Cpnhelp.org

Blog 5/08
Warning: this is a lengthy one as it's been a while.

It’s been quite a while since I posted a blog. I’ve been experimenting with some things and don’t like to report too much until I have a clear trend going, and that takes months. Now that the experimental protocol is public I can give my own report. I’m also the “old man” of the site, and if newbies see that I’m doing things differently than the “standard” CAP’s it tends to confuse. One of the side costs of our success in bringing more people to the site is that it’s more problematic for me to “think out loud” about my own treatment like I used to here. My musings and speculations tend to be followed with more attention than perhaps they deserve,  and all sorts of questions or concerns pop up for people.

I’ve been following an emerging protocol Dr. Stratton has been developing with a friend of his who is a patient-expert on Cpnⁱ. The intention of this has been to find ways to alleviate some of the onerous effects of Cpn treatment so that it is easier on people, and to make the treatment process less lengthy. A number of people previously unable to tolerate CAP treatment, older folks especially with GFA syndrome (Generally Falling Apartⁱ from Cpn related diseasesⁱ) have been able to tolerate treatment and benefit from it in a number of months.

(Some of the explanation below has been repeated in the Handbook post on the experimental protocol)
Emerging research has been suggesting that Cryptic Cpn is not benign even if it is not replicating. Cryptic Cpn is essentially a stressed form of Cpn, and stress causes it to generate of Heat Shock Protein (HSP60), which is many times more inflammatory than LPSⁱ endotoxinⁱ. LPS endotoxin is the one that causes the fever and chills and is released mostly when RB’s are killed and lyse, or when EB’s are killed. The inflammationⁱ of plaques in cardiovascular disease has been associated specifically with Cpn HSP60 (this is a blog, so I’m not going to try to reference all this stuff here, you can look it up in Pubmed) and with the persistent (cryptic) form of Cpn. This is probably why those “big” studies of 6 months of azithromycin showed not lowering of risk of heart disease… it’s not caused by the replicating form of Cpn and the idiots never asked a microbiologist about what might kill cryptic Cpn!

Dr. Stratton has been thinking that a lot of the reactions people have to antibioticsⁱ in treating Cpn is not all the LPS endotoxin release or porphyrins, but could in large part be from the highly inflammatory effect of forcing Cpn into Cryptic formⁱ, causing it to generate a big wave of HSP60, and then a lower but chronic amount until it’s killed by the flagyl. He speculates that some of the reports of IV treatment causing little or no reaction is because it floods the system with so much antibiotic so quickly that the Cpn is killed before it starts to be stressed and generate HSP60 as part of it’s survival strategy. Paul Griffith, a non-medical friend researching this whole area, found that supplementing pyruvate might do the trick.

Basically, this approach uses 6grams of calcium pyruvate one hour before taking the antibiotics, and an additional 6 grams if needed later for reactions when the antibiotics exert their effect. In theory the first dose of pyruvate encourages the cryptic/persistent form of Cpn to convert back into RB (replicating) form by supplying it with a ready source for generating cellular energy. In RB form it is:
a) Susceptible to the regular antibiotics and,
b) Can be killed when it is not in “stress” so it is not stimulated into producing and releasing so much the highly inflammatory HSP60.

In essence, you are feeding it until it is comfy and sprawling in it’s chair at the dining table, and then whacking it upside the head!

In theory this approach should limit turning Cpn into cryptic form by the treatment and make it more directly susceptible to the protein synthase inhibitors (like doxyⁱ and azith).

In theory, it should also winnow down the cryptic load one has acquired, along with it’s inflammatory affects, without needing to kill it directly with flagyl.

Also in theory, the second dose of pyruvate for reactions to the antibiotics should supply the fundamental cellular energy needed to help lower the generation of porphyrins.

Back to my blog…
So for the past three months I’ve been experimenting with this using different antibiotic agents, without and pulses. I finally did a tiniⁱ pulse last week to see whether I had indeed reduced the cryptic load—based on how much reaction I would have to the pulse. My personal speculation is that, if I’ve been building up lots of cryptic load by going so long without a pulse I’d have a strong reaction. If this new approach was itself winnowing down my cryptic load, I would have a relatively mild reaction.

Well, it’s only one pulse, but it was the easiest pulse I’ve ever had, and no noticeable post-pulse reaction. So it does seem that this new approach is useful. More importantly to me personally is that I’ve improved noticeably in my energy and cognition after these three months. I had been at a glacially slow improvement phase for a while, so this is really significant for me.

Month One- I first did a month of Biaxin (clairithromycin) twice a day in combination with about 4 grams of  pyruvate, without any doxycycline. This combination was not easier on me. In fact I had stronger die-off reactions from this than I’d had in a long time. This was surprising, as I don’t have any significant reactions to the regular antibiotics, only to pulses. It suggested that I was indeed getting previously untouched Cpn to be vulnerable to the antibiotics. In fact, the reactions I was having were more like old pulses used to be: I was getting aches in joints, knees, trapezius muscle, sacroiliac joint, etc. which I only have gotten during pulses.

I had a couple weeks of flare up like this on the Biaxin/pyruvate combo. The second dose of pyruvate didn’t help a lot to counter these reactions, but I was only doing 4 grams for these post-antibiotic dose reactions and was told later by Dr. Stratton that this was not sufficient.

Month Two- The next month I did roxithromycin and Bactrim DS. I had some roxy left from a past experiment, and wanted to try the Bactrim to see if it helped with urinary symptoms. I had less reactions than on the Biaxin. After about two weeks I actually felt mentally clearer and more energy than I had in a long time! I was still only doing about 4 grams of the pyruvate, but love that roxy/bactrim!

Month Three- I ran out of the roxy after a month, and switch back to azithromycin briefly, 250mg daily preceeded by the pyruvate. I got an initial kick, again, but it settled down shortly. About this time I started to use 6grams pyruvate instead of 4. This eliminated most reactions and seemed to improve my energy and mood. Shortly, I got more roxy and switched back to it but also added doxy back as I ran out of Bactrim. I’d say during this month I was functioning well although at about the same level end of the month as at the beginning of the month.

He Hits, He Scores, He Pulses… I finally did my usual pulse of 500mg tini twice a day for five days. I had some reaction to the first dose of 1000mg. I usually double the first dose to 1000mg to bring my blood levels up quicker. These reactions were mostly alleviated by additional pyruvate. The rest of the pulse was uneventful: some short periods of irritability and aches that were easily countered by some pyruvate  and a dose of ibuprophen. Post pulse now a week, no post pulse reactions to speak of.

I have to say that it does appear that this approach is clearing some stubborn areas of Cpn and also contributing to more energy, cognitive clarity and less inflammation.

Almost forgot: the unforgettable rifampin… Ah yes. Somewhere in the middle of all this I tried the pyruvate and rifampin. SLAMMED! I did 150mg rifampin twice a day and could only manage 4 days. Even lots of pyruvate didn’t counter my reactions to this one! So there is still some way to go here for me, as the “acid test” of rifampin is not approachable.

In Conclusion- Some of you who have noted how bloody long I’ve been on this protocol may be wondering if it’s really worth it. I’m the poster child (maybe along with Willow?) for starting out with an incredibly high bacterial loadⁱ and pervasive infection. Every step-up of the protocol, every addition of a stronger agent, cost me in miserable reactions. But I told a friend the other day that I can look back at the last three birthdays and truly say that I have felt better than the last one each time. Not bad for reaching my 55th this weekend! Worth it? You bet. I am living more life than I was able to last year, and so much more than when I started. My patient story spoke of the narrowing tunnel of illness when I started the CAP.  I’m out of the tunnel, in the sunshine and on level ground. That's good!

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CAPⁱ for Cpnⁱ 11/04. Dxⁱⁱ: 25yrs CFSⁱⁱ & FMSⁱⁱ. Currently: 250 aithromycin mwf, doxycycline 100mg BIDⁱⁱ, Tiniⁱ 1000mg/day pulses; Vit D2000 units, T4 & T3, 12mg Iodoral