info..please check out, Controlling Seizures: A Nutritional Approach

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hi-

maybe some of you have seen this site before or at least seen

something similar but I had to pass it on, in case some have not.

Below is a copy of info or website address is;

http://www.worldwidehealthcenter.net/articles-115.html

shelly

Controlling Seizures: A Nutritional Approach

3rd Dec 2002

Controlling Seizures: A Nutritional Approach

September 2000

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. 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.

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