From: manfred on
http://www.pdazzler.com/archives/359#more-359

Over the past 20 years there have only been a few supplements that
have made huge impressions on me. Two are Vitamin C and Vitamin D.
CoQ10 is a third that just cannot be ignored by cancer patients.

My initial impression was CoQ10, found in all of us and important for
a healthy heart and cardiovascular system, did not have a lot of
application for cancer patients.

I was clearly wrong in that assessment. Not only does this powerful
antioxidant play a direct role in ATP (energy) production in the cells
but CoQ10 is required for our bodies to absorb and process Vitamin D.

The significance of CoQ10 in Vitamin D absorption was brought home to
me personally with my own specific experience. I have known of the
importance of Vitamin D in cancer survival for at least 10 years. I
wrote about Vitamin D, supplemented COD Liver oil and Vitamin D-3,
purchased a Vitamin D Lamp and sunned daily during the summer
specifically to ensure I had adequate Vitamin D levels.

A couple of years ago I had my first experience with Vitamin D
Hydroxy-25 testing. I was flabbergasted to find my level of Vitamin
D wholly insufficient. With my Vitamin D awareness, supplementation,
and sunning my Vitamin D Hydroxyl-25 level was below 26ng/ml at the
end of summer.

It was about this same time I stumbled on some little known research
about Ubiquinol, the new activated form of CoQ10. The manufacturer
of Ubiquinol had used several retirement centers to validate the super
viability of Ubiquinol , establish safe dose levels and monitor
Ubiquinols effects.

Buried in the back pages of the study was a paragraph about a number
of cancer patients that participated in the test by happenstance.
(They just happened to have cancer and be living in the retirement
centers used for the Ubiquinol studies.)


Kaneka QH
Those cancer patients receiving 100mg of Ubiquinol daily saw a
leveling off in their cancer’s progression. Those cancer patients
receiving 200mg of Ubiquinol daily saw some reduction in cancer and
those cancer patients receiving 400mg of Ubiquinol daily saw a
complete regression in their cancers.

Well, that paragraph caught my attention in a big way. I added 400mg
daily to my current preventative cancer regimen immediately. I took
400mg of Ubiquinol for 120 days (the length of the manufacturer’s
study) and then tapered down to 100 mg of Ubiquinol daily which I
still maintain.

During this same period I increased Vitamin D-3 intake to 6,000 i.u.
daily hoping to raise hydroxyl-25 test scores to sufficiency level
(above 40 ng/ml). What a pleasant surprise when I next Vitamin D
Hydroxy-25 tested and the level came back at 96 ng/ml.

Obviously, the increased levels of CoQ10 from taking Ubiquinol had
assisted me in absorbing the needed Vitamin D.

I have subsequently concluded part of my inability to absorb Vitamin D
previously was due to a serious deficiency in CoQ10. Further study
indicates lack of CoQ10 is at least partially responsible for
difficulty in absorbing any number of nutrients including Vitamin E
and Vitamin C.

This limited National Cancer Institute Study leads one to the probable
conclusion cancer patients in general are deficient in CoQ10. And a
number of limited studies of interest to cancer patients are linked
from the reference.

My own inclination, it is likely Vitamin D and CO Enzyme Q10
deficiency are common across all cancer patients. Thus it stands to
reason all cancer survivors and all cancer patients should consider
supplementing with the activated form of Ubiquinol to dramatically
raise CoQ10 levels in their bodies. And without saying, they should
Vitamin D Hydroxy-25 test and supplement Vitamin D-3 if needed to
reach between 75 ng/ml and 100 ng/ml Vitamin D levels.

BTW, the activated form of Ubiquinol is manufactured by Kaneka
Corporation. A number of vitamin and supplement manufacturers
market activated Ubiquinol under their own brand names.
....

Much of the information on CoQ10 is available through the
International Co Enzyme Q10 Association. Don’t be afraid to do a
little digging. It is quite enlightening, including information on
problems with Lipitor and similar statins depleting the body of needed
CoQ10. Vibrant Life Publishing also did a nice booklet on C0Q10.
Though no longer available through Vibrant Life I have made the
CoQ10 / Ubiquinol booklet available here in pdf format.
From: randall on
On Mar 29, 10:00 pm, manfred <manfre...(a)lycos.com> wrote:



Manfred,


Good one...


When the flag goes up (VDR) looking for some D3 i wonder
what is happening. Exactly haPPening?

In normal and psor folks..

Did find some confirmation for coQ10 potentiating vitamin D
on the cellular level.

Would be an interesting trial that NO one will ever do i suppose.

100 psor's and 100 controls, take baseline on vitamin D and
then pump em with coQ10 to see what goes on next.

In clearing of skin and VD levels.


Exp Gerontol. 2007 Aug;42(8):798-806. Epub 2007 May 10.

Modifications of plasma proteome in long-lived rats fed on a coenzyme
Q10-supplemented diet.
Santos-González M, Gómez Díaz C, Navas P, Villalba JM.

Departamento de Biología Celular, Fisiología e Inmunología, Facultad
de Ciencias, Campus Rabanales, Ed. Severo Ochoa, 3a planta,
Universidad de Córdoba, E-14014 Córdoba, Spain.

Dietary coenzyme Q(10) prolongs life span of rats fed on a PUFAn-6-
enriched diet. Our aim was to analyze changes in the levels of plasma
proteins of rats fed on a PUFAn-6 plus coenzyme Q(10)-based diet. This
approach could give novel insights into the mechanisms of life span
extension by dietary coenzyme Q(10) in the rat. Serum albumin, which
decreases with aging in the rat, was significantly increased by
coenzyme Q(10) supplementation both at 6 and 24 months. After
depletion of the most abundant proteins by affinity chromatography,
levels of less abundant plasma proteins were also studied by using 2D-
electrophoresis and MALDI-TOF mass fingerprinting analysis. Our
results have shown that lifelong dietary supplementation with coenzyme
Q(10) induced significant decreases of plasma hemopexin,
apolipoprotein H and inter-alpha-inhibitor H4P heavy chain (at both 6
and 24 months), preprohaptoglobin, fibrinogen gamma-chain precursor,
and fetuin-like protein (at 6 months), and alpha-1-antitrypsin
precursor and type II peroxiredoxin (at 24 months). On the other hand,
coenzyme Q(10) supplementation resulted in significant increases of
serine protease inhibitor 3, vitamin D-binding protein (at 6 months),
and Apo A-I (at 24 months). Our results support a beneficial role of
dietary coenzyme Q(10) decreasing oxidative stress and cardiovascular
risk, and modulating inflammation during aging.

PMID: 17587521

It took six months in an animal (rat) that lives how long? LOL

For this long livid rat...


Have to admit I did find CoQ10 to be extremely beneficial in my
personal trials taken in high enough dosages.

But it is rather expensive, but certainly cheaper then what's going on
with cardio
care these days.

If it does the same for cancer and autoimmune plus cardiovascular
effects then it
certainly mitigates ROS and downstream or uPstream inflammation.

Just imagine if you combine CoQ10 with magnesium and iodine plus ALA,
ALC and NAC
and fish oils (dha, epa etc) and and and...

To the MOON ALICE... LOL


But adjust the retinol down while doing the D3 i suspect. <G>


And we can get this formula in Hungary. <w>
http://www.ncbi.nlm.nih.gov/pubmed/16711261
Orv Hetil. 2006 Apr 23;147(16):747-52.

[Recent changes in concepts of antioxidant treatment]
[Article in Hungarian]

Matkovics A.

Gyógy-ITT Bt., Felnott Háziorvosi Rendelo, Budapest.

The promising theoretical possibilities of antioxidant prevention and
protection against vascular diseases and neoplasms could not have been
realized as yet. The author searches into the causes of this failure
by analyzing data of recent literature. Previous preventive trials as
well as newly discovered pharmacological and molecular biological
effects of antioxidants are reviewed. Results of meta-analyses on
prevention trials of vascular disease by vitamin-E and those of
gastrointestinal cancers are also included. The lately recognized
properties of antioxidants are surveyed with special regard to their
capability of modulating apoptosis, inducing gene expressions and
their transformation into pro-oxidants. The harmful consequence of
high doses of a single antioxidant is emphasized. The retinoids,
vitamins D and K possess both pro-apoptotic and antiproliferative
activity, while N-acetylcysteine exerts mainly anti-apoptotic effects.
Since the effects of the eight vitamin E homologues are different in
many respects, alpha-tocopherol can not be regarded as vitamin E of
full value. Antioxidant supply from natural sources does not seem to
be sufficient for an adequate preventive effect. The author recommends
such a combination in which physiological amounts of vitamins C, D, K
and B-complex, N-acetylcysteine, vitamin E of natural origin might be
complemented by allopurinol, co-enzyme Q-10 and alpha-lipoic acid. A
diet rich in flavonoids and carotenoids is essential. Application of
appropriate laboratory methods is of great value in the
individualization, monitoring and control of antioxidant treatment.

PMID: 16711261


I just wish i knew why Cannell and the vitamin D council are calling
retinol and D3 absorption on the carPet... <w> <w>


Ok, if i go through these 106 returns for VDR + retinol on pubmed:
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=retinol+vdr&log$=activity

Does this have an answer?


Cancer Biol Ther. 2009 May;8(10):951-62. Epub 2009 May 20.

Mechanisms underlying the induction of the putative human tumor
suppressor GPRC5A by retinoic acid.
Ye X, Tao Q, Wang Y, Cheng Y, Lotan R.

Department of Thoracic/Head and Neck Medical Oncology, University of
Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA.

Comment in:

Cancer Biol Ther. 2009 May;8(10):963-5.

Retinoic acid regulates the expression of genes involved in cell
proliferation, differentiation and survival by direct control of gene
transcription via activation of nuclear retinoid receptors bound to
response elements in the promoters of target genes or by indirect
mechanisms. Herein, we investigated the mechanism by which retinoic
acid induces the expression of the human tumor suppressor GPRC5A. The
proximal 5' upstream region of the GPRC5A gene was found to contain
two potential RAR/RXR binding sites (RAREs) and one VDR/RXR binding
site with direct repeat 5 (DR5) motifs designated DR5I (-489 to -473),
DR5II (-136 to -120) and DR5III (-81 to -65). DR5II and DR5III but not
DR5I were conserved among vertebrates. However, only DR5III (5'-TGT
CCC TCT GCT CAC CC-3') was found to be the functional RARE for
mediating induction of GPRC5A as indicated by electrophoretic mobility
shift assay using wild type and mutated synthetic oligonucleotides
representing different fragments of the promoter for competition with
retinoic acid receptor beta RARE. Chromatin immunoprecipitation assay
confirmed the binding of retinoic acid receptors alpha and gamma and
retinoid X receptors alpha and beta to DR5III in intact cells. These
results demonstrate the importance of functional analysis for
validating the activity of predicted response elements.

PMID: 19279407


Ok this is not helping.

Back to P and D via the nb-uvb laser with retinol on the side (or
rubbed in the plaques).


J Rheumatol Suppl. 2009 Aug;83:71-2.

Retinoids and phototherapy for psoriasis.
Monfrecola G, Baldo A.

Department of Dermatology, University Federico II, 80131 Napoli,
Italy. monfreco(a)unina.it

Retinoids are the most widely used agents for systemic treatment of
psoriasis; as structural and functional analogs of vitamin A, they are
involved in the regulation of several biologic functions. Acitretin is
the oral retinoid currently used, alone or in combination with other
treatments, for plaque type, erythrodermic, and pustular psoriasis.
Due to its high teratogenic effect, therapeutic contraception is
required for women taking the drug. Narrowband ultraviolet B (nbUVB,
311 +/- 2 nm) is effective for guttate and plaque-type psoriasis. At
the molecular level, UV light acts (1) directly (type I reaction)
inducing the formation of pyrimidine dimers that, in turn, cause a
transient cellular growth arrest; and (2) indirectly (type II
reaction) through the generation of reactive oxygen species that act
on key molecules such as lipids (in particular lipid membranes),
proteins, and nucleic acids. Several studies show that UV rays can
cause a transient decrease in DNA, RNA, and protein synthesis. These
events are accompanied by a temporary normalization of cell kinetics
of psoriatic keratinocytes. Phototherapy is carried out 3 times a week
alone or in combination with topical treatments and/or acitretin.
Several studies have confirmed that oral retinoids together with nbUVB
(ReUVB) reduce the recovery time and also the doses of both acitretin
and nbUVB. The regimen is carried out treating the patient with
acitretin alone (0.5 mg/kg bw) for 2 weeks, then the dose of acitretin
is reduced to 0.3 mg/kg bw, and the nbUVB is added 3 times a week
until complete resolution of disease. As retinoids exert an
anticarcinogenic effect, the ReUVB regimen could lower skin cancer
risk resulting from longterm UVB therapy.

PMID: 19661548


But what genes?


J Cell Physiol. 2009 Aug;220(2):427-39.

Retinoid-responsive transcriptional changes in epidermal
keratinocytes.
Lee DD, Stojadinovic O, Krzyzanowska A, Vouthounis C, Blumenberg M,
Tomic-Canic M.

New York University School of Medicine, Department of Dermatology,
Biochemistry and The Cancer Institute, New York, NY, USA.

Retinoids (RA) have been used as therapeutic agents for numerous skin
diseases, from psoriasis to acne and wrinkles. While RA is known to
inhibit keratinocyte differentiation, the molecular effects of RA in
epidermis have not been comprehensively defined. To identify the
transcriptional targets of RA in primary human epidermal
keratinocytes, we compared the transcriptional profiles of cells grown
in the presence or absence of all-trans retinoic acid for 1, 4, 24,
48, and 72 h, using large DNA microarrays. As expected, RA suppresses
the protein markers of cornification; however the genes responsible
for biosynthesis of epidermal lipids, long-chain fatty acids,
cholesterol, and sphingolipids, are also suppressed. Importantly, the
pathways of RA synthesis, esterification and metabolism are activated
by RA; therefore, RA regulates its own bioavailability. Unexpectedly,
RA regulates many genes associated with the cell cycle and programmed
cell death. This led us to reveal novel effects of RA on keratinocyte
proliferation and apoptosis. The response to RA is very fast: 315
genes were regulated already after 1 h. More than one-third of RA-
regulated genes function in signal transduction and regulation of
transcription. Using in silico analysis, we identified a set of over-
represented transcription factor binding sites in the RA-regulated
genes. Many psoriasis-related genes are regulated by RA, some induced,
others suppressed. These results comprehensively document the
transcriptional changes caused by RA in keratinocytes, add new
insights into the molecular mechanism influenced by RA in the
epidermis and demonstrate the hypothesis-generating power of DNA
microarray analysis.

PMID: 19388012


Calling ALL UNITs one ADAM10

------------

FASEB J. 2009 Jun;23(6):1643-54. Epub 2009 Jan 14.

Up-regulation of the alpha-secretase ADAM10 by retinoic acid receptors
and acitretin.
Tippmann F, Hundt J, Schneider A, Endres K, Fahrenholz F.

Institute of Biochemistry, University of Mainz, Becherweg 30, D-55099
Mainz, Germany.

Late-onset Alzheimer's disease is often connected with nutritional
misbalance, such as enhanced cholesterol intake, deficiency in
polyunsaturated fatty acids, or hypovitaminosis. The alpha-secretase
ADAM10 has been found to be regulated by retinoic acid, the
bioreactive metabolite of vitamin A. Here we show that retinoids
induce gene expression of ADAM10 and alpha-secretase activity by
nonpermissive retinoid acid receptor/retinoid X receptor (RAR/RXR)
heterodimers, whereby alpha- and beta-isotypes of RAR play a major
role. However, ligands of other RXR binding partners, such as the
vitamin D receptor, do not stimulate alpha-secretase activity. On the
basis of these findings, we examined the effect of synthetic retinoids
and found a strong enhancement of nonamyloidogenic processing of the
amyloid precursor protein by the vitamin A analog acitretin: it
stimulated ADAM10 promoter activity with an EC(50) of 1.5 microM and
led to an increase of mature ADAM10 protein that resulted in a two- to
three-fold increase of the ratio between alpha- and beta-secretase
activity in neuroblastoma cells. The alpha-secretase stimulation by
acitretin was completely inhibited by the ADAM10-specific inhibitor
GI254023X. Intracerebral injection of acitretin in APP/PS1-21
transgenic mice led to a reduction of Abeta(40) and Abeta(42). The
results of this study may have clinical relevance because acitretin
has been approved for the treatment of psoriasis since 1997 and found
generally safe for long-term use in humans.

PMID: 19144697


http://en.wikipedia.org/wiki/ADAM10


=============



manfred posted:

> http://www.pdazzler.com/archives/359#more-359
>
> Over the past 20 years there have only been a few supplements that
> have made huge impressions on me.   Two are Vitamin C and Vitamin D.
> CoQ10 is a third that just cannot be ignored by cancer patients.
>
> My initial impression was CoQ10, found in all of us and important for
> a healthy heart and cardiovascular system, did not have a lot of
> application for cancer patients.
>
> I was clearly wrong in that assessment.    Not only does this powerful
> antioxidant play a direct role in ATP (energy) production in the cells
> but CoQ10 is required for our bodies to absorb and process Vitamin D.
>
> The significance of CoQ10 in Vitamin D absorption was brought home to
> me personally with my own specific experience.   I have known of the
> importance of Vitamin D in cancer survival for at least 10 years.   I
> wrote about Vitamin D, supplemented COD Liver oil and Vitamin D-3,
> purchased a Vitamin D Lamp and sunned daily during the summer
> specifically to ensure I had adequate Vitamin D levels.
>
> A couple of years ago I had my first experience with Vitamin D
> Hydroxy-25 testing.   I was flabbergasted to find my level of Vitamin
> D wholly insufficient.   With my Vitamin D awareness, supplementation,
> and sunning my Vitamin D Hydroxyl-25 level was below 26ng/ml at the
> end of summer.
>
> It was about this same time I stumbled on some little known research
> about Ubiquinol, the new activated form of CoQ10.   The manufacturer
> of Ubiquinol had used several retirement centers to validate the super
> viability of Ubiquinol , establish safe dose levels and monitor
> Ubiquinols effects.
>
> Buried in the back pages of the study was a paragraph about a number
> of cancer patients that participated in the test by happenstance.
> (They just happened to have cancer and be living in the retirement
> centers used for the Ubiquinol studies.)
>
> Kaneka QH
> Those cancer patients receiving 100mg of Ubiquinol daily saw a
> leveling off in their cancer’s progression.  Those cancer patients
> receiving 200mg of Ubiquinol daily saw some reduction in cancer and
> those cancer patients receiving 400mg of Ubiquinol daily saw a
> complete regression in their cancers.
>
> Well, that paragraph caught my attention in a big way.  I added 400mg
> daily to my current preventative cancer regimen immediately.    I took
> 400mg of Ubiquinol for 120 days (the length of the manufacturer’s
> study) and then tapered down to 100 mg of Ubiquinol daily which I
> still maintain.
>
> During this same period I increased Vitamin D-3 intake to 6,000 i.u.
> daily hoping to raise hydroxyl-25 test scores to sufficiency level
> (above 40 ng/ml).    What a pleasant surprise when I next Vitamin D
> Hydroxy-25 tested and the level came back at 96 ng/ml.
>
> Obviously, the increased levels of CoQ10 from taking Ubiquinol had
> assisted me in absorbing the needed Vitamin D.
>
> I have subsequently concluded part of my inability to absorb Vitamin D
> previously was due to a serious deficiency in CoQ10.    Further study
> indicates lack of CoQ10 is at least partially responsible for
> difficulty in absorbing any number of nutrients including Vitamin E
> and Vitamin C.
>
> This limited National Cancer Institute Study leads one to the probable
> conclusion cancer patients in general are deficient in CoQ10.   And a
> number of limited studies of interest to cancer patients are linked
> from the reference.
>
> My own inclination, it is likely Vitamin D and CO Enzyme Q10
> deficiency are common across all cancer patients.   Thus it stands to
> reason all cancer survivors and all cancer patients should consider
> supplementing with the activated form of Ubiquinol to dramatically
> raise CoQ10 levels in their bodies.    And without saying, they should
> Vitamin D Hydroxy-25 test and supplement Vitamin D-3 if needed to
> reach between 75 ng/ml and 100 ng/ml Vitamin D levels.
>
> BTW, the activated form of Ubiquinol is manufactured by Kaneka
> Corporation.    A number of vitamin and supplement manufacturers
> market activated Ubiquinol under their own brand names.
> ...
>
> Much of the information on CoQ10 is available through the
> International Co Enzyme Q10 Association.   Don’t be afraid to do a
> little digging.   It is quite enlightening, including information on
> problems with Lipitor and similar statins depleting the body of needed
> CoQ10.   Vibrant Life Publishing also did a nice booklet on C0Q10.
> Though no longer available through Vibrant Life I have made the
> CoQ10 / Ubiquinol booklet available here in pdf format.

-----------


OTOH maybe this person wrote this to sPur sales?


Hate to be cynical but this is the net.



randall.... or i may do the trial on top of my udder trials?