thoughts on cryptic bodies: is there evidence for two classes? And have they different properties?

D W

There has been quite a bit of discussion on new strategies of treatment. I thought I should add my two pence.

There are a few conjectures which I would be very pleased to be able to air. I can hear William of Occam in the background, honing that famous razor of his.
Here are my assertions:

a) The naturally occurring Cryptic (NOC) form occurs when chronic host stressors are applied to the Reticulate form.

b) In the NOC, bacterial protein synthesis is not inhibited. Heat Shock Protein genes are upregulated. Excess HSPs are made. HSPs are highly irritant, molecular mimics. This is why the NOC is dangerous. It is certainly not inert.

c) The antibiotic-induced Cryptic (AIC) form occurs when protein-synthesis inhibitors (tetracyclines, macrolides and rifampicin or rifamycins) are given.

d) The AIC is an abnormal form which has a limited ability to produce HSPs. Heavily infected host cells may therefore regain the capacity to undergo systematic cell-death via the caspase route. (This may account for the unpleasant die-off reactions some people get with antibiotics usually considered bacteriostatic.)

e) The AIC will have a limited ability to form actin filaments which steers the endosome away from host lysosomes. The AIC is likely to become depleted over months of bacteriostatic treatment even in host cells which do not undergo apoptosis.

f) NOCs do not seem to be susceptible to Nitroimidazoles. You can give Metronidazole to someone with an obvious large Cpn load, and they get no die-off reaction.

g) AICs are highly susceptible to Nitroimidazoles, in that die off reactions are often severe.

Summarizing, I would say that the evidence points to there being two classes of Cryptic Body. These two classes are radically different. I agree that HSP overproduction plays a huge role in the natural chronic infection with Cpn, but I would find it hard to believe that it becomes more important when treatment is begun. I daresay that pyruvate may well be able to convert the NOC back into the RB form, but I doubt if it could convert the AIC form back into a RB form. The AIC form should be well and truly stalled.

DW:] There, William. I rest my case. Have I multiplied entities without need, or does it escape your razor?

W of O:] Tu me defendas calamo; ego te defendam novaculo!
(Defend me with your pen; I'll defend you with my razor!)

DW:] I knew I could rely on you! I'll buy you a beer this evening!

Interesting-thanks a lot for this! It would mean that on the regular protocol would never kill naturally occurring Cryptic (NOC)? As flagyl has no effect on it...
doxy200, azith250, NAC 2400, Metro 1250(once a month), supplements, vitamins.

David- Thanks for presenting your thinking on this. I've been just trying to keep up with Dr. Stratton on phone discussions, plus the reams of papers he sends me to review, and I don't know the nuances of the different bacterial forms. Have you talked to him about your schema? It seems ripe for being fairly easily tested in the new Chlamydia lab.

I have some, admittedly less educated thoughts and questions about the schema you present.

What evidence are you drawing from in making the division between NOC's and AIC's? I've not seen anything that makes this distinction before.

"In the NOC, bacterial protein synthesis is not inhibited." It would seem to me that the presence of concentrations of antibiotics would inhibit the particular protein synthesis those antibiotics affect in any cryptic form exposed to it. As well, in my understanding at least, protein synthase inhibition is fairly specific for particular proteins, so the inhibition of replicating proteins would not necessarily inhibit HSP60. HSP60 seems a widely conserved bacterial stress response, and either antibiotics or natural antibacterials (tnf-alpha) can induce it, as can starvation, etc..

Point "e" is interesting, as it might help explain the unexpected waves of die-off when nothing else seems to have changed in the protocol, months into the treatment process. 

Again, I'm not sure (point f) where the assertion that NOC's, if there are such things, are not susceptible to Nitroimidazoles. Yes, you can give someone with Cpn doses of flagyl and have little reaction, but that may just mean that they have at that point little cryptic load. For example, if their immune system is suppressed, or they are Vitamin D deficient, etc., they may not be putting out enough endogenous antibiotics to cause much cryptic formation. It's only when they start taking exogenous antibiotics that enough threat is created to generate a larger cryptic load. Occam's razor means that alternative explanations could suffice, yes?

"I daresay that pyruvate may well be able to convert the NOC back into the RB form, but I doubt if it could convert the AIC form back into a RB form."- The "test," at least clinically, would be taking people already using the CAP antibiotics (protein synthase inhibitors) who have fairly predictable reactions to Nitroimidazole pulses, and starting them on the pyruvate regimen for a number of months without use of Nitroimidazoles. On re-initiating the Nitroimidazole pulse one would expect a lessor reaction to the pulse than had been so previously.

Obviously, there is some subjectivity to this, but this is a personal experiment anyone on the CAP could try. Most of us on this for 6 pulses or more have a pretty good idea of what kind of reactions they have on average. It would only take a couple of pulses to get an "after pyruvate intensity of reaction average."

The other clinical observation would be that starting antibiotic naive subjects on pyruvate + antibiotics might encourage NOC's to convert to RB's where they can be killed in your schema, but it would not prevent the formation of AIC's. Therefore, you would expect the addition of Nitroimidazole pulses somewhere down the line would be just as severe as it always has been for starters. According to Dr. Stratton's reports this has not been the case. He has seen elders who he would have said could not tolerate CAP treatment treated with few reactions and significant improvements in health, with little reaction to flagyl when it has been tried. Again this is all provisional, but argues against the division you present.

More importantly, I have missed your posts here and your erudite discursive style, and our spirited and free-wheeling discussions! I always learn a tremendous amount from your speculations and from your kindly responses to my non-professional thoughts on a subject. I'll summon a virtual beer for our next round of discussion. May I some day join you in your local pub for a pint and a chat!

CAP for Cpn 11/04. Dx: 25yrs CFS & FMS. Protocol: 200mg Doxy, 300mg Roxithromycin, Tini 1000mg/day pulses; Vit D1000 units, Iodoral 50mg, T4 & T3

 

CAP for Cpn 11/04. Dx: 25+yrs CFS & FMS. Currently: 250 aithromycin mwf, doxycycline 100mg BID, restarted Tini pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

Red

Hi Jim,

Can't comment on this much, but here's a review article that seems to divide the cryptic form into three categories: "Antibiotic-induced persistence", "Deficiency-induced persistence" and "Cytokine-induced persistence":

Chlamydial Persistence: beyond the Biphasic Paradigm

The article unfortunately discusses multiple species, but some key points:

  • Antibiotic-induced persistence:
    •  "exposure of C. pneumoniae AR-39 infections in HeLa cells to 50 µg of ampicillin/ml led to the development of aberrant, giant RB (122). Interestingly, when directly compared to C. trachomatis infections subjected to the same conditions, the persistent C. pneumoniae infections were extremely inefficient in reactivation after the removal of ampicillin (122). The explanation for this result is unclear at present, since observations of C. pneumoniae exposed to gamma interferon (IFN-Image removed.) or deprived of tryptophan (72) (see below) argue against slow recovery from persistence as a distinguishing feature of this species"
  • Deficiency-induced persistence:
    • "In contrast to persistence induced by antibiotics, the depletion of essential nutrients from cell culture medium temporarily arrests the growth of both chlamydiae and their host cells until the missing nutrients are replaced (78)."
    • "Exposure of C. trachomatis serovar E-infected polarized endometrial epithelial (HEC-1B) cells to 100 µM concentrations of the iron chelator deferoxamine mesylate (DAM) inhibited infectivity and caused significant morphological changes in the chlamydiae that were generally distinct from those observed in other persistence systems (95) (Table 1). The persistence of C. pneumoniae TW-183 in HEp-2 cells was similarly induced by exposure to 30 µM DAM and maintained for as long as 6 days, although not all of the morphological features described for the C. trachomatis cultures were observed (3)."
  • Cytokine-induced persistence:
    • " Persistent chlamydial infections are induced by exposing cultures to moderate IFN-Image removed. levels, usually following infection. In this way, persistence was established for C. trachomatis serovar A in HeLa cells at IFN-Image removed. levels as low as 0.2 ng (2.4 U)/ml (7) and for C. pneumoniae A-03 in HEp-2 cells at a level of 25 U/ml (87). Persistence of C. trachomatis serovar A was maintained for several weeks (10). Ultrastructurally, the IFN-Image removed.-induced persistent chlamydiae were enlarged and aberrant (7, 87) (Table 1)"
    • " In C. trachomatis serovar A, there was also evidence of budding and endopolygeny, the production of multiple progeny from a single enlarged form, during resumption of productive infection after removal of IFN-Image removed. from the cultures (10). These morphological observations were consistent with those from other persistence induction systems (26, 69). However, a direct comparison of IFN-Image removed.- and amino acid depletion-induced persistent C. trachomatis serovars E and L2 in HeLa cells revealed different growth characteristics between the two systems, since only IFN-Image removed.-exposed cultures showed decreases in inclusion size and the number of infected cells (52)."

There's a lot more, but it's difficult reading for we lay people... 

 

On Combined Antibiotic Protocol for Cpn in Rosacea 01/06 - 07/07, On Vit D3 + NAC since 07/07 and daily FIR Sauna since 08/07

Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-
Red

Hi Jim,

I think my previous attempt at this was considered spam, so I'll shorten it.   

I can't weigh in much on this since it is well beyond my level of comprehension, but it appears that the following review article discusses this division of cryptic forms, but breaks the division down even further, discussing differences between antibiotic-induced persistence, deficiency-induced persistence and cytokine-induced persistence: 

Chlamydial Persistence: beyond the Biphasic Paradigm

 

On Combined Antibiotic Protocol for Cpn in Rosacea 01/06 - 07/07, On Vit D3 + NAC since 07/07 and daily FIR Sauna since 08/07

Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-

Protein synthesis inhibition by antibiotics is nonspecific; it commonly involves the antibiotics binding on to part of the ribosome (the assembly that translates RNA into proteins) and jamming it. However, it's not an absolute barrier -- some proteins (especially small ones) can sneak past the jam. For that matter, the jam, like everything at the molecular level, is a probabilistic thing, which can spontaneously unjam itself.

 Long time since I've seen this article, and I probably can understand a bit of it now! Amazing. 

I'll have to dig into it, but I noted a couple of things germaine to Dr. Stratton's comments about persistance being associated with HSP60:

...many studies have reported enhanced production of cHSP60-specific antibodies in various chronic chlamydial infections...

...Another potential explanation for the relative abundance of cHSP60 during C. trachomatis persistence is its function as a stress response chaperone (77), which is likely to be of particular importance under the conditions that induce persistence. In support of this view, the production of five proteins thought to be major heat shock proteins, including cHSP60, was strongly increased...

At any rate, it's helpful in defining some of the differences in morphology from different persistance inductions, but doesn't expressly make David's case. The debate is still on! Tally ho!

CAP for Cpn 11/04. Dx: 25yrs CFS & FMS. Protocol: 200mg Doxy, 300mg Roxithromycin, Tini 1000mg/day pulses; Vit D1000 units, Iodoral 50mg, T4 & T3

 

CAP for Cpn 11/04. Dx: 25+yrs CFS & FMS. Currently: 250 aithromycin mwf, doxycycline 100mg BID, restarted Tini pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

One thing to keep in mind, in these discussions, is that most of the chlamydiae, most of the time, have got to be in the cryptic/persistent form. This is because if they were constantly replicating, they'd quickly become so numerous as to kill their host. The life cycle of Cpn, when replicating, is about 72 hours; that takes it from a single EB, through the RB stage, to about 100 EBs that are released at the end of the cycle. So each 72 hours brings about a factor of 100 increase. This is not something that is sustainable -- not even for a month (ten periods of 72 hours, which would yield a factor of 100000000000000000000), let alone the years that Cpn infections last for. Of course that rate of multiplication is slowed by the time taken for the released EBs to encounter new host cells, and further slowed by the action of the immune system in destroying EBs and infected cells. But for the immune system to constantly be, in each 72 hours, destroying 99% of the infection, as would be required to keep the infectious load about the same under conditions of constant replication, is most improbable: normally it'll destroy either more or less than that. As for EBs, those can indeed serve as an alternative non-growth form; but if one were to try to force it to entirely take the place of the cryptic form, that would mean that the chlamydial population would have to consist almost entirely of EBs, with only a few RB-infected cells to keep their numbers up. But uninfected cells (which that model assumes to be predominant) take up EBs quite readily, so that model doesn't work. The only thing that is left is to suppose that the cryptic form, plus whatever EBs are somehow stuck in places where they can't infect anything, accounts for the vast majority of the infectious load, during the vast majority of the time.

Another thing this line of thought shows is that intentionally forcing chlamydiae into the replicating form is 'tickling the tail of the dragon'... perhaps a good thing to do, but rather risky.

Good "in vivo" thinking, Norman. Of course, the whole speculated role of pyruvate is just that, speculation. It's one of the things they wish to examine first in the new Chlamydia lab. It could be that pyruvate acts to mitigate treatment responses in a whole different way than is theoreticaly supposed. It reminds me of the person who argued that all those William Shakespeare plays weren't written by him at all, but by another man with the same name!  

CAP for Cpn 11/04. Dx: 25yrs CFS & FMS. Protocol: 200mg Doxy, 300mg Roxithromycin, Tini 1000mg/day pulses; Vit D1000 units, Iodoral 50mg, T4 & T3

 

CAP for Cpn 11/04. Dx: 25+yrs CFS & FMS. Currently: 250 aithromycin mwf, doxycycline 100mg BID, restarted Tini pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

 

Jim, I think David's idea would be an excellent thing to test when the new lab opens because  you mention the calcium pyruvate idea being started with a non medical friend:

Paul Griffith, a non-medical friend researching this whole area, found that supplementing pyruvate might do the trick. Pyruvate may also have other beneficial effects. Basically, this approach uses 6 grams of calcium pyruvate one hour before taking the antibiotics, and an additional 6 grams if needed later for reactions when the antibiotics exert their effect. In theory the first dose of pyruvate encourages the cryptic/persistent form of Cpn to convert back into RB (replicating) form by supplying it with a ready source for generating cellular energy.

I don't like the idea of whole protocols, whether experimental or not, being based around the ideas of someone who could for all we know, be doing his experiments on the kitchen table with the family alsatian padding around on the floor.  I don't want to see the new lab becoming a laughing stock before it has hardly got off the ground.  If medical doctors are to take this seriously they want to see evidence published in PubMed.  "A non medical friend finding that something might do the trick" is not good enough............Sarah

An Itinerary in Light and Shadow...........Completed Stratton/Wheldon regime for aggressive secondary progressive MS in June 2007, after four years, three of which intermittent.   Still slowly improving and no exacerbation since starting. EDSS was 7, now 2, less on a good day.

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

 I should add that Dr. Stratton has been using the protocol himself with a number of people and has found the results he has seen and his understanding of the biochemistry to be sound and consistent. And he's the only person I know that can look at a diagram of a molecule and tell you whether it would effect the particular bacteria!

But that's why I've listed it as an experimental protocol. No one here should see this as anything but experimental. There is no lab evidence that it is working the way Dr. Stratton believes it is working, and he is clear that this is "a work in progress." He clearly felt that the beneficial results he was seeing in a variety of patients warranted releasing the information prior to the full lab investigation, and that the potential for harm was minimal. 

CAP for Cpn 11/04. Dx: 25yrs CFS & FMS. Protocol: 200mg Doxy, 300mg Roxithromycin, Tini 1000mg/day pulses; Vit D1000 units, Iodoral 50mg, T4 & T3

 

CAP for Cpn 11/04. Dx: 25+yrs CFS & FMS. Currently: 250 aithromycin mwf, doxycycline 100mg BID, restarted Tini pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

 

Jim, I know you list it as an experimental protocol, but not enough people are taking any notice of the word "experimental" and are convinced that they have to down globs of calcium pyruvate to stand any chance of getting better.

To put people's minds at ease me reiterate here was my regime:

Straight away I started on 200mg of doxycycline.  I was delirious with fevers and chills for about two weeks.

I began roxithromycin after few weeks, experienced no additional reactions.

After three months I did my first five day pulse of metronidazole and experienced a kind of disconnectedness.  In subsequent pulses, on a cycle of four weeks off, five days on,  I experienced some sharp pains in my right arm, the one that was virtually paralysed when I started, but nothing more.

I changed doxycycline for rifampicin at about six months, but just before this I experienced a bout of severe reflex sympathetic dystrophy in my right arm, which started during a metronidazole pulse and continued for a week or so after. (More details in my Patient Story.)

The addition of rifampicin made my walking worse due to the lack of immunomodulation, but I gradually got used to it.

Before the year was out, I had stopped getting any reactions so it was decided that I should go onto intermittent therapy, with the proviso that I should restart the full protocol, but with doxycycline this time rather than rifampicin.  Since I never felt anything coming back, this was never needed, so I took abx for two week bouts, every two months at first, moving to every three months.  Metronidazole was taken with the other abx for the last five days each time but I soon swapped to tinidazole because metronidazole can make some people feel sad and depressed no matter what.  (So does tinidazole but to a lesser extent.)

Apart from this I never got any reactions when restarting antibiotics, so one could theorise that I had already killed the organism after a year.  We were neither of s brave enough to try, though.  Finally after nearly four years I finished yet I am still showing subtle improvements, posted from time to time in my blogs.

I only started NAC after eighteen months and I never took amoxicillin.  I still take NAC every day, along with D3 and  variety of antioxidants and B12.

Many people, even some doctors like my former neurologist, don't understand the nature of progressive disease say that either this remission is just in the nature of the disease, or in the neuro's case, spontaneous remissions do sometimes happen, but I did have very aggressive SPMS which just stopped progressing from the day I first took doxycycline, so what did I do that didn't require the addition of calcium pyruvate?  Large amounts of glucose from the Happy Brewer, maybe?

Incidentally David and I both think the world of both Sriram and Stratton and also of the birthday boy, but I'm just not so sure about non medical researchers who do it as a hobby.................Sarah

An Itinerary in Light and Shadow...........Completed Stratton/Wheldon regime for aggressive secondary progressive MS in June 2007, after four years, three of which intermittent.   Still slowly improving and no exacerbation since starting. EDSS was 7, now 2, less on a good day.

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

Believe me, I would not publish a protocol that was not from The Man himself. Credit is due, however, to anyone's contribution to a new line of thinking. The protocol as published was reviewed and approved by Dr. Stratton.

I had a big concern about putting this on the site, as it is experimental and theoretical. But once there was someone blogging about it, or was it a forum question, I knew that shortly there would be lot's of anxiety and questions. It felt more responsible to ask Dr. Stratton what he wanted represented as a reference so that at least the theoretical and experimental scheme was available.  But I'm glad you reiterated your protocol, Sarah, because as far as I'm concerned this is the most tried and true, safe, protocol with the clearest track record.

Should probably move these comments off David's thread and into a forum of their own, yes? 

CAP for Cpn 11/04. Dx: 25yrs CFS & FMS. Protocol: 200mg Doxy, 300mg Roxithromycin, Tini 1000mg/day pulses; Vit D1000 units, Iodoral 50mg, T4 & T3

 

CAP for Cpn 11/04. Dx: 25+yrs CFS & FMS. Currently: 250 aithromycin mwf, doxycycline 100mg BID, restarted Tini pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

Red

Hi Jim,

I'm all for searching for new and better ways to get rid of this nasty infection, as you know. This is reflected in my own current regimine even, although I certainly plan to finish up treatment on a more standard protocol if need be once I've stabilized in my reactions.

As you're probably well aware though too, I also probably have an initial bias towards any agent that seems to decrease reactions due to my experience with the 5-LOX inhibitor, Boswellia, which seemed to greatly decrease my symptoms for a period, but then seemed to leave me with a much increased burden (i.e. when I went off the boswellia, I was much, much worse than before I took it).

I've known for quite some time that Ibuprofen almost completely eliminates reactions for me, and it thus it both intrigues me and scares the heck out of me, if this makes any sense. Could Ibuprofen be preventing the killing of Cpn in some way for me? Is this why all reactions shut down so completely and so quickly for me, very much like what I saw with the boswellia? I haven't been able to find anything that would suggest it might, but I'm still very afraid to take Ibuprofen for anything other than a one time shot here and there when I absolutely need it.

The reported decreased reactions when taking pyruvate made me wonder if it could in some way be due to a decreased kill rate of Cpn, etc. I've been searching for any potential mechanisms that might bring this about, and I may have run across one this morning.  Pyruvate appears to reduce apoptosis, as some studies suggest by blocking caspase-3 activation, which is the same mechanism, as you know, that Cpn seems to use (see page 24 of the Stratton TWAR slide presentation for anyone who wants to read more on this):

Sodium pyruvate protects against H(2)O(2) mediated apoptosis in human neuroblastoma cell line-SK-N-MC.

"Sodium pyruvate protected cells significantly (P<0.05) against apoptosis in a dose dependent manner as assessed for cell viability by dye exclusion method and apoptosis by TUNEL. Sodium pyruvate significantly inhibited caspase 3 activity, cleavage of PARP and breakdown of mitochondrial membrane potential."

Enhanced survival effect of pyruvate correlates MAPK and NF-kappaB activation in hydrogen peroxide-treated human endothelial cells.

"Activation of caspase-3 and the cleavage of procaspase-6 and procaspase-7 were strongly inhibited by pyruvate"

 

There are quite a few other studies in pubmed suggesting this same effect. Could the decrease in symptoms you are experiencing be somehow related to reduced apoptosis of parasitized cells (i.e. less dumping of porphyrins and other inflammatory components upon apoptosis)? I wonder...

Has Dr Stratton looked into this potential? If so, am I just over worrying? As you know, I have no medical background so I certainly could be missing something very important.

Thanks again, and I am very happy you are experiencing better health these days. What better gift could you have for your birthday?!!!

On Combined Antibiotic Protocol for Cpn in Rosacea 01/06 - 07/07, On Vit D3 + NAC since 07/07 and daily FIR Sauna since 08/07

Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-

Jim was very clear in stating that the introduction of calcium pyruvate was experimental. Sarah, you were very fortunate to not have experienced more reaction from Flagyl.. But I dont want for people to think that your experience is typical. I would say a good portion of us with CPN have a much harder time in introducing Flagyl into the protocol. I would recommend that people not start with a 5 day pulse for their first flagyl pulse. Also, reading from MSers blog, you are also fortunate that your very aggressive SPMS just stopped progressing from the day you took your first doxycycline. again, from my reading on this site, i dont see this has been typical response either. Red, you bring up some good points about the pyruvate. But I do wonder if Jim would have experienced improvements if he was not knocking down the CPN load..I would love to read Jim response to your blog.

From what i understand from reading, a non medical person may have come up with the idea. however, stratton is the one who felt that this idea may have merit to it, and has experimented with the pyruvate.

Also, I would have to wonder the benefit of use of calcium pyruvate for MS vs nonMS. does the pyruvate even cross the BBB?

Mphs, TN. CFS, hypoT (Hashi), adrenal fatigue, 37 w/hormones of 80,. right arm neuropathy. + cpn, myco, EBV, CMV. NAC 4000mg, doxy 100-2xday, azith 250 m/w/f/sun, progesterone, estriol, synthroid, pulse flagyl, tini<

Mphs, TN. CFS, hypoT (Hashi), adrenal fatigue, hormonal inbalance. right arm neuropathy-getting better. cpn, myco, EBV, CMV, HHV-6. Cap began in 6/07. NAC 2400mg, mino 100mg bid, biaxin 500mg bid. cytomel, flagyl bid continuously.

Hmmm, I think there are many examples of non-professionals contributing to research in a specialized area of study. John Kanzius and his anti-cancer machine comes to mind: http://tinyurl.com/6lft2n Let's hope his machine becomes a big success! Raven CAp since 8-05 for Cpn and Mycoplasma P. for MS and/or CFS

Feeling 98% well-going for 100. Very low test for Cpn. CAP since 8-05 for Cpn/Mycoplasma P.,Lyme, Bartonella, Mold exposure,NAC,BHRT, MethyB12 FIR Sauna. 1-18-11 begin new treatment plan with naturopath

 

Jim, no!  He wants them kept here.  I know that without even asking him, but please, don't move anything..............Sarah

An Itinerary in Light and Shadow...........Completed Stratton/Wheldon regime for aggressive secondary progressive MS in June 2007, after four years, three of which intermittent.   Still slowly improving and no exacerbation since starting. EDSS was 7, now 2, less on a good day.

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

I'd like to add a voice to Sarah's in advocating a "watchful waiting" stance with respect to altering the protocol on our own.

First: David makes a good case for a necessary multiplication of entities. Is it true? Are there NOC and AIC bodies, and do they act as described? We don't know -- and the fact that we don't know something that basic is a good reason to stay with the established protocol. Many of us here are struggling to get out of the swamp. I have two years in the protocol, and I am having minimal progress right now, so I know how attractive a shortcut looks. Still, we have professional scouts here, so we should let them explore the shortcuts and eliminate the dead ends for us. We can't afford to chase down a dead end on our own.

 Second: as Sarah points out, we are not just a group of private persons with a common interest in a protocol for CPn. We are public advocates for the protocol, we are public advocates for microbial etiologies for a number of difficult to treat diseases, and we are public advocates for the other sufferers who come here. Conjecture is a good thing, but running from one to the next doesn't serve any of our advocacy roles very well.

 So, my vote: read with interest everything that comes along, all the scouting reports, but don't follow the scout until he or she comes back and says it wasn't a dead end.  Stay on the proven path: show that the protocol works, show that microbial etiology explains many diseases, and show that anyone can start down the current protocol path with confidence that it won't lead to a dead end. Then it will be easier to find more scouts to develop good shortcuts; maybe even a paved road.

Ron

On CAP for CFS starting 01/06 (NE Ohio, USA)

Currently: doxy & zith -- continuous; metronidazole -- 5 days on, 9 days off.

Get the research results you paid for: support Open Access

Ron

On CAP for CFS starting 01/06 (NE Ohio, USA)

Began rifampin trial 1/14/09

Currently: on intermittent

man, oh man, I wish I had a crystal ball to look at 10 years down the road. This is somewhat exciting..well, has much has cpn can be exciting.  

Mphs, TN. CFS, hypoT (Hashi), adrenal fatigue, 37 w/hormones of 80,. right arm neuropathy. + cpn, myco, EBV, CMV. NAC 4000mg, doxy 100-2xday, azith 250 m/w/f/sun, progesterone, estriol, synthroid, pulse flagyl, tini<

Mphs, TN. CFS, hypoT (Hashi), adrenal fatigue, hormonal inbalance. right arm neuropathy-getting better. cpn, myco, EBV, CMV, HHV-6. Cap began in 6/07. NAC 2400mg, mino 100mg bid, biaxin 500mg bid. cytomel, flagyl bid continuously.

Wow so much information to take in, and especially to ponder and understand and make choices and wow, yes its alot. I'm somehwat nervous though because i feel like the treatment protocol is going to come full circle and reflect my past experiences...and then I will be right up the creek because there will be no treatment left for me. Ive done the biaxin before, I feel like Im going backwards now. Im just trying to process all of this and decide what is best for me, Its not easy, but yes knowing the enemy is half the battle, so thankyou for all the ongoing overwhelming info, its very appreciated.

 

 

 

 

 

&nbs

So what I understand is that the new protocoll should work even better with the noc (converting with pyruvate) and the aic killing with metro !

 

Right? 

 

 

Male 35 (Hamburg-Germany),CFIDS, IBS, Enterovirus, Cpn,treated Enterovirus with Inf-y,Inf-a.,Ribavirin. Started Wheldon Cap on 02/19/08, Currently NAC 2400, Doxy 2x100, Biaxin 2x500, Metro pulses,pyr

Male 38 years (Germany),CFIDS, IBS, Enterovirus, Cpn and Bartonella, Dientamoeba fragilis positive. Started Cap on 02/19/08, Currently taking Bactrim, Flagyl, soon adding Malarone and Clindamycin for suspected protozooa. 

[Quote]We are public advocates for the protocol, we are public advocates for microbial etiologies for a number of difficult to treat diseasesi, and we are public advocates for the other sufferers who come here. Conjecture is a good thing, but running from one to the next doesn't serve any of our advocacy roles very well.[endquote]

I'm with Paron on this. If everyone keeps jumping form one thing to the next and switching to experimental protocols without any monitoring it takes away any authority CAP has as a treatment.

We have enough trouble getting GPs on board as it is, even those who are working with people are going to start to question it if they're being asked to change everything every time somebody hears that Stratton is trying something new. Add to that, newcomers to this site are totally confused by the existing information, all this new stuff just makes things worse.

Jim I'm seriously concerned about all this and I'm wondering if you need to make all this part of an Experimental Protocols area so it's clear to everyone and only put it back in Protocols Compared once it's proven..

Berkshire, UK. Diagnosed RRMS Feb 4th 2008.

NAC 2400mg. All supplements. Doxy 200mg. Zith 250mg M/W/F.
No GP/Neuro support. Self medicating with help from David Wheldon.
Started CAP 20th April 2008.

Berkshire, UK. Diagnosed RRMS Feb 4th 2008.

NAC 2400mg. All supps. Doxy 200mg. Zith 250mg. Metro 400mg.
No GP/Neuro support. Self medicating with help from David Wheldon.
Started CAP 20th April

great post, i can understand your frustration Andesine.  Although it was an exciting possibility, it has taken some jaw-gnashing on my part to get to grips with, and was not something I relished.  But essentially, the experiment protocol mainly amounts to the difference regarding Calcium Pyvurate, which may end up an essential supplement in the way NAC is.  IT doesn't feel particularly like a revolutionary change, despite my first 'take' on the matter.  Actually its just something additional that may help, hopefully significantly.  As someone who has suffered considerably on CAP I am hopeful and grateful if this is the case.  I think because it is experimental, it does add some confusion, and I'm not sure how this is going to be cleared up.  But there is a sense in which the whole protocol is experimental, and personally, I would not like to be denied something useful because it may potentially be confusing for newcomers (who may also benefit).  How that circle is squared is another matter!  By the way, however we respect what is being done here, and however we hope the outcome is personally good for ourselves and others, not everyone who comes to the site is a 'public advocate'.  We are just trying something new based on some research and experience, that sounds promising and makes sense.  All medicine is 'Emerging', just like the title of CPNhelp.org.  Any doctor can be reminded of that fact, or else we'd all still be living in the Stone Age and he/she would be a shamen singing to the skyImage removed.

M.E./CFS 20 years, intermittent.  Wheldon Protocol - Started NAC and supplements Sept 2007. Doxy and Roxy full dose by Dec '07.  First Flagyl pulse January 2008.

M.E./CFS 20 years, intermittent.  Wheldon Protocol - Started NAC and supplements Sept 2007. Doxy and Roxy full dose by Dec '07.  First Flagyl pulse January 2008.  Changed to Tini in December 2008.  Stopped CAP in February 2009 at pulse 16.

 Andesine, et al- Susan is right, essentially this only changes three things about Dr. Stratton's protocol:

  1. The addition of the pyruvate before and if needed, after the antibiotics.
  2. The particular macrolide used (either Clarithromycin or Roxithromycin).
  3. And that he is pulsing the metronidazole as does Dr. Wheldon's protocol.

The only thing theoretical here is what exactly the action of pyruvate is in moderating reactions and, at least in some cases, speeding up the rate of treatment because of that. Everything else is consistent with his prior discussions, including the judicious use of low dose steroids to manage inflammation appropriately.

The discussion in this thread is on the theoretical mechanisms proposed currently. This is a theory discussion. As we are a free information website and don't have special categories that only some members can get into, everyone, even new folks, can read everything including the theory discussions. They will have to learn to distinguish the suggested protocols from the theory discussions about them. That's the way it is with internet info.

Perhaps this thread should be moved to "theoretical discussions" forum label to make that clearer. David? May I? 

CAP for Cpn 11/04. Dx: 25yrs CFS & FMS. Protocol: 200mg Doxy, 300mg Roxithromycin, Tini 1000mg/day pulses; Vit D1000 units, Iodoral 50mg, T4 & T3

 

CAP for Cpn 11/04. Dx: 25+yrs CFS & FMS. Currently: 250 aithromycin mwf, doxycycline 100mg BID, restarted Tini pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

Maybe the two forms are why I reacted to pyruvate as I did. The first time I did it, a few hours after I took my morning antibiotics, I got so nauseated I threw up. This is the first time this has happened in over a year. The next two times I took pyruvate, I felt worse for a couple of hours. I think the pyruvate must be stirring up something. Combined Antibiotic Protocol minocycline, azithromycin, continuous metronidazole for muscle pain, insomnia, interstitial cystitis, sinus, disphonia, dry eyes, stiff neck, veins, thyroid, TMJ.

minocycline, azithromycine, metronidazole 2007-2009, chelation for lead poisoning, muscle pain, insomnia, interstitial cystitis (almost well), sinus, dry eyes, stiff neck, veins, hypothyroid, TMJ, hip joints (no longer hurt)

[Quote]They will have to learn to distinguish the suggested protocols from the theory discussions[Endquote]

 

I'm sorry Jim but that's a bit harsh. I thought the whole idea of this place was to inform and help new people not dump loads of confusion and let them wallow around in it. We've just been going through discussions about people on the Lyme forum saying how confusing they find the site.

There are many on here who are well versed in microbiology, understand all the terms, have had all the weird and wonderful tests, and therefore results, you seem to get out in the US and been on the Protocol or a version of it for some considerable time.

You forget that others of us have trotted off to Royal Berkshire Hospital, or other large medical establishment, and been told by an overworked Neuro that we have MS or whatever, based on an MRI scan. Full stop. The only blood tests I had were to check my thyroid and to make sure I didn't have diabetes. We don't get to see those results.

We have no idea what all these raised xxx, yyy, zzz things are that you all go on about. We haven't had and aren't likely to get all the blood tests you do. We're not GP supported and we can't just waltz into a lab and ask for them. I'll be lucky to be able to get another MRI down the line unless I go private and pay for it. Our Private insurance certainly won't cover it as it's not GP referred.

Brain fog apart, we don't have the same background information available to us that many of you seem to have so we stick with the tried and tested; but, some of us are already on CAP and have seen David so we have confidence in the Protocol as it stands.

Anyone new on here sees a massive amount of information, a huge number of terms they don't have a clue about. We direct them to Getting Started precisely because they need plain English. They then wander round the site and find theoretical discussions that aren't clearly theoretical due to some people immediately diving in. There have been several posts outside of this thread about Pyruvate and they aren't clearly marked as Theoretical.

I've noticed a number of long termers saying it's newbie responsibility to dig out the information. I think that's doing the Protocol and the aims of this site a big disservice and turning away a lot of people that this could help as they just can't get their head round it.

In the UK we're conditioned, due to the NHS, to doing everything supported by a GP. Going out on your own is pretty much unheard of and tends to make the News when people do. For us, it's a super scary prospect not to mention super expensive so we need hand holding. I kind of thought that was what this site was about, not, here's all the info, get on with it.

I'm pretty lucky as Carol was already on here, she and her husband had researched this and directed me here. I don't have bad foggies so although it took me a while to understand it, I got there. I'd hate to think what some people must make of it.

Most of the regular posters on here are pretty intelligent, quick on the uptake and fairly sharp, fog or no fog but I think we need to remember that not everyone who comes here is as fortunate. I suspect there are a lot of "lurkers" too terrified to join/post. Is that what we want?

 

Berkshire, UK. Diagnosed RRMS Feb 4th 2008.

NAC 2400mg. All supplements. Doxy 200mg. Zith 250mg M/W/F.
No GP/Neuro support. Self medicating with help from David Wheldon.
Started CAP 20th April 2008.

Berkshire, UK. Diagnosed RRMS Feb 4th 2008.

NAC 2400mg. All supps. Doxy 200mg. Zith 250mg. Metro 400mg.
No GP/Neuro support. Self medicating with help from David Wheldon.
Started CAP 20th April

'Going out on your own'   is exactly what we lyme patients have been doing for years and years before Cpn was even heard of so I think you may be underestimating how resourceful such patients can be.   There are very, very few patients either here on cpnhelp or on many of the lyme sites that have the backing of their GPs and one of the first things it is absolutely necessary to learn in tackling these illnesses is that we have  to get out of the mindset of relying on the NHS or any other 'official' body.  The people who come here and stay have got what it takes.

Elinor ..... from England  on CAP, doxy/roxi/tini  for ME/CFS/lyme borreliosis, positive Cpn and borrelia. Started Aug05, stopped Jan06, started again Sept 06.

Elinor ..... from England  on CAP, doxy/roxi/tini  for ME/CFS/lyme borreliosis, positive Cpn and borrelia. Started Aug05, stopped Jan06, started again Sept 06.

Andesine,  The truth in your words is undeniable, and they get right to the root of the difference between what we can do and what we should do, even what is sustainable.  It's heart-wrenching to think about the vast need of not only the newcomers who stumble in, but also of those who never do.  Because the protocol in its various forms is experimental, anyone, doctor or patient, who chooses to administer a CAP is dabbling in "unknown" medical territory.  Therefore, the responsibility for learning as much as possible about this emerging treatment lies with whoever makes the decision to do it.  While most of us strive to stay on top of the information about the CAP, old and new, we are not doctors, we can't take the responsibility of directing "do this" or "do that."  Even if we were doctors, what doctor would dare to direct treatment by the proxy of the internet, sight of patient unseen? 

I agree that it all needs to be set out as clearly as possible, but we can never ignore the user's necessary learning burden whether they be doctor or patient or both. 

Joyce~caregiver-advocate in Dallas for Steve J (SPMS).  CAP since August 06, Cpn, Mpn, B. burgdorferi, systemic candidiasis, EBV, CMV & other herpes family viral infections, elevated heavy metals, gluten+casein sensitivity. 

Joyce~caregiver-advocate in Dallas for Steve J (SPMS).  CAP since August 06, Cpn, Mpn, B. burgdorferi, systemic candidiasis, EBV, CMV & other herpes family viral infections, elevated heavy metals, gluten+casein sensitivity. 

I think that's it.   If people want this badly enough (and we did) they will do what it takes to get it.   I'm not a science high flyer, (I'm no slouch either) but it took me two years to feel confident enough to write Getting Started.   We don't have Private Insurance, we pay for our drugs ourselves, but it is a small price to pay in time, effort and money for a chance of improvements in our health.   It is not just people in the UK who come, have a look and go away again.   This must happen across the board. 

In the UK we are lucky to have the NHS, warts and all, even if we don't have access to the same kind of blood tests as other countries; but that does not exonerate us from taking responsibility for ourselves or preclude us from researching, thinking and consulting with others about might be affecting our health.   I remember asking the doctor what caused Ella's relapses the answer was:"any number of things might, but no one really knows".   I think it was at that time that I started looking for solutions myself rather than asking questions of professionals.   It was that answer that made me realise that they did not know everything, and there was more to discover about MS than doctors knew about.   This is when I started pestering my daughter for health event details, trying to make connections, and this is what prompted me to do the google search that brough me here following the observation that ABX seemed to help her symptoms...

Michèle (UK) GFA: Wheldon CAP 1st May 2006. Daily Doxy, Azi MWF, metro pulse. Zoo keeper for Ella, RRMS, At worse EDSS 9, 3 months later 7 now 5.5 Wheldon CAP 16th March 2006

Michèle (UK) GFA: Wheldon CAP 1st May 2006. Daily Doxy, Azi MWF, metro pulse.

Andesine, I have to share some of your sentiments. I am not educated in the medical field and did find the site intimidating for sure. I think that maybe there are those here that are getting fatigued with the newbies and all of their babysteps and that is  completely understandable to me. I would never have the patience to explain and reexplaing the basics. On the other hand, I believe that the people that are participating in the protocol are generally pretty free thinking, self motivated individuals that won't be held down by limitations. I read the material for weeks before approaching my doc and did ask some very basic questions at first. Bottom line seems to be to me, if someone is not able or willing to do extensive research and reading, this CAP will not be comfortable to them. There's a lot to each disease and illness so to imagine that the treatment will be simple and straight forward seems unlikely. I would hope that new people will continue to be treated gently and with care as I believe they will because of my limited experience with the caring and gentle people that are administering here.

The discussion of the experimental changes to the protocol will likely muddy the waters somewhat I agree. I am glad that I learned the basics before I encountered it but this is an open forum named Cpn Help and I guess it has it's place here as well. I have made my decision to do the Wheldon Protocol and the discussions won't change my mind but I do try to read the threads to try to keep up with what is happening.

Thanks Andesine for speaking up on the behalf of the starters.

SPMS< Supplements & NAC, Doxy 100 mg, Azith 250 mg 3X/wk

Lived with MS since 1991. Completed 16 months of full CAP plus supplements. Currently in full remission. Not on any antiobiotics anymore but taking all supplements incl NAC.

I can only say, that I have never seen such kind and caring atmosphere as on cpnhelp is, on any other website. I was able to start protocol, even when I was foreigner, non native english speaker, non medicaly or biologicaly educated. None in Czech Republic had ever heard about longterm CAP in 2006, when I started. My doctors did not speak english at all. Despite this I started- due to help of people from cpnhelp. Well, it took some time, but if you do not have choice, you care. Prague, The Czech Republic, On Wheldon protocol since 02/18/2006, CFS and many problems 30 years (cpn and mycoplasma), 3rd year on protocol- doxy, azi, tini pulses

Stratton/Wheldon protocol 02/2006 - 10/11 for CFS and many problems 30 years