27 Apr 2018

Long term NAC -- would it eventually eliminate C.Pn.?


Would NAC administered for a sufficient time eliminate C.Pn? Here's my reasoning:The C.Pn. spreads in the body by means of Essential Bodies. NAC kills them. The replicating body has to work in a cell -- and all cells eventually die, killing the replicating bodies in them (I think that's what I read.)The Cryptic Body is kind of "out of the loop." Mysterious, but if it can't get energy from a cell, and it can't reproduce, what does it really do?Does anyone know, or can they set me straight, please?Ron 


Despite all my research I am still confused by this myself.

I also don't understand how CPn survives in its cryptic form after the particular cell it is inhabiting, dies, especially given that the patient is taking antibiotics that will attack all of its other forms...I am definitely not a biologist.

Frankly not a lot is understood about the Cryptic form. Remember that the Cryptic form is inside the cell, so it is not threatened by NAC, your immune cells, or other extracellular events. Second, it is originally an RB which when faced with nutrient starvation, antibiotics, or other threat to its survival reverts to a non-replicating form, still within the cell, and apparently very low metabolizing. It seems to go from aerobic metabolism (using oxygen) to anearobic metabolism (not using oxygen) which is why metronidazole kills it.

Under the return of favorable conditions, some of the Cryptic forms can covert back into RB's and begin replicating again. This is one of the major sources, along with accumulated EB's in extracellular tissues, of persistance and reinfection. Actually it is not reinfection, as the organism is still infecting us, just not fulminating while in cryptic form.

Elsewhere (I can't find the post) David Wheldon has commented that, at least theoretically, once you kill all the RB's, EB's and Cryptic organisms through the protocol, by staying on NAC the rest of your life you should be able to kill any infecting EB's from other persons and avoid reinfection.

Now, I suppose that it's possible that we could be harboring some Cryptic bugs, deep in some tissues which don't get penetrated well by flagyl or the like. But it is a relatively slow growing infection. So one would only have to be alert to the early, prodromal symptoms and treat immediately if they crop up. 

On Wheldon/Stratton protocol for Cpn in CFS/FMS since December 2004.

Its technical, but Guangming Zhongs work is interesting to study (or just glance over the abstracts). His group has identified a factor, CPAF, which chlamydiae secrete into host cytosol to degrade a certain protein that governs host DNA transcription.

Chlamydiae also interfere with the programmed death of host cells. Zhong has a molecular observation that rationalizes this fact: several important cell-death-governing proteins are degraded in infected cells. But Zhong doesnt know how the chlamydiae are bringing this about.

This stuff tallies with the broadest facts of immunity against intracellular parasites. The body wants to kill infected cells; the parasites dont want their homes destroyed. Theres probably no strong argument (at least I am unaware of one) that infected cells ought to die in time the way most types of normal human cells do. Absent evidence to the contrary, I would assume that they can live indefinitely.

Lately I've been reading surprising things about the well-proven immune diseases (MS, IBD, sarcoidosis, scleroderma, RA, Wegeners granulomatosis, ReA, systemic lupus, etc; but not CFS). Most of these diseases (but apparantly not MS?) are reported to usually remit at the clinical onset of AIDS, and some are shown to do so by formal studies. The strong response of many of these diseases to extreme doses of cytotoxic drugs (which unfortunately is a risky and very serious procedure) is also very striking. It appears that most of these diseases probably depend on the specific immune system, unlike normal infectious diseases. Nevertheless, I am still focused on bacterial antigens as the likeliest engines of these diseases. Daunted notes that antibacterials other than NAC attack all the other forms of Cpn. Thats so, but phenotypic resistance is a huge force. Most people probably know of the Gieffers paper, PMID 11157684, which suggests Cpn may be very hard to kill when it infects monocytes. Recently I've found several papers showing that this is a general phenomenon shown by many bacterial taxa:

10858369 Mycobacterium avium grown in Acanthamoeba castellanii is protected from the effects of antimicrobials.

16419973 Intracellular Staphylococcus aureus and antibiotic resistance:
implications for treatment of staphylococcal osteomyelitis.

8593002  Intraphagocytic growth induces an antibiotic-resistant phenotype of Legionella pneumophila.

Paper 3 (or was it another paper by Barker?) is notable for showing that the resistant phenotype lasts for some time after the host cell is lysed and the legionellae liberated.

Papers 1 and 2 (tho 2 doesnt give the raw data, which is bad form) are notable for showing an actual increase in numbers of the intracellular bacteria despite concentrations of abx that should be effective. This could be an artifact; a stressed bacterium might divide & disperse upon cessation of growth in order to increase the chances that one of the "seed" cells will soon fall on better days. Thus bacterial CFUs might increase without bacterial biomass increasing. However, if this is not such an artifact, then it is inexplicable and most important.

Paper 2 is notable because no professional phagocyte is involved; rather, osteoblasts are the host cell confering resistance on staph.

1634816, Fibroblasts protect the Lyme disease spirochete, Borrelia burgdorferi, from ceftriaxone in vitro, might also be added to this list of papers. So might 12924489, The effect of combined therapy according to the guidelines for the treatment of Mycobacterium avium complex pulmonary disease, which contains data suggesting that HIV-negative MAC pulmonary disease, a fully-accepted bacterial disease, may be harder to improve using antibacterial therapy than CFS is. The common denominator here is intracellularity of the bacteria. Despite looking at lots of data, I havent found out what physiological factors, other than slow growth, might contribute to this sort of extremely robust phenotypic resistance. This is not a hot research topic. There is some work going on that touches on this question but there isnt anyone out there directly asking how this stuff could work.

My point is simply that any bacteria contributing to any of our diseases may be real, real tough to kill.  

I guess this is all the more reason to consider the use of INH which has been shown to eradicate CPn from macrophages and monocytes. Unfortunately, I couldn't tolerate it daily, but I am going to consult with my doctor about pulsing INH.

Wow....that's interesting and also kind of frightening.


Hubby DX 10-05 by LLMD; positive for Borreliosis; took 200-400 mg Doxy for 2 mons; followed by zith daily for 6 wks; small does of flagyl daily for 3 mons; tested by ID for Cpn 6-06;  Tested positive and took Ketek for 6 weeks; Began Cap protocol

Lately I've been reading surprising things about the well-proven immunei diseasesi (MSi, IBD, sarcoidosis, scleroderma, RAi, Wegeners granulomatosis, ReA, systemic lupus, etc; but not CFS). Most of these diseases (but apparantly not MS?) are reported to usually remit at the clinical onset of AIDS, and some are shown to do so by formal studies. The strong response of many of these diseases to extreme doses of cytotoxic drugs (which unfortunately is a risky and very serious procedure) is also very striking.


I agree that these AIDS drugs probably would be very effective but are a little over the top for general use. If you are looking for a crazy novel drug that probably has excellent effect against Cpn, you might try Thalidomide. It is a little too intense for my own personal comfort what with the bad press and birth defects in children but it probably would be one of the better Cpn drugs.


Also it is my opinion that there is no free lunch (at least so far) when going after the persistent form of Cpn. Anything that works well has significant side effects and potential liver problems. The best so far are probably tetracyclines, rifamycins, and probably INH. I am partial to rifamycins but unfortunately Cpn develop reistance to these drugs quickly if used alone.

You could always try and starve them out. They need Vitamin C to replicate [Effects and applications of ascorbic acid on the proliferation of Chlamydia trachomatis] but you would probably end up with scurvy long  before the last Cpn was gone ;) And speaking of starving them out, you can't do better than old fashioned excercise for this. It is a time limited starvation for your own cells and will probably as often as not causes the Cpn to reduce to EBs, which all things being equal is the better state to have them.

- Paul 

Paul, your comments are very intriguing.

I am fortunate in that I am still able to exercise- I was losing the ability when I went on the protocol. But it is certainly not the fun it used to be. I know it has some positive effects on the immune system (not to mention my mental state!) but I am interested in this idea that CPn would reduce to EBs when subjected to exercise.

Any more details or thoughts on this idea?

I have also heard of people using infrared saunas to raise their body temperature. I wonder if this is effective. Fever therapy worked for syphillis in some cases...

Hi Daunted ! I have a very fond feeling when I see your name on here, you were so supportive in thisisms in my first quest to understand this thing. Thanks again for being there and participating
have you posted a blog for a while? I am very curious about how you are doing after all this time...exercise does not feel like it used to? what do you mean? in what way? Are you well in general now? all that kind of stuff. What do you take now, where are you at in terms of treatment? Just curious...
BLessings to you

On CAP since Sept '05 for MS, RA, Asthma, sciatica. EDSS at start 5.5.(early cane) Now 6 (cane full time) Originally on: Doxy 200, Azith 3x week, Tini cont. over summer '07, Revamp of protocol in Summer '08 by Stratton due to functional loss; clarithro


Thanks so much for your nice words. Good to see you active over here.

It is a roller coaster ride. I talked to my doctor right after a Flagyl pulse and I'm sure it looked like I was getting much worse- and right now I am having one of those days when I feel almost NORMAL. (Wish I could figure out what is causing it!)

According to my neurologist I am CFS/FMS but on many days I probably wouldn't even formally qualify for those diagnoses- but on other days I definitely would. Most of my symptoms are now more Fibro-esque, pain, stiffness, etc.

I'm still on the protocol and still reacting to Flagyl (especially when INH was there also). It's hard for me to tell where I am at, let alone tell someone else, but today I am feeling great.


Paul, thanks for that explanation. I thought that when I exercised in the heat (I live in a very hot, humid area) that it resulted in die-off reactions, but I was never sure- hard to tell. I agree that it's a bad idea to kill all the Cpn if you kill the host at the same time!


Exercise uses up the available ATP in your cells. Replicating Cpn can use both glucose for energy to make their own ATP or use the cell's ATP with their ATP/ADP exchange mechanism. However persistent Cpn only use the ATP/ADP exchange. So presumably when you excercise, many of the Cpn are forced to reduce down to the metabolically inactive EB state or die. (Hopefully some of both.). I would guess that some of the drugs like doxycycline really add to their challenge here as doxy damages Cpn and they would lack the energy to make repairs. I am not advocating large doses of doxy, intense excercise and starvation to eliminate Cpn though. There are lots of things you can do that will kill Cpn including jumping off a bridge but are not neccessarily good ideas Image removed.

- Paul 

 Daunted- I'm seeing a potential headline here: "Daunted discovers the cause of feeling normal..."

Please, please, let us know if you do. 

On Wheldon/Stratton protocol for Cpn in CFS/FMS since December 2004.

Headed off at the pass! lol  I was just writing a response to the question about excercise and boy am I too slow! lol Here's what I wrote...

I posed a similar question a week or two ago about excercise and it's effect on CPn and whether or not the protocol would be impacted by it.  Either Jim or Paul wrote back and suggested that the excercise uses up the excess ATP, preventing RBs from using it within the cells.  I think that's probably going on to an extent that depends upon how much you excercise and how vigorous what you do is. 


best, JohnRRMS/EDSS was 4.5, 5, 6, 6.5, 6.9999, 6.5 on Wheldon/Stratton Protocol beginning 04/12/2006nac 4x600 mg/daydoxycycline 2x100mg/dayazithromycin 3x250mg/day MWFmetronidazole 3x400mg/day then 3x500mg/day

Paul, the cytotoxic/lymphoablative regimes I mentioned arent in use for HIV (tho the idea has been explored). Theyre only in use for some lymphomas and, now, for tough cases of the immune diseases I listed.

Do you have any information on thalidomide being antibacterial? I think (not certain here) HIV generally replicates only in activated leucocytes; that may explain why a TNF antagonist could hinder HIV.

Regarding ATP, during exercise it is utilized at a higher rate, but also generated at a higher rate, so I'm not sure whether its concentration declines very dramatically or not. Even at rest the turnover is very rapid - all of the ATP in your body is hydrolysed to ADP and recycled back into ATP every minute (or less). I think I recall that a person hydrolyses a total of ~50 kg of ATP per day (whereas I think the total amount in the body at a given moment is on the order of 20 g).

This is the first opportunity I've had to catch up on this thread when my brain is working and I am not.

 I think Eric's idea that C.Pn. host cells can basically live forever puts the kibosh to the question I started with -- NAC by itself probably wouldn't work -- certainly not soon enough. And if I miss a day or two -- Bam! Back to "square one" for me. No joy.

As far as exercise/ATP starving the beasties:

  • if it comes to a showdown, they've got first dibs on my ATP -- I wouldn't be sick, else, right?
  • on the CFS discussions/sites, there's a lot of talk about CFS setbacks caused by exertion. I know the research available is highly suspect, in its definition of CFS (basically, anyone who is chronically fatigued), its definition of exercise (tai chi, yoga, gentle stretching, daily activity as tolerated by the patient), and its sponsorship.
  • I understand (no, I hear, I don't really understand) that in a pinch, the cells will "burn" ADP to AMP -- but that there's no recycling AMP to ADP; they have to start all over from scratch. I always thought that might be what happened when I over-exerted myself. I was OK at the time, but hammered for a day or two after (which I thought of as the time required to rebuild the ADP/ATP cycle.)
  • And, as both Paul and Eric implied, the lack of ATP might hurt me more than the bugs. For instance, some experts consider CFS a form of heart failure, where exertion merely hastens the disease.

Some very interesting discussion, though -- thank you all for chiming in!



On Stratton protocol for CFS starting 01/06 (NE Ohio, USA).

RonOn CAP for CFS starting 01/06 (NE Ohio, USA)Began rifampin trial 1/14/09Currently: on intermittent

Ron I seem to recall ADP is regenerated from AMP in the reaction ATP + AMP --->  2 ADP. But as usual :) I'm not really certain.

I looked in my text to see if the concentration of ATP declines much during exercise, but found no info. By the way in case anyone is looking for info on this, concentration is indicated with square brackets. "[ATP]" means "concentration of ATP."

the cytotoxic/lymphoablative regimes I mentioned [...] [are] only in use for some lymphomas and, now, for tough cases of the immune diseases I listed.

Oops I got this wrong. Its been (at least) tried in some other cancers as well. In breast cancer for example, it looks like there were some trials that showed it wasnt better than conventional chemo... then a further trial showed it was a bit better (but that trial was criticized for not employing taxols, which are apparantly the best breast cancer drugs). Still, from what I read it sounds like it may be used in select cases of breast cancer.

Wow, what an interesting thread. IT has many angles and theories in it for mental digestion. thanks for posting this

On CAP since Sept '05 for MS, RA, Asthma, sciatica. EDSS at start 5.5.(early cane) Now 6 (cane full time) Originally on: Doxy 200, Azith 3x week, Tini cont. over summer '07, Revamp of protocol in Summer '08 by Stratton due to functional loss; clarithro

Excellent forum.  A word of caution on some of the abx - beware of possible resistance.  I realise the contributors will research this before devising their program.  Less technical readers need to be cautious of Rifampicin and similar 'TB' drugs and get good advice before taking them.  Abx are freely available in many areas of the world, unlike the control in the USA/UK..............Mark.

Mark Walker - Oxford, England.
RRMS since 91, Dx 97, CFS Jan03.  Patient of David Wheldon Feb06, started CAP Mar06. Pharmaceutical Consultant (until I stopped working in Jan03).<

Mark Walker - Oxford, England.RRMS Nov 91, Dx 97. CFS Jan03. Copaxone + continuous CAP (NAC, Dox, Rox) Feb06 to May 07. Met pulses from Jun06. Intermittent Abx from June 07 onwards.