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wytnez
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| Joined: | Mon Nov 29th, 2004 |
| Location: | Texas USA |
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Posted: Sat Dec 1st, 2007 17:49 |
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This was in the AMS Novermber 25th discussing new research for Alzheimers. I know that Dr.M is not going to be surprised.
A variety of medications already being used by millions to control high blood pressure actually may prove to help protect individuals from memory and cognitive declines. Recently, researchers were encouraged by studies with mice when one drug in particular - valsartan- significantly reduced the buildup of protein in the brain. The plan now is to assess its effectiveness in humans.
For those of us who have been using Benicar know of its reduction of brain fog, memory loss and a host of other IPs. They are so slow in research. ARF is miles and miles ahead.
Saj
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sarc lymph nodes. ph1 1/05,125D 33,25D 10,ph2 5/05,ph3 12/05,125D 21, 25D less than 7
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jcwat101
Research Professional
| Joined: | Tue Jul 20th, 2004 |
| Location: | Pasadena, USA |
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Posted: Sun Dec 2nd, 2007 04:15 |
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Interesting! I didn't find that study when I looked just now, but I found this one and there apparently have been others too, along the same lines:
Angiotensin II Type-2 Receptor Stimulation Prevents Neural Damage by Transcrip
Joyce Waterhouse
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20 yrs with CFS/FM/Lyme/IBS, food sensitivities; 1,25D/25D 8/04:64/11 http://SynergyHN.com
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Ute
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| Joined: | Sun Sep 30th, 2007 |
| Location: | Germany |
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Posted: Tue Oct 13th, 2009 07:50 |
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http://tinyurl.com/yzp2h45
Blocking angiotensin-converting enzyme induces potent regulatory T cells and modulates TH1- and TH17-mediated autoimmunity. Department of Neurology and Neurological Sciences, Beckman Center for Molecular Medicine, Stanford University, Stanford, CA 94305, USA. michael.platten@med.-uni-heidelberg.de
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CFS/FM/IBS part.thyroidectomy osteopenia food sensit 125D71 25D15.2 Ph1Nov07 Ph2Jan08 Ph3May08 T3/T4 cal/mag Tri-Est Progest.
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ChrisMavo
Member in Phase 2
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Posted: Tue Oct 13th, 2009 08:52 |
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Very interesting study! This ties in very well with an article I posted a few months back:
http://www.marshallprotocol.com/forum11/13418.html
I am more and more confident that the MP is totally correct and that by using a Olmesartan blockade with low-dose pulsed antibiotics... I will recover in time from this terrible disease ALS.....
Chris Mavo
San Francisco
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PLS/ALS, speech difficulty, dizziness, leg weakness, overly emotional, Ph1Aug2609, 11/09: 25D-20, 9/09: 25D-27, 7/09: 25D-38, 1,25D-46, Mod Ph2Oct09, 100mg Mino + 150mg Clindy
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Bane
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Posted: Tue Oct 13th, 2009 14:48 |
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Angiotensin Receptor Blocker Prevented {beta}-Amyloid-Induced Cognitive Impairment Associated With Recovery of Neurovascular Coupling.
http://www.ncbi.nlm.nih.gov/pubmed/19805638
Benefits of the angiotensin II receptor antagonist olmesartan in controlling hypertension and cerebral hemodynamics after stroke.
http://www.ncbi.nlm.nih.gov/pubmed/19745828
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Oral Lichen Planus(mild)/Clubbed Finger (digital clubbing)Last 25D 5.6ng/ml, phase3
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Phillyguy
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Posted: Tue Oct 13th, 2009 15:21 |
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From wikipedia:
"Experimental evidence from mouse models suggests that some pathogens may have evolved to manipulate regulatory T cells to immunosuppress the host and so potentiate their own survival. For example, regulatory T cell activity has been reported to increase in several infectious contexts, such as retroviral infections (the most well known of which is HIV), mycobacterial infections (like tuberculosis), and various parasitic infections including Leishmania and malaria."
Any concern that part of the palliation from ARBs is due to Treg induced immunosuppression? There are several references in the literature about ATII blockade inhibiting the maturation of dendritic cells. What long-term effect would this have on us?
Perhaps, this is one of the trade-offs to therapy? In this context, some of the other ARBs that block the VDR would appear to be dangerous because we at least get a boost in cell-mediated immunity by olmesartan.
Could the ARB's be immunomodulatory exerting a "push down, pop up" effect which we often see with the immune system. In other words, an upreg of Tregs and some other component of the immune system (cell-mediated) and a depression of adaptive immunity.
Either way, I'm thankful for having something that allows me to feel better while I attack the bacteria.
The other thing that we need to keep in mind is that per one of Dr. Marshall's earlier papers, olmesartan exhibits some direct inhibitory effects against certain strains of bacteria - one of the staph bugs as I recall.
Last edited on Tue Oct 13th, 2009 17:04 by Phillyguy
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eClaire
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Posted: Wed Oct 14th, 2009 00:38 |
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Wow, what a wealth of recent research. I'm definitely tagging this thread for my doctor.
Claire
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38mo on MP; CFS FMS MCS COPD hypermob. IBS/GERD osteopor.; 125D48 25D<4;
NoIRs during most daylight outings & covered up; home w/o NoIRs
Ph1.Dec06 * ModPh2.Jun07 * AbxBrk.Mar-May08 * Ph2.Oct-Nov08 * Ph1.Jan2009
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Phillyguy
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Posted: Wed Oct 14th, 2009 19:11 |
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Thought this image may provide a visual representation of my comment regarding push down pop up effect - assuming it is correct.
http://edrv.endojournals.org/cgi/content/full/29/6/726/F9
The way that I read this is that 1,25D leads to an increase in CAMP activity and Tregs and a decrease in antigen presentation and auto-reactive T cells. Based upon this information is it fair to assume that olmesartan should not only remove the underlying cause of disease (underlying infection) but also provide a direct reduction in auto-reactive T cells - TH17?. Could a reduction in antigen-presentation also cause a reduction in antigen-antibody immune complex deposition and therefore reduction in certain sequelae like glomerulonephritis?
How critical is reduced expression of VDR in the disease process? Is reduced VDR a highly important confounding factor to disease onset and progression in addition to blockade of the receptors themselves? I know that Dr. Marshall has included the concept of pathogen mediated VDR reduction in many of his recent presentations (TB, EBV, Borellia). Any thoughts on increasing expression of VDR in combination with olmesartan? Interestingly, silymarin in milk thistle may be an estrogen receptor agonist. Because ER beta expresses VDR, perhaps milk thistle serves as an important adjunct to the protocol? Just a couple of musings, hopefully not too off base.
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Silymarin/ERBeta references:
Update: Sorry - my memory didn't parse the information between rat and human studies.
Silymarin is a selective estrogen receptor beta (ERbeta) agonist and has estrogenic effects in the metaphysis of the femur but no or antiestrogenic effects in the uterus of ovariectomized (ovx) rats.
Seidlová-Wuttke D, Becker T, Christoffel V, Jarry H, Wuttke W.
Department of Clinical and Experimental Endocrinology, University of Goettingen, Robert-Koch-Strasse 40, 37075 Goettingen, Germany.
Silymarin is a widely used standardized mixture of flavonolignans and its major component Silybinin binds to cytosolic estrogen receptors. Here, we demonstrate that this binding is exclusive to the estrogen receptor beta (ERbeta). Treatment of ovariectomized (ovx) rats with silymarin or estradiol (E2) may allow differentiation of biological effects mediated by the ERalpha or ERbeta. E2 inhibited serum LH, cholesterol, LDL and HDL concentrations in the blood and increased gene expression of IGF1, HbEGF and C3 in the uterus, while silymarin was totally ineffective or antagonistic in altering these parameters. Both, E2 and silymarin inhibited expression of uterine ERbeta gene. Hence, in the pituitary, liver (where the lipoproteins are synthesized) and uterus E2 acts primarily via the ERalpha. Exclusive estrogenic effects of silymarin were observed in the metaphysis of the femur (MF), on osteoblast parameters (gene expression of IGF1, TGFbeta1, osteoprotegerin, collagen-1alpha1, osteocalcin (OC)) and on the osteoclast activity marker tartrate resistant acid phosphatase (TRAP) gene expression of adult ovx rats. Our RT-PCR method detects ERbeta gene expression in all organs including developing bones but not in the MF of adult ovx rats. We conclude therefore, that the effects of silymarin in this part of the bone cannot be exerted via the ERalpha because it does not bind to this receptor subtype. Despite the failure to detect ERbeta mRNA in the MF of our animals the possibility exists that ERbeta protein is present and may mediate the effects of silymarin. Another possibility may be that the effect of silymarin and therefore possibly also of E2 in the MF may be mediated via other possibly not yet identified receptors or via an ERbeta splice variant which is not detected by our PCR-method.
PMID: 14568570 [PubMed - indexed for MEDLINE
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Hopefully I can redeem myself by the following silymarin/caspase 3 reference with the following in mind:
1) Caspase 3 degrades the VDR.
2) Silibinin is the major active constituent of silymarin, the mixture of flavonolignans extracted from milke thistle consisting of silibinin A and B, isosibilinin A and B, silicristin, silidianin.
Silymarin prevents UV irradiation-induced A375-S2 cell apoptosis.
Biol Pharm Bull. 2004 Jul;27(7):1031-6.
Silymarin, a plant flavonoid from milk thistle (Silybum marianum) was first evaluated for its protective effect against UV irradiation-induced apoptosis in human malignant melanoma cells. Treatment with silymarin significantly inhibited UV irradiation-induced apoptosis. Activities of caspase-9 and caspase-3 in UV-irradiated cells were effectively reduced by silymarin in a dose-dependent manner. It is suggested that the inhibitory effect of silymarin is exerted by blockage of the caspase/ICAD pathway after increased expression of Bcl-x(L) protein and activation of the ERK/MAPK pathway.
Then a contradictory reference relating to silibinin component of silymarin:
Silibinin modulates CDKI-CDK-cyclin cascade and activates caspase 3 causing growth inhibition and apoptotic death of human TCC cells, providing a strong rationale for future studies evaluating preventive and/or intervention strategies for silibinin in bladder cancer pre-clinical models.
Carcinogenesis. 2004 Apr 29
So perhaps there are compunds in milk thistle that activate caspase 3 (which ones) and some that degrade it (silibinin). I guess the take home message is that we need to be careful about which milk thistle products we consume. Many milk thistle supplements contain large amounts of silibinin, in fact, some are comprised excusively of silibinin, while others contain silymarin which includes various compounds including silibinin.
Last edited on Wed Oct 14th, 2009 23:03 by Phillyguy
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eClaire
Member in Phase 2
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Posted: Wed Oct 14th, 2009 20:01 |
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Am waiting to read your posts about silymarin. I had a very good source back in the early 90's but it was taken off the market. (Good in that I had very good results with it... to the extent that I believe it may have slightly slowed my descent into totally disability and removed one type of pain I had... I believe as a result of its affect on helping my liver to detox.)
Prior to the MP, I had taken silymarin for over 10 years, but once I got on the MP, I found that it made me feel worse. I've not tried it since even though my body might be doing better and I might be able to handle the MP and silymarin again... though, my gut says, "Not so fast."
At any rate, looking forward to your post. Claire
Last edited on Wed Oct 14th, 2009 20:03 by eClaire
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38mo on MP; CFS FMS MCS COPD hypermob. IBS/GERD osteopor.; 125D48 25D<4;
NoIRs during most daylight outings & covered up; home w/o NoIRs
Ph1.Dec06 * ModPh2.Jun07 * AbxBrk.Mar-May08 * Ph2.Oct-Nov08 * Ph1.Jan2009
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Jeff
Member in Phase 3
| Joined: | Tue Jun 5th, 2007 |
| Location: | Delaware USA |
| Posts: | 31 |
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Posted: Wed Jan 27th, 2010 18:47 |
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ARBs Linked to Lower Dementia Risk
More grist for the mill: http://www.medpagetoday.com/Neurology/AlzheimersDisease/17928
For full PDF: http://www.medpagetoday.com/upload/2010/1/13/b5465.pdf
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Lyme/neuro Parkinson's 125D41 Ph1Sep07 Ph2 Mar08 Ph3 May08 NoIRs coverup 2h lite daily driving D25<7 May08
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