Re: Finally found a simply worded study explaining Vitamin 25D has no impact on 1,25

[Guest guest]

Thank you for another reference where supplementation of Vitamin D

does not increase 125D for the vast MAJORITY of people.

" > Vitamin D increased mean serum 25-PHD from 30 +/- 4 to 99 +/- 15

> ng/ml (P < 0.001) and did not change mean serum 1 alpha,25(OH)2D

> (32 +/- 3 vs. 29 +/- 3 pg/ml) or mean serum calcium (9.5 +/- 0.1 >

vs. 9.6 +/- 0.1 mg/dl) in the normal subjects. "

In this case, 1,25 D ACTUALLY DROPPED (32-> 29) -- demonstrating the

point that low 25D levels will cause high 125D in the majority of

people.

The very special case of sarcoidosis should be treated the same as

people for diabetes - a special case [not the NORM], the normal

response is cited above.

> In contrast, vitamin D increased mean serum 25-OHD from 19 +/- 3 to

> 65 +/- 19 ng/ml (p < 0.05), increased mean serum 1 alpha,25(OH)2D

> threefold from 40 +/- 7 to 120 +/- 24 pg/ml, and increased mean

serum

> calcium from 9.4 +/- 0.2 to 9.8 +/- 0.2 mg/dl (P < 0.01).

>

I found that it was interesting with normal patients that it

increases by 69 ng/ml but with sarc only 46 ng/ml -- and far more

interesting, the variation was +/-3 versus +/-19 which suggests that

the response was all over the map with sarc patients -- to do the

class +/- / value we have normals with < 3% variation with normal in

response versus ~30% with sarc patients. Sound like they should have

attempted to identify the subclasses of sarc patients --- the numbers

suggests that there are major variations.

I have notices a lot of recent research on VDR defective genes and

been wondering if sarc patients happen to have these defects.

A.D.Hock in Germany publications with Vitamin D supplementation do

not appear to suggest any responses. One size do not fit all. The

majority of people do not have any change. A person with a Protien S

deficiency should avoid vitamin K --- it is not wise to avoid Vitamin

K unless there is a clear documented reason to do so. If you looked

at the title " abnormal regulation " -- which means NOT NORMAL, and

thus does not apply to most people.

Yes - something is going on for those patients (which are people WITH

sarc -- like you). On CFSProtocol, many people who had sunlight

sensitivity has found that disappears with Vitamin D supplementation -

-- the cause of THEIR sensitivity is that the Vitamin D triggered an

immune response and they appeared to have herx badly -- with more D,

this sensitivity dropped.

All of those patients are CFS patients, not Sarc.

I give no opinion on Sarc or TB patients (which also have abnormal

regulation of D). For CFS/FM and Lyme patients --- I see no evidence

of any abormal regulation of D.

I am saying what the literature is saying : Optimal is 100-400

approximately. Do not go over 400. The case below that you cite some

people with a reading over 1800 -- I AGREE with you for THOSE

LAYERS. Those levels of Vitamin D should not happen. The literature

say 100-400, and I would recommend just reaching 45-50 ng/ml or 115-

128 nmol/l per Dr. ph Mercola MD. " Do not become a vegan because

very heavy meat eaters have a health problem --- that is knee-jerk

over reacting " .

> > Pippit,

> > I am in COMPLETE AGREEMENT that you do NOT supplement with

> > 1,25D. Every study that I have read indicates problems -- in

short,

> > the body sets the 1,25D level (using any and all available 25D

> > reserves) that most effectively handles the infection. That is

what

> > all of your studies are saying. You are mucking with the body

> immune

> > response (aka disrupting the immune system) when you supplement

> with

> > 1,25D.

> >

> > At the same time (I spent many hours in January reading every

thing

> I

> > could find --- in full text, dropped a lot of $ buying PDFs -

which

> > is fine, I'm fully recovered [and those in the Seattle CFIDS

groups

> > will VERY MUCH attest to that] and back to good earnings), every

> > study that I could find (including those for Sarc) had the

positive

> > results for supplementation with 25D3. " All D's are not equal "

> >

> > A study showing that 1,25D SUPPLEMENTATION has bad outcomes does

> not

> > show that having 1,25D levels is bad. It is EQUIVALENT to saying

> that

> > because normal people get sick from insulin injections [even die

> from

> > insulin shock!] that we should reduce out insulin levels to the

> > absolute minimum!!!![ah, we should have lower insulin levels than

> > diabetics!]. You are doing that type of logic.

> >

> > It seems logical to a physical engineering type, but makes no

> senses

> > to those familar with biological illnesses. I give " Mother

Nature "

> > or " Intelligent Design " or ??? far more credit --- the immune

> system

> > has far more smarts than any PhD, and will adjust itself to what

is

> > needed (if you give it the needed raw material). Give it the

> storage

> > form of Vitamin D, 25D. Give it the storage form of iron,

> ferretin.

> > Get those levels up to the recognized optimal ranges and you will

> > likely see very significant improvements! (and a few remissions)

> >

> > IMHO

[Guest guest]

KEN wrote:

" I found that it was interesting with normal patients that it

increases by 69 ng/ml but with sarc only 46 ng/ml -- and far more

interesting, the variation was +/-3 versus +/-19 which suggests that

the response was all over the map with sarc patients -- to do the

class +/- / value we have normals with < 3% variation with normal in

response versus ~30% with sarc patients. Sound like they should have

attempted to identify the subclasses of sarc patients --- the numbers

suggests that there are major variations. "

Actually Ken, if you look at the abstract carefully, you'll see that the N for

sarc patients

is only 6, thus it is not a subclass issue but rather just high variability in

very few

observations. (and the N for controls was only 17, way too low in both

groups...). Given

the low N, if we could see the individual data points of the sarc patients, 4-5

could have

actually reacted as normals and this finding could be due to only 1-2 of the

people given

the crazy low N. Bayesian issues rule the day once again...

> > > Pippit,

> > > I am in COMPLETE AGREEMENT that you do NOT supplement with

> > > 1,25D. Every study that I have read indicates problems -- in

> short,

> > > the body sets the 1,25D level (using any and all available 25D

> > > reserves) that most effectively handles the infection. That is

> what

> > > all of your studies are saying. You are mucking with the body

> > immune

> > > response (aka disrupting the immune system) when you supplement

> > with

> > > 1,25D.

> > >

> > > At the same time (I spent many hours in January reading every

> thing

> > I

> > > could find --- in full text, dropped a lot of $ buying PDFs -

> which

> > > is fine, I'm fully recovered [and those in the Seattle CFIDS

> groups

> > > will VERY MUCH attest to that] and back to good earnings), every

> > > study that I could find (including those for Sarc) had the

> positive

> > > results for supplementation with 25D3. " All D's are not equal "

> > >

> > > A study showing that 1,25D SUPPLEMENTATION has bad outcomes does

> > not

> > > show that having 1,25D levels is bad. It is EQUIVALENT to saying

> > that

> > > because normal people get sick from insulin injections [even die

> > from

> > > insulin shock!] that we should reduce out insulin levels to the

> > > absolute minimum!!!![ah, we should have lower insulin levels than

> > > diabetics!]. You are doing that type of logic.

> > >

> > > It seems logical to a physical engineering type, but makes no

> > senses

> > > to those familar with biological illnesses. I give " Mother

> Nature "

> > > or " Intelligent Design " or ??? far more credit --- the immune

> > system

> > > has far more smarts than any PhD, and will adjust itself to what

> is

> > > needed (if you give it the needed raw material). Give it the

> > storage

> > > form of Vitamin D, 25D. Give it the storage form of iron,

> > ferretin.

> > > Get those levels up to the recognized optimal ranges and you will

> > > likely see very significant improvements! (and a few remissions)

> > >

> > > IMHO

[Guest guest]

Many thanks --- I completed missed the N. And as you point out, with

such a small sample just one odd ball reaction (such as something

else triggering the 1,25D production IN ONE INDIVIDUAL) could account

for the change -- in which case, the ability to identify Vitamin D as

the causality is almost totally undermined.

On the plus note, it was a reasonable example of data showing that

1,25D goes down with 25D supplementation for normal people -- which

was requesting earlier.

Bayesians rule! CFIDS is a Markovian Process!

>

> " I found that it was interesting with normal patients that it

> increases by 69 ng/ml but with sarc only 46 ng/ml -- and far more

> interesting, the variation was +/-3 versus +/-19 which suggests

that

> the response was all over the map with sarc patients -- to do the

> class +/- / value we have normals with < 3% variation with normal

in

> response versus ~30% with sarc patients. Sound like they should

have

> attempted to identify the subclasses of sarc patients --- the

numbers

> suggests that there are major variations. "

>

>

> Actually Ken, if you look at the abstract carefully, you'll see

that the N for sarc patients

> is only 6, thus it is not a subclass issue but rather just high

variability in very few

> observations. (and the N for controls was only 17, way too low in

both groups...). Given

> the low N, if we could see the individual data points of the sarc

patients, 4-5 could have

> actually reacted as normals and this finding could be due to only 1-

2 of the people given

> the crazy low N. Bayesian issues rule the day once again...

[Guest guest]

> KEN wrote:

> > I have notices a lot of recent research on VDR defective genes

and

> > been wondering if sarc patients happen to have these defects.

No, but they may have other defective genes:

Eur J Hum Genet. 2005 Feb 9;

Association between SLC11A1 (formerly NRAMP1) and the risk of

sarcoidosis in Poland.

SLC11A1, formerly known as NRAMP1 (natural resistance-associated

macrophage protein 1), controls the transport of certain metal ions

into monocyte/macrophage cells, and thus may control resistance to

pathogens. In humans, it is linked to several infectious and

autoimmune diseases, including HIV, rheumatoid

arthritis,sarcoidosis, and Crohn's disease.

Also:

Hum Genet. 2004 Apr;114(5):503-9. Epub 2004 Mar 5.

Association between IFNA genotype and the risk of sarcoidosis

" In healthy subjects, IFNA allele 2, which is over-represented in

patients with sarcoidosis, was significantly associated with

increased IFN-alpha and IL-12p70 production induced by Sendai virus

in vitro. This study suggests that possession of the IFNA allele

with higher levels of IFN-alpha significantly increases the risk of

sarcoidosis. "

IFN-alpha increases Th-1 responses, increasing levels of IFN-gamma,

and IFN-gamma is known to be able to stimulate macrophage production

of vitamin D. (IFN-alpha therapy for hepatitis has been known to

cause cases of sarcoidosis).

Mark

[Guest guest]

> KEN wrote:

> > I have notices a lot of recent research on VDR defective genes

and

> > been wondering if sarc patients happen to have these defects.

No, but they may have other defective genes:

Eur J Hum Genet. 2005 Feb 9;

Association between SLC11A1 (formerly NRAMP1) and the risk of

sarcoidosis in Poland.

SLC11A1, formerly known as NRAMP1 (natural resistance-associated

macrophage protein 1), controls the transport of certain metal ions

into monocyte/macrophage cells, and thus may control resistance to

pathogens. In humans, it is linked to several infectious and

autoimmune diseases, including HIV, rheumatoid

arthritis,sarcoidosis, and Crohn's disease.

Also:

Hum Genet. 2004 Apr;114(5):503-9. Epub 2004 Mar 5.

Association between IFNA genotype and the risk of sarcoidosis

" In healthy subjects, IFNA allele 2, which is over-represented in

patients with sarcoidosis, was significantly associated with

increased IFN-alpha and IL-12p70 production induced by Sendai virus

in vitro. This study suggests that possession of the IFNA allele

with higher levels of IFN-alpha significantly increases the risk of

sarcoidosis. "

IFN-alpha increases Th-1 responses, increasing levels of IFN-gamma,

and IFN-gamma is known to be able to stimulate macrophage production

of vitamin D. (IFN-alpha therapy for hepatitis has been known to

cause cases of sarcoidosis).

Mark