This Is MS Multiple Sclerosis Knowledge & Support Community

Insights to CCSVI, Infections and degenerative diseases.

My line of thought and research has focused lately from my prospective, MS dx and CPn dx and how the two could be linked.
I have read much and found many other PwMS that test positive for Intracellular Bacteria which have similar capabilities to CPn.
There is also studies showing that combinations of infections of virus' and bacteria are implied in co-incidence with MS and many degenerative diseases.
The finding that blood flow is consistently tested being lower in PwMS by Beggs, Shepherd and Zamboni, http://koti.mbnet.fi/hiihoo/ccsvi/PLETH ... 0BEGGS.pdf
is also reason to be concerned that the method of crossing the BBB and maintaining a healthy BBB is dependant on quality of blood flow!

"C pneumoniae–infected macrophages can infect endothelium and smooth muscle cells

C pneumoniae can be found to infect all of the major cellular players involved in the pathogenesis of atherosclerosis, including endothelium, smooth muscle, and monocytes/macrophages.16–18 When cocultured, C pneumoniae–infected macrophages can infect endothelium and smooth muscle cells,5 thereby demonstrating a mode of transference of a respiratory pathogen to the vasculature.
http://circres.ahajournals.org/content/102/8/861.full"

My next pondering is about the effect of CPn cells on the hypothalamus-pituitary-adrenal axis;
"Impaired hypothalamus-pituitary-adrenal axis activity and more severe multiple sclerosis with hypothalamic lesions.
Abstract
In this postmortem study, we investigated the relationship between multiple sclerosis (MS) lesions in the hypothalamus and the state of activity of corticotropin-releasing hormone (CRH)-producing neurons that control the hypothalamus-pituitary-adrenal (HPA) axis. A high incidence (15/16) of MS lesions was found in the hypothalamus, of which more than 50% was active, that is, contained activated macrophages. MS patients have increased numbers of CRH-immunoreactive neurons coexpressing vasopressin (CRH/VP neurons), a sign of chronic activation of CRH neurons and increased CRH mRNA expression. Active MS lesions correlated with a low number of hyperactive CRH/VP neurons. High human leukocyte antigen (HLA)-DR, -DP, -DQ expression, a measure for macrophage and microglial activation, correlated with low CRH mRNA expression. The nearer the HLA expression was situated to the CRH neurons, the stronger the inhibiting effect, suggesting that activated microglial cells or macrophages suppress these neurons. The more active MS lesions were present in the hypothalamus, the shorter was the disease duration until the moment of death, indicating an unfavorable course of the disease. Thus, MS patients have a chronically activated CRH system, but, in the subgroup of patients with active MS lesions in the hypothalamus, this activation is impaired and the disease course is worse.
http://www.ncbi.nlm.nih.gov/pubmed/14705110"

Hey NZer,
Regarding the hpa axis, I think the study you linked was a bit misleading. Yes, we need crh and its cascading hormones to be healthy...hence worse progression with greatly impaired hypothalamus. However, I think the constantly activated hpa axis is detrimental to a number of ms related conditions (endothelial health, bbb, peripheral nerves, muscle tension/blood flow, etc).

Here's a more current study that sees hpa axis dysregulation in MS in a more negative light.
http://www.sciencedirect.com/science/ar ... 7213000438

I'm pretty sure the crh is being released in response to cytokines. I'm experiencing the same improvements by inhibiting cytokines associated with MS damage that I did when I was just inhibiting ACTH (step after crh). Fenofibrate also affects lipid metabolism and d3 production so those might be contributing factors too. The difference between feno and the interferons in respect to immunomodulation is that feno, unlike interferons, doesn't cause hpa axis hikes and depressions...which I believe might be the cause of negative reactions and what I observe to be faster decline in those taking interferons (totally unscientific observation).

I don't think we need cpn to mess up our endothelium. Our chronically activated hpa axis can do that on its own. It could be that if there is cpn, it and our immune response to it are crossing the bbb because our hormones are making it weak and permeable. Just my opinion. . Though I do wonder what is triggering the cytokines if we don't currently have an active breach of bbb.

Hi Anonymoose:
At one point you were recommending clonidine. And then I think you stopped taking it. Why?

vesta wrote:Hi Anonymoose:
At one point you were recommending clonidine. And then I think you stopped taking it. Why?

Hi Vesta,
After about two and a half months on clonidine my blood pressure suddenly got really low and stayed low on the tiniest of doses. I quit and it came back up after about 22 hours. In the month or so between clonidine and fenofibrate, I took clonidine a few times to ease returning neck tension. It still worked and didn't lower my blood pressure if I only took it for a day or two (didn't try longer).

I tried to unrecommend it in multiple threads for people with low or normal blood pressure but I must not have done a very good job.

Anonymoose wrote:Hey NZer,
Regarding the hpa axis, I think the study you linked was a bit misleading. Yes, we need crh and its cascading hormones to be healthy...hence worse progression with greatly impaired hypothalamus. However, I think the constantly activated hpa axis is detrimental to a number of ms related conditions (endothelial health, bbb, peripheral nerves, muscle tension/blood flow, etc).

Here's a more current study that sees hpa axis dysregulation in MS in a more negative light.
http://www.sciencedirect.com/science/ar ... 7213000438

I'm pretty sure the crh is being released in response to cytokines. I'm experiencing the same improvements by inhibiting cytokines associated with MS damage that I did when I was just inhibiting ACTH (step after crh). Fenofibrate also affects lipid metabolism and d3 production so those might be contributing factors too. The difference between feno and the interferons in respect to immunomodulation is that feno, unlike interferons, doesn't cause hpa axis hikes and depressions...which I believe might be the cause of negative reactions and what I observe to be faster decline in those taking interferons (totally unscientific observation).

I don't think we need cpn to mess up our endothelium. Our chronically activated hpa axis can do that on its own. It could be that if there is cpn, it and our immune response to it are crossing the bbb because our hormones are making it weak and permeable. Just my opinion. . Though I do wonder what is triggering the cytokines if we don't currently have an active breach of bbb.

'Moose I think you are missing my drift, and that's ok!
I look at things from a cause and effect way of Life rather than a replace or modify aspect which infinitely confuses Life and Illness.

I have been looking for a reason and or connection as to why degenerative diseases, are over the last few years as technology has caught up with testing methods, are becoming known to share symptoms.

The technology used now for detection of the 0.4% of labelled Bacteria within our systems is showing statistical commonality of many pathogens, not one singular, but multiple known disease causing bacteria together in autopsy studies across a broad group of diseases from atherosclerosis to Dementia. Co-Incidence?

The technology is still not accurate and only about 40-65% trustworthy, mostly because the antigens that are looked for are only mildly understood in the disease process of the individual pathogen.

By modifying or killing of a pathogen you are not confronting the reason it is flourishing in your system and more importantly you are allowing the pathogen to evolve and re-express itself in a stronger form. Pathogens are far more adaptive than most people realise and that can happen multiple times within our systems before our system can develop a defence within one's Life time, we are slow learners so to say in the big picture of Life!

So my search has been about connecting the dots of HOW can these de-generative diseases be occurring rather to than first modify the disease process before you know what it is!


Nigel

Anonymoose wrote:

vesta wrote:Hi Anonymoose:
At one point you were recommending clonidine. And then I think you stopped taking it. Why?

Hi Vesta,
After about two and a half months on clonidine my blood pressure suddenly got really low and stayed low on the tiniest of doses. I quit and it came back up after about 22 hours. In the month or so between clonidine and fenofibrate, I took clonidine a few times to ease returning neck tension. It still worked and didn't lower my blood pressure if I only took it for a day or two (didn't try longer).

I tried to unrecommend it in multiple threads for people with low or normal blood pressure but I must not have done a very good job.

'Moose, has anyone worked out why you are unwell?

Calling or labelling a disease is only a minor part of wellness return of course and I wonder what the disease process is that you are combating?


Nigel

Hello NZer1:
I submitted my post (CCSVI Evolved and the Missing Infectious Link) a few hours after yours. We take different approaches to the same subject. I'm not equipped to take a scientific approach and don't pretend to, but feel I (and others) can take care of ourselves with the aid of appropriate professionals, the basic elements are now in place. Cheers.

Hi vesta, great post you have placed!

I agree with your thinking and my outstanding remaining thought is that you have an active infection happening at the moment and identifying it or them would be hugely beneficial to your Health now and in the future.
I am not saying that you need to bomb the infection and illuminate all of it from your system, quite the opposite. If you find out what the bacteria/virus/pathogen is you will have some insight as to what your body is doing overall when you have treats from 'dis-ease'.

I don't see anywhere in my studies that one bacteria can cause all the problems in any disease. Professor Nicholson is a great source of information on Stealth Bacteria ;)

What I do see is that a life time of imbalance in diet, exercise, stress management, injury healing, mindfullness and so on will allow dis-ease to develop into disease.

The straw that breaks the camels back is but one factor in a cascade of outcomes from the journey of Life.

Having enough straws will load us into a known disease format and then we have to work on many aspects to regain health. Having CCSVI is for instance a mechanism to breach the BBB, Infection by intracellular bacteria is a method to damage the Immune Systems function and cells of all sorts, Spinal alignment is a symptom generating issue that can also cause back jets and reflux, poor diet weakens the entire system of Wellness and repair to Health and so on.

Vesta my insights from reading many research papers brings me to the same thinking as you, ,
I have posted many more articles and papers on my site,
https://www.facebook.com/pages/CCSVI-in ... 1636357984
and on there is also the forum pages with many more articles from over the last few years of searching for answers.

;)
Nigel

NZer1 wrote:Moose, has anyone worked out why you are unwell?

Calling or labelling a disease is only a minor part of wellness return of course and I wonder what the disease process is that you are combating?


Nigel

Nope. I'm in the same boat as everyone else here.

I'm trying to target a proven/documented element of rrms (actually 2 now, hpa axis dysregulation and cytokines/inflammation) hoping to reduce damage. I get your point about trying to find the cause but at this point, no one knows what it is and we can't just sit around doing nothing while we wait for the answers.

I do love your posts and exploration of ideas...good food for thought. How is CAP going? Your year is up in August, right?

Hi 'Moose,
the treatment is rolling along like a steam roller as predicted and time doesn't stand still!
Don't know how many anniversaries there will be on the Protocol yet, 22nd Sept I began the official pill popping process, had been on the NAC treatment since mid Feb as a trial.

What tests have you had regarding the possible causes and effects of your symptoms?
Bloods for indications?
MRI's of Spine and brain?
MRI's done over time/years?
CCSVI tests Doppler or treatments IVUS, PTA?
CFS flow tests?
Spinal alignment assessment?
Personal Health History study for interconnected outcomes?

What methods/treatment are you using at present?


Nigel

NZer1 wrote:Hi 'Moose,
the treatment is rolling along like a steam roller as predicted and time doesn't stand still!
Don't know how many anniversaries there will be on the Protocol yet, 22nd Sept I began the official pill popping process, had been on the NAC treatment since mid Feb as a trial.

What tests have you had regarding the possible causes and effects of your symptoms?
Bloods for indications?
MRI's of Spine and brain?
MRI's done over time/years?
CCSVI tests Doppler or treatments IVUS, PTA?
CFS flow tests?
Spinal alignment assessment?
Personal Health History study for interconnected outcomes?

What methods/treatment are you using at present?


Nigel

Nzer,
I don't know how you manage to keep your brain working on CAP. I thought I was doing great on it...now I can't even remember most of those months! I hope it's over for you sooner rather than later.

Aside from my initial MRI in August, I don't have much other data that I find to be super useful. Ive done the usual nutrients, cortisol, cholesterol and liver tests. I'm starting to think about that csf flow and ao though.

Right now I'm just taking 96mg/day of fenofibrate, a multi, and 400mg magnesium.

A random oddity, since I've been thinking about it all day...maybe you can figure it out as it is CAP related. Since around the time of my first flare (janish 2010, whever the olympics were) I've had a small amount of clear fluid leaking out my nose (after I tip my head down and lift) and ears (when I sleep). It stopped whilst I was on CAP and just started again this week. With all this csf pressure talk, I'm wondering if it isn't csf leaking. Any idea about how CAP might stop that? (Clonidine would have reduced csf pressure and I was on that about a week after I completely stopped CAP). Also found something about vitamin d being something to avoid if you have iih. It made me think of that video you posted in the d3 thread a while ago. I need to dig into it more and will post if its worth it...tomorrow.

Anonymoose wrote:

NZer1 wrote:Hi 'Moose,
the treatment is rolling along like a steam roller as predicted and time doesn't stand still!
Don't know how many anniversaries there will be on the Protocol yet, 22nd Sept I began the official pill popping process, had been on the NAC treatment since mid Feb as a trial.

What tests have you had regarding the possible causes and effects of your symptoms?
Bloods for indications?
MRI's of Spine and brain?
MRI's done over time/years?
CCSVI tests Doppler or treatments IVUS, PTA?
CFS flow tests?
Spinal alignment assessment?
Personal Health History study for interconnected outcomes?

What methods/treatment are you using at present?


Nigel

Nzer,
I don't know how you manage to keep your brain working on CAP. I thought I was doing great on it...now I can't even remember most of those months! I hope it's over for you sooner rather than later.

Aside from my initial MRI in August, I don't have much other data that I find to be super useful. Ive done the usual nutrients, cortisol, cholesterol and liver tests. I'm starting to think about that csf flow and ao though.

Right now I'm just taking 96mg/day of fenofibrate, a multi, and 400mg magnesium.

A random oddity, since I've been thinking about it all day...maybe you can figure it out as it is CAP related. Since around the time of my first flare (janish 2010, whever the olympics were) I've had a small amount of clear fluid leaking out my nose (after I tip my head down and lift) and ears (when I sleep). It stopped whilst I was on CAP and just started again this week. With all this csf pressure talk, I'm wondering if it isn't csf leaking. Any idea about how CAP might stop that? (Clonidine would have reduced csf pressure and I was on that about a week after I completely stopped CAP). Also found something about vitamin d being something to avoid if you have iih. It made me think of that video you posted in the d3 thread a while ago. I need to dig into it more and will post if its worth it...tomorrow.

'Moose, are you going to answer my questions or are you only wanting answers from me and the audience?

I also now assume you have some sort of ABx history?

Have you been tested for the 'MS mimics' such as CPn, mycoplasma's and Lyme?

Have you had CSF pressure tests like Lumbar Punch or Cine flow tests?

Who do you have as advisers or on your health team and what are their opinions?

Without this sort of info it is impossible to discuss any cherry picked symptom or things such as weeping nose and ears.


Nigel

Nzer,
Thus far, my "team" consists of my neurologist and myself (and the Internet lol). I was diagnosed in August 2012 and started CAP September 11, 2012 without testing because cpn can be there without showing up on tests. I managed 3 pulses before I stopped CAP towards end of December to pursue the hpa axis angle (continued doxy until a week or so before starting clonidine in mid January).

My neurologist didn't think CAP would work but prescribed for me anyway. He basically prescribes what I ask for and monitors the "danger zones" and anything else I ask him to test. To be clear, I have had one MRI and the other blood tests I mentioned. I have had no other tests.

I always thought the fluid thing was just a sinus thing. Only yesterday I read of csf leaks presenting in the same way so I've not gotten my neuro's opinion yet. Frankly, I'd like to be armed with a plan of action before I throw myself down at to command and control of doctors because if it is a csf leak it may be protecting me in a way from other MS symptoms.

I only mentioned it because I thought it was interesting that CAP and clonidine seemed to have stopped whatever is leaking...thought you might be interested in CAP angle.

Thanks 'moose for making a clearer picture.
I would like to ask why you stopped the ABx treatment, if you were having side effects, whether they were detox issues, herx issues, endo-toxin issues or secondary porphyria issues they all indicate an issue with bacterial infection.
Three pulses, depending of course on the protocol ABx and method is not very long imo and if you had done bloods at that time a quality Lab would have been good indications for any of the bacterial and viral infection antigens because the die off would have stirred the immune response.
If it was me I would have continued and learned more from others who were on the protocol and or the experts in protocol such as David Wheldon, if there was hope from a reaction or side effects I would have jumped at it!

The fluid leakage from nose and ears does ring a bell with me as well and I thought it was due to CSF pressure build up, I may be wrong as well.

Has your disease profile been sporadic episodes or steady progression?

The two forms seem to respond to different treatment approaches and have different lesion expression which I think gives clues of what to look for from a history angle. You can sometimes find injury history, or stress history in recent past and if there is infection history over life times then that has a profile as well.

1. If there is a positive response to using steroids it points to a format in the disease expression. If there is nil or a negative reaction it is hinting at a form of disease profile.
2. If diet makes a difference then looking at the life time of diet habits and life events can be educational.
3. The onset of symptoms whether they are grouped by sensory or motor nerve changes is a lead.
4. The disability progress as it occurs around the body for instance motor, sensory, cognitive, bladder/bowel, mobility are hinting at regions of the CNS or the Spine that are being damaged and the timing of progression gives clues of treatment possibilities.
5. If there is responses from AO Chiropractic treatments over time (aka more than 5 treatments) it is another positive lead.
6. Having Doppler Ultrasound of the neck veins will give a 'glimpse' of blood flows, not only the Zamboni protocol also the flow analysis calculations.
7. Having CSF cine flow tests will give insights to general brain and cord health.
8. Upright MRI will be very, very helpful for quality assessments, especially if it is through Dr Rosa in Albany USA and is CSF flows as well as MRI.

I find that now that there has been some access to historic studies and PwMS are using the Internet to assess research there have been big advances and Hope that hasn't been committed to by Specialists in the past.
The realisation that the Disease Modifying Drug (DMD) approach in MS doesn't do anything positive for PwMS (but to Drug Company Investors it's a saviour,) and that piece of insight is a step forward by breaking the mould of silence that had occurred.

;)
Nigel

"Those with MS or ALS type symptoms appear to have huge biofilm issues. Some people can have such a huge problem with biofilm it's said strings can come out when donating blood. Course these guys are incredibly ill though. All my research really goes towards MS, ALS, Alzheimer's, Lyme, Autism, and similar. and they are all very connected with a biofilm problem and with detox pathways being overloaded and/or faulty. Hair loss just happens to overlap with biofilm problems like the above issues. "
http://immortalhair.forumandco.com/t693 ... d-biofilms


Nigel