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

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Hi Ken

Would you, post this on the accidental patient message board please.

People are being told very low vid D with a high ratio of D125 means

having to reduce their already low vit D levels even lower, everyone

needs to see why the interretations of the d tests results on the MP

are misleading.

Cheers, Tansy

> Concerning vitamin D, I finally came across an article that states

> some important items very clearly based on actual studies --

instead

> of speculative theories. I have been frustrated because I have seen

> the same thing stated in many articles -- but it has not been

> sufficiently simply stated that a CFIDS mind could understand it.

>

> Source:Vitamin D: importance in the prevention of cancers, type 1

> diabetes, heart disease, and osteoporosis, American Journal of

> Clinical Nutrition, Vol. 79, No. 3, 362-371, March 2004 The full

text

> is available at: http://www.ajcn.org/cgi/content/full/79/3/362

>

> " neither increased exposure to sunlight nor increased oral intake

of

> vitamin D raised blood concentrations of 1,25(OH)2D " (3 studies

> cited)

>

> Furthermore, the author states:

>

> " as a person becomes vitamin D-deficient, there is an increase in

the

> concentration of parathyroid hormone (PTH), which increases the

renal

> production of 1,25(OH)2D, the circulating concentrations of which

> often become normal or even elevated "

>

> So 1,25D increases with Vitamin D deficiency has been established

in

> medical literature. It seems clear that Vitamin D supplementation

> until Vitamin D is at the optimal levels should be done before you

> can be sure of meaningful 1,25D levels

> * 45-50 ng/ml or 115-128 nmol/l. Mercola, MD

> http://www.mercola.com/2002/feb/23/vitamin_d_deficiency.htm

>

> I found it interesting that low levels of Vitamin D may induce a

> false elevation of 1,25D levels (even a HIGH reading).

>

> This is what medical science study states and have found to be the

> case.

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Just finished reading this paper. What a clear, lucid explanation of how Vit. D

is

working -- plan to follow up on some of the references as well... I have a VERY

low

25D level and a 45ish 1,25D level. Ordering supplements later today as I am

still

bedbound (just started treatment) and can't get out to the sun....

Thanks for posting this.

--- In infections , " Ken " <ken_lassesen@y...>

wrote:

> Concerning vitamin D, I finally came across an article that states

> some important items very clearly based on actual studies -- instead

> of speculative theories. I have been frustrated because I have seen

> the same thing stated in many articles -- but it has not been

> sufficiently simply stated that a CFIDS mind could understand it.

>

> Source:Vitamin D: importance in the prevention of cancers, type 1

> diabetes, heart disease, and osteoporosis, American Journal of

> Clinical Nutrition, Vol. 79, No. 3, 362-371, March 2004 The full text

> is available at: http://www.ajcn.org/cgi/content/full/79/3/362

>

> " neither increased exposure to sunlight nor increased oral intake of

> vitamin D raised blood concentrations of 1,25(OH)2D " (3 studies

> cited)

>

> Furthermore, the author states:

>

> " as a person becomes vitamin D-deficient, there is an increase in the

> concentration of parathyroid hormone (PTH), which increases the renal

> production of 1,25(OH)2D, the circulating concentrations of which

> often become normal or even elevated "

>

> So 1,25D increases with Vitamin D deficiency has been established in

> medical literature. It seems clear that Vitamin D supplementation

> until Vitamin D is at the optimal levels should be done before you

> can be sure of meaningful 1,25D levels

> * 45-50 ng/ml or 115-128 nmol/l. Mercola, MD

> http://www.mercola.com/2002/feb/23/vitamin_d_deficiency.htm

>

> I found it interesting that low levels of Vitamin D may induce a

> false elevation of 1,25D levels (even a HIGH reading).

>

> This is what medical science study states and have found to be the

> case.

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Any idea what it means when you don't have a low D,25, but it is

also high. My D,25 was high at 59 (range 9-54) and then my D 1,25

was was really high at 78 (range 15-60). Do I need to cut back on D,

do I need to supplement, what? Very confused. Do I have calcium

leaching into my muscle tissue and not getting enough into my bones

due to to much D? Does this explain the muscle cramps everytime I

consume calcium?

I seemed to have noticed less cramping and my heart may have settled

a bit since avoiding Vit. D in my food and supplements. I don't

avoid the sun at all though. I just am having a hard time

understanding all of this and what I see happening in my own body.

> Concerning vitamin D, I finally came across an article that states

> some important items very clearly based on actual studies --

instead

> of speculative theories. I have been frustrated because I have

seen

> the same thing stated in many articles -- but it has not been

> sufficiently simply stated that a CFIDS mind could understand it.

>

> Source:Vitamin D: importance in the prevention of cancers, type 1

> diabetes, heart disease, and osteoporosis, American Journal of

> Clinical Nutrition, Vol. 79, No. 3, 362-371, March 2004 The full

text

> is available at: http://www.ajcn.org/cgi/content/full/79/3/362

>

> " neither increased exposure to sunlight nor increased oral intake

of

> vitamin D raised blood concentrations of 1,25(OH)2D " (3 studies

> cited)

>

> Furthermore, the author states:

>

> " as a person becomes vitamin D-deficient, there is an increase in

the

> concentration of parathyroid hormone (PTH), which increases the

renal

> production of 1,25(OH)2D, the circulating concentrations of which

> often become normal or even elevated "

>

> So 1,25D increases with Vitamin D deficiency has been established

in

> medical literature. It seems clear that Vitamin D supplementation

> until Vitamin D is at the optimal levels should be done before you

> can be sure of meaningful 1,25D levels

> * 45-50 ng/ml or 115-128 nmol/l. Mercola, MD

> http://www.mercola.com/2002/feb/23/vitamin_d_deficiency.htm

>

> I found it interesting that low levels of Vitamin D may induce a

> false elevation of 1,25D levels (even a HIGH reading).

>

> This is what medical science study states and have found to be the

> case.

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This may explain the results a long time ago when 6 or 9 or whatever

it was, sarc patients were given vitamin D and half got well...I

asked Trevor Marshall what he made of that and he couldn't answer.

Now it makes sense.

> > Concerning vitamin D, I finally came across an article that

states

> > some important items very clearly based on actual studies --

instead

> > of speculative theories. I have been frustrated because I have

seen

> > the same thing stated in many articles -- but it has not been

> > sufficiently simply stated that a CFIDS mind could understand it.

> >

> > Source:Vitamin D: importance in the prevention of cancers, type 1

> > diabetes, heart disease, and osteoporosis, American Journal of

> > Clinical Nutrition, Vol. 79, No. 3, 362-371, March 2004 The full

text

> > is available at: http://www.ajcn.org/cgi/content/full/79/3/362

> >

> > " neither increased exposure to sunlight nor increased oral intake

of

> > vitamin D raised blood concentrations of 1,25(OH)2D " (3 studies

> > cited)

> >

> > Furthermore, the author states:

> >

> > " as a person becomes vitamin D-deficient, there is an increase in

the

> > concentration of parathyroid hormone (PTH), which increases the

renal

> > production of 1,25(OH)2D, the circulating concentrations of which

> > often become normal or even elevated "

> >

> > So 1,25D increases with Vitamin D deficiency has been established

in

> > medical literature. It seems clear that Vitamin D supplementation

> > until Vitamin D is at the optimal levels should be done before

you

> > can be sure of meaningful 1,25D levels

> > * 45-50 ng/ml or 115-128 nmol/l. Mercola, MD

> > http://www.mercola.com/2002/feb/23/vitamin_d_deficiency.htm

> >

> > I found it interesting that low levels of Vitamin D may induce a

> > false elevation of 1,25D levels (even a HIGH reading).

> >

> > This is what medical science study states and have found to be

the

> > case.

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<ken_lassesen@y...> wrote:

> " neither increased exposure to sunlight nor increased oral intake of

> vitamin D raised blood concentrations of 1,25(OH)2D " (3 studies

> cited)

But - is that in healthy mammals or inflamed ones? The 25 --> 1,25

conversion is very different in inflamed states than what it is in

health.

> Furthermore, the author states:

>

> " as a person becomes vitamin D-deficient, there is an increase in the

> concentration of parathyroid hormone (PTH), which increases the renal

> production of 1,25(OH)2D, the circulating concentrations of which

> often become normal or even elevated "

Aha, very interesting.

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Wouldn't having an infecion /inflammation problem cause

abnormalities that make this finding irrelevant. I would comfortably

sit in a porphyria diagnosis with a sun explanation(impact on

infection) instead of trying to explain the many abnormalities of

minerals and vitamins from having an untreated infection.

To sum up I basically needed to hear that having suffered from an

untreated infection you develop something along the lines of

porphyria and getting the toxins out of the blood and/or soft

tissue makes a lot more sense than focusing on D vitamin status

good bad or otherwise.I feel th issue at hand is to test thoroughly

for what's missing and if it's low D maybe testing the water with

upping the D may be the smart end of the spectrum instead of giving

it to us cut and dried.

-- In infections , " Hodologica "

<usenethod@y...> wrote:

> <ken_lassesen@y...> wrote:

> > " neither increased exposure to sunlight nor increased oral

intake of

> > vitamin D raised blood concentrations of 1,25(OH)2D " (3 studies

> > cited)

>

> But - is that in healthy mammals or inflamed ones? The 25 --> 1,25

> conversion is very different in inflamed states than what it is in

> health.

>

> > Furthermore, the author states:

> >

> > " as a person becomes vitamin D-deficient, there is an increase

in the

> > concentration of parathyroid hormone (PTH), which increases the

renal

> > production of 1,25(OH)2D, the circulating concentrations of

which

> > often become normal or even elevated "

>

> Aha, very interesting.

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Hey --

Do you have references for your comment " The 25 --> 1,25 conversion is very

different in inflamed states than what it is in health. " I would be VERY

interested in

reading that...

Thanks.

> > " neither increased exposure to sunlight nor increased oral intake of

> > vitamin D raised blood concentrations of 1,25(OH)2D " (3 studies

> > cited)

>

> But - is that in healthy mammals or inflamed ones? The 25 --> 1,25

> conversion is very different in inflamed states than what it is in

> health.

>

> > Furthermore, the author states:

> >

> > " as a person becomes vitamin D-deficient, there is an increase in the

> > concentration of parathyroid hormone (PTH), which increases the renal

> > production of 1,25(OH)2D, the circulating concentrations of which

> > often become normal or even elevated "

>

> Aha, very interesting.

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" neither increased exposure to sunlight nor increased oral intake of

vitamin D raised blood concentrations of 1,25(OH)2D " (3 studies

cited)

So Ken, would you agree that if someone (or a group of someones) has

1,25(OH)2D levels that do increase with exposure to sunlight or oral

intake of vitamin D, then they would have a disregulated system and

the D studies you site would be meaningless for them? That would be

fairly easy for people to check, if they can get the tests done.

" as a person becomes vitamin D-deficient, there is an increase in the

concentration of parathyroid hormone (PTH), which increases the renal

production of 1,25(OH)2D, the circulating concentrations of which

often become normal or even elevated "

There is a much better discussion of this at http://www.bonekey-

ibms.org/cgi/content/full/ibmske;2/5/7 The Relation Between Serum

Calcidiol and Calcitriol

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Regarding inflammation affecting 1,25 vitamin D,

http://edrv.endojournals.org/cgi/reprint/14/1/3.pdf section III

Cutaneous Production of 1,25(OH)2D, the authors state:

" These cells are exquisitely sensitive to IFN with

stimulation of 1,25(OHbD production seen at concentrations

less than 10 PM. Higher concentrations are inhibitory,… "

" TNF stimulates 1,25(OH)2D production

and transglutaminase activity in preconfluent cells

(76), and it can reverse the inhibition seen with the higher

concentrations of IFN (Fig. 6). The effects of TNF and IFN

are not additive at the lower and "

In keratinocytes the inflammatory cytokines tnf-alpha, and inf-gamma

together significantly increase 1,25(OH)2D production.

From http://www.jleukbio.org/cgi/content/abstract/54/1/17 :

" Alveolar macrophages acquire 1 alpha-hydroxylase activity in

inflammation, and thereby metabolize 25 hydroxyvitamin D3 (25 D3) to

the active metabolite, 1 alpha,25-dihydroxyvitamin D3 (1,25 D3,

calcitriol). "

The study also shows that in the presence of the inflammatory

cytokines tnf-alpha and inf-gamma, moncytes are also capable of

producing calcitriol.

> > > " neither increased exposure to sunlight nor increased oral

intake of

> > > vitamin D raised blood concentrations of 1,25(OH)2D " (3

studies

> > > cited)

> >

> > But - is that in healthy mammals or inflamed ones? The 25 -->

1,25

> > conversion is very different in inflamed states than what it is

in

> > health.

> >

> > > Furthermore, the author states:

> > >

> > > " as a person becomes vitamin D-deficient, there is an increase

in the

> > > concentration of parathyroid hormone (PTH), which increases

the renal

> > > production of 1,25(OH)2D, the circulating concentrations of

which

> > > often become normal or even elevated "

> >

> > Aha, very interesting.

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Hi Tansy,

Don't be misled by this study. There are alot of these sponsored by

these nutritional special interest groups, so I wouldn't let it

change your lifestyle just yet. This one was sponsored by the

American Society for Clinical Nutrition. The author attempts to apply

a wellness model and generalize it to include people with chronic

disease (whose Vitamin D metabolism is dysregulated). This study

looks good on the surface, but there is no way the author can make

this fit for all of the populations he cites, because the

biochemistry doesn't work the same way in all these populations. He

has put together a patchwork quilt of studies and drawn a larger

conclusion than one can reasonably draw in this instance.

The one part I thought was illuminating was the reference to storage

in fat cells in people who are obese, making the Vitamin D not

bioavailable, but he then erroneously draws the conclusion from this

that these people are D-deficient, which is actually a

misinterpretation.

This is a prime example of a sufficient amount of Vitamin D in the

body but where a breakdown in normal Vitamin D metabolism is taking

place.

Similarly, in immune disease, 25-D converts very rapidly to 1,25-D

and this is where the breakdown in normal metabolism occurs; in

otherwords 1,25-D stays elevated by rapidly depleting 25-D or

inhibiting its manufacture in the liver(making it appear when 25-D is

tested as though there is a deficiency).

Here is a study which supports this hypothesis;

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?

cmd=Retrieve & db=pubmed & dopt=Abstract & list_uids=6332830 & itool=iconpmc & q

uery_hl=38

J Clin Invest. 1984 Oct;74(4):1540-4.

Evidence that 1,25-dihydroxyvitamin D3 inhibits the hepatic

production of 25-hydroxyvitamin D in man.

Bell NH, Shaw S, RT.

Previous in vitro studies in rachitic rat liver suggested that 1,25-

dihydroxyvitamin D inhibits the hepatic production of 25-

hydroxyvitamin D (25-OHD).

An investigation therefore was carried out in eight normal subjects

to determine whether concomitant administration of 1,25-

dihydroxyvitamin D3 [1,25(OH)2D3] would alter the response of serum

25-OHD to challenge with vitamin D.

In control studies, vitamin D, 100,000 U/d for 4 d, significantly

increased mean serum 25-OHD, from 26.3 +/- 2.9 to 66.7 +/- 12.6 ng/ml

(P less than 0.01).

In contrast, 1,25(OH)2D3, 2 micrograms/d for 4 d, completely

prevented an increase in serum 25-OHD in response to the same dose of

vitamin D in the same individuals (25.1 +/- 2.2 vs. 27.4 +/- 5.3

ng/ml, NS).

In a post-control study in seven of the normal subjects, vitamin D

again significantly increased mean serum 25-OHD, from 18.2 +/- 3.1 to

42.8 +/- 4.7 ng/ml (P less than 0.001).

In each of the three studies, mean serum calcium, phosphorus, and

creatinine did not change and remained within the normal range.

Whereas mean urinary calcium did not change in response to vitamin D

alone during the 4 d of the two control studies, it increased

significantly in the study in which vitamin D and 1,25(OH)2D3 were

given together.

A dose-response inhibition of the response of serum 25-OHD to vitamin

D by 1,25(OH)2D3 was demonstrated in two of the normal subjects.

The results provide evidence that 1,25(OH)2D3 inhibits the hepatic

synthesis of its precursor 25-OHD in man.

PMID: 6332830 [PubMed - indexed for MEDLINE]

The Vitamin D is still in there, it hasn't left the body, only it's

been rapidly converted to 1,25-D. It's a matter of rate-of-

utilization; not a true deficiency.

The following study suggests that plasma (25-D) readings are likely

to reflect a lower level after 19-25 hours than what is actually

stored in fat cells. This doesn't support the hypothesis that there

is a deficiency, but instead that low 25-D levels are deceptive. It

also suggests that we have plenty of Vitamin D which builds

cumulatively from each exposure.

VITAMIN D DISAPPEARS FROM PLASMA WITH HALF-LIFE OF 19-25 HR, BUT IS

STORED IN BODY FOR PROLONGED PERIODS (6 MO OR LONGER IN RAT)...IN FAT

DEPOSITS THROUGHOUT BODY. /VIT D/

[Gilman, A. G., L. S. Goodman, and A. Gilman. (eds.). Goodman and

Gilman's The Pharmacological Basis of Therapeutics. 6th ed. New York:

Macmillan Publishing Co., Inc. 1980., p. 1543]**PEER REVIEWED**

Below is a paper in which (contrary to the study Ken cited)found a

direct correlation between increased circulating 1,25-D and Rheumatic

Disease;

J Bone Miner Res. 1986 Apr;1(2):221-6.

Abnormal calcium metabolism caused by increased circulating 1,25-

dihydroxyvitamin D in a patient with rheumatoid arthritis.

Gates S, Shary J, RT, Wallach S, Bell NH.

Veterans Administration Medical Center, Albany, NY.

A 35-year-old white male with rheumatoid arthritis who had developed

hypercalcemia, hypercalciuria, and nephrolithiasis was found to be

abnormally sensitive to vitamin D as a result of lack of regulation

of circulating 1,25-dihydroxyvitamin D (1,25-(OH)2D).

An increase in daily intake of vitamin D from 10 micrograms (400

units) per day to 50 micrograms (2000 units) per day produced an

abnormal elevation in serum 1,25-(OH)2D, hypercalcemia, and

hypercalciuria which were corrected by prednisone. Serum 25-

hydroxyvitamin D initially was abnormally low, and increased with

vitamin D to values which were in the low normal range.

There were significant positive correlations between serum 1,25-(OH)

2D (p less than .05) and serum calcium and between serum 1,25-(OH)2D

and urinary calcium (p less than .05).

Serum immunoreactive parathyroid hormone, initially in the lower

range of normal, decreased further during hypercalcemia. A radiograph

of the chest, gallium scan, and serum angiotensin-converting enzyme

activity were normal.

No granulomas or evidence of lymphoma were found in biopsies of the

liver and of several lymph nodes. It is concluded that the abnormal

calcium metabolism in this patient resulted from increased

circulating 1,25-(OH)2D and that the defect in vitamin D metabolism

was not related to sarcoidosis, other granulomatous disease,

Hodgkin's disease, or lymphoma.

The relationship, if any, of the abnormal metabolism of vitamin D and

calcium to rheumatoid arthritis remains to be established.

PMID: 3503540 [PubMed - indexed for MEDLINE]

In addition, the study that Ken cited suggests that adequate vitamin

D in the diet and from sunlight can " prevent " autoimmune disease, yet

with all the fortification being done in food nowadays I don't know

how that could be the case because the incidence of it seems to be

increasing, not decreasing, over time, and I doubt it can be

explained away by the advent of sunscreen.

Before I knew this was harmful, I used to eat lots of Salmon and

shellfish (rich in Vitamin D), I ate lots of cheese, lots of sour

cream, and raw Spinache in salads, and used Vitamin D fortified milk

and cream.

I got as much sun exposure as most healthy average citizens. I was

definitely not Vitamin D deficient. Yet I developed a whopping

autoimmune disease! In fact, several, simmering for many years, and

then right smack in the middle of the summer (during blaring hot,

sunshiny days) I became deathly ill.

I clearly found that when I restricted D I began to feel better, and

on days when I was outside too much, I felt worse. Sometimes the

reaction was immediate and other times it took until the next day for

me to feel it.

I have noticed that when I accidentally ate something with a high

level of Vitamin D in it my pain grew much worse, I had heart

arrythmias, chest pain, and pounding heart, difficulty breathing,

nausea, body temperature dysregulation, motor slowing, and brain fog

and confusion.

It really didn't take much convincing for me to see that this was

true. Life pretty much proved for me.

It's like that joke about the patient who comes into the doctor's

office and says, " Doctor, when I poke this straw into my eye it

hurts " , and the doctor says, " Well don't do it. "

Pippit

> > Concerning vitamin D, I finally came across an article that

states

> > some important items very clearly based on actual studies --

> instead

> > of speculative theories. I have been frustrated because I have

seen

> > the same thing stated in many articles -- but it has not been

> > sufficiently simply stated that a CFIDS mind could understand it.

> >

> > Source:Vitamin D: importance in the prevention of cancers, type 1

> > diabetes, heart disease, and osteoporosis, American Journal of

> > Clinical Nutrition, Vol. 79, No. 3, 362-371, March 2004 The full

> text

> > is available at: http://www.ajcn.org/cgi/content/full/79/3/362

> >

> > " neither increased exposure to sunlight nor increased oral intake

> of

> > vitamin D raised blood concentrations of 1,25(OH)2D " (3 studies

> > cited)

> >

> > Furthermore, the author states:

> >

> > " as a person becomes vitamin D-deficient, there is an increase in

> the

> > concentration of parathyroid hormone (PTH), which increases the

> renal

> > production of 1,25(OH)2D, the circulating concentrations of which

> > often become normal or even elevated "

> >

> > So 1,25D increases with Vitamin D deficiency has been established

> in

> > medical literature. It seems clear that Vitamin D supplementation

> > until Vitamin D is at the optimal levels should be done before

you

> > can be sure of meaningful 1,25D levels

> > * 45-50 ng/ml or 115-128 nmol/l. Mercola, MD

> > http://www.mercola.com/2002/feb/23/vitamin_d_deficiency.htm

> >

> > I found it interesting that low levels of Vitamin D may induce a

> > false elevation of 1,25D levels (even a HIGH reading).

> >

> > This is what medical science study states and have found to be

the

> > case.

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Hi Pippet

Thanks.

I do a lot of research and have read all the debates and opposing

hypotheses.

I have raised my vit d, and now when it's not too hot (have heat

intolerance) get as much as I can from direct sunlight. My

improvements from increased vitamin D make me feel more confident I

have made the right informed choice. What's more it would take a lot

more than I have read to make me give up the benefits I get from my

fish oil and all the other things that have allowed me to increase my

physical and mental activities, lower my pain levels, and no longer

look as ill as I felt.

Our opposite responses highlight yet again that so far there is no

one size fits all for PWME/CFIDS, FM and lyme disease.

Cheers, Tansy

> > > Concerning vitamin D, I finally came across an article that

> states

> > > some important items very clearly based on actual studies --

> > instead

> > > of speculative theories. I have been frustrated because I have

> seen

> > > the same thing stated in many articles -- but it has not been

> > > sufficiently simply stated that a CFIDS mind could understand

it.

> > >

> > > Source:Vitamin D: importance in the prevention of cancers, type

1

> > > diabetes, heart disease, and osteoporosis, American Journal of

> > > Clinical Nutrition, Vol. 79, No. 3, 362-371, March 2004 The

full

> > text

> > > is available at: http://www.ajcn.org/cgi/content/full/79/3/362

> > >

> > > " neither increased exposure to sunlight nor increased oral

intake

> > of

> > > vitamin D raised blood concentrations of 1,25(OH)2D " (3

studies

> > > cited)

> > >

> > > Furthermore, the author states:

> > >

> > > " as a person becomes vitamin D-deficient, there is an increase

in

> > the

> > > concentration of parathyroid hormone (PTH), which increases the

> > renal

> > > production of 1,25(OH)2D, the circulating concentrations of

which

> > > often become normal or even elevated "

> > >

> > > So 1,25D increases with Vitamin D deficiency has been

established

> > in

> > > medical literature. It seems clear that Vitamin D

supplementation

> > > until Vitamin D is at the optimal levels should be done before

> you

> > > can be sure of meaningful 1,25D levels

> > > * 45-50 ng/ml or 115-128 nmol/l. Mercola, MD

> > > http://www.mercola.com/2002/feb/23/vitamin_d_deficiency.htm

> > >

> > > I found it interesting that low levels of Vitamin D may induce

a

> > > false elevation of 1,25D levels (even a HIGH reading).

> > >

> > > This is what medical science study states and have found to be

> the

> > > case.

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Just wanted to say thanks Ken for your diligence in shining some

light on this subject. I have saved everyones response as well to now

go and read. I feared that if started reading,I'd never make my way

to saying Thanks.

I have much to digest as this has been a topic of frustration for me.

To the point that two weeks ago ,when I again showed deficient

Vitamin D, I didn't even attempt my usual questions.

I've been low in Vit D since 2001 and have made attempts to get my

questions answers with no success. It has been that when I try to pin

the doctor's down in how this affects the blood concentrations of

1,25d as you wrote, that my appointment goes sour.I always get the

inquisition as to why I want to know this information which my

answers are never adequate for their best answer. Sometimes knowing

that I was confused already, they would throw a slew of other big

words and haughty facts to dig me deeper or I would get equally

disturbing blank looks.Either way I feared the doctor's didn't know

any more than I did.

I note that it is expected for the parathyroid to be elevated, but I

believe mine was also reducedalong with abnormalities in the renal

results.? I need to double check that. Maybe that is tied in with my

low aldersterone levels though.

Despite ++ supplementation (even IV)I am not making any headway in

increasing my vitamin d nor my calcium. ly I'm low in several

nutritional areas, but have not had any luck with finding answers.

Armed with this information here and a little cutting and pasting, I

should be mightily armed.

Thanks again.

Peg

> Concerning vitamin D, I finally came across an article that states

> some important items very clearly based on actual studies --

instead

> of speculative theories. I have been frustrated because I have seen

> the same thing stated in many articles -- but it has not been

> sufficiently simply stated that a CFIDS mind could understand it.

>

> Source:Vitamin D: importance in the prevention of cancers, type 1

> diabetes, heart disease, and osteoporosis, American Journal of

> Clinical Nutrition, Vol. 79, No. 3, 362-371, March 2004 The full

text

> is available at: http://www.ajcn.org/cgi/content/full/79/3/362

>

> " neither increased exposure to sunlight nor increased oral intake

of

> vitamin D raised blood concentrations of 1,25(OH)2D " (3 studies

> cited)

>

> Furthermore, the author states:

>

> " as a person becomes vitamin D-deficient, there is an increase in

the

> concentration of parathyroid hormone (PTH), which increases the

renal

> production of 1,25(OH)2D, the circulating concentrations of which

> often become normal or even elevated "

>

> So 1,25D increases with Vitamin D deficiency has been established

in

> medical literature. It seems clear that Vitamin D supplementation

> until Vitamin D is at the optimal levels should be done before you

> can be sure of meaningful 1,25D levels

> * 45-50 ng/ml or 115-128 nmol/l. Mercola, MD

> http://www.mercola.com/2002/feb/23/vitamin_d_deficiency.htm

>

> I found it interesting that low levels of Vitamin D may induce a

> false elevation of 1,25D levels (even a HIGH reading).

>

> This is what medical science study states and have found to be the

> case.

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Vitamin D lab ranges only indicate where you are relative to those in

the same lab area. It is generally accepted that 95% of US residents is

deficient in Vitamin D. Dr. Mercola recommendations agree with the

nutritional research scientists that I have read (and I purchased a

stack of their full text articles in PDF -- most dated from 2004 and

2005 back in January when I did a criticial review of someone works --

prior to that I was PRO-him [as those in the Seattle CFIDS group will

testify] -- after the review (personal threats did not help) -- I

became very very concerned about the lack of hard science).

Back to topic: The BOTTOM of the optimal range is:

* 45-50 ng/ml or 115-128 nmol/l. Mercola, MD

http://www.mercola.com/2002/feb/23/vitamin_d_deficiency.htm

I beleive that your measurement is in nmol/l, in which case your are at

half the optimal range. If not, if it is in ng/ml, you are perfectly

fine according to the literature. The beginning of the high range

(where there is a change in the body according to the nutritionist

scientists is about 400 nmol/l or 200 ng/ml.)

The optimal range is around 110-400 nmol/l.

So the one thing that is certain --- you are not at a risk of excessive

Vitamin D.

> Any idea what it means when you don't have a low D,25, but it is

> also high. My D,25 was high at 59 (range 9-54) and then my D 1,25

> was was really high at 78 (range 15-60). Do I need to cut back on D,

> do I need to supplement, what? Very confused. Do I have calcium

> leaching into my muscle tissue and not getting enough into my bones

> due to to much D? Does this explain the muscle cramps everytime I

> consume calcium?

>

> I seemed to have noticed less cramping and my heart may have settled

> a bit since avoiding Vit. D in my food and supplements. I don't

> avoid the sun at all though. I just am having a hard time

> understanding all of this and what I see happening in my own body.

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On CFSProtocol there is one person's experience that may totally

explain things:

She started at 200 IU/day and had to cut back because of temperature

increase and feeling bad. To her VERY GREAT CREDIT, she follow the

advise of scaling back the dosage to 50 IU/day and she has been able

to increase by 50 IU/day each week afterwards. She is still

increasing vitamin D and is glad that she is doing so --- she has

noticed improvement in several areas.

If those SARC patients were similar, they probably were given far too

high dosages of vitamin D and to put it simply, HERX LIKE PURGATORIO!

For people starting vitamin D, taking body temperature (ear is best),

when you take it and every 30 minutes afterwards seem to be a way of

judging whether the dosage is too high or not. My kid hit 103F on 2

successive days after taking 800 IU of D, feeling sick -- this was

what clued me in to D, because the temperature rise (in ~ 30 minutes)

and duration (4-6 hours) fit a herx pattern/immune response increase.

Many on CFSProtocol reported the same pattern when they started.

So --- start slowly, and if you feel too bad (or get too hot), go to

lower dosages! Generally the Calcium + D capsules are 1-200 IU each,

so you could cut them in half for a lower dosage.

> This may explain the results a long time ago when 6 or 9 or

whatever

> it was, sarc patients were given vitamin D and half got well...I

> asked Trevor Marshall what he made of that and he couldn't answer.

> Now it makes sense.

>

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Check the three referenced studies --- or alternatively, can you post a

citation from a study that cleanly and clearly state that there is a

difference (and how)?

> But - is that in healthy mammals or inflamed ones? The 25 --> 1,25

> conversion is very different in inflamed states than what it is in

> health.

>

> > Furthermore, the author states:

> >

> > " as a person becomes vitamin D-deficient, there is an increase in

the

> > concentration of parathyroid hormone (PTH), which increases the

renal

> > production of 1,25(OH)2D, the circulating concentrations of which

> > often become normal or even elevated "

>

> Aha, very interesting.

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Thanks Ken. The D,25 was measuered in ng/mL and the D, 1,25 was

pg/mL. Both say I am out of range, high. My doctor did believe that

even though according to their range I was high, he believes the

numbers should be higher from his research. If they were where he

believe they should be, then I was good. He also said that

my " ratios " , were good according to that other guys protocol. He

felt that he was really trying to squeeeze me into the box, even

though the ratio was looking pretty good and I really didn't fit the

criteria.

The LLMD that I saw today, said of those tests that they looked

pretty good to him and he did have at least some knowledge of that

other protocol. He said that I shouldn't worry about taking D

supplements, but not to avoid it either. The way the sun is here in

NM, I'll get all the D I need considering my #s.

Thanks for your help!

> > Any idea what it means when you don't have a low D,25, but it is

> > also high. My D,25 was high at 59 (range 9-54) and then my D

1,25

> > was was really high at 78 (range 15-60). Do I need to cut back

on D,

> > do I need to supplement, what? Very confused. Do I have calcium

> > leaching into my muscle tissue and not getting enough into my

bones

> > due to to much D? Does this explain the muscle cramps everytime

I

> > consume calcium?

> >

> > I seemed to have noticed less cramping and my heart may have

settled

> > a bit since avoiding Vit. D in my food and supplements. I don't

> > avoid the sun at all though. I just am having a hard time

> > understanding all of this and what I see happening in my own

body.

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What I read is that there is localized production of Vitamin 1,25D

due to IFN and other cytokines. The production levels of 1,25D is not

tied back to:

* Supplementation of Vitamin D

* Sunlight exposure

* Or even Vitamin 25D levels.

The localized production of Vitamin 1,25D may be a different process

than the normal production of 1,25D and may take different

precursors. The cytokines may be causing localized PTH disruptions --

or it may be a totally different process. I recall reading discussion

on the what the pathway of the ***localized production*** of 1,25D

may be.

Am I missing something in your quote?

> Regarding inflammation affecting 1,25 vitamin D,

> http://edrv.endojournals.org/cgi/reprint/14/1/3.pdf section III

> Cutaneous Production of 1,25(OH)2D, the authors state:

>

> " These cells are exquisitely sensitive to IFN with

> stimulation of 1,25(OHbD production seen at concentrations

> less than 10 PM. Higher concentrations are inhibitory,… "

> " TNF stimulates 1,25(OH)2D production

> and transglutaminase activity in preconfluent cells

> (76), and it can reverse the inhibition seen with the higher

> concentrations of IFN (Fig. 6). The effects of TNF and IFN

> are not additive at the lower and "

>

> In keratinocytes the inflammatory cytokines tnf-alpha, and inf-

gamma

> together significantly increase 1,25(OH)2D production.

>

> From http://www.jleukbio.org/cgi/content/abstract/54/1/17 :

>

> " Alveolar macrophages acquire 1 alpha-hydroxylase activity in

> inflammation, and thereby metabolize 25 hydroxyvitamin D3 (25 D3)

to

> the active metabolite, 1 alpha,25-dihydroxyvitamin D3 (1,25 D3,

> calcitriol). "

>

> The study also shows that in the presence of the inflammatory

> cytokines tnf-alpha and inf-gamma, moncytes are also capable of

> producing calcitriol.

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The first thought that crosses my mind (from recent readings) is

micro-thrombosis in various organs. This seems to be often reported

with APS (which CFIDS may be a variation of -- per Berg/Hemex).

Have you had coagulation testing? (I forget)

Have you done the enzyemes: bromelain, serrapetase, nattokinease and

lumbrokinease? [ taking all four should reduce microthrombosis - each

one impacts different parts of deposits from thrombosis].

Just a quick thought that came to mind....

> Despite ++ supplementation (even IV)I am not making any headway in

> increasing my vitamin d nor my calcium. ly I'm low in several

> nutritional areas, but have not had any luck with finding answers.

> Armed with this information here and a little cutting and pasting,

I

> should be mightily armed.

> Thanks again.

> Peg

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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

> > > Concerning vitamin D, I finally came across an article that

> states

> > > some important items very clearly based on actual studies --

> > instead

> > > of speculative theories. I have been frustrated because I have

> seen

> > > the same thing stated in many articles -- but it has not been

> > > sufficiently simply stated that a CFIDS mind could understand

it.

> > >

> > > Source:Vitamin D: importance in the prevention of cancers, type

1

> > > diabetes, heart disease, and osteoporosis, American Journal of

> > > Clinical Nutrition, Vol. 79, No. 3, 362-371, March 2004 The

full

> > text

> > > is available at: http://www.ajcn.org/cgi/content/full/79/3/362

> > >

> > > " neither increased exposure to sunlight nor increased oral

intake

> > of

> > > vitamin D raised blood concentrations of 1,25(OH)2D " (3

studies

> > > cited)

> > >

> > > Furthermore, the author states:

> > >

> > > " as a person becomes vitamin D-deficient, there is an increase

in

> > the

> > > concentration of parathyroid hormone (PTH), which increases the

> > renal

> > > production of 1,25(OH)2D, the circulating concentrations of

which

> > > often become normal or even elevated "

> > >

> > > So 1,25D increases with Vitamin D deficiency has been

established

> > in

> > > medical literature. It seems clear that Vitamin D

supplementation

> > > until Vitamin D is at the optimal levels should be done before

> you

> > > can be sure of meaningful 1,25D levels

> > > * 45-50 ng/ml or 115-128 nmol/l. Mercola, MD

> > > http://www.mercola.com/2002/feb/23/vitamin_d_deficiency.htm

> > >

> > > I found it interesting that low levels of Vitamin D may induce

a

> > > false elevation of 1,25D levels (even a HIGH reading).

> > >

> > > This is what medical science study states and have found to be

> the

> > > case.

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IFN-g-induced local inflammatory production comes from the same

precursor, as I vaguely recall. At least that was the impression I

got from the Vidal paper likes (a paper which is rather

dense). But I am no close student of the subject.

> > Regarding inflammation affecting 1,25 vitamin D,

> > http://edrv.endojournals.org/cgi/reprint/14/1/3.pdf section III

> > Cutaneous Production of 1,25(OH)2D, the authors state:

> >

> > " These cells are exquisitely sensitive to IFN with

> > stimulation of 1,25(OHbD production seen at concentrations

> > less than 10 PM. Higher concentrations are inhibitory,… "

> > " TNF stimulates 1,25(OH)2D production

> > and transglutaminase activity in preconfluent cells

> > (76), and it can reverse the inhibition seen with the higher

> > concentrations of IFN (Fig. 6). The effects of TNF and IFN

> > are not additive at the lower and "

> >

> > In keratinocytes the inflammatory cytokines tnf-alpha, and inf-

> gamma

> > together significantly increase 1,25(OH)2D production.

> >

> > From http://www.jleukbio.org/cgi/content/abstract/54/1/17 :

> >

> > " Alveolar macrophages acquire 1 alpha-hydroxylase activity in

> > inflammation, and thereby metabolize 25 hydroxyvitamin D3 (25 D3)

> to

> > the active metabolite, 1 alpha,25-dihydroxyvitamin D3 (1,25 D3,

> > calcitriol). "

> >

> > The study also shows that in the presence of the inflammatory

> > cytokines tnf-alpha and inf-gamma, moncytes are also capable of

> > producing calcitriol.

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Hi Pippit:

Nice to see you here... your post is very well thought out

and an excellent reply to Kens post.

It's too long for me to reply to specific points but I will makes

some comments.

" Don't be mislead by this study " ... and I'll add " Don't be mislead

by any study " .

From my own past, I positively know that my symptoms overlapped with

Sarc (as you know from previous communications) and lupus. One of

the most startling symptoms I had was the classic " S " swelling -

which is edema between the eyebrow and the top crease of the eye lid.

And I positively could not tolerate sunlight in doses longer than 15

minutes or I'd get nauseous and often would vomit - and be so ill as

to have to go to bed. This was in the 70's - so of course I had no

idea about vit D dysregulation - or autoimmune disease - or chronic

infection for that matter. But I could track feeling ill (and UV

exposure) to food. i.e. I felt much better if I didn't eat anything.

So I thought there was something in the food that exacerbated the

problem - but I never figured out what.

I was operated on in 1980 and samples of every internal tissue was

sent to the path lab. Every single one of them showed signature

inflitrates of chronic inflammation. So I positively know I had

system chronic inflammation - hense that bolstered my lupus diagnosis

even more... Insite of all this 'evidence' my root problem was

infection as evidenced by my total remission after treatment for Lyme.

The point I want to make in this post, is that if chronic infection

is allowed to proliferate - wide spread inflammation and

dysregulation of MANY of the body's (regulation) mechanisms occurs.

Dysregulation of D is probably just one - and we know it's tied

into hormone dysregulation , probably pain and alsoregulation of

minerals and so on down the dysregulation path.....

So, in my opinion, treatment has to be flexible and tailored to the

stage of infection, and taking into consideration the persons drug

tolerance (liver/metabolism genetics)..

So I really think that instead of pushing one particular product or

another - or trying to disprove or PROVE any particular theory - we

should discuss them on their merits, and short comings openly and

honestly. If that can't be done- we don't get anywhere IMO.

And I'm not interested in staying static.

And I do have one question taht's been pressing on my mind for over a

year.

Is there anyone who has been able to stop Benicar and not have their

symptoms return?

Thanks.

Barb

> > > Concerning vitamin D, I finally came across an article that

> states

> > > some important items very clearly based on actual studies --

> > instead

> > > of speculative theories. I have been frustrated because I have

> seen

> > > the same thing stated in many articles -- but it has not been

> > > sufficiently simply stated that a CFIDS mind could understand

it.

> > >

> > > Source:Vitamin D: importance in the prevention of cancers, type

1

> > > diabetes, heart disease, and osteoporosis, American Journal of

> > > Clinical Nutrition, Vol. 79, No. 3, 362-371, March 2004 The

full

> > text

> > > is available at: http://www.ajcn.org/cgi/content/full/79/3/362

> > >

> > > " neither increased exposure to sunlight nor increased oral

intake

> > of

> > > vitamin D raised blood concentrations of 1,25(OH)2D " (3

studies

> > > cited)

> > >

> > > Furthermore, the author states:

> > >

> > > " as a person becomes vitamin D-deficient, there is an increase

in

> > the

> > > concentration of parathyroid hormone (PTH), which increases the

> > renal

> > > production of 1,25(OH)2D, the circulating concentrations of

which

> > > often become normal or even elevated "

> > >

> > > So 1,25D increases with Vitamin D deficiency has been

established

> > in

> > > medical literature. It seems clear that Vitamin D

supplementation

> > > until Vitamin D is at the optimal levels should be done before

> you

> > > can be sure of meaningful 1,25D levels

> > > * 45-50 ng/ml or 115-128 nmol/l. Mercola, MD

> > > http://www.mercola.com/2002/feb/23/vitamin_d_deficiency.htm

> > >

> > > I found it interesting that low levels of Vitamin D may induce

a

> > > false elevation of 1,25D levels (even a HIGH reading).

> > >

> > > This is what medical science study states and have found to be

> the

> > > case.

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I dono, no idea. Personally I dont modulate D. I havent been

following the porphyria discussion so I dont know anything about that.

> > > " neither increased exposure to sunlight nor increased oral

> intake of

> > > vitamin D raised blood concentrations of 1,25(OH)2D " (3

studies

> > > cited)

> >

> > But - is that in healthy mammals or inflamed ones? The 25 -->

1,25

> > conversion is very different in inflamed states than what it is

in

> > health.

> >

> > > Furthermore, the author states:

> > >

> > > " as a person becomes vitamin D-deficient, there is an increase

> in the

> > > concentration of parathyroid hormone (PTH), which increases the

> renal

> > > production of 1,25(OH)2D, the circulating concentrations of

> which

> > > often become normal or even elevated "

> >

> > Aha, very interesting.

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Ken,

So you're suggesting that people with autoimmune disease get more

iron and that will induce remission?

Pippit

> > > > Concerning vitamin D, I finally came across an article that

> > states

> > > > some important items very clearly based on actual studies --

> > > instead

> > > > of speculative theories. I have been frustrated because I

have

> > seen

> > > > the same thing stated in many articles -- but it has not been

> > > > sufficiently simply stated that a CFIDS mind could understand

> it.

> > > >

> > > > Source:Vitamin D: importance in the prevention of cancers,

type

> 1

> > > > diabetes, heart disease, and osteoporosis, American Journal

of

> > > > Clinical Nutrition, Vol. 79, No. 3, 362-371, March 2004 The

> full

> > > text

> > > > is available at: http://www.ajcn.org/cgi/content/full/79/3/362

> > > >

> > > > " neither increased exposure to sunlight nor increased oral

> intake

> > > of

> > > > vitamin D raised blood concentrations of 1,25(OH)2D " (3

> studies

> > > > cited)

> > > >

> > > > Furthermore, the author states:

> > > >

> > > > " as a person becomes vitamin D-deficient, there is an

increase

> in

> > > the

> > > > concentration of parathyroid hormone (PTH), which increases

the

> > > renal

> > > > production of 1,25(OH)2D, the circulating concentrations of

> which

> > > > often become normal or even elevated "

> > > >

> > > > So 1,25D increases with Vitamin D deficiency has been

> established

> > > in

> > > > medical literature. It seems clear that Vitamin D

> supplementation

> > > > until Vitamin D is at the optimal levels should be done

before

> > you

> > > > can be sure of meaningful 1,25D levels

> > > > * 45-50 ng/ml or 115-128 nmol/l. Mercola, MD

> > > > http://www.mercola.com/2002/feb/23/vitamin_d_deficiency.htm

> > > >

> > > > I found it interesting that low levels of Vitamin D may

induce

> a

> > > > false elevation of 1,25D levels (even a HIGH reading).

> > > >

> > > > This is what medical science study states and have found to

be

> > the

> > > > case.

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Ken,

IMHO, one shouldn't supplement with 25-D either. Since 25-D ends up

synthesizing more 1,25-D in the body, the end result in an autoimmune

patient is the same as if you were to supplement straight 1,25-D.

When I say this I'm not referring to people whose immune systems are

functioning normally. For those, your model is probably appropriate,

but with someone whose system is extra-sensitive to Vitamin D, some

counter-adjustments need to be made to compensate for the particular

metabolism difficulty. If we make more 1,25-D than what normally

would happen in those who are not ill, it follows that our disordered

metabolisms can't handle the same amount of its precursor (25-D)as

other well people can.

SARC AND THE SYTHESIS OF 1,25-D IN GRANULOMATOUS TISSUE;

Endocrine complications of sarcoidosis.

Bell NH.

Veterans Affairs Medical Center, ton, South Carolina.

Sarcoidosis is a multisystem disorder of unknown etiology that

frequently involves the lymph nodes, lungs, eyes, and skin. The

disease can involve any organ system, and noncaseating granulomas are

characteristically present.

Synthesis of 1,25-dihydroxyvitamin D, the most biologically active

form of vitamin D, occurs in granulomatous tissue and may give rise

to increases in its concentration in the peripheral circulation and

to hypercalcemia and hypercalciuria.

PMID: 1935922 [PubMed - indexed for MEDLINE]

THE EFFECTS OF 25-D INCREASED 3-FOLD IN SARC PATIENTS W/O

HYPERCALCEMIA;

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?

cmd=Retrieve & db=pubmed & dopt=Abstract & list_uids=7419722 & itool=iconpmc & q

uery_hl=38

J Clin Invest. 1980 Oct;66(4):852-5.

Evidence for abnormal regulation of circulating 1 alpha,25-

dihydroxyvitamin D in patients with sarcoidosis and normal calcium

metabolism.

Stern PH, De Olazabal J, Bell NH.

The effects of vitamin D, 2.5 mg (100,000 U)/d for 4 d, on serum

calcium, serum 25-hydroxyvitamin D (25-OHD), and serum 1 alpha,25-

dihydroxyvitamin D [1 alpha,25(OH)2D] were compared in 17 normal

subjects and 6 patients with sarcoidosis who had normocalcemia and no

history of hypercalcemia.

The diagnosis was confirmed histologically in each of them.

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 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).

There was a significant positive correlation between the serum 1

alpha,25(OH)2D and serum calcium in these individuals (r = 0.663, P <

0.01) but not in the normal subjects.

The results (a) provide further evidence for abnormal regulation of

circulating 1 alpha,25(OH)2D in sarcoidosis and

(B) indicate that the abnormality may exist in patients with normal

calcium metabolism. Thus, the defect in vitamin D metabolism in

sarcoid apparently is more common than was previously recognized.

PMID: 7419722 [PubMed - indexed for MEDLINE]

If one eats a reasonable diet (not high in D, but reasonable),we

should have enough not to be deficient, but it's the added vitamin D

and that naturally occuring in foods in which Vitamin D is

particularly high that we need to be careful not to eat, and sunlight

for many people puts it over the top. For people who already

manufacture too much 1,25-D naturally, taking 25-D could put them in

the ER.

I'm not only using a scientific perspective, but also a practical

one. If X number of patients (including myself) get sick upon Vitamin

D ingestion or absorbtion through the skin via sunlight, then there's

obviously something going on and it's more than just an isolated

incident. If I eat shrimp for instance, then I get sick within only

15-20 minutes (at least I did last time I ate it several years ago

when I was alot sicker), and there's no mistaking it. There was a

time before I was so sick when shrimp didn't bother me but as soon as

my disease got really out of control that was it, I could no longer

tolerate it.I have a similar reaction to MSG and Folic Acid.

Here are a few more studies which support the idea that in people

with a dysregulated Vitamin D metabolism should not supplement with

25-D, and that 25-D can in fact raise 1,25-D too much in susceptible

populations;

Clin Sci (Lond). 1985 Feb;68(2):135-41.

Vitamin D metabolism in patients intoxicated with ergocalciferol.

Mawer EB, Hann JT, Berry JL, Davies M.

Vitamin D metabolites were measured on admission in eight patients

intoxicated with ergocalciferol (serum calcium 3.01-4.05 mmol/l) and

also during the subsequent 2 months in six of the eight.

Serum concentrations of 25-hydroxyergocalciferol, on admission, were

grossly elevated in all patients (range 583-1843 nmol/l). Serum

calcium concentration was related significantly only to the

concentration of 25-hydroxyergocalciferol (P = 0.003).

Concentrations of 25-hydroxyergocalciferol in serum were

significantly related to those of calciferol (P = 0.004).

Elevated initial concentrations of 1,25-dihydroxycalciferol, mainly

as 1,25-dihydroxyergocalciferol, were found in seven of the eight

patients (range 179-313 pmol/l).

It is suggested that the hypercalcaemia in these patients may be

explained by the action of 25-hydroxyergocalciferol at high

concentration in competing for 1,25-dihydroxycalciferol receptors,

thus exerting a biological effect per se, and also by increasing the

synthesis of 1,25-dihydroxycalciferol through a mass-action effect on

the renal 1 alpha-hydroxylase.

PMID: 3871380 [PubMed - indexed for MEDLINE]

25-D AND ARTHRITIS;

http://toxnet.nlm.nih.gov/cgi-bin/sis/search/r?dbs+hsdb:@term+@rn+67-

97-0

....IT IS CONTRAINDICATED IN CONDITIONS SUCH AS ARTHRITIS...

[American Medical Association, Council on Drugs. AMA Drug

Evaluations. 2nd ed. Acton, Mass.: Publishing Sciences Group, Inc.,

1973., p. 203]**PEER REVIEWED**

If you believe in intelligent design or Mother Nature, then maybe

He/She is trying to tell us something here with this live sampling of

people, many of whom feel better when they have less D rather than

more. Although vitamin D is only a part of this intricate metabolic

problem, it makes good sense to heed this piece of the puzzle when

you find a large number of people who respond the same way in a

direct trial.

There are other fine-points of the biochemistry of these diseases

that remain a mystery, which is where we should be investing our

energies at this point.

Pippit

> > > > Concerning vitamin D, I finally came across an article that

> > states

> > > > some important items very clearly based on actual studies --

> > > instead

> > > > of speculative theories. I have been frustrated because I

have

> > seen

> > > > the same thing stated in many articles -- but it has not been

> > > > sufficiently simply stated that a CFIDS mind could understand

> it.

> > > >

> > > > Source:Vitamin D: importance in the prevention of cancers,

type

> 1

> > > > diabetes, heart disease, and osteoporosis, American Journal

of

> > > > Clinical Nutrition, Vol. 79, No. 3, 362-371, March 2004 The

> full

> > > text

> > > > is available at: http://www.ajcn.org/cgi/content/full/79/3/362

> > > >

> > > > " neither increased exposure to sunlight nor increased oral

> intake

> > > of

> > > > vitamin D raised blood concentrations of 1,25(OH)2D " (3

> studies

> > > > cited)

> > > >

> > > > Furthermore, the author states:

> > > >

> > > > " as a person becomes vitamin D-deficient, there is an

increase

> in

> > > the

> > > > concentration of parathyroid hormone (PTH), which increases

the

> > > renal

> > > > production of 1,25(OH)2D, the circulating concentrations of

> which

> > > > often become normal or even elevated "

> > > >

> > > > So 1,25D increases with Vitamin D deficiency has been

> established

> > > in

> > > > medical literature. It seems clear that Vitamin D

> supplementation

> > > > until Vitamin D is at the optimal levels should be done

before

> > you

> > > > can be sure of meaningful 1,25D levels

> > > > * 45-50 ng/ml or 115-128 nmol/l. Mercola, MD

> > > > http://www.mercola.com/2002/feb/23/vitamin_d_deficiency.htm

> > > >

> > > > I found it interesting that low levels of Vitamin D may

induce

> a

> > > > false elevation of 1,25D levels (even a HIGH reading).

> > > >

> > > > This is what medical science study states and have found to

be

> > the

> > > > case.

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Hi Barb,

Nice to see you too. Sorry for the length of my other post with all

the studies in it. I agree with you that Vitamin D isn't the only

part of this pathogenesis, and that was in my most recent response to

Ken. We were just looking into that one aspect deeply (on both sides

of the issue)and I think that is part of the discernment process and

ultimately making treatment flexible. One has to look at the micro

view (one idea, and close-up, from one side to the other)to determine

whether or not something holds true for all, for some, or for none of

the population you're researching.

I have actually learned alot of new information in the past several

months, through reading as well as experience and observation, and am

applying it and have been integrating it with the knowledge base I

had before.

I've never been one to just blindly " trust " anyone because they say

so, but instead if I come to the conclusion that something is true

(or not true), it's based on alot of groundwork and alot of weighing

back and forth. If I'm presented with information that causes me to

re-evaluate my view (and that does happen at times), I'm willing to

re-evaluate.

I look at a theory as a basic framework, not a political position per

se. If you find (or put one together) that basically works in

practice, you can adjust it as need dictates.

I've found that there are some physical laws that prove themselves to

me again and again, no matter how many times I consider the opposite

(or other) explanation.

By the same token, there are other new considerations that I take

into account, as I continue to observe, read, and talk to patients

about their experience with treatment.

I believe there are some common threads that run through all

approaches that work for Lyme, Sarc, CFS, Lupus, etc...and finding

out what those commonalities are will save us alot of time, because

in the end we're more the same than different as human beings.

I, like you, will never remain static. That's why I read material

encompassing all sides of an issue, go to alot of different sites,

and engage in discussion with patients and professionals of every

variety.

I want these diseases gone from the earth, and I won't rest until

that happens. I'm not satisfied with remission, or symptom-control. I

want to take it further than that. I want to see the day when we know

that stealth pathogens will never again parasitize our cells (not

because we think they won't) but with proof that the blueprint for

them to do so has been changed to what it should have been, pre-

illness.

By the way, I read your article on Fibroblast Growth Factor and it's

very interesting. This is another facet worth looking into further.

In answer to your question about Benicar, I'd have to check on that.

I do know that a number of people (including myself) have been able

to reduce their daily intake of Benicar, as they improve. It may be

too early to assess whether someone off Benicar entirely will remain

stable without symptoms returning because it's really only been a

year since Phase III was introduced. Probably, if anybody has tried

it, they wouldn't have been off it for long yet.

Pippit

> > > > Concerning vitamin D, I finally came across an article that

> > states

> > > > some important items very clearly based on actual studies --

> > > instead

> > > > of speculative theories. I have been frustrated because I

have

> > seen

> > > > the same thing stated in many articles -- but it has not been

> > > > sufficiently simply stated that a CFIDS mind could understand

> it.

> > > >

> > > > Source:Vitamin D: importance in the prevention of cancers,

type

> 1

> > > > diabetes, heart disease, and osteoporosis, American Journal

of

> > > > Clinical Nutrition, Vol. 79, No. 3, 362-371, March 2004 The

> full

> > > text

> > > > is available at: http://www.ajcn.org/cgi/content/full/79/3/362

> > > >

> > > > " neither increased exposure to sunlight nor increased oral

> intake

> > > of

> > > > vitamin D raised blood concentrations of 1,25(OH)2D " (3

> studies

> > > > cited)

> > > >

> > > > Furthermore, the author states:

> > > >

> > > > " as a person becomes vitamin D-deficient, there is an

increase

> in

> > > the

> > > > concentration of parathyroid hormone (PTH), which increases

the

> > > renal

> > > > production of 1,25(OH)2D, the circulating concentrations of

> which

> > > > often become normal or even elevated "

> > > >

> > > > So 1,25D increases with Vitamin D deficiency has been

> established

> > > in

> > > > medical literature. It seems clear that Vitamin D

> supplementation

> > > > until Vitamin D is at the optimal levels should be done

before

> > you

> > > > can be sure of meaningful 1,25D levels

> > > > * 45-50 ng/ml or 115-128 nmol/l. Mercola, MD

> > > > http://www.mercola.com/2002/feb/23/vitamin_d_deficiency.htm

> > > >

> > > > I found it interesting that low levels of Vitamin D may

induce

> a

> > > > false elevation of 1,25D levels (even a HIGH reading).

> > > >

> > > > This is what medical science study states and have found to

be

> > the

> > > > case.

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