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Dr Trevor Marshall
Research Team
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Posted: Sat Feb 23rd, 2008 06:29 |
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If you are interested in the conflicts of interest swirling around the Vit D advocates, then you will enjoy reading this article from the Canadian Broadcasting Commission:
"The Vitamin D Debate"
http://www.cbc.ca/news/viewpoint/vp_strauss/20080213.html
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Rico
Member in Phase 3
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Posted: Sat Feb 23rd, 2008 11:57 |
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Ah, so that's why they want us all to ingest more Vitamin D. Now it all adds up! $$$$$
I'm glad to see that we, the population, are served by such well-meaning scientists.
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No diagnosis/some symptoms; wife with Sarc on MP; Olm 40mg q6h| avoid D| 1,25D=63 25D=32 (May 2006) 1,25D=44; 25D=10(Dec 2006)PhaseI(May06) PhaseII(Aug06) PhaseIII(Aug07)
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Frans
Member in Phase 2
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Posted: Sat Feb 23rd, 2008 17:14 |
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Oh man, if it weren't such an important issue, I would be rolling on the floor laughing my tushy off...
It surely gives those of us trying to get through to people some ammunition.
Our beloved Vieth's wife made 30.000 times 20 dollars, equalling 600.000 dollars from this paper in two days, but he still says he has no conflicting interests...
Wow, did I make the wrong career choice...
Frans
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Burn-out/nervous breakdown Jan01 125D 48 25D8.48 Ph1Nov06 ModPh2Jan07 Ph2Apr08 Cipramil Seroquel NoIRs lite exp r/t work cover up 25D3.9(Oct07)
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laura1814
Member in Phase 2
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Posted: Mon Feb 25th, 2008 05:05 |
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| Great article! Thanks for sharing it!
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CFS, EBV, PCOS, POF, TMJ, hypoglycemia, hyperlipidemia, MP Ph1 1/08, MP Ph2 4/08; enzymes, & ranitidine PRN, NoIRs, low lux home, limited outings, covered up, 1,25D=37, 25D=9.
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joedegs
Member
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Posted: Tue May 6th, 2008 13:37 |
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Dr. Marshall,
Just found this article online...don't know if you have seen it or not but it talks about Vit D causing several bladder conditions. Just thought you might be interested in it.
http://jcem.endojournals.org/cgi/content/full/90/2/962
Joe
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Res MP, Pulmonary and Cardiac sarc, avoiding sunlight/vitamin D.
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inge
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Posted: Tue Jul 22nd, 2008 09:10 |
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I haven't checked things thoroughly, but to me it seems that during the winter months there is no vitamin D production at all in individuals living in countries situated at latitudes far from the equator (PMID: 2839537). Knowing that the skin has the ability to produce vitamin D it seems that it has this ability for a reason. I get the impression from the MP site that you really can't get vitamin D so low that you will experience adverse health effects. But why does the skin then only have the abiltity to produce vitamin d (as it appears from the study I linked to) from sunlight? Is anyone aware of findings showing that a minimum of vitamin D can be produced without sunlight? After all, a minimum of vitamin D production appears to be necessary for optimal health, knowing how many genes are transcribed by the VDR.
Last edited on Tue Jul 22nd, 2008 09:14 by inge
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CFS/ME 125D64 25D12(dec 07) Ph1De06 daily lite exp NoIR use Ph2Mar07 ModPh2 Jun07 abx brkOct 07 r//t KFTs freq abx chg to control kidney IP Apr 08 phase 2 abx
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kenc
Member in Phase 2
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Posted: Tue Jul 22nd, 2008 09:57 |
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inge,
Have you considered the possibility that the purpose of the skin producing vitamin D in the presence of sunlight is to activate the innate immune system to repair the damage to the skin caused by sunlight?
kenc
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Crohn's Disease 1984, 24May05 1,25D=33 25D=8.4 6Sep05 1,25D=29 25D=12, 12Jul05 Beni+pred, 27Sep05 Mino, 12Jul06 Phase2+dexa ,12Jul07 1,25=16.7 25D<10, 14Aug07 Phase2
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Dr Trevor Marshall
Research Team
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Posted: Tue Jul 22nd, 2008 11:39 |
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Inge, that study is based on a model which was absolutely incorrect. Their early in-vitro work was not thorough, yet a generation of researchers did not question it.
The model was based on an in-vitro experiment which showed that skin keratinocytes expressed Vitamin D when exposed to high intensity UV light of a few key wavelengths. Recently, another study found that monocytes and other cell lines also generated D metabolites when exposed to UV radiation. So what is the reason for that? Those cells, unlike keratinocytes, are never exposed to such radiation. It is now clear that an incorrect and insufficient conclusion was drawn from the initial Vit D stidies of UV on keratinocytes.
Every pragma about sunlight on the skin producing Vitamin D or 25-D is probably incorrect, IMO, as there was a study a few years ago which showed that, especially in the presence of the inflammatory cytokine TNF-alpha, the keratinocytes produced 1,25-D directly, and did not stop at 25-D. This is what the model in my recent paper suggests.
http://www.ncbi.nlm.nih.gov/pubmed/15225839
The human body, just like the bodies of the nocturnal mice and rats in which we test all our medicines  does not need to be exposed to sunlight in order for its D metabolism to function correctly, and deliver activated 1,25-D to its VDR to enable transcription. Full stop. Holick, Vieth, and the others, were just incorrect.
You might like to read these recent articles by Stephen Strauss of the CBC. The first deals directly with misreading epidemiological studies so that they prove what you expect them to prove:
http://www.cbc.ca/technology/story/2008/07/07/strauss-vitamind.html
and
http://www.cbc.ca/news/viewpoint/vp_strauss/20080213.html
Vitamin D is not a nutrient. A nutrient would have a first-order mass-action model for its metabolism. AFAIK, only Cannell has been reckless enough to claim that it does. Figure 1 of my Bioessay makes it quite clear that we are dealing at least with a 6th order metabolism, probably even higher.
Last edited on Tue Jul 22nd, 2008 11:54 by Dr Trevor Marshall
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inge
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Posted: Fri Jul 25th, 2008 22:10 |
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Dr Trevor Marshall wrote: The model was based on an in-vitro experiment which showed that skin keratinocytes expressed Vitamin D when exposed to high intensity UV light of a few key wavelengths. Recently, another study found that monocytes and other cell lines also generated D metabolites when exposed to UV radiation. So what is the reason for that? Those cells, unlike keratinocytes, are never exposed to such radiation. It is now clear that an incorrect and insufficient conclusion was drawn from the initial Vit D stidies of UV on keratinocytes.
I hope that you can clarify the above a bit:
- why does it matter that monocytes and other cell lines also generated D metabolites? There are no enzymes needed for the 7-DHC to previtamin D conversion are there? So as long as 7-DHC is present in these cells, when they are exposed to radiation vitamin d will be generated (however unnatural radiation may be for them).
- From the abstract of the study you mentioned (http://www.ncbi.nlm.nih.gov/pubmed/15225839) it does not seem that TNF-alpha singlehandedly induced production of vitamin D metabolites (i.e. all cells were exposed to radiation as well) , or does the full text reveal other findings?)
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CFS/ME 125D64 25D12(dec 07) Ph1De06 daily lite exp NoIR use Ph2Mar07 ModPh2 Jun07 abx brkOct 07 r//t KFTs freq abx chg to control kidney IP Apr 08 phase 2 abx
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Dr Trevor Marshall
Research Team
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Posted: Fri Jul 25th, 2008 23:55 |
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Inge,
There is a pathway from 7-dehydrocholesterol to pre-vitamin-D which does not involve radiation, but which involves enzymatic, or some other energy (eg body heat) to cleave the benzene ring. It is likely that the reason macrophages and other cell lines react to UVB is that the UVB synthesis is incidental to the normal and usual way that pre-Vitamin-D is synthesised (eg enzymatic).
Other mammalian species, even invertebrates such as the Lamprey, have an active VDR metabolism in the absence of UVB radiation. You need to be thinking of the corollary, the alternate hypothesis, and not the pragma that you have been taught in medical school. That pragma doesn't fit the data If high intensity UVB was absolutely necessary for the Vitamin-D metabolism to function, then your countrymen would be sick and weakly by comparison with those in Africa
The importance of the TNF-alpha study was to demonstrate that 25-D is not necessarily the result of irradiation of keratinocytes, that the cells are acting under other influences as well, going straight to 1,25-D metabolite. Again, this is in violation of the pragma in your textbooks We are dealing with the complex, multi-factorial feedback metabolism of my Figure 1, not the simple reactions we would expect from a nutrient.
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didierchretien
Member in Phase 2
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Posted: Sat Aug 16th, 2008 11:04 |
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Hi,
A recent Belgian epidemiological study on Low-level 21-month microwave exposure on rats shows that there is an increased mortality of the exposed rats with respect to non-exposed rats. They also noticed a loss of some cognitive functions after a few monthes of exposure.
It may due to a weakening of the immune system, favouring the genesis of decay processes wich may result in life-threatening disorders including cardiovascular and pulmonary diseases, cancer or premature aging.
http://home.scarlet.be/~tsf94646/001/documents/Thesis%20Dirk%20Adang%20-%20Synthese.pdf
This would be a good opportunity for our CWD bacteria...
Didier
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Sarcoidosis 25D10(Jan08) 25D6.9ng(May08) 25D7.1ng(July08) BeniFeb08 to wean prednisone Ph1Jun08 Ph2Jul08 Zolpidem Xyzall NoIRs low lux home limited outings covered
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Dr Trevor Marshall
Research Team
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Posted: Sat Aug 16th, 2008 11:21 |
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Didier,
The answer almost certainly lies in the VDR / Vitamin D axis )that they didn't even bother to measure). Note that in my Figure 1 I note that 7-dehydrocholesterol is changed to Vitamin D by the addition of ENERGY (I have UVB only as an example). There is also strong evidence for enzymatic catalysis.
Monocytes differentiate from hematopoetic stem cells, at least in part based on 1,25-D levels. This study found monocytes to be the most profoundly affected cell type.
I once took a quick look at the Atomic Radiation poisoning after Chernobyl, and certainly the chronic deaths of children there look awfully like an upset innate immune system. What the effect of any Th1 pathogens might be is not clear, as these folk seem to succumb to acute disease pretty readily, probably before the chronic pathogens become a significant factor.
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Pat McKinzie
Member in Phase 3
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Posted: Sun Aug 17th, 2008 11:46 |
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Dear Dr Marshall,
My wife Pat started pn the MP 4 month ago, after years of sickness and declining helth, despite all efforts by her physicians. The protocoll, as harsh as it is to follow, is the first treatment which gave her hope for recovery and I am immensely gratefull to you for that.
She is doing very well in my opinion (she is almost ready for phase 3) but I do have a big concern with the low vitamin D level which are required.
I am not, by far, a medical expert, but have found many publications stating that low level of vitamin D lead to a cerain death, especially by elevating the heart failure's risks.
As far as I have understood the MP, the low vitamin D level is required to prevent the system from producing 25D & 1.25 D.
How long does this process generally last ? Is there a time when it is possible to go back to "normal" vitamin D levels ?
I would be gratefull if you could give me some hints on this topic, as I did not want to discuss it with her without knowing enough, in order to not stress her even more than she already is.
Many thanks.
Gérald lechault
(Switzerland)
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Lyme CFS FM 25D39 Ph1 Apr08 levothyroxin Co-Dafalgan fluoxetine Sinqan NoIRs, covered up lite exp r/t to work|
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Dr Trevor Marshall
Research Team
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Posted: Sun Aug 17th, 2008 12:10 |
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Gérald,
Next month I will be co-Chairman of a special session on "VDR, Vitamin D, and Autoimmune Disease" at the 6th International Congress on Autoimmunity. I, and my colleagues, will be presenting our data and science to that august gathering of expert researchers:
http://www.marshallprotocol.com/forum39/12376.html
Last year I published a paper which explained why the addition of Vitamin D to the food chain is responsible for the current epidemics of chronic disease. I opined that the mistake of calling Vitamin D a nutrient, which it is most certainly not, will go down in history as the biggest mistake Medicine has ever made:
http://TrevorMarshall.com/BioEssays-Feb08-Marshall-Preprint.pdf
Vitamin D is not a nutrient. The reason that people are recovering their lives on the MP is because it is based on 21st century science, and not on 20th century mistakes Vitamin D is a seco-steroid transcriptional activator, the body produces all that it needs.
Anyway, there is a lot of detailed material here, and at the other sites on this topic. I trust it will set your mind at ease. For example:
http://mp-lifestyles.org/forum1/46.html
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Pat McKinzie
Member in Phase 3
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Posted: Sun Aug 17th, 2008 13:38 |
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Dear Dr Marschall,
Many, many thanks for such a prompt reply.
I will read through this material and, hopefully, understand it. Ha !
Gérald
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Lyme CFS FM 25D39 Ph1 Apr08 levothyroxin Co-Dafalgan fluoxetine Sinqan NoIRs, covered up lite exp r/t to work|
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eClaire
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Posted: Sun Aug 17th, 2008 18:05 |
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Gerald,
You might also want to read (an easier read) Amy's "The Truth About Vitamin D: Fourteen Reasons Why Misunderstanding Endures."
http://bacteriality.com/2007/09/15/vitamind/
Claire
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CFS FMS MCS COPD hypermobility IBS/GERD osteoporosis 125D48 25D8 Ph1Dec06 ModPh2Jun07 NoIRs limited outings covered up low lux home abx brk 3/2-5/25/08; Temazepam 9/26/08; Ph2Oct29
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inge
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Posted: Mon Aug 18th, 2008 19:26 |
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| How can massive amounts of vitamin D supplementation lead to hypercalcemia if all other vitamin D forms than vitamin D 1,25 inactivate the VDR?
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CFS/ME 125D64 25D12(dec 07) Ph1De06 daily lite exp NoIR use Ph2Mar07 ModPh2 Jun07 abx brkOct 07 r//t KFTs freq abx chg to control kidney IP Apr 08 phase 2 abx
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Dr Trevor Marshall
Research Team
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Posted: Mon Aug 18th, 2008 19:56 |
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Inge,
Pse look at my Bioessay figure 1.
Note that the VDR transcribes the Calcium Sensing Receptor, CASR. The function of CASR is to regulate the levels of calcium:
http://en.wikipedia.org/wiki/Calcium-sensing_receptor
So, if you knock out the VDR you take away the ability of the CASR to regulate calcium, as you reduce the expression of CASR.
Of course, the complete detail is a lot more complex than this, as there are many other pathways involved in the regulation of such a critical body function as calcium homeostasis.
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Russ
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Posted: Tue Aug 19th, 2008 14:28 |
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I have often wondered why for millions of years primitive man ate no dairy foods and yet did not suffer from calcium deficiency and yet today people risk deficiency if they do not keep calcium intake at the 1000-1500mg RDA which is surely much more calcium than primitive man got on his hunter-gatherer diet. Is this the answer, that widespread TH1 disease which has shut down VDR function has messed up calcium homeostasis?
Some of the advocates of a "paleolithic" diet claim that it was the addition of grains and the move to a high carb diet that has caused the need for more calcium and they claim that on a paleo-diet, which forbids dairy foods, one does not need to supplement calcium because the need for it drops. Since my understanding is that too much calcium can be as bad as too little, I've wondered how much calcium one should aim for if they are eating paleo/low-carb and I guess if one is taking a VDR agonist as we are that might factor in to the amount needed as well.
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Lyme/Borrelia, Connective Tissue Disease | May '06: 1-25D=59 25D=30 | Jul '06: Phase 1 | Aug '06 25D=16 | Oct '06 25D=6 | Nov '06: Phase 2 | Jul '07: Phase 3 | covering up & wearing NOIRs | no other meds or supplements
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Knochen
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Posted: Tue Aug 19th, 2008 15:16 |
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yet today people risk deficiency if they do not keep calcium intake at the 1000-1500mg RDA which is surely much more calcium than primitive man got on his hunter-gatherer diet.
A real hunter/gatherer ate a lot of small beasties whole, bones and all, just like other animals. Lots of calcium there! Same for small birds eggs. Our forebears were not so fastidious as we! 
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Reiter's Syndrome 25+ yrs, fatigue, joints, muscles, migraine, brainfog| 25D 6 ng/ml |Benicar May06|Ph1 June06|Ph 2 Sept06|Ph 3 Jan 07|NoIRs K-Cream Zinc Oxide cream - Always covered!
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