From: sbharris@ix.netcom.com(Steven B. Harris)
Newsgroups: sci.med.nutrition
Subject: Re: Vitamin D and calcium
Date: 3 Dec 1997 22:20:09 GMT

In <34858B79.3E48@erols.com> physical@erols.com writes:

> Interestingly, dark-skinned
>people get 25% less D from sunlight than light-skinned people, yet, are
>reputed to have higher bone density (at least Africans), despite much
>lower calcium intakes (but also much lower protein!).

   If they get their D from other sources.  In the days before vitamin
D it was added to milk, black people in higher latitudes had terrible
problems with rickets.  Quiz: what famous black former football star,
recently accused of murdering his wife, had rickets as a child in San
Francisco, in the days before fortified milk?  I know, it's a tough one
<g>.

   Vitamin D is "added" to milk, BTW, by zapping it with UV.  Nature
can't make D without UV.  Even D in fish is from plankton which have D
in them, and need UV themselves to make it.  Vitamin D was the only
vitamin the "Biospherians," who got no UV through the glass, knew
absolutely they'd have to get in pills.


                                       Steve Harris, M.D.

From: sbharris@ix.netcom.com(Steven B. Harris)
Newsgroups: sci.med.nutrition
Subject: Re: Vitamin D and calcium
Date: 5 Dec 1997 00:09:58 GMT

In <666s5b$748@clam.Hi.COM> wright@nospam.clam (David Wright) writes:
>
>In article <664lup$3i1@sjx-ixn3.ix.netcom.com>,
>Steven B. Harris <sbharris@ix.netcom.com> wrote:
>
>>   Vitamin D is "added" to milk, BTW, by zapping it with UV.  Nature
>>can't make D without UV.  Even D in fish is from plankton which have D
>>in them, and need UV themselves to make it.  Vitamin D was the only
>>vitamin the "Biospherians," who got no UV through the glass, knew
>>absolutely they'd have to get in pills.
>
>Was there something special about the glass used in Biosphere II?  I
>was under the impression that ordinary glass did allow some UV to pass
>through it.


   No, it was standard glass.  And standard glass doesn't pass enough
UV to let you make much vitamin D.

From: sbharris@ix.netcom.com(Steven B. Harris)
Newsgroups: sci.med.nutrition
Subject: Re: Feline Nutriton Question
Date: 22 Aug 1998 05:25:20 GMT

In <cjfuller-2108980748030001@c-fuller1.uncg.edu>
cjfuller@mindspring.com (C. J. Fuller) writes:

>Liz-Cats can synthesize their own vitamin D in the skin, IF they are
>exposed to sunlight or another source of UV light.  The pathway is the
>same as for humans:


  Thanks, Cindy.  I suspected as much.  Humans have a terrible problem
making enough vitamin D at high latitude if they have dark skins, and I
suspect that cats with dark hair have the same problem.

   In fact, the thought just occurs-- it may be that white Siberian
tigers got selected for in nature (before we started doing it
artificially) partly because of this.  Polar bears get all the D they
need in the diet, but Siberian tigers might have a problem there, and
need some sunlight D to supplement.  White hairs have recently been
shown to conduct UV to the skin like little light fiber conduits.  One
reason that polar bears have nearly black skin under all that white
fur.  In the UV, polar bears are very dark against snow--- UV vision
would be very useful to seals.

   As you know, current theory suggests that the human race started out
with very dark skin, and lighter skin is a mutation-- a response to
having to live at high latitudes with clothing and no fish.

                                       Steve Harris, M.D.

From: reinhold.vieth@utoronto.ca (Reinhold Vieth)
Newsgroups: sci.med.nutrition
Subject: Re: Vit D - A very urgent case
Date: 14 Mar 2002 20:36:57 -0800
Message-ID: <22ca11f.0203142036.1779fb5f@posting.google.com>

Dear Nayer:
YOU ASKED about vitamin D toxicity, because you
> have used Vitamin D3 - 50.000 I.U. made by Merck , about 60 capsules in a
> period of 3 months or less.

I am a clinical researcher specializing in vitamin D nutrition.
I am regularly asked similar panick questions about vitamin D, and
have read with interest the many previous recommendations offered you
since you posted your  request for advice.

NUMBER ONE: what any responsible physician MUST do for a patient
presenting as you did, MEASURE THE 25(OH)D LEVEL !!!!  If the level is
less than 300 nmol/L (for Americans, that works out to < 120 ng/mL)
you can rest assured there is nothing toxic going on.  There have been
lots of people getting your kind of dose for therapeutic purposes, and
without problem.  At a guess, from what you say, if you were taking
vit D3 (which I doubt, since 50000 formulations in the US have to my
knowledge been vit D2 - not D3), then I would predict your 25D
concentration would be close to 300 nmol/L.  If higher, than this, and
your serum and urine calcium levels are normal, then again, you have
no problem.  If you still find out you have a toxicity problem, then
your Dr should discuss treatment with a corticosteroid and/or
bisphosphonate with you.

In Canada, there is no problem in getting a 25D level done by any
physician if toxicity is a concern.  I am surprised you have not
reported to this discussion group what your 25D result is.

If you really want to see what vitamin D toxicity is like, check the
Feb 23, 2002 issue of the Lancet, in which two people each consumed
over 1 million IU of vit D3, daily, for SEVEN MONTHS!  From what you
say, you would have only taken a grand total of 1.5 million units -
what these patients took in just one day.  The patients we reported in
the Lancet showed all the classic signs: hypercalcemia,
hypercalciuria, kidney calcium deposits, dehydration, nausea,
vomiting, weight loss.  The symptoms are long term, if not treated.
When the patient first presented at the emergency room, the symptoms
were thought to be gastroenteritis (part of the initial differential
diagnosis).  You evidently don't show any of those symptoms.

Vitamin D continues to be the boogey-man of nutrition.  I would not
recommend taking 50000 IU per day without a reason, but a few days of
it should not be a problem for a healthy adult.  I note one person
responding here to your query stated that liver enzymes would be
affected by high vitamin D levels - there is NO WAY that happens!  (If
anyone knows of peer-reviewed evidence contradicting my bold
statement, please let me know, because from what I have been able to
find, such liver notions are groundless).

Three questions for you:
1.  Where did you get the 50000 IU capsules, because this dose is only
available by prescription?
2.  Are you sure it was vit D3 that you took?  To my knowledge all the
50000 IU doses available in North America are actually vit D2, which
probably has a different toxicity profile.  i.e. Was it D2 or D3 ?
3.  Would you please let us know your 25D level when you find out what
it is?

I would appreciate clarification on these 3 points.

Best wishes, and I assume you are doing well,
Reinhold Vieth

From: "Steve Harris" <sbharris@ix.RETICULATEDOBJECTcom.com>
Newsgroups: sci.med.nutrition
Subject: Re: Vit D - A very urgent case
Date: Fri, 15 Mar 2002 13:54:41 -0700
Message-ID: <a6tn7n$ldo$1@slb7.atl.mindspring.net>

"JEDilworth" <bactitech@nospamhortonsbay.com> wrote in message
news:3C9197AD.7E914E1B@nospamhortonsbay.com...
> Thanks for clearing up the liver enzyme question.  As I have stated many
> times, I am not a chemistry technologist.  I enjoy learning about case
> histories, and the one you have presented is very interesting.  I was
> looking at this in a very simplistic mode and obviously got it all
> wrong.  My apologies.  I was looking at it totally from the viewpoint of
> liver damage = elevated liver enzymes.  Obviously it's much more
> complicated than that.


It really is that simple, as liver damage always does cause elevation of
liver enzymes (while it's going on). The reason you don't see this with
vitamin D poisoning is simply that it doesn't cause liver damage!  That's
vitamin A poisoning.

I'm glad to get Dr. Vieth's input on this as the recognized expert in the
field, but I still don't know why he's recommending testing 25-OH-D levels,
as I cannot see how they would change your treatment in the eucalcemic
patient. In the patient who has stopped vitamin D and who has normal calcium
levels, it seems unlikely to impossible that they'll rise in the future, so
it doesn't matter what his blood levels for D are-- you're never going to
see or test him again unless he becomes symptomatic (nauseus, anorexic,
polyuric, etc). If he does become symptomatic, then you'll have to test him
for calcium anyway, and there's no point in testing for D levels if the
calcium continues to be normal. Only if it's ABNORMAL do you have to go on
to test for D levels, as you then need to differentiate some latent weird D
toxicity from some new and unrelated medical problem, like parathyroidosis
or Ca hormone-active tumor. Otherwise, it appears to me you're wasting
money.

Steve

From: reinhold.vieth@utoronto.ca (Reinhold Vieth)
Newsgroups: sci.med.nutrition
Subject: Re: Vit D - A very urgent case
Date: 16 Mar 2002 21:59:59 -0800
Message-ID: <22ca11f.0203162159.20be4262@posting.google.com>

Concerning the diagnosis question:
> Medical insurance companies don't like to pay out for extremely
> expensive testing unless a diagnosis code supports the test request.  It
> seems perfectly reasonable to me from the monetary standpoint to run the
> Ca levels first and then go to the esoteric testing if the Ca screening
> is abnormal.

  I am not in the US, so I wonder, Is there not a "diagnostic code"
for a poisoning?  It makes sense to me, that if there is a medical
query about an overdose or a poisoning, and if a diagnostic test for
that poison is available, then that test should be done.
The 25D level will certainly affect followup in this case:
1.  if the patient thought he took vitamin D, but the 25D is low or
normal, then obviously the patient was wrong, and no more followup is
justified, and the patient can take calcium supplements
2.  if the 25D is elevated, but without hypercalcemia, then there
should be a followup medical visit, to ensure the situation continues
to subside.  If the 25D is elevated beyond 250-300 nmol/L (higher than
naturally possible for the human) then the patient should be advised
to keep away from calcium supplements for at least 6 months.

3.  The final justification for doing the 25D test is that it contains
knowledge.  There is very little record of what the 25D level will be
for given vitamin D intakes, and unless the suspected toxicology is
appropriately documented, then vitamin D will continue to be the
bogeyman of nutrition, just because we don't document the suspected
cases of toxicity properly.  If this does not happen in the public
ongoing practice of medicine, then how can we learn about what happens
with high doses?  I doubt that there is anybody out there willing to
take part in a toxicological clinical study of this, even if funded by
the NIH.  I know that responsible manufacturers of vitamins keep very
close watch out for reports of cases of overdose.  Occurrence and
effects of excessive intake are fundamental to public health.

You see, the 25D level does affect medical practice.

I am still waiting for a response from Nayyer to the 3 questions I
posed previously.  Perhaps this case is not "very urgent" any more.

From: "Steve Harris" <sbharris@ix.RETICULATEDOBJECTcom.com>
Newsgroups: sci.med.nutrition
Subject: Re: Vit D - A very urgent case
Date: Thu, 14 Mar 2002 12:41:07 -0700
Message-ID: <a6quh8$n9i$1@slb7.atl.mindspring.net>

"Martin Banschbach Ph.D." <mbansch314@aol.com> wrote in message
news:20020313102612.24444.00000362@mb-ch.aol.com...

> A serum calcium is a "snapshot".  It can be used to confirm vitamin D
> toxicity but it can't be used to rule it out.

And why not?  If your calcium level is normal NOW, you can't have vitamin D
toxicity NOW.  The worst you can have is calcification from it in the PAST,
or enough unabsorbed vit D in your stomach (if you just swallowed a bottle)
to give you problems later, but that's unlikely here.

> A normal total calcium indicates that the 25-hydroxy D levels are
> probably not high enough to cause a significant movement of calcium out
> of bone.


I don't believe that high 25-hydroxyD causes *much* calcium to move out of
bone.  A little goes in that direction, but certainly not enough to cause
condromalacia per se (as low vit D does). The high serum calcium and tissue
calcification in vit D in poisoning is generally caused by overabsorption.
The calcium for it mostly does not come from the bones.


> The only way to determine exactly how much vitmain D is stored in your
> liver is through a 25-hydroxy D lab test.  I don't recall what the cost
> is.  It's not a routine clinical lab test.


Actually it is commonly done on non-milk drinking non-supplement using women
in workups for osteoporosis, in higher latitudes (anything where you get
snow in winter) where sunlight is scarce. I've ordered many a 25-hydrox D
test.

By the way, here's a fascinating article suggesting that the presently
recognized upper safe vitamin D limit of 2,000 IU (5 standard OTC pills) a
day is probably low by a factor of at least 5, since people working in
sunlight get 10,000 a day, and all known tox cases have been at more than
40,000 IU a day (and that for a long time).  So our poster doesn't have that
much to worry about

============================================

Am J Clin Nutr 1999 May;69(5):842-56
Comment in:
Am J Clin Nutr. 1999 May;69(5):825-6.

Vitamin D supplementation, 25-hydroxyvitamin D concentrations, and safety.

Vieth R.

Department of Laboratory Medicine and Pathobiology, University of Toronto,
Mount Sinai Hospital, Ontario, Canada. rvieth@mtsinai.on.ca

For adults, the 5-microg (200 IU) vitamin D recommended dietary allowance
may prevent osteomalacia in the absence of sunlight, but more is needed to
help prevent osteoporosis and secondary hyperparathyroidism. Other benefits
of vitamin D supplementation are implicated epidemiologically: prevention of
some cancers, osteoarthritis progression, multiple sclerosis, and
hypertension. Total-body sun exposure easily provides the equivalent of 250
microg (10000 IU) vitamin D/d, suggesting that this is a physiologic limit.
Sailors in US submarines are deprived of environmentally acquired vitamin D
equivalent to 20-50 microg (800-2000 IU)/d. The assembled data from many
vitamin D supplementation studies reveal a curve for vitamin D dose versus
serum 25-hydroxyvitamin D [25(OH)D] response that is surprisingly flat up to
250 microg (10000 IU) vitamin D/d. To ensure that serum 25(OH)D
concentrations exceed 100 nmol/L, a total vitamin D supply of 100 microg
(4000 IU)/d is required. Except in those with conditions causing
hypersensitivity, there is no evidence of adverse effects with serum 25(OH)D
concentrations <140 nmol/L, which require a total vitamin D supply of 250
microg (10000 IU)/d to attain. Published cases of vitamin D toxicity with
hypercalcemia, for which the 25(OH)D concentration and vitamin D dose are
known, all involve intake of > or = 1000 microg (40000 IU)/d. Because
vitamin D is potentially toxic, intake of >25 microg (1000 IU)/d has been
avoided even though the weight of evidence shows that the currently
accepted, no observed adverse effect limit of 50 microg (2000 IU)/d is too
low by at least 5-fold.


SBH

From: reinhold.vieth@utoronto.ca (Reinhold Vieth)
Newsgroups: misc.health.diabetes
Subject: Re: Vitamin D and Type 1
Date: 3 Nov 2001 19:45:39 -0800
Message-ID: <22ca11f.0111031945.69d376ea@posting.google.com>

Concerning the Finnish study of vitamin D supplementation and
prevention of juvenile diabetes, as initiated by William C Biggs MD:

The study is very interesting and potentially important.

I point out that the epidemiologic study focused on babies born in the
1960's in Finland.  And at that time, the infant recommended dose of
vitamin D in Finland was TEN TIMES the current US recommendation for
infants !!!  I point out to the reader that the study followed these
babies for 30 years into adulthood.  The Lancet article goes on to
wonder, whether the apparent increase in juvenile diabetes in Finland
might be attributable to their falling into line with US vitamin D
recommendations.

Note that a quick PubMed search using the terms "vitamin D, diabetes"
should direct the reader to the EURODIAB study showing similar, but
less impressive diabetes prevention using cod-liver oil delivering a
smaller amount of vitamin D (400 IU/day), and to other similar
studies.  This connection between vitamin D and diabetes is NOTHING
NEW, but just part of a growing pile of evidence for something good.
Just imagine how quick conventional medicine would eagerly snap up and
accept comparable evidence if the opposite had been reported.  Why are
we so eager to accept bad news, and pretent to play the cool waiting
game when people report something good, like the Finns just did in the
Lancet?

I highly doubt it would be ethically possible or feasible to do the
double blind prospective study the accompanying Lancet editorial so
coolly recommends should be done.  Are we going to have to wait
another 40 years for that confirmative study to be completed?

The Finns are living north of 60 degrees latitude, and are taking the
issue of vitamin D very seriously.  Their research output along these
lines is amazing, considering the country's population is only 5
million.

I hope they keep up the good work.  In the meantime, we on this side
of the Atlantic need to support the research necessary to move the
science along.

From: reinhold.vieth@utoronto.ca (Reinhold Vieth)
Newsgroups: sci.med.diseases.osteoporosis
Subject: vitamin D
Date: 25 Nov 2001 19:44:52 -0800
Message-ID: <22ca11f.0111251944.2d6a42c1@posting.google.com>

Nobody in these osteoporosis discussions has pointed out that the
SUCCESSFUL osteoporosis studies showing what we all think we know,
that "you need vitamin D along with your calcium" to lower fractures
of osteoporosis, used 800 IU/day of vit D3.  Note, 800 of D2 failed to
work.  400 IU of D3 did not work.

Simply put, if you are worried about osteoporosis, then take at least
800 IU of vitamin D3 (also known as, cholecalciferol) per day.  Less
has NEVER been shown to do anything, and more is absolutely safe and
physiological.

Think about it.  Humans are the only primates living north of 40
degrees latitude.  Humans evolved to expose 100% of skin surface to
abundant sunlight (could you really imagine that Nature designed us to
wear clothes?).

Thus, if one asks, "what is natural or normal for vit D?"  Then,
surely, the dose must be at least as much as you could get lying on
the beach in your bathing suit - almost every day.  Nobody has ever
considered this to be harmful in terms of getting too much vitamin D.
Instead, we wear clothes, live in the north, and avoid the sun.  There
is no way that the 400 IU of vit D3 in the teaspoon full of cod-liver
oil designed to prevent rickets in a baby will do you any good as an
adult.

It is a fantasy to think 400 IU of vit D will be of much use to an
adult.  The lowest dose shown to have a detectable benefit in adults
is 800 IU/day.  We know the lowest proven toxic patient took at least
40000 IU/day for many months.

Take your vitamin D, at a generous dose.  And if you are worried about
"toxicity" I contend that the most likely risk of "poisoning" is
because of the harm from modern humans having taken too little vitamin
D, not too much.

From: reinhold.vieth@utoronto.ca (Reinhold Vieth)
Newsgroups: alt.support.mult-sclerosis
Subject: Re: Vitamin D-Anyone tried high dose?
Date: 27 Nov 2001 12:06:57 -0800
Message-ID: <22ca11f.0111271206.18c5feb7@posting.google.com>

Concerning the question:
> 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

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.

From: reinhold.vieth@utoronto.ca (Reinhold Vieth)
Newsgroups: alt.support.mult-sclerosis
Subject: Re: Vitamin D-Anyone tried high dose?
Date: 2 Dec 2001 19:34:40 -0800
Message-ID: <22ca11f.0112021934.33febf74@posting.google.com>

Nick
Concerning the statement:

> 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

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

From: reinhold.vieth@utoronto.ca (Reinhold Vieth)
Newsgroups: alt.support.mult-sclerosis
Subject: Re: Vitamin D derived from tanning bed exposure
Date: 28 Dec 2001 20:51:55 -0800
Message-ID: <22ca11f.0112282051.eec7ebd@posting.google.com>

AN IMPORTANT DISTINCTION: FOCUS ON 25D, NOT 125D

A point of clarification about which vitamin D metabolite to pay
attention to: it is NOT "the therapeutic hormone", but rather
25-hydroxyvitamin D, also written as 25(OH)D, or 25D, or as calcidiol.

The 25(OH)D from circulation is used by brain and immune tissues to
make  1,25-dihydroxy vitamin D  ( 1,25(OH)2D , or 125D) which is NOT
released into the bloodstream.  That 125D which is found in blood is
from the kidney, and is relevant to calcium homeostasis.

Yes, 135 picomol/L (or pmol/L) of 125D is reasonable number, but
unless you have a kidney defect, you should be focusing on the vit D
nutrition marker, the 25D.

I suggest that circulating 25D should exceed 100 nmol/L for those
concerned about non-bone forms of D-deficiency.

The following quotes are thus a bit misleading, and I suspect Nick
just misprinted the form of vitamin D he was referring to.  It surely
is supposed to say, "25-hydroxy", not "1,25-dihydroxy".

> > level of 1,25-dihydroxy  must exceed 100 nmol/L in order for it to be an
> > effective immunosuppressant.

> > After two months of using a full body tanning bed my 1,25-dihydroxy levels
> > are 135 nmol/L. The bed I used has twenty four, 100 Watt bulbs. There are 12

From: reinhold.vieth@utoronto.ca (Reinhold Vieth)
Newsgroups: alt.support.mult-sclerosis
Subject: Re: Vitamin D derived from tanning bed exposure
Date: 30 Dec 2001 09:40:26 -0800
Message-ID: <22ca11f.0112300940.e5275ab@posting.google.com>

Response to the question about:
"last winter there was discussion about not bathing after the tanning
bed.  Is this still the understanding?  If so, for how long?  > Diane"

  Nobody has done the research on the issue of bathing and
sun-acquired vitamin D.  The question is a logical one and should be
looked into.

But since in human skin, vitamin D is generated beneath the protective
keratin layer of the skin, it probably does not make much difference
whether you bathe or not.  Your sun-made vitamin D is absorbed from
the lower skin layers directly into the bloodstream.

There is some vitamin D produced in the oils of the skin, but
relatively little of that is absorbed back into the bloodstream.

Fur-bearing animals get their vitamin D by grooming their fur --
licking their fur, removing the oils with the vitamin D3.  Thereby
most mammals take the sun-generated vitamin D by mouth.  Thus, if one
were a fur-bearing animal, the bathing would make a difference, and
wash off the vitamin D.

Interesting note: most vit D3 for supplement use is derived from the
oil of defatted lamb's wool, exposed to UV light and purified from
that.  Thus wool keeps you warm, and the oils from it can nourish you.

(Take care to note that vit D2 is NOT the natural product, be sure to
take vit D3, or get sunshine.)

Best wishes, Reinhold Vieth

From: reinhold.vieth@utoronto.ca (Reinhold Vieth)
Newsgroups: alt.support.mult-sclerosis
Subject: Re: Vitamin D derived from tanning bed exposure
Date: 8 Jan 2002 18:18:31 -0800
Message-ID: <22ca11f.0201081818.4a516ce2@posting.google.com>

Response to the following comment from Ed Hill

" > dr vieth seems to be saying here that serum levels of 1,25D3 don't
have the same effect as that produced by the individual cell.
> i respect and appreciate dr. vieth's opinion here but i'm not sure that
> the research bears this out.  especially in cases of autoimmune disease
> where supplementation of the hormone may be helpful."

I agree that the "research" suggests that doses 1,25(OH)D or its
analogs have effects when they are given to people with some high-risk
conditions.
Similar evidence for "dosing" with vitamin D3 (cholecalciferol)
supplementation does not exist.  However, the observational
epidemiology based on UV light all points to ONLY vitamin D nutrition
as being helpful.

One needs to realize that for some strange reasons, nobody has ever
considered the obvious possibility that doses of vitamin D that match
what the skin can make from sunshine might actually do anything.  The
dose-administration "research" to this point, has all been supported
by drug companies that make the 1,25(OH)2D or its analogs.

The research funded by drug companies has always avoided comparisons
with plain and simple vitamin D3, because the companies don't want to
compromize the chance of showing an effect for their own products.

Yes, research needs to be done for use of nutritional vitamin D.  It
is an agent that has been overlooked, and for which public research
funds need to be made available.  No corporation can justify an
investment in a clinical study of an agent like vitamin D, that is
guaranteed to be of no financial value for the company.

One must never confuse vitamin D with 1,25(OH)2D or its analogs.
There is no such thing as a safe, "non-calcemic" vitamin D analog.
The drugs are all far more toxic and risky than plain vitamin D,
because their use involves addition  to the whole body a powerful
agent that many tissues make locally when they need it.

Use of 4000 IU/d of vitamin D3 has never been shown to cause harm, and
it is the dose of vitamin D that should do for you what we think UV
light does.

Best wishes, Reinhold Vieth

From: reinhold.vieth@utoronto.ca (Reinhold Vieth)
Newsgroups: sci.med.nutrition,sci.bio.misc
Subject: Re: safety of vit D, related to MS
Date: 11 Jan 2002 11:47:10 -0800
Message-ID: <22ca11f.0201111147.37eb984c@posting.google.com>

This is in response to the following statements by
"Martin Banschbach PhD" <mban...@osu-com.okstate.edu> wrote in message

> Total body (no clothes on at all) is estimated to produce about 2,000 IU of
> vitamin D in a person with light skin.  Without the darkening of the skin,
> any dietary intake of vitamin D could lead to vitamin D toxicity since the
> amount formed in the skin is not regulated at all by what is already stored
> in the liver.
>
> Skin darkening is believed to have been an adaptation to decrease the risk
> of both skin cancer and vitamin D toxicity.

The comments are based on old assumptions.

First, There is no way that simply taking 2000 IU of vit D daily will
produce 25D concentrations over 100 nmol/L (40 ng/mL).  People taking
sun-lamp treatments (10 min, 2-3 times weekly) always have 25D over
100 nmol/L.
As a rule of thumb, 1 microgram (40 IU) of vitamin D3 daily will
increase 25D by about 0.7 nmol/L.  We showed this a year ago, Feb 2001
Am J Clin Nutrition.

Thus, 2000 IU = 50 mcg => 0.7 X 50 nmol/L = 35 nmol/L increase,
approximately.

Second.  The concept that black skin protects against vit D toxicity
makes no sense when it is noted that we all, black and white, can make
the same amount of vitamin D from sunshine exposure.  The toxicity
concept Dr Banschbach refers to is found in old anthropology texts,
and it stems back to a speculative article in the journal, Science, by
Loomis in the 1960's.  I highly recommend a more recent article by
Nina Jablonski (Journal of Human Evolution 39:57-106, 2000) in which
she explains the role of skin colour is to protect micronutrients in
the capillaries under the skin surface, as well as to prevent the
burning of skin.  Given that, she goes on to explain that the pressure
for the natural selection that favours lighter skin away from the
equator is to permit sufficient production of vitamin D.

i.e. if it were not for our need for enough vitamin D to prevent a
mishapen pelvis of rickets, making a vaginal delivery of a baby
impossible, none of us would have white skin.

The discussions posted by all of you here are excellent, and a
pleasure to read, thank you for them.

From: reinhold.vieth@utoronto.ca (Reinhold Vieth)
Newsgroups: sci.med.diseases.osteoporosis
Subject: Re: Vit D - A very urgent case
Date: 23 Mar 2002 01:08:13 -0800
Message-ID: <22ca11f.0203230108.68551646@posting.google.com>

Concerning the POWDER Study: Prevention of Osteoporosis With vitamin
D: Evaluation of Responses as quoted here

>     Well -- when I look at my various vitamins some count Vitamin D in
> UI and others as mg. I'm really not up on these measurements --
> perhaps they mean the same thing?
>    Regarding the study: It's called POWDER, phone number 416 946 7553
> Participants will receive either 600 or 400 units per day, taken once
> weekly in a drink. No placebos, all participants will get Vitamin D
> After 2 years, density will be tested.
>   I forgot to see who was doing the study -- maybe the university?

The POWDER study is aimed at answering the question, "if you are a
postmenopausal woman who has had bone density done, and it is reported
back to you as normal, will a physiologically natural supply of
vitamin D slow down the progression of bone loss?"

I am the principal investigator of this study, supported by Canadian
Institutes for Health Research.  We randomize volunteers to receiving
vitamin D3 in a dose that what works out to either 800 IU or 4200 IU
per day.

Note that the teaspoon-ful of cod-liver oil given to infants contains
400 IU/day to prevent rickets, thus the 4000 IU/day we are trying to
evaluate for adults is only the adult equivalent of the rickets
prevention dose for babies.  We have published in Dec 2001 European J
Clin Nutrition that you cannot detect the effect in the blood, of the
officially "recommended" intake of vit D, and thus adults do need a
higher dose of vitamin D to produce a detectable benefit.  What needs
to be proven is whether more than 800 IU/day will offer any added
benefit. The research must be done to prove it one way or the other.

In the new units for nutrients (by weight) used in our POWDER study
are daily supplementations of either 20 microgram (often mistakenly
written as mg because the greek letter "mu" is replaced by the roman
"m"; ug to mg errors are common misprints) or 100 microgram (1/10th of
a milligram).  Note, that a white person spending 20 min in summer sun
with a bathing suit easily produces 250 microgram of vit D3, so you
see we are well within the "natural" supply of vit D for adults.
Black people, depending on darkness of skin are reported to need up to
6 times longer than white people to produce the SAME dose of vit D via
the skin.

We have had a hard time promoting the POWDER study, and it is
difficult to find healthy people willing to see whether disease can be
prevented.  Unfortunately, research is far easier to do on people who
are already sick.  We need women who recently had bone density
measured to take part.  Right now we are changing our study protocol
to make participation easier for volunteers to take part in the study
(i.e. no visits needed to Mt Sinai Hospital in Toronto, just take the
vitamin D we plan send ).


Reinhold Vieth

p.s. I am curious how you learned of our study.

From: reinhold.vi...@utoronto.ca (Reinhold Vieth)
Newsgroups: sci.med.diseases.osteoporosis
Subject: Re: Vit D - too much !
Date: 23 Mar 2002 01:47:18 -0800
Message-ID: <22ca11f.0203230147.2ad3350d@posting.google.com>

Concerning the question raised above about evidence relating to
inadequacy of "RDA" for vitamin D, as quoted here

> I disagree wholeheartedly with your conclusion. ...
> as to the RDA values being low - from where did that
> information arise? Can you give us a reference so we cal
> enlighten ourselves further...
> John

In response,
I direct you to the following articles, and several more similar cited
in them, that 200-400 IU daily of vit D has practically NO detectable
effect in the adult.  I also point out to you that contrary to popular
belief, there is NO RDA established for vit D.  The current FNB
recommendation, and what you get in your multivitamins, is a
guesstimate, called an "adequate intake" (AI).  That is, there was NO
appropriate scientific evidence to support the Food and Nutrition
Board's 1997 recommendations for how much vitamin D adults should be
taking.  Since then, the data have been coming in, from Toronto, and
several other groups.

Eur J Clin Nutr 2001 Dec;55(12):1091-7
Wintertime vitamin D insufficiency is common in young Canadian women,
and their vitamin D intake does not prevent it.
Vieth R, Cole DE, Hawker GA, Trang HM, Rubin LA.
Here is a shortened version of its abstract:
OBJECTIVE: We asked whether women self-reporting the recommended
consumption of vitamin D from milk and multivitamins would be less
likely to have low wintertime 25-hydroxyvitamin D (25(OH)D) levels.
METHODS: This cross-sectional study enlisted at least 42 young women
each month (age 18-35 y, 796 women total) through one year. We
measured serum 25(OH)D and prevalence of low 25(OH)D (<40 nmol/l) was
21% of the 146 consuming no vitamin D, in 26% of the 140
reporting some vitamin D intake, up to 5 microg/day (median, 2.5
microg/day), and in 20% of the 149 women reporting vitamin D
consumption over 5 microg/day (median, 10 microg/day).
INTERPRETATION: The self-reported vitamin D intake from milk and/or
multivitamins does not relate to prevention of low vitamin D
nutritional status of young women in winter. Recommended vitamin D
intakes are too small to prevent insufficiency.

2: Am J Clin Nutr 2001 Feb;73(2):288-94
Efficacy and safety of vitamin D3 intake exceeding the lowest observed
adverse effect level. Vieth R, Chan PC, MacFarlane GD.
This article shows just how much vit D3 an adult needs to hit
desirable targets in terms of the 25D level in the blood.  And the Dec
2001 issue of AJCN has editorial followup on this.

John, if you still think the "RDA" is appropriate for vit D in adults,
then I would ask you to cite evidence to show that it is.  I am
comfortable in predicting that you will find nothing solid on that.
Best wishes,
Reinhold Vieth

From: reinhold.vieth@utoronto.ca (Reinhold Vieth)
Newsgroups: alt.support.mult-sclerosis
Subject: Re: Dietary Calcium As A Supplement To Vitamin D Compound Treatment Of 
	Multiple Sclerosis
Date: 5 May 2002 17:51:25 -0700
Message-ID: <22ca11f.0205051651.56035222@posting.google.com>

> What do you think of the Calcium, Vitamin D idea?   John

Since I don't know what the details of the patent are, there is no
reasonable way to comment.

A speculation:  DeLuca's MS work has so far all focused on a mouse
model of MS, and ways to use his patented analogs of the hormone
derived from vitamin D -- he never actually uses vitamin D, the
nutrient!  Thus, there is no way the mouse work could be mimicked by
someone without access to his magic molecules.  We'll have to await
details of his clinical trials; however, to this point, that hormone
derived from vitamin D ( 1,25(OH)2D, and its analogs ) has always been
used with special precautions to AVOID calcium.

The epidemiologic data still points to plain and simple "nutrition"
i.e. vitamin D3 itself as the most likely MS preventive agent.  The
evidence in real people does NOT point me toward use of any other
molecule.  If it were me, I would stick to vitamin D3, and if DeLuca's
patent seems to inspire you, add calcium supplements or whatever you
wish, it will do no harm if you stick to the nutrients, and avoid the
hormone (which you can't get anyway).
Best wishes,
Reinhold

From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med.nutrition
Subject: Re: Vitamin D supplementation and increased CO2 levels
Date: 8 Jul 2005 16:04:03 -0700
Message-ID: <1120863843.821715.63250@g43g2000cwa.googlegroups.com>

Bob Prichard wrote:
> I started Vitamin D supplementation at the beginning of this year and have
> noticed a big improvement in mood. I am now taking 4,000 IU a day. My blood
> calcium level has remained the same, but my blood CO2 level has risen from
> 22 mmol/L to 33 (lab says normal range is 20-32). I didn't think much of it,
> but a friend has just reported the same results with the same regimen. Can
> Vitamin D raise CO2 levels, or is this a coincidence?

COMMENT:

Coincidence with the vitamin D. But not coincidence that the "total
CO2" level rises with each draw. This is very common as people get less
anxious about blood draws over time.  The first time they
hyperventilate and pCO2 (what you meansure on an ABG) and total CO2
(mostly bicarbonate, what you measure in a blood draw), are often low.

SBH