NEUROMUSCULAR DISEASE
Neuromuscular Disease and Creatine Monohydrate
THE EXPERTS SPEAK-Clinical Pearls, 1999
Mark A Tarnopolsky, MD, PhD, FRCPC
Department of Neurology
McMaster University Medical Centre
Hamilton, Ontario, Canada
"Creatine Monohydrate Increases Strength in Patients with Neuromuscular Disease"
Kirk Hamiltion: Can you tell is a little bit about your study and the basic results?
MT: This paper presents the results of our pilot work in that we study the effects of creatine (10 gm/day for five days), administered to 81 patients with a variety of neuromuscular disease (muscular dystrophy, inflammatory myopathy, metabolic myopathy, neuropathy) in an open trial. We measured body weight and foot, knee extension and hand grip strength before and after treatment. There were improvements in all variables ranging grom 5-15 percent.
KH: Were there any side effects to the creatine?
MT: Only for one patient. However, we recommend all patients be followed by their physician, as the possibility of idiosyncratic reactions are possible with any drug or nutraceutical compound.
KH: Was the benefit from creatine sustained or just short-term?
MT; The benefit was only evaluated in the short term period.
KH: What was the optimal maintenance dose of creatine?
MT: Studies in young, healthy individuals demonstrate that between two and three grams per day is sufficient to maintain creatine levels in the muscle. The optimal dosage is unknown for those with already low concentrations. However, we recommend five grams at this point.
ALSO-Kerry Bone BSc (Hons) Dip Phyto, MNIMH (UK), MNHAA-Founder of Mediherb recommends Skullcap for neuromotor
conditions.
"Neurodegeneration from mitochondrial insufficiency; nutrients, stem cells, growth factors, and prospects for brain rebuilding using integrative management," Kidd PM, Altern Med Rev; 2005;10(4):268-293.
SUMMARY: In this review article, the author discusses brain energetics as an emerging focus for intervention in individuals with degenerative brain disorders. Studies of the brain in Alzheimer's and other dementias, Down syndrome, stroke, Parkinson's disease, multiple sclerosis, amyotrophic lateral sclerosis, Huntington's disease, Friedreich's Ataxia, and related disorders. Intervention with orthomolecular nutrients including essential minerals, the B vitamin group, vitamins E and K, alpha-lipoic acid, coenzyme Q10, and nictinomide adenine dinucleotide, have been shown to provide clinical benefit. Additionally, cognition has been found to improve with L-cartinine, glycerophosphocholine, and phosphatidylserine, which improve mitochondrial support and conserve growth factors. Furthermore, the omeg-3 fatty acid docosahexaenoic acid(DHA) is involved in nerve cell expansion.
"Neurodegenerative Disorders in Human: The Role of Glutathione in Oxidative Stress-Mediated Neuronal Death," Bains JS, Shaw CA, Brain ResRev, 1997;25:335-338.
SUMMARY: In this review oxidative stress-mediated neuronal loss may be initiated by a decline n the antioxidant molecule glutathione. Glutathione in the nervous system acts as a free radical scavenger, redox modulator of ionotropic receptor activity and possibly a neurotransmitter. Gluthathione depletion can enhance oxidative stress and may increase levels of excitotoxic molecules, which may initiate cell death in specific neuronal populations. Evidence for a role of oxidative stress and reduced glutathione status is found in Lou Gehrig's disease, Parkinson's disease and Alzheimer's disease. (Gluthathione levels can be increased through NAC N-Acetylcysteine.
PARKINSON'S DISEASE
"Treatment of Parkinson's Disease With l-Methionine" Smythies JR, Halsey JH, South Med J, 1984;77:1577.
Five g/day of l-methionine in Parkinson's disease patients improved akinesia and rigidity in approximately 3 weeks. Seven out of 11 patients with Parkinson's disease showed a positive improvement in akinesia and/or rigidity.
"Vitamin E Therapy in Parkinson's Disease", factor SA Sanchez-Ramos JR, Weine WJ. Adv. Neurol, 19990,53:457-461.
IN 14 Parkinson's Disease patients (mean age 68.6 years, with duration of Parkinson's disease of 6.9 years) subjects too 400 and 3200 IU day of vitamin E and a mean daily dose of levodopa of 512 mg. They were matched with 14 patients who did not take the vitamin E. The study showed that the Parkinson's disease patients taking vitamin E had significantly less severe disease compared with those not taking vitamin E.
"Nicotinamide Adenine Dinucleotide (NADH)- A New Therapeutic Approach to Parkinson's Disease", Birkmayer, J.G. D., et al, Acta Neuro. Scand., 1993;87:Suppl. 146:32-35.
Summary: In an open trial of 885 Parkinson's disease patients, half of the patients received NADH by intravenous infusion over 30 minutes and another group of patients obtained 5 mg. of NADH orally in the form of capsules. The oral administration of NADH resulted in an overall improvement in disability similar to the other form. In about 80 per cent of the patients, a beneficial clinical effect was observed, 19.3 per cent of the patients showed a very good improvement of disability, 58.7 per cent showed a moderate improvement and 21 per cent did not respond to NADH.
EPILEPSY
Niacin:
Supplementation may potentate the effect of anticonvulsants.
Clinical Observation: Several pts. were unable to achieve good control with anticonvulsants as the required dosages made them so drowsy and sluggish that they were unable to function normally. They were supplemented with vitamin B3 1 gram 3 times daily. After they were on the supplement for several months the anticonvulsant dose could be slowly reduced while monitoring for increased seizure activity. (Hoffer A. Niacin Therapy in Psychiatry. Springfield, Ill., Charles C. Thomas 1962).
MUSCULAR DYSTROPHY
Reference: "Nutritional Muscular Dystrophy for Deficiencies of Selenium and vitamin E in Ruminants,
Garcia-Belennguer, S, et al, Med. Vet, 1992;9(2):84-92.
Summary: It is known that selenium and vitamin E deficiency in ruminants causes a nutritional muscular dystrophy. The treatment should attempt to measure and correct the vitamin and selenium deficiency.
Duchenne Muscular Dystrophy-Glutamine, Isonitrogenous Amino Acid, Whole Body Protein Degradation
Oral Glutamine and amino acid supplementation inhibit whole-body protein degradation in children with Duchenne muscular dystrophy? Mok E. Violante CE et al. Am J Clin Nutr., 2006;83(4):82-8.
Article review: The author reviews a study with 26 children with Duchenne Muscular Dystrophy. He states oral glutamine supplementation and oral amino acid supplementation were equally effective in inhibiting whole-body degradation. The subjects received a daily oral supplement of glutamine (.5 g/kg.) or an amino acid mixture .8g/kg. for 10 days. The author does not make any specific references to observable improvements in the 26 children.
MULTIPLE SCLEROSIS
"Vitamin B-12 Metabolism in Multiple Sclerosis", Reynolds, MD Archives of Neurology, June 1992;49:649-652.
Summary: The authors evaluated 29 MS patients and found low vitamin B12 levels in all subjects. The authors feel that vitamin B12 deficiency should always be looked in for patients with multiple sclerosis.
"Magnesium Concentration in Plasma and Erythrocytes of Multiple Sclerosis ", Stelmasiak, Z., et al. ACTA Neurol Scand, 1995;92:109-111.
Summary: Red blood cell magnesium was evaluated in 24 men and women between 29 and 60 years of age. A statistically significant decrease in magnesium concentrations in the erythrocytes was found but not in the plasma of multiple sclerosis patients.
Multiple Sclerosis-Vitamin D
Summary: It has been shown that 1,25 dihydroxyvitamin D3, the hormonal form of vitamin D3, can completely prevent a mouse model of MS. This opens up the possibility that MS may be preventable in genetically susceptible individuals with early intervention strategies that provide hormonally active levels of 1,25 dihydroxyvitamin D3 or its analogs.
Experimental and observational study: 16 pts. were found to have abnormal blood rheology and were supplemented with primrose oil (brand name Effamol) 4 gm. daily. After 3 wks., both blood rheology and hand grip strength were improved, suggesting that there was improved capillary perfusion in muscles. (Simpson LO et al. Dietary supplementation with Effamol and multiple sclerosis. N Z Med J 98(792);1053-54,1985).
ADAPTRIN: Adaptrin is a Tibetan Formula blending 24 Herbs-
Experimental Double-blind Study: 100 pts. suffering from chronic progressive form of multiple sclerosis randomly received Adaptrin, 2 tablets 3 times daily or only systomatic treatment for 1 year. 44% of pts. showed improvement of their general condition, increase of muscle strength, and decrease or disappearance of weakness in afflicted sphincters. A decrease in paresis was observed in 36%. In 41% of those pts. with initially an abnormal tracing of visual evoked potentials, an improvement or normalization was achieved. Pts. with both recurrent attacks and slowly progressive MS both improved, although the improvement was higher (55%) in the former gp. than the latter (33%). No side effects were reported. Of the patients who did not receive Adaptrin, none felt better and 40% of them showed a detioration(Korwin-Piotrowska T et al. Experience of Adaptrin in multiple sclerosis. Phytother Res 6:133-6,1992).