Hi all,
I'd like to know, what is the physical sensation of bursting a lot of EBi [1]'s at once?
I have a good reason for asking - related to the quote Daisy managed to pull up from the Stratton patent regarding the use of dithiol reducing agents to counter EB's.
many thanks,
garcia.
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Hunter: Don't think - experiment
Links:
[1] http://www.cpnhelp.org/taxonomy/term/46
[2] http://www.cpnhelp.org/chlamydia_pneumoniae/supp
[3] http://www.cpnhelp.org/taxonomy/term/64
[4] http://www.cpnhelp.org/taxonomy/term/38
[5] http://www.cpnhelp.org/chlamydia_pneumoniae/ca_0
[6] http://www.cpnhelp.org/taxonomy/term/44
[7] http://www.cpnhelp.org/taxonomy/term/63
[8] http://www.cpnhelp.org/glossary/term/167
[9] http://www.cpnhelp.org/taxonomy/term/127
[10] http://www.cpnhelp.org/glossary/term/163
[11] http://www.cpnhelp.org/glossary/term/168
[12] http://www.cpnhelp.org/taxonomy/term/39
[13] http://www.cpnhelp.org/glossary/term/183
[14] http://www.cpnhelp.org/glossary/term/170
[15] http://www.cpnhelp.org/glossary/term/120
[16] http://www.cpnhelp.org/taxonomy/term/58
[17] http://www.cpnhelp.org/glossary/term/185
[18] http://www.cpnhelp.org/glossary/term/171
[19] http://www.cpnhelp.org/glossary/term/162
[20] http://www.cpnhelp.org/glossary/term/184
[21] http://www.cpnhelp.org/taxonomy/term/49
[22] http://www.cpnhelp.org/print/2396#comment-15309
[23] http://www.cpnhelp.org/nac_and_mercury
[24] http://www.cpnhelp.org/taxonomy/term/142
[25] http://www.cpnhelp.org/glossary/term/177
[26] http://www.cpnhelp.org/chelation_cap_question
[27] http://null/user/daisy
[28] http://null/taxonomy/term/46
[29] http://null/chlamydia_pneumoniae/supp
[30] http://null/taxonomy/term/58
[31] http://null/glossary/8#term114
[32] http://www.cpnhelp.org/taxonomy/term/34
[33] http://null/taxonomy/term/34
[34] http://null/taxonomy/term/64
[35] http://null/taxonomy/term/49
[36] http://www.cpnhelp.org/print/2396#comment-15346
[37] http://www.cpnhelp.org/print/2396#comment-15348
[38] http://www.cpnhelp.org/glossary/term/88
[39] http://www.cpnhelp.org/taxonomy/term/24
[40] http://www.cpnhelp.org/chlamydia_pneumoniae/anti
[41] http://www.cpnhelp.org/chlamydia_pneumoniae/an_0
[42] http://www.noamalgam.com/
[43] http://www.cpnhelp.org/print/2396#comment-15403
I found, on taking N-acetyl
I found, on taking N-acetyl cysteine, symptoms of sinusitis similar to those which had troubled me all through adolescence, but without the heavy dull ache of sinusitis. This was accompanied by a profuse watery nasal discharge. Also, I developed a productive cough with thin sputum. This lasted for about six weeks and then tailed off. NACi [2] doesn't have any effect on me at all now - I take 2,400 mg every day. Not everyone has 'NAC-flu'; it seems to depend on organism numbers and probably the state of the immunei [3] response. I only started NAC after taking cidal antibioticsi [4], so I had been exposed to lots of chlamydial proteins.
D W - [Myalgia and hypertensioni [5] (typically 155/95.) Began (2003) taking doxycycline and macrolide and later adding metronidazolei [6]. Now on intermittent treatment. No other antihypertensive therapy. BP 8th June 114/75.]
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D W - [Myalgia and hypertensioni [5] (typically 155/95.) Began (2003) taking doxycycline and macrolide and later adding metronidazolei [6]. No medication now; just supplementsi [7] and IR sauna. Morning BP typically 105/75]
Thanks very much for posting
Thanks very much for posting your experiences David.
Before I had CPni [8] I was chelating for mercury toxicity with alpha lipoic acidi [9] (ala).
However 10 months after getting infected with CPn I found I could no longer tolerate ala - it would give me the strange symptom of muscle pain & stiffness in my left neck/shoulder area. After 3 days of chelating I would be in excrutiating pain and virtually unable to move my neck/shoulder. I now know that this is where my CPn infection is most active.
All this time I've been wondering exactly what was going on.
Given Stratton's comments on the role of disulfide reducing agents in breaking apart EBi [1]'s, I wonder if that was what I was experiencing? Massive numbers of EB's being broken apart by ALA after 10 months of unfettered growth.
Any comments much appreciated.
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CFSi [10] since 2001. Infected CPn Jan 2006. Dx'd March 2007. Started CAPi [11] March 2007. Currently taking: Azith 250mg MWF, 100mg doxyi [12] every other day.
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Hunter: Don't think - experiment
garcia, I don't think it
garcia, I don't think it was the breaking apart of the EBs that you were feeling, but inflammation caused by your immune system's clean-up crew after the EBs croaked and broke up. It makes a mess, and the clean-up is rough.
Joyce~caregiver-advocate in Dallas for Steve J (SPMSi [13]). CAPi [11] since August 06, antivirals, heavy metals chelation, LDNi [14], Metanx, Lunesta, GF/CF diet, Lauricidin, oral IgG/lactoferrin/IGF-1 booster, astaxanthin, gamma oryzanol.
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Joyce~caregiver-advocate in Dallas for Steve J (SPMSi [13]). CAPi [11] since August 06, Cpni [8], Mpn, B. burgdorferi, systemic candidiasis, EBVi [15], CMV & other herpes family viral infectionsi [16], elevated heavy metals, gluten+casein sensitivity.
Well said, Joyce! I do
Rica PPMSi [17] EDSSi [18] 6.7 at beginning - now 2. Began CAPi [11] Sept, 2004 with Rifampin 150 mg 2xd, Doxyi [12] 100 mg 2xd, added regular pulses Jan 2005. Jan 2006 switched to Doxy, Azith, cont. flagyli [6] total 43 pulses NC USA
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Rica PPMSi [17] EDSSi [18] 6.7 at beginning - now 2. Began CAPi [11] Sept, 2004 with Rifampin 150 mg 2xd, Doxyi [12] 100 mg 2xd, added regular pulses Jan 2005. Jan 2006 switched to Doxy, Azith, cont. flagyli [6] total 52 pulses LDNi [14] NC USA
Whatever causes Cpn to die
Whatever causes Cpni [8] to die in its different stages will have an effect which we will feel at the site of the clean up operation. It does not matter, in my experience, what substance it is that has caused it, it all feels the same to me. Nausea, guidiness, pain and sometime depression is my experience.
Michele (UK) GFAi [19]: Wheldon CAP1st May 2006 . Daily Doxyi [12], Azi MWF, Flagyli [6] at 400mg for 7 days prior to 5 day pulses at 1200mg three weeks cycle. Spokesperson for Ella, RRMSi [20] Wheldon CAP 16th March 2006
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Michèle (UK) GFAi [19]: Wheldon CAPi [11] 1st May 2006. Daily Doxyi [12], Azi MWF, metroi [6] pulse. Zoo keeper for Ella, RRMSi [20], At worse EDSSi [18] 9, 3 months later 7 now 5.5 Wheldon CAP 16th March 2006
Thanks very much everyone
Thanks very much everyone for the responses.
Joyce, I think you are right that it is an immunei [3] response which is being felt.
Katman, thanks for the words of encouragement. Its good to know you have the same symptoms.
My point in posting the above was that I can't tolerate either NACi [2] or amoxicillini [21], so need another anti-EBi [1] agent. As far as I know no one is looking at alternatives - ALA certainly sounds like it could be a potential candidate.
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CFSi [10] since 2001. Infected CPni [8] Jan 2006. Dx'd March 2007. Started CAPi [11] March 2007. Currently taking: Azith 250mg MWF, 100mg doxyi [12] every other day.
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Hunter: Don't think - experiment
Initially, the CAP is going
Initially, the CAPi [11] is going to be hard to tolerate and maybe you should consider taking a smaller dose of NACi [2], the Wheldon cap suggest that you take ALA additionally to NAC. This is not going to be a bed of roses whichever drugs you start with. If you don't have some unpleasant reactions to taking the ABXi [4] in the beginning you are probably not treating Cpni [8].
Michele (UK) GFAi [19]: Wheldon CAP1st May 2006 . Daily Doxyi [12], Azi MWF, Flagyli [6] at 400mg for 7 days prior to 5 day pulses at 1200mg three weeks cycle. Spokesperson for Ella, RRMSi [20] Wheldon CAP 16th March 2006
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Michèle (UK) GFAi [19]: Wheldon CAPi [11] 1st May 2006. Daily Doxyi [12], Azi MWF, metroi [6] pulse. Zoo keeper for Ella, RRMSi [20], At worse EDSSi [18] 9, 3 months later 7 now 5.5 Wheldon CAP 16th March 2006
Michelle, I can't take NACi
Michelle, I can't take NACi [2] because I'm mercury poisoned, not because I'm expecting things to be "a bed of roses".
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CFSi [10] since 2001. Infected CPni [8] Jan 2006. Dx'd March 2007. Started CAPi [11] March 2007. Currently taking: Azith 250mg MWF, 100mg doxyi [12] every other day.
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Hunter: Don't think - experiment
In that case I imagine that
Michele (UK) GFAi [19]: Wheldon CAP1st May 2006 . Daily Doxyi [12], Azi MWF, Flagyli [6] at 400mg for 7 days prior to 5 day pulses at 1200mg three weeks cycle. Spokesperson for Ella, RRMSi [20] Wheldon CAP 16th March 2006
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Michèle (UK) GFAi [19]: Wheldon CAPi [11] 1st May 2006. Daily Doxyi [12], Azi MWF, metroi [6] pulse. Zoo keeper for Ella, RRMSi [20], At worse EDSSi [18] 9, 3 months later 7 now 5.5 Wheldon CAP 16th March 2006
Hi Garcia, FYI, if you [22]
Hi Garcia,
FYI, if you haven't already seen it, you may find an older thread on NACi [2] and Mercury interesting and potentially useful for discussion with your doctor:
http://www.cpnhelp.org/nac_and_mercury [23]
Hang in there...
On Combined Antibiotic Protocol for Cpn in Rosaceai [24] since 01/06
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On Combined Antibiotic Protocol for Cpni [8] in Rosaceai [24] 01/06 - 07/07, On Vit D3 + NACi [2] since 07/07 and daily FIRi [25] Sauna since 08/07
garcia,
garcia, You might benefit from reading this comment from another current thread [26]:
"Submitted by Daisy [27] on Fri, 2007-06-08 08:36.
Eureka - Some neuron in the back 40 kicked in and I found it - in Yguner's antibiotic log on THISISMS. Thanks Guner! Here it is below for anyone else who is interested.
Looks like those who are chelating with oral DMSA are getting some EBi [1]i [28] killing to boot in addition to the NACi [29]! Could also help explain chelation related brain fog in some !
Here is document about succimer (DMSA) and its use in the treatment of Cpn. I highlighted the relevant in yellow.
As described in previous sections. it is also believed that persistance of chlamydial infectionsi [30], in part, may be due to the presence of cryptic forms of Chlamydia within the cells. This cryptic intracellulari [31] chlamydial form apparently can be activated by certain host factors such as cortisone (Yang et al., Infection and Immunity, 39:655-658 (1983); and Malinverni et al., The Journal of Infectious Diseasesi [32]i [33], 172:593-594 (1995)). Antichlamydial therapy for chronic Chlamydia infections must be continued until any intracellular EBs or other intracellular cryptic forms have been activated and extracellular EBs have infected host cells. This reactivation/reinfection by chlamydial EBs clearly is undesirable as it prolongs the therapy of chlamydial infections, as well as increases the opportunity for antimicrobial resistance to occur.
Physiochemical agents have been identified that can inactivate chlamydial EBs in their respective hosts by reducing disulfide bonds which maintain the integrity of the outer membrane proteins of the EBs. For Chlamydia, disruption of the outer membrane proteins of EBs thereby initiates the transition of the EB form to the RB form. When this occurs in the acellular milieu where there is no available energy source, the nascent RB perishes or falls victim to the immunei [34] system. Thus, disulfide reducing agents that can interfere with this process are suitable as compounds for eliminating EBs.
One such class of disulfide reducing agents are thiol-disulfide exchange agents. Examples of these include, but are not limited to, 2,3-dimercaptosuccinic acid (DMSA; also referred to herein as "succimer"); D,L,-.beta.,.beta.-dimethylcysteine (also known as penicillamine); .beta.-lactam agents (e.g., penicillins, penicillin G, ampicillin and amoxicillini [35], which produce penicillamine as a degradation product), cycloserine, dithiotreitol, mercaptoethylamine (e.g., mesna, cysteiamine, dimercaptol), N-acetylcysteine, tiopronin, and glutathione. A particularly effective extracellular antichlamydial agent within this class is DMSA which is a chelating agent having four ionizable hydrogens and two highly charged carboxyl groups which prevent its relative passage through human cell membranes. DMSA thus remains in the extracellular fluid where it can readily encounter extracellular EBs. The two thiol (sulfhydryl) groups on the succimer molecule (DMSA) are able to reduce disulfide bonds in the MOMP of EBs located in the extracellular milieu."
Of course, my thought was that you might "kill two birds with one stone." A personal comment on the prospect of depending on NAC to chelate mercury: I've been using NAC since Spring "06. Most of the time, the dosage has been 2400mg/day. When I was recently tested for heavy metals, they were elevated, especially mercury. There is no way of knowing what my mercury level was before starting the NAC, so I don't know how much it accomplished. Given that the mercury was high even after that year of NAC, I suspect that NAC chelation of mercury is something that happens at a comparatively creeping pace. I hope you try again with NAC, though, starting out with a low dosage and titering-up. You need it for EB killing even if you are on chelation therapy, and the glutathione boosting property is something all of us need. The starting is tough, but that's because it's killing something. Extra vitamin C and activated charcoal helped both Steve and me through the NAC flu.
Joyce~caregiver-advocate in Dallas for Steve J (SPMSi [13]). CAPi [11] since August 06, antivirals, heavy metals chelation, LDNi [14], Metanx, Lunesta, GF/CF diet, Lauricidin, oral IgG/lactoferrin/IGF-1 booster, astaxanthin, gamma oryzanol.
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Joyce~caregiver-advocate in Dallas for Steve J (SPMSi [13]). CAPi [11] since August 06, Cpni [8], Mpn, B. burgdorferi, systemic candidiasis, EBVi [15], CMV & other herpes family viral infectionsi [16], elevated heavy metals, gluten+casein sensitivity.
Hi Joyce, thanks for posting [36]
Hi Joyce,
thanks for posting that but you could have saved yourself the effort - if you look along Daisy's thread you will see that I actually posted there. It was Daisy's quote which got me started.
A couple of points.
NACi [2] is not a chelator of mercury. Never has been, never will be. The word chelator comes from the greek word "chele" which means claw - reason being is because a chelator is defined as a compound which forms a bond with a metal ion in 2 (or more) places. The crucial thing is that there has to be 2 bonds.
The reason this is a meaningful definition is that we want a chelator to hold on tightly to a substance before escorting it out of the body (either via urine or bile). Now chemical bonds are made and lost all the time. If you have a substance which holds onto a metal in 2 places, even if one of the bonds is temporarily lost the other bond will most likely hold.
DMSA, DMPS, ALA are all examples of chelators - they each form 2 bonds with a metal ion, thus holding on to it tightly much like a claw.
NAC is a single thiol - it is not a chelator. It is more properly called a "mobilizer" of mercury. The bond that NAC forms with mercury is no stronger than the bond mercury makes with the thiols in your body.
Now NAC has many health benefits, raising GSH amongst them (as you point out). However many/most people who are mercury poisoned have deranged sulphur chemistry and a tendency to already be high in cysteine. As such taking NAC rapidly and markedly worsens the symptoms of mercury poisoning. Such people often have to limit their intake of dietary sulphur as foods high in sulphur can produce the same symptoms.
When I talk about mercury poisoned people I don't mean anyone who has mercury in their body (which is pretty much everyone). I'm talking about a specific subset of people whose ability to deal with their body-burden of mercury has broken down.
Measuring urine mercury (either with or without challenge) is meaningless as an indicator of chronic mercury poisoning. Everyone has mercury in their body. Also what is important is not the mercury in the kidneys, but the mercury in the brain because it is here that Hg causes the most damage.
There is no direct way of measuring brain mercury (other than by autopsy). The next best thing is the "hair test interpretation rules" as defined by Andrew Cutler Phd (the world's foremost expert on chronic mercury poisoning - think of him as the equivalent of Dr Stratton). Basically mercury poisoned people have a unique "fingerprint" in the mineral pattern on their hair.
You actually don't need NAC for killing the EBi [1]. If you read the quote which you yourself pasted you will see that Dr Stratton talks about a multitude of agents (DMSA amongst them) which are productive against elementary bodies. In fact he singles out not NAC, but DMSA for special consideration.
Garcia.
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CFSi [10] since 2001. Infected CPni [8] Jan 2006. Dx'd March 2007. Started CAPi [11] March 2007. Currently taking: Azith 250mg MWF, 100mg doxyi [12] every other day.
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Hunter: Don't think - experiment
Michele, Joyce isn't [37]
Michele,
Joyce isn't chelating - she is using NACi [2] which is not a chelator. BTW I was chelating before I caught CPni [8]. The first effect of the CPn was to render me unable to chelate.
> I think it will be difficult to replace the drugs you are not able to take with others that are as effective.
I'm curious as to what you base that assesment on (btw NAC isn't a drug but a supplement made from animal hair).
If you read the patent of Dr Stratton you will see that he mentions a multitude of anti-elementary bodyi [1] substances. NAC is just one of many. In fact he singles out not NAC, but DMSA for special consideration. It might be an idea to read the patent when you have time.
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CFSi [10] since 2001. Infected CPn Jan 2006. Dx'd March 2007. Started CAPi [11] March 2007. Currently taking: Azith 250mg MWF, 100mg doxyi [12] every other day.
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Hunter: Don't think - experiment
Garcia- Your comments on
Garcia- Your comments on NACi [2] as a mobilizer but not chelator, and on the more extensive mercury poisoning you are dealing with are helpful. I've commented before that we become "experts by necessity" of those particular aspects of illness from which we are particularly afflicted. You obviously have had to develop expertise in this one. No need to get snippy with each other over differences in terms, you are actually getting somewhere here in the discussion.
By the way, I've read all the different patents more than once, but frankly don't recall all the details. I recalled more, of course, when they were fresh and I was desperate for understanding, but many details drop out-- I had not recalled all the agents cited as being anti-EBi [1] such as DMSA for example-- as some details weren't relevant to me at the time. It's a bit arrogant of you to tell someone who has been here for years and made a massive study of Cpni [8] to read the patent materials. Although I daresay that I could stand to reread them myself. No matter, we are all snippy when sick, and give each other latitude. That's why we rely on each other here as a community, to be a group-mind for the ill, brain fogged, inexpert and forgetful to draw on each other's expertise.
Frankly, I think you could forgo the EB's and get started on the doxyi [12] and azith. Why? Well for one, Dr. Stratton has often altered the order of the meds he uses and sometimes will go for "clean up of EB's" after a person is well into treatment. The other is that by bringing down the overall active and cryptic Cpn load you are restoring impaired organ function. I think particularly of liver and kidneys which may help improve your processing and excretion of mercury. Additionally, apoptosisi [38] of infected cells will likely liberate some tissue mercury which can be chelated out with Vitamin C and other agents (cilantro, chlorella, etc). And, it halts and reverses the disease progression. You can clear EB's and mercury better when your system is less impaired by Cpn.
I'm sure, also, you are familiar with FIRi [25] sauna as a detox method. It turns out that one Cpn doc has found regular use also has anti-Cpn effect producing distinct and recognizable die-off symptoms. He often uses it as a first-line treatment prior to using antibioticsi [4]. This might be an especially appropriate adjunct to both mercury and CAPi [11] treatment for you.
CAP for Chlamydia pneumonia since 11/04. 25yrs CFSi [10] & FMSi [39]- Currently: 150mg INHi [40], 200 Doxycycline, 500mg MWF Azithromycin, 500mg Tinii [41] daily (Continuous protocol)
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CAPi [11] for Cpni [8] 11/04. Dx: 25yrs CFSi [10] & FMSi [39]. Currently: 150mg BID Roxithromycin, Doxycycline 100mg BID, Tinii [41] 1000mg/day pulses; Vit D2000 units, T4 & T3
I had a look at Andrew
I'm rather surprised that someone with a background in chemistry would think that the hair levels of elements like sodium and potassium, which are highly soluble, were a useful basis for determining anything except personal hygiene habits. Yet they're one of the things Cutler looks at, to diagnose mercury poisoning.
Maybe Cutler (again unlike Stratton) has hidden away all his evidence in the parts of his books that he charges money for; but there doesn't seem to be enough of a chance of that to induce me to buy them.
Jim, I certainly don't [43]
Jim,
I certainly don't expect people to recall all the details of the various Stratton patents. They are extremely long & complex documents, which probably need to be read repeatedly and ideally discusssed to gain an understanding. I'd hoped that this thread would initiate some discussion (at least on the anti-EBi [1] aspect of the various agents) so that my own understanding could be furthered.
I actually started on the doxyi [12]/azith a while back (see my sig).
Thanks for reminding me of Dr Stratton's altered approach. I remember reading this a while back but had forgotten. Going after the active/cryptic load sounds like good advice. Personally I suspect the benefits will be more to do with reducing oxidative stress than helping the liver/kidneys, but either way its bound to be helpful.
Thanks also for the sauna advice. On the rare occasions that I do manage to sweat I certainly feel much better, so its certainly something worth looking into (although being mercury poisoned I have problems sweating so its not so straight forward).
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CFSi [10] since 2001. Infected CPni [8] Jan 2006. Dx'd March 2007. Started CAPi [11] March 2007. Currently taking: Azith 250mg MWF, 100mg doxy every other day.
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Hunter: Don't think - experiment