Carolyn

[Guest guest]

Carolyn,

I am happy to help.

I am concerned about him having so many seizures right now though. Status

seizures can be very dangerous. I would inform my doctor.

I pray you will get the help you need.

Hallie

From: caronath

To: ketogenic

Sent: Monday, July 19, 2004 5:09 PM

Subject: Re: Re: about the meal planner from excel/Hallie

Hallie,

I wrote to Emma and saw her website, she helps me as she can and she's so

nice.

I think there is better team in England than here in France, I'm pretty

alone with aël's disease and the seizures!

Unfortunatelly, at the moment aël is not transportable, so I can't

take him anywhere.

Thanks a lot

Carolyn

Re: Re: about the meal planner from excel

Carolyn, The Stanford site has a download to figure Ketogenic meals too.

In fact, Tanners nutritionist uses it and figured out a weeks supply of meals

for them before they left the hospital.

There is a hospital in England that does the diet. There is a girl named

Emma from my other list that works there. Her website is

www.matthewsfriends.org

She works with the team at Great Ormond Street. You could contact her if

you want to.

Hallie

[Guest guest]

Carolyn-

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.