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Linda J
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Posted: Wed Oct 31st, 2007 11:04 |
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I'm not real sure whether this should be posted here on on the Marshall Protocol Forum, but I thought this would be of interest to someone. I'll let someone else post about this over there if this is the wrong place to put this. I came across this news article on Fox News that I thought was relevant to the Marshall Protocol that says that they're finding that Valsartan has the ability to stop the progression of Alzheimers.
http://www.foxnews.com/story/0,2933,305318,00.html
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Dr Trevor Marshall
Foundation Staff
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Posted: Wed Oct 31st, 2007 11:43 |
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Indeed, I published a paper during 2001 pointing out that Valsartan was active in the immune diseases. There is a later copy here:
http://clinmed.netprints.org/cgi/content/full/2002080006
It is a pity that these researchers were just using trial and error on a murine model to stumble upon what we had already shown so long ago. You would think that Google would have been a much better study methodology 
Something about monkeys at typewriters starts to enter my consciousness about now...
ps: During my presentation to the FDA I explained why Olmesartan was a much better choice than Valsartan, and better again than the statins, in immune disease. These 'researchers' didn't even bother to test Olmesartan.
Such is the power of molecular biology...Real answers, real understanding...
Last edited on Wed Oct 31st, 2007 12:01 by Dr Trevor Marshall
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wrotek
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Posted: Fri Nov 2nd, 2007 21:50 |
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Dr M told me on Jun, 2005
Other ARBs that you might have in Poland Irbesartan 150mg every 8 hours Valsartan 80mg every 6-8 hours neither are anywhere near as good as Olmesartan but if they are cheap they may get you going towards healing and you can change to Benicar later ..trevor..
Irbesartan is VDR agonist too ? How many other ARBs are, i wonder...
Last edited on Fri Nov 2nd, 2007 21:53 by wrotek
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Dr Trevor Marshall
Foundation Staff
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Posted: Sat Nov 3rd, 2007 03:35 |
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I also think Simvastatin is a weak VDR agonist. No proof yet, but staring at the molecules docked together does make me think there could agonistic action. This is quite distinct from the activity of the other statins (except for Lovastatin, which is an essentially identical chemical compound to Simvastatin).
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wrotek
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Posted: Sat Nov 3rd, 2007 10:13 |
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Simvastatin has 4. Is it possible for a drug to have a higher affinity and still be a weaker agonist ?
P.S. i wonder, can there be any significant changes in VDR structures in different individuals that can determine whether drug works for them or not ?
Polymorphisms, i guess.... ?
Last edited on Sat Nov 3rd, 2007 11:47 by wrotek
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cheryl b
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Posted: Tue Nov 6th, 2007 14:44 |
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looks like they are trying to re-invent the wheel.
the one that Dr. Marshall already invented.
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Dr Trevor Marshall
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Posted: Tue Nov 6th, 2007 15:41 |
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Wrotek,
A high binding affinity, a low Ki, just means that the two molecules lock together tightly. It does not mean that the molecules lock into a position where the receptor is activated.
In fact, I would say that 99% of binding is as antagonist, only 1% as agonist. To understand which is which takes a lot of analysis of the way the receptor works, and I find that the (moving) molecular dynamics simulations help a lot.
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wrotek
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Posted: Wed Nov 7th, 2007 22:59 |
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Still Dr Marshall, You could find 3 (possibly 4) vdr agonists -
Olmesartan, Valsartan, Irbesartan and Simvastatin...
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Dr Trevor Marshall
Foundation Staff
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Posted: Wed Nov 7th, 2007 23:35 |
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Yes, but Valsartan and Irbesartan are weak VDR agonists, if at all.
Note today's study on Simvastatin and Pravastatin, though. This gives a clue as to Simvastatin's unusual activity in the Statins group:
http://www.reuters.com/article/healthNews/idUSN0751116520071107
Of course, it also shows how PhRMA will go to great lengths to find a competitive advantage for their products. The money which funded this study could have gone to many other more worthy causes...
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wrotek
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Posted: Thu Dec 13th, 2007 11:54 |
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Another study about Simvastatin
Simvastatin is associated with a reduced incidence of dementia and Parkinson's disease
http://www.biomedcentral.com/1741-7015/5/20Last edited on Thu Dec 13th, 2007 11:54 by wrotek
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nickbowler
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Posted: Fri Dec 28th, 2007 16:40 |
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So some statins may have some VDR activity. Is the converse also possible - might Benicar have any effect on HMG Co-A reductase?
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Dr Trevor Marshall
Foundation Staff
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Posted: Mon Dec 31st, 2007 22:22 |
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You are assuming that the statins primary therapeutic effect is due to their actions on HMG Co-A reductase. That is a dangerous assumption, there is no real science to back that up.
Far more likely, IMO, that these Nuclear receptor effects are what endow statins with their LDL lowering properties, and that's what I told the FDA.
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nickbowler
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Posted: Thu Jan 3rd, 2008 12:55 |
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| Thanks I am sure that you are correct, so I will re-phrase my question - does activation of the VDR affect HMG Co-A reductase and if so how?
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Dr Trevor Marshall
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Posted: Thu Jan 3rd, 2008 16:11 |
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No idea. I haven't looked, because HMG Co-A reductase is not what causes the LDL/HDL imbalance. This ratio is restored only after the Th1 disease disappears.
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nickbowler
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Posted: Fri Jan 4th, 2008 07:36 |
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OK thanks it appears to be a complete red herring then. I was just concerned at the overlap with statins because I know that they deplete CoQ10 supposedly by affecting HMGCoAR and I wondered if it might be prudent to look at taking supplemental CoQ10 whilst on the MP.
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Dr Trevor Marshall
Foundation Staff
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Posted: Fri Jan 4th, 2008 14:01 |
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I know that they deplete CoQ10 supposedly by affecting HMGCoAR
How do you know that Nick? How do you know that such an action would be important?
Those are the questions which have to be asked. Conversely, there is no doubt that the Statins affect the operation of the Nuclear Receptors, the body's font-line in gene transcription. And we also know that the manufacturers have not figured this out yet, or are being dishonest when they explain the drug actions to the FDA solely in terms of HMGCoAR.
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nickbowler
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Posted: Fri Jan 4th, 2008 14:43 |
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Trevor, I certainly don't know it for a fact, but I know that there is a lot of noise out there about the possibility of problems so I merely suggested that if there was a link then it might be prudent to take precautions. Of course if the Mevalonate pathway is not really affected anyway then it is all probably a storm in a teacup.
These are examples of what is being said about HMGCoAR inhibitors:
http://mb.rxlist.com/rxboard/lipitor.pl?noframes;read=4002
http://www.townsendletter.com/FebMar2006/coq100206.htm
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Dr Trevor Marshall
Foundation Staff
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Posted: Fri Jan 4th, 2008 18:55 |
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But Nick, these references are fixated on CoQ10. yet the nuclear receptors are responsible for transcribing a majority of the genes in the human genome. Not just CoQ10. These authors are all suffering from the same myopia as folk who see EBV virus as the cause of CFS, or Sarcoidosis, or MS, or any one of the chronic diseases with which it has been associated. That myopia prevents them from seeing the magnitude of the problem.
The whole reason the MP exists is because, in 2001, I knew that the explanations being given for the actions of the ARBs was probably incorrect. We wrote this early paper:
http://clinmed.netprints.org/cgi/content/full/2002080006
and then started to search for the true science. That search eventually led to the understanding of chronic disease that we have today. The people who wrote the material you linked to have not even begun to traverse the path of knowledge. True, there are a lot of them, but there are also still a lot of sick people in this world. Take a look at what I said at the start of my presentation to the AAEM about "Weight of Evidence":
http://www.youtube.com/watch?v=RpocxjKJxag
http://www.youtube.com/watch?v=ZMn-zUTTHgw
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nickbowler
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Posted: Sun Jan 6th, 2008 20:19 |
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OK Trevor, I think I am getting there. Thanks for your patience. So these guys are stuck in ‘iceberg mode’ and not seeing the whole web of interactions beneath the obvious ones because they are focusing on the wrong things. It’s all about the VDR stupid! Or more correctly modulation of the nuclear receptors and the turning on or off of many genes at once, so trying to highlight just one thing is daft.
On another matter entirely, would you say that TH1 inflammation is a likely contributor to (particularly female) infertility? I note that 1,25D is naturally increased in pregnancy and so perhaps TH1 disease emulates a pregnant hormonal state and makes conception difficult, much as the pill emulates pregnancy progesterone levels with the same end result?
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Chris
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Posted: Mon Jan 7th, 2008 14:59 |
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Nick, here's evidence that infertility can be TH1 related. Look, for the
post by Martha, July 14 2007.
http://www.marshallprotocol.com/view_topic.php?id=1827&forum_id=35&highlight=martha+nikki+infertility
____________________
sarcoid since 1983 (or much earlier), MP since summer 2004 Chris' story
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nickbowler
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Posted: Tue Jan 8th, 2008 07:08 |
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Sorry Chris, I can't seem to access that link - it keeps saying I am do not have permission or am not logged in when I am. Also searching under 'Martha' doesnt show any posts for that day.
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Chris
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Posted: Wed Jan 9th, 2008 14:36 |
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Sorry, here's the text.
------------------------------------------------
Please be careful of pregnancy now as your hormones are returning to normal on the MP. At 45 after 6 months on the MP, I became pregnant (almost immaculate conception ) after 16 years of infertility. I don't think it was the antibiotics because I had been on high dose minocycline for 4 years prior to beginning the MP and never worried about pregnancy...I believe the benicar was normalizing my hormones and maybe the combo of the benicar with the antibiotics.
Last edited on Wed Jan 9th, 2008 14:36 by Chris
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sarcoid since 1983 (or much earlier), MP since summer 2004 Chris' story
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Dr Trevor Marshall
Foundation Staff
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Posted: Wed Jan 9th, 2008 15:19 |
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And here are two reprints of early papers (from the 1980's) when our research team was successfully treating infertility:
http://autoimmunityresearch.org/transcripts/Keogh_Ovulation_Induction.pdf
http://autoimmunityresearch.org/transcripts/Keogh_Pulsatile_GnRH.pdf
I obtained copies of these two papers from the collection of the US National Library of Medicine. Of the dozens of papers we published at that time, these are the only two which have survived, although I expect there may be more hidden away in Australian libraries
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