Motor Neurone Disease and the Life of
Motor Neurones. Is Low B3/Peilagra
Aggravating It?
Christopher M Reading B.Sc., Dip.Agr.Sc., M.B.,
B.S., F.R.A.N.Z.C.P., F.A.C.N.E.M.
I read with interest an article by Garth Nicholson and following
correspondence concerning the cell death of the motor neurone. 1-4
In 1975, I wrote to Professor John Lance about measuring vitamins
Bi and B6 in patients with motor neurone disease (ALS) because of
clumping and condensation of chromatin in the dying anterior hom
cells in ALS patients. From my research,"? this suggests the cells
were not getting enough Bi (for cAMP, etc.) and B6 (for PGEl
series) and that low Bland B6 could be aggravating or causing the
condition. (It is known Isoniazid given to animals can cause low B6
and cause an ALS picture.) Professor Lance agreed to look at serum
Bland B6 and other vitamin levels in a group of ALS patients.
The tests were done by Dr Sylvia Nobile of Roche Laboratory in
1975/6 and were as follows:
Patient 1. Low B 1, B6;
Patient 2. Low vitamin A (total carotenoids), vitamin C, folic
acid, vitamin Bl2 (but not Bt, B6);
Patient 3. Low vitamin A (total carotenoids), vitamins C, Bs,
Bl andB6;
Patient 4. Bi and B6 only were assayed and was low in B6;
Patient 5. Low vitamin A (total carotenoids), vitamin E, vitamin
C,Bl,B2.
(Unfortunately B3 was not assayed in any of these patients.)
In 1976 Professor Lance advised me per phone that I was correct as
ALS patients seem to be low in B 1 (3/5) and B6 (4/5). The next 14
patients to 1995 (Bi 8114 and B6 10114) and most ALS patients since
then have been shown to be low in Bland B6. However, on extra B 1
and B6 there were temporary improvements but the patients still
succumbed to the illness.
From 1983 to 1985 it was possible to measure serum B3 and 5/6 proved
to be low in Bs/niacin, having pellagra which can cause bulbar palsy and
paralysis. My ALS patients since 1983 have been treated with Bi, B6
and B3. Low Bi, B6, B3 can all cause depression and so most have been
less depressed and have lived for longer than three years.
One ALS patient had a B3 of 130 (160-200), the lowest level of Bs I
have recorded in over 300 patients showing low B3. She lived from
1983 to 1994 (when she stopped the B3). Another ALS patient in
May 1988 had a low B3 of 157 (160-200) and on B3, etc., is still
alive - playing tennis and riding a bicycle.
Giving Bi and B6 alone is not enough if one is low in B3. B3 is not
enough unless 2 gram of niacinamide is given. One patient with low
B3 (but not ALS), on 1800 mg of Bs/day was losing the ability to talk
(and was still low in B3). However, on 500 mg niacinamide QID this
problem went.
Another patient with low B3 and also on 1800 mg of Bs/day was still
low in B3 as measured and was losing the ability to swallow. On
500 mg B3 QID this problem also went.
journal of the Australasian
Correction of low B3 appears to be very important for ALS patients
since low B3 can per se cause bulbar palsy, paralysis, coma, etc.
Unfortunately, I thought, for years, that B3 500 mg TDS and B3 in
a Multi-B cover or 1800 mg was sufficient - it wasn't and, in
retrospect, earlier ALS patients most likely, unfortunately, still
died of pellagra. I would now start patients on 500 mg QID of
niacinamide and they may require Bi from 500 mg to 750 mg and
B6 from 500 mg to 1250 mg to have normal levels (P-5-P;
EGOT:EGOT+P5P enzyme test).
Why are ALS patients low in B3?
Since tryptophan requires Bt, B2, B6, vitamin C, magnesium, zinc,
manganese to be converted to B3 then all these are important for the
synthesis of Bs. Professor Lance was correct to give Bi and B6 but
only years later, by measuring these vitamin levels and rechecking
on heavy supplementation, is it clear that high amounts of Br, B6, B3
are necessary in ALS patients, due to severe food sensitivity/
intolerance to cows milk, gluten-containing grains, legumes, beans
and resultant malabsorption state. Nowadays, GMI ganglioside
antibodies and anterior hom cell antibodies can be measured. I find
these are positive in ALS patients (and anti-nerve antibodies and
anti-myelin antibodies in MS) and antibodies can be reversed to
negative on a diet free of cows milk/gluten-containing grains/legumes/
beans and on supplements of Bi, B6, B3, vitamin C, etc., if low.
(Two cases so far).
Do the anterior hom cells die because of not enough B i, B2, B6,
vitamin C and thus B3 and thus low cAMP, causing clumping and
condensation of chromatin? (cAMP can cause dispersal of chromatin).
Are neurotoxic peptides in legumes/beans (compare ricin in castor
oil bean) and in cows milk and gluten-containing grains damaging
neurological tissue causing an 'autoimmune neuritis' involving
anterior hom cells (hence antibodies to these) and are thus toxic
to these cells?
(A copy of the vitamin assays in 20 ALS patients and autoimmune
disease in 16 ALS patients is available on request).
References
1. Nicholson GA, "Motor neurone disease and the life of motor neurones." Med
J Aust 1996; 165:80-181.
2. Bansal AS, Bansal JA, "Motor neurone disease and the life of motor neurones."
Med J Aust 1997; 166:109.
3. Vaux DL, Hawkins CJ, Uren AG, et al., "Motor neurone disease and the life of
motor neurones." Med J Aust 1997; 166: 109.
4. Nicholson GA, "Motor neurone disease and the life of motor neurones." Med
J Aust 1997; 166: 109-110.
5. Reading CM, McLeay AC, Nobile S, "Down's Syndrome and thiamine
deficiency." J Orthomolecular Psychiatry 1979; 8: 1,4-12.
6. Reading CM, Down's Syndrome: Nutritional Intervention. Address to 13th
Annual Conference, McCarrison Society 23.8.93. "Nutritional and Mental
Health; Links between food and behaviour, 1983." J Nutrition and
Health. 1984; 3:90-111.
7. Reading CM, "Down's Syndrome: is gluten/alpha-gliadin sensitivity/coeliac
disease the cause?" Int J Biosocial Research 1984; 6: 1:62-65.
College of Nutritional and Environmental Medicine - December 1997 - 21