A Paul Thibault study


This link should go to a 1 page description on a study by Dr. Paul Thibault (Australia's Vein Specialist), the Dr in the MSi Cure video. He used the CAPi treatment on MS patients to fight cpni and measures blood flow in the CCSVI model.


Paul Thibault's Current Position on CCSVI

From CCSVI / CCSVO specialist Dr Paul Thibault :

The concern I have is that people (medical doctors, patients, and the general public) will become disillusioned by the many studies (including Zamboni et al), which refute the use of venoplasty to achieve a "cure" for MSi<i<. Zamboni has highlighted the connection between MS and a chronic venous disease, which I appreciate. However, since 2011 I have suspected his theory that venous obstructions cause demyelinationi<i< (due to iron-deposition which accompanies vascular reflux) to be incorrect.

In a published pilot study<<, we showed that venoplasty appeared to improve cerebral perfusion and I feel this is the mechanism which explains why some pwMS experience symptomatic improvement following venoplasty. But this effect was short term in most, and only occurred in approximately 30% of those treated. We analysed 2 pilot studies in NSW, one at St Vincents Hospital and a later one at Prince of Wales Private Hospital. Both came to the conclusion that venoplasty was generally ineffective in improving the symptoms of pwMS in the long term. The major participants had no enthusiasm for publishing negative results from pilot studies, and no randomised placebo controlled trials were planned. We abandonded venoplasties for CCSVO (Chronic CerebroSpinal Venous Obstruction) in MS in 2012. At that stage, we had performed over 200 procedures. Never-the-less, the objective diagnostic ultrasound examination<< that we developed to diagnose obstructive venous disease in the neck veins (in contrast to the subjective Zamboni ultrasound) appeared to be accurate, reproducible and indicated that the venous obstructions were due to a chronic inflammatory venous condition that resulted in obstructions to both the internal jugular veins AND the vertebral veins. Interestingly, the vertebral veins have been largely ignored by Zamboni and others - perhaps because they can't be treated by venoplasty. After seeing David Wheldoni<i<'s website suggesting that a chronic persistent chlamydophila pneumonia infection was the likely cause of disease in a large sub-group of pwMS, I developed the theory that MS was due to a chronic infective cerebrospinal phlebitis and venulitis (published in Phlebology in 2012.)<<. From that time, we have treated pwMS with the combined antibiotic protocol developed by the Stratton group (Vanderbilt University, Nashville) and David Wheldon. My observations are that the results have been superior to venoplasty, particularly in RRMSi<i< with positive serologyi<i< to Cpni<, with relapses completely suppressed and only rare instances of new lesions developing on MRI examinations. Our 6-month follow-up with ultrasound flow measurements in the affected neck veins (published in Phlebology) shows significant improvements in those with positive serologyi<i< testing to chlamydophila pneumonia (Cpn) infection. This article also highlights the possibility that chronic persistent infection with Cpn is widespread in the community but only a small percentage go on to develop MS. Some other factor, such as a genetic or concurrent infection with an agent like EBVi<i<, is likely to be involved at a critical time early in life. Therefore CCSVI (O) is likely to be observed in many "normal" people who are included in randomised trials, which explains why so many studies have shown that the neck vein obstructions are observed in the "normal" population, but generally not at the rate found in pwMS. This is consistent with the epidemiology studies of the most famous MS neurologist, Prof John Kurtzke who concluded that MS was caused by an infection that was widespread through the community, but only a SMALL proportion went on the exhibit MS.

So why do some people have such a good result with venoplasty alone? I suspect that they have a "burnt-out" Cpn infection, that has been completely controlled by their immunei<i<system, but has left resultant venous obstructions that cause reduced cerebral perfusion. These people test negative to Cpn. This state will be improved by successful venoplasty. As for the other > 90% who have chronic persistent Cpn infection but don't have MS, they will be prone to other vascular and "auto-immune" disease including coronary artery disease, cerebro-vascular diseasei<i<, thyroid disease, CFSi<i<, polymyalgia, reactive arthritis, thrombo-embolic disease, rosaceai<i< and possibly lymphomas of the head and neck. PwMS have a high co-morbidity with these diseasesi<i<.

So this is why I have entered into this argument, as the only doctor in Australia with a real interest in investigating the association of MS with CCSVO. I will be presenting the evidence at the UIP 2018 meeting to be held in Melbourne in February in a special "Masterclass on CCSVO". There will also be a demonstration of our Objective Ultrasound Examination, which will show that this is a real entity that needs to be addressed. I apologise that this reply has been so long, but it is an extremely complex problem.

Dr Paul Thibault publications referenced:

1 – A Prolonged Antibiotic Protocol to Treat Persistent Chlamydophila Pneumoniae Infection Improves the Extracranial Venous Circulation in MS. 

2 - Objective duplex ultrasound evaluation of the extracranial circulation in multiple sclerosis patients undergoing venoplasty of internal jugular vein stenoses: A pilot study 

 3 - Multiple sclerosis: a chronic infective cerebrospinal venulitis? 


Doing Thibault protocol (NACi/minoi/roxi/tinii/nattokinase)...but considering morphing to Stratton protocol

Cpn treatment and effect on venous circulation in the neck

I have finally written up the results and conclusions of the study involving 91 MSi patients on a CAPi aimed at treating chronic persistent Cpni infection. This will be published in Phlebology shortly and should be available to read from my website: www.cosmeticcentre.com.au<. The contents are consistent with what I have described previously in this discussion with a few added insights. We are currently starting phase 2 of our research, which is targetting diagnostic reliability of our methods (this may be a bit boring for the MS sufferers but is important for our scientific credibility) which is crucial to have the venous Cpn infective theory accepted.

The direct link

The direct link: http://cosmeticcentre.com.au/client_images/1905173.pdf

Thanks for all you do Dr Thibault


Doing Thibault protocol (NACi/minoi/roxi/tinii/nattokinase)...but considering morphing to Stratton protocol

"burnt out" and other factors

Hi Dr Thibault,

if you're still frequenting this page, I'd like to know what you mean when you say CPni could be "burnt out" in some patients? Does that mean it's all contained inside their macrophages in Cryptic Body state...or something else? You also mention there is likely another factor involved in MSi (in addition to CPn/CCSVI)? I reckon it's likely it's something to do with iron homeostasis....perhaps the infection exploits an underlying genetic weakness such as these polymorphisms:


Or even an underlying genetic porphyriai?


Doing Thibault protocol (NACi/minoi/roxi/tinii/nattokinase)...but considering morphing to Stratton protocol

Burnt out

My concept of "burnt out" means that the Cpni infection is no longer active, although it may have caused considerable long-term effects due to tissue damage (scarring) which will not respond to Abxi treatment. It may respond to interventional procedures such as venoplasty but these will be in the minority of cases. So the primary aim is to achieve a state where the Cpn is inactive.

Symptomatic improvements on the CAP

My overall informal assessment of trends in symptomatic response to the CAPi in this group of 91 MSers is positive. As would be expected the best symptomatic improvements are seen in early disease and the great majority of so-called relapsing remitting subjects no longer have relapses.with many of their symptoms such as fatigue and heat intolerance subsiding. Some who required walking aids for mobility have been able to do away with the aids.  Most will show no further activity on their MRIs. Progressive types are more problematical. Many observe a definite deterioration in their mobility when they start the CAP and this may not improve even though they may show evidence of improvements in blood flow. You may note from the results that the the primary progressive types have the greatest improvement although the difference from the RR types was not statistically significant. Those that present in wheelchairs do not get any restoration of their mobility, and I do question the suitability of this group to enter this therapeutic program. Having said that, I did observe one of these wheelchair bound subjects, able to lift her arms above her head after 6 months which she wasn't able to do before hand, but eventually she withdrew from the CAP after 2 years. I certainly believe that the CAP should be offered to all MSers with early, RM disease, as this appears to be the time to stop MS in its tracks, and obtain complete recovery from the early symptoms and signs. With the progressive types, we aim to stop further progression, and in general this is achievable. However, this group are often disappointed that significant improvements in mobility are not achieved (which is explained prior to starting), and are more likely to drop out of the program, as it is this symptom that defines their condition.

The complementary Diet helps fatigue

Ive been on this treatment and regard it as successful. I want to point out that the fatigue went away after going on the recommended diet of 70% carbohydrates, before the antibioti treatment had progressed very far. This indicates to me that the fatigue is caused by the porphyriai. I was already on the Swank diet, but had to adjust it to reduce the protein I was consuming (all low saturated fat protein such as fish, beans and tofu). I was not able to implement the diet successfully without assistance. I got it wrong for quite some time before I had a dietitian draw up a diet for me that was 70% carbohydrate but balanced. I got my energy back within a week on the professionalply monitored diet. if you've got enough know-how and energy, you could build your own diet using an online app which tells you the protein/fat/carb composition of foods. 


Doing Thibault protocol (NACi/minoi/roxi/tinii/nattokinase)...but considering morphing to Stratton protocol

My own experience of treating

My own experience of treating people with MSi using antibioticsi is that relapsing-remitting illness is usually very amenable to treatment. I have had patients who have not had a relapse in ten years. Early secondary progressive disease generally responds to treatment, though the response may be slow. Some SP people continue to gain improvements years after treatment has been stopped. Clonusi and extensor plantar reflexes can slowly fade away. Late progressive disease tends to be less responsive. I have seen some good results in patients confined to wheelchairs though; one 40 year old woman responded very well; she had been a very athletic person in health (a county-class tennis player) and developed SP disease and had been confined to a wheelchair for two years. Now, 11 years after treatment was begun, she is able to walk a couple of kilometres and play a little mild badminton. I suspect her athleticism aided her recovery.

I am not a neurologist, but I studied neuropathology at the Radcliffe Infirmary, Oxford. My teacher was David Oppenheimer, the doyen of his specialty. One of the characteristics of MS is the immense variation in the placement of the lesions. I suspect that this variation determines not only the course of the disease but the response to treatment. If the lesions are predominantly in the brain then there is often great improvement due to the ability of undamaged areas of cerebral cortex to take over the function of areas whose axons are compromised; this is called ‘cortical plasticity’. Cord and midbrain lesions seem to be more problematic, but even so I have seen improvements in people  with very aggressive extensor plantar responses indicating damage to the corticospinal tract.

David Wheldoni<


I think it prudent to advise patients not to have too much expectation. Any improvement is a bonus.

D W - [Myalgia and hypertension">i (typically 155/95.) Began (2003) taking doxycycline and macrolide and later adding metronidazolei. No medication now. Morning BP typically 110/75]

Hi Doctor,To me, halting

Hi Doctor,

To me, halting Rick's MSi is very encouraging, and more than we could have hoped for 18 months ago.  I appreciate your comments about both folks with SPMSi who have improved and the points you made about brain vs. spinal chord lesions.  Per Rick - he has a fair number or large in extent lesions in his spinal chord.

There is one thing that I want to mention in this context.  That is that the results for Biotin - phase I or II I don't recall, are very encouraging for folks with spinal chord lesions.


and - a very salient extract - is this:

Sixteen patients out of 18 (89%) with prominent spinal cord involvement were considered as improved as confirmed by blinded review of videotaped clinical examination in 9 cases. In all cases, improvement was delayed from 2 to 8 months following treatments onset.

My take is that Rick should be patient and "steady as she goes" with his current course of treatment.  My concern is that he may be unduly influenced by his eagerness to get better and a no doubt very fine Neurologist with nothing but good intentions, but who may be inclined to recommend a course of treatment that could actually be a set back for Rick!

The good news is that Rick is very thoughtful and thorough, and is open to talking about the subject.  Plus his current stated plan is to have another MRI and see if there are "objective" signs of improvement visible there.  If that turns out to be the case - - he will not undertake a course of treatment that might include signficant and negative potential side-effects.  In other words - no Tysabri, no Lemtrada - no HSCT.  He will still likely want to get involved in a trial for a medicine that might help with remyelinationi (lingo 1 or II, biotin, clemastine - which he is already on, etc.).

Best & Highest Regards,

Tom C


Proud Parent of Rick - R started CAPi in Nov. 13. Small measurable improvements as of 7/14, more by 10/14.  Holding Steady in early 2017.  "I will leave no stone unturned, no theory unexamined, to help my son." Tommi

Thank you.We now have some

Thank you.

We now have some idea of reasonable expectations for Rick - who by the time he started this protocol, was wheelchair bound.  He has indeed experienced a bit more deterioration as noted above while on CAPi

Perhaps it just takes longer on CAP to first halt then reverse the disease.  Perhaps it will take yet another therapy to repair what damage can be repaired.

Folks here have wondered again and again, me and Rick included, what might be reasonable to expect from this treatment, and how long it might take.  There has really been mostly anecdotal information available here until now.

To complete the above thought about "anecdotal" information - what I've gleaned is that there are cases where "initial glimmers" only showed up after 3 years of treatment, but that some of those folks did get substantial improvements after many more years.  I've also read that there is at least one case where all that seems to have happened was that they halted the progress (note that I don't mean to diminish "halting the progress" with that phrase, that's huge in and of itself). 

I think it's important for folks to get some kind of a sense of what to expect - how long it might take - etc.  We have a lot of very encouraging and supportive folks here - with their own stories, but what's been lacking is specific information about the expected "prognosis" - how long to stay on the protocol, when and what to expect in the way of improvements, etc. I believe there are folks here who are still on a CAP protocol - after as many as 8 years.  I believe it's very possible in those cases that the germ has long been obliterated, and that a CAP protocol continued for that long may not actually be beneficial.  I don't know of course...

Doctor, your comments above at least start to provide that in more tangible form - thank you!

Your information rises above anecdotal, and while some of it is dissapointing (your comments about folks who present wheelchair bound are to me and will be to Rick) at the least it provides more insight into what a specific individual might expect.

Damn it.  I wish I had found out about CAP 6 years ago...

I'm concerned Dr. - you made a comment about wheelchair bound folks:

"Those that present in wheelchairs do not get any restoration of their mobility, and I do question the suitability of this group to enter this therapeutic program."

Given Rick is currently on his CAP protocol, and appears to be deteriorating a bit (something we expected, possibly due to the die-off reaction or herx, but expected to change after a bit too) - is there any reason to believe that CAP itself is potentially harming him in some way, and that the horse itself (the active cpni infection) is long gone, and therefore there may be no reason for Rick to continue his CAP treatment? 

He has appeared to have less or no relapses on his CAP, and certainly he has not had a major relapse.  Might the minocycline be in some way robbing energy from his mitochondria (as it's been reported to do elsewhere)?

I'm very reluctant to have him consider going off of his CAP protocol, but would appreciate your thoughts on the matter.

Best & Highest Regards,

Tom C

Proud Parent of Rick - R started CAPi in Nov. 13. Small measurable improvements as of 7/14, more by 10/14.  Holding Steady in early 2017.  "I will leave no stone unturned, no theory unexamined, to help my son." Tommi

in severely immobile

in severely immobile patients, I try to determine the current activity of Cpni. I suspect that in some, it is "burnt out" and CAPi treatment is unlikely to have any effect at all (good or bad). I depend largely on Cpn serologyi results, particularly IgAi levels, and blood flow abnormalities in the extra cranial duplex ultrasound examination that I have described elsewhere. Anyone with IgA antibodies, I strongly advise to go onto the CAP for at least 2 years. If there are definite obstructions in the ECVs I advise the CAP for an initial period of 6 months with re-evaluation after that time. It may be of interest to those non-MSi Cpn sufferers that I have found extra cranial vein obstructions in other conditions including rosaceai and CFSi. The pattern is the same as in MS. Therefore I suspect that there is some other factor present that turns the venous vasculitisi that is a signature of chronic Cpn, into MS. This is consistent with the observations of Kurtzke, who predicted that only a small proportion of those infected go on to develop MS. The other factor may be a co-infection such as EBVi occurring at a susceptible time that allows breakdown of the BBBi.

Hi Doctor,Thank you for

Hi Doctor,

Thank you for writing - and thank you for having whatever it takes to be involved in and sponsor a clinical trial for CPNi / CAPi and MSi

Rick's Doctor who is treating him with a CAP protocol - did run several tests for CPN - I don't recall all the specifics, but he concluded Rick should be treated for CPN.  And - it does appear at least to me - that his CAP protocol has at the least started to stabilize his disease.  He's had no further major relapses in a bit over a year - and has been on his protocol about 18 months.

Rick's protocol is minocycline, azithromycin and rifampin.  No pulsing with tinii or metroi.  His protocol also includes a number of targeted supplementsi and chelation (he hasn't done much of that with IMD or whatever it is). 

I believe we are on the right track - given his apparent stabilization relapse wise.  It is possible he's transitioned from RRMSi with active relapses to SPMSi - with no more relapses but steady slow deterioration too - I understand that is one course that SPMS can take.

It's time we had a published clinical trial - as you are involved in - for CAP and CPN.  I'm curious about how you got any funding for that given most or all of the drugs are off-patent and therefore the big pharma companies might not have an interest in funding a trial.

Best & Highest Regards,

Tom C

Proud Parent of Rick - R started CAPi in Nov. 13. Small measurable improvements as of 7/14, more by 10/14.  Holding Steady in early 2017.  "I will leave no stone unturned, no theory unexamined, to help my son." Tommi

Funding for further clinical trial

Hi Tom

Up to this time, I have funded all my clinical research personally. Fortunately, due to the benevalence of several contributors to this website, I can now go on and investigate the role of Cpni in MSi to the next level. I am not interested in receiving funding from any pharmaceutical companies, as this can only distort the final outcome of such research.

Wow!To both yourself and the


To both yourself and the benevalent contributors from this website!  I'd join in on that but Rick's care has been very expensive, and any contribution I could reasonably make would be laughingly small. 

My Hat's off to you and the folks who have contributed!

Best & Highest Regards,

Tom C

Proud Parent of Rick - R started CAPi in Nov. 13. Small measurable improvements as of 7/14, more by 10/14.  Holding Steady in early 2017.  "I will leave no stone unturned, no theory unexamined, to help my son." Tommi

Very interesting....Thank you

Very interesting....

Thank you so much ..



The Greatest Risk of all is Not taking the Risk...

To make sure

that cpni is gone , I was tested four times by LTT test.  The progression stopped, since 4 years I have no signs of inflammationi. What finally  helped me , is Stephen Buhners herbal antibioticsi, because they stimulated my immunei function, which is important to get rid of any infection.

Being on CAPi my immune function was reduced.

I´m glad that I´m not scared anymore to become more disabled every year.

I´m still wheel-chair bound and working on it , but I feel good . My hopes to get out of the wheel- chair, well ...


 Wheldon CAPi May 2008,   52  Tinii pulses - stopped Nov.2013- Buhner´s protocol Dec. 2013 till  June 2014 - cpni free Oct. 2014

Awesome, Sphinx...I am

Awesome, Sphinx...

I am convinced that CAPi is the right thing for Rick - afterall his relapses have virtually stopped, after 8 years with 2-4 major relapses a year - the last year Rick may have had a minor relapse - minor enough that he's not even sure.

I've long told him that first we need to stop this nasty disease, then figure out how to improve things.  He's pretty impatient, and is exploring options like getting involved in a clinical trial of drugs that are supposed to help with remyelinationi.  I hope he has the patience and the personal werewithal to resist being persuaded to try something like Tysabri or Lemtrada.  I think he should stay on his current treatment and give it time.

I'm curious, you mentioned herbal antibioticsi.  Did you do those while you were on a CAP protocol - as an addition, or did you stop CAP then start the herbal antibiotics?

Best & Highest Regards,

Tom C

Proud Parent of Rick - R started CAPi in Nov. 13. Small measurable improvements as of 7/14, more by 10/14.  Holding Steady in early 2017.  "I will leave no stone unturned, no theory unexamined, to help my son." Tommi

The CAP and other therapies

I agree that the CAPi is not the total solution to chronic Cpni infection. Diet and selected supplementsi are important. One has to have a total understanding of how Cpn operates and this is well covered by this website. However I suspect that the judicious use of the CAP in most affected people will be of benefit, and will augment any valid natural measures. I do favour natural therapies that have valid scientific basis to their efficacy.

Hi Paul,In your opinion what

Hi Paul,

In your opinion what natural therapies with scientific basis did you find effective... and what supplementsi?

Kind Regards


The Greatest Risk of all is Not taking the Risk...

Supplements and diets

These are my practical observations, which are evolving. 

Vitamin B12 injections given weekly appears to be of benefit early.

Vitamin Di supplementsi are advised due to the uniformly low levels that are found on initial presentation. But don't expect any short-term response.

Low iron diet, which means no red meat in order to suppress Cpni<

Minimal dairy

Broad spectrum anti-oxidant ( I recommend a concentrated fruit and vegetable extract)

low fat, low sugar diet.

I think that's enough for most people to take on initially.

Update on supplements

Following positive scientific reports in the medical literature, I now recommend Resveratrol (the active anti-oxidant in red wine) 250mg -300mg twice daily in patients diagnosed with chronic persistent Cpni infection. Resveratrol inhibits Cpn. Its early days, but I have seen some good responses to this so far. I therefore now include a specific question to my Cpn patients "Do you drink red wine?". Interestingly, the majority say no. The other supplement that I have an interest in at the moment is curcumin which also inhibits Cpn. I understand that it is not aborbed well orally. There is a transdermal product available in Austalia that contains Vitamin B12, Vitamin Di and tetrahydrocurcumin (THC). There is another product with just THC at a higher concentration. The theory behind this is that it is absorbed transdermally and will be taken up by the lymphatic system, exactly what we want. It can be massaged into the neck (good for those with neck symptoms) or applied to various dermatological manifestations of Cpn.

Alcohol and porphyria

Red wine definitely cranks my immunei system up. I'm loving it now the porphyriai has subside - a great way to ward off a looming cold/flu. dr Thibault, I was highly alcohol-sensitive for years before i was diagnosed with MSi. this alcohol sensitivity may be due to the porphyria, and the reason why many with MS avoid alcohol!


Doing Thibault protocol (NACi/minoi/roxi/tinii/nattokinase)...but considering morphing to Stratton protocol

With curcumin, it's not just

With curcumin, it's not just that it's not absorbed well, it's also that when it does get absorbed the half-life is about five minutes.  Oh, and also that the stuff is quite reactive, a nasty toxin, and the body shows excellent wisdom in not absorbing it.  It attacks a wide variety of proteins.  It disrupts cell membranes.  It has frequently been reported as killing cancer cells, but according to a recent review,

Surprisingly, data on the cytotoxicity of [curcumin] against normal (noncancerous) cell lines are sparse. A recent report demonstrated cytotoxicity of [curcumin] against a murine macrophage cell line and human kidney cells at IC50 values of 31 and 15.2 μM, respectively. These values are at or below those reported for several therapeutic targets or cell lines [...] suggesting that [curcumin] might be generally cytotoxic and does not show a preference for normal versus cancerous cells.

That's from the article referenced here:


curcumin vs tetra hydra curcumin

Norm, you are totally correct about the curcumin. It has a short half life! The tetra hydra curcumin (which we have been using calling it curcumin) is highly soluble. It is the biologically active anti-inflammatory version in the body. Using it transdermally overcomes any issues with poor gut absorption. In addition you can apply it directly to the site where you want the anti-inflammatory effect. In comparative anti-inflammatory trials in small animals it was better and less toxic that NSAIDsi. Some references for you below,

Osawa, T. et al. (1995) Antioxidative activity of the Tetrahydrocurcuminoids. Biosci. Biotechnol. Biochem. 59(9): 1609-12.

Sugiyama, Y. (1996) Involvement of the beta-diketone moiety in the antioxidative mechanism of Tetrahydrocurcumin. Biochem Pharmacol, 52(4):519-25 Aug 23

Nakamura, Y. et al. (1998) Inhibitory effects of curcumin and Tetrahydrocurcuminoids on thetumor- promoter-induced reactive oxygen species generation in leukocytes, in vitro and in vivo. Jpn JCancer Res, 89(4):361-70

Hope that alleviates any confusion!

Curcumin is really good at

Curcumin is really good at messing up vitro assays like those.  (There's one in vivo assay in the last of those linked papers, but even it has a biochemical endpoint.)  I'm not a biochemical wizard, so I'm not going to try to look at the particulars of those studies and guess how exactly it might have short-circuited their measurements, but as Derek Lowe put it in the blog post I linked to earlier:

"...curcumin participates in pretty much every undesirable behavior possible in an assay: it reacts with proteins, it’s a redox cycler, it coordinates metal ions, it aggregates, it disrupts membranes nonspecifically, it interferes with fluorescent readouts, and it decomposes."

(In case it isn't clear, the idea here is that biochemical assays are complicated, and rely on the chemical being measured not doing things like directly making a fluorescent molecule glow.)

By the way, how is it supposedly getting through the skin?  Diffusion through skin is slow.  Applying things to the skin is normally about the least effective way of getting them into the body.  (Of course if the skin is actually the target organ, that can be fine.)  Maybe if you add lots of DMSO, though?

Norm, I think you are

Norm, I think you are skeptical about skin absorption. There seems to be a huge market out there in testosterone patches, nicotine patches, scopolamine patches, and then there are all the topical SNAIDs that are on the market. THC is oil soluble - they put it with a carrier (the carrier ingerdients are patented & I am not privy to that) however i know it is not DMSO. There is a lady in the UK adding DMSO to everything i think. 

When i put the THC oil on i get a herx. Somewhere somehow the stuff is getting through the skin. Irrespective of how curcumin behaves in an assay there are quite a few of us now who have herxes from it. We have found quite a few other benefits as well. The inventor in australia has just finished clinical trials with the transdermal B12. it might be another year though before we get some "good scientific numbers". the wheels turn slowly! My B12 levels have also increased on the transdermal B12. 

I hope that helps


If it's patented, the patent

If it's patented, the patent should say how it's supposed to work.  (One of the selling points of patents is that they provide public disclosure, so that companies don't have to keep things as trade secrets.)  Is there a patent number printed on your bottle?

Anyway, it's not that things can't get through the skin, it's that it takes time -- that's the idea with the sorts of patches you list: to slow down absorption -- and for a highly-reactive molecule with a half-life of five minutes, it's rather hard to see how a slow absorption could result in any of it actually getting through.  That you get a reaction doesn't necessarily mean it's the curcumin that is getting through; it might be some other part of the mixture.

For that matter, just because it makes you feel sick doesn't mean it's a Herxheimer reaction; there are lots of ways of feeling sick besides killing pathogens.

I am pretty sure it's die off

I am pretty sure the  thyme essential oil I have used causes a genuine die off reaction 

I say that because it's a similar response when I go on a Flagyli pulse 

Tinctures are well absorbed too 

DAILY:  NACi 2400MG , DHEAi sublingual , vit D3 , multi vits,./ Three times  a week: B12 injections (Hydroxycobalamin). Deer antler./  Once every few months methyl B12 Methyl injections

Essential Oil on the skin created a significant Herx

When I use a Cpni killing essential oil  rubbed into my skin I get a pretty good herx 

DAILY:  NACi 2400MG , DHEAi sublingual , vit D3 , multi vits,./ Three times  a week: B12 injections (Hydroxycobalamin). Deer antler./  Once every few months methyl B12 Methyl injections

Interesting article on

Interesting article on pubmed 




The Greatest Risk of all is Not taking the Risk...

That's a paper by Bharat

That's a paper by Bharat Aggarwal, the honesty of whose research has come under great question recently, with the result that many of his papers have been retracted.


Turmeric has that problem but

Turmeric has that problem but consuming natural fats like coconut, avocado, almond or black pepper will help a lot in its absorption. Turmeric and black pepper work the best in my opinion. Black pepper enhances turmeric’s bioavailability. I use a product from source naturals with black pepper added.



The Greatest Risk of all is Not taking the Risk...

Thanks, Paul!

Thanks, Paul!

The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi

Curcumin Vitamin B12 Vitamin D transdermal product

It is the combined Vit B12, Vit D, curcumin combination that clinically seems to have benefit. So I have no idea what ingredient is important. But I feel that transdermal application so that the active ingredient is absorbed directly into the lymphatic system in the region affected is essential. Oral ingestion of these substances is less likely to be effective.

Thanks Paul for your

Thanks Paul for your observations and comment..

Kind Regards


The Greatest Risk of all is Not taking the Risk...

Be careful when mixing herbs

Be careful when mixing herbs and antibioticsi... Remember some herbs have similar actions and reactions like antibiotics.... 



The Greatest Risk of all is Not taking the Risk...

Hi Darren,Thank you for your

Hi Darren,

Thank you for your cautionary note.  Rick doesn't make changes or additions to his regime without a lot of thought - he doesn't rush in and try something on a whim.

Best & Highest Regards,

Tom C

Proud Parent of Rick - R started CAPi in Nov. 13. Small measurable improvements as of 7/14, more by 10/14.  Holding Steady in early 2017.  "I will leave no stone unturned, no theory unexamined, to help my son." Tommi

I stopped CAP

, you can see it under my signature, then switched to Buhner`s protocol.

As I understood Stephen Buhner, you can take both in addition.

Have you seen the protocol? I posted it here some time ago.And you are lucky to get his herbs without the problems European people have.

I can understand Rick, being impatient, but it means to me , he has hope to change things.

Hope kept me going and still does, you never know what might be possible.


 Wheldon CAPi May 2008,   52  Tinii pulses - stopped Nov.2013- Buhner´s protocol Dec. 2013 till  June 2014 - cpni free Oct. 2014

Hope is vitally

Hope is vitally important...

And, with no new relapses in a year - Rick now has a lot more confidence in his future.  He's also impatient, but very thoughtful too.  He has a new neurologist - who MAY agree or suggest he try Tysabri - with very close monitoring (every 3 week) for the JC virus.  I'm hoping that either the Neurologist does not agree to that, or that Rick doesn't agree if he's offered the chance.  Rick does have that virus evidently.

I like his current plan - and it may well be an adequate plan to keep him from making a rash decision.  He plans to get an MRI and have it compared with his last MRI to see if there is any sign of stabilization or improvement.  My concerns about that milestone are centered around how accurate a comparison might be made, who does tha analysis - and are they both competent and un-biased, and if the MRI will actually show any improvement yet as it's only been 16 months.

It is wonderul to see him have no relapses - or none that he can be certain of - in a full year.  That has raised his HOPE considerably.

Best & Highest Regards,

Tom C

Proud Parent of Rick - R started CAPi in Nov. 13. Small measurable improvements as of 7/14, more by 10/14.  Holding Steady in early 2017.  "I will leave no stone unturned, no theory unexamined, to help my son." Tommi

Isn't this the same study

Isn't this the same study Marco posted here last year?


The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi

Similar but different

Similar but different numbers: he is probably using it as a work in progress, putting it on a cloud site so people can see it, but it isn't on pub-med yet......................Sarah

Completed Stratton/Wheldon regime for aggressive secondary progressive MSi in June 2007, after four years, three of which intermittent.   Still improving bit by bit and no relapses since finishing treatment.

Study progressing

when study presented at earlier conference it involved fewer subjects



Doing Thibault protocol (NACi/minoi/roxi/tinii/nattokinase)...but considering morphing to Stratton protocol

Thanks, Sarah.  The beginning

Thanks, Sarah.  The beginning verbiage is identical and I remembered reading it months ago. We have people on the site who are his patients; perhaps they can get us some ongoing information, as this progresses.

The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi

Very interesting indeed.

Very interesting indeed. Where did you find it?

D W - [Myalgia and hypertension">i (typically 155/95.) Began (2003) taking doxycycline and macrolide and later adding metronidazolei. No medication now. Morning BP typically 110/75]

Presented at conference

Was presented at a recent conference. Full paper not published yet.



Doing Thibault protocol (NACi/minoi/roxi/tinii/nattokinase)...but considering morphing to Stratton protocol


It showed up on a CCSVI Austrailian facebook link. Before cpni I looked into CCSVI and had that treatment done, so a while back I had collected CCSVI friends. On facebook I get to review CCSVI articles all the time. This one combined cpn subject with ccsvi and thought it interesting.

7th mo on CAPi. NACi 2400, doxyi 200mg, azith 250mwf, pulse met 500, chorella 1600

Effect of CAP on neck vein blood flows

I have closed this study at 91 patients. I plan to submit it for publishing in the next few months. My last study describing the quantitative ultrasound examination of the blood flows in the neck veins  took approximately 2 years to appear in print. So you will need to be patient. The present study has impressed the local neurologist in charge of the MSi clinic enough to offer co-operation in future studies, initially to verify correlation between the ultrasound findings and MRI venography. This would then lead on to randomised control trials using the CAPi. We will see!

That's good news.  I hope the

That's good news.  I hope the full writeup will include some indications of how the patients are doing in terms of symptoms and disabilities, not just blood flow measurements.

CAP in MS study.

This is Phase 1 of our pathway to investigate the benefits of a CAPi in MSi. Unfortunately this study didn't examine symptoms and disabilities. Those were beyond its capabilities as I am a vascular doctor without the necessary skills and knowledge in neurological disease to be able to accurately provide the data you would require. That will be included in the randomised control trial we plan to do as Phase 3 of this investigation in co-operation with the neurologists. We need significant funding for that trial and it isn't easy to obtain. Phase 2 is to confirm correlation between my ultrasound protocol and MRI venography. Then we aim to proceed to Phase 3. which will include  progress disability scores and MRI for disease activity. There are still many hurdles to overcome.

Well, those sorts of results

Well, those sorts of results would be interesting to see.  When I looked at Zamboni's ultrasound measurements, they seemed a bit murky -- as in "well, maybe you have something here, and maybe you don't".  Transcranial ultrasound is inherently difficult, with the reflections and such that you get from the skull, so checking the results against MRI seems quite appropriate.

Still, symptoms and disabilities are what people really care about.  Patients here often make guesses at their own EDSSi values, and the concept doesn't seem difficult to apply, but I suppose to make a formal publication-quality assessment one needs to be a member of the neurologists' guild.  Of course there's an upside to this: if you're not going to publish that sort of data on this group of patients, there's nothing stopping you from telling us your informal assessment here (with appropriate caveats about it being purely informal, preliminary, and so forth).