Dietary Calcium As A Supplement To Vitamin D Compound Treatment Of Multiple Sclerosis
John Sykes Fletcher
Vitamin D is a recent arrival in the roster of agents that are known to
regulate the immune system. Vitamin D is converted in a two-step process to
the hormone, 1,25-dihydroxycholecalciferol (1,25-(OH).sub.2D.sub.3).sup.1
that is a key factor in regulating serum calcium, phosphorus and bone
(DeLuca, 1997). This hormone acts in a steroid hormone-like mechanism
through a nuclear receptor, the vitamin D receptor (VDR), which is a member
of the steroid hormone receptor superfamily (Pike, 1991; Ross, et al.,
1993). The discovery of VDR in peripheral blood lymphocytes (Bhalla, et al.,
1983; Provvedini, et al., 1983) is a factor that led to the realization that
1,25-(OH).sub.2D.sub.3 is a significant regulator of the immune system. The
most striking evidence of a role for 1,25-(OH).sub.2D.sub.3 as an immune
system regulator comes from in vivo experiments. 1,25-(OH).sub.2D.sub.3 can
prevent the development of EAE (Cantorna, et al., 1996 and U.S. Pat. No.
5,716,946; Lemire and Archer, 1991), experimental arthritis (Cantorna, et
al., 1998a), and 1,25-(OH).sub.2D.sub.3 can markedly inhibit transplant
rejection (Bouillon, et al., 1995; Hullett, et al., 1998).
EAE is mediated by CD4+ T cells, which mount an inappropriate
immune-mediated attack on the central nervous system (CNS). Type-1 helper
(Th1) cells specific for CNS antigens induce the disease and the Th1
cytokines interferon (IFN)-y and tumor necrosis factor (TNF)-.alpha. are
associated with EAE in mice (Holda and Swanborg, 1982; Powell, et al.,
1990). Conversely, type-2 helper (Th2) cells and other cell types which
produce interleukin (IL)-4 and transforming growth factor (TGF)-.beta.1 in
response to CNS antigens are known to ameliorate EAE. In vivo
1,25-(OH).sub.2D.sub.3 treatments result in a net loss in the total number
of lymphocytes and a net increase in the expression of IL-4 and TGF-.beta.1
(Cantorna, et al., 1998b). Conversely the in vivo 1,25- treatments had no
effect on IFN-.gamma. or TNF-.alpha. expression (Cantorna, et al., 1998b).
The role, if any, for calcium in the regulation of the immune response
remains unclear.
The present invention is a method of more effectively treating multiple
sclerosis patients. The method comprises the step of administration of an
amount of calcium that renders a vitamin D compound effective in preventing
or markedly reducing MS symptoms. Preferably, this amount of calcium is
0.5-2 g per patient per day. Most preferably, the amount is between 1 and 2
g of calcium as a salt with a variety of anions, e.g. Co.sub.B.sup.=,
PO.sub.4.sup.=, Cl.sub.2.sup.- acetate, gluconate, citrate, etc.
David SH
it say who was trying to patent it?
And how the devil did you find that anyway?
Rgds
"John Sykes Fletcher" <harvest%20this@%20abuse%40localhost%20.com> wrote in
message news:jUuz8.2660$2N4.4...@news02.tsnz.net...
John Sykes Fletcher
"David SH" <whitepjsR...@aol.com> wrote in message
news:aamblb$it8$1...@news7.svr.pol.co.uk...
> How can you patent a calcium supplement?
It's only an application ... I personally doubt that you can but who knows
http://appft1.uspto.gov/netacgi/nph-Parser?TERM1=20020016313&Sect1=PTO1&Sect
2=HITOFF&d=PG01&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.html&r=0&f=S&l=50
> Did
> it say who was trying to patent it?
DELUCA, HECTOR F. ; et al.
Department of Biochemistry, University of Wisconsin-Madison, Madison,
Wisconsin
He's done a lot of research into Vitamin D and autoimmunity
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=Display&DB=PubMed
Guess he decided not to publish the results from this study and patent them
instead.
> And how the devil did you find that anyway?
:-)
All the best
John
Nick Topolnyski
Quite the contrary, Vieth promotes taking plenty of vitamin D (4,000 IU/d)
and with 800 mg/d each of calcium and magnesium in order for a therapeutic
level to be attained. The reason for taking vitamin D, magnesium and calcium
together is because each other functions best in the body whilst in the
presence of one another (synergy).
Here is more information on MS and vitamin D3.
1. In 1988 Webb et al determined that an individual in Edmonton derives no
vitamin D3 from the sun from mid-October through to mid-April. Edmonton is
in Alberta, Canada. Alberta has an MS prevalence of 300 per 100,000 people.
See
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=2839537&dopt=Abstract
2. In 1999, University of Toronto researcher Reinhold Vieth published a
seminal paper indicating humans require dramatically more (ten to twenty
times) vitamin D3 than the commonly recommended amount. See
http://www.direct-ms.org/articles/VitaminDSupplementation.pdf
3. In 2000, DIRECT-MS researcher Ashton Embry published data providing solid
support for the role of vitamin D in seasonal fluctuations in MS disease
activity. See http://www.direct-ms.org/seasonal.html
4. In 2000, Embry published a paper collecting previous medical experiments
demonstrating immune-regulating actions for vitamin D hormone. See
http://www.direct-ms.org/vitamind.html
5. Again in 2000, Embry et al identified vitamin D3 supply as the only
reasonable explanation for the large variations in the prevalence of MS in
British and Irish immigrants to Australia which Hammond et al. (2000)
documented. See http://www.direct-ms.org/british.html
6. Also in 2000, Hayes et al published evidence indicating that vitamin D
may be a natural inhibitor of MS by virtue of experiments with autoimmune
encephalomyelitis (EAE), an animal model of MS. Hayes et al completely
inhibited EAE induction and progression with treatment of vitamin D hormone.
See http://www.direct-ms.org/articles/VitaminDInhibitorOfMS.pdf
7. In 2001, Dosch et al from the U of T released an analysis concluding that
MS and juvenile diabetes are virtually identical disease processes except
for their end result and that dairy is a risk factor for diabetes and
possibly for MS. See http://www.Direct-MS.org/articles/IDDMandMS.pdf
8. Also 2001, van der Mei et al demonstrated that the regional variation in
MS prevalence in the continent of Australia could be closely predicted (with
a 95 % degree of confidence) by variations in regional ultraviolet radiation
levels (ie vitamin D supply). This contribution can be regarded as smoking
gun evidence that adequate vitamin D can prevent MS onset in most, if not
all cases. See http://www.direct-ms.org/articles/australia-uv.pdf
9. Again in 2001, Elenkov et al found that women in their third trimester of
pregnancy had serum levels of 1,25-dihydroxyvitamin (the vitamin D3 hormone)
2- to 3-fold higher than postpartum values. In light of the
immunosuppressive characteristics of vitamin D3, this finding is supportive
of clinical observations that multiple sclerosis sufferers frequently remit
during pregnancy but exacerbate, or have their onset, in the postpartum
period. See
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMe
d&list_uids=11600565&dopt=Abstract
10. In November 2001, Hypponen et al published their findings that increased
dietary vitamin D is associated with reduced risk of type 1 diabetes and
ensuring adequate vitamin D supplementation for infants could help to
reverse the increasing trend in the incidence of type 1 diabetes. See
http://neuro-mancer.mgh.harvard.edu/ubb/Forum215/HTML/010777.html
Cheers
Nick
ed hill
i don't think calcium has a role in the immune modulation of 1,25 D3.
and if you read down that's pretty much what's said in the transcript.
>>| The role, if any, for calcium in the regulation of the immune response
>>| remains unclear.
the VDR or Vitamin D Receptors invo;ved in immune function are found mostly in
the cell nucleus and nearly always require that 1,25D3 be mated to a retinoid
molecule before joining and becomming active in triggering a VDTE or
Vitamin D Transcription Element. which is actually a region on the cellular DNA
that upon encountering an occupied VDR starts the process of transcribing a
region of the DNA "downstream" into RNA on the way to being expressed as a protein
or protieins.
the calcium issue is another whole ball of wax that seems pretty much unrelated.
that generally happens in the serum, not within the cells.
best regards
ed
"David SH" <whitepjsR...@aol.com> writes:
>Rgds
--
-----------------------------------------------------------------------
"The whole business of his life was in the plunder of his gaze..."
Daniel Halevy on Degas
| <include>ed's 3d stuff | http://world.std.com/~ehill | 617-629-4625 |
ed hill
what i refer to as a VDTE "vitamin d transcriptional element"
is actually called a VDRE "vitamin d response element'.
as i said the VDRE is a transcriptional response element.
it's a region on the cellular DNA that upon encountering
an activated VDR starts the transcriptional process.
VDR's are most often linked to a retinoid receptor or RXR.
this assemblage of two different receptors is called a
VDR-RXR heterodimer.
in cases where an VDR joins another VDR that's a homodimer.
either way both sides of the receptor molecule must be
occupied by their subtrate to activate the VDRE.
now
aren't you glad you asked?
regards
ed
ok....so you didn't ask....
John Sykes Fletcher
> >i don't think calcium has a role in the immune modulation of 1,25 D3.
Neither do I. Just looks like it clears the path somehow for Vitamin D to be
more effective. Interesting also that this therapy (Vitamin D + Calcium) is
one of the few approved ones for RA?
Just started B12 + Vitamin D + Calcium + Evening Primrose oil and arguably
feeling slightly more energetic / brighter. Might also be because of some
marked success I'm having with a pinhole camera contemporary art project
I've been theorising about.
Cholestrol levels also a borderline high 5.7 mmol/L and apparently this is
common with auto-immune diseases. I can do little to modify it though as my
diet is very good for low Cholestrol ... bar a few slices of cake with eggs
in a week :'-(.
Are you on minocycline? If so how is it?
All the best
John
David SH
Rgds
"John Sykes Fletcher" <harvest%20this@%20abuse%40localhost%20.com> wrote in
message news:B54A8.3022$2N4.5...@news02.tsnz.net...
John Sykes Fletcher
Blackmores BIO Calcium: Calcium Phosphate 570mg, Calcium Hydrogen Phosphate
600mg, Vitamin D3 (Colecalciferol 2.5mcg)
Blackmores Cod Liver Oil: Vitamin A 275mg, Vitamin D3 (Colecalciferol 1.45
mcg)
Rationale (both) : The patent discussed here.
Blackmores B12: Vitamin B12 (cyanocolbalamin) 50 mcg
Rationale : Dr Patrick Kingsley gives v high doses of this as part of his
treatment, help fatigue and nerve repair.
Natures Own Evening Primrose Oil: Gamma Linolenic Acid 100mg
Rationale : Mother swears by the stuff for her psoriasis
Blackmores E: Vitamin E (d-alpha-Tocopherol 168mg)
Rationale : General antioxidant and shown to enhance longevity
My partner reckons she has seen some improvement in youthfulness since
starting these and I arguably feel better. Time will tell though.
All the best
John
"David SH" <whitepjsR...@aol.com> wrote in message
news:aar6pt$fgl$1...@newsg4.svr.pol.co.uk...
John Sykes Fletcher
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=11726533&dopt=Abstract
Vitamin D: its role and uses in immunology.
Deluca HF, Cantorna MT.
Department of Biochemistry, University of Wisconsin-Madison, Madison,
Wisconsin 53706, USA. del...@biochem.wisc.edu
In recent years there has been an effort to understand possible noncalcemic
roles of vitamin D, including its role in the immune system and, in
particular, on T cell-medicated immunity. Vitamin D receptor is found in
significant concentrations in the T lymphocyte and macrophage populations.
However, its highest concentration is in the immature immune cells of the
thymus and the mature CD-8 T lymphocytes. The significant role of vitamin D
compounds as selective immunosuppressants is illustrated by their ability to
either prevent or markedly suppress animal models of autoimmune disease.
Results show that 1,25-dihydroxyvitamin D3 can either prevent or markedly
suppress experimental autoimmune encephalomyelitis, rheumatoid arthritis,
systemic lupus erythematosus, type I diabetes, and inflammatory bowel
disease. In almost every case, the action of the vitamin D hormone requires
that the animals be maintained on a normal or high calcium diet. Possible
mechanisms of suppression of these autoimmune disorders by the vitamin D
hormone have been presented. The vitamin D hormone stimulates transforming
growth factor TGFbeta-1 and interleukin 4 (IL-4) production, which in turn
may suppress inflammatory T cell activity. In support of this, the vitamin D
hormone is unable to suppress a murine model of the human disease multiple
sclerosis in IL-4-deficient mice. The results suggest an important role for
vitamin D in autoimmune disorders and provide a fertile and interesting area
of research that may yield important new therapies.
Publication Types:
Review
Review, Tutorial
PMID: 11726533 [PubMed - indexed for MEDLINE]
John Sykes Fletcher
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=3537648&dopt=Abstract
Multiple sclerosis: decreased relapse rate through dietary supplementation
with calcium, magnesium and vitamin D.
Goldberg P, Fleming MC, Picard EH.
A group of young patients having multiple sclerosis was treated with dietary
supplements containing calcium, magnesium and vitamin D for a period of one
to two years. The experimental design employed self-pairing: the response of
each patient was compared with his/her own case history as control. The
number of exacerbations observed during the program was less than one half
the number expected from case histories. No side effects were apparent. The
dietary regimen may offer a new means of controlling the exacerbation rate
in MS, at least for younger patients. The results tend to support a theory
of MS which states that calcium and magnesium are important in the
development, structure and stability of myelin.
Publication Types:
Clinical Trial
PMID: 3537648 [PubMed - indexed for MEDLINE]
Mona
--
Laura
So ignore the 90% of the studies that conclude otherwise and boom,
pee brain is correct.
"John Sykes Fletcher" <harvest%20this@%20abuse%40localhost%20.com>
wrote in message news:VbiA8.152$A07....@news02.tsnz.net...
John Sykes Fletcher
"Mona" <thehap...@yahoo.co.uk> wrote in message
news:aasdvi$d5r7s$1...@ID-95032.news.dfncis.de...
> um..anything more current? This is 15 years old.
Sad isn't it? Just like Copaxone was discovered in 1974 and nothing was done
about it for 20 years.
All the best
John
Nick Topolnyski
See my post of may 1 for recent research regarding vit D and MS.
N
"Mona" <thehap...@yahoo.co.uk> wrote in message
news:aasdvi$d5r7s$1...@ID-95032.news.dfncis.de...
John Sykes Fletcher
All the best
John
DISCUSSION
The effects of dietary calcium and 1,25-(OH).sub.2D.sub.3 are critically
linked for the prevention of EAE in mice. When mice are fed a diet
containing high calcium (approaching that found in nonpurified diets),
1,25-(OH).sub.2D.sub.3 at appropriate doses is 100% effective in preventing
EAE. In contrast, if calcium is removed from the diet,
1,25-(OH).sub.2D.sub.3 reduced the incidence of EAE by only 50%. When an
intermediary level of calcium is fed, the effectiveness of
1,25-(OH).sub.2D.sub.3 is intermediate between low calcium and a high
calcium diet. These results argue strongly that calcium is involved in the
action of 1,25-(OH).sub.2D.sub.3 in the prevention and treatment of this
autoimmune disease (Holda and Swanborg, 1982; Powell, et al., 1990).
It is of some interest that in mice given a low calcium diet, doses of
1,25-(OH).sub.2D.sub.3 that nevertheless produce frank hypercalcemia, show
little or no further reduction in the incidence of EAE. Thus, in the absence
of a dietary source of calcium 1,25-(OH).sub.2D.sub.3 mediated increases in
serum calcium are ineffective for the further suppression of EAE. On the
other hand, there are doses of 1,25-(OH).sub.2D.sub.3 that do not cause
hypercalcemia but that nevertheless reduce the incidence of EAE. Overall,
our results argue that the 1,25-(OH).sub.2D.sub.3 may function by both
calcium dependent and calcium independent mechanisms to suppress EAE.
Manipulating only dietary calcium had no effect on the immune response to
EAE. The total cell number in the LN of mice with EAE was inversely related
to the amount of dietary calcium fed in the 1,25-(OH).sub.2D.sub.3 treated
mice. Similarly, thymic atrophy resulted as a consequence of
1,25-(OH).sub.2D.sub.3 induced hypercalcemia (Mohamed, et al., 1996). The
decreased cell number in the LN may be due to 1,25-(OH).sub.2D.sub.3 induced
decreases in cell expansion or increases in cell death. IL-4 was increased,
but not TGF-.beta.1, relative to the amount of calcium fed. In the absence
of added dietary calcium, 1,25-(OH).sub.2D.sub.3 had no effect on IL-4
expression. 1,25-(OH).sub.2D.sub.3 and calcium may actually be selectively
inhibiting the differentiation and/or expression of cells that do not make
IL-4. The result would seem to be an increase in IL-4 expression. Therefore,
it is possible that IL-4 expression has not changed but instead the
proportion of cells making IL-4 has increased. Conversely, TGF-.beta.1
increased in response to 1,25-(OH).sub.2D.sub.3 regardless of dietary
calcium. This finding is consistent with our previous work suggesting
TGF-.beta.1 gene expression is directly regulated by 1,25-(OH).sub.2D.sub.3
(Cantorna, et al., 1998b). Calcium is an important intracellular messenger,
but how dietary calcium might affect intracellular calcium is unknown. More
work is needed to understand the relationship of 1,25-(OH).sub.2D.sub.3 and
calcium as immune system regulators.
We note that low dietary calcium reduces the incidence of EAE, while at the
same time it reduces the effectiveness of 1,25-(OH).sub.2D.sub.3 in
preventing EAE. The animals used in these experiments are not vitamin D
depleted and thus contain stores of vitamin D and 25-hydroxyvitamin D. It is
well known that low dietary calcium markedly stimulates the production of
1,25-(OH).sub.2D.sub.3 (DeLuca, 1983). This endogenously produced hormone
may well play a role in reducing the incidence of EAE. On the other hand, it
is clear that even large doses of 1,25-(OH).sub.2D.sub.3 cannot completely
prevent EAE in these mice. Low dietary calcium must, therefore, play more
than one role.
Reinhold Vieth
> Vieth promotes taking plenty of vitamin D (4,000 IU/d)
> and with 800 mg/d each of calcium and magnesium in order for a therapeutic
> level to be attained.
Nick, I have no major disagreement about practically all that you
wrote in the preceding posting. However, I am sure you must have
gotten the wording wrong about atribution to me anything about
magnesium. I concentrate on vitamin D alone in my science, and make a
point of remaining silent about calcium and magnesium.
You misphrased it, and I just want to keep the record straight.
Best wishes,
Reinhold
John Sykes Fletcher
"Reinhold Vieth" <reinhol...@utoronto.ca> wrote in message
news:22ca11f.02050...@posting.google.com...
Hi
What do you think of the Calcium, Vitamin D idea?
All the best
John
Reinhold Vieth
Since I don't know what the details of the patent are, there is no
reasonable way to comment.
A speculation: DeLuca's MS work has so far all focused on a mouse
model of MS, and ways to use his patented analogs of the hormone
derived from vitamin D -- he never actually uses vitamin D, the
nutrient! Thus, there is no way the mouse work could be mimicked by
someone without access to his magic molecules. We'll have to await
details of his clinical trials; however, to this point, that hormone
derived from vitamin D ( 1,25(OH)2D, and its analogs ) has always been
used with special precautions to AVOID calcium.
The epidemiologic data still points to plain and simple "nutrition"
i.e. vitamin D3 itself as the most likely MS preventive agent. The
evidence in real people does NOT point me toward use of any other
molecule. If it were me, I would stick to vitamin D3, and if DeLuca's
patent seems to inspire you, add calcium supplements or whatever you
wish, it will do no harm if you stick to the nutrients, and avoid the
hormone (which you can't get anyway).
Best wishes,
Reinhold
Jim Carter
>A speculation: DeLuca's MS work has so far all focused on a mouse
>model of MS, and ways to use his patented analogs of the hormone
>derived from vitamin D
A further speculation: DeLuca owns the patents on the analogs. If his trials
with a certain analog show improvement, DeLuca benefits financially.
John Sykes Fletcher
discovery in his trial was not further investigated. It seems his work was
taken over by researchers interested in polyunsaturated lipids which failed
to show any benefit.
Goldberg also speculated upon the reason why the highest rates of MS are in
communities with high oat consumption or high phytate consumption in
addition to northern latitudes. Phytates bind with calcium and are
antagonistic to vitamin D. In Northern Scotland where the MS rates are the
highest in the world, both oats, low seafood diets, and lack of sunshine
combine to produce the perfect environment for MS.
Unfortunately, no dietary studies were tried using cod liver oil and
avoidance of phytates for those subject to MS to test Dr. Goldberg's theory
that dietary changes might help new creation of myelin by the addition of
calcium-magnesium, and fish or fish oil sources of vitamin D, with their
omega 3's or linoleic acids, to see to what extent damaged myelin might be
rebuilt and repaired.
Apparently the coastal Norwegians consumed the equivalent of about 1300 IU
of vitamin D3 daily, about 3-fold higher than individuals living in inland
(Goldberg 1974a). In his small clinical trial in 1974 MS patients ingested
cod liver oil (20 g/day; 5000 IU/day of vitamin D), along with calcium and
magnesium supplements. This reportedly lowered their rate of exacerbations
(Goldberg et al. 1986). This trials involved very few subjects and had other
methodological shortcomings. The experimental design employed self-pairing:
the response of each patient was compared with his/her own case history as
control. Never the less the number of exacerbations observed during the
program was less than one half the number expected from case histories. No
side effects were apparent.
Dosage was estimated between the 3800 IU/day that Goldberg calculated might
prevent MS (Goldberg 1974b), and the 5000 IU/day that was given in the small
clinical trial of fish oil (Goldberg et al. 1986). Very high doses of
vitamin D can cause hypercalcemia, which is potentially fatal. Accordingly,
a tolerable safe upper limit for vitamin D supplementation has been set at
2000 IU/day for age >1, and 1000 IU/day for age <1 (Holick 1998). However,
the panel that established this limit overlooked information indicating that
the safe upper limit is actually much higher. Adults living or working in
sunny environments easily generate >10,000 IU/day of vitamin D through sun
exposure without adverse effects, so the safe upper limit for total vitamin
D nutrition is at least 10,000 IU/day (Vieth 1999). Moreover, all documented
cases of vitamin D toxicity with hypercalcemia involved intakes >40,000
IU/day (Vieth 1999). Thus, the 4000 IU/day needed by an adult without sun
exposure to maintain serum 25-hydroxyvitamin D3~100 nmol/L would be safe,
since it is well below the 10,000 IU/day generated by adults living or
working in sunny environments
Goldberg was responsible also for finding that neurological disease doesn't
exist at the equator (International Journal of Environmental Studies). There
sunshine produces 2 to 4 thousand IUs of vitamin D per day in contrast to
the 400 IUs of the official Recommended Dietary Allowance. Nor is the risk
of MS high at high altitudes. High altitude above 1000 feet intensifies
ultra violet exposure and reduces MS risk. Multiple Sclerosis begins to
develop as human populations move away from the most intense sunlight.
Fascinatingly also he discovered that on the Shetland and Orkney islands,
multiple sclerosis rates are among the highest in the world, much higher
than the 1 in 1000 people who are subject to the disease in northern
latitudes or smog polluted cities elsewhere. On the Faeroe Islands with
exactly the same sunlight, dampness, overcast, and gloom, less than normal
incidence of MS exists. What accounts for the difference? On Faeroe Islands,
seafood is abundant; on the other, it is virtually non-existent in the diet.
Does anybody have any more information?
All the best
John
Goldberg P. (1974a) Multiple sclerosis: Vitamin D and calcium as
environmental determinants of prevalence (A viewpoint). Part 1: Sunlight,
dietary factors and epidemiology. International Journal of Environmental
Studies 6, 19-27.
Goldberg P. (1974b) Multiple sclerosis: Vitamin D and calcium as
environmental determinants of prevalence (A viewpoint). Part 2: Biochemical
and Genetic Factors. International Journal of Environmental Studies 6,
121-129. Goldberg, P. Fleming M. C., & Picard E. M. (1986) Multiple
sclerosis: decreased relapse rate through dietary supplementation with
calcium, magnesium, and vitamin D. Medical Hypotheses 21, 193-200
"Jim Carter" <jimc...@gmx.net> wrote in message
news:nstcdu4stfqvatu3i...@4ax.com...
Nick Topolnyski
redundant...
1. In 1986 Goldberg et al treated a group of young patients having multiple
sclerosis with dietary supplements containing calcium, magnesium and vitamin
D for a period of one to two years. The number of exacerbations observed
during the program was less than one half the number expected from case
histories. See
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=3537648&dopt=Abstract
2. In 1988 Webb et al determined that an individual in Edmonton derives no
vitamin D3 from the sun from mid-October through to mid-April.
3. In 1999, University of Toronto researcher Reinhold Vieth published a
seminal paper indicating humans require dramatically more (ten to twenty
times) vitamin D3 than the commonly recommended amount. See
http://www.direct-ms.org/articles/VitaminDSupplementation.pdf
4. In 2000, DIRECT-MS researcher Ashton Embry published data providing solid
support for the role of vitamin D in seasonal fluctuations in MS disease
activity. See http://www.direct-ms.org/seasonal.html
5. Also 2000, Embry et al identify vitamin D3 supply as the only reasonable
explanation for the large variations in the prevalence of MS in British and
Irish immigrants to Australia which Hammond et al. (2000) documented. See
http://www.direct-ms.org/british.html
6. Again in 2000, Embry writes an essay combining scientific evidence which
supports the concept that vitamin D likely plays an important role in
controlling autoimmunity and MS. Such evidence consists of epidemiological
data, animal experiments, immunological analyses, genetics and the results
of small clinical trials which used vitamin D or a metabolite as the
therapeutic agent. See http://www.direct-ms.org/vitamind.html
7. In 2001, Dosch et al from the U of T release an analysis concluding that
MS and juvenile diabetes are virtually identical disease processes except
for their end result and that dairy is a risk factor for diabetes and
possibly for MS. See http://www.Direct-MS.org/articles/IDDMandMS.pdf
8. Again in 2000, Hayes publishes evidence indicating that vitamin D may be
a natural inhibitor of MS by virtue of experiments with autoimmune
encephalomyelitis (EAE), an animal model of MS. Hayes completely inhibited
EAE induction and progression with treatment of vitamin D hormone. See
http://www.direct-ms.org/articles/VitaminDInhibitorOfMS.pdf
9. In 2001, van der Mei et al demonstrated that the regional variation in MS
prevalence in the continent of Australia could be closely predicted (with a
95 % degree of confidence) by variations in regional ultraviolet radiation
levels (i.e. vitamin D supply). This contribution can be regarded as smoking
gun evidence that adequate vitamin D can prevent MS onset in most, if not
all, cases. See http://www.direct-ms.org/articles/australia-uv.pdf and
below.
10. Also in 2001, Elenkov et al found that women in their third trimester of
pregnancy had serum levels of 1,25-dihydroxyvitamin (the vitamin D3 hormone)
2- to 3-fold higher than postpartum values. In light of the
immunosuppressive characteristics of vitamin D3, this finding is supportive
of clinical observations that multiple sclerosis sufferers frequently remit
during pregnancy but exacerbate, or have their onset, in the postpartum
period. See
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list
_uids=11600565&dopt=Abstract
11. In November 2001, Hyppönen et al published their findings that increased
dietary vitamin D is associated with reduced risk of type 1 diabetes and
ensuring adequate vitamin D supplementation for infants could help to
reverse the increasing trend in the incidence of type 1 diabetes. See
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=11705562&dopt=Abstract
It would thus appear that Canada has the highest rates of MS (Alberta = 300
per 100,000) as well as juvenile diabetes in the world because of its high
latitude position and a consequent very low vitamin D supply and a chronic
gluten and dairy consumption( http://www.direct-ms.org/nutritional.html ).
This weekend of April 6 & 7 saw the MS Society of Canada bring together the
world's leading researchers, including Ashton Embry of DIRECT-MS, of vitamin
D3 (the sunshine vitamin) and MS for a conference. One of the concepts
arising from this conference was that vitamin D is probably most effective
as a preventative measure. It appears that once the disease is active, that
getting sufficient vitamin D3 might not completely suppress the disease
process.
Thus eliminating the http://www.direct-ms.org/nutritional.html]causal
factors (dietary proteins in DIRECT-MS' opinion) and getting sufficient
vitamin D3 (4,000 IU/d) are necessary for the best possible therapy.
As a result of this recent collaboration in Toronto, a trial involving
vitamin D3 supplementation in high-risk candidates (i.e. offspring of people
with MS) will be conducted by the MSSC. There is no information regarding
this on their site likely because this occurred very recently.
Cheers
Nick
"John Sykes Fletcher" <harvest%20this@%20abuse%40localhost%20.com> wrote in
message news:uSBB8.992$A07.1...@news02.tsnz.net...
Pauline
| Fascinatingly also he discovered that on the Shetland and
| Orkney islands, multiple sclerosis rates are among the
| highest in the world, much higher than the 1 in 1000
| people who are subject to the disease in northern
| latitudes or smog polluted cities elsewhere. On the Faeroe
| Islands with exactly the same sunlight, dampness,
| overcast, and gloom, less than normal incidence of MS
| exists. What accounts for the difference? On Faeroe
| Islands, seafood is abundant; on the other, it is
| virtually non-existent in the diet.
In reference to the above, I have just read a short article
about the high & increasing incidence of MS in Sicily:
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
**"Studies of the distribution of MS in different pops. have
shown that MS is more common in northern areas.
Therefore many regions in the Med. would be expected
to have low incidence of the condition. However, 2
large Med. islands, Sicily & Sardinia, have unexpectedly
high levels of MS.
The 1st survey to show this unusual pattern was carried
out 25 yrs ago in the town of Enna, Sicily. The overall
pop. of Enna remained stable in the 20 yrs from 1975
to 1995. The level of public medicare is high with a
neurology unit & other similar services available. In 1995,
a follow up study was performed to assess whether MS
levels were still high.
Various strategies were employed to identify pwMS.
People dx in the past were reappraised, contacts were
made with all the GPs and neuros & the study was
advertised through local TV. The local Italian MS assoc.
was involved, as were all rehab & other relevant centres.
The study found an incidence of 120.2 per 100,000 pop.
(a rise from 53 in 1975) & a rate of 5.7 cases per 100,000
pop. per yr (from 1986-1995). These are among the
highest numbers found in the Med. area, second only
to Sardinia, and level with N. European countries. They
indicate that MS is still increasing.
It is unknown what this increase is relevant to. It could
be due to environmental or socio-economic changes. The
research points out that dx has always been efficient, &
even though the dxstic procedure has improved, this alone
cannot account for the increases observed. Genetic
predisposition may play a role....Enna was one of the major
areas to be taken over by Vikings and according to the
'Viking hypothesis', the global distribution of MS may be
attributed to the spread of northern European susceptibility
genes."
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
The Shetland & Orkney Isles, being much closer to the
Viking source, would appear to also apply to the
'Viking hypothesis'. Scotland may also apply and
Canada where many Scots went after the 'clearances'.
I am in the UK & of Scottish descent.
There is also evidence that the Vikings discovered
the American continent centuries before Columbus.
Take care,
Pauline
**published in Neurology, Dec 2001, vol 57, pp 1891-1893.