment, therefore, is to try to find the cause.
However when a cause cannot be readily determined, I recommend a shotgun approach, using a variety of supplements which have been demonstrated to be effective in treating this bothersome and often disabling condition.
First, one of the most common causes of peripheral neuropathy is a thiamin deficiency – or an abnormal requirement for thiamin. For example, a child in Japan suffered from relapsing cases of severe neuropathy, debilitating muscle weakness, and difficulty maintaining his balance each time he had a febrile illness. Finally, the childs physicians began using high doses of thiamin every time he became sick. Using doses of 500 mg of thiamin per day, neuropathy symptoms would resolve within two weeks (as opposed to two months, without thiamin). In addition, the frequency of illness was reduced from 2 to 4 episodes per year when thiamin was not used, compared to no more than one seasonal illness per year with thiamin. Thiamin was effective in preventing further episodic neurologic attacks at 500 mg per day in this patient. Thiamin, in doses of 20 to 2400 mg/day, has been given to patients with various metabolic diseases, without adverse effects. (Kinoshita 1997).
In one double-blind study of 24 diabetic patients who suffered from peripheral neuropathy, a high-dose B-Complex regimen was used. The dosages were: Thiamin, 320 mg/d for the first 2 weeks, and 120 mg/d thereafter; Vitamin B6, 720 mg/d for the first 2 weeks, and 270 mg/d thereafter; and Vitamin B12, 2,000 mcg/day for the first 2 weeks and then 750 mcg/day thereafter. The treatment resulted in significant improvement in nerve conduction velocity in the peroneal nerve and an improvement of the vibration perception threshold. (Stracke, 1996).
Many physicians and supplement users are concerned by the reports of peripheral neuropathy with high doses of vitamin B6. Dr. Bernard Rimland, whom I consider one of the worlds foremost experts on clinical use of B6, claims there has never been a serious illness or death associated with ingestion of large amounts of B6. He points out that eighteen studies have been published since 1965 on the role of high dose B6 in autism which show that benefits occur in about half of all autistic children and adults, with no reported toxicity whatsoever.
Abnormal substances in the urine of autistic children are often eliminated by vitamin B6, and brain waves tend to normalize with B6. Magnesium and other B vitamins may help prevent reversible toxicity of vitamin B6 even when taken at doses of 2,000 to 6,000 mg per day.
Dr. Rimland has followed thousands of autistic children and adults on megadoses of vitamin B6 over 30 years, and has only encountered four cases of peripheral neuropathy. In those four patients, the symptoms went away very quickly and completely when the dosage was reduced. Resumption of therapy was reinitiated without problems.
Dr. Rimland notes his own son, who is now 40, has been taking one gram of vitamin B6 along with 400 mg of magnesium and other nutrients for almost 30 years.
In addition to its benefits in autism and peripheral neuropathy, Vitamin B6 when taken in dosages of 100-300 mg/day for several years has resulted in a 27% reduction in the risk of heart disease in the elderly. (Rimland, 1996).
Biotin is another B vitamin that helps with neuropathy. In one study, three patients with severe diabetic peripheral neuropathy were given high doses of biotin (10 mgs intramuscularly [IM]) daily for six weeks; then 10 mgs IM three times per week for six weeks, and then 5 mg/d orally. These biotin dosages were 50-100 times higher than the recommended daily allowances.
Within four to eight weeks after the biotin administration there was objective improvement in the symptoms of peripheral neuropathy, specifically painful muscle cramps, paresthesias, ability to stand, walk and climb stairs, and disappearance of restless leg syndrome in all patients. After one year of treatment with biotin all patients were free of paresthesias and could walk more than 300 meters without help.
It may be that diabetics have an abnormality in the biotin dependent enzyme pyruvate carboxylase, thereby causing accumulation of pyruvate and/or depletion of aspartate, both of which play important roles in nervous system function. The authors concluded that Biotin supplementation should be recommended for every diabetic patient for the prevention and management of peripheral neuropathy (Koutsikos, D., 1990).
In another case, an elderly man with mild diabetes had peripheral neuropathy, and could not open his right eyelid. After six weeks on vitamin B12, the eyelid and the eye became perfectly normal. (Chicola, 1996).
Folate deficiency (or increased folate requirement) is also an often unrecognized cause of neuropathy. Dosage ranges that have been found effective for folic acid in peripheral neuropathy are: 10 mg, 2 to 3 times daily (Parry, T.E., 1990).
Diabetics may have impaired conversion of linoleic acid to gamma-linolenic acid (GLA), which may lead to defective nerve function. This is because the metabolites of gamma-linolenic acid are known to be important in nerve membrane structure, nerve blood flow, and nerve conduction. GLA supplementation corrects impaired nerve function in animals.
In three randomized, placebo-controlled human studies of GLA supplementation in patients with diabetic neuropathy, the subjects received a placebo or 480 mg of GLA/day. One study was done in 22 patients for 6 months and showed improvement in diabetic neuropathy in the GLA group, with deterioration in the placebo group. The other two trials lasted 12 months. The first trial involved 111 patients in 7 centers, while the second involved 293 patients in 10 centers. The results in the trials were virtually identical. In the first trial, 25 of 28 parameters improved over baseline in the first year. In the second trial, 23 of 28 parameters improved. In the first trial, 26 of 28 parameters deteriorated from baseline in the placebo group; and in the second trial, 28 of 28 parameters deteriorated. (Heroin, 1997).
Vitamin E deficiency is also known to result in peripheral neuropathy and ataxia. It is usually related to fat mal-absorption or genetic abnormalities in lipoprotein metabolism. Vitamin E may be of benefit in ischemic heart disease, atherosclerosis, diabetes, cataracts, Parkinsons disease, Alzheimers disease and impaired immune function. Therapeutic doses of vitamin E have been used in the above conditions between 100 and 800 IU. per day (Traber and Sies, 1996).
A home exercise program appears to be an important component of the treatment of persons with chronic peripheral neuropathy. The home exercise program should include resistance exercise, stretching, and aerobic conditioning (Ruhland and Shields, 1997).
Three hundred and twenty non-insulin-dependent diabetic patients with symptomatic peripheral neuropathy were evaluated in a three week multicenter trial using infusions of lipoic (thioctic acid) at 3 doses of 1200 mg, 600 mg and 100 mg or a placebo. The total symptom score in the feet decreased from baseline to day 19 with the 1,200 mg dose and the 600 mg dose versus the placebo.
Each of the four symptom scores, which included pain, burning, paresthesia and numbness, were significantly lower in the 600 mg group than in the placebo after 19 days. By day 19, improvement in total symptom scores was noted to be 70.8% in the 1200 mg dose, 82.5% in the 600 mg dose, 65.2% in the 100 mg dose and 57.6% in the placebo group. The reduction in pain with 1200 mg and 600 mg of lipoic acid were significant when compared to placebo after 19 days. The 600 mg dose of lipoic acid over three weeks was superior to placebo in reducing symptoms of diabetic neuropathy without significant side effects.
The authors conclude that intravenous alpha-lipoic acid at 600 mg/day over 3 weeks is safe and effective in reducing symptoms of diabetic neuropathy, and oral treatment with 800 mg/day for four months may improve cardiac autonomic dysfunction in non-insulin-dependent diabetes mellitus (Ziegler, 1995; Ziegler and Griess, 1997).
It is interesting to note that it took three weeks to see significant improvement using the intravenous route, so if people are going to take alpha-lipoic acid orally it may take several months for improvement to occur.
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4. Kinoshita, H., and Nonaka, I. Recurrent Muscle Weakness and Ataxia in Thiamine-Responsive Pyruvate dehydrogenase Complex Deficiency J Child Neurology, February 1997, 12(2) 141-144.
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13. Ziegler, Dan and Gries, F. Arnold. Alphalipoic acid in the Treatment of Diabetic Peripheral and Cardiac Autonomic Neuropathy. Diabetes, September, 1997, 46 (Suppl. 2):S62-S66.
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