Chlamydia Pneumonia + CCSVI

[Kinora]

Hello,
I can not look at the computer for extended periods and can not reasearch the science, but has anyone made the connnection between CCSVI and Chlamydia Pneumonia? I see a relationship.

CPn Help/thoughts_appertaining_ccs

http://www.cdc.gov/ncidod/eid/vol4no4/campbell.htm

http://www.med.wayne.edu/Scribe/scribe0 ... rigger.htm

Audrey

[cheerleader]

Hi Kinora-
Marie Rhodes, a frequent poster on TIMS and the RN who wrote the book CCSVI: the science behind the controversial theory www.ccsvibook.com
was treated for many years for Cpn, using the Wheldon antibiotic protocol. It wasn't the answer for her, but it has helped many.

Marie believes that it is the venous congestion and reflux found in CCSVI which allows many viruses and bacteria to break the blood brain barrier and harm the central nervous system...which is why we see neurological Lyme, EBV, etc. The blood brain barrier should protect brain and spinal tissue from these invaders, but cannot, due to venous congestion.

It is very important that pwMS understand what their nutritional status is (vit. B12, vit D levels, etc., co-infection status (Lyme, Cpn, EBV, herpes, etc) may be, as treating CCSVI with venoplasty may not be the complete answer for some. But it is impossible to find one, exclusive pathogen linked to MS. Many have been implicated. None have been isolated.
cheer

[Kinora]

Dear Cheerleader,

A very interesting and enlightening idea. I will look at the book maybe.

Thanks,

Kinora

[MarkW]

Hello Joan,
You and Maria are oracles on CCSVI, sometimes I feel your advocacy oversteps the science. You posted:
Maria, who wrote the book CCSVI: the science behind the controversial theory www.ccsvibook.com was treated for many years for Cpn, using the Wheldon antibiotic protocol. It wasn't the answer for her, but it has helped many.
Marie believes that it is the venous congestion and reflux found in CCSVI which allows many viruses and bacteria to break the blood brain barrier and harm the central nervous system...which is why we see neurological Lyme, EBV, etc. The blood brain barrier should protect brain and spinal tissue from these invaders, but cannot, due to venous congestion.

I have a problem with your statement:
The blood brain barrier should protect brain and spinal tissue from these invaders, but cannot, due to venous congestion.

The BBB problem is poorly understood. I have not seen firm evidence that venous congretion causes BBB porosity. I have not seen good evidence when BBB porosity occurs nor what triggers it. Happy to receive any evidence you have.

I suggest we stick with the mantra for CCSVI:
"if you have stenosed veins get them treated"

I have used the Wheldon protocol and it helped slow my MS progression. I agree with Maria, it is worth trying if you have MS (the Wheldon protocol is cheap).
As a first step, I recommend getting a diagnosis for CCSVI but for many people this is not possible for financial reasons.

CCSVI is a syndrome says Zamboni, let's treat it while we try to understand the science.

Said as gently as I know how..........

MarkW

[CureOrBust]

I have a problem with your statement:
The blood brain barrier should protect brain and spinal tissue from these invaders, but cannot, due to venous congestion.

The BBB problem is poorly understood. I have not seen firm evidence that venous congretion causes BBB porosity. ... Happy to receive any evidence you have.

The only evidence I remember seeing on the BBB porosity being adversely affected by blood flow, was a reference made by Dr Simka to a bovine (ie cow) study. The only other study that even came close (I have not actually seen the paper) is the"Pullman" (I think that was his name) paper which was performed on dogs. Now that study I would love to read.

I have not seen good evidence when BBB porosity occurs nor what triggers it.

Not sure that you actually meant what this statement says at face value. MS has long been associated with BBB porosity, which from my understanding increases during a relapse; and I would assume has been shown to do such. In the past, I have read many articles discussing how steroids are used to not only reduce the immune system attack, but to also reduce the BBB porosity.

[NHE]

I have not seen good evidence when BBB porosity occurs nor what triggers it.

Not sure that you actually meant what this statement says at face value. MS has long been associated with BBB porosity, which from my understanding increases during a relapse; and I would assume has been shown to do such. In the past, I have read many articles discussing how steroids are used to not only reduce the immune system attack, but to also reduce the BBB porosity.

I am also confused. Gadolinium is used to highlight active lesions in MRI as it crosses the BBB where the BBB has broken down. This not only indicates areas of active inflammation, but also demonstrates that the BBB has increased porosity. I know this seems obvious, but maybe I'm missing something in the prior discussion.


NHE

[MarkW]

Hello CureOrBust and NHE,

I meant exactly what I wrote:
MarkW: I have not seen good evidence when BBB porosity occurs.
It is commonly stated that BBB porosity increases during relapses. I have not seen any research which shows that the BBB does this. Blood cells need to pass through the BBB during a relapse but not during remission if the commonly held view is correct.
I hoped to see research on when the BBB porosity alters in pwMS over disease progression. Please share any info you have.

My understanding is that Gandolinium passes thru the BBB in relapses and remission. It just highlights active lesions.

My main point is that we do not understand the BBB in pwMS because there is little evidence available. This is also important for the red blood cell/iron theory of myelin damage.

MarkW

Discusion history:

CureOrBust wrote:
MarkW wrote:
I have not seen good evidence when BBB porosity occurs nor what triggers it.

Not sure that you actually meant what this statement says at face value. MS has long been associated with BBB porosity, which from my understanding increases during a relapse; and I would assume has been shown to do such. In the past, I have read many articles discussing how steroids are used to not only reduce the immune system attack, but to also reduce the BBB porosity.

NHE posted:
I am also confused. Gadolinium is used to highlight active lesions in MRI as it crosses the BBB where the BBB has broken down. This not only indicates areas of active inflammation, but also demonstrates that the BBB has increased porosity. I know this seems obvious, but maybe I'm missing something in the prior discussion.

[HappyPoet]

I have not seen good evidence when BBB porosity occurs nor what triggers it.

Not sure that you actually meant what this statement says at face value. MS has long been associated with BBB porosity, which from my understanding increases during a relapse; and I would assume has been shown to do such. In the past, I have read many articles discussing how steroids are used to not only reduce the immune system attack, but to also reduce the BBB porosity.

I am also confused. Gadolinium is used to highlight active lesions in MRI as it crosses the BBB where the BBB has broken down. This not only indicates areas of active inflammation, but also demonstrates that the BBB has increased porosity. I know this seems obvious, but maybe I'm missing something in the prior discussion.


NHE

My understanding is the same as NHE's understanding of when Gad crosses the BBB -- during relapses. If the BBB hasn't broken down anywhere, the Gad won't cross the BBB.

This link is to a fascinating article that provides new insights into the BBB; there is also a great live video of T-cells crossing in/out of the BBB (Ewwww):

http://www.physorg.com/news176652011.html

[Cece]

http://www.direct-ms.org/sites/default/ ... n%2003.pdf

This does not answer the question but it is an indepth article on the BBB with some useful images.

[MarkW]

Thanks for the posts. However these do not answer the basic question:
When does the BBB porosity change in pwMS ? What triggers the change is even more difficult.
I am looking for evidence rather than opinions, which may be correct.
MarkW

[Cece]

Besides loss of the BBB solute barrier, enhanced
transendothelial leukocyte migration into the CNS is
observed early in the course of MS, and likely contributes
to disturbances in neural integrity.19 21

19 Kermode AG, Thompson AJ, Tofts P, MacManus DG, Kendall
BE, Kingsley DP et al. Breakdown of the blood-brain barrier
precedes symptoms and other MRI signs of new lesions in
multiple sclerosis. Brain 1990; 113: 1477¡/89.

21 Springer TA. TrafŽc signals for lymphocyte recirculation and
leukocyte immigration: the multistep paradigm. Cell 1994;
76: 301¡/14.

I'd look at #19. Breakdown of the BBB precedes symptoms and MRI signs of new lesions in MS. I wonder how they define the breakdown of the BBB. I haven't read it, these were cited in the article listed above, which is where my quote is from.

[CureOrBust]

However these do not answer the basic question:
When does the BBB porosity change in pwMS ? What triggers the change is even more difficult.

Are you questioning if MS is associated with BBB porosity? or if it changes during the course of MS?

[CureOrBust]

I have not seen firm evidence that venous congretion causes BBB porosity. I have not seen good evidence when BBB porosity occurs nor what triggers it. Happy to receive any evidence you have.

How about one from your own post. By "congretion" I am guessing you mean flow changes such as reflux? which to me would mean non-laminar flow

http://www.thisisms.com/ftopict-17538-.html

http://phleb.rsmjournals.com/cgi/reprint/25/6/269

and it has been established that steady laminar shear stress promotes a
release of factors from endothelial cells that inhibit migration of leukocytes.20,21


20 Bergan JJ, Schmid-Schonbein GW, Smith PD, Nicolaides
AN, Boisseau MR, Eklof B. Chronic venous disease. N
Engl J Med 2006;355:488–98
21 Sorescu GP, Song H, Tressel SL, et al. Bone morphogenic
protein 4 produced in endothelial cells by oscillatory
shear stress induces monocyte adhesion by stimulating
reactive oxygen species production from a nox1-based
NADPH oxidase. Circ Res 2004;95:773–9

I haven't read the referenced studies, but I would guess they trump the cow study.

Is this the sort of thing you were looking for above?
....edit...
I'm still reading this same paper, and thought this may also count.

Raised venous pressure can stretch vein
walls sufficiently to separate the tight junctions
between endothelial cells forming the blood–brain
barrier.33

33 West JB, Tsukimoto K, Matheu-Costello O, Prediletto R.
Stress failure in pulmonary capillaries. J Appl Physiol
1991;70:1731–42

[CureOrBust]

I remember looking at steroids effects on the BBB a number of years back (2007). I found the old posts, and this quote basically covers it I think.

http://www.nationalmssociety.org/Meds-M ... solone.asp

Methylprednisolone is one of a group of corticosteroids (cortisone-like medications) that are used to relieve inflammation in different parts of the body. Corticosteroids are used in MS for the management of acute exacerbations because they have the capacity to close the damaged blood-brain barrier and reduce inflammation in the central nervous system.

Although it talks of anti-inflamatory properties to start with, I read that sentence as more of a background on steroids

http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=1619410

http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=1866009

Even Statins which I think were originally thought to be anti-inflamatory, are being found to affect the BBB

Statins reduce human blood-brain barrier permeability and restrict leukocyte migration: relevance to multiple sclerosis.
Ann Neurol. 2006 Jul;60(1):45-55.

ummmm..this is meant to be a partial answer to the questions "When does porosity change in pwMS? What triggers it?" Steroids change the porosity. Steroids trigger a change.