MediTest

I've read several posts on Porphyria, including the interview with Dr. Stratton (I think is who it was).  I'm still left wondering what I can do to combat porphyria as I definitely have it going on and it's something I want to deal with.

As far as I know, the only thing that can be done is the following...

  • take activated charcoal in either powder or capsule form
  • wash it away with water
  • avoid eating protein / eat a diet consisting of 70% carbohydrate

Have I left out something?  I'm left wondering if there is anything that can be done medically?  Would a medical measure to address it also lead to other undesireable side affects?

take care

John

p.s.  signature not omitted intentionally

Don't forget:

  • avoid sucrose and fructose, seek glucose.
  • Red meat, tuna, and dark turkey are verboten, too. Chicken, fish, nuts, and eggs -- and, as you say, not too much of them.
  • Alcohol is a real promoter of porphyria as well.

I've never been quite sure whether the dairy prohibition is because of porphyria or because of rendering the doxy ineffective, so I didn't include that.

Now, what else -- I'm sure that's not everything.

Ron

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

Ron

On CAP for CFS starting 01/06 (NE Ohio, USA)

Began rifampin trial 1/14/09

Currently: on intermittent

John- Other than those the only other one suggested is low-dose Plaquinal (125mg two or three times a week). Severe porphyria requires IV Hematin, which is a human blood product, very expeinsive and only obtainable for proven porphyric condition (mostly genetic in origin).

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

 

CAP for Cpn 11/04. Dx: 25+yrs CFS & FMS. Currently: 250 aithromycin mwf, doxycycline 100mg BID, restarted Tini pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

D W

Cimetidine has been used in both hereditary and secondary porphyrias [Horie Y, et al., Cimetidine in the treatment of porphyria cutanea tarda. Intern Med. 1996 Sep;35(9):717-9.] It is very inexpensive.

D W - [Myalgia and hypertension (typically 155/95.) Began (2003) taking doxycycline and macrolide and later adding metronidazole. No medication now. Morning BP typically 110/75]

Thank you for posting this.

http://www.journalarchive

Kim's been having die-off reactions and and we're hoping to supplement the charcoal she takes at night.

I looked Cimetidine up and found out that it's sold as Tagamet, which is an over the counter heartburn/ulcer medication. I further followed up to try and find out what the dosage might be. The way Tagamet is sold, dosage is:

Tablets for Oral Administration : Each light green, film-coated tablet contains cimetidine as follows: 300 mg-round, debossed with the product name TAGAMET, SB and 300; 400 mg-oval Tiltab® tablets, debossed with the product name TAGAMET, SB and 400; 800 mg-oval Tiltab® tablets, debossed with the product name TAGAMET, SB and 800. I found this at: http://www.rxlist.com/cgi/generic/cimet.htm

I'm hoping you might be able to recommend a dosage and or any other thoughts about taking this to help relieve die-off reactions. Thank you, Ken

PS: I've also been looking into Oregano oil as noted in the CPn handbook. I checked this out at the Vitaminshoppe and found Oregano oil is mixed with olive oil, is this what folks are using? I'm not sure how much to use if we try this also. Is anyone using Oregano Oil? Are softgels ok?

In pursuit of ABX

Don't Allow What You Know To Get In The Way Of What Might Be

Hi Ken, I am using the oregano oil in liquid form.  I put 1 -2 drops in my morning vitamin cocktail drink!

I believe it helps keep yeast in check!

CFIDS/ME 26yrs, FMS, IBS, EBV, CMV, Cpn, chronic insomnia, Lymes, HME, Natural HRT peri-M, NAC 2.5 gm, 6-07 Doxy 200 mg day pm, Azith 375 mg M/W/Fday, Pulse#9 750mg 5.5 day, 4-25-8

CFIDS/ME, FMS, MCS, IBS, EBV, CMV, Cpn, H1, chronic insomnia, Chronic Lyme, HME, Babesia, Natural HRT-menopause, NAC 2.4 gm,Full CAP 6-2-07, all supplements+Iodorol, Inositol-depression, ultra Chitosan, L lysine Pulse#27 04-19-10 1gm Flagyl/day-5 days<

 Are you smooshing all your vits into a drink? I keep reading that you shouldn't do this as it can affect the potency, but others say it's OK with some coatings and not with others. Confused.

Berkshire, UK. Diagnosed RRMS Feb 4th 2008.

NAC 2400mg. All supplements. Doxy 200mg. Zith 250mg M/W/F.
No GP/Neuro support. Self medicating with help from David Wheldon.
Started CAP 20th April 2008.

Berkshire, UK. Diagnosed RRMS Feb 4th 2008.

NAC 2400mg. All supps. Doxy 200mg. Zith 250mg. Metro 400mg.
No GP/Neuro support. Self medicating with help from David Wheldon.
Started CAP 20th April

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

I was also thinking that vitamin B12 counteracts porphyria 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

best, John

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

More on glucose & porphyria-

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 Cpn 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 Syndrome &amp; Fibromyalgia- Currently: 150mg INH, Doxycycline/Zithromycin, Tinidazole pulses. Northern Ohio, USA

 

CAP for Cpn 11/04. Dx: 25+yrs CFS & FMS. Currently: 250 aithromycin mwf, doxycycline 100mg BID, restarted Tini pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

On B12 from David Wheldon-

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 homocysteine. Vitamin B12 (together with B6 and folate) 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 apoptosis 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 dementia. 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, demyelination, remyelination 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 Syndrome &amp; Fibromyalgia- Currently: 150mg INH, Doxycycline/Zithromycin, Tinidazole pulses. Northern Ohio, USA

 

CAP for Cpn 11/04. Dx: 25+yrs CFS & FMS. Currently: 250 aithromycin mwf, doxycycline 100mg BID, restarted Tini pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

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 supplements and abx. We have to have some freedom to indulge and it appears that for Paron and me, it may be dairy. As for porphyria, 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  EDSS 6.7 at beginning - now 2.  Began CAP Sept, 2004 with Rifampin 150 mg 2xd, Doxy 100 mg 2xd, added regular pulses Jan 2005. Jan 2006 switched to Doxy, Azith,  cont. flagyl  total 39 pulses NC USA

3/9 Symptoms returning. Began 5 abx protocol 5/9 Rifampin 600, Amox 1000, Doxy 200, MWF Azith 250, flagyl 1000 daily. Began Sept 04 PPMS EDSS 6.7 Now good days EDSS 1 Mind, like parachute, work only when open. Charlie Chan  In for the duration.&am

Hi Rica, thank you for writing me on this topic.  You may not be aware, but this is an old thread of discussion that I haven't touched since May of 2006, or so I believe.  Be that as it may, I am glad that you brought it up as there is a question I've had brewing on the topic of porphyria for a bit.

I don't know if it was Jim K or Eric or someone else who created it, but there was a post some time ago that summarized the effects of porphyria.  I noted that the way in which I experience porphyria wasn't on the list which makes me wonder if what's going on with me is really porphyria at all.  It seems to coincidental not to be but that may be the case.

In my case, I get the symptoms I thought/have believed were porphyria after eating.  Indeed, taking glucose before eating seems to alleviate much of it unless I really eat a lot.  My symptoms are that I become more lethargic, less coordinated, sometimes to the point where I have to be very careful with walking as I tend to drag my right foot which is exacerbated after eating.

I had talked about these symptoms in another thread some time ago and had mentioned that if I begin drinking lots of water after having eaten, it tends to more quickly relieve these symptoms.  I believe it may have been Jim K who suggested that the water was sweeping away water soluble porphyrins, which sounds likely to me.

Anyway, to summarize, I'm wondering whether or not these symptoms are actually porphyria or something else.  I think DW posted earlier on this thread about an imbalance in homocysteine or some such in people with MS.  I wonder if it's that instead, but have no real clue.  I guess the best thing I can do to have a better idea and understanding is probably do the poor man's porphyria test and see for myself. 

all my best

John

RRMS/EDSS 4.5 on Wheldon Protocol (nac, doxycycline, azithromycin, metronidazole) since 04/12/2006

best, John

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

John, the symptoms you describe just sound to me like a person recovering from multiple sclerosis digesting his food.  Your body is concentrating on digesting the food rather than bothering about whether you drag your foot a bit.  Although I can now use a knife and fork very well, towards the end of the meal I can lose  lot of strength in my wrists and fingers and make really heavy going of cutting up the remaining food.  I can then drag my feet whereas previously I wasn't simply because I can't be bothered not to.  For a few minutes I just want to close my eyes.  Half an hour later, digestion nearly finished, I am back to my normal, alert self........Sarah   An Itinerary in Light and ShadowWheldon regime since August 2003, for very aggressive SPMS.  Intermittent therapy after one year. 2006 still take this, now two weeks every three months.  EDSS was about 7, now 2. United Kingdom.
Completed Stratton/Wheldon regime for aggressive secondary progressive MS in June 2007, after four years, three of which intermittent.   Still improving bit by bit and no relapses since finishing treatment.

Sarah       

I'm at a loss to decide whether or not you're right about it being a digestive energy issue.  It doesn't seem to be as when I take glucose before eating, it does alleviate the problem either entirely or mitigates it to a great degree.

Also, for those of you following this thread, my reponse to Rita yesterday stated I take glucose before eating.  As one might expect, taking it after eating has no effect, or at least, has no effect on me when I've done that in the past.  Definitely take it before eating, and at least about 10 minutes and not much less or more.  The longer the time, the less the effect, the shorter the time, the less time your body has to respond to it before responding to digestion/eating.

all my best

John

RRMS/EDSS 4.5 on Wheldon Protocol (nac, doxycycline, azithromycin, metronidazole) since 04/12/2006

best, John

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

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 Cpn 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 heme... ie porphyria 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.

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

 

CAP for Cpn 11/04. Dx: 25+yrs CFS & FMS. Currently: 250 aithromycin mwf, doxycycline 100mg BID, restarted Tini pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

John said he takes the glucose after eating...I thought the glucose was supposed to be taken before eating. Which is right?

Joyce~caregiver-advocate in Dallas for Steve J (SPMS) / Cpn indicated by reactions; Mpn, EBV, CMV positive; elevated heavy metals; gluten+casein sensitive / Wheldon CAP since Aug. '06 - doxycycline+azithromycin+flagyl pulses; antivirals; chelation; LDN.

Joyce~caregiver-advocate in Dallas for Steve J (SPMS).  CAP since August 06, Cpn, Mpn, B. burgdorferi, systemic candidiasis, EBV, CMV & other herpes family viral infections, elevated heavy metals, gluten+casein sensitivity. 

Joyce        

See my last reply to Sarah.  I take glucose before eating, not after Image removed. 

all my best

John

RRMS/EDSS 4.5 on Wheldon Protocol (nac, doxycycline, azithromycin, metronidazole) since 04/12/2006

best, John

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

 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 porphyria from the energy it takes to digest! At least that's the hypothesis. We see all kinds of twists and turns in this.

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

 

CAP for Cpn 11/04. Dx: 25+yrs CFS & FMS. Currently: 250 aithromycin mwf, doxycycline 100mg BID, restarted Tini pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

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 IBS, sinusitis, alopecia, asthma, peripheral neuropathy. Spokesperson for Ella started Wheldon CAP 16th March 2006 for RRMS. Sussex UK

Michèle (UK) GFA: Wheldon CAP 1st May 2006. Daily Doxy, Azi MWF, metro pulse.

Red

Hi all, just reading again about secondary porphyria 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 Cpn 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 heme-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 intracellular 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-apoptosis effects)?

BTW, I've also noticed caffeine seems to increase porphyria symptoms greatly for me now that I've added Vit D3 (particularly on flagyl 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 Rosacea since 01/06

Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-

Amazing, Red. Could this be one of the reasons that D is not metabolized in Cpn 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 porphyria for me---but I seem to have musch less porphyria these days. What a complex puzzle. Thanks for th elinks, Raven

Feeling 98% well-going for 100. Very low test for Cpn. CAP since 8-05 for Cpn/Mycoplasma P.,Lyme, Bartonella, Mold exposure,NAC,BHRT, MethyB12 FIR Sauna. 1-18-11 begin new treatment plan with naturopath

Red

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) porphyria symptoms. I'm currently trying to cut it out slowly (one half mug at a time)...

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

Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-

Red, the short story is that you are correct about both Vitamin D and caffeine being sources of making you sick, and your belated understanding of the role of Cpn in causing porphyria due to mitachondrial ATP theft.

Both Vitamin D and caffeine require Phase I hepatic metabolism. In order to become bioactive, Vitamin D undergoes Phase I hepatic hydroxylation followed by another hydroxylation by the kidneys. Finally, when the body is done with Vitamin D, the liver hydroxylates it a third time to allow it to be excreted.

Phase I hepatic metabolism first involves the synthesis of one or more of several different P450 isoenzymes. These isoenzymes have a half life of only a few seconds at most, and therefore can not be stored. In fact, they are synthesized upon demand, and the trigger for their synthesis is the presence of the substance that must be metabolized.

Every one of these isoenzymes contains a heme entity, which itself must be manufactured upon demand. It is this induction of heapatic heme manufacture that ultimately results in porphyria for those of us who are prone to it.

Porphria is a consequence of heme synthesis gone awry. Once triggered, heme synthesis takes eight sequential steps. If all goes well, completed heme falls out of the bottom of the synthetic pipeline and feeds back to signal the first step to halt, thereby halting all subsequent steps.

If something goes wrong at one of the eight steps once the process starts, and finished heme does not result, the process does not stop, and intermediate precursors pile up at one or more of the steps. These precursors are called porphyrins, and are EXTREMELY potent radical oxygen species that are EXTREMELY neurotoxic, bringing on terrible systemic nervous system disruption and a consequently broad array of symptoms when released into the bloodstream.

Cpn infection is one of the things that can damage the heme making machinery. Cpn sets up shop near the mitochondria and steals their ATP output, which is the body's principal source of energy. This ATP theft also clobbers the ability of mitachondria to perform their role in heme manufacture, since as it turns out, half of the steps to make heme occur INSIDE of the mitachondria.

Cpn liver infection is thus particularly vicious because the liver is needed to metabolize many of the very substances that one needs to cure the infection, but because of damage by Cpn, those substances trigger porphyria. Nice survival mechanism, hey?

Vitamin D, caffeine, alcohol, tobacco, about 80% of all pharmaceuticals, many food substances, and many endogenous substances require Phase I metabolism for activation and/or elimination. Those of us who are prone to porphyria must be extremely careful with the drugs we take and some of the foods we eat. Substances that are good for healty people, like blueberries and cruceriferious vegetables (for example), can be bad for us. And substances that might normally be unhealthy for healthy people, like grapefruit juice and cimetidine (for example), can be beneficial for us.

Vitamin D made me extremely ill, and not just from its antibiotic effect, which is what lead me to do the research that made me realize that Vitamin D is just one more substance that can trigger porphyria.

basil.

If cats are outlawed, only outlaws will have cats.

The quantities of Vitamin D involved are low enough that I doubt that the need to synthesize enzymes to modify Vitamin D has much to do with porphyria. 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.)
Red

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 porphyria symptoms for me too through this method (rather than just through apoptosis 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 Cpn in Rosacea since 01/06

Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-

Red, glucose and cimetidine provide me immediate relief as well when I realize I'm becoming porphyric. Actually, this immediate relief is not something I really expected, because I've always been under the impression that porphyrins are long-lived chemicals that are difficult to eliminate. And yet, such immediate relief would contradict that impression. Perhaps the body has the ability to deal with a certain amount of porphyrins rather handily, but if that amount is exceeded, the porphyrins accumulate.

Regarding the congestion, one thing that could happen is that if you are prone to blood-sugar instability, a big dose of glucose or carbs could cause your insulin to rapidly spike and then drop, along with a rapid drop in blood glucose. This would be consistent with the time frame of your congestion onset. The above is a form of hypoglycemia disorder. Regarding symtoms that can result from the above process, I found this:

"The symptoms of 'hypoglycemia' (the term we will continue to use here) are many. They consist of fatigue, irritability, nervousness, depression, insomnia, flushing, impaired memory and concentration. Anxieties are common as are frontal or bitemporal headaches, dizziness, faintness or actual syncope. There is often blurring of vision, nasal congestion, ringing in the ears, numbness and/or tingling of the hands, feet or face. Excessive gas, abdominal cramps, loose stools or diarrhea are common. Many complain of leg or foot cramps. These are the chronic symptoms of this condition and are present even during periods of normal blood sugar."

I'm wondering if you perhaps have any of the above symptoms besides just the nasal congestion.

basil.

If cats are outlawed, only outlaws will have cats.
Red

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 porphyria and congestion/inflammation. 

Thanks again and take care... 

 

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

Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-

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 - CFIDS/ME.

When my intestinal flora gets out of what I know because I crave sugar.  It is a challenge being on abx & 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 

CFIDS/ME, FMS, MCS, IBS, EBV, CMV, Cpn, H1, chronic insomnia, Chronic Lyme, HME, Babesia, Natural HRT-menopause, NAC 2.4 gm,Full CAP 6-2-07, all supplements+Iodorol, Inositol-depression, ultra Chitosan, L lysine Pulse#27 04-19-10 1gm Flagyl/day-5 days<

 Basil- Reading your post on the azith thread:

Finally, I personally have suffered repeated porpyria attacks triggered by CAP, even though none of the substances I take require Phase I metabolism (and therefore would not be porphyria triggers). My attacks are not simply the result of porphyrin release from liver-cell apoptosis, 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 intracellular 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 CFS & FMS- Currently: 150mg INH, 200 Doxycycline, 500mg MWF Azithromycin, 500mg Tini daily (Continuous protocol)

 

CAP for Cpn 11/04. Dx: 25+yrs CFS & FMS. Currently: 250 aithromycin mwf, doxycycline 100mg BID, restarted Tini pulses; Vit D2000 units, T4 & T3, 6mg Iodoral

Jim, I think you may have hit the nail on the head. Phase 1 processing is usually the first step in converting fat soluable compounds into water soluable compounds, with Phase 2 conjugation being the second and final step.

The body has very very poor(almost non-existent) mechanisms for eliminating fat soluable compounds, hince the need for conversion to water soluability.

I too just recently briefly wondered about the fat soluable porphyrins and whether they would undergo Phase I metabolism. But I didn't pursue the thought like I should have. But you did.

That is, you've hypothesized that the body would attempt to utilize Phase I metabolism for the inital step in converting fat soluable porphyrins into water soluable compounds. However, this attempt at conversion would result in either triggering and/or sustaining a self-perpetuating porphyria attack.

In the case where a porphyria attack had not yet started, but in which a person was prone to secondary porphyria attacks, if CAP-induced apoptosis of infected liver cells released too much intracellular porphyrins from diseased liver cells, then a secondary porphyria attack would be triggered, actually producing new porphyrins on top of the porphyrins released by the CAP. Furthermore, such an attack would be self-sustaining until abated by treatment with glucose/cimetidine/Panhematin, producing far more porphyrins than those originally dumped by cell apoptosis.

This hypothesis very neatly explains why CAP induces self-sustaining secondary porphyria attacks. Based on my own experience, and others here, I've simply never believed that the amount of porphyrins dumped by cell apoposis was enough to make people as sick as they get. Furthermore, I have no doubt that CAP has triggered self-sustaining porphyria attacks in myself, and others here. One reason for this belief is that glucose and cimetidine should have no effect on porphyria symptoms produced by simple porphyrin dumping as a consequence of cell apoptosis, and yet myself and others have reported that these remedies bring relief from CAP-induced porphyria symptoms.

I really think you may have discovered a very important piece of the puzzle.

If this is all true, then this would also be one of the mechanisms that would sustain primary (genetic) porphyria attacks as well. Experimentally, this hypothesis shouldn't be too difficult to prove. Perhaps a murin model with induced porphyria cutanea tarda could be used. Once the mice are made PCT with the appropriate toxin, fat solulable porphyrins could be injected and it could be easily determined if a self-sustaining porphyria attack resulted. I wish I had the money to fund the research.

I would be very, very interested in what Charles Stratton has to say about all of this.

Great thinking! I'm jealous that I didn't figure this out myself!

basil

If cats are outlawed, only outlaws will have cats.

yikes, all this talk about the liver & porphyrins.  scary.  I am glad I backed off the flagyl/metro 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 Cpn 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 

CFIDS/ME, FMS, MCS, IBS, EBV, CMV, Cpn, H1, chronic insomnia, Chronic Lyme, HME, Babesia, Natural HRT-menopause, NAC 2.4 gm,Full CAP 6-2-07, all supplements+Iodorol, Inositol-depression, ultra Chitosan, L lysine Pulse#27 04-19-10 1gm Flagyl/day-5 days<