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About a year ago, there were several posts here introducing an experimental pyruvate protocol against Cpn. The general idea of the protocol is to awaken Cpn from its cryptic state (aka "persistent state"), so that it can be killed using antibiotics other than metronidazole or tinidazole.

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Norman, Once again, you've given me enough to read and study for an entire evening. Thanks again for your intelligent and cogent posts. I kind of like stretching my brain (Image removed. now that it's working again, that is).

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

Thank you Norman. Your review of the protocol that you are using is most useful. I've only just started my treatment and just joined this network. I'm encouraged that I'll find here very useful recommendations and common experiences. Straight away I asked my self - How can I speed this up? You see, I am hoping for a 12 month treatment. But I've had CFS for 20yrs, that's probably not realistic. In Australia, there are so few doctors who know enough about CP to be of much help. So I'm my own researcher and physician to a degree.

Leanne

Norman, its becoming clearer now, thank you!!............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 improving bit by bit and no relapses since finishing treatment.

Norman, did you ever try Tinidazole instead of metronidazole from any of your pulses?  Tinidazole has been OK for me in many respects.  I have not substitute minocycline for doxycycline but may need to do that in the future. And I may substitute clarithromycin for roxithromyin or azithromycin because it is a daily dosed medication and available easily here in the USofA.  I am using calcium Pyruvate have been for a number of months now mid-afternoon for an energy booster in my mid-afternoon energy sink hole and it works for me in that application.   I have not used it for augmenting the intensity of abx effect as it has been done in some instances by members physicians for their personal treatment plans.   I am satisfied with the progress of the basic Stratton/Wheldon CAP for my abx treatment at present, as it has allowed me some time to begin to participate once again in a more functional lifestyle.  Guess that may be because I have been ill with CFS for many, many years and my onset of trouble was not an acute experience or was it a rapidly reached diagnosis as it is for some folks with MS in the early stages.  

It is wonderful to hear your process and I am very glad that this is working for you and may give some insight to others here to ponder.   I will be looking forward to reading your continued personal insights.   

  • CAP(TiniOnly): 06/07-02/09 for CFS
  • MethylationProtocolSupplements: Started08/08
  • Intermtnt CAP: 02/09-02/10
  • Full MethylProtocol & LDN 02/09
  • Off CAP: 02/10, cont LDN & MethlyProtocol support

Norman- I always appreciate your thoughtful, clear observations and well reasoned suppositions and experiments. This experiment is the epitome of them all. I particularly appreciate your care in noting the difference between reason and supposition from observations and what we factually know from scientific data, the latter of which is so little.

Not understanding the chemistry as you do, it never occurred to me  to question why pyruvate and not glucose directly. Assuming the health issues with glucose are accounted for, it certainly is a cheaper an more efficient way of stimulating Cpn growth. I'll have to try it and see.

One of the criteria that Dr. Stratton felt was useful in this type of protocol is to use shorter half-life antibiotics, so that you are gearing up replication the most by amping up the ATP (glucose or pyruvate) when there was little or no replication-inhibiting abx in the cell to hold Cpn in cryptic state. Both niacin and rifampin qualify for this, and you might further experiment with this by changing your longer half life abx (azith and mino) for shorter varieties. This was part of my switch to roxy since I was playing with the pyruvate protocol at the time, and roxy is shorter half-life than azith. Biaxin also meets this criteria, as does doxy.

I've thought similarly about tryptophan, since that is one of the main ways of inducing cryptic state in the lab (tryptophan starvation) and of feeding to re-ignite cryptic to replicating form. I also suspect that some of the sleep and mood problems in Cpn related CFIDS is from tryptophan depletion by Cpn. Timing is the issue here, since tryptophan may induce sleepiness and is usually taken at night for this reason, so if you have some thoughts about this let me know. It may be enough to take it before bedtime and let your morning abx dose get at the replicating phase, although this violates your principle of not letting it be stimulated to replication too long before kicking it's butt. 

All in all you've stimulated much to think about. I'll pass this on to see what Dr. S might have to add.

 

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

Hi Norman, Lots to chew on here...thanks for the mind-meal.

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. 

No, I've never tried tinidazole. Its advantage in causing milder reactions seems like it might be due to being less effective in killing Cpn; maybe not, but in any case I've been leery of it.

As for clarithromycin, I might try that; but the switch to it seemed largely predicated on the idea of waking the bacteria up and then suddenly slamming them with antibiotics; a pulse of antibiotics is necessary for that. Though that's possible, I find it more plausible that the effect is from simultaneously waking the bacteria up and subjecting them to antibiotics; for that, antibiotic pulses aren't necessary (although if your antibiotic is of the pulsed sort anyway, like rifampin is, you should make sure its pulses coincide with the pulses of pyruvate).

I haven't done a head-to-head test of these two theories, which could be done by comparing the reactions I get from taking pyruvate an hour before antibiotics against the reactions I get from taking it at the same time or half an hour later. I've just done the latter things, and found that they seem to be effective in increasing die-off, and in the long run in making me feel better. If I'm right, then taking pyruvate an hour before would result in some overlap of the two pulses, but a bunch of unnecessary bacterial growth, and thus die-off symptoms without as much progress in clearing the infection. But to judge that progress, I'd have to do a rather long test -- at least a month, and probably much more; and I don't care to. Judging die-off symptoms could be done quicker, but die-off symptoms aren't what we're after. I also somewhat doubt my own ability to judge my long-term progress; it's not something that's easy to measure. Only when there's a rather large degree of progress (or regress) does the signal emerge from the noise enough that I get confident about it. And it's especially easy to misjudge when I start off disliking one of the theories, and liking the other, as is the case here.

There's nothing exclusive about the two theories, of course: it could easily be a little bit of both.

No, no - no pulsing of rifampin!

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

By 'pulsing', as regards rifampin, I don't mean that rifampin should be pulsed like metronidazole is in the CAP; I just mean that since rifampin's half-life is only about three hours, what you get when you take it on the usual schedule (once or twice a day) are pulses of it, rather than continuously high blood levels.

I picked out the following 6 assertions from that 5000 word tome:

1. People have varying responses to flagyl, could be due to different immune reactions to HSP60

2. Instead of whacking chlamydia, pyruvate works by sending mixed messages

3. Why pyruvate, why not glucose?

4. Flagyl pulses have a very long tail - due to autoimmune reaction?

5. Cautious diet may alleviate symptoms, but in long-run doesn't lure out Cpn to be killed by abx

6. Tryptophan?

 

1 wasn't something I'd considered, and it seems plausible. But it would be very difficult to quantify this vis-a-vis how much of the variation in responses is simply due to e.g. degree of illness. But interesting nevertheless.

2 I think could well be true. It certainly explains the fact that the chronology (pyruvate or abx) doesn't seem to matter much.

3 you pretty much answer yourself. Glucose seems to be working for you, but there are real risks for those of us who aren't as healthy as you.

4 is the real problem with pulsing - the long tail. I don't know if it is an autoimmune reaction but I certainly think it is a runaway (over-?) reaction. If it is autoimmune, given that higher doses of Vitamin D will drag out pulses much much longer, does that mean D is potentiating autoimmunity?

5 is the gem in all this. Its probably the core question regarding Cpn treatment, and so deserves its own thread.

6 I mention because Jim said that tryptophan may induce sleepiness, but surely tryptophan gets converted to 5-htp. I take 5-htp during the day and at night. During the day it increases neurotransmitters and if anything wakes me up. At night I seem to get some conversion to melatonin, but the effect is subtle. Has anyone actually experienced sleepiness firsthand from supplemental tryptophan taken during the day?

 

Hunter: Don't think - experiment

My guess with vitamin D would be that it increases die-off in the first place, and thus increases the consequences of die-off, rather than doing anything that specifically promotes autoimmunity.

As for tryptophan, that gets converted to a variety of things, most of which I am only dimly aware of. But as regards 5-HTP, this caution is probably worth reading.

Norman- great link on dangers of 5-HTP use. Sounds like the thing to do is stick to tryptophan if you are going to use any of these serotonin precursors either for sleep or depression. And given the cautions in the original Vanderbilt patent for serotonin and porphyrins, probably not the first choice in any case. I've put it on a seperate page so as not to space on your thread as the info is of interest to the discussion and hard to locate: http://www.cpnhelp.org/tryptophan_serotonin_chla

 

 

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

Some of the background information in that patent text quote seems to come from the world of stroke and heart attack treatment; that's the sort of place where one finds references to "the post-ischemic neurological score" -- ischemia being lack of blood flow, as is produced by a heart attack or stroke, and "post-ischemic" implying that the ischemia would be a brief incident rather than an ongoing problem. While ischemia is a possible factor even in a slow Cpn infection, strokes and heart attacks do much quicker and more intense damage. So lessons from that world don't necessarily carry over; one would have to look hard at the numbers.

The bit about tryptophan interfering with gluconeogenesis, on the other hand, is definitely relevant. Still, if you're eating plenty of glucose or starches, you might not need to worry about gluconeogenesis, since your liver might not need to do much of it.