Anyway, there were enough points that hit home, and the cost of Vitamin D3
is very low, so I thought I'd give it a try. I'm concerned about the
toxicity of the high dose, although the report recommended a level that it
said shouldn't be a problem.
Have any of you more experienced/educated cynics out there tried this
before? Any warnings? Just low cost snake oil or worth a try?
TIA
Dawn LaFrance
Please clarify what you mean by high dose. Toxcity of what? Vit d3 or what
is with it??
Jack
I wouldn't. Vitamins, like any substance on earth, are toxic in too high of
doses. I've had MS for 10 yrs (that I know of), & have never gotten back any
test results that showed I had a vitamin deficiency.
There are people who have written on the effectiveness of vitamins, diet,
magnets, bee stings, & all sorts of things as being "miraculous" in
treating - even curing - MS. As far as I see it, if it wasn't the subject of
a multi-site double-blind study, & if the results are not reproducable in
other studies, it's not anything I'd waste my time or buckage on.
Just my opinion....
Lin
The recommendation in Ashton Embry's article
(www.direct-ms.org/vitamind.html) is 4000 IU per day of Vitamin D3, along
with increased amounts of calcium & magnesium so the Vitamin D3 works
properly. These levels are far above suggested daily intake from the
Canadian government. Excessive Vitamin D in the system can cause various
problems, such as kidney problems, as it is not flushed through the system,
but accumulates.
Dawn LaFrance
"jack n dalton" <jda...@ix.netcom.com> wrote in message
news:9tv823$k01$1...@slb4.atl.mindspring.net...
Jack
P.S. I included additional studies for those who like to connect the dots.
P.S. I take SOLGAR TWO(2) 1000 IU caps Vit D3 (Cholecalciferol) which
together has 6000 IU of Vit A total.
Study points to positive results from vitamin D supplements for MS sufferers
Public release date: 2-Apr-2001
Study points to positive results from vitamin D supplements for MS sufferers
University Park, Pa. --- A small study conducted by researchers at Penn
State
and Helen Hayes Hospital in New York has shown that a daily dose of vitamin
D -
1000 IU or two and a half times the recommended dose for adults -- causes
changes in blood chemistry that indicate positive effects for multiple
sclerosis
patients.
Dr. Margherita Cantorna, assistant professor of nutrition, says the study
has
not been in progress long enough to observe changes in the clinical symptoms
of
the disease in the patients who participated. However, blood samples drawn
after
just 6 months of Vitamin D supplementation, show an increase in transforming
growth factor beta-1 (TGF-Beta) which is associated with the remission and
suppression of the immune response which produces symptoms in MS patients.
In
addition, the researchers found a decrease in interleuken-2 which is
associated
with the cells that induce MS.
Cantorna's student, Brett Mahon, a doctoral candidate in nutrition, detailed
the
study results today (April 3) at the Experimental Biology 2001 conference in
Orlando, Fla. The paper, "Altered Cytokine Profile in Patients with Multiple
Sclerosis Following Vitamin D Supplementation," is co-authored by Dr.
Felicia
Cosman, medical director, Clinical Research Center, S. A. Gordon and J.
Cruz,
all of Helen Hayes Hospital, and Cantorna. Mahon is first author.
As a postdoctoral fellow at the University of Wisconsin, Madison, Cantorna
and
others had shown, in experiments with mice, that vitamin D supplementation
could
completely prevent the development of MS in susceptible animals. After
Cantorna
joined the faculty at Penn State, she learned of Dr. Cosman's research
program
which centers on investigating whether a low level vitamin D deficiency in
MS
patients might account for the incidence of brittle bones.
Cantorna asked Cosman for blood samples from the participating patients to
see
if the same changes she had observed in mice also occur in humans who
receive
vitamin D supplementation. She found that the results were, in fact, similar
at
the blood chemistry level. Multiple sclerosis is an autoimmune disease in
which
the victim's own immune system attacks the spinal cord and brain. The
disease
afflicts about 350,000 people in the United States alone and its cause is
thought to be a complex interaction of genetics and environmental forces
that
are not completely understood.
Cantorna and others hypothesize that one crucial environmental factor
involved
in the development of the disease is the amount of sunlight a person
receives.
Exposure to sunlight catalyzes the production of vitamin D in the skin. In
low
sunlight, the skin produces significantly less vitamin D.
In support of a connection among sunlight, vitamin D and multiple sclerosis,
Cantorna points out that the incidence of the disease is nearly zero near
the
equator and increases with latitude in both hemispheres. In addition,
Switzerland has high MS rates at low altitudes and low MS rates at high
altitudes. Ultraviolet light is more intense at higher altitudes, resulting
in
the skin manufacturing more vitamin D.
Other evidence of an MS/vitamin D link comes from Norway where MS rates are
higher inland than on the coast where larger quantities of fish are consumed
which are rich in vitamin D.
While Cantorna's research and MS's geographical distribution suggest a
connection between vitamin D and MS, she cautions that the vitamin's exact
role
is still unclear.
"I think that if you are an MS patient, it would be best to continue to
follow
your personal physician's advice," says the College of Health and Human
Development faculty member. Since vitamin D can be toxic in high doses, it
would
not be a good idea to begin taking vitamin D pills available
over-the-counter in
large amounts.
"On the other hand, since adequate amounts of vitamin D are difficult to get
from diet and because MS patients often have to stay out of the sun, you
might
want to consider taking a vitamin D supplement at the current recommended
daily
requirement level. There are potential benefits for bone health and for the
immune system as well."
The project was supported by two grants from the National Multiple Sclerosis
Foundation
Vitamin D3 AbstractVitamin D3 reduces the apoptotic effect of IFN-but does
not
facilitate HLA
class II inducibility in RB-defective cells.
B. Schmidt, S. S. Carter, D.E. Berry, and G. Blanck.
1996. in press, Cancer Letters.
The retinoblastoma protein (RB) regulates the cell cycle by binding and
inactivating the E2F transcription factors, which prevents transcription of
genes required for DNA synthesis. RB has been shown to inhibit
IFN-gamma-mediated apoptosis, possibly by regulating premature entry into S
phase. RB is also required for high level IFN-gamma induction of HLA class
II
genes, which encode antigen presenting molecules, but not for other
IFN-gamma
inducible genes as demonstrated in previous reports describing the analysis
of
RB-transformants of the RB-defective cell lines, MDA-468-S4(S4) and H2009.
The
IFN-gamma response of the HLA class II genes takes much longer than does the
response of other the other IFN-gamma inducible genes, raising the question
of
whether RB facilitates HLA class II inducibility by maintaining cell
viability
over the long time course required for HLA class II induction. Thus, we
sought
to learn whether IFN-gamma induced apoptosis in an RB-defective cell line
could
be prevented independently of RB and whether doing so would facilitate HLA
class
II inducibility in the RB-defective line. Our results indicated that
cotreating
the RB-defective S4 cells with IFN-gamma and Vitamin D3 decreased the number
of
cells containing subdiploid DNA compared to cells treated with IFN-gamma
alone,
suggesting that Vitamin D3 reduced IFN-gamma-mediated apoptosis. S4 cells
cotreated with Vitamin D3 and IFN-gamma also had decreased cell detachment,
further indicating that Vitamin D3 decreased IFN-gamma induced apoptosis.
However, Vitamin D3 cotreatment resulted in no detectable increase in
HLA-DR,
the most prominent HLA class II molecule, indicating that the effect of RB
on
HLA class II induction is not exclusively due to its ability to inhibit
IFN-gamma induced apoptosis.
Copyright (c) 1996, George Blanck, Ph.D.
This page was designed by George Blanck, Aaron Osborne and Alex Sheppard
and is currently maintained by Aaron Osborne.
1: Expert Opin Investig Drugs 2000 Apr;9(4):747-64
Apoptosis modulators in the therapy of neurodegenerative diseases.
Deigner HP, Haberkorn U, Kinscherf R
Anatomy and Cell Biology III University of Heidelberg, Germany.
Apoptosis is a prerequisite to model the developing nervous system. However,
an
increased rate of cell death in the adult nervous system underlies
neurodegenerative disease and is a hallmark of multiple sclerosis (MS)
Alzheimer's- (AD), Parkinson- (PD), or Huntington's disease (HD). Cell
surface
receptors (e.g., CD95/APO-1/Fas; TNF receptor) and their ligands (CD95-L;
TNF)
as well as evolutionarily conserved mechanisms involving proteases,
mitochondrial factors (e.g. , Bcl-2-related proteins, reactive oxygen
species,
mitochondrial membrane potential, opening of the permeability transition
pore)
or p53 participate in the modulation and execution of cell death. Effectors
comprise oxidative stress, inflammatory processes, calcium toxicity and
survival
factor deficiency. Therapeutic agents are being developed to interfere with
these events, thus conferring the potential to be neuroprotective. In this
context, drugs with anti-oxidative properties, e.g., flupirtine,
N-acetylcysteine, idebenone, melatonin, but also novel dopamine agonists
(ropinirole and pramipexole) have been shown to protect neuronal cells from
apoptosis and thus have been suggested for treating neurodegenerative
disorders
like AD or PD. Other agents like non-steroidal anti-inflammatory drugs
(NSAIDs)
partly inhibit cyclooxygenase (COX) expression, as well as having a positive
influence on the clinical expression of AD. Distinct cytokines, growth
factors
and related drug candidates, e.g., nerve growth factor (NGF), or members of
the
transforming growth factor-beta (TGF-beta ) superfamily, like growth and
differentiation factor 5 (GDF-5), are shown to protect tyrosine hydroxylase
or
dopaminergic neurones from apoptosis. Furthermore, peptidergic cerebrolysin
has
been found to support the survival of neurones in vitro and in vivo.
Treatment
with protease inhibitors are suggested as potential targets to prevent DNA
fragmentation in dopaminergic neurones of PD patients. Finally, CRIB
(cellular
replacement by immunoisolatory biocapsule) is an auspicious gene
therapeutical
approach for human NGF secretion, which has been shown to protect
cholinergic
neurones from cell death when implanted in the brain. This review summarises
and
evaluates novel aspects of anti-apoptotic concepts and pharmacological
intervention including gene therapeutical approaches currently being
proposed or
utilised to treat neurodegenerative diseases.
Publication Types:
Review
Review, academic
PMID: 11060707
> "mdlafrance" <mdlaf...@home.com> wrote in message
> news:JRFM7.70094$Ud.33...@news1.rdc1.bc.home.com...
--
Best regards, Meg
www.livergood.net
"Lin" <kt...@woh.rr.com> wrote in message
news:%SFM7.68567$z55.8...@typhoon.neo.rr.com...
Thanks for the reply. Your position re the double blind studies, etc is
pretty much the stand I've taken over the last ten years also - despite the
insistance of my "alternative health" mother pushing every snake oil she
hears about at me.
In all my blood work I've never been told I had any deficiencies either -
except for severe anemia while on betaseron. But I don't know that they ever
tested for something as simple as Vitamin D either.
I guess because I feel like I'm on a slow, downward slope I was a bit more
open to looking into Vitamin D at this time. In doing a bit of research it
sounds like women should be increasing their intake as they age, expecially
if you don't get a lot of natural sunshine (not here on the wet coast
anyway - either too hot to be outside, or liquid sunshine only). Maybe I'll
increase the dosage slowly, as the study that Jack pointed out has shown a
lower amount may be beneficial, and it will only cost a couple of dollars
per month. (and that's Canadian dollars!)
Dawn
"Lin" <kt...@woh.rr.com> wrote in message
news:%SFM7.68567$z55.8...@typhoon.neo.rr.com...
Vitamin D is a perfectly reasonable and safe nutrient to take.
My lab has been looking into the safety of 4000 IU/day for several
years
and we have published results this year. There is discussion on
the issue of the safety limit for vitamin D located at this web
address:
http://www.ajcn.org/cgi/reprint/74/6/862
Consider some of the scientific rationale for vitamin D. Go to PubMed
at the following address, and type in "vitamin D and multiple
sclerosis"
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
Please consider: the double-blind randomized studies get done for
patented drugs. But for something without a patent, you really have
to
think the problem through. Without a profit potential at the end of
the research, there can be no private money to support the research.
Why should anybody bother to find out if nutritional vitamin D
does anything, when drug companies keep enticing physicians able to
look
into the problem... enticing them to take the free, effortless money
to
look into another drug.
Any physician wanting to consider vitamin D at NATURAL, physiological
doses
has to jump through many hoops:
1. the toxicity issue (grossly overblown for vitamin D - you are
worrying about taking 1000 to 4000 IU of it, when the absolute lowest
dose anyone has ever implicated as bad is 40,000 IU/day. That is a
ten-fold safety margin!)
2. the money issue, why bother with all the effort needed to
apply to a granting agency when drug company money is effortlessly
available
to the physician (I have nothing against drug companies, they do good
work,
but my point is, they do distract the focus into the things that just
might
be money-making products for themselves)
3. Where would the patients for such a study come from? Unlike some
new miracle drug that you couldn't get any other way than to take part
in a study, would study patients with MS not just opt to buy the
vitamin D themselves, and let somebody else figure out whether it
works?
If I were someone with MS, I would certainly take on anything that I
would consider to be a "no-lose proposition". Vitamin D is cheap!!,
safe, and
there is a lot of reason to think it will do good. Perhaps the
problem
is that the jury is still out whether it really does good. Imagine
how hard it is to do the appropriate research.
So there you have it, patented drugs will end up with the
placebo-controlled evidence (through no fault of any drug company,
since they are playing their role as they should). On the other hand,
something like vitamin D, which is natural, and stands just as good a
chance of being an answer in MS, falls by the wayside....... by
default.
Sadly, though, no-one will fund a multi-site double-blind study if the
results were to prescribe cheap-as-dirt D3 that doesn't lock you into an
ever-increasing spiral of additional, more expensive drugs to combat the
effects of the first one. What pharmaceutical company would sign up for
that ? And that's why it's never been done.
Is there anything else that might convince you (and me) of its efficacy ?
"Lin" <kt...@woh.rr.com> wrote in message
news:%SFM7.68567$z55.8...@typhoon.neo.rr.com...
But that's not entirely true. I posted this article a few months ago. It
is from the North American Research Committee on MS. I post it again:
Study Points to Positive
Results from Vitamin D
Supplements
A small study conducted by researchers at Penn State and Helen
Hayes Hospital in New York has shown that a daily dose of vitamin
D-1,000 IU, or two and a half times the recommended dose for
adults-causes changes in blood chemistry that indicate positive
effects for patients with MS.
Blood samples drawn after 6 months of vitamin D
supplementation show an increase in transforming growth factor
beta-1 (TGF-beta), which is associated with the remission and
in suppression of the immune response, which produces symptoms
in patients with MS. In addition, the researchers found a decrease in
interleukin-2, which is associated with the cells that induce MS.
It has previously been shown, in experiments with mice, that vitamin
D supplementation could completely prevent the development of MS
in susceptible animals.
Tbe hypothesis suggested by the investigators is that one crucial
environmental factor involved in the development of the disease is
the amount of sunlight a person receives. Exposure to sunlight
catalyzes the production of vitamin D in the skin. In low sunlight,
the skin produces significantly less vitamin D. In support
of a connection among sunlight, vitamin D, and MS,
they point out that the incidence of the disease is nearly
zero near the equator and increases with latitude in both
hemispheres. In addition, Switzerland has high MS rates
at low altitudes and low MS rates at high altitudes.
Ultraviolet light is more intense at higher altitudes,
resulting in the skin manufacturing more vitamin D.
Other evidence of an MS/vitamin D link comes from
Norway, where MS rates are higher inland than on
the coast where larger quantities of fish, which is rich in
vitamin D, are consumed.
However, although circumstantial evidence suggests a
connection between vitamin D and MS, researchers
caution that the vitamin's exact role is still unclear and that
high doses of the vitamin can be toxic. They urge patients with MS
to follow the advice of their personal physician.
(www-eurekalert.org).
1: Proc Soc Exp Biol Med 1997 Oct;216(1):21-7Related Articles,
Books, LinkOut
Vitamin D and multiple sclerosis.
Hayes CE, Cantorna MT, DeLuca HF.
Department of Biochemistry, University of Wisconsin-Madison 53706, USA.
Recently, it has been clearly demonstrated that exogenous
1,25-dihydroxyvitamin D3, the hormonal form of vitamin D3, can
completely prevent experimental autoimmune encephalomyelitis (EAE), a
widely accepted mouse model of human multiple sclerosis (MS). This
finding has focused attention on the possible relationship of this
disease to vitamin D. Although genetic traits certainly contribute to MS
susceptibility, an environmental factor is also clearly involved. It is
our hypothesis that one crucial environmental factor is the degree of
sunlight exposure catalyzing the production of vitamin D3 in skin, and,
further, that the hormonal form of vitamin D3 is a selective immune
system regulator inhibiting this autoimmune disease. Thus, under
low-sunlight conditions, insufficient vitamin D3 is produced, limiting
production of 1,25-dihydroxyvitamin D3, providing a risk for MS.
Although the evidence that vitamin D3 is a protective environmental
factor against MS is circumstantial, it is compelling. This theory can
explain the striking geographic distribution of MS, which is nearly zero
in equatorial regions and increases dramatically with latitude in both
hemispheres. It can also explain two peculiar geographic anomalies, one
in Switzerland with high MS rates at low altitudes and low MS rates at
high altitudes, and one in Norway with a high MS prevalence inland and a
lower MS prevalence along the coast. Ultraviolet (UV) light intensity is
higher at high altitudes, resulting in a greater vitamin D3 synthetic
rate, thereby accounting for low MS rates at higher altitudes. On the
Norwegian coast, fish is consumed at high rates and fish oils are rich
in vitamin D3. Further, experimental work on EAE provides strong support
for the importance of vitamin D3 in reducing the risk and susceptibility
for MS. If this hypothesis is correct, then 1,25-dihydroxyvitamin D3 or
its analogs may have great therapeutic potential in patients with MS.
More importantly, current research together with data from migration
studies opens the possibility that MS may be preventable in genetically
susceptible individuals with early intervention strategies that provide
adequate levels of hormonally active 1,25-dihydroxyvitamin D3 or its
analogs.
Publication Types:
Review
Review, Tutorial
PMID: 9316607 [PubMed - indexed for MEDLINE]
PMID: 11060707
"Lin" <kt...@woh.rr.com> wrote in message
news:%SFM7.68567$z55.8...@typhoon.neo.rr.com...
I have supplemented at this level with vitamin D3.As a precaution I had my liver
enzymes assessed in the same analysis taken to determine my serum vitamin D3
levels. Unfortunately my enzymes were quite elevated upon taking vitamin D
supplements, even with as little as 1000IU/d. The issue then, is do I have a
dysfunctional liver or am I sensitive to vitamin D supplements? Prior to my
winter time supplementing I had consisently sun bathed every summer day for 20
minutes and despite having ideal serum vitamin D3 concentrations, my liver
enzyme levels were very normal.
The reason for assessing my liver enzymes is that I have suspected a problematic
liver for some time. My liver problems predated my supplementing with vitamin D.
I inferred this on my own by interpreting symptoms (according to traditional
Chinese medicine) such as dark circles under the eyes, dry skin, weak ligaments,
poor circulation and prominent veins .
This self diagnosis has been corroborated by health practitioners such as
nutritionists ( they also say I have gall bladder irregularities)and
naturopaths.
I contacted R. Vieth about this and while he has never looked specifically for
liver enzymes in his trials with VD3, he said there is absolutely nothing in the
medical literature alluding to this concern.This doesn't mean it is not a
potential concern though. In accordance with Vieth recommended vitamin D3
supplement levels, Ashton Embry had normal liver enzymes the last time he had
his serum VD3 assessed.
Presently I am undergoing nutritional therapies (specific vitamins & cleanses)
to address my liver & gall bladder concerns. My method to my madness being if I
can resolve the problems in my organs which are responsible for digestion of
fats then I won't have a problem taking fat soluble vitamins such as VD3. I am
now going to a tanning salon to get my VD3 but my preference would be to get
VD3 fron pills during the winter.
Should you embark on taking VD3 in supplement form you should first assess your
1. serum VD3 level and 2. liver enzyme levels. This assessment will give you a
baseline by which to compare to. Beyond that I advise you to follow Vieth's and
Embry's guidelines regarding the amounts of VD3, Ca and Mg.
All during my experimenting phase I didn't feel any different, with or without
out the elevated liver enzymes. This is good because I feel quite
well(attributable to diet revision). However the elevated liver enzymes leads me
to think maybe the elevated liver enzymes are either: irrelevant (since I fell
well) or a precursor to ill health. Discretion is the better part of valor so I
decided to halt the supplements.
Getting sufficient vitamin D3 from the tanning bed is not an exact science. I
am presently trying to correlate how much VD3 I receive from regular exposure
durations. This not necessarily a critical pursuit though since I have my MS
under control via the diet prescribed at http://www.direct-ms.org/.
Cheers
Nick
High dose vitamin D3 increases need for magnesium. This was recently cited
in Townsend Letter article on low stomach acid...but here is a bit from
http://www.lef.org/magazine/mag97/dec-late97.html
"Vitamin D3: The AntiCancer Vitamin
Vitamin D3 and its metabolites are currently being studied by researchers
worldwide for cancer prevention and treatment. The anticancer mechanisms of
D3 are different from the antioxidant and antimutagenic effects of other
nutrients that may prevent cancer.
Vitamin D3 induces certain types of cancer cells to differentiate into
normal cells. What does cell "differentiation" mean? Normal cells go through
cell cycle growth processes that enable them to mature into functional cells
(differentiate), and then naturally die (undergo apoptosis) after so many
cell divisions have occurred. Cancer cells, on the other hand, often fail to
differentiate, which means they divide rapidly without turning into the kind
of specialized cells needed to support the body. Instead of differentiating
into normal functioning cells, cancer cells divide forever until they
overwhelm the host with nonfunctional cancer cells.
Vitamin D3 induces cells to differentiate throughout the body, but its
intake must be limited because of its potential toxicity. Too much vitamin
D3 can lead to hypercalcemia (too much calcium in the blood), which can
cause sudden death, or can induce calcification to accelerate the aging
process. Calcification causes cells to "clog up" and stop functioning. The
safest calcium channelblocking therapy is to make sure you have plenty of
magnesium in your bloodstream to inhibit excess calcium infiltration into
your cells.
Life Extension Mix contains 300 IU of vitamin D3 in each daily dose. Some
members concerned with prostate or breast cancer have been taking an
additional 1,000 IU of vitamin D3 a day.
For cancer patients, we suggest 3,000 to 4,000 IU of vitamin D3 a day on an
empty stomach, with frequent blood tests to make sure that too much calcium
is not building up in the bloodstream."
Well, technically no, but it was New York and Penn State so that makes
it multi site. As far as anything else goes, nobody is forcing anybody
to to take vit D in any quantity. I don't care. Just passing on some
information that was inquired about. Vitamn D is cheap and MAY help.
That's good enough for me to give it a try. Don't think it can hurt.
> Attached is the D3/MS Prevalence world map that's been thrown around a fair
> bit. One thing I'm struggling with, is the large discrepancy between US and
> UK MS rates, both on a similar latitude. I believe (please correct me if
> I'm wrong), MS in the US is at around 350K for the 260M population (0.135%).
> The MS Society in the UK puts the figure at around 10% in Scotland. Factor
> in or out lots of considerations and there's still a huge difference. It
> may be sunlight (Scotland hardly gets any) but what about the northern areas
> of Russia, e.g. Siberia which is put at a lower risk than Scotland ?
I'm not really worried about nor interested enough to do a lot of
computational exercises. I also didn't conduct nor participate in the
survey(s) so I am an outside party.
Bottom line is that if you want to try taking vitamin D for whatever
reason -- try it. I am. If not, not a problem and I wish you good luck.
uh, its been done several times. With inconclusive results I might
add.
>
> Is there anything else that might convince you (and me) of its efficacy ?
Just simple logic. There is a direct link between UVA/B exposure and
MS. As well as with vit d, parathyroid hormone, and skin meletonin
content. Vit d is a component of the cause of MS. But certainly not
the soul cause. Do as he suggests. 4000IUs Unless you go tanning.
WHich is much more benificial.
>
> "Lin" <kt...@woh.rr.com> wrote in message
> news:%SFM7.68567$z55.8...@typhoon.neo.rr.com...
> > I've never tried it, & I'm certainly no expert, but...
> >
> > I wouldn't. Vitamins, like any substance on earth, are toxic in too high
> of
> > doses.
Which is irrelivant in regard to therepeutic doses.
I've had MS for 10 yrs (that I know of), & have never gotten back
> any
> > test results that showed I had a vitamin deficiency.
The background of vit d therepy has nothing to do with having a
deficiancy. A deficiancy doesnt/cant cause MS. Its not that simple.
> >
> > There are people who have written on the effectiveness of vitamins, diet,
> > magnets, bee stings, & all sorts of things as being "miraculous" in
> > treating - even curing - MS. As far as I see it, if it wasn't the subject
> of
> > a multi-site double-blind study, & if the results are not reproducable in
> > other studies, it's not anything I'd waste my time or buckage on.
Well, dunno what to say? It seems an education is in order. There
are hundreds of studies in regard to MS, fish, sunshine, and vitamin
d. Maybe looking into those might be a good start.
> >
> > Just my opinion....
> >
> > Lin
And my .o2 ;^)
Rob
A fine example demonstrating the influence vitamin D has upon MS is found at
http://www.direct-ms.org/british.html. The article discusses a genetically
homogenous group of Irish immigrants that have moved to Australia and how their
MS prevalence in Aus is less than in their country of origin and the variable
prevalence with latitude in their new country of Australia.
The US straddles two regions of MS prevalence on this map. It wouldn't be valid
to use the national prevalence in the US as a value to compare to a country such
as the UK, which is in a single prevalence region.
> One thing I'm struggling with, is the large discrepancy between US and
> UK MS rates, both on a similar latitude. I believe (please correct me if
> I'm wrong), MS in the US is at around 350K for the 260M population (0.135%).
> The MS Society in the UK puts the figure at around 10% in Scotland. Factor
> in or out lots of considerations and there's still a huge difference.
The map indicates Siberia as a probable high risk area. To me this indicates a
lack of hard or available statistics.
> It
> may be sunlight (Scotland hardly gets any) but what about the northern areas
> of Russia, e.g. Siberia which is put at a lower risk than Scotland ?
>
> > But that's not entirely true. I posted this article a few months ago. It
> > is from the North American Research Committee on MS. I post it again:
> >
> > A small study conducted by researchers at Penn State and Helen
> > Hayes Hospital in New York has shown that a daily dose of vitamin
> > D-1,000 IU, or two and a half times the recommended dose for
> > adults-causes changes in blood chemistry that indicate positive
> > effects for patients with MS.
>
> [Image]
After 8 years of drugs that were supposed to prevent things from getting
worse with an initial diagnostic of 'demyelinating disease'. I had a scare
with a follow up MRI showing 'advanced MS' with a lot of obvious
deterioration since my diagnostic MRI.
Without going into a long letter and a lot of detail I revised my self-
treatment with complementary supplements. Among the changes I made - I
started 400IU vitamin D3 after reading Ashton Embry's article.
One year later I had another follow up MRI with improvement noted by both
the radiologist and the neurologist. My brain actually got better! I
consider this pretty overwhelming proof that I am doing something right.
Celeste
Was it 400 IU of D3, or 4000 IU that you are taking?
Dawn LaFrance
"Celeste Wood" <celes...@qwest.net> wrote in message
news:jkzN7.658$Ah4.1...@news.uswest.net...
"mdlafrance" <mdlaf...@home.com> wrote in message
news:W3FN7.7826$nm3.3...@news1.rdc1.bc.home.com...
>
>Have any of you more experienced/educated cynics out there tried this
>before? Any warnings? Just low cost snake oil or worth a try?
>
From an old book source on vitamins:
VITAMIN D
Both vitamins (A & D) are vital in virtually all body functions, but
specifically in effective mineral assimilation and synergistic action of other
vitamins.
1. 400 IUs per capsule/1 or 2 capsules daily (separate meals).
2. Fat soluble.
3. Toxicity: 2,000 IUs a day.
4. Rich sources: milk.
5. Other sources (IU per 3 oz.):
20,000 = Cod liver oil
360 = Salmon
225 = Tunafish
135 = Mushrooms
135 = Shrimp
83 = Sunflower seeds
45 = Eggs
45 = Liver
36 = Butter
36 = Fortified milk
27 = Cheese
Grace
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4524E9FD843
I checked the above web link, and honestly see very little credible
data there. I don't like being so negative, but it is an opinion I
developed through a lot of thought and research.
I would love to see the evidence (peer-reviewed, published medical
literature) that vitamin D plays any role in magnesium biology.
Likewise, I would love to see the published evidence about the concept
prevailing in the alternative medicine literature about the severe
focus on magnesium. If you can, please direct me to something
published on this that I can find on Medline. I have searched to no
avail, I have asked colleagues about this, and likewise come up empty
on real evidence for much of a need for magnesium supplementation.
Unlike calcium, magnesium is pretty available in many foods because Mg
is the major intracellular cation (and most foods are comprised of
cellular material).
Lastly, I have not seen any data from our hospital patients that
suggests any correlation between alkaline phosphatase (an enzyme that
goes up with gall-bladder, liver problems). Like I have said before,
there is no obvious reason why vitamin D should affect the liver.
Also, note that vitamin D can be taken orally and be thus taken by its
natural route. How else would fur-bearing animals get their vitamin D
other than by licking the vitamin D generated in the oils of their
fur.
The fears about vitamin D are grossly overblown, and the a need for
magnesium supplementation seems only to be based on promotions derived
from nutrient manufacturers, not real science.
Best wishes,
Reinhold
Thank you for your participation in this forum.
I profess an absence of knowledege on the topic of vitamin D and magnesium. I
simply have followed Ashton's recommendation of 800 mg/d of both Ca and Mg.
My understanding was that the Mg is necessary to help the body in utilizing
Ca and that Ca in turn was symbiotic in it's relationship to vitamin D.
In re-reading your papers on vitamin D it is evident you don't recommend
supplementing with Ca or Mg.I haven't consulted Ashton on this discrepency.
Perhaps it is because he strongly suggests dairy is to be avoided for PwMS (I
do avoid it) and a Ca supplement is thus needed.
In regards to the liver enzymes and VD3 supplement situation that I have
encountered, I feel my results are valid. The levels of alkaline phosphatase,
ALT and GGT were all well above the reference ranges provided on my analyses.
I had these monitored for periods in which I supplement with amounts of
4,000, 3,000 and 1,000 IU/d. During this investigative phase I stopped taking
all vitamin supplements aside from consistently taking vitamin D3, Ca and Mg.
I rarely drink alcohol these days and was moderate boozer prior to being
diagnosed with MS 10 years past. My diet is low in saturated fats yet I
supplement daily with EFA's and suffer no ill feeling from consuming these
fats. This is no liver or gall bladder disease in my family heritage.
When I was either receiving my VD3 from the sun or not taking any VD3
supplements at all my enzymes were all well within the reference ranges. I am
aware of your work indicating the availability of vitamin D taken either
orally or au natural.
Given that Ashton's enzymes have come back normal I would conclude that I am
a unique beast in this respect. Perhaps this is an unfortunate trait shared
by PwMs and /or those with autoimmune diseases in general. This is why in
good conscience I advise people to assess the liver enzymes prior and during
vitamin D supplementing. Methinks it's a reasonable precaution. My efforts
are certainly not intended to be part of the overblown fears (which I concur
with) you allude to.
Maybe my enzyme response could be circumvented by stossing although this does
not seem intuitively obvious. Your thoughts are appreciated.
Cheers
Nick
PS This week I am going to assess my hydroxy levels resulting from two months
of salon tanning. I'll keep you apprised.