Winnowing down EBs?

Hi.  I'm wondering how possible it would be to willow down the EBs gradually so that when Flagyli is started, there isn't the herx reaction to a massive die off of EBs?  What I have in mind is a lower dose of NACi, taken over time.

So ultimately my question is this:  is it necessary to take the full 2x600mg / day of NAC to achieve die off of EBs, or can a smaller dose eradicate a smaller portion of them?  My "mini-trial" of NAC was using 2x600 mg / day and I got a massive reaction (by my definition) on the third day.  I want to mitigate that somewhat in the future so that when I get to the Flagyl stage, it won't incapacitate me.  A smaller dose of NAC would theoretically kill off fewer EBs, right?  It would still be effective, just not as effective?

Farandwide- Flagyli doesn't kill EBi's, so winnowing them down (I think that's the word you wanted) won't mitigate the pulse reactions. They are a separate thing. Flagyl is intended to kill the anearobic Cryptic phase, and may have some kill effect for RB's as well.

As a separate issue, you can certainly start slower on NACi and work up over time, just like it is suggested in the rest of the protocol. It is the working up to full protocol eventually that will assure you are killing all phases adequately. Strong reaction to NAC just means that you have a big EB load built up, or are very sensitive to the endotoxini/porphyriai from the die off. 

On Wheldon/Stratton protocol for Cpni in CFSi/FMSi since December 2004.

 

CAPi for Cpni 11/04. Dxi: 25+yrs CFSi & FMSi. Currently: 250 aithromycin mwf, doxycycline 100mg BIDi, restarted Tinii pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

Indeed, winnowing is the word I meant but my impulse to hit the post button won over my impulse to perform spell and grammar check.  By the time I realized my mistake, there had already been views and your reply.  My bad, lol!  Anyhow, thanks for your reply.

Ok, so NACi is effective against EBs.  I think I've confused Flagyl and INHi (I think thats the one?) with the intent of referring to the one that's effective against EBs.  However, allow me to pose this question for sake of clarification.  I've read about the Wheldon protocol on his site and as I recall, there were only three preferred antibioticsi--doxycycline, roxithromycin (or azi), and metronidazol.  Metronidazol is Flagyl, correct?  Okay, so assuming that's correct, which of those are effective against EBs, if any, or is NAC the only portion of that protocol that's effective against EBs? 

I've read in other posts about something else that's effective at breaking the disulphide bonds in the outer membrane of EBs, but I fail to recall just what that was.  Niacini perhaps? 

I'll take a look around the site and the handbook to see what I can find.  I'll also endeavor to shake the morning off and wake up! lol Wink

thanks again

John

best, John

RRMSi/EDSSi was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
naci 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day

NACi or Amoxicillini takes out EBs. I gather that most of the data showing the efficacy of NAC is unpublished, it's found primarily in the patents and in communications with Drs. Stratton and Wheldon.

NAC is preferred by most I believe because of the lack of side effects as compared to Amoxicillin.

Daunted is correct. NACi is known as a disulphide bond reducer in other contexts but not tested in the original Mitchell/Stratton research. David Wheldoni and Mike Powell both independently began testing NAC as an alternative to amoxicillan to destroy the disulphide bonds of the EBi cell membrane, and both found it efficacious. Dr. Stratton gave his "seal of approval" to using NAC as an alternative to amoxi. You will see on David's current protocol that NAC is considered an important part, not only as anti-EB but also for it's use as a precursor to glutathione which is a major liver detox agent, and as an antioxidanti in it's own right.

INHi is an anti-replicant (RB) agent, having particular efficacy in clearing Cpni from macrophages and monocytes-- immunei cells. This tends to restore immune dysfunction from Cpn as these cells are then fully functioning, and since these cells are one of the ways Cpn spreads via the blood stream (along with EB shedding) it limits the spread to other organs.

The only similarities between INH and Flagyli is that both function as antibioticsi by their metabolites (what they are broken down into in the body) inducing free radical damage within the bacteria, but at very different phases of the bacterial cycle.  The other similarity is that it has been proposed by Dr. Stratton that INH could be pulsed along with Flagyl in some cases, since it's effects are more immediate unlike the other anti-replicants which act by inhibiting proteins rather than destroying them.

On Wheldon/Stratton protocol for Cpn in CFSi/FMSi since December 2004.

 

CAPi for Cpni 11/04. Dxi: 25+yrs CFSi & FMSi. Currently: 250 aithromycin mwf, doxycycline 100mg BIDi, restarted Tinii pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

I don't want to beat a dead horse here, but just for my own mental comfort, I want to ask again about winnowing down the EBs.  What I've been thinking of doing is to take 1 x 600 mg of NACi every other day to begin with; however, I also had the thought that it might be necessary for a certain blood level of NAC to be reached before NAC is effective.  Is that the case?  In addition, is it not possible for Cpni to develop a resistance or toleration of NAC?  Just want to make sure I don't  create a problem in how I approach things.

many thanks!

John

best, John

RRMSi/EDSSi was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
naci 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day

The only answer to both your questions (blood level required and resistance) about NACi is: we don't know!

That said, start as you need to, and work up as tolerance requires. That's the watchword here.

On the resistance issue I could speculate that, since they are not metabolizing nor reproducing, EBi's can't develop resistance to an agent in of themselves. They would have to replicate to pass on genesi to the next generation of EB's. If you are taking antireplicants (eg Doxyi, Zithi) this is less likely to happen. 

On CAPi's protocol for Cpni in CFSi/FMSi since December 2004.
Currently: 150mg INHi, Doxy/Zith, Tinii pulses 

"I really didn't say everything I said." Yogi Berra

 

CAPi for Cpni 11/04. Dxi: 25+yrs CFSi & FMSi. Currently: 250 aithromycin mwf, doxycycline 100mg BIDi, restarted Tinii pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

Thanks Jim, I will take your suggestion and see how it goes.  I've just been apprehensive about it since my fist experience with NACi was so horrible.  But then I had no idea at the time what kind of bacterial loadi I might have.  It clearly must be substantial despite the fact that I'm only RRMSi.  I think the reaction I had was a peek at what others who have had more severe experiences with MS have dealt with.  Not fun.  I can at least still walk under my own power.  I'll be careful going forward with the NAC.  1 x 600 mg every other day it is...

John

best, John

RRMSi/EDSSi was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
naci 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day

I thought I would follow up on this thread with an update.  I have taken 1 x 600 mg, Monday, Wednesday, and Friday of this week with no major ill affects.  This is in stark contrast to my first go with NACi about 1.5 months ago where I did 2x600mg for 3 straight days and had a massive reaction on the fourth day.  I think it's entirely possible that I knocked down my load of EBs that first time, substantially, and that it's now lower.  But I'm not assuming that and continuing to take it slow.  I don't want the same sort of dibilitating reaction I had the first time to happen again.  What I may do is in a couple of weeks, increase my dosage to 1x600mg x 1/day instead of every other day as I am now.

John

best, John

RRMSi/EDSSi was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
naci 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day

 John- It's good to hear of your progress on this. When you take an obviously innocuous amino acid like NACi, and get such strong reactions, you know it ain't for no reason. No reason at all to push the limit, as your slow-and-steady is winning the race!

On CAPi's protocol for Cpni in CFSi/FMSi since December 2004.
Currently: 150mg INHi, Doxyi/Zithi, Tinii pulses 

"I really didn't say everything I said." Yogi Berra

 

CAPi for Cpni 11/04. Dxi: 25+yrs CFSi & FMSi. Currently: 250 aithromycin mwf, doxycycline 100mg BIDi, restarted Tinii pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

Another follow-up to my earlier one...I have now been taking NACi every other day since last Monday (not yesterday but a week ago).  While I haven't had the same reaction to NAC I did the first time (due to the lower dosage), I have had a reation.  My reaction is that my MSi symptoms are a little worse.  I started doxyi just a few days before I began NAC, but I don't think that the increase in MS symptoms is due to doxy.  More specifically, the increat in symptoms is that I have a little bit harder time walking and my balance is a little worse.  Now, it's not constant and seems to be greater in the morning than the late afernoon evening, which would correspond to when I take NAC wherease I take doxy 2 x per day, in mid afternoon and late evening.

As stated in my last post, I'm now considering when to increase to 1 dose of NAC a day vs. 1 every other day as I am now taking.  I may wait until the second week in May when I should be starting azi for the first time to see how I respond to that when it's added.  So far, my reaction to treatment has been uncofortable but manageable/doable.  I know that I've got a long way to go yet but look forward to down the road when I can look back and say that I'll never have to deal with any of that again.  Sky-diving anyone?  Rock-climbing?

John

RRMSi/disability 4.5 on Wheldon Protocol since 04/12/2006

best, John

RRMSi/EDSSi was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
naci 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day

John, I must say you are being very calm and collected about all this.  I never took NACi until not yet a year ago, so I don't know how it would have affected me in the early days.  When I first started the antibioticsi, I was a bit too loopy to register how I was affected, but David says that my MSi symptoms became slightly worse.  I don't remember but I do remember having an awfully runny nose. When I first started taking NAC this also made me rather sniffly for a few weeks.  Not all day, but fairly shortly after taking the stuff.  I was taking three of them so I just took them all together, to avoid it happening more than once.  I very shortly after starting, did this with the doxycycline as well.

I think I'll choose rock-climbing.Undecided

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

John,

My opinion, which is not neccessarily shared by Dr. Wheldon or Dr. Statton, is that NACi should not be taken early on. I think focusing on the most important thing, which is in my opinion replicating Cpni, makes the most sense. It is a nice plus to kill some EBs outside of cells and NAC has some liver protective properties. However you can only address some stages of Cpn initially and have to choose between replicating organisms which are making more Cpn and causing the most side effects, elementary bodies which are doing no harm until you cause them to start replicating with NAC, and cryptic bodies which only cause modest side effects and rarely replicate, so I would choose to expend all of my resources on the replicating organisms initially. Anyway while anecdotal this has worked very well for me. I cannot say that it would work for everyone but if it were me I would be adding NAC later rather than sooner.

- Paul

 Paul- Your rationale makes sense logically in terms of the dynamics of the bacteria, but leaves out the possible medical dynamics of the patient. The winnowing down of EBi's is not actually the reason for starting a CAPi with NACi, although it is the question of the thread here.

The rationale for starting with NAC is in terms of protocol safety: that likely many people with Cpni have compromised liver functioning, both from porphyrin toxicity and endotoxini, and from Cpn infecting the liver itself. The protectant effects of NAC build in safety and lower the risk of the CAP overall. Since we don't have a way to measure Cpn infection of the liver ahead of starting a CAP, it makes the most sense to build in protection of this vital organ first. In addition, Dr. Stratton feels that, clinically, patient reaction to NAC gives him some rough idea of the total Cpn load.

It is an individual choice, of course, to pursue the biggest energy drain and porphyrin producing phase of the organism first by starting with antireplicant drugs first. Remember, too, that you had already gone through a CAP and had a lot of experience in dealing with Cpn and likely had a better sense of how effected your liver was from your symptoms and experience. So your margin of safety was added to by this. Most people starting in don't have any sense of this. I know now that my liver was effected by Cpn, after having felt the improvements in my liver symptoms!

Actually, most people report building up within weeks on the NAC and starting in with the other CAP drugs. Given the relatively slow rate of repilication of Cpn, this is probably not a big deal.

On CAP's protocol for Cpn in CFSi/FMSi since December 2004.
Currently: 150mg INHi, Doxyi/Zithi, Tinii pulses 

"I really didn't say everything I said." Yogi Berra

 

CAPi for Cpni 11/04. Dxi: 25+yrs CFSi & FMSi. Currently: 250 aithromycin mwf, doxycycline 100mg BIDi, restarted Tinii pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

Paul

You may be under the misconception that I am only taking NACi - I'm not.  I'm on Doxyi as well.  The two are not mutually exclusive and I see no reason why I can't do both at the same time.  My hope is that by the time I get to the metroi/flagyl stage that I will have smacked down my EBi load such that any effects I'm feeling from taking it can be if not entirely, mostly attributed to the die-off of RBs and the cryptic formi of Cpni.  I hope to be able to continue taking NAC through that process and hope that I've winnowed down the EBs such that I'm feeling nothing or almost nothing as a result of taking it.

John

RRMSi/disability 4.5 on Wheldon Protocol since 04/12/2006

best, John

RRMSi/EDSSi was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006
naci 4x600 mg/day
doxycycline 2x100mg/day
azithromycin 3x250mg/day MWF
metronidazole 3x400mg/day then 3x500mg/day

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