Cpnhelp.org - Chlamydia Pneumoniae Treatment

Thanks for all the replies, I'm glad to get the additional information.

I was also thinking that vitamin B12 counteracts porphyriai due to being similar in molecular structure to a porphyrin but I can't remember if that's the case.  Does that sound correct? 

all my best

John

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

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all my best

John

RRMS/EDSSi was 4.5, was 4.???, now 5 on Wheldon Protocol (naci, doxycycline, azithromycin, metronidazolei) since 04/12/2006. Added Rifampin 2x150mg/daily 08/19/2007. Added INHi 300mg/daily 03/17/2008 but stoppe

More on glucose & porphyriai-

Glucose has been the standard treatment for serious porphyric attachs, usually IV. This quote explains it further:

Intravenous administration of glucose (a pure form of carbohydrate) is part of the standard treatment of acute attacks of porphyria. Glucose is given by vein because the stomach and intestine usually do not function properly during an attack, and material taken by mouth is not properly propelled through these organs. Glucose and other carbohydrates can repress the pathway for synthesis of herne in the liver. As a result, the overproduction of prophyrin precursors and porphyrins is repressed by carbohydrate administration. 

http://theaipforum.tripod.com/

The site above has some excellent dietary guidlines for porphyria.

From the Cpni Handbook, Mitchell and Stratton note further:

Increasing the availability of glucose provides optimal conditions for the cells to produce energy. However, sucrose is not the best way to increase the glucose availability. Sucrose is a mixture of glucose and fructose. Fructose is the sugar contained in fruit. Because high levels of fructose act as a signal to the liver to store glycogen, an excess of fructose may temporarily reduce the availability of glucose at the cellular level. Fructose should be avoided as much as possible.

 I think the molecular symetry of B12 is accurate but speculative about it's function. I think it's strong methylation effects and that it is used up rapidly for this purpose in porphyria is the original idea.

Combined Antibiotic Protocol for Chlamydia pneumonia in Chronic Fatigue Syndromei & Fibromyalgiai- Currently: 150mg INHi, Doxycycline/Zithromycin, Tinidazole pulses. Northern Ohio, USA

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CAPi for Cpni 11/04. Dx: 25yrs CFSi & FMSi. Currently: 150mg BID Roxithromycin, Doxycycline 100mg BID, Tinii 1000mg/day pulses; Vit D2000 units, T4 & T3

On B12 from David Wheldoni-

I'll add this nice bit from David Wheldon's site on B12:

High-dose sublingual Vitamin B12 (methylcobalamin) should be taken; initially 4000 - 5000 micrograms several times a day, reducing to once daily after three months. This is to flood the system with methylcobalamin as there is often a functional B12 deficit, as evidenced by raised serum methylmalonate or homocysteinei. Vitamin B12 (together with B6 and folatei) counteracts the hyperhomocysteinaemia which frequently accompanies chronic Chl pneumoniae infection and which is thought to cause connective tissue damage. Excess homocysteine is a potent neurotoxin with activity against cortical and hippocampal neurones. [1. Kruman II, Culmsee C, Chan SL, et al., Homocysteine elicits a DNA damage response in neurons that promotes apoptosisi and hypersensitivity to excitotoxicity. J Neurosci 2000;20:6920-6:] [2. Den Heijer T, Vermeer SE, Clarke R, Oudkerk M, Koudstaal PJ, Hofman A, et al. Homocysteine and brain atrophy on MRI of non-demented elderly. Brain 2002;126:170-5:] [3. Leblhuber F, Walli J, Artner-Dworzak E, Vrecko K, Widner B, Reibnegger G, et al. Hyperhomocysteinemia in dementiai. J Neural Tansm 2000;107:1469-74.] An excellent review of Vitamin B12 and multiple sclerosis can be recommended here: [Miller A, Korem M, Almog R, Galboiz Y. Vitamin B12, demyelinationi, remyelinationi and repair in multiple sclerosis. J Neurol Sci 2005 Jun 15;233(1-2):93-7.]

http://www.davidwheldon.co.uk/ms-treatment.html 

 

Combined Antibiotic Protocol for Chlamydia pneumonia in Chronic Fatigue Syndromei & Fibromyalgiai- Currently: 150mg INHi, Doxycycline/Zithromycin, Tinidazole pulses. Northern Ohio, USA

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CAPi for Cpni 11/04. Dx: 25yrs CFSi & FMSi. Currently: 150mg BID Roxithromycin, Doxycycline 100mg BID, Tinii 1000mg/day pulses; Vit D2000 units, T4 & T3

Hi John Most of us try very hard to avoid or consume as required. I never had any luck avoiding milk and cheese. I do not eat much red meat (maybe a couple of ounces a couple of times a month) and my preferred fowl has always been dark but I have conformed to the rest for the most part. But I do eat lots of cheese, - 3 to 4 ozs a day at least - lots of raw vegetables, few eggs, very few fried foods and lots of fish. I always take all my supplementsi and abxi. We have to have some freedom to indulge and it appears that for Paron and me, it may be dairy. As for porphyriai, I took charcoal my last pulse (I have not needed it for a few months!) because I was so obviously having a really, really good one but it does get lots, lots better!

 

Rica PPMS  EDSSi 6.7 at beginning - now 2.  Began CAPi Sept, 2004 with Rifampin 150 mg 2xd, Doxyi 100 mg 2xd, added regular pulses Jan 2005. Jan 2006 switched to Doxy, Azith,  cont. flagyli  total 39 pulses NC USA

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Rica PPMS EDSSi 6.7 at beginning - now 2. Began CAPi Sept, 2004 with Rifampin 150 mg 2xd, Doxyi 100 mg 2xd, added regular pulses Jan 2005. Jan 2006 switched to Doxy, Azith, cont. flagyli total 51 pulses NC USA

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Neat to pop this discussion up again accidently. John, putting together Sarah's comment about energy going into digesting food and some comments made by Dr. Stratton: since Cpni is an ATP (energy molecule) parasite there's less available for other cellular and organ functions. Any other heavy use of ATP such as muscle activity or even digestion (active transport processes) will leave some cells at a deficit and incomplete hemei... ie porphyriai can result. Isn't there some old saw about the energy to digest celery is more than it provides, hence the perfect diet food?

Another factor- Cpn up-regulates the host cell to absorb more glucose from the bloodstream, so it can make more ATP for the Chlamydia. So these big blood sugar crashes, which then result in more porphyria, all get rolled up together.

Your symptoms are familiar to me from times past, but without the foot-drop:"...lethargic, less coordinated, sometimes to the point where I have to be very careful with walking." My kids used to call me a klutz because I was always banging into things, especially when low blood sugar and porphyric from die-off.

CAPi for Chlamydia pneumonia since 11/04. 25yrs CFSi & FMSi- Currently: 150mg INHi, 300mg Rifampin, 200 Doxycycline, 500mg mwf Azithromycin, plus 500mg Tinidazole 2x/day pulses every two weeks. Whew! That's a lot!

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CAPi for Cpni 11/04. Dx: 25yrs CFSi & FMSi. Currently: 150mg BID Roxithromycin, Doxycycline 100mg BID, Tinii 1000mg/day pulses; Vit D2000 units, T4 & T3

 It depends-- some people (Ella for example) need the glucose to help suppress porphyric nausea and get back appetite. John appears to be needing it after eating to avoid blood sugar drop and porphyriai from the energy it takes to digest! At least that's the hypothesis. We see all kinds of twists and turns in this.

CAPi for Chlamydia pneumonia since 11/04. 25yrs CFSi & FMSi- Currently: 150mg INHi, 300mg Rifampin, 200 Doxycycline, 500mg mwf Azithromycin, plus 500mg Tinidazole 2x/day pulses every two weeks. Whew! That's a lot!

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CAPi for Cpni 11/04. Dx: 25yrs CFSi & FMSi. Currently: 150mg BID Roxithromycin, Doxycycline 100mg BID, Tinii 1000mg/day pulses; Vit D2000 units, T4 & T3

Jim's right, when Ella is in a porphyric state, and she is about to eat when hungry her mouth starts to water to such an extent that it pours out of her mouth, and she feels very sick.   When she is feeling this way now, she takes a glucose tablet and the symptoms stop more or less immediately.  If she ignores the symptoms she usually sicks up what she has eaten some 10 minutes after eating.

This does not happen very often now but she still gets the following symptoms: stomach hunger and the feeling of nausea at the same time.   She has to make an effort to eat, as she does not feel like putting food in her mouth, but if she does she usually manages to keep it down.  

Michele: Wheldon CAP1st May 2006 for ailments including IBSi, sinusitis, alopeciai, asthmai, peripheral neuropathy. Spokesperson for Ella started Wheldon CAP 16th March 2006 for RRMS. Sussex UK

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Michèle (UK) GFAi: Wheldon CAPi 1st May 2006. Daily Doxyi, Azi MWF, metroi pulse. Zoo keeper for Ella, RRMS, At worse EDSSi 9, 3 months later 7 now 5.5 Wheldon CAP 16th March 2006

Hi all, just reading again about secondary porphyriai and came across something interesting in Dr Stratton's article The Pathogenesis of Systemic Chlamydial Infections: Theoretical Considerations of Host Cell Energy Depletion and Its Metabolic Consequences that just didn't sink in before.

Forgive me if you understood this before, but although I'd read the article before I guess I didn't catch this. In the last paragraph he mentions the implications of Cpni infection of liver cells and states:

"Moreover, if chlamydiae were to infect hepatic cells, the use of any pharmacologic agents that are metabolized in the liver will increase the need for cytochrome P-450 which is a hemei-based enzyme. Hence, the biosynthesis of heme in the liver is increased. If hepatic cells were infected with Chlamydia species, the decreased energy in the host cell would not allow heme biosynthesis to go to completion, and porphyrins in the liver/entero-hepatic circulation would increase."

He also goes on to mention that when the antimicrobial agents kill the Cpn the accumulated intracellulari porphyrins would be released. Luckily I managed to catch this concept the first time I read it prior to beginning treatment.

The concept of increasing the need for P-450 by pharmacologic agents intrigues me in that I've noticed Vit D3 seems to increase porphyria symptoms for me. I recently read that apparently Vit D3 synthesis also requires P-450 enzymes in the liver and kidney:

CYTOCHROME P450, SUBFAMILY IIR, POLYPEPTIDE 1; CYP2R1

CYTOCHROME P450, SUBFAMILY XXVIIB, POLYPEPTIDE 1; CYP27B1

I'm wondering if increased need for P450 might be a good part of the reason Vit D3 seems to increase porphyria symptoms (in addition to its pro-apoptosisi effects)?

BTW, I've also noticed caffeine seems to increase porphyria symptoms greatly for me now that I've added Vit D3 (particularly on flagyli pulses), and I just read that apparently P450 CYP1A2 is involved in caffeine metabolism:

CYTOCHROME P450, SUBFAMILY I, POLYPEPTIDE 2; CYP1A2

Does this make sense?

On Combined Antibiotic Protocol for Cpn in Rosaceai since 01/06

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On Combined Antibiotic Protocol for Cpni in Rosaceai 01/06 - 07/07, On Vit D3 + NACi since 07/07 and daily FIRi Sauna since 08/07

Amazing, Red. Could this be one of the reasons that D is not metabolized in Cpni infected bodies because of this liver enzyme being in short supply? "I recently read that apparently Vit D3 synthesis also requires P-450 enzymes in the liver and kidney" BTW, caffeine is a big trigger for porphyriai for me---but I seem to have musch less porphyria these days. What a complex puzzle. Thanks for th elinks, Raven

Gosh, interesting question Raven, but I'm not sure what if anything might cause a short supply of the P-450 enzymes involved in Vit D metabolism. I'll see if I can find anything.

Up to this point caffeine has been more of a help than a problem for me, but I'm now wondering if cutting it out might help with some of my remaining (and sort of still increasing) porphyriai symptoms. I'm currently trying to cut it out slowly (one half mug at a time)...

On Combined Antibiotic Protocol for Cpni in Rosaceai since 01/06

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On Combined Antibiotic Protocol for Cpni in Rosaceai 01/06 - 07/07, On Vit D3 + NACi since 07/07 and daily FIRi Sauna since 08/07

The quantities of Vitamin Di involved are low enough that I doubt that the need to synthesize enzymes to modify Vitamin D has much to do with porphyriai. Only micrograms of Vitamin D are present; in comparison, gluconeogenesis needs to operate on gram quantities, since it's generating the main fuel used by the body. (Avoiding gluconeogenesis is the reason for eating glucose to stop a porphyria attack.)

Thanks so much Basil. I cannot tell you how helpful this information is. It really confirms my suspicions that Vit D3 seems to be causing porphyriai symptoms for me too through this method (rather than just through apoptosisi mechanisms). I found immediately upon starting Vit D3 that I became extremely alcohol intolerent. This explains why. I believe I now (after 6 months of 4000iu of Vit D3) that I've reached a point where I may be intolerent of caffeine as well. I'll continue to try to eliminate it slowly from my diet (to avoid withdrawal symptoms).

Here's another question for you, glucose tabs seem to almost immediately provide relief of my symptoms (within @ 20 minutes or so). But within a couple of hours I notice greatly increased congestion symptoms that last for @ 8-12 hours or so. High carb meals seem to do the same. While I'm worried about candida/yeast problems, the quick onset of these symptoms (and then clearance) doesn't seem to make a lot of sense along these lines. I'm wondering if the increased glucose/carbs sets off some kind of inflammatory or oxidative type reaction with the porphyrins (to eventually help scavenge and clear them), but haven't been able to find much on this. Does this make any sense?

Thanks again so much as always....

On Combined Antibiotic Protocol for Cpni in Rosaceai since 01/06

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On Combined Antibiotic Protocol for Cpni in Rosaceai 01/06 - 07/07, On Vit D3 + NACi since 07/07 and daily FIRi Sauna since 08/07

Thanks Basil.   Many of these symptoms are VERY familiar to me, and I've always been more than a little sensitive to foods high in sugars so potentially this explanation makes a lot of sense in my case too.

I think I'll continue to try to cut out caffeine and try bumping up my intake of complex carbs a bit to see if I can reach a happy medium state between porphyriai and congestion/inflammationi. 

Thanks again and take care... 

 

On Combined Antibiotic Protocol for Cpni in Rosaceai since 01/06

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On Combined Antibiotic Protocol for Cpni in Rosaceai 01/06 - 07/07, On Vit D3 + NACi since 07/07 and daily FIRi Sauna since 08/07

Thanks basil for the information on Hypoglycemia.  I have this disorder and keep the simple carbs down to a dull roar.  I see, like many other ailments, there are cross over symptoms - CFIDSi/ME.

When my intestinal flora gets out of what I know because I crave sugar.  It is a challenge being on abxi & keeping the balance as in the past I have had a candida problem (I just did a cleanse in February).

The change in the diet recommended during the protocol I feel will have me gaining alot of weight?  When I am able to do more exercise I increase the complex carbs accordingly.

I hope I will be ok; I continue down the path

Mad CAPper

With Christ in Faith

Ruth 

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CFIDSi/ME 32 yrs, FMSi, IBSi, EBVi, CMV, Cpni, chronic insomnia, Lymes, HME, Natural HRT peri-M, NACi 2.5 gm, 6-07 Doxy 200 mg day pm, Azith 375 mg M/W/Fday, Pulse#12 2 gm oops then 1250 mg 4 days 6-14-08

 Basil- Reading your post on the azith thread:

Finally, I personally have suffered repeated porpyria attacks triggered by CAPi, even though none of the substances I take require Phase I metabolism (and therefore would not be porphyriai triggers). My attacks are not simply the result of porphyrin release from liver-cell apoptosisi, but full blown, out-of-control, continuous-porphrin production attacks that can be stopped only by taking large amounts of gluecose and cimetidine (a P450 inhibitor).

It got me thinking: could apoptosis and dump of intracellulari porphyrins require Phase 1 processing by the liver, ie how are the fat soluble porphyrins processed by the liver? That would put a big demand on the liver which would trigger immediate porphyrin attack, and round and round.

CAP for Chlamydia pneumonia since 11/04. 25yrs CFSi & FMSi- Currently: 150mg INH, 200 Doxycycline, 500mg MWF Azithromycin, 500mg Tinii daily (Continuous protocol)

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CAPi for Cpni 11/04. Dx: 25yrs CFSi & FMSi. Currently: 150mg BID Roxithromycin, Doxycycline 100mg BID, Tinii 1000mg/day pulses; Vit D2000 units, T4 & T3

yikes, all this talk about the liver & porphyrins.  scary.  I am glad I backed off the flagyl/metroi as my liver, gallbladder, spleen area was very sore.  I guess that is porphyrin attack as after I cut the doseage in 1/2, about 4 days I had less pain in that area.

The Nasty Cpni already triggered my Hemochromatosis - excess iron storage.  My inner Physician has been working overtime for years, I blame everything on the bacteria!! lol

My best wishes

With Christ in Faith

Ruth 

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CFIDSi/ME 32 yrs, FMSi, IBSi, EBVi, CMV, Cpni, chronic insomnia, Lymes, HME, Natural HRT peri-M, NACi 2.5 gm, 6-07 Doxy 200 mg day pm, Azith 375 mg M/W/Fday, Pulse#12 2 gm oops then 1250 mg 4 days 6-14-08