Guest guest Posted September 29, 2004 Report Share Posted September 29, 2004 Greetings- I am reposting this article for all the new members and the ones that never got to read it the first time. Its long but worth printing out and saving. Below is a list of all the vitamins that our kids should be on. I found > this in an article, written for controlling seizures with nutrition. I > posted it before but don't know if you saw it, Adding these to Nath, > diet maybe worth a try. > > > > Magnesium: 500-1,000 mg/day > Selenium: 100-200 mcg/day > Taurine: 1-3 gm/day > L-carnitine: 1-3 gm/day > GABA (gamma amino butyric acid): 500-1,000 mg/day > Vitamin B complex, w/special emphasis on; > Vitamin B1: 50-100 mg/day > Vitamin B6: 200-500 mg/day > Folic Acid: 400-1,000 mcg/day > Vitamin E: 400-800 IU/day > DMG (dimethylglycine): 50-200 mg/day > Pregnenolone: 100-500 mg/day > Kava Kava: 200-800 mg/day > > > > > > Seizures can be attributed to a number of causes including metabolic > abnormalities, infections, nutritional deficiencies, or trauma. > Emotional stress also increases the frequency of seizures. But most > seizures occur due to unknown reasons. > > In the 1920s, before anticonvulsant medications were available, high fat > diets were used to control seizures in epileptics. Clinical trials are > now confirming that high-fat diets work " better than any other regimen " > according to Dr. M. Freeman, director of the Pediatric Epilepsy > Clinic at Children's Center in Baltimore, land. He recommends a > stringent diet consisting of high fat, low protein, low carbohydrate > foods. Some experts estimate that this diet can lead to a 50 to 70 > percentage reduction of seizures, a record which few drugs can claim. > Dr. Freeman has written a book titled, The Epilepsy Diet Treatment: An > Introduction to the Ketogenic Diet, Demos Publications, 1994, New York > (Maltz, 1994). > > Gamma-aminobutyric acid (GABA), the brain's major inhibitory > neurotransmitter, tends to be in lower than normal levels in > seizure-prone rats (1) and humans with epilepsy. (2) Seizure-prone > preeclamptic patients (hypertensive condition during late pregnancy) > also have decreased brain GABA concentrations. (3) Brain GABA levels > depend on both zinc and vitamin B6. Zinc is involved in the maintenance > of pyridoxal phosphate concentrations by the activation of pyridoxal > kinase. Pyridoxal kinase is important in decarboxylation, and lack of > this enzyme results in lowered brain levels of GABA. Consequently, zinc > deficiency may increase the risk of preeclamptic seizures by reducing > brain GABA concentrations and lowering the seizure threshold. > Unfortunately, plasma pyridoxal phosphate measurements alone do not > appear to accurately reflect vitamin B6 status or true tissue pyridoxal > phosphate levels. (3) > > Glutamate concentrations in the brain are higher in some seizure > patients, and these concentrations can increase to potentially > neurotoxic concentrations during seizures. Thus, it appears that a rise > in brain glutamate may precipitate seizures. These concentrations may > reach levels capable of causing cell death. (2) The importance of > relative concentrations of glutamate, gamma-aminobutyric acid, and > pyridoxal-5-phosphate with respect to seizures is illustrated by a > 33-month-old male seizure patient whose cerebro-spinal fluid glutamate > levels were 200 times normal! When he was given vitamin B6 at a dose of > 5 mg/kg body weight per day (350 mg), his EEG normalized and his > seizures stopped, but the CSF glutamate concentration was still 10 times > normal. With a higher dose of B6 (10 mg/kg bw/d-700 mg), the CSF > glutamic acid normalized. These results indicate that the optimal dose > of B6 for epileptics should be the dose that normalizes CSF glutamate > levels, not just the control of seizures. (4) > > Dr. Lasley (1) found that brains of rats that are genetically > prone to seizures also have reduced levels of taurine as well as > increased levels of aspartate. Therefore, I believe that avoidance of > aspartame should be a key element in an anti-seizure diet. Also, > taurine, in doses of 1-3 grams per day may be helpful. > > In addition to vitamin B6, magnesium and dimethylglycine have also > frequently resulted in a rapid, sometimes overnight, appearance of > speech in formerly non-speaking autistic children. Magnesium, vitamin B6 > and dimethylglycine all have strong anti-seizure properties and can be > effective even when other anti-seizure medications fail. (5) The > deficiency of another member of the B-complex, B1, has also been > reported as a cause of epileptic seizures. (6) > > Vitamin E has been helpful in patients with complex partial seizures, > which are often resistant to drug therapy, and may compensate for > vitamin E deficiencies induced by anticonvulsant medications. Dr. > Sheldon Levy (7,8) believes that vitamin E, although not an > anticonvulsant or an antiepileptogenic agent, plays a useful role in > anticonvulsant therapy as an adjunctive therapy which compensates for > anticonvulsant-induced vitamin deficiencies. > > Carnitine is an amino acid that is excreted in large amounts when > anti-seizure medications like valproic acid (Depakote) or > Tegretol are taken. Depakote is a very effective antiepileptic drug > but has limited use due to risk of fatal hepatotoxicity. The > hepatotoxicity is probably due to valproate-induced carnitine > deficiency. Carnitine transports long chain fatty acids into the > mitochondria. Valproic acid treatment results in a reduction of free > carnitine levels. Carnitine is supplied both by the diet and by > endogenous biosynthesis from lysine. Carnitine's primary metabolic role > is to transport 12-20 carbon long-chain fatty acids into the > mitochondria where they are catabolized to acetyl-CoA for synthesis of > mainly citrate and acetoacetate. Carnitine also is involved in a variety > of fatty acid and organic acid transacylation reactions, where the acyl > moieties of acetyl-CoA esters are transformed to or from carnitine. > > There are four metabolic actions of carnitine that have been utilized as > therapeutic rationales: to correct an absolute relative carnitine > deficiency, to enhance fatty acid oxidation, to accept and shuttle > unmetabolized acyl groups from the mitochondria and to increase levels > of free unesterified coenzyme A and thereby increase the intracellular > free-CoA/acyl-CoA ratio, an important regulator of enzyme > activation/deactivation. (9) Carnitine supplementation is effective in > reducing valproic acid-associated hyperammonemia. (10) Recommended > dosages for carnitine replacement are 50-100 mg/kg/day in children, and > 1 to 3 gm per day for adults in 2 or 3 divided doses. (11) > > In many cases of epilepsy, there is an association with celiac disease > and cerebral calcifications. Gluten-free diet, a mainstay in the > treatment of celiac disease, often reduce the incidence of seizures, > especially if the diet is started soon after the onset of seizures. The > efficacy of the gluten-free diet in epilepsy appears to be inversely > related to the duration of epilepsy before the diet, and to the age at > the beginning of the diet. (12) The possibility of celiac disease should > be investigated in all cases of epilepsy, especially if cerebral > calcifications are identified. > > In this regard, Dr. A. Ventura reported on two females, 5 and 23 years > old, who had focal occipital epilepsy with cerebral calcifications and > who were not responding well to anti-epileptic therapy. (13) Both > females also had celiac disease as well as documented folic acid > deficiency. It is well-known that antiepileptic drugs may induce a > folate deficiency. The patients were placed on gluten-free diets with > supplementary folic acid (dosage unknown). This led to complete > normalization of the EEG in the five year-old and a cessation of > seizures. The 23-year-old's EEG improved significantly and seizure > frequency was reduced. Folic acid levels returned to the normal range > within several months. This report suggests that there is an association > between folic acid deficiency and neurologic diseases such as epilepsy. > Dr. Ventura believes that the mucosal abnormalities of celiac disease > may have caused the folate deficiency, which precipitated the seizures. > (13) The causative relationship of cerebral calcifications to seizures > is unknown, but this may be a condition that may be helped by EDTA > chelation therapy. EDTA chelation is probably the treatment of choice > for metastatic calcification in any tissue. Whether resolution of > cerebral calcification would help in reducing seizures is unknown, but > it certainly wouldn't hurt. > > Magnesium sulfate is standard therapy for pregnancy-induced hypertension > (eclampsia and pre-eclampsia) to prevent seizures. 10 gm of magnesium > are administered intramuscularly initially, followed by 5 gm > intramuscularly every 4 hours. If administered intravenously, a 6 gm > bolus over 15 minutes is given, followed by 1 to 3 gm per hour. In a > comparative study, Dilantin was compared to magnesium in preventing > seizures and reducing blood pressure. The investigators found no > differences in the patient's tolerance, adverse reactions or outcomes > between the two groups. The authors then made the amazing conclusion > that Dilantin " is a well tolerated alternative to magnesium sulfate for > seizure prophylaxis in patients with mild pregnancy-induced > hypertension. " (14) My question is, " what about magnesium as a > well-tolerated alternative to Dilantin? " > > Seizures may also result from glutathione peroxidase deficiency, which > could be from lack of bioavailable selenium. (15) Selenium > supplementation in children resulted in a reduction in seizures and > improvement in EEG recordings after 2 weeks. Selenium is important in > the formation of glutathione peroxidase which may play a role in > protecting neuronal cells against oxygen radicals and peroxidative > damage. Selenium deficiency in the brain of patients with epilepsy may > be an important triggering factor for the origin of intractable seizures > and subsequent neuronal damage. (16) > > Recently, a colleague related a story of a patient with a history of > multiple, intractable, daily grand mal seizures for over 50 years. > Because of the frequency of her daily seizures, the patient has been > unable to attend school, and is illiterate. She was treated with > pregnenolone, with immediate and near-total resolution of her seizures, > being reduced in frequency from several each day to less than one per > month. She repeats over and over that pregnenolone has finally given her > a life. Although this anecdotal report is without precedent or > confirmation, pregnenolone certainly seems to be worth trying. I > recommend starting with 10 mg each morning for one month, increasing the > dose to 30 mg, then to 100 mg, at monthly intervals. > > Kava Kava, which I believe to be a nutritional precursor to the > now-outlawed GHB, has been used traditionally for its anti- convulsant > properties. Consequently, Kava Kava might also be considered for its > sedative, muscle relaxant and anti-convulsant effects. (20, 21, 22) > > In summary, for seizure disorders I recommend using a nutritional > " shotgun " therapy, which includes: > > Magnesium: 500-1,000 mg/day > Selenium: 100-200 mcg/day > Taurine: 1-3 gm/day > L-carnitine: 1-3 gm/day > GABA (gamma amino butyric acid): 500-1,000 mg/day > Vitamin B complex, w/special emphasis on; > Vitamin B1: 50-100 mg/day > Vitamin B6: 200-500 mg/day > Folic Acid: 400-1,000 mcg/day > Vitamin E: 400-800 IU/day > DMG (dimethylglycine): 50-200 mg/day > Pregnenolone: 100-500 mg/day > Kava Kava: 200-800 mg/day > References: > 1. Lasley, S. M. Role of Neurotransmitter Amino Acids in Seizure > Severity and Experience in the Genetically Epilepsy-Prone Rat. Brain > Res, 1991; 560:63-70 > > 2. During, M.J. and Spencer, D. D. Extracellular Hippocampal Glutamate > and Spontaneous Seizure in the Conscious Human Brain. The Lancet, June > 26, 1993; 341 (8861): 1607-1610 > > 3. Anonymous. Zinc, Preeclampsia, and Gamma-Aminobutyric Acid. Am Jnl of > Obst & Gyn, July 1990, 163, 1, (Part I): 242-243 > > 4. Baumeister, F. Glutamate in Pyridoxine-Dependent Epilepsy: Neurotoxic > Glutamate Concentration in the Cerebrospinal Fluid and Its Normalization > by Pyridoxine. Ped, September 1994, 94 (3): 318-321 > > 5. Seizures, Vitamin B6, DMG, and Sudden Speech Autism, Res Rev Intl, > 1996, 10 (2): 1 > > 6. Keyser, A. Epileptic Manifestations and Vitamin B1 Deficiency. Eur > Neuro, 1991, 31: 121-125 > > 7. Levy, S. L. An Evaluation of the Anticonvulsant Effects of Vitamin E. > Epilepsy Res, 1990, 6: 12-17 > > 8. Levy, S. L. The Anticonvulsant Effects of Vitamin E: A Further > Evaluation. Can Jrnl Neurosci, 1992, 19: 201-203 > > 9. Kelley, R. I. The Role of Carnitine Supplementation in Valproic Acid > Therapy. Ped, June 1994, 93 (6): 891-892 > > 10. Sakemi, K., Tohoku, J. The Effect of Carnitine on the Metabolism of > Valproic Acid. Exp Med, 1992, 167: 89-92 > > 11. Coulter, Da. L., M.D. Carnitine, Valproate, and Toxicity. Jrnl Child > Neuro, January 1991, 6 (1): 7-14 > > 12. Gobbi, G. Celiac Disease, Epilepsy and Cerebral Calcifications. The > Lancet, August 22, 1992, 340: 439-442 > > 13. Ventura, A. Celiac Disease, Folic Acid Deficiency and Epilepsy With > Cerebral Calcifications. ACTA Pediatrica Scandinavica, 1991, 80: 559-562 > > > 14. Appleton, M. P. Magnesium Sulfate Versus Phenytoin for Seizure > Prophylaxis of Pregnancy-Induced Hypertension. Am Jnl of Obst & Gyn, > October 1991, 907-913 > > 15. Weber, G. Glutathione Peroxidase Deficiency and Childhood Seizures. > The Lancet, June 15, 1991, 337: 1443-1444 > > 16. Ramaekers, V., Th. Selenium Deficiency Triggering Intractable > Seizures. Neuro Ped, 1994, 25: 216-223 > > 17. Dean, W. Stop criminalization of GHB, VRP Nutrition News, Vol 11, > Number 4, April 1997 > > 18. Klunk, W.E., Covey, D.F., and Ferendelli, J.A. Anticonvulsant > properties of alpha, gamma, and alpha, gamma-substituted gamma > butyrolactones. Molecular Pharmacology, 1982, 22: 438-443. > > 19. Ikeda, M., Dohi, T., and Tsujimoto, A. Protection from local > anesthetic-induced convulsions by gamma amino butyric acid. > Anesthesiology, 1982, 56: 365-368. > > 20. Klohs, M.W., and Keller, F. A review of the chemistry and > pharmacology of the constituents of Piper methysticum Forst. J Med, > Pharm, Chem 1963, 1(1): 95-103. > > 21. Klohs, M.W.F., Keller, F., , R.E., Toekes, M.I., and > Cronheim, G.E. A chemical and pharmacological investigation of Piper > methysticum Forst. J Med, Pharm, Chem, 1959, 1: 95-103. > > 22. Nickl, J. and Keck, J. Medicines containing lactones from Piper > methysticum, Brit Patent 943,121, Nov 27, 1963. > > The information in this article is not intended to provide personal > medical advice, which should be obtained from a medical professional, > and has not been approved by the U.S. FDA. > > Copyright 2001 by Vitamin Research Products, Inc. (VRP) The use of > information found in Vitamin Research News for commercial purposes is > prohibited without written permission from VRP. > > Quote Link to comment Share on other sites More sharing options...
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