This Is MS Multiple Sclerosis Knowledge & Support Community

I hate to poo-poo any of our strategies to beat MS but having been on CAP and felt improvements along with a lot of suffering and some new neurological symptoms, I feel it only right I share this with CAP'ers and those looking into CAP.

HPA axis dysregulation and resulting excess cortisol and aldosterone are known to be a part of MS. Doxycycline and minocycline suppress cortisol and aldosterone release. I think the reason CAP works for some is that it resets the HPA axis dysregulation by suppressing cortisol production, allowing the hippocampus to 'regenerate' and properly do it's job to shut down the production of ACTH, cortisol and aldosterone. A little scientific background here http://www.thisisms.com/forum/general-d ... 21536.html A TIMS search of hpa axis dysregulation, or cortisol, or aldosterone will bring up more supporting info.

There are less harmful ways to accomplish this correction of HPA axis than taking antibiotics. You could try Jimmyleg's aggressive dosing of Vitamin D and magnesium. You could try Clonidine (my current experiment). You could try taking GABA which is also known to reduce cortisol levels. I'm sure there are other ways. I don't know if these methods will work, but I would try them before I tried CAP.

Many, many people live with cpn and don't have MS. It may not be the cause of your disease.

(actually my approach is optimizing a constellation of nutrients that have been found in research to be low in ms. you only have to be aggressive with therapeutic supplementation when levels are not high enough. which tends to be the case..)

Right Anonymoose, so you hate to poo-poo my husband's strategies. Fair enough, but what about the people on the Vanderbilt protocol who have never taken doxycycline bur rifampicin, which is not immunomodulatory.

My treatment had to be aggressive because my neuro had me in line for a nursing home. Before my progression my diet was very similar to Jimmylegs' but for me it stopped working.

Sarah

Anecdote wrote:Right Anonymoose, so you hate to poo-poo my husband's strategies. Fair enough, but what about the people on the Vanderbilt protocol who have never taken doxycycline bur rifampicin, which is not immunomodulatory.

My treatment had to be aggressive because my neuro had me in line for a nursing home. Before my progression my diet was very similar to Jimmylegs' but for me it stopped working.

Sarah

Sarah,

Please don't try to make this personal. We know that for some reason CAP "cured" you and many others (but certainly not everyone). However, we do not know why as it has not been proven that cpn causes MS (or, for that matter, that hpa-axis dysregulation causes it). That leaves the various CAP protocols open to speculation and scrutiny.

By Vanderbuilt, I assume you are referring to the Stratton protocol which is outlined on the CPn Help site. Doxycycline is a part of this protocol. I didn't follow Stratton. I did the Wheldon protocol so I don't really know much about people who have done Stratton w/o taking doxycycline. I imagine that doxy is not the only part of the protocol which influences the hpa axis.

There are many elements of the full Wheldon and Stratton protocols which work to push the hpa axis towards a proper balance. Vitamin D and magnesium supplements are among these (links somewhere in my wandering aldosterone thread in the CCSVI forum). NAC is also a major part of CAP for multiple protocols and it has been proven to attenuate some of the damage from a hyper-responsive hpa axis. http://www.sciencedirect.com/science/ar ... 4010644549

I have no doubt that DW's protocol does cure cpn. He was right. I have no doubt that his protocol "cured" you of MS. I only doubt the reason why your MS was cured. The medications and supplements in the plan affect far more than bacteria. There are people suffering greatly and struggling with the antibiotics because they think they will heal them. If the antibiotics "cure" MS for some reason other than the eradication of CPn, those people may have a path towards healing that is gentler. I think your brilliant DW could be the one to figure out what is really happening with CAP and MS.

My best to you both.

You all know I am the "resident insulin-believer;" I ask your tolerance and permission to jump in with more of my unconventional ideas.

Many different courses of action seem to improve individual cases of MS – antibiotics help some, but not all; diet and exercise help some, but not all; even the CRAB drugs seem to help some, but not all; etc.. But WHY? What is the common denominator?

Let me propose… wait for it… INSULIN, or more precisely the pancreas. Can there be a bacterium (maybe CPN, maybe the one causing tuberculosis – Dr. Denise Faustman has used the Bacillus Calmette-Guérin to increase insulin production, or perhaps yet another one) infecting the pancreas of some MSers, who then see improvement with antibiotics?

Diet and exercise might reduce insulin in some who have not developed intractable insulin resistance (as I seem to have).

In some cases, inflammation may be causing internal fat, which triggers cytokines, which lead to increased insulin. Anti-inflammatory diet, drugs, or even interferons may help in those cases.

I propose this route as a possibility for what is really happening. I am not a scientist, but sometimes I think WE ALL can have good ideas, too. I encourage ALL of us to continue searching in our particular areas of interest!

Anonymoose, I wasn't meaning to sound personal, but I was getting worked up about my malfunctioning printer: so sorry.

The current Vanderbilt protocol uses rifampicin and azithromycin. My experience of rifampicin is that there is no immunomodulation: I walked a lot worse when I started taking it. That passed when I became used to it but when people start straight off with it they often give up. I started it after six months but I don't know how I would have been with it had I started it straight away. It is the cause of most people's ill effects when taking abx before starting metro or tinidazole.

Sarah

No worries. A printer on the fritz would make the best of us grumpy.

I just found this.
http://aac.asm.org/content/44/6/1761.full

rifampin is a glucocorticoid receptor ligand with the ability to transactivate the receptor (6). Following this hypothesis, rifampin could act as an immunosuppressive agent, reactivating persistent infection and thus allowing azithromycin to act on replicating pathogens,

Couldn't rifampin, by plugging into the GRs, give the hippocampus a break from cortisol and a chance to resensitize to it?

Also, didn't DW do the protocol for high blood pressure? Aldosterone is a much targeted bad guy in the treatment of hypertension...

Especially a very expensive large format photo printer, not old but well out of guarantee period!

You might be right about rifampicin, especially for DW, but surely if something works as an immunosuppressive, it is anti-inflammatory but it wasn't with me, unless, of course, the fact that it suddenly made my walking worse was a sign that it was working better than the doxycycline which I had been taking. Perhaps that is the reason why I improved so quickly.

Sarah

I had one of those huge photo printers too. It was a temperamental beast...couldn't color calibrate the thing to save my life so it just sat there until I passed it off to hubby...who's just letting it sit there.

I don't really believe rifampin is immunosuppressive. That doesn't make any sense. Glucocorticoids are immunosuppressive. That's why they try to shoot us up with steroids when we relapse. I think the rifampin blocks the effect of endogenous glucocorticoids by docking in the GRs...maybe that's why it makes people so miserable.

Pubmed 11371760 wrote:The tropism of C. pneumoniae to the neural tissue suggests it may play a role in diverse neurologic diseases, including Alzheimer's disease, multiple sclerosis and giant-cell arteritis.

That's only one of many citations, but, to a small extent, you are right: there are a vast number of people that are infected with C. pneumoniae whom have not developed MS. They may develop altogether different kinds of diseases, either fulminant or forme fruste, including reactive arthritis, atherosclerosis and even asthma. That does not mean one can outright exclude C. pneumoniae's involvement with multiple sclerosis.

The very nature of the bacterium, and the disease it is capable of producing, especially after prolonged chronic infection, is almost impossible to study according to Koch's postulates, the standard for associating pathogen with disease: 1. culturing the pathogen from diseased individuals [accomplished, Sriram et al. 1999.]; 2. infecting healthy organism with said cultured bacterium and observing subsequent disease state [not likely to happen with C. pneumoniae, but Barry Marshall did it with H. pylori and gastric ulcers, e.g., simply because of how quickly gastric ulcers develop]; 3. observing similarities between original culture and newly-infected culture [again, unlikely to happen in an experiment].

This is precisely why DW writes the following:

David Wheldon wrote:An elucidation of the possible events which may happen in the course of persistent infective states with this organism will present one of the greatest challenges in medical microbiology in this century.

http://www.davidwheldon.co.uk/peer-review.html

Curious,

You may not have taken note of my use of the words "if" and "may" in my posts. They are there. I have not excluded CPn as a possible cause for MS.

Not everyone with MS has CPn. Based on the papers I have read, most if not all, PwMS have hpa-axis dysregulation and hippocampal atrophy early in the disease, as early as CIS. Many people who develop MS do so within a few years of a life event/situation that causes chronic high stress and excessive cortisol release which can atrophy the hippocampus leading to hpa-axis dysregulation...cortisol and aldosterone gone wild (along with a slew of other things the body releases in response).

I think it's worthwhile to investigate the effects CAP protocols have on this dysregulation. The coincidence that CAP "cures" MS and at least temporarily alters hpa axis activity is just too great to ignore. Why would you close your eyes to the possibility? I thought you were a curiousrobot.

I am always open to the possibility & this thread can be a perfect environment for stating your case for hpa-axis disregulation. However, citing anecdotal failure and making claims such as "not everyone with MS has Cpn" is far from enough to pique my curiosity.




;)

CuriousRobot wrote:I am always open to the possibility & this thread can be a perfect environment for stating your case for hpa-axis disregulation. However, citing anecdotal failure and making claims such as "not everyone with MS has Cpn" is far from enough to pique my curiosity.
;)

I don't even know how to politely respond to this except to say that you seem to be missing the gist of what I am saying whilst reading things that aren't there. If your curiosity hasn't been piqued, perhaps you should stop wasting your time reading this thread.

,,,,,,,,,,,,,

Lib, the medical community in the West would not take too seriously any trial conducted on C pn involving herbal drugs.

As far as I know there aren't any current trials, but there are people working in their laboratories to find an easier solution to get rid of what is a very problematic pathogen. Never mind the money, all these things take time. There have been trials in the United States to substantiate the theory, as have been listed on this forum, but you can't force people at knife point to take part and since trials are by and large for relapsing remitting people, there are plenty of easier things for them to try.

Sarah