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  • Taurine

    I would like to know more about Taurine and its effect on epilepsy
    and possible adverse effect. Thank you.


  • #2
    Below is one study, I found. However it's on mice. I'm looking for a better study. What info where you looking for? It's actual effectiveness? Dosagages? real world evidence?

    Adv Exp Med Biol. 2003;526:515-25. Related Articles, Links

    Prevention of epileptic seizures by taurine.

    El Idrissi A, Messing J, Scalia J, Trenkner E.

    New York State Institute for Basic Research in Developmental Disabilities and The Center for Developmental Neuroscience, The City University of New York, Staten Island, NY 10314, USA.

    Parenteral injection of kainic acid (KA), a glutamate receptor agonist, causes severe and stereotyped behavioral convulsions in mice and is used as a rodent model for human temporal lobe epilepsy. The goal of this study is to examine the potential anti-convulsive effects of the neuro-active amino acid taurine, in the mouse model of KA-induced limbic seizures. We found that taurine, (43 mg/Kg, s.c.) had a significant antiepileptic effect when injected 10 min prior to KA. Acute injection of taurine, increased the onset latency and reduced the occurrence of tonic seizures. Taurine, also reduced the duration of tonic-clonic convulsions and mortality rate following KA-induced seizures. Furthermore, taurine, significantly reduced neuronal cell death in the CA3 region of the hippocampus, the most susceptible region to KA in the limbic system. On the other hand, supplementation of taurine, in drinking water (0.05%) for 4 continuous weeks failed to decrease the number or latency of partial or tonic-clonic seizures. To the contrary, we found that taurine, -fed mice showed increased susceptibility to KA-induced seizures, as demonstrated by a decreased latency for clonic seizures, an increased incidence and duration of tonic-clonic seizures, increased neuronal death in the CA3 region of the hippocampus and a higher post-seizure mortality of the animals. We suggest that the reduced susceptibility to KA-induced seizures in taurine, -injected mice is due to an increase in GABA receptor function in the brain which increases the inhibitory drive within the limbic system. This is supported by our in vitro data obtained in primary neuronal cultures showing that taurine, acts as a low affinity agonist for GABA(A) receptors, protects neurons against kainate excitotoxic insults and modulates calcium homeostasis. Therefore, taurine, is potentially capable of treating seizure-associated brain damage.

    PMID: 12908638 [PubMed - indexed for MEDLINE]


    • #3

      Neurochem Res. 2004 Jan;29(1):319-24. Related Articles, Links

      Plasma and cerebrospinal fluid amino acids in epileptic patients.

      Rainesalo S, Keranen T, Palmio J, Peltola J, Oja SS, Saransaari P.

      Brain Research Center, Medical School, University of Tampere, Finland. [email protected]

      Altered plasma and cerebrospinal fluid amino acid levels may be associated with human epilepsy. We studied three groups of patients, those with a generalized epileptic syndrome, juvenile myoclonic epilepsy, patients with refractory localization-related epilepsies, and patients with acute seizures (within 24 h). Plasma levels of amino acids were studied in all patient groups, as were those in the cerebrospinal fluid (CSF) of patients with acute seizures. After acute seizures, the amino acid changes in the CSF were limited to a reduction in the level of taurine, whereas the levels of most amino acids in plasma were decreased. On the other hand, levels of the excitatory amino acids glutamate and aspartate were increased. The most notable finding in the juvenile myoclonic epilepsy patients was an increase in glutamate level in the plasma. Our study supports the conception of an altered metabolism of glutamate in generalized epilepsies.

      PMID: 14992292 [PubMed - in process]


      • #4
        Also, Taurine is very cost effecient as far as amino acids go.
        I use Taurine regularly for cramping due to depletion induced by exertive activites, I know several references that claim it to be very effective for hypertension. I'm also unclear on it for the purposes you have stated.

        Last edited by Anonymous; 07-08-2011, 03:48 PM.


        • #5
          Another good article

          by Ward Dean, MD
          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. John M. Freeman, director of the Pediatric Epilepsy Clinic at Children’s Center in Baltimore, Maryland. 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. Stephen 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 diets, 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
          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., Williams, 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.


          • #6
            Dr. Dean, I don't know where you got your nutrition training, but a couple of your recommendations are dangerous.

            1) An epileptic should NEVER take GABA because it is rapidly converted to glutamic acid and/or glutamates. In fact, researchers think that a subset of epileptics may have a disordered metabolism of GABA/glutamates that so that both forms are primarily kept in glutamate form.

            2) The level of standard vit B6 (pyridoxine) you prescribe is excessive and may cause neuropathy, among other things. That problem is avoided if the patient takes P5'P (type of B6 active in the body) instead.

            Also a couple of your other recommendations are questionable. The dosage of pregnenolone you recommend is fairly high and will definitely disorder the sex hormones w/ some negative side effects, especially in women. The KavaKava, especially taken on a daily basis, gives some people headaches. It is also somewhat psychoactive, but not as much as conventional anti-epileptics, so I suppose if it works (questionable) it could be considered an improvement.

            An improvement in tolerability and effectiveness of magnesium is gained if the patient uses the new sustained release magnesium malate supplements.
            Last edited by Anonymous; 07-08-2011, 09:36 AM.