When Stratton et al describe pulsing antibioticsi it is not a clear-cut concept. Correct me if I am wrong but basically their "pulse" is a pretty high dose of an antibiotic for a few days to weeks.
There is currently a fair amount of research on a concept of pulsing that is relatively low dose and dosed every other day or even every 2nd or 3rd day. It is looking like this type of dosing actually prevents bacteria resistance. In laymen's terms I would describe it as the bacteria know some poison is out there, they hide, and then when they think the coast is clear they venture out, only to find that the level of bacteria killer suddenly goes up, ie the patient takes another dose, and the bacteria get killed.
This is the concept that the Roadback Foundation and Dr. Trevor Marshall were/are following. Here is a link to a biotech in Germantown, MD doing studies on the same concept.
http://www.middlebrookpharma.com/BREAKTHROUGH_technology/NOVEL_infectious.aspx
Unfortunately for us sickies, the studies are nowhere near concluded. We kind of have to play it by ear in terms of what is working for us. But my general point is this: more high-dose antibiotics may not be better in terms of resistance or in terms of killing more bacteria. In fact feeling better on a consistant high dose may mean that fewer bacteria are dying. They are just hiding out.
I can post more studies on this, but hopefully this will give some food for thought and not food for the critters.
Paula Carnes
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Paula Carnes
One quick clarification.
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Paula Carnes
Paula- I'm not sure how you
Paula- I'm not sure how you can assert that "pulsing antibioticsi is not a clear-cut concept" here. It may be unclear to you as of yet, but the concept is quite clearly laid out here. My concern is that it seems to me that you are really posting an editorial comment here, and one which inaccurately reflects the information here, under the guise of presenting "research." If you had posted this under the "Theoretical speculations" forum I'd be happy to discuss it... as speculations is what these are.
We are quite clear througout this site that "a pulse" refers to a periodic course (3-10 days depending on the protocol) of bacteriocidal agent such as flagyli or tinidazole. None of the antibiotics (such as doxycycline or azithromycin, etc.) are pulsed, they are always used continuously and the bacteriocidal pulse is used against the background of the continous antibiotics. Have you not read the handbook yet?
The idea of pulsing the flagyl/tinidazole actually was the development made by Dr. Wheldon, as Dr. Stratton previously had use all the agents of the CAPi continuously. Dr. Stratton now believes , in terms of practical treatment, that the use of flagyl/tinidazole in a pulsed manner as described by Dr. Wheldon is the most practical and usable approach for most patients.
The science behind the use of bacteriocide is that this indeed addresses the way in which the particular bacteria Cpni escapes being killed by the regular antibiotics. As you say, the bacteria reacts to the antibiotic by "hiding" but is killed in it's hiding phase (cryptic) by the bacteriocide. Bacterial resistance to an antibiotic, and it's persistance by changing forms, are different mechanisms altogether. What I can gather from the Middlebrooke notion is that it is trying to prevent resistance, but does nothing for persistance.
You've probably gathered that we are not fans of the MPi here and one of the reasons is it is based on theoretical speculations that simply don't match up with what is known about bacteria, and what is known about Vitamin Di (for anyone other than sarcoid patients), and does not even have minimal laboratory findings to support it. The greatest body of evidence around bacterial resistance is that, while normal inhibitory dosing of antibiotics may have it's problems as we well know from the endotoxini and porphyrin issues here, sub-inhibitory dosing is guaranteed to generate bacterial resistance.
There are legitimate reason to consider alternating different kinds of antibiotics at their recommended clinical doses in order to overcome the efflux pumps that bacteria turn on to pump out certain molecules. But this is not the same as using low doses in alternation. I don't know the methodology or rationale behind the Middlebrooke approach, and they give little info on it other than their declarative statements. It's an interesting idea, worth discussing and knowing more about.
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CAPi for Cpni 11/04. Dx: 25yrs CFSi & FMSi. Currently: 150mg BID Roxithromycin, Doxycycline 100mg BID, Tinii 1000mg/day pulses; Vit D2000 units, T4 & T3
You are welcome to move my
You are welcome to move my post to the theoretical forum. Yes, I am new here and have trouble navigating the board or figuring out where the forums even are.
I am bringing up an issue in regard to "pulsing." I don't think I made my point very clear. And you bring up even more issues.
First let me say that I am in no way promoting the Marshall Protocol except in their concept of pulsing. This is also the concept being explored by Middlebrooke. They are (or were) doing studies pulsing minocycline for instance. The point of this type of pulsing is that bacteria expose themselves and die at some point when the level of antibiotic is declining. When the level is constant they simply hide.
I have read the various protocolsi here. I don't see where any of the "pulses" fit this notion. I tried to make the point that Zithromax is certainly not being pulsed at 500 mg three days a week. But then Stratton isn't pulsing doxycycline at all as you mention. Furthermore, on another topic, I tend to think that minocycline would generally be preferable since it crosses the blood brain barrier more effectively than doxy. Given that most Lyme and cfs patients have neuroi symptoms I don't think doxycycline would be a first choice.
Of course, it goes without saying that these bacteria are BOTH persistent and resistant. But the trick is to not continue the antibiotic constantly at the same level or the persistent bacteria will simply hide out indefinitely and then blithely emerge unscathed.
Do I know that pulsing as I describe it will work? No. And that is really my point. No one knows what will work. I suspect Stratton would be the first to admit that, especially when you consider that we have multiple infectionsi going on, not just c. pneumoniae.
Again, please move this to the more speculative section. Unfortunately that will not mean that much of what we hope is true is not also speculation. I look forward to discussing this with Dr. Powell until he throws me out or charges me extra - just kidding.
Hey, I hope this works, but I've been on this stuff - all of it - before and still relapsed. I do know that doxycyline does NOTHING for me. Minocycline is another story in my case. We are all an experiment in progress at this point in time.
I'll try to post a few more actual published studies asap.
Paula Carnes
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Paula Carnes
What we understand here as
What we understand here as a pulse affects only the Flagyli or tinidazole, these are the bacteriacide antibioticsi. The other two antibiotics are antireplicative and not considered to be pulsed, even though in the case of Azithromycin it is not taken every day. As you say this is not pulsing as it has a long life in the body.
Different doctors prescribe different antibiotics, for different patients. The reason behind the choice of Doxycycline, Azithromycin and Flagyl as the basic protocol is that a sizeable number of people have to pay for their drugs themselves and they are the most affordable to the effective drugs available. It is certainly worth starting this CAPi using these drugs as we know they work. There may come a time (maybe two years into the treatment) when it is advisable to change antibiotic for the reasons that Jim states.
Taking two antibiotics to stop bacteria replicating will mean that there they will not be able to mutate to become immunei to the antibiotics providing the antibiotics are used in effective doses. And yes the Cryptic formi of Cpni is the result of an unfriendly environment but that is why we use Flagyl which kills it in its cryptic form.
We have to remember that dying Cpn is toxic to the body and takes some getting rid of which is another reason why the Flagyl is usually pulsed, especially in the beginning.
There have been extensive discussions here on the differences between what we consider appropriate treatment for Cpn and the Marshall protocol. You could do a site search for this if you are interested, but when it comes down to it, on Cpnhelp, we think that the CAP is the right way to go for us. There has been some extensive research done on the problems of treating Cpn by some highly qualified medical doctors and researchers and on the whole we are confident that we are on the right track. There is always room for new discoveries but we would not consider them worth following unless they were approved by our very competent doctors.
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Michèle (UK) GFAi: Wheldon CAPi 1st May 2006. Daily Doxyi, Azi MWF, metroi pulse. Zoo keeper for Ella, RRMSi, At worse EDSSi 9, 3 months later 7 now 5.5 Wheldon CAP 16th March 2006
Paula- I'll move this to
Paula- I'll move this to the Theoretical forum for clarity.
The trouble with the broad brush statements like "that bacteria expose themselves and die at some point when the level of antibiotic is declining. When the level is constant they simply hide..." is that this really depends on the particular bacteria, how fast it is growoing,and how they "hide" and a whole bunch of other factors. We know pretty well how Cpni hides on exposure to anti-replicants (converts to cryptic), and by the remainder of EB'si. The CAPi here takes care of those and of resistance as well, as Michele mentioned.
I don't know if the Middlebrooke method is geared at particular bacterial or what because they don't say, but their method might only work with bacteria which are fast replicators, or who those that down-reguate efflux pumps quickly and so get slammed when the concentrations increase. Each bacteria has different methods of adaptation, so without speaking of a particular bug we really can't know what way to attack them.
On a theoretical note, I do think this strategy has validity. Somewhere on the site, Norman Yarvin published a "medical hypotheses" paper on how fluctuating dosing of antibioticsi due to people normally missing does and such may actually have benefit, in a similar fashion to what you are talking about. Dr. Stratton tells me that a future strategy with Cpn may be rotating different antibiotics on a week to week basis to hit them with an antibiotic that they have not upregulated their efflux pumps for at that moment, but this would be at full inhibitory dosing, and he was specific that this works best if you also have a cidal drug rather than only inhibitory, in part of the cycle (one of the reasons he likes levaquin for short use is it is cidal, and yes, I know of the many problems people have had with this drug).
Anyway, interesting discussion. I hope Norman chimes in at some point, or some other techies, to continue the speculations.
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CAPi for Cpni 11/04. Dx: 25yrs CFSi & FMSi. Currently: 150mg BID Roxithromycin, Doxycycline 100mg BID, Tinii 1000mg/day pulses; Vit D2000 units, T4 & T3
The Wheldon nitroimidazole
The Wheldon nitroimidazole pulses are actually not tradiitional antibiotic pulses, as you are not allowing the Cpni to change form. All the while you are still taking bacteriostatics which keep the Cpn stuck in the cryptic formi. So this is very different from the roadback concept of pulsing. The reason you "pulse" in CAPi is because the nitroimidazoles can be very rough, and time off is needed for the body to recover/heal.
Antibiotic Pulsing in general is certainly an interesting concept worthy of exploration (at least intellectually - I'm not advocating that anyone experiment on themselves).
The middlebrookpharma is doing something slightly different. They are releasing several beads from a single capsule which have a variable release rate. So instead of one max, you get a staircase effect. However over a period of 24 hours, the 2nd half does seem to be pretty much antibiotic-free, and in a sense this is "pulsing" the antibiotic, though every 24 hours, rather than the 2-3 days of Roadback. What middlebrookpharma refer to as "pulses" though seem to be the staircase effect, rather than the 12-hour on, 12-hour off part of their protocol. As far as Cpn is concerned 12 hours off may not be enough for a signifcant number of cryptic bodies to become replicating (though I could be wrong).
Jim wrote: There are legitimate reason to consider alternating different kinds of antibiotics at their recommended clinical doses in order to overcome the efflux pumps that bacteria turn on to pump out certain molecules
I was reading about efflux pumps recently, and apparently efflux pumps can work across a range of drugs (e.g. antibiotics in the same class):
"Expression of several efflux pumps in a given bacterial species may lead to a broad spectrum of resistance when considering the shared substrates of some multi-drug efflux pumps, where one efflux pump may confer resistance to a wide range of antimicrobials."
So although rotating should be helpful, its by no means a perfect strategy. Also I strongly suspect that once you've used an antibiotic once for a significant period, it will never be as effective again no matter how long you avoid using it for.
Paula wrote: But the trick is to not continue the antibiotic constantly at the same level or the persistent bacteria will simply hide out indefinitely and then blithely emerge unscathed.
I agree with this 100%. That is basically what Cpn does. Once you have spent a few months on the bacteriostatics, they no longer produce any overt die-off, and you are largely reliant on the nitroimidazoles to do the killing (though other abxi may affect cryptic forms to a limited degree).
The bottom line is that pulsing (in the CAP-sense) can be rough due to the extremely inflammatory nature of Heat shock proteins. I certainly think that alternative methods of winnowing down the bacterial population are worth exploring.
garcia.
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Hunter: Don't think - experiment
Thanks Jim. I don't think
Thanks Jim. I don't think I've seen Norman's paper. Anyone have a link??
Dr. Stratton tells me that a future strategy with Cpni may be rotating different antibioticsi on a week to week basis to hit them with an antibiotic that they have not upregulated their efflux pumps for at that moment, but this would be at full inhibitory dosing, and he was specific that this works best if you also have a cidal drug rather than only inhibitory, in part of the cycle (one of the reasons he likes levaquin for short use is it is cidal, and yes, I know of the many problems people have had with this drug).
This is actually close to what my lyme doc (who diagnosed me with cpn) does. He basically rotates antibiotics. After I had read this site I decided to follow the standard CAPi though, because at the time it made more sense to me, having a sound theoretical basis. Have we come across the perfect strategy in the existing CAP? Almost certainly not. I'm sure there are many advances to be made.
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Hunter: Don't think - experiment
Interesting thread.
Interesting thread.
Here’s an extract from an unpublished paper (Chuck Strattoni and I) which goes into the microbiology of metronidazolei action. Basically, it causes single-strand DNA breaks which multiply until the DNA is non-viable. Bacteria can repair these breaks, but require a whole platoon of proteins to effect repair. And, of course, the tetracycline and the macrolide seriously impair bacterial protein synthesis. So you can safely pulse the metronidazole.
The bactericidal effect of metronidazole involves its reduction to create short-lived but highly reactive intermediates (here designated M▪), which damage the DNA of the target cell. This can take place only within a strongly reducing environment where electrons will be donated preferentially to metronidazole. The direct donors of electrons in anaerobic bacteria are a family of electron transport proteins which include ferredoxin [32]. If C. pneumoniae has the ability to utilise an anaerobic pathway it should have the potential to fabricate ferredoxin or a ferredoxin-like protein, and, indeed, C. pneumoniae has recently been found to possess a gene which codes for ferredoxin [33]. M▪ damages DNA by acting on the AT base-pair and causing strand-breakage (reviewed by Edwards D [34].) The death or survival of an organism in the presence of metronidazole rests on the equation of the rate of M▪ induced DNA damage versus the rate of DNA repair [35]. If the rate of M▪ induced DNA damage outstrips the ability of the cell to effect DNA repair, then the cell will die. The dynamics of metronidazole have been extensively studied in the Enterobacteriacae [35-38]. Escherichia coli is normally highly resistant to metronidazole, surviving concentrations in excess of 500 μg/mL [39]. However, metronidazole is not inert within this bacterium. E. coli mutants with a defective ability to repair damaged DNA are much more susceptible to metronidazole than strains not possessing this mutation [37,38]; this implies that metronidazole is actively reduced to M▪ in E. coli, and that highly efficient DNA repair takes place under normal circumstances. Anaerobic co-cultivation of E. coli with Bacteroides fragilis in the presence of metronidazole results in enhanced killing of the Bacteroides [36,40] indicating that E. coli growing under anaerobic conditions effectively converts metronidazole to M▪ and then passes M▪ out into the substrate with such efficiency that other, more susceptible, bacilli are more rapidly killed. Production of M▪ in E. coli is likely to be a continuous process; although metronidazole enters the cell by passive diffusion, inward flow is maintained by a concentration gradient as intracellulari metronidazole is removed by irreversible reduction [41]. DNA repair mechanisms in bacteria call upon complex and ancient pathways which operate by way of induced proteins (reviewed in detail by Kuzminov A [42].) Nitroimidazoles are known to activate the S.O.S. ‘last resort’ repair system in bacteria [43]; this system requires at least 15 enzymes. It is not surprising that repair of DNA damage is curtailed by low-nutrient conditions [44,45]. Blocking the induction of proteins involved in DNA repair mechanisms should enhance the effects of DNA damage. This has been shown to be so: preincubation of E. coli with the protein-synthesis inhibitor rifampicin interferes with the organism’s ability to repair damage to DNA caused by X radiation [46]. One might hypothesize that nutritionally-starved intracellular Gram-negatives, surrounded by a double membrane system derived from host as well as bacterium, may be unable to pass M▪ efficiently beyond the phagosome and so may accrue higher concentrations of active intermediates.
32. Edwards DI (1980) Mechanisms of selective toxicity of metronidazole and other nitroimidazole drugs. British Journal of Venereal Diseasesi 56:285-290
33. Chlamydia genome project (2004). [Online] http://chlamydia-www.berkeley.edu:4231/cpn/ident2.html (22 September 2004, date last accessed).
34. Edwards DI (1992) Nitroimidazole drugs — action and resistance mechanisms. I: Mechanisms of action. Journal of Antimicrobial Chemotherapy 31: 9-20.
35. Chrystal EJ, Koch RL, McLafferty MA, Goldman P (1980) Relationship between metronidazole metabolism and bactericidal activity. Antimicrob Agents Chemother 18:566-573
36. McLafferty MA, Koch R L, Goldman P (1982) Interaction of Metronidazole with Resistant and Susceptible Bacteroides fragilis. Antimicrob Agents Chemother 21:131-134
37. Yeung TC, Beaulieu BB Jr, McLafferty MA, Goldman P (1984) Interaction of Metronidazole with DNA Repair Mutants of Escherichia coli. Antimicrobial Agents Chemother 25:65-70
38. Jackson D, Salem A, Coombs GH (1984) The in-vitro activity of metronidazole against strains of Escherichia coli with impaired DNA repair systems. J Antimicrob Chemother 13:227-236
39. Tally FP, Goldin BR, Sullivan N, Johnston J, Gorbach SL (1978) Antimicrobial activity of metronidazole in anaerobic bacteria. Antimicrob Agents Chemother 13:460-465
40. Soriano F, Ponte MC, Gaspar MC (1982) Reciprocal antimicrobial synergism between Escherichia coli and Bacteroides fragilis in the presence of metronidazole. J Clin Pathol 35:1150-1152
41. Ings RMJ, McFadzean JA, Ormerod WE (1974) The mode of action of metronidazole in Trichomonas vaginalis and other microorganisms. Biochem Pharmacol 23:1421-1429
42. Kuzminov A (1999) Recombinational repair of DNA damage in Escherichia coli and bacteriophage lambda. Microbiol Mol Biol Rev 63:751-813
43. Widdick DA, Edwards DI (1991) A comparison of the relative activities of 8 radiosensitizers in the SOS chromotest. 259:89-93
44. Sargentini NJ, Diver WP, Smith KC (1983) The effect of growth conditions on inducible recA-dependent resistance to X rays in Escherichia coli. Radiat Res 93:364-380
45. Dzidic S, Salaj-Smic E, Trgovcevic Z (1986) The relationship between survival and mutagenesis in Escherichia coli after fractionated ultraviolet irradiation. Mutat Res 173:89-91
46. Sargentini NJ, Smith KC (1985) Growth-medium dependent repair of DNA single-strand and double-strand breaks in X-irradiated Escherichia coli. Radiat Res 104:109-115
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D W - [Myalgia and hypertensioni (typically 155/95.) Began (2003) taking doxycycline and macrolide and later adding metronidazolei. No medication now; just supplementsi and IR sauna. Morning BP typically 105/75]
Wow, I am impressed. You
Wow, I am impressed. You guys and ladies have added so much to my simple beginning points here. Let me just add a couple of thoughts.
One is that no one has the answers yet, because the research has not been done -which bacteria get killed which ways? Which different antibioticsi are key to killing which particular bacteria? Are some antibiotics too dangerous to risk?
Two is that the kind of pulsing I described is not what Stratton/Wheldon are doing. I totally agree with the need to use two or three antibiotics with a different mode of action. I understand stopping Flagyli for a rest period as it is so hard to tolerate. But that is not my use of the word "pulsed." I was describing the up and down LEVEL of the antibiotic every few hours or days in order to get the bacteria back out in the open.
I hasten to add that IF this type of pulsing works it may make the patient much sicker for awhile due to constant die-off or every other day die-off. It would feel like a good day when the dose was high followed by a bad day when you didn't take the antibiotic. Of course, the nice solution to this is to extend the off days, ie take the pill every 3rd day instead of every other day etc.
I am no friend of Dr. Marshall. Indeed, I was the first moderator there who got kicked out due to thinking. <grin> But I do sometimes respect the brains of folks with narcissistic personality disorder. Some of the MP is actually good science. The reason I bought into the particular antibiotics he chose and the pulsing aspect is because of my history with the Roadback Foundation using low dose, pulsed minocycline. Also, my study and personal history suggest that minocycline is much more effective. Indeed, if one of your infectionsi happens to be mycoplasma incognitus you can flush your doxycycline down the toilet. Maybe it will kill germs there. It simply will not work for m. incognitus. Yes, I have a study to document this done for a full year on Gulf war vets with mycoplasma. The doxy did not work. Too bad, because the gov. scientists then concluded that mycoplasma was not a key player in GWI. But I digress.
I'll post more on my own case once I see Dr. Powell and try to figure out what the heck I am going to do.
Best wishes to all here and thanks so much for all the work you do for all of us.
Paula Carnes
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Paula Carnes
David, thanks very much for
David, thanks very much for that. Its great that you and Dr Stratton are writing a paper on this. I think the fact that the nitroimidazoles work against Cpni deserves to be more widely known. And personally I'm very interested in their mechanism of action.
The death or survival of an organism in the presence of metronidazolei rests on the equation of the rate of M▪ induced DNA damage versus the rate of DNA repair
From a practical point of view your extract is very interesting as it confirms what many of us have suspected all along - that the real beneficial effect of a pulse occurs after the pulse itself. Its one thing damaging the DNA of the CB's, but its only when you stop subsequent repair that the actual kill occurs.
It is not surprising that repair of DNA damage is curtailed by low-nutrient conditions
Presumably this implies that "high-nutrient conditions" will effect an efficient repair of DNA damage? This would relate directly to my personal experiences that its possible to "sabotage"/cut-short a pulse by giving Cpn enough breathing room and allowing the cryptic forms to repair themselves. For me high levels of cortisol and/or sugar do the trick. The real discipline in a pulse is in enduring the post-pulse reaction and not giving the damaged Cpn a chance to repair themselves.
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Hunter: Don't think - experiment
Paula, I would personally
Paula, I would personally have used more minocycline if it wasn't so darn expensive (about 4 times the price of doxyi). The first time I used mino I could barely walk straight, so I know its powerful stuff with great CNSi penetration.
Also although we don't advocate pulsing here, you might want to investigate the pyruvate protocol, which is a modification of the original Stratton/Wheldon protocolsi. Although not strictly pulsing, there are certainly similarities between that protocol and antibiotic pulsing. In particular you are trying to draw out the cryptic forms into the replicating forms. Not by withholding antibioticsi, but by supplying the Cpni with extra energy.
Here are a couple of threads to get you started:
http://www.cpnhelp.org/calcium_pyruvate_discussi
http://www.cpnhelp.org/experiences_new_protocol
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Hunter: Don't think - experiment
Paula, I could be wrong
Paula, I could be wrong here, but it seems we're talking about two different things. I am here to treat cpni. This protocol works against cpn. Now, if I had a co-infection, that's another matter, and of course I would be seeking treatment for it.
To say, "if you're infected with 'incognitus' you can flush your doxyi", is irresponsible. Being co-infected with 'incognitus' does not mean I cannot treat my cpn with doxy. The statement only makes sense if the sole illness I have is 'incognitus'!!!
If I'm infected with cpn and that's what I'm treating, doxy is just fine. But if I'm infected with 'incognitus', then I'm not expecting or intending that my cpn treatment will be effective against that (or any number of other infectionsi). I would be seeking additional treatment for my additional disease.
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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
David, Thanks once again
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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
Paula, May I suggest you
Paula,
May I suggest you read "The Potbelly Syndrome." After reading this Book Review I read it and it helped answer alot of questions for me.
For starters, the theory alot of researchers believe is that eradicating ONE infection (ie; CPni) we heal enough of the immunei system so that it will be able to heal itself of the henchmen and/or other co-infectionsi. The Potbelly Syndrome further explains this.
IMHOi, being able to eradicate one infection (CPn) which may have much harder phases of this bacteria (EBs, RBs, Cryptics) to deal with than some of the other so called infections or co-infections might just give our immune systems enough of a fighting chance. That's how I'm viewing this treatment regardless of whatever other infections my body is eradicating while I'm dealing with the CPn.
BTW, I am still planning on (eventually) using an antiviral due to the high viral titers I now have but I don't think treating with an antiviral alone is enough to make me well. Just my nickel's worth based on all I've learned to date.
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NACi 2.4g, Zithi 250mg/MWF, minoi 200mg, Tinii 1g/day pulses, Iodoral 25mg, Supps, CFIDSi/FMSi, Hashimoto's, Psoriasis, PA, IBSi, Secondary Addisons
Don't believe everything you think!David- Really glad you two
David- Really glad you two are publishing on the nitro impact on Cpni. It is a critical principle and as Garcia noted, completely unknown in the medical field other than readers here and your site.
I'm curious if Garcia's linking the post-pulse effects we observe to the timing of a cumulative inability for DNA repair fits. What is the time frame of this repair (or failure of repair) function? Could the bacterium be hanging on, lamely trying to repair while the protein synthase inhibitors limit it, and then go into mass failure? How many hours or days past the clearance of flagyli from the bloodstream? Curiouser...
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CAPi for Cpni 11/04. Dx: 25yrs CFSi & FMSi. Currently: 150mg BID Roxithromycin, Doxycycline 100mg BID, Tinii 1000mg/day pulses; Vit D2000 units, T4 & T3
I will try to write a bit
I will try to write a bit more another day. It's 11:30 pm pacific time.
Quick comments:
Since doxycycline and minocycline are the same family but mino crosses the blood/brain barrier I can't see using doxy unless you develop lupuslike symptoms from the mino. The government study on mycoplasma and doxycycline is located here.
http://www.cfids-cab.org/rc/Donta.pdf
Minocycline would be at least as effective against c. pneumoniae, and probably more-so based on the similarities. If one had cognitive and CNSi symptoms I would certainly think mino would be better.
I recently posted notes on "Potbelly Syndrome" on another couple of email lists. This book is a breakthrough. However, it is not encouraging at this time in terms of cure. If we control even one chronic intracellulari infection we are doing well. But then we all have to die of something. I guess the best we can hope for is a reasonably healthy life as long as we live. I'm actually once again looking at Stratton's work after 8 years because of what I read in "Potbelly Syndrome." Per Marin puts the pieces together nicely even if he doesn't have the magic fix.
At some point I would be most interested to hear this group's take on borrelia, and then there is babesia. How about the two viruses Montoya is looking at? I know at least a few patients who have borrelia, mycoplasma and EBVi and HHV6 at high titres. They recover, as I did to maybe 80%, but then the viruses increase and they tend to relapse.
Okay, enough. I'm gonna get some sleep. Strangely, I have had 4 good days now and no clue as to why. Still doing Allimed, but stopped the NACi after getting the NAC flu. I'm waiting now to see Powell in one month before just trying things out of ignorance.
One more thing - just read Powell's patent. Hum. It's better than "Potbelly" but I keep thinking of poor Kenny DeMeirleir who got crucified for owning his patent. I think I am going to claim to own the dirt in my back yard and create life.
Paula Carnes
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Paula Carnes
Paula, as I suggested above
Paula, as I suggested above and I think Mac also mentioned, doxycycline was chosen for the basic protocol because there are quite a few people who have to pay for their drugs and it is considerably cheaper than minocycline and is effective against Cpni. We must not forget that our main focus here is Cpn, not the multitude of other bacteria that we as a group are possibly infected with.
The theory is that if we can erradicate or at least reduce the levels of Cpn sufficiently our immunei system will be better able to cope with the rest of the parasites we carry around.
David, thank you for letting us have a glimpse of you and Dr Stratton's article. Who would have thought that E. coli could have its uses...
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Michèle (UK) GFAi: Wheldon CAPi 1st May 2006. Daily Doxyi, Azi MWF, metroi pulse. Zoo keeper for Ella, RRMSi, At worse EDSSi 9, 3 months later 7 now 5.5 Wheldon CAP 16th March 2006
The post of mine that was