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Belinda Research Team

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Posted: Thu Mar 15th, 2007 01:11 |
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Dr. Marshall is busily working on a new paper about vitamin D, so I am sharing some of his latest work with you, which he communicated via e-mail.
A paper published in March 2007 by Demay, Sabbagh and Carpenter Calcium and vitamin d: what is known about the effects on growing bone, should finally put the vitamin-D deficiency rickets myth to bed. The Demay group found that the metabolic cause of rickets is hypophosphatemia.
Dr. Marshall wrote the author, asking what evidence there is to back the statements in that paper that Vitamin D helps the gut absorb calcium. The reply he received said:
"We have no data that 1,25 has any effect on the prevention of rickets ..
Absence of ligand or receptor in the presence of normal mineral ions leads to a normal growth.."
Dr. Marshall wrote to me saying, in any case, this “study clearly shows only lack of circulating phosphate induces rickets. Indeed, any amount of calcium, in the absence of the correct amount of phosphorous, does not prevent or cure rickets. Neither does Vitamin D. Here is yet another paper confirming that:
Hypophosphatemia leads to rickets by impairing caspase-mediated apoptosis of hypertrophic chondrocytes.
The full text is available online here.
So let me repeat those email comments:
"normal mineral ions prevent skeletal disease in the absence of the VDR .. Absence of ligand or receptor in the presence of normal mineral ions leads to a normal growth.. "
There we have it: in-vitro, murine and in-vivo (PubMed 15531695) results all failed to show that Vitamin D is important in either causing or curing rickets, and further that calcium doesn't help either, unless adequate phosphorous is present.
Dr. Marshall did note that “the VDR does transcribe CASR and PTH and TRPV5 and TRPV6, all of which are active in calcium homeostasis.”
It really is a shame that the same old pragma about vitamin D is put into papers just to appease the industry or the reviewers so that papers can be published.
Belinda
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wrotek Member in Phase 3

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Posted: Thu Mar 15th, 2007 11:11 |
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| So children simply don't have a right diet between 3rd month and second year of life, when rickets occurs ?
____________________ Lyme reflux chronic pain fatigue depression 125D36 Ph1Sep05 Ph2Oct06 Ph3Apr07 homebound in low lux NoIRs 25D<7 Oct06
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Gus Member
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Posted: Thu Jun 28th, 2007 09:26 |
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Trevor,
I quote:
Dr. Marshall wrote the author, asking what evidence there is to back the statements in that paper that Vitamin D helps the gut absorb calcium. The reply he received said:
"We have no data that 1,25 has any effect on the prevention of rickets ..
Absence of ligand or receptor in the presence of normal mineral ions leads to a normal growth.."
Rather than deny any effect of 1,25D on prevention of rickets, I see that the reply stated that they had no data of an effect. And doesn't preventing rickets in any case generally pre-suppose abnormal mineral ions (which administration of 1,25D migh be instrumental in normalising??)
There was a paper quoted by someone recently which researched the effect of IV and oral 1,25D on spontaneous and hypocalcemia-induced PTH secretion. It showed that Ca ++ concentration did not change in the short term with 1,25D administration and according to the paper, this was because in the limited period of study, the increase in gut absorption was exactly nullified by increased excretion. Is the measured increased level of excretion and constant ionised Ca not evidence of increased gut absorption? The alternative would appear to be that the source of increased Ca excreted derived from mobilisation of Ca directly by PTH. Is this what you are suggesting?
It also seems to me that asserting that ionised Ca depends only on Ca intake and correct phosphorus level ignores the fact that intestinal phosphate absorption is increased by 1,25D - or do you take issue with this as well?
Gus
____________________ Pre MP, Symptoms typical FMS or Lyme (tick bite 1964) 25D 1.4 ng/ml 1,25D 29pg/ml, Noirs on order, avoiding D but not sun/lights, Benicar/Mino available but start date not decided.
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jcwat101 Research Professional

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Posted: Thu Jun 28th, 2007 12:10 |
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From what I understand, I don't think there is any question that one does need adequate calcium and phosphorus intake and that VDR activation (usually by 1,25D, but on the MP, it can be by Benicar) does increase absorption of both. Many focus too much on 25D (vitamin D) levels and we know that is a common mistake in Th1 disease.
Patients on the MP are usually recommended to get near the RDA of calcium and phosphorus (when one adds up dietary and supplemental sources, with dietary sources much preferred). An exception is in cases of hypercalcemia and then one should consult one's doctor on the level of mineral intake.
There seems to be usually a greater emphasis on calcium intake because it is more often deficient in the diet. Phosphorus occurs in a wider array of foods. But inadequate phosphorus intake has been known to cause Rickets. The above study actually focuses on the proximate role of phosphorus in the mechanism of Rickets rather than the amount in the diet. As I recall, in that study they avoid the issue of absorption and dietary intake through giving and manipulating the minerals intravenously.
Calcium and phosphorus are also intertwined because deficient calcium increases PTH, which then causes too much phosphorus to be excreted and thus causes too low a phosphorus level, which then affects the bone formation in Rickets.
Joyce Waterhouse
____________________ 20 yrs with CFS/FM/Lyme/IBS, food sensitivities; 1,25D/25D 8/04:64/11 1/05:22/6 9/05:1,25D=12 10/06:22/8, 4/07:25/<4 chewed Ben. 40mg q8h; Mod. P2: 2/23/05, P2: 4/06; P3: 1/1/07
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eClaire Member in Phase 2

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Posted: Tue Nov 27th, 2007 02:26 |
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Yet another Vitamin D Rickets story. (It gets scarier and scarier.)
"Little milk, exercise hurts kids' bones"
http://news.yahoo.com/s/ap/20071126/ap_on_he_me/healthbeat_kids__bones
Claire
____________________ CFS FMS MCS COPD hypermobility IBS/GERD osteoporosis 125D48 25D8 Ph1Dec06 ModPh2Jun07 NoIRs limited outings covered up low lux home abx brk 3/2/08 to 5/25/08
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Kas Member in Phase 2

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Posted: Tue Nov 27th, 2007 14:52 |
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If you think of children in Africa, who live in a sunshine climate virtually year round, and have great skin exposure to the sun in their early years, especially, it makes sense that Vitamin D does not cure or prevent rickets, as African children have a particularly high incidence of the disease. I guessed it was because they were not consuming / absorbing sufficient calcium from their diets, and now I have also learned about phosphoros.
Out of interest, which foods are rich in phosphoros? Are almonds and other nuts?
Moderator's note: Because the increasing volume of requests for assistance is threatening to overwhelm our small staff of volunteers, before you post a question, we ask that you type key words into the search feature of this site or an Internet search engine.
____________________ Sarc Dx by splenectomy 03- Lungs, lymph nodes, liver. Non MP meds: natural progesterone cream three weeks a month; cal/mag; probiotics; milk thistle daily; cranberry caps prn; quercetin prn.Noirs outdoors and under flourescent work lights, Spectra 3 cream
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eClaire Member in Phase 2

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Posted: Tue Nov 27th, 2007 15:27 |
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Note that both too much phosphate and too little phosphate in the blood can be bad for bones (if this site is to be believed).
http://www.merck.com/mmhe/sec12/ch155/ch155h.html
____________________ CFS FMS MCS COPD hypermobility IBS/GERD osteoporosis 125D48 25D8 Ph1Dec06 ModPh2Jun07 NoIRs limited outings covered up low lux home abx brk 3/2/08 to 5/25/08
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Dr Trevor Marshall Research Team

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Posted: Tue Nov 27th, 2007 15:39 |
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Here is a recent paper from the Dept of Agriculture which deals with the issues
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=169216
"Rickets in toddlers is a large problem in parts of Africa, especially Nigeria. It is not due to vitamin D deficiency but is caused by not having enough calcium in the diet"
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eClaire Member in Phase 2

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Posted: Tue Nov 27th, 2007 16:03 |
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Thanks for that link Dr. Marshall!
That is why the article in the newspaper is so scary. The information is out there and yet researchers/doctors are continuing to be quoted as saying D matters when it comes to rickets. There's the whole fear factor involved with these headlines (to sell copy), and I see, in my mind's eye, worried parents pressing even more milk "fortified" with vitamin D on their children. Sigh....
____________________ CFS FMS MCS COPD hypermobility IBS/GERD osteoporosis 125D48 25D8 Ph1Dec06 ModPh2Jun07 NoIRs limited outings covered up low lux home abx brk 3/2/08 to 5/25/08
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inge Health Professional

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Posted: Tue Nov 27th, 2007 16:24 |
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There is not nescessarily only one cause of a disease, and although in some populations vitamin d plays no role in causing rickets, this does not preclude that it can play a role in other populations, where vitamin d is lower than in Africa. As I understand vitamin d was discovered due to it's role in curing rickets (Mellanby T. The part played by an “accessory factor” in the production of experimental rickets.Physiol. 1918;52:11–14. and Hess A.F., Unger L.J. The cure of infantile rickets by sunlight. JAMA. 1921;77:39–41.), i.e if it hadn't been for rickets vitamin d would have been discovered at a later stage.
Any critisisms to these studies? (sorry don't have the full text)
Inge
____________________ 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: Tue Nov 27th, 2007 17:12 |
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Inge,
'Experimental Rickets' is useless, as the mouse/rat VDR is different from that of man. Additionally, the rodent VDR does not decode the gene for Cathelicidin, nor for many other proteins having functional commonality with man.
Actually, the very first description of Rickets, in 1857, had the mineral pathogenesis pretty well correct:
http://ije.oxfordjournals.org/cgi/content/full/32/3/336
Vitamin D has some role in assisting the absorption of minerals, but anybody with anywhere near a normal Vit D metabolism will not have difficulty. Supplementation has no purpose, as it fails in "Vitamin D Resistant Rickets" anyway
Marie DeMay wrote to me saying:
"We have no data that 1,25 has any effect on the prevention of rickets, absence of ligand or receptor in the presence of normal mineral ions leads to a normal growth plate"
when I asked her why she had mentioned Vitamin D in the abstract to her paper
http://tinyurl.com/yspko3
while the fulltext showed no benefit at all to vitamin D. Yes, yes, I know that was in a model of experimental rickets  
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Rico Member in Phase 3
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Posted: Wed Nov 28th, 2007 00:52 |
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Sorry for diverging from the topic, but I'm not sure where to post this - this has upset me. I quote from the 17th edition (1993) of the Taber's Cyclopedic Medical Dictionary (which I believe is a reputed book in the conventional medicine circles), under the topic of steroid:
| Term applied to any one of a large group of substances chemically related to sterols. Includes sterols, D vitamins, bile acids, certain hormones, saponins, glucosides of digitalis, and certain carcinogenic substances. |
Ok, what's the deal?! I don't get it. If the medical community has known since at least 1993 that D vitamins are a steroid, why is the public being supplemented with steroids and told it's good for you? I thought that Vitamin D being considered a steroid was relatively new and that it hadn't quite made its way to the FDA, Health Canada, etc. Seems to me the industry has long known of this. I thought it was common knowledge that steroids are not good for you long term.
I wonder what the FDA and Health Canada would say if patients started writing them asking why they've approved overdosing us with steroids?!
____________________ 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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JCB Member in Phase 3

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Posted: Wed Nov 28th, 2007 16:40 |
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I think this New York Times Health article yesterday about so-called "good" and "bad" bacteria is a useful indication of where the conventional wisdom is and perhaps is going, and the direction isn't great. Take a look.
http://www.nytimes.com/2007/11/27/health/27book.html?_r=1&oref=slogin&ref=health&pagewanted=print
There are some amazing contradictions, e.g. chronic "drug resistant" infection has been with us for a long time, but at the same time it is implied to be due to modern abx resistance. Similarly the writer observes that the human bacterial load may be huge, but at the same times posits that "auto-immune" diseases may be due to germ free environments.
(An interesting mention is made however of a 19th century immunologist - Elie Metchnikoffoc - who linked "senility, atherosclerosis and an altogether shortened life span" to bacterial pathogens, but that is seemingly discredited by the article.)
____________________ teenage daughter with chronic Lyme Jul 28 04 25D-23, 1,25D-60 ratio 2.8, Benicar init Sep 14 04 Mino Nov 4 04 Phase 2 Jan 25 05, Mod Ph 2 w/ C currently
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eClaire Member in Phase 2

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Posted: Thu Nov 29th, 2007 02:32 |
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| There was a similar bizzare article in Time a month or so ago about kids and food allergies. (Sorry I don't have the link.) The authors were touting the germ-free environment theory as well. I found it so scary (really, the direction mainstream seems to be taking me is truly frightening) that I couldn't finish reading the article (afraid of bad dreams). Claire
____________________ CFS FMS MCS COPD hypermobility IBS/GERD osteoporosis 125D48 25D8 Ph1Dec06 ModPh2Jun07 NoIRs limited outings covered up low lux home abx brk 3/2/08 to 5/25/08
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