B1& Magnesium for Tourette's Syndrome

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B1/Mg Deficiencies Cause TS Symptoms

 

" Hypothesis: Vitamin B1 and/or Magnesium Deficiency Cause Symptoms

Associated

with Tourette's Syndrome in Children with Alcoholic Relatives "

 

by Frances Jurnak

 

I would like to comment on the role of diet in Tourette's syndrome. There

are

likely to be several causes of the symptoms of Tourette's Syndrome. A

deficiency in vitamin B1 (thiamine) or Mg is probably one of the MAJOR

causes, particularly in those cases in which there is a family history of

ALCOHOLISM. B1 affects the proper metabolism of sugar/carbohydrates and some

amino acids found in proteins. Vitamin B1 is also involved in the synthesis

of neurotransmitters, particularly acetylcholine and GABA, which affect

brain

functions.

 

Vitamin B1 (<400 mg/day) must always be administered with magnesium

(Mg)(<400

mg/day), otherwise a high dose of B1 could deplete the body's Mg reserves

and

lead to death. There are a few reports of an adverse reaction to B1 at doses

higher than 400 mg/day. In be effective in children, B1/Mg must be given

thrice daily or with every meal, otherwise the B1/Mg is passed quickly into

the urine. Studies in Germany have shown that ALL children require a much

higher level of B1/Mg, particularly during the years of 2-5 and 7 to 10.

Because these years correspond to the years in which the brain is most

active

in development, it would make sense that brain development must be

accompanied by an increase in the components, including B1, necessary for

neurochemical reactions. The need for B1 decreases with the onset of

puberty,

thus many children who are on the threshold of B1 deficiency before puberty

will become symptom free after the onset of puberty. Other children are not

so lucky because there is likely to be a genetic defect in a B1-utilizing

enzyme in those families with a history of alcoholism, particularly if the

family has a European heritage. B1/Mg deficiency can also be caused by a

malabsorption of the vitamin, particularly in cases of a viral, bacterial or

parasitic infection. B1/Mg deficiencies can also be found in children with

carbohydrate-rich diets or in critically ill children who are unable to eat

properly.

 

Physicians, especially pediatricians, are no longer trained to recognize the

clinical symptoms of vitamin B1/Mg deficiency. Symptoms of mild B1

deficiency

include nausea, lack of appetite, irritability, depression, fatigue, lack of

energy, lack of automatic reflexes 2-3 hours after a meal, and rage tantrums

4-6 hours after a meal. With prolonged B1 deficiency, the peripheral nervous

system is affected, leading to mental confusion as well as to muscle

coordination problems, particularly in the eyes and extremities. In

children,

these symptoms are displayed as visual processing learning disabilities,

dyslexia, fine motor skill problems, inability to focus, excessive

daydreaming, inability to notice fine details, clothing sensitivities (eg

socks), numbness in hands/feet, and/or motor/vocal tics, particularly those

involving the eyes/face. Most children do not exhibit all of the

B1-deficient

symptoms, thus it may be difficult to recognize. In some children, the

aggregate symptoms may appear to be hypoglycemia, in layman's terms, but not

in the strictest definition of the medical disorder. In families with a

history of alcoholism, children often exhibit symptoms of ADHD (mixed

inattentive and hyperactivity type), visual learning disabilities and,

depending upon the severity of the B1/Mg deficiency, tics. The problems are

likely due to a genetic defect in a metabolic process that utilizes vitamin

B1. A B1/Mg deficiency may also be responsible for some cases of

hyper-insulinism (a form of pre-diabetees) and for the hyperactive sugar

effect seen in some children. If a low-carbohydrate diet ameliorates some

behavioral problems, then a B1/Mg deficiency should be suspected.

 

The metabolically active form of B1 is thiamine pyrophosphate (TPP). This

involves a number of enzymes to absorb, transport and convert B1 into TPP.

Mg

and TPP are both essential for converting glucose into energy and into the

neurotransmitters, acetylcholine and GABA. In glucose metabolism, TPP and Mg

are the cofactors for two complex enzymes called pyruvate dehydrogenase and

alpha-ketoglutarate dehydrogenase. Glucose is obtained by direct ingestion

of

sugar or by the metabolic breakdown of simple and complex carbohydrates,

such

as those found in grains. Glucose is the only form of energy used by the

brain. If there is a B1 or Mg deficiency or a genetic defect in the

TPP-dependent enzymes, the brain would not be able to synthesize the proper

amounts of GABA or acetylcholine. Insufficient supply of acetylcholine is

likely to cause a poor automatic reflex. This is usually accompanied by

daydreaming. Moreover, the receptor for this neurotransmitter is the same

one

to which nicotine binds, causing tobacco addiction in these susceptible

individuals. It is well established that moderate B1 deficiency causes

Wernicke-Korsakoff syndrome, particularly in a subpopulation of alcoholics

of

European heritage. In addition to the symptoms of B1 deficiency already

mentioned, a more severe deficiency leads to ataxia (very poor muscle

coordination), ophthalmoplegia (loss of eye coordination, nystagamus), and

mental confusion. Autopsies of the brains of such individuals usually

display

lesions or soft spots in certain areas of the brain. No one has considered

the possibility that prolonged, mild B1 deficiency may cause similar, but

smaller brain lesions in children, which ultimately result in tics and the

long-term neurological damage behind visual learning disabilities and

inability to focus. In alcoholics, the Wernicke part of the syndrome is

usually reversible with proper thiamine/Mg administration, but the Korsakoff

part responsible for mental confusion (inability to focus) may not be

completely reversible.

 

In addition to the generation of energy, GABA and acetylcholine in glucose

 

metabolism, TPP is also utilized by an enzyme called transketolase, This

enzyme converts one of the products of glucose into ribose used in the

synthesis of nucleic acid precursors and into NADPH used in fatty acid

biosynthesis. Transketolase is particularly important because it forms the

basis of the most sensitive clinical assay for measuring B1 deficiency in

red

blood cells. In addition to the enzymes involved in glucose metabolism, TPP

is also used by a B1-dependent enzyme, called branched-chain alpha-keto acid

dehydrogenase, in the degradation of several amino acids found in protein

(leucine, isoleucine and valine). Thus, a low-carbohydrate diet, may not

resolve all symptoms, because a B1-dependent enzyme is required in the

digestion of proteins.

 

The clinical assays for B1 typically measure serum levels and this may be

quite unrelated to B1 levels in the brain. The best test is called a

transketolase assay, in which the activity of the enzyme is measured with

and

without added TPP to obtain the TPP differential. A TPP differential of 14%

or greater is considered to be a significant B1 deficiency. This assay used

to be commonly carried out among alcoholic populations but it is rarely done

in children. It may be difficult to find a laboratory in the USA that does

the assay properly. Please note that the transketolase assay is not able to

detect a B1-deficiency in the brain or if the B1-utlizing enzymes in the

brain are properly binding to TPP. Thus, an individual may have

B1-responsive

symptoms, but no known serum assay will detect a B1 deficiency.

 

Who am I and how do I know all of this and why do I care? I am a professor

who has conducted biochemical research for more than 20 years. Since my son

was eight months old, I suspected that something was wrong with his

metabolism. I took him to over 20 physicians, including pediatricians and

numerous kinds of specialists. All missed clinical signs of vitamin B1 and

vitamin C deficiencies. When my son was 8 years old, he was diagnosed with

ADHD, Tourette's syndrome and visual learning disabilities. I started

researching the medical literature myself, with some key references given

below. When I realized he displayed all symptoms of Wernicke-Korsakoff's

syndrome (albeit in a milder form), I began the proper administration of 350

mg of B1 and 400 mg Mg, split into 3 daily doses. Within 30 hours, his mood

changed from depressed to very happy; within a week, all tics disappeared;

within four weeks, his nearly constant nausea disappeared; and his focus

continues to improve, albeit more slowly. I am now looking into ways to

reverse the neurological damage that has occurred over the first eight years

of his life.

 

I am not a physician and cannot help individuals with their problems.

However, I would like to collect antidotal stories and the names of

individuals who think that B1-Mg supplementation may be helping their

children.

 

Six Important References:

 

1. L. Pantoni, L. Poggesi, A. Repice and D. Inzitari. " Disappearance of

motor

tics after Wernicke's encephalopathy in a patient with Tourette's syndrome. "

Neurology, 48:381-383 (1997).

 

2. A. Brenner. " The effects of megadoses of selected B complex vitamins on

children with hyperkinesis: controlled studies with long-term follow-up. "

Journal of Learning Disabilities, 15(5):258-264 (1982).

 

3. L. Reinken, H. Stolley and W. Droese. " Biochemical assessment of thiamine

nutrition in childhood. " European Journal of Pediatrics, 131:229-235 (1979)

 

4. A.B. Mukherjee, S. Svoronos, A. Ghazanfari, P.R. Martin, A. Fisher, B.

Roecklein, D. Rodbard, R. Staton, D. Behar, C.J. Berg and R. Manjunath.

" Transketolase abnormality in clutured fibrobnlasts from familial chronic

alcoholic men and their male offspring. " The Journal of Clinical

Investigation, 79:1039-1043 (1987).

 

5. J.P. Blass and G.E. Gibson. " Abnormality of a thiamine-requiring enzyme

in

patients with Wernicke-Korsakoff syndrome " . The New England Journal of

Medicine, 297:1367-1370 (1977).

 

6. R.L. Hoffman. " The natural approach to attention deficit disorder:

drug-free ways to treat the roots of this childhood epidemic. " Good Health

Guide published by Keats Publishing, Inc., New Canaan, Connecticut, 1997.

 

In the course of my research, I have learned of physicians who have

expertise

in the field of vitamin B1, including Dr. Arnold Brenner from Randallstown,

Maryland; Dr. Derrick Lonsdale in the Chicago area; and Dr. Ronald Hoffman

in

the New York City area.

 

 

 

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[Guest Jonathan c]

I am currently on 1500mg of magnesium citrate and 300mg of b1 is order to help my stutter, I have read a few articles that claim it helps (in some cases cures) stutters.

Been on it a few days and so far only noticed a runny tummy which is a common side effect of high dose magnesium. I will post on here again in a couple weeks with my results

[Guest Jonathan c]

After two weeks noticed no noticeable effect from the supplement besides a runny tummy. My speech got a little worse tho I'm blaming that on environmental factors.

Did not work for me