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Meg Mangin R.N.
Research Team
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Posted: Sun Jan 14th, 2007 11:58 |
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Don't I need vitamin D to prevent bone loss?
Vitamin D supplementation will not prevent bone loss.
Until we standardize the clinical evaluation of vitamin D metabolites, assessing both 1,25-dihydroxycholecalciferol D and the inactive precursor, 25-dihydroxyvitamin D, patients with dysregulated vitamin D metabolism will continue to be misdiagnosed as Vitamin D deficient. These folks suffer from excess production of the biologically active metabolite (1,25D) and all the impact of this hormone, which includes activation of the immune macrophage system. http://tinyurl.com/6gbgq
Bone remodeling is a continuously ongoing process. The bone cells that resorb bone are osteoclasts. The ones that lay down new bone are osteoblasts. If the two processes are in balance, then things are normal. But 1,25-D is a cytokine that induces increased production of osteoclasts from stem cells. In addition, 1,25-D increases osteoclastic activity. When osteoclasts outnumber osteoblasts (bone builders) and when they are working faster than osteoblasts, then existing bone is resorbed faster than new bone can be laid down and bone loss results. That's what happens when 1,25-D is unregulated and elevated.
Bone resorption can be stimulated by oral 1,25-D in healthy men taking a dose as small as .75 micrograms every 6 hours. See http://tinyurl.com/dktzm
1,25-D plays a crucial role in bone reformation by stimulating bone osteclast formation and activity. See the final two paragraphs of the paper at http://edrv.endojournals.org/cgi/content/full/23/6/763 Note that much of the previous research of 1,25-D has been done "in vitro" (in labs) rather than "in vivo" - in life. That's a big part of the reason why there has been such misconception about how 1,25-D functions.
Much of the misconception about vitamin D goes back decades, back before 1,25-D was identified and understood - when 25-D was thought to be the active hormone. That's where the notion that "more D is better" originated (when the only D known was 25-D).
Here is a link to a tutorial on vitamin D that provides a relatively simple explanation:
VITAMIN D TUTORIAL
Because the body can make 1,25-D from 7-dehydro-cholesterol, there is a link between the lipid metabolism and the immune system. It's a very complex subject that, unfortunately, is not being taught correctly in medical schools because their curriculum has not caught up with the latest reserach.
http://www.endotext.org/parathyroid/parathyroid3/parathyroidframe3.htm
Vitamin D is actually a secosteroid hormone, and is critical to many functions throughout the body. A drawing showing some of the organs it affects is at UC Riverside, URL http://vitamind.ucr.edu/Images/metab.gif
The definitive work on vitamin D metabolism is being done by Dr. Anthony Norman:
http://biochemistry.ucr.edu/faculty/norman.html
Industrial forces that have a financial conflict of interest are promoting increased vitamin D supplementation. To increase the sales of vitamin D, they have called on self-appointed vitamin D experts to raise the level of 25-D that is accepted as normal. The studies their claims are based on are seriously flawed and/or based on an outdated understanding of vitamin D.
It used to be accepted that vitamin D was synthesized via the skin, and then metabolized via the liver and kidneys. Now we know that human skin can completely synthesize the active hormone D, 1,25-dihydroxycholecalciferol, independent of other organs. http://tinyurl.com/65nrc
Conventional medicine says that 25-D is produced when the skin is exposed to sunlight, but they are incorrect, and especially inocrrect in the Th1 diseases. Keratinocytes in the skin primarly produce 1,25-D and not 25-D. You can read the details in: "Role for tumor necrosis factor-alpha in UVB-induced conversion of 7-dehydrocholesterol to 1alpha,25-dihydroxyvitamin D3 in cultured keratinocytes" You will note that the process seems to be energized by the presence of the inflammatory hormonal cytokine, TNF-alpha. That cytokine would exist at high concentrations in the inflamed tissue. While there is substantial evidence for other extra-renal sources of hormone 1,25-D, it has been known for decades that activated macrophages produce 1,25-D in diseases such as sarcoidosis.
The vitamin D used by the healthy body (1.25-D) comes mostly (90 to 100%)from exposure to sunlight. Ten to fifteen minutes of daylight exposure two times per week to the face, arms, hands, or back is enough exposure to provide an adequate amount to a healthy person. People can get that in only a fraction of the amount of time they spend outside each week. The keratinocytes in the skin of people who have Th1 inflammatory disease are especially sensitive to any light, and even infra-red radiation. Most folk with inflammatory disease manufacture too much 1,25-D even in the absence of sunlight, as the activated macrophages of the immune system also produce it.
We know now that hormone D activates the immune system. However, the increased use of nutritional vitamin D is suppressing the immune systems of people with immune disease who can be made ill by additional vitamin D. You do not need to ingest vitamin D to be healthy.
Regarding nutritional sources of vitamin D:
- There is no Recommended Daily Allowance (RDA) for vitamin D, because it is endogenously produced by humans in the presence of a few minutes of sunlight.
- The alternative Recommended Dietary Intake (RDI) of nutritional vitamin D is based on the absence of adequate sunlight. http://www.iom.edu/Object.File/Master/7/296/0.pdf
- When studies of dietary needs for vitamin D are conducted, people with diseases that result in dysregulated vitamin D metabolism (such as sarcoidosis) may be excluded. One example is the Food Standards Agency's Expert Group on Vitamin and Minerals: Safe Upper Levels for Vitamins and Minerals May 2003
http://www.food.gov.uk/multimedia/pdfs/vitmin2003.pdf
That report noted, "Excessive vitamin D intake may lead to hypercalcaemia and hypercalciurua. Vitamin D promotes the absorption of calcium and the resorption of bone resulting in the deposition of calcium in soft tissues, diffuse demineralization of bones and irreversible renal and cardiovascular toxicity. It has long been known that (as the report continues), "Patients with sarcoidosis are abnormally sensitive to vitamin D, due to uncontrolled conversion of the vitamin to its active form in the granulomatous tissue."
25-D displaces 1,25-D from the Vitamin D Receptor. Too much 25-D is able to turn off the immune system response which is necessary to prevent chronic inflammatory disease.
Why has there been so much detection of low 25-D, called "Vitamin D deficiency," when people consume vitamins and foods containing supplemented Vitamin D? Uncontrolled conversion of vitamin D to its active form, hormone 1,25-D, is rarely investigated in any research of vitamin D deficiency. Based on results that have been reported to our study sites, we believe this uncontrolled conversion of 25-D to 1,25-D is a common cause of measured 25-D "deficiency," and the underlying reason is the existance of Th1 disease.
Studies have shown that nutritional vitamin D can be toxic to vascular tissues. http://tinyurl.com/45he3
This study shows that vitamin D doesn't slow bone loss in black women http://tinyurl.com/nu7r4
Vitamin D has been used to induce an animal model of arthrosclerosis in research: http://tinyurl.com/664sv
Too much vitamin D can result in illness ranging from dental changes http://tinyurl.com/66e98 ,
to bone loss Gains in Bone Mineral density with Resolution of Vitamin D Intoxication
or even death. http://tinyurl.com/4cfsg
Hypothesis: etiology of atherosclerosis and osteoporosis: are imbalances in the calciferol endocrine system implicated? states: The use of vitamin D as a food supplement coincides with epidemic onsets of atherosclerosis and osteoporosis, and excess vitamin D induces both conditions in humans and laboratory animals.
The standard practice, in assessing vitamin D status, has been to evaluate only serum 25-D, which is the inactive metabolite. The best way to know whether sunlight and vitamin D would be dangerous is to test the two major vitamin D metabolites (25-D and hormone 1,25-D) to detect any evidence of dysregulated vitamin D metabolism.
We have an amazing depth of knowledge about the complexity of 1,25-D actions in the human body, but it is in the molecular-medicine literature, and often very hard to read. The easy-to-read material comes from observational studies in clinical medicine. Studies which are invariably badly flawed, because they fail to acknowledge the manner in which the metabolites of Vitamin D actually affect the human body.
There are a plethora of clinical concepts about the actions of Vit D, and nearly everyone of them has been shown by molecular medicine to be totally incorrect. Ours is a catalyst which will allow clinical medicine to start to catch up with the molecular scientific knowledge.
..Trevor..
Members experiences
Saw the Dr this morning.. confirmed my bone density reading was 5% above the population norm for my age after 2.5 years on a low Vit D diet !! He was a bit surprised and delighted that the regime of small, regular doses of calcium rich foods each day has avoided any issues in this area. ~Sydney Chris
My BMD dropped a bit in the past 3 yrs on the MP but the rate of bone loss has slowed by 50%. ~Meg Mangin R.N
After one year on the MP, was doctor was surprised by my bone scan results......I no longer have osteopenia! ~Lynda
Related topics:
What does my bone density test mean?
My 25-D is low and/or my 1,25-D is high. Should I be concerned about osteoporosis?
The Importance of Reducing 25-D
A Review - Vitamin D and Calcium in Sarcoidosis (7-5-03)
http://www.sarcinfo.com/calcium.htm
rickets(osteomalacia)
Nutritional Sources of Vitamin D
Don't I need to take a calcium supplement?
Calcium Fact Sheet
Osteoporosis, osteopenia and Th1 illness
In the new 2006 medical textbook titled Vitamin D: New Research, published by Nova, you will find a chapter written by Waterhouse JC, Marshall TG, Fenter B, Mangin M, Blaney G on High levels of active 1,25-dihydroxyvitamin D despite low levels of the 25-hydroxyvitamin D precursor - Implications of dysregulated vitamin D for diagnosis and treatment of Chronic Disease A copy of the chapter can be found at this Internet address:
http://winmlm.neostrada.pl/vitamindbook/vitamindnewresearch.pdf
Marshall TG: VDR Nuclear Receptor Competence is the Key to Recovery from Chronic Inflammatory and Autoimmune Disease. Abstract presentation, Days of molecular medicine, 2006.
Copy available from URL http://autoimmunityresearch.org/karolinska-handout.pdf
Vitamin D does not reverse osteoporosis.
Vitamin D insufficiency: Disease or no disease?
Last edited on Sun Mar 9th, 2008 23:02 by Meg Mangin R.N.
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