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High doses of methylcobalamin have been used to treat degenerative neurological diseases in rodents and humans. People with amyotrophic lateral sclerosis (Lou Gehrig's disease) took 25 mg a day of methylcobalamin for a month. In this disease, the neurons that control muscle movements deteriorate. The double-blind, controlled study showed that methylcobalamin improved muscle response after a month of treatment. [100]
A study published in the journal Internal Medicine investigated the daily administration of 60 mg of methylcobalamin to patients with chronic progressive MS, a disease that has a poor prognosis and widespread demyeli-nation in the central nervous system. Although motor disability did not improve, there were clini-cal improvements in visual and auditory MS-related disabilities. The scientists stated that methylcobalamin might be an effective adjunct to immunosuppressive treatment for chronic progres-sive MS. This again suggests a potential benefit, but no clinical studies on ALS patients using methylcobalamin have been conducted. [101]
The effects of methylcobalamin were studied on an animal model of muscular dystrophy. This study published in Neuroscience Letters, looked at the degenera-tion of axon motor terminals. In mice receiving methylcobalamin, nerve sprouts were more fre-quently observed and regeneration of motor nerve terminals occurred in sites that had previously been in a degenerating state. [102]
In a study published in the Journal of Neuro-logical Science, sci-entists postulated that methylcobalamin could up-regulate protein synthesis and help regener-ate nerves. The scientists showed that very high doses of methylcobalamin produced nerve regen-eration in laboratory rats. The scientists stated that ultra-high doses of methylcobalamin might be of clinical use for patients with peripheral neu-ropathies. The human equivalent dose to dupli-cate this study would be about 40 mg of sublingually administered methylcobalamin. [103]
In humans, a subacute degeneration of the brain and spinal cord can occur by the demyelina-tion of nerve sheaths caused by a folic acid or vita-min B12 deficiency. In a study published in the Journal of Inherited Metabolic Diseases, it was shown that some people have genetic defects that preclude them from naturally producing methylcobalamin. The scientists stated that a deficiency of methylcobalamin directly caused demyelination disease in people with this inborn defect that prevents the natural synthesis of methylcobalamin. [104]
An early study published in the Russian journal Farmakol Toksikol showed that the daily administration of methylcobalamin in rats markedly activated the regenera-tion of mechanically damaged axons of motor neu-rons. [105]
An even more pronounced effect was observed in laboratory rats whose sciatic nerves were mechanically crushed. Two studies published in the Japanese journal Nippon Yakurigaku Zasshi showed that the administration of methylcobalamin caused signifi-cant increases in the in vivo incorporation of the amino acid leucine into the crushed sciatic nerve. This resulted in a stimulating effect on protein synthesis repair and neural regeneration. [106, 107]
Acetyl-L-carnitine has produced dramatic results in protecting neurons in a wide range of disease states. Alzheimer's disease and amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig's disease) also respond to higher doses of acetyl-l-carnitine combined with other neuroprotective supplements.
One study of exercise tests in six ALS patients and six matched untrained controls indicated that the exercise-induced increase in plasma free fatty acids, beta-hydroxybutyrate, esterified carnitine, and muscle esterified carnitine was significantly retarded in ALS patients. [108]
It is therefore suggested that ALS patients take 3000 mg a day of acetyl-L-carnitine.
Neuronal damage can be caused by degeneration of the mye-lin sheath, a fatty layer that wraps the signal-moving neuronal fibers. Omega-3 and omega-6 fatty acids may help to repair the myelin sheath required for proper neuron conduction.
New studies show pregnenolone to be a specific memory-enhancing hormone. Pregnenolone maintains the “program” brain cells need to store and retrieve short-term memories. As stores of pregnenolone (and DHEA) are depleted with advancing age, we see a marked and often dramatic decline in the neuronal synchronization required for optimal mental function. [109]
DHEA is a hormone primarily made in the adrenal glands. Production peaks around the age of 25-30 and then drops by 85-90% by the age of 70. DHEA has been associated with the ability to stay thin, make muscle, improve memory, resist stress, and produce a sense of “well-being”.
Since pregnenolone and DHEA are involved in the regulation of neurologic function, supplemen-tation with 50 mg 3 times a day of pregnenolone, and/or 25 mg 2 to 3 times a day of DHEA should be considered.
The phytoestrogen genistein, found in soy prod-ucts, may also help the survival rate in ALS patients, according to research results in the journal Biochemical and Biophysical Research Communications.
Researchers at the Hughes Institute in Minne-sota studied the effects of genistein on male and female mice with familial ALS. The researchers propose that the higher incidence of the disease and earlier onset in the male mice could be related to the presence of estrogen in females. Results of the study indicated that the genistein provided neuroprotective effects that were both estrogen-dependent and independent. Genistein warrants further study as a preventive agent against condi-tions such as ALS and stroke. Because there are insufficient research studies on humans, a physi-cian must be consulted for dosage and prophylactic effectiveness. [110]
Progesterone is synthesized in the peripheral nervous system in glial cells, which comprise the supporting structure of the nervous system. Studies have shown that progesterone stimulates neuron growth, accelerates the maturation of the regenerating axons, and enhances the remyelination of nerve fibers. The progesterone-induced myelination is probably mediated by progesterone receptors, as it is impaired by mifepristone (RU486), a progesterone antagonist. [111]
Continue to Part 6 of the ALS Article
© 2002