Does D Do Dastardly Deeds
- From: ironjustice <ironjustice@xxxxxxxxx>
- Date: Sat, 9 May 2009 03:06:24 -0700 (PDT)
On May 8, 4:49 pm, Rusty the Canuck Dicksucker
<flakey...@xxxxxxxxxxxxx> wrote: snip <<
ALL you shteaters were TOLD to stay off my threads ..
Understand .. shteater .. ?
You shteaters have NO .. input .. ON ..
**my** threads ..
That too hard for you shteaters to understand .. ?
You shteaters ha've been TOLD numerous times .. you are NOT
welcome ..
You shteaters are a fkg .. looooooons ..
STAY .. off .. my .. threads .. you fkg .. loooooon ..
Dooooo .. it .. looooon ..
------------------
Autoimmune Disease May Be Exacerbated By Vitamin D
Deficiency in vitamin D has been widely regarded as contributing to
autoimmune disease, but a review appearing in Autoimmunity Reviews
explains that low levels of vitamin D in patients with autoimmune
disease may be a result rather than a cause of disease and that
supplementing with vitamin D may actually exacerbate autoimmune
disease.
Authored by a team of researchers at the California-based non-profit
Autoimmunity Research Foundation, the paper goes on to point out that
molecular biologists have long known that the form of vitamin D
derived from food and supplements, 25-hydroxyvitamin D (25-D), is a
secosteroid rather than a vitamin. Like corticosteroid medications,
vitamin D may provide short-term relief by lowering inflammation but
may exacerbate disease symptoms over the long-term.
The insights are based on molecular research showing that 25-D
inactivates rather than activates its native receptor - the Vitamin D
nuclear receptor or VDR. Once associated solely with calcium
metabolism, the VDR is now known to transcribe at least 913 genes and
largely control the innate immune response by expressing the bulk of
the body's antimicrobial peptides, natural antimicrobials that target
bacteria.
Written under the guidance of professor Trevor Marshall of Murdoch
University, Western Australia, the paper contends that 25-D's actions
must be considered in light of recent research on the Human
Microbiome. Such research shows that bacteria are far more pervasive
than previously thought - 90% of cells in the body are estimated to
be
non-human - increasing the likelihood that autoimmune diseases are
caused by persistent pathogens, many of which have yet to be named or
have their DNA characterized.
Marshall and team explain that by deactivating the VDR and
subsequently the immune response, 25-D lowers the inflammation caused
by many of these bacteria but allows them to spread more easily in
the
long-run. They outline how long-term harm caused by high levels of
25-
D has been missed because the bacteria implicated in autoimmune
disease grow very slowly. For example, a higher incidence in brain
lesions, allergies, and atopy in response to vitamin D
supplementation
have been noted only after decades of supplementation with the
secosteroid.
Furthermore, low levels of 25-D are frequently noted in patients with
autoimmune disease, leading to a current consensus that a deficiency
of the secosteroid may contribute to the autoimmune disease process.
However, Marshall and team explain that these low levels of 25-D are
a
result, rather than a cause, of the disease process. Indeed,
Marshall's research shows that in autoimmune disease, 25-D levels are
naturally down-regulated in response to VDR dysregulation by chronic
pathogens. Under such circumstances, supplementation with extra
vitamin D is not only counterproductive but harmful, as it slows the
ability of the immune system to deal with such bacteria.
The team points out the importance of examining alternate models of
vitamin D metabolism. "Vitamin D is currently being recommended at
historically unprecedented doses," states Amy Proal, one of the
paper's co-authors. "Yet at the same time, the rate of nearly every
autoimmune disease continues to escalate."
Notes:
For the past five years, Autoimmunity Research Foundation has been
running an observational study in which patients are administered
pulsed low dose antibiotics and a VDR agonist in order to kill
chronic
bacteria implicated in their diseases. Specific data on the cohort
was
recently presented by CAPT Thomas H. Perez, USPHS (ret) at the
International Congress on Autoimmunity in Porto, Portugal: Transcript
Resources
Citation: Albert PJ et al. In press. Autoimmunity Reviews. "Vitamin
D:
The alternative hypothesis." Full-text preprint:
http://autoimmunityresearch.org/transcripts/AR-Albert-VitD.pdf DOI:
http://dx.doi.org/10.1016/j.autrev.2009.02.011
Presentation on clinical data: Transcript
Video: http://vimeo.com/1789735
Foundation website: http://AutoimmunityResearch.org/
Source:
Paul Albert
Autoimmunity Research Foundation
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Tom
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