Left field insight to Vit D, There are comments on the effects of Vit D metabolism;
http://buhnerhealinglyme.com/miscellane ... -protocol/
"Nevertheless, his finding still stands true – there are people, myself included – whoi do not metabolize vitamin D in the normal way and thus these people should never be given vitamin D supplements as this will create a huge problem for their immune system."
and
http://www.natmedtalk.com/f50/1643-mars ... y-one.html
"The Marshall Protocol was developed by Trevor Marshall, PhD, in 2002 to treat certain diseases that involve Th1 immune system dysfunction.
Dr. Marshall's papers describe how numerous Th1 diseases such as sarcoidosis, Lyme disease, chronic fatigue syndrome, fibromyalgia, lupus and rheumatoid arthritis (among others) are caused by Cell Wall Deficient (CWD) bacteria of various species......
An essential part of the Marshall Protocol is avoidance foods and vitamin supplements containing vitamin D to reduce the level of this hormone which suppresses the immune system......
and
The protocol also includes the introduction of carefully, selected low dose antibiotics in a pulsed schedule"......
http://www.marshallprotocol.com/forum2/364.html
"Ingested Vitamin D is an immune-suppressant, similar to the function that prednisone performs. Ingested Vitamin D suppresses the action of the VDR (Vitamin D Receptor) and thus turns-off the immune system's Th1 response so it cannot fight the intra-phagocytic bacteria. People feel better in the short-term, but will succumb to the infection more rapidly in the long-run"......
http://www.marshallprotocol.com/forum2/4062.html
"The MP coordinates the use of Benicar (Olmesartan medoxomil), and specific, pulsed, low-dose, bacteriostatic, oral antibiotics to enable the immune system to destroy the persistent bacteria [5]. Correctly dosed, Benicar reduces inflammatory cytokine production by blocking the angiotensin II, type I receptors to inhibit, inter alia, the release of tumor necrosis factor-alpha during the Th1 immune reaction"......
http://autoimmunityresearch.org/phase1.pdf
and
http://www.prweb.com/releases/2008/1/prweb639651.htm
New Research Challenges Concept of Vitamin D Deficiency
The vitamin D deficiency long interpreted as a cause of disease is more likely the result of the disease process and increasing intake of vitamin D often makes the disease worse.
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Thousand Oaks, CA (PRWEB) January 21, 2008
Low blood levels of vitamin D have long been associated with disease, and the assumption has been made that vitamin D supplements may protect against disease. In the light of new knowledge that hundreds of genes are dependent on vitamin D, this assumption needs to be reconsidered.
In a report published in the current issue of the journal BioEssays(1), Trevor Marshall, Ph.D., professor at Australia's Murdoch University School of Biological Medicine and Biotechnology, explains how increased vitamin D intake affects much more than just nutrition or bone health. The paper explains how the Vitamin D Nuclear Receptor (VDR) acts in the repression or transcription of hundreds of genes, including genes associated with diseases ranging from cancers to multiple sclerosis.
"The VDR is at the heart of innate immunity, being responsible for expression of most of the antimicrobial peptides, which are the body's ultimate response to infection," Marshall said. "Molecular biology is now forcing us to re-think the idea that a low measured value of vitamin D means we simply must add more to our diet. Supplemental vitamin D has been used for decades, and yet the epidemics of chronic disease, such as heart disease and obesity, are just getting worse."
"Our disease model has shown us why low levels of vitamin D are observed in association with major and chronic illness," Marshall added. "Vitamin D is a secosteroid hormone, and the body regulates the production of all it needs. In fact, the use of supplements can be harmful, because they suppress the immune system so that the body cannot fight disease and infection effectively."
Marshall's research has demonstrated how ingested vitamin D can actually block VDR activation, the opposite effect to that of Sunshine. Instead of a positive effect on gene expression, Marshall reported that his own work, as well as the work of others, shows that quite nominal doses of ingested vitamin D can suppress the proper operation of the immune system. It is a different metabolite, a secosteroid hormone called 1,25-dihydroxyvitamin D, which activates the VDR to regulate the expression of the genes. Under conditions that exist in infection or inflammation, the body automatically regulates its production of all the vitamin D metabolites, including 25-hydroxyvitamin D, the metabolite which is usually measured to indicate vitamin D status.
Vitamin D deficiency, long interpreted as a cause of disease, is more likely the result of the disease process, and increasing intake of vitamin D often makes the disease worse. "Dysregulation of vitamin D has been observed in many chronic diseases, including many thought to be autoimmune," said J.C. Waterhouse, Ph.D., lead author of a book chapter on vitamin D and chronic disease (2). "We have found that vitamin D supplementation, even at levels many consider desirable, interferes with recovery in these patients."
"We need to discard the notion that vitamin D affects a disease state in a simple way," Marshall said. "Vitamin D affects the expression of over 1,000 genes, so we should not expect a simplistic cause and effect between vitamin D supplementation and disease. The comprehensive studies are just not showing that supplementary vitamin D makes people healthier."
and
http://trevormarshall.com/BioEssays-Feb ... eprint.pdf
Conclusion
This BioEssay has examined a number of ways in which,
while the widespread use of Vitamin D as a food supplement
may be providing short term benefits to a subset of the
population, epidemic expansion of obesity and chronic
disease are quite possibly the legacies to be bestowed upon
future generations.
This BioEssay has examined a number of ways in which,
while the widespread use of Vitamin D as a food supplement
may be providing short term benefits to a subset of the
population, epidemic expansion of obesity and chronic
disease are quite possibly the legacies to be bestowed upon
future generations.
The concept that “The Sunshine Vitamin” really is just a
vitamin, with the consequent implication of a linear ‘vitamin
in, benefit out’ model, is clearly no longer tenable. At any
level of molecular analysis, the Vitamin D metabolites are
part of the delicate homeostasis which allows our bodies to
express genes, and to express them when the need arises.
The concept that “The Sunshine Vitamin” really is just a
vitamin, with the consequent implication of a linear ‘vitamin
in, benefit out’ model, is clearly no longer tenable. At any
level of molecular analysis, the Vitamin D metabolites are
part of the delicate homeostasis which allows our bodies to
express genes, and to express them when the need arises.
The conviction that one can, with impunity, continue to add
higher and higher concentrations of this secosteroid to the
food chain is still firmly held by many of our clinical
colleagues. This is a recipe which could easily lead to a
public health disaster. Yet the ‘vitamin’ model has a
seductive simplicity, a simplicity which offers a welcome
escape from the complex world of modern molecular
medicine.
The conviction that one can, with impunity, continue to add
higher and higher concentrations of this secosteroid to the
food chain is still firmly held by many of our clinical
colleagues. This is a recipe which could easily lead to a
public health disaster. Yet the ‘vitamin’ model has a
seductive simplicity, a simplicity which offers a welcome
escape from the complex world of modern molecular
medicine.
Molecular biologists have a duty to share their new-found
genomic knowledge with their clinical colleagues. They
need to help them understand the steroidal nature of Vitamin
D. To help them understand that this substance is intimately
involved in the transcription of hundreds, probably
thousands, of genes. Genes which determine the course of
immune disease, and cancers. At the very least, we must
ensure that every researcher understands the importance of
measuring the concentration of the actual transcriptional
activator, 1,25-dihydroxy-vitamin-D.
Molecular biologists have a duty to share their new-found
genomic knowledge with their clinical colleagues. They
need to help them understand the steroidal nature of Vitamin
D. To help them understand that this substance is intimately
involved in the transcription of hundreds, probably
thousands, of genes. Genes which determine the course of
immune disease, and cancers. At the very least, we must
ensure that every researcher understands the importance of
measuring the concentration of the actual transcriptional
activator, 1,25-dihydroxy-vitamin-D.
Biologists need to raise their voices and help Federal
regulators understand what is being discovered about the
wonderful genetic tapestry which has historically allowed
Homo sapiens to thrive, and to control its environment.
Biologists need to raise their voices and help Federal
regulators understand what is being discovered about the
wonderful genetic tapestry which has historically allowed
Homo sapiens to thrive, and to control its environment.
While it is true that molecular biology can still only precisely
describe a very small fraction of the human experience,
what it can describe it does so in exquisite detail. It is critical
that Medicine revisits the role which has been assigned to
"The Sunshine Vitamin," properly recognizing its function as
a secosteroid, a transcriptional activator, key to the proper
operation of the innate immune system.
and
http://mpkb.org/home/pathogenesis/vitamind
Science behind vitamin D
A number of studies have suggested that patients with chronic inflammatory diseases are deficient in 25-hydroxyvitamin D (25-D) and that consuming greater quantities of vitamin D, which further elevates 25-D levels, alleviates disease symptoms.
Some years ago, molecular biology identified 25-D as a secosteroid. Secosteroids would typically be expected to depress inflammation, which is in line with the reports of short-term symptomatic improvement. The simplistic first-order mass-action model used to guide the early vitamin studies is now giving way to a more complex description of action.
When active, the Vitamin D nuclear receptor (VDR) affects transcription of at least 913 genes and impacts processes ranging from calcium metabolism to expression of key antimicrobial peptides. Additionally, recent research on the Human Microbiome shows that bacteria are far more pervasive than previously thought, dramatically increasing the possibility that the spectrum of chronic diseases is bacterial in origin.
Emerging molecular evidence suggests that symptomatic improvements among those administered vitamin D is the result of 25-D’s ability to temper bacterial-induced inflammation by slowing VDR activity. While this results in short-term palliation, persistent pathogens that influence disease progression proliferate over the long-term.....................
