281 replies to this topic

[Frans]

Look at post #24 again. 25-D is active. This is physical reality. It has about 1% the activity of 1,25-D, and since there's so much more of it than 1,25-D, it accounted for about 1/8 of total D activity in that study. 4 ng/ml 25-D is stupid unless you have out of control macrophages churning out excessive 1,25-D.

Krillin, I read the paper, but you can not be taking this serious?

I will explain:
- they shuffeled calcium into these people
- calcium leads to higher PTH
- higher PTH leads to higher CYP27B1
- higher CYP27B1 leads to faster conversion of 25D to 1,25D
- so, in fact, the 25D they gave these people was simply converted into 1,25D at a higher rate, which is a well documented pathway, which accounts for their results

Another simple observation why this is misleading and just dead wrong is that they never even measured PTH nor CYP27B1, so their are missing an enormously big piece of the puzzle. Intentionally? I don't know, I guess it is because this paper is from 1997... things have changed in the last 10 years.

So, 25OHD does NOT activate the VDR or have you some more papers I can explain to you?

Sincerely, Frans

Edited by Frans, 23 January 2008 - 10:38 AM.

[pro-d]

Calcium leads to higher PTH...are you sure about that and the rest of the chain? You might want to triple check.
I'm going by clinical data.

[Frans]

Krillin, about post #24:

We agree that the VDR does the job.

You say: "I have yet to see any in-vivo or in-vitro evidence that 25-D is a VDR antagonist. The first study below found that 25-D cannot displace 1,25-D from the VDR"

Since serumlevels of 1,25D have never been found to be zero, it will bind the VDR. Ok?


Now how does 25OHD do the job if it can NOT displace 1,25D from the receptor ? It is bound by 1,25D....


I hope you see now that as long as you don't know the level of 1,25D, you ARE MISSING an important part of the puzzle...

Sincerely, Frans

BTW: The only instance I know in which serumlevels of 1,25D go down to zero was in a paper about AIDS patients.

[krillin]

Krillin, I read the paper, but you can not be taking this serious?

I will explain:
- they shuffeled calcium into these people
- calcium leads to higher PTH
- higher PTH leads to higher CYP27B1
- higher CYP27B1 leads to faster conversion of 25D to 1,25D
- so, in fact, the 25D they gave these people was simply converted into 1,25D at a higher rate, which is a well documented pathway, which accounts for their results

Another simple observation why this is misleading and just dead wrong is that they never even measured PTH nor CYP27B1, so their are missing an enormously big piece of the puzzle. Intentionally? I don't know, I guess it is because this paper is from 1997... things have changed in the last 10 years.

So, 25OHD does NOT activate the VDR or have you some more papers I can explain to you?

Sincerely, Frans

These are two of the most embarrassingly stupid posts I've seen in some time. You'd do Marshall a favor by shutting up now and letting a smarter person defend him.

Calcium lowers PTH. And you're also ignoring this information provided in the abstract.

25(OH)D was also active in elevating absorption and did so without raising total 1,25(OH)2D levels.

Now how does 25OHD do the job if it can NOT displace 1,25D from the receptor ? It is bound by 1,25D....

Because all of the VDRs are not continuously occupied by 1,25-D.

[pro-d]

Frans, you need to deeply read the article in post #53, and then look over some other basic level knowledge.

Stepping back from all this, do you honestly think it's normal to feel 'worse' on a treatment? Is it normal to be taking a combo of antibiotics for an almost infinite amount of time and not worry about long term health? I see some people have been on them for a few years, still holding out for hope of being fully cured. If you ask me, withholding D and remaining on antibiotics is what keeps some probably feeling fine without addressing the cause - which is to match man as nature intended.

I read Marshall once said he sees no reason why the body needs vitamin D from sun/supplementation.
If our bodies are averse to vitamin D, why does our skin have a material that turns into D3 in sunlight? Why then does it then get sent to the liver? People aren't meant to be couped up all day long.
Excuse me, but I thought our bodies try and protect us. As do the bodies of other animals. Conversion of skin cholesterol is not an autoimmune disease!
Furthermore, mainstream supplementation (typically 400IU) and fortification of foods doesn't reach anywhere near the levels that the sun can give us with sensible exposure.

On common sense alone, the Marshall Protocol is ludicrous. If you must, try the FWIW Zero Based Protocol which combines D and antibiotics for diseases associated with D hypersensitivity. Everyone else would do fine optimising their D levels alone.

Edited by pro-d, 23 January 2008 - 11:14 PM.

[stephen_b]

Science daily article:

With skin that was more transparent to sunlight, humans were better able to produce sufficient vitamin D in their new climate.

U. scientist says human evolution is going strong:

Other mutations concern "broken pigment genes," giving Europeans white skin, blond hair and blue eyes. The cause of this mutation is that after people moved out of Africa and into Europe, they needed a better way to get vitamin D.

If the hypothesis that development of light skin among Europeans happened to allow sufficient amount of vitamin D to be made is true, then that's a strong argument for just how vital it is.

Stephen

[ortcloud]

Frans, you need to deeply read the article in post #53, and then look over some other basic level knowledge.

On common sense alone, the Marshall Protocol is ludicrous. If you must, try the FWIW Zero Based Protocol which combines D and antibiotics for diseases associated with D hypersensitivity. Everyone else would do fine optimising their D levels alone.

I agree, it is ludicrous. It is also a convoluted approach to a TH2 dominant disease. There are many options to balancing the immune system to mount a defense against intracellular bacteria. But rationality and options are not what Trevor is interested as it threatens his power and notoriety. Sure, I have made some cult jokes about him but only because it is the best way to describe him and his followers. The leader is closed minded and only spews rhetoric and dogma and refuses to be challenged only allowing unquestioned devotion. So just like other religous fanatcs you then get the followers that believe the dogma and then attempt to preach the dogma to others like what we have seen with Frans and AmyP, but their dogma is easily shot down with science and logic as you and krillin and others have. They dont know what to do other than to refer to their false teachings from their leader. It is sad and futile to discuss logic or science with them as we have witnessed. Eventually though like a jehovahs witness that knocked on your door, if you throw enough tough questions at them they will quietly go away.

Edited by ortcloud, 25 January 2008 - 04:12 AM.

[pro-d]

Yeah, that's another thing. From what I've read, I detect a certain arrogance from Marshall. Someone who doesn't allow open critique of their work isn't someone to follow at all.
MP seems to be only somewhat popular because it's controversial. The assumption that controversial is ground breaking shouldn't be jumped on - not without clear evidence. Marshall states that all these cases are best left to molecular biologists because simply "I know better than you." And yet he has no unanimous peer support.

Also, it's been noted that a lot of those coming to the MP often have insufficient or deficient 25-D. I've not heard them mention if someone with consistently optimal 25-D levels has developed conditions like sarcoidosis and come to them. This would crash Marshallsoft's VDR simulator.

While some people on the MP have shown benefits or rare recovery cases (most likely due to the antibiotics that physicians haven't entirely disputed. regardless of 25-D status), the number of people benefiting from physiological vitamin D is vast. The no. of people with adverse effects is minimal. Deficiency is much more a worry than hard-to-achieve toxicity.

Edited by pro-d, 24 January 2008 - 02:48 PM.

[tham]

Supplemental vitamin D is critical for preventing falls in
the elderly, which should be at least 50 nmol/L, and preferably
above 80 nmol/L. I think this is about 20 ng/dL and 32 ng/dL
respectively.

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum


http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

Edited by tham, 26 January 2008 - 03:29 PM.

[tham]

Reviewing some of the above studies, it would appear that
a 1,000 i.u. D3 or D2 supplement drastically reduces the risk
of falling when we grow old, regardless of deficiency.

" Older people in residential care can reduce their incidence
of falls if they take a vitamin D supplement for 2 years even
if they are not initially classically vitamin D deficient. "

http://www.ncbi.nlm....l=pubmed_docsum


" The majority of patients who were vitamin D insufficient
consumed more than the recommended 400 to 600 IU/d of
vitamin D. Obese patients were found to have significantly
lower 25(OH)D concentrations and higher PTH concentrations
than nonobese patients. "

http://www.ncbi.nlm....l=pubmed_docsum


" Participants in the 800 IU group had a 72% lower adjusted-
incidence rate ratio of falls than those taking placebo. "

http://www.ncbi.nlm....l=pubmed_docsum

Edited by tham, 26 January 2008 - 06:03 PM.

[tham]

I prefer to supplement my father with 0.25 mcg of alfacalcidol
or calcitriol rather than plain D3 or D2, taken every two or three
days to minimize risks of vascular, soft tissue and brain calcification.

Vitamin D's importance in neuromuscular system appears to
be critical in its prevention of falls in the elderly :

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum


While some studies do not prove that vitamin D is important
in the neuromuscular system, they confirm that 1,25 OHD3
is the critical metabolite for preventing falls in the elderly due
to poorer renal function impairing its conversion from plain D3.
Part of the fall in renal function in aging is the rise of
inflammatory cytokines, particularly TNF-alpha and IL-6. Giving
the metabolites circumvents this.

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum


Alfacalcidol, amongst other benefits over that of plain D3,
itself inhibits TNF-alpha and IL-6.

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

http://www.ncbi.nlm....l=pubmed_docsum

Edited by tham, 27 January 2008 - 03:06 PM.

[rabagley]

I prefer to supplement my father with 0.25 mcg of alfacalcidol
or calcitriol rather than plain D3 or D2, taken every two or three
days to minimize risks of vascular, soft tissue and brain calcification.

Wow. It seems like the need for precision dosing and careful serum level measurement is extremely important there to avoid the hypercalcemia. But I guess that if you know your dad has impaired renal function, that's pretty much the only way to go.

Thank goodness my kidneys are still going strong, so I'll let my body make whatever it wants from an adequate supply of 25(OH)D.

[ortcloud]

I prefer to supplement my father with 0.25 mcg of alfacalcidol
or calcitriol rather than plain D3 or D2, taken every two or three
days to minimize risks of vascular, soft tissue and brain calcification.

Wow. It seems like the need for precision dosing and careful serum level measurement is extremely important there to avoid the hypercalcemia. But I guess that if you know your dad has impaired renal function, that's pretty much the only way to go.

Thank goodness my kidneys are still going strong, so I'll let my body make whatever it wants from an adequate supply of 25(OH)D.

vitamin K2-mk7 would reduce soft tissue calcification risk. But does he indeed have impaired renal function in the first place ? Dosing with calcitriol is too risky unless you are checking frequent blood levels of it and calcium levels. I understand what you are trying to do, but I would check to see if he does have high cytokine levels in the first place, did you check these ? Have you considered looking at a few things that would reduce the inflammatory cytokines in the first place rather than trying to treat the after effects ?

[tham]

vitamin K2-mk7 would reduce soft tissue calcification risk. But does he indeed have impaired renal function in the first place ? Dosing with calcitriol is too risky unless you are checking frequent blood levels of it and calcium levels. I understand what you are trying to do, but I would check to see if he does have high cytokine levels in the first place, did you check these ? Have you considered looking at a few things that would reduce the inflammatory cytokines in the first place rather than trying to treat the after effects ?

Thanks, Ortcloud and Rabagley.

He doesn't have seriously impaired renal function, but
when last checked some years ago, it was already
compromised, largely due to congestive heart failure.
I'll test his renal function again.

I don't think the primitive labs in Malaysia are equipped
to test inflammatory cytokines - they can't even test for
Lp(a). I'll check them out again though.

He has been taking this to reduce cytokine production.
He can't really tolerate Omega-3 fish oils due to gaseous
disturbances, so I place him on minimal doses of cod liver
oil instead.

http://www.betterlif...p?prod_id=20972


I'm thinking about replacing the Kal's product with this :

http://www.betterlif...p?prod_id=17264


Thanks for the info on vitamin K2-MK7.

His orthopedician had actually placed him on 0.5 mcg calcitriol
long term for his osteoporosis, so I reduced him to 0.25 mcg
alfacalcidol on alternate days. I will review this again though,
and see if I can start him back on some plain D3.

[ortcloud]

His orthopedician had actually placed him on 0.5 mcg calcitriol
long term for his osteoporosis, so I reduced him to 0.25 mcg
alfacalcidol on alternate days. I will review this again though,
and see if I can start him back on some plain D3.

I understand, well do you know what his serum calcium levels are ?

[neogenic]

I had this article (trevor's) sent to me by a friend and I was about to post it over here...only to find there was this thread already. The debate seemed like scientology (MP) vs. science. With the collective data on Vitamin D being the most established nutrient in terms of clinical research, one would need to expect to push back that mountain with some pretty compelling information that clearly negates what millions have come to believe over a group of thousands with a few researchers. Not saying that there isn't a possiblity that the established thought can't be wrong, but with so much research it less than likely. Again, one should not be suprised when trying to refute all that data...but expect it. Thrive on it even. I've yet to see anything truly compelling and the point about none of this research being on PubMed...pretty much makes it worthless to me as well. If it ain't peer reviewed, it ain't jack.

I've always wondered why people don't supplement with the "active" form of 1,25-D. Someone in here said the range between therapeutic and toxic...is that the case? What would be an expected difference by bypassing conversion and supplementing with 1,25-D? Also, what if one supplemented with both in a specific ratio? Just some questions I've wondered and this thread seems like a good place ask.

[pro-d]

That's exactly it. When challenged, "Marshalls" seem to get defensive rather than presenting disarming information.
A theory often starts out with a minority view, concrete facts get cherished by the majority and I don't think that protocol will reach that stage.

1,25D (Calcitriol) has been, as said above, been used to treat patients with poor renal function in certain conditions. But as a healthy body knows how much to convert, the mechanics are best left to the body. With poor renal function, measurements and apt dosage are needed.
Calcitriol has a short half-life, but if you get it wrong you can invoke hypercalcemia. Invoking hypercalcemia by 25D is a hard feat and usually caused by industrial accidents in the creation of pills (rare). Your body welcomes a certain degree of too much 25D than too little.

The crux is that supplementation mirrors nature where adequate sunlight cannot be obtained and your kidneys are fine. Your skin makes D3 on exposure, so it's only wise you supplement with D3 as the alternative.

Edited by pro-d, 28 January 2008 - 07:36 PM.

[tham]

I understand, well do you know what his serum calcium levels are ?

His serum calcium was last tested at about 2.4 mmol/L,
which works out to 9.6 mg/dl.

I'll try to get him to test it again sometime. Thanks.

[amyproal]

Guys,

The paper discussed in this thread "Vitamin D deficiency outpaces FDA decision making" was published in BioEssays which is a peer reviewed journal. Dr. Marshall has another Autoimmunity Reviews Paper in PubMed.

It's sad to see this thread go from what seemed like a good, open-minded discussion at the start to a bunch of criticism about Dr. Marshall's personality written by people who have never met him or got on the MP board directly. And discussion of cults which have no relevance to the MP.

It could be said that the media, supplement companies, and doctors who have careers built around promoting vitamin D have developed more of a cult mentality among most of you, as I see little effort from most of you to approach this issue with an open mind.

Take a look at the patient interview on my website (www.bacteriality) and listen to people who are getting better on the MP. Are you telling all these people that they are crazy and liars? Give them the benefit of the doubt. Marshall's model is holding up in a clinical setting and if it weren't I wouldn't be here writing this message. Don't discount the Marshall Protocol before you actually take the time to learn about it in great depth. There are too many rumors being spread about Dr. Marshall on the internet these days. Rather than believing everything you hear get on the study site and talk to people who have actually done the treatment and thus can speak about it with more authority.

Best,

Amy

[pro-d]

I don't dispute that there aren't people benefiting from the MP - it's an avenue for those with D hypersensitivity - but you have to concede that there are people who have shown no improvement or have got worse. And there are many people doing well with D. Dr. Davis' treatment - involving D - removes calcium from the arteries. This is not a suppression of symptoms, this is treatment for the hypothesis of arterial calcium and not bacteria. It has many success stories.
I can see your defence of the MP is due to enthusiastic personal experience but because of that there is a heavy bias and I sense no iota of stepping back and looking outside the box. D on it's own aside, there are other protocols that have shown effectiveness so my question is how do you not know it's not the antibiotics alone and not D reduction that is beneficial? The antibiotics the MP use have never been outright disputed by physicians.

As for a vitamin D cult mentality, that can be disputed. Pharmaceutical companies are interested in creating (and have created) analogues of vitamin D for treatments such as BPH. They believe an analogue is safer, but they probably mean that for their own pockets. Supplements aside, I don't think nature has anything to gain from giving us sun exposure. Even then, there's not much money to be made from supplementation. Does Marshall gain from Benicar?

It's hard not to criticise the MP, if not Marshall himself, because you must understand that an image exists of a protocol that does not tolerate dissent, doesn't have transparent workings, and there are articles that can be followed up that show up discrepancies in his character that are notable to people who have designs to join the MP. I find it eyebrow easing alone that Marshall uses the Dr. title when there is no good reason other than to show authority.
No one ever said D supplementation (at least in a straight forward manner) was good for people with D hypersensitivity states, but only the MP seems to say that D is bad for everyone. An immense number of trials will show you this is not so.

Guys,

The paper discussed in this thread "Vitamin D deficiency outpaces FDA decision making" was published in BioEssays which is a peer reviewed journal. Dr. Marshall has another Autoimmunity Reviews Paper in PubMed.

It's sad to see this thread go from what seemed like a good, open-minded discussion at the start to a bunch of criticism about Dr. Marshall's personality written by people who have never met him or got on the MP board directly. And discussion of cults which have no relevance to the MP.

It could be said that the media, supplement companies, and doctors who have careers built around promoting vitamin D have developed more of a cult mentality among most of you, as I see little effort from most of you to approach this issue with an open mind.

Take a look at the patient interview on my website (www.bacteriality) and listen to people who are getting better on the MP. Are you telling all these people that they are crazy and liars? Give them the benefit of the doubt. Marshall's model is holding up in a clinical setting and if it weren't I wouldn't be here writing this message. Don't discount the Marshall Protocol before you actually take the time to learn about it in great depth. There are too many rumors being spread about Dr. Marshall on the internet these days. Rather than believing everything you hear get on the study site and talk to people who have actually done the treatment and thus can speak about it with more authority.

Best,

Amy

Edited by pro-d, 30 January 2008 - 12:42 PM.

[Frans]

Krillin, I read the paper, but you can not be taking this serious?

I will explain:
- they shuffeled calcium into these people
- calcium leads to higher PTH
- higher PTH leads to higher CYP27B1
- higher CYP27B1 leads to faster conversion of 25D to 1,25D
- so, in fact, the 25D they gave these people was simply converted into 1,25D at a higher rate

Another simple observation why this is misleading and just dead wrong is that they never even measured PTH nor CYP27B1, so their are missing an enormously big piece of the puzzle.

Intentionally? I don't know, I guess it is because this paper is from 1997... things have changed in the last 10 years.

So, 25OHD does NOT activate the VDR or have you some more papers I can explain to you?

Sincerely, Frans

These are two of the most embarrassingly stupid posts I've seen in some time. You'd do Marshall a favor by shutting up now and letting a smarter person defend him.

Calcium lowers PTH. And you're also ignoring this information provided in the abstract.

I'm back.

I see you guys have been bashing away at Amy and me, we (I) have been called stupid, a yehova's wittness, ludicrous has passed, some bs was delivered on my doorstep, etc., etc., so I guess the moderators here will give me some leeway while answering.


So, Krillin, let's talk about this. Calcium lowers PTH?

You are absolutely right. You deserve a point for that one.

I must say it sounded ludicrous, since it leads to 2 pathways to take care of excess calcium shutting down. PTH and VDR.

But hey, this is a paper by mr Holick, a world renowned expert on vitamin D, he can not be wrong, can he?

So I sat down, opened pubmed and looked at what I was missing.

Well, you won't like what I found, which must be the understatement of the century, actually...


Please bear with me, you scored your point, now it's my turn again.


The whole thing hinges on activation of the PTH receptor, right? Well, it turns out there is another molecule that can turn that receptor on. It is called PTHrP, parathyroid hormone related peptide.

You can check a lot of the knowledge about it here:
- http://www.ncbi.nlm....m.cgi?id=168470

Now, the fun is, that this molecule is actually UPregulated by Calcium via the CASR.
- you can check this at, eg: PMIDs: 10942719, 11108243, 15336602, 16019433


So, where does that leave us?


Well, to reiterate:

- they shuffeled calcium into these people
- calcium leads to higher PTHrP
- higher PTHrP leads to higher CYP27B1 by activating the PTH receptor
- higher CYP27B1 leads to faster conversion of 25D to 1,25D
- so, in fact, the 25D they gave these people was simply converted into 1,25D at a higher rate, which probably accounts for their results


Funny how they were not measuring the right things, right? It makes this research worthless.


got it now ?


So, when working through this article we are discussing which is of mr. Holick's, I found that other so-called vitamin D 'experts' are still quoting this article as being proof that 25OHD activates the VDR, rather strange, since I think have proven this 'landmark paper' absolutely and totally wothless now...

To see who is referring to this worthless article, see:
- http://jcem.endojour...full/82/12/4111
and scroll all the way down.

I even found a paper in that list by mr Vieth (another so-called vit. D 'expert') stating:
"Although intestinal calcium absorption was not assessed in this trial, this effect of vitamin D is unequivocal"... where he refers to mr Holick's paper. This paper, by the way, is from 2006 !! See:
- http://jcem.endojour...t/full/91/2/405


Still with me guys ?


Makes one wonder how it is possible that mr Vieth never stumbled across this information on PTHrP, right?

Reeks of criminal negligence if you ask me. Of both Vieth and Holick.

One thing is sure: they have been cutting some corners, not doing their homework, which sounds bizarre, since we are talking about a serious thing like cancer, right?


But it gets even more bizarre.


One might argue that they possibly didn't know about this pathway via PTHrP, still rather negligent and telling about your vitamin D 'experts', but hey, they are only human.


The main problem I have with that concept is that mr Holick published a paper in 1994, 3 years before the worthless paper we are discussing here.

This paper was about PTHrP... Yes, about PTHrP... he knew about it, but still didn't think it prudent to test it...
(see PMID: 08058749)


I don't know how you would call this, but in The Netherlands this goes even further than unethical, we would call it downright criminal.


Got it now ?


Someone here said you are critical thinkers. Boy I hope he/she is right, even though, until now, you have only been critical about other's thoughts and insights.


You guys have a lot of questions to ask yourself, like:

- did Holick suddenly develop a severe case of amnesia in 1997 that still hasn't ended a decade later ?

- why didn't Vieth, or the other so-called vitamin D 'experts' stumble upon this information, when someone as stupid as I am did ?

- you should be asking yourself what else these so-called 'experts have been missing during their countless research, since the knowledge about PTHrP upregulating 1,25D was already known in 1997 ! Eleven years ago. see PMID: 9062504; what else have they been missing during that decade ? Funny how someone as stupid as I am can find more knowledge in a weekend than they have in a decade, isn't it? makes one wonder...

- you should ask yourself what all this tells you about the level of competence of the so-called 'experts', is this what you call 'critical thinking'?

- you should ask yourself if you really want to follow someone like Holick's lead, I sure won't

- you should start looking into the sponsors that paid for these persons' research; I have been on the MP for 2 years now and it has not cost me a dime, all insured and Marshall's work does not cost me a penny, rather telling, right?

- you should start asking yourself why all those hundreds of scientists keep calling 1,25D the active metabolite

- you should start thinking if there may, perhaps, be a reason, why 25OHD is synthesized to 1,25D; did mother nature pull a prank on us? or no, better still, she must also be a disciple of Marshall's little cult, right? Well, as mother nature, she definitely gets in the sun a lot, so yes, she probably wears sunglasses like us on the MP

- you should ask yourself I you really want to stay on believing people who behave as I have just tried to reiterate to you... or will you start believing those guys that are telling us that at least 1,25D is a critical thing to measure, not just 25OHD

- you should ask yourself if you should keep on holding on to research that has only been measuring 25OHD; not calcium, not PTHrP, not CYP27B1, not 1,25D to mention a few examples

- the ones posting here should really think if they should keep on pushing vit. D like they have, they have clearly not been doing their homework as the 'critical thinkers' they portend to be

- you should ask yourself if that black box the 'experts' are shuffeling full with vitamin D is perhaps a little more complicated than these 'experts' want to make you think; especially since that black box is your own body...


- pro-d, you said: I go by clinical data; I understand, black boxes are scary things, aren't they?

- you also said Marshall uses his Dr title in a dubious way, well, guess what, he has been appointed Adjunct professor at Australia’s Murdoch University School of Biological Medicine and Biotechnology, so maybe he does know what he is talking about, or no, probably they are also just members of Marshall's cult...
- see: http://wwwcoms.murdo...ywords=marshall


I sincerely hope you guys see the light and if it gets too bright, I know somewhere you can buy sunglasses...


Just some thoughts,

Sincerely, Frans


PS Neogenic, you seem ok, you might want to check out the following paper:
- http://www.pnas.org/...full/104/8/2927
You might want to start with the discussion chapter.

What they are basically saying is that the Pretri dish as golden standard for finding and identifying bacteria in and on humans is hopelessly outdated; also something that has been around for a century or so that is being challenged by molecular medicine...

[pro-d]

Er, taking calcium decreases PTH and will in turn decrease 1,25D levels.
http://www.ncbi.nlm....Pubmed_RVDocSum
PTHrP is often secreted by tumours adding to a large serum amount and causes hypercalcemia, so it's the other way 'round.
You didn't read the article in post #53 either did you?

I said ludicrous, because on my observation it is. As other animals synthesise vitamin D3, you don't think it's going to elicit a laugh that they should keep away from sunlight and wear shades?
I don't know how you're processing this debate, but for me this isn't about point scoring. I'm saying sell MP to those who come to your shop, don't go door to door when people are achieving results on D that are *not* simply attributed to suppression.
Everyone else will not want a product that gives these risks:
http://lassesen.com/...otocolRisks.htm
I quote Lassesen due to him having completely recovered from CFS with a method that involved optimising D 'and' using kinds of antibiotics that are low risk and natural.
Neither you or Amy have produced off-model evidence that 25-D is immunosuppressive above 20ng/ml. Computers or human trials? There are more visible, open trials, outside of the MP. Also, show me another molecular biologist who has either observed and/or praised Marshall's model?

If I'm not mistaken, Holick didn't discover PTH reduces calcium. This was a previously established fact. Also, Holick has been a leading figure in vit D advocacy for at least 20yrs. I'm sure he would've abandoned his viewpoint had he discovered anything that would be detrimental to patients. He also advises zoos and has helped maintain animal health. He found pet Iguanas (removed from light) developed osteoporosis unless given a pet form of D3 along with cream cheese!
Whereas, Marshall? A few years ago he rose from the ashes of a defunct electronics co.

May I point 'adjunct' means tempororary or assisting. If he was a bonafide prof he could use Prof. But he prefers to use Dr. which he is just about qualified to use. This adjunct role was likely only given because of mild interest, which in time I do believe will be attributed to his choice of antibiotics than his his anti-D policy.

Also, not only do I go by clinical data. My brother had seizures and muscle weakness corrected by D and calcium. Your protocol, from my understanding doesn't mention treatment for this and would foam about how 'everything' is related to bacteria. The MP allows calcium, but since 25-D aids intestinal absorption the calcium is metabolised sloppily without it. Which can lead to arterial calcium deposits which Dr. Davis reverses with his Track Your Plaque system (by surprise, vitamin D as core to his treatment).

I vehemently defend D because fundamentally I know at a personal level that it is advantageous to match nature. A Pascal's Wager indicates it's better to match nature than not and become susceptible to illness and rely on long-term antibiotics.

Until you show me off-model evidence...I can't hear you.

Edited by pro-d, 31 January 2008 - 12:21 AM.

[luminous]

For those not totally familiar with the marshall cult, he tell his disciples to wear special sunglasses
that block out all sunlight and to stay indoors so they reduce any evil vitamin d production.

So you can always spot one of the cult members by the glasses.


Here is a glimpse of what a meeting looks like.

I don't know whether to do the D or not, but I have to say, this image and post had me laughing out loud--hilarious.

[Frans]

Er, taking calcium decreases PTH and will in turn decrease 1,25D levels.
http://www.ncbi.nlm....Pubmed_RVDocSum
PTHrP is often secreted by tumours adding to a large serum amount and causes hypercalcemia, so it's the other way 'round.

And you guys are calling me stupid?

Look at these quotes from these papers in pubmed, which I already referred to in my earlier post btw, but you never read them did you?

10942719:
- CaR agonists stimulate PTHrP secretion (Calcium is CAR agonist)

11108243:
- Elevated extracellular calcium (Ca2+(o)) also stimulates PTHrP secretion
- Furthermore, elevated Ca2+(o) and the polycationic CaR agonists, neomycin and spermine, stimulated PTHrP secretion dose dependently

15336602:
- high extracellular Ca2+ stimulates parathyroid hormone-related protein (PTHrP) release from human prostate and breast cancer cell lines as well as from H-500 rat Leydig cancer cells, an action mediated by the calcium-sensing receptor (CaR)
- High extracellular Ca2+ stimulates PTHrP release

16019433:
- the calcium-sensing receptor (CaR) stimulates PTHrP release and proliferation

It's the other way 'round? Sure, keep on dreaming kid.

The paper you are quoting is from 1979, is that the last time you looked at the literature?

Furthermore, it is clear you didn't read what I said and referred to, so, I really have to quote Krillin on this one:

This the most embarrassingly stupid post I've seen in some time. You'd do yourself a favor by shutting up now and letting a smarter person defend supplementing vit. D

So again, for those that have some understanding of how to read the literature:

- they shuffeled calcium into these people
- calcium leads to higher PTHrP
- higher PTHrP leads to higher CYP27B1 by activating the PTH receptor
- higher CYP27B1 leads to faster conversion of 25D to 1,25D
- so, in fact, the 25D they gave these people was simply converted into 1,25D at a higher rate, which probably accounts for their results


Sincerely, Frans

[pro-d]

If you read my posts, I actually never insulted you personally, but with your attitude it seems justified.

Just because a publication has dated doesn't suddenly mean it becomes incorrect.
"Long story short, taking 800 mg/day of calcium citrate w/o any D and w/o raising my level of 25D, I have lowered my 1,25D AND my PTH is back within normal limits." (2007)
http://www.marshallp...rum11/8193.html
Or do you not even believe those within your own camp any more?

The reason why 25D alone reduces PTH is because it increases intestinal absorption of even minimal amounts and metabolises it correctly.
Calcium on it's own is fine, but is like painting by throwing paint on a wall than using a brush. And raises the risk of arterial calcium. An effect most MP candidates won't see until when heart diseases strikes later in life.

You rave on about how 1,25D is the active metabolite but don't seem to acknowledge that many tissues have 25(OH)D-1-alpha-hydroxylase which convert 25 to 1,25D to satisfy local tissue requirements in a tightly controlled way. This is why PTH has a strong association with 25-D levels.

I think you'll find when a tumour secretes PTHrP (which is otherwise virtually undetectable in generally healthy persons) it can lead to hypercalcemia.
"Parathyroid hormone-related peptide (PTHrP) is thought to mediate the hypercalcemia that develops with many malignancies. Assays to measure this peptide are available."
http://www.emedicine...rg/topic260.htm
The reports you refer to talk about excess extracellular calcium from normal *and malignant* cells. The 300mg in Krillin's post alone is not excessive considering many are given 500-1000mg.
At the end of 11108243 note:
"PTHrP-secreting breast cancers metastatic to bone, the CaR could potentially participate in a vicious cycle in which PTHrP-induced bone resorption raises the levels of Ca2+(o) and TGFbeta within the bony microenvironment, which then act in concert to evoke further PTHrP release and worsening osteolysis."

I also beg you to read http://stuff.mit.edu...on/universe.htm It is a long read so I recommend reading a little a day. I have nothing further to say on this matter.

Edited by pro-d, 01 February 2008 - 07:48 PM.

[krillin]

I've always wondered why people don't supplement with the "active" form of 1,25-D. Someone in here said the range between therapeutic and toxic...is that the case?

It is in chickens.

Poult Sci. 1990 Oct;69(10):1702-12.
Optimal dietary level of 1 alpha,25-dihydroxycholecalciferol for eggshell quality in laying hens.
Tsang CP, Grunder AA, Narbaitz R.
Animal Research Centre, Agriculture Canada, Ottawa, Ontario.

The optimal dietary level of 1 alpha,25-dihydroxycholecalciferol [1,25-(OH)2D3] for eggshell quality was established. White Leghorn hens, 59 wk of age, were fed one of eight diets that contained the same basal ingredients, including 3.1% calcium, but different levels (microgram/kg) or forms of calciferol supplements: no calciferol supplement of any form (56 hens); 27.5 (control) or 55.0 micrograms of cholecalciferol (56 hens each); 3, 5, or 7 micrograms of 1,25-(OH)2D3 (28 hens each); 5 micrograms of 24,25-dihydroxycholecalciferol [24,25-(OH)2D3] with 28 hens; 5 micrograms each of 1,25-(OH)2D3 and 24,25-(OH)2D3 (28 hens). All groups were fed the control diet prior to the 21-wk treatment. The group fed 5 micrograms 1,25-(OH)2D3/kg diet ranked first in specific gravity (SG), e.g., 1.081 versus 1.077 for the control group at Week 21 (P less than .05). The group fed 7 micrograms 1,25-(OH)2D3/kg consumed 30% less feed and laid 20% fewer eggs than the control, but shell quality was not affected. The groups receiving no calciferol supplement or receiving only 24,25-(OH)2D3 laid eggs with significantly lower SG than the control after 2 wk of treatment (1.072 or less versus 1.082 at Week 2). The rest of the treatment groups mentioned were comparable to the control in eggshell quality and egg production. Groups fed the combination of 1,25-(OH)2D3 and 24,25-(OH)2D3 per kilogram of feed, or 1,25-(OH)2D3 alone at 5 micrograms/kg, had significantly higher tibial weights relative to the control group. All groups receiving the diets without cholecalciferol supplementation had markedly reduced hatchability. It was concluded that the optimal dietary level of 1,25-(OH)2D3 for improving eggshell quality without affecting egg production was approximately 5 micrograms/kg and the toxic level was 7 micrograms/kg.

PMID: 2263546

[krillin]

- so, in fact, the 25D they gave these people was simply converted into 1,25D at a higher rate, which probably accounts for their results

- you should ask yourself if you should keep on holding on to research that has only been measuring 25OHD; not calcium, not PTHrP, not CYP27B1, not 1,25D to mention a few examples

They did measure 1,25-D, and it didn't change. I again quote from the abstract:

25(OH)D was also active in elevating absorption and did so without raising total 1,25(OH)2D levels.

Did you ignore this sentence, or are your dark glasses interfering with your vision?

[krillin]

Frans, you are not allowed to use the quote function if you substitute your own words for the quoted person's. You have just committed libel.

Furthermore, it is clear you didn't read what I said and referred to, so, I really have to quote Krillin on this one:

This the most embarrassingly stupid post I've seen in some time. You'd do yourself a favor by shutting up now and letting a smarter person defend supplementing vit. D

[neogenic]

Vitamin D related inflammation could be systemic and muscular inflammation would ensue, Frans. Hans warned us of this years ago as well. Ever since you've left his side you've seemed angry. Find your way back to Hans. He's out there and he still wants you.

Edited by neogenic, 02 February 2008 - 03:31 PM.

[Frans]

You rave on about how 1,25D is the active metabolite but don't seem to acknowledge that many tissues have 25(OH)D-1-alpha-hydroxylase which convert 25 to 1,25D to satisfy local tissue requirements in a tightly controlled way. This is why PTH has a strong association with 25-D levels.

Pro-d, to avoid misunderstandings, I have mentioned 25(OH)D-1-alpha-hydroxylase several times, albeit with another name, since CYP27B1 is actually 25(OH)D-1-alpha-hydroxylase, which is why PTHrP also has a strong association with 25D and 1,25D levels.

- calcium leads to higher PTHrP
- higher PTHrP leads to higher CYP27B1 by activating the PTH receptor
- higher CYP27B1 leads to faster conversion of 25D to 1,25D

I hope this clears this misunderstanding.
See: - http://www.ncbi.nlm....m.cgi?id=609506

I was being a little lazy, CYP27B1 is shorter than 25(OH)D-1-alpha-hydroxylase.

ok?

I will answer the other's posts another time. I am looking into PTHrP a little further, but Krillin, my post isn't libel I hope, I just updated, or freely quoted your remark so as to make it fit to the situation at hand, I hoped you guys understood that.

Another remark for Krillin, please look again at my original post, you'll find a link to several papers about PTHrP that make clear it is extremely (granted, not exclusively) active in the tissues. If it generates CYP27B1 in the cells, that then leads to faster conversion of 25OHD to 1,25D in the cells themselves, in the mitochondria if I am not mistaken, which accounts for the serumlevels staying the same.
- http://www.ncbi.nlm....m.cgi?id=168470

Sincerely, Frans