The Marshall Protocol Study Site Home

Search
   
Members

Calendar

Help

Home
Search by username
   Not logged in - Login | Register 


Host Defences - UCSD 2006
 Moderated by: Prof Trevor Marshall Page:    1  2  Next Page Last Page  
 

New Topic

Reply

Print
AuthorPost
Prof Trevor Marshall
Foundation Staff


Joined: Fri Jul 9th, 2004
Location: Thousand Oaks, California USA
Posts: 15734
Status:  Offline
 Posted: Sun Oct 8th, 2006 13:18

Quote

Reply
University of California-San Diego
Frontiers of Clinical Investigation Conference
Host Defense 2006: From Bench to Bedside
Oct5-7 La Jolla, CA

................................................

Quotable quotes that stuck in my mind:
"Everybody knows Inflammation induces Cancer"- Francesco Marincola MD, Senior Investigator, NIH

"Vitamin D is Immunosuppressive" - Hans-Dieter Volk MD, PhD, Head of the Institute for Medical Immunology, Charite-University Medicine Berlin.
---------------
Wow! What an amazing conference. Over 100 top researchers who were actually interested in what we have been doing, and who didn't recoil in horror whenever I mentioned "Vitamin D":)

For anybody that is interested, the detailed schedule can be found here:
http://cfdev.ucsd.edu:89/b2b2006/program.html

I took a video aide-memoire for my own use on a small pocket camera, the quality is atrocious, and many of the slides are washed out. Nevertheless, one of the presentations was so compelling I have taken the effort to put it online. It explains how the antimicrobial peptides (the body's own antibiotics) are employed against the pathogens which cause Crohn's disease.

Many of you have heard me talk about how important it is to get the VDR Nuclear Receptor working properly (one of the things Benicar does) because the VDR is responsible for the Cathelicin Anti-Microbial Peptides. It is also responsible for transcribing the genes of the Beta Defensins.

This presentation explains how those, and the other Defensins, are important, and I think that those of you who track the science will find it very interesting indeed.

The 24 Mbyte RealVideo 9 presentation runs for 30 minutes. You can stream it from URL

http://autoimmunityresearch.org/crohns.ram

and the more technically astute can download the whole presentation by right-clicking on this link.

As my mind starts to relax I am sure I will think of more "interesting stuff," and your questions (on the molecular biology topic, please) will also help fuel the discussion.


paulalbert
Research Team


Joined: Thu Jul 15th, 2004
Location: New York USA
Posts: 1034
Status:  Offline
 Posted: Sun Oct 8th, 2006 13:52

Quote

Reply
Nice video. Here's my favorite quote. Here's an inexact transcription. It comes at minute 20:

Why are these data important? I think these data provide a rationale for alternative therapies. Right now, almost all of the therapies target inflammatory cells; they try to suppress the inflammatory response.

Don't get me wrong, I'm very happy we have these drugs, because right now that's the only thing we do have for these patients but I still think it's based on the wrong strategy because the entire secondary reaction or response to the bacteria.

[Slide text: Current therapy targets a secondary response to bacteria!!!]

I think the therapy of the future could in addition try to somehow target or strengthen barrier function and restore antibacterial host defense.

Paul

Last edited on Sun Oct 8th, 2006 13:56 by paulalbert



____________________
Diag CFS 6.03 / sympt since 9.02 / exercise, food intol, sleep prob / 1,25D: 16, 4.06; 1,25D:27, 25D:26 7.04; 1,25D:43, 25D:6 6.05; 1,25D:17, 25D:8 8.05; / MP: 7.04 / Ph. 3 / Bacteriality
Freddie Ash
...


Joined: Fri Apr 8th, 2005
Location: LeSage, West Virginia USA
Posts: 1019
Status:  Offline
 Posted: Sun Oct 8th, 2006 16:06

Quote

Reply
HI ALL

This is Fred in WV. Here is some infomation I just read in my Oct issue of Prevention magazine. This was found in the article,"Take Your Vitamins." Under the vitamin D, it said: "There's no doubt about it: vitamin D is required to get calcium into the bones. Yet in the WHI study, volunteers given D plus calcium were as likely as other women to suffer fractures. Same thing with colon cancer: Although a 2005 review at the Naval Health Reach Center in San Diego concluded that people who took extra vitamin D halved their risk of the cancer, the WHI reported last year that D supplements did nothing to ward it off."

WHI is Women's Health Initiaive.

Remember, we are all in this together and I am pulling for us.

Your friend in sarcoidosis

Freddie



____________________
Freddie: dx-sarc 2/82 lymph; skin, eyes, joints, esophagus, intestines, spleen, heart,lungs-25D-7; 125-D43
Prof Trevor Marshall
Foundation Staff


Joined: Fri Jul 9th, 2004
Location: Thousand Oaks, California USA
Posts: 15734
Status:  Offline
 Posted: Mon Oct 9th, 2006 03:17

Quote

Reply
Freddie,
What you are seeing is a clash of cultures. Clinicians have come to rely upon observations of disease, of studies of people who are sick. Molecular Biologists have focused on an understanding of the complexities of the disease process itself.

It is not possible for either group to fully understand the overview unless they listen to all inputs. An excellent example of this is my Letter to the Editor which was just published in The Lancet. The editors of The Lancet, the premiere British clinical journal, had no idea what I was talking about. They could not understand the depth of my knowledge about Statins and Vitamin D, or even that such knowledge was possible. Consequently they were promoting the views of Dr Grimes, who has some pea-brained concept that Statins improve health because they are "like Vitamin D."

The Editors changed around the words I had written into a form which greatly diluted my message. Sigh... I am sure they had the best of intentions, but not the ability to comprehend:)

..Trevor..

ps: the Citation to my Lancet correspondence is:
Marshall TG: Are statins analogs of vitamin D?. Correspondence to Grimes, DS. The Lancet 2006; 368:1234 doi:10.1016/S0140-6736(06)69509-3

and a copy is at URL http://tinyurl.com/r2gtl
(I think you will have to register to get access)

UshiAad
member


Joined: Tue Jul 19th, 2005
Location: Rotterdam, Netherlands
Posts: 76
Status:  Offline
 Posted: Mon Oct 9th, 2006 05:51

Quote

Reply
Very interesting indeed and agree with Paul's remark.

PD Although i don't have crohn's disease (as far as i am aware) before the unset of my ME/CFS in 1993 i had bowel problems and breakdown for years .......




____________________
Diagnosis ME 1993, D free diet and low light since 7/05, Benicar since 9/05; Benicar/Mino since 10/05; 25D 10/05: 6, 11/06: 17, 7/07: 29, 12/07: 25; 1,25D 10/05: 21 ?, Phase 2 since 12/05; Phase 3 since 6/06|
Frans
Member*


Joined: Sun Feb 20th, 2005
Location: Near Rotterdam, Netherlands
Posts: 1034
Status:  Offline
 Posted: Mon Oct 9th, 2006 09:01

Quote

Reply
Trevor, wow !

How did you get this published in the Lancet, of all magazines?

This is fantastic ! I can't wait to read any comments to your comment  :D:D:D

If everyone is paying attention, it will blow a lot of people away !!

I haven't seen anyone contesting that D3/25oh D act as ANTAgonist for the VDR.

Let's see what happens with this information.



____________________
Burn-out/nervous breakdown Jan01 125D 48 25D8.48 Ph1Nov06 ModPh2Jan07 Ph2Apr08 Cipramil Seroquel NoIRs lite exp r/t work cover up 25D3.9(Oct07)
Frans
Member*


Joined: Sun Feb 20th, 2005
Location: Near Rotterdam, Netherlands
Posts: 1034
Status:  Offline
 Posted: Mon Oct 9th, 2006 09:13

Quote

Reply
Trevor,

I have a question. I understand you applied for a CME certification.

(For the ones who don't know: CME stands for Continuous Medical Education)

Can we assume that the status of a CME certification is as much as a peer review?

I ask since my company doc. last said: I will follow the literature...

Does a CME-certification equal ... the literature... ?

Did you also get a CME-certification for this conference in particular? And Karolinska?

Sincerely, Frans



____________________
Burn-out/nervous breakdown Jan01 125D 48 25D8.48 Ph1Nov06 ModPh2Jan07 Ph2Apr08 Cipramil Seroquel NoIRs lite exp r/t work cover up 25D3.9(Oct07)
Prof Trevor Marshall
Foundation Staff


Joined: Fri Jul 9th, 2004
Location: Thousand Oaks, California USA
Posts: 15734
Status:  Offline
 Posted: Mon Oct 9th, 2006 10:17

Quote

Reply
Frans,
The CME presentation is at the AAEM conference in Hilton Head later this month. I will be speaking to several hundred physicians, who will get CME points (they need a certain number each year to keep their licence) for listening to my presentation, and answering some simple 'exam-type' questions.

This means that not only was the AAEM presentation invited, the abstract went through their Peer Review committee, objectives were set for what the audience is expected to learn, and then my final slides were also submitted for the Peer Review committee to approve.

So the presentation has been made to jump through the hoops. I will be trying to get a video version of this presentation which we can put online for you all. It will be about 1 hour 15 minutes in length, and cover the MP science from end to end.

..Trevor..

tickbite
inactive member


Joined: Mon Apr 24th, 2006
Location: Tulsa, Oklahoma, USA
Posts: 399
Status:  Offline
 Posted: Mon Oct 9th, 2006 10:57

Quote

Reply
Hi Trevor,

By the sounds of this presentation, most probiotics don't really do a darn thing, unless you are using a Nissle strain. And even this is just another palliative approach. Would this be correct in your opinion?

No doubt this presentation is very compelling. Did I hear the presenter say "Chromosomal DNA" being the true cuplrit to Crohn's and not the initial bacterial infection? Thanks so much for putting up the video for us. I for one, love to absorb as much as possible!



____________________
"Lyme","CFS", Meningitis
Phase3 8-2-07, MP on hold 11/2007

Prof Trevor Marshall
Foundation Staff


Joined: Fri Jul 9th, 2004
Location: Thousand Oaks, California USA
Posts: 15734
Status:  Offline
 Posted: Mon Oct 9th, 2006 11:10

Quote

Reply
The slide showing that 30% of Crohn's patients have a defect in the NOD gene was discussed a little, as well as the fact the Crohn's patients generally had fewer gene replications in the region of the Defensin genes. But the presenter understood that these were merely interesting associations, and did not present them to be causal. When I was speaking with him during the coffee breaks he semed to have a very good overview of the disease process, and he certainly took a copy of my Karolinska paper when I offered it:)

Ival
inactive member


Joined: Mon Mar 14th, 2005
Location: Pensacola, Florida USA
Posts: 139
Status:  Offline
 Posted: Tue Oct 10th, 2006 13:49

Quote

Reply
I find this video very interesting. The mutation in the intestines in crohn’s disease somehow are similar to my version of rheumatoid arthritis. One of my worst herxs in my intestines is right where the small intestine and the colon are connected right were 40 to 50% of the crohn’s disease cases occur. Whenever that part of my intestine would herxs my arthritis would double or triple for weeks at the beginning of the protocol. I know that’s the area where the herxs is because I had an Appendectomy in my early twenties and it hurts in the exact same spot. I’m sure I have other mutations like in my joints that affect my disease but the GI tract is definitely involved in RA at least in my version.

That observation leaves me with a lot of questions. The first one being the barrier of the intestine is being compromised because of the mutations in the genes. Since we’re getting rid of the infections will those cells that are mutated eventually be replaced with healthy cells or will they always be a problem. My experience so far is they must be getting replaced or somehow repairing their self because when I herxs in that area now I very rarely have the arthritis symptoms follow and the herxs is only about half of what it used to be.

The stem cells that he’s talking about in the video are located where. The intestinal tract or are they in other parts of the body. When is the mutations happening in those cells right when the stem cells makes them or is the mutation happening after the new cell becomes infected again with the infection in the area.

Watching the video gives you one possibility of what the appendix does in the first place. That is a transition area between very little bacteria to a lot of bacteria. One of the possibilities is it delivers a special kind of peptides or at least just more of them in the area to make the transition easier.



____________________
MP 4/12/05/Benicar Q6h Ph1 4/26/05/ 25D13ngml 125D44pgml Ph2/6/1/05 Ph3/1/25/06 diag RA 2001 Male 47
Prof Trevor Marshall
Foundation Staff


Joined: Fri Jul 9th, 2004
Location: Thousand Oaks, California USA
Posts: 15734
Status:  Offline
 Posted: Tue Oct 10th, 2006 14:09

Quote

Reply
Ival,
I wish I could describe the mechanism of DNA mutation to you. But I am not convinced by anything I have read. Which is sorta crazy - we have known for decades that radiation induces the DNA to mutate - but we don't yet seem to know how.

Once I understand the exact mechanism, and whether the host DNA is changed by bacteria early in life, or whether it never changes, and whether it is reversible, only then I will be able to give you an answer.

Maybe I will find out at the upcoming conference (at the start of November) "Nuclear Receptors - Bed to Bedside" as that seems to have some pretty smart people on the list of attendees, and we will have plenty of time to mix and chat...

ps: here is a recent suggestion on mechanisms

Last edited on Tue Oct 10th, 2006 14:17 by Prof Trevor Marshall

RobertTownsend
health professional
 

Joined: Tue Oct 18th, 2005
Location:  
Posts: 129
Status:  Offline
 Posted: Wed Oct 11th, 2006 13:09

Quote

Reply
Trevor

Not sure where to post this but there is a really interesting piece in this week's New Scientist

"Researchers have cured viral meningitis in mice by blocking the action of an anti-inflammatory immune molecule"

Researchers at the La Jolla Institute for Allergy and Immunology in California have found that an anti-inflammatory response ( in this case IL-10) was preventing the immune system from attacking the virus

The piece is at

http://www.newscientist.com/article.ns?id=dn10264&feedId=online-news_rss20

Seems to add much to your immmune-enabling proposals. I have not tracked back to the original research paper - but if you cannot get it from your own sources, I expect my Uni Online subscriptions should be able to turn it up for you.

Regards

RobertTownsend



____________________
CFS 4yrs,crippled knees;Oct05 Phase 1;Feb 06 Phase 2 ; Mar06 1,25D-61pMol/L 25D-23nMol/K;Jul06 Ph3 start ;July 08 dose tapering some abx,daytime fatigue much lower, skin still very light sensitive ;knee mobility very constrained with limited walking
RobertTownsend
health professional
 

Joined: Tue Oct 18th, 2005
Location:  
Posts: 129
Status:  Offline
 Posted: Wed Oct 11th, 2006 13:11

Quote

Reply
Trevor

PS

The headline writer for the New Scientist got it wrong - it should read

"
Inflammation turned OFF "

RobertTownsend



____________________
CFS 4yrs,crippled knees;Oct05 Phase 1;Feb 06 Phase 2 ; Mar06 1,25D-61pMol/L 25D-23nMol/K;Jul06 Ph3 start ;July 08 dose tapering some abx,daytime fatigue much lower, skin still very light sensitive ;knee mobility very constrained with limited walking
Prof Trevor Marshall
Foundation Staff


Joined: Fri Jul 9th, 2004
Location: Thousand Oaks, California USA
Posts: 15734
Status:  Offline
 Posted: Wed Oct 11th, 2006 14:09

Quote

Reply
Robert,
Now that you mention it, there was a lot of talk about blocking IL-10 at the conference. I have to admit I thought it was such a stupid idea that I usually left the lecture hall and spent the time mixing/talking in the corridors during that type of presentation:) Also left during the ones examining the minutia of T-cell activation in mice... (those folk can't see the forest for the trees)

RobertTownsend
health professional
 

Joined: Tue Oct 18th, 2005
Location:  
Posts: 129
Status:  Offline
 Posted: Wed Oct 11th, 2006 14:43

Quote

Reply
Trevor

I think this is wholly consistent with your work, and indeed corrobates it becuase it is a different "entrenched pathogen" albeit a viral one.

If you assume for the moment the simplified model that TH1 responses are to bacteria and TH2 responses are to viruses, then the dominant pro-inflammatory responses are

Bacterial : TH1 elevated IL12 and IFNgamma ( I think these are the right ILs, though IL1 and IL6 will also be elevated)

Viral : TH2 elevated IL10

Then this work of von Herrath on the immune systems elevated inflammatory response ( in this case elevated IL10 to a viral pathogen) blocking innate immunity is

exactly equivalent

to your observations that elevated Th1 inflammatory cytokines in bacterial infections are blocking innate immunity

RobertTownsend

PS incidentally we don't here subscribe to the full text of the source document

Last edited on Wed Oct 11th, 2006 14:55 by RobertTownsend



____________________
CFS 4yrs,crippled knees;Oct05 Phase 1;Feb 06 Phase 2 ; Mar06 1,25D-61pMol/L 25D-23nMol/K;Jul06 Ph3 start ;July 08 dose tapering some abx,daytime fatigue much lower, skin still very light sensitive ;knee mobility very constrained with limited walking
tickbite
inactive member


Joined: Mon Apr 24th, 2006
Location: Tulsa, Oklahoma, USA
Posts: 399
Status:  Offline
 Posted: Wed Oct 11th, 2006 15:40

Quote

Reply
I'm a little confused here on Robert's evaluation of LCMV creating an elevated inflammatory response. From the news article it sounds to me like the IL-10 creates an decreased immune response. Not that these cytokine reactions don't have any relavance to each other, they abosultely do. I love the article. It sounds like the two states of Th1 and this particular Th2 response are exact opposite in as far as inflammatory response. Is this a wrong observation? Thank you for the post Robert.



____________________
"Lyme","CFS", Meningitis
Phase3 8-2-07, MP on hold 11/2007

Prof Trevor Marshall
Foundation Staff


Joined: Fri Jul 9th, 2004
Location: Thousand Oaks, California USA
Posts: 15734
Status:  Offline
 Posted: Wed Oct 11th, 2006 18:08

Quote

Reply
I haven't had time to look at the paper, but many think that the best way to treat disease is just to suppress the inflammation. There is no thought of long-term prognosis. For example, the TNF-alpha blockers work in this way. I haven't had time to look into the IL-10 papers, but what little I did listen to, sounded as though the IL-10 blockade was a similar concept - stop the immune system creating inflammation - this was the stated goal.

Very few scientists understand the concept of persistent bacteria. I was looking at this paper earlier today, for example, which found bacterial ribosomal DNA in the blood of supposedly healthy individuals, and did not know what conclusions to draw from this
http://jcm.asm.org/cgi/content/full/39/5/1956?view=long

RobertTownsend
health professional
 

Joined: Tue Oct 18th, 2005
Location:  
Posts: 129
Status:  Offline
 Posted: Wed Oct 11th, 2006 20:44

Quote

Reply
Trevor

The abstract is at

http://www.jem.org/cgi/content/abstract/jem.20061462v1

We don't have access to the full article

RobertT



____________________
CFS 4yrs,crippled knees;Oct05 Phase 1;Feb 06 Phase 2 ; Mar06 1,25D-61pMol/L 25D-23nMol/K;Jul06 Ph3 start ;July 08 dose tapering some abx,daytime fatigue much lower, skin still very light sensitive ;knee mobility very constrained with limited walking
tickbite
inactive member


Joined: Mon Apr 24th, 2006
Location: Tulsa, Oklahoma, USA
Posts: 399
Status:  Offline
 Posted: Wed Oct 11th, 2006 22:23

Quote

Reply
This may or may not be of any relevance, but IL-10R blockade is pro-inflammatory. I'm not sure what the researchers were saying at the conference but elevated IL-10 is anti-inflammatory from these references:

http://www.eurekah.com/abstract.php?chapid=1690&bookid=118&catid=19

http://en.wikipedia.org/wiki/Interleukin_10

So, perhaps the headline writer for the New Scientist article got it right...

"Inflammation 'turned on' to fight killer viruses"

Sometimes not enough pro-inflammatory cytokines is bad? i.e. HIV? However, I realize that the whole concept of only looking at cytokines is lacking and the truth is an infectious etiology. By the way, i'm only an amateur. If i'm totally wrong about this please harass me.



____________________
"Lyme","CFS", Meningitis
Phase3 8-2-07, MP on hold 11/2007


 Current time is 19:48
Page:    1  2  Next Page Last Page  



* We can help you understand chronic disease, but only your physician is licensed to give you medical care *

Powered by WowBB 1.7 - Entire site Copyright © 2004-2019 Autoimmunity Research Foundation, All Rights Reserved
Click here to view our PRIVACY POLICY
Page processed in 0.0473 seconds (69% database + 31% PHP). 17 queries executed.