|Amino Acid / Protein|| L-Carnitine
| ||L-Acetyl Carnitine (LAC) was effective and well tolerated in improving neurophysiological parameters and in reducing pain over a 1-year period. LAC is, therefore, a promising treatment option in patients with diabetic neuropathy. [Drugs R D. 2002;3(4):223-33]|
Another study conducted in a British Hospital found that LAC can greatly reduce the damage caused to nerves by certain HIV drugs, even promoting nerve regeneration. [AIDS 2004;18: 1549-1560, 2004] The dose in this study was 3 grams per day (1500mg bid).
Evening Primrose Oil / GLA
| ||See Neuropathy and Alpha Lipoic Acid.|
Mistletoe (Viscum album)
| ||Mistletoe has a history of use in the treatment of neuritis, an inflammatory condition of the nerves or nerve sheath resulting in shooting or other pains throughout the body. It has been used for those with vertigo attacks and "pins and needles" sensations in the limbs.|
| ||An alkaline diet can reverse the effects of an overly acidic diet which may be contributing to nerve irritation and inflammation.|
| ||In severe cases, a short juice fast for four or five days with carrot, beet, citrus fruits, apple and pineapple may be used to hasten the recovery process prior to an alkalinizing diet.|
Conventional Drugs / Information
| ||Atenolol, a beta-blocker, is one of any number of drugs that can have side effects. Fatigue is a common side-effect and paraesthesia, peripheral neuropathy and myopathies have been reported.|
Alpha Lipoic Acid
| ||There was a marked synergy between GLA and alpha lipoic acid which produced compounds that had at least an order of magnitude increase in efficacy over either one alone in correcting motor nerve conduction velocity and endoneural blood flow defects. A 1.3:1 GLA:alpha lipoic acid ratio appears to be optimal against experimental diabetic neuropathy. [Diabetologia (1998), 41: pp.390-399 (rat study)]|
Experimental work confirms that GLA-aLA (equimolar) conjugate is so effective that it completely reverses the effects of the broken neurotrophic mechanisms that correlate with diabetic neuropathy. [Diabetologia 1998 Jul; 41(7): pp.839-843]
Vitamin B Complex
| ||All vitamins of the B group have proven beneficial in the prevention and treatment of neuritis. The disorder has been helped when vitamins B1, B2, B6, B12, and pantothenic acid have been given together.|
Vitamin B1 (Thiamine)
| ||In a study of the efficacy of vitamin B1, it was given to 133 people who had headaches, joint pain, nerve pain, or neuritis. 1-2 grams of B1 once or twice daily caused 78% of headaches to improve, 71% of spine or joint pains to improve, and 62% of patients with neuralgia reported relief. Start with lower amounts and work your way up, making sure to take all of the B vitamins during this trial. [Bibl Nutr Dieta (38):pp.110-1]|
| || Increasingly, it appears that vitamin D plays a role in nerve growth and maintenance and may have important pharmaceutical applications for treatment of neurodegenerative conditions.|
The therapeutic potential of ergocalciferol - the plant-derived form of vitamin D, named vitamin D2 - was assesed in a rat model of peripheral nerve injury and repair. The left peroneal nerve was cut out on a length of 10 mm and immediately autografted in an inverted position. After surgery, animals were treated with ergocalciferol (100 IU/kg/day) and compared to untreated animals. Functional recovery of hindlimb was measured weekly, during 10 weeks post-surgery, using a walking track apparatus and a numerical camcorder. At the end of this period, motor and sensitive responses of the regenerated axons were calculated and histological analysis was performed. We observed that vitamin D2 significantly (i) increased axogenesis and axon diameter; (ii) improved the responses of sensory neurons to metabolites such as KCl and lactic acid; and (iii) induced a fast-to-slow fiber type transition of the Tibialis anterior muscle. In addition, functional recovery was not impaired by vitamin D supplementation. Altogether, these data indicate that vitamin D potentiates axon regeneration. Pharmacological studies with various concentrations of the two forms of vitamin D (ergocalciferol vs. cholecalciferol) are now required before recommending this molecule as a potential supplemental therapeutic approach following nerve injury. [J Neurotrauma. 2008 Oct;25(10):1247-1256]
Previous research has found that vitamin D deficiency is common in patients with Type 2 diabetes, but its effect on neuropathic pain has not previously been tested, say study authors Drs Paul Lee and Roger Chen from Concord Repatriation General Hospital.
Their study, published in today�s Archives of Internal Medicine (168:771-772) involved 51 patients with Type 2 diabetes and typical neuropathic pain. All patients were vitamin D deficient with a mean serum 25D concentration of 18 ng/mL.
After three months, vitamin D repletion with cholecalciferol (vitamin D3) tablets resulted in a significant reduction in pain scores using two separate assessments, one suggesting the pain severity was reduced by 40% the other suggesting pain severity had been halved.
How vitamin D reduces the severity of diabetic neuropathic pain is uncertain, but the researchers suggest that vitamin D insufficiency may potentiate diabetic nerve damage and impair nociceptor function. The results could not be explained by a decrease in parathyroid hormone as testing did not show any statistically significant difference in hormone level following the vitamin D repletion, they say.
Vitamin B12 (Cobalamine)
Vitamin B2 (Riboflavin)
Vitamin B6 (Pyridoxine)
| ||The medical literature contains reports of neuritis or nerve damage caused by using large amounts of vitamin B6 (1000-6000mg per day) for long periods. Lower doses have been helpful in treating neuritis. Some susceptible people may develop neuritis from as little as 300-400mg a day when the other B vitamins are not taken along with the B6. Examine your vitamin and supplement combinations to ensure that you are not taking excessive doses, but getting enough to learn if you are helped by it.|
However, there has been an association with B6 supplementation at lower doses and neuropathic damage and so caution is advised.
Characteristics of pyridoxine overdose neuropathy syndrome.
A neurotoxic syndrome due to pyridoxine (B6) overdose is described. It is the largest series of B6 intoxication hitherto reported. A raised serum B6 level was present in 172 women of whom 60% had neurological symptoms, which disappeared when B6 was withdrawn and reappeared in 4 cases when B6 was restarted. The mean dose of B6 in the 103 women with neurological symptoms was 117 +/- 92 mgs, compared with 116.2 +/- 66 mgs in the control group. There was a significant difference (P less than 0.01) in the average duration of ingestion of B6 in the neurotoxic group of 2.9 +/- 1.9 years compared with 1.6 +/- 2.1 years in controls. The symptoms were paraesthesia, hyperaesthesia, bone pains, muscle weakness, numbness and fasciculation, most marked on the extremities and predominantly bilateral unless there was a history of previous trauma to the limb. These women were taking a lower dose of B6 than previously described (1,2), which may account for the complete recovery within 6 months of stopping B6. [Acta Neurol Scand. 1987 Jul;76(1): pp.8-11]