I can't sleep...some of you are very much on my mind. In fact, you could say that my head is very much like a can of rusty worms here in these wee small hours. The common thread to all these thoughts is iron, but am I trying to connect dots that just don't want to be connected? I'm off on a splintering tangent of investigation along which I am openly inviting the more scientific minds of this site to join in and take over or straighten me out. Sometimes it's helpful for an idiot to ask simplistic questions that might spark the right thoughts in the more learned and then get out of the way. In any case, I've bitten off more than I can chew, but my intuition tells me this is worth the chewing. Please help.
Background: basil's thread "Some more thoughts on porphyria and Cpn" and paron's thread "Lactoferrin and porphyria" . The latter post set me onto a line of investigation where I unearthed a very interesting CDC article "Iron Loading and Disease Surveillance " by Eugene D. Weinberg of Indiana University in Bloomington. Topics in this article included Hazards of Iron Loading, How Microbes Acquire Iron: A Determinant of Host Range and Tissue Localization, Microbial genera with strains whose growth in body fluids, cells, tissues, and intact vertebrate hosts is stimulated by excess iron (yes, Chlamydia was listed), The Iron Withholding Defense System, Conditions that can compromise iron withholding, Strengthening the Iron Withholding Defense (including a list of methods), and Perspectives and Conclusions.
From there, I googled "chlamydia pneumoniae iron," and what I got could keep me reading for a long time, but I'll mention this article: "Iron and the role of Chlamydia pneumoniae in heart disease" by Jerome L. Sullivan and Eugene D. Weinberg. The closing paragraph really grabbed my attention: "We suggest that, above a modest threshold level of stored iron in vivo, C. pneumoniae acquires the ability to colonize coronary arteries. Invasion and colonization by the organism in vivo probably require a concentration of available iron similar to that needed for growth in cell culture. Even in a state of total iron depletion, iron is still present in the body in abundance. However, in iron depletion virtually all iron in the body is functional iron. Functional iron, i.e., iron in hemoglobin, may not be readily accessible to the organism. Our hypothesis implies that stored iron can be mobilized by C. pneumoniae for growth. An approach to testing the hypothesis would involve comparing the ability of C. penumoniae to colonize macrophages from stored iron-replete persons with those from persons without stored iron. If the hypothesis is confirmed, maintenance of an iron-depleted state under medical supervision could be recommended as a preventive strategy against recolonization after a course of antibiotic therapy."
Hmmmm. That last sentence made me think of Wiggy and Jim and the other site users who are anemic or who have a history of anemia. From there I came back to cpnhelp.org and did a search for simply "iron." I re-read some postings by Marie and Red that touched on iron and nitric oxide that contributed to this line of thought, but I particularly re-read Jim's post on Dr. Stratton's recent observations. There it was again...anemia...and bone marrow.
Many thoughts on the table: iron loading~Cpn, excess iron-loading more prevalent in men than in women, the speculation of purposefully maintaining "an iron-depleted state under medical supervision...as a preventive strategy against recolonization after a course of antibiotic therapy...," and the obvious conflicting interest of Cpners with anemia. Beyond those thoughts are more questions. Is there a relationship between iron loading and Cpn-related secondary porphyriai? Are men with Cpn infection more prone to it? If so, what has been the effect of the recommended iron supplementation for women in recent years? Does that smudge the line? How might dairy product consumption play a role in this? And particularly, besides porphyria and Cpn infection, what might Jim's daughter and Elinor have in common?
Joyce~caregiver-advocate in Dallas for Steve J (SPMSi) / Mpn, EBVi, CMV positive; strong indications of Cpn; elevated heavy metals / Wheldon CAPi since Aug '06-doxycycline 200mg/day+azithromycin 375mg ever other days+pulsed metronidazolei 375mg 3X/day; antivirals; chelation; LDNi.
PS: Happy Thanksgiving Day...finding this site and all the help Steve and I have been blessed to receive here will be tops on my list of thanks.
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Joyce~caregiver-advocate in Dallas for Steve J (SPMSi). CAPi since August 06, Cpni, Mpn, B. burgdorferi, systemic candidiasis, EBVi, CMV & other herpes family viral infectionsii, elevated heavy metals, gluten+casein sensitivity.
 Joyce, I remember Jim
Joyce, I remember Jim saying his daughter has lyme disease, so do I. When I googled iron and lyme I got this
http://www.uga.edu/columns/000828/campnews.html
I'm doing the same as you, presenting information then going for lunch
Elinor from England, UK..... on Wheldon protocol for ME/lyme borreliosis , positive for borrelia and Cpni. Started Aug 05, stopped Jan06, started again Sept 06.
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Elinor ..... from England on CAPi, doxyi/roxi/tini for ME/CFSi/lyme borreliosis, positive Cpni and borrelia. Started Aug05, stopped Jan06, started again Sept 06.
Hi Joyce, happy
As far as using an iron depleted state under medical supervision as a preventative strategy against recolonisation, this surely isn't necessary if one just carries on taking n acetyl cysteine.......Sarah
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Hello all, and Happy
Hello all, and Happy Thanksgiving!
If you want to be food-paranoid: dark meat turkey contains a lot of tryptophan, hence all that sleepiness after Thanksgiving meal! Tryptophan is one of the main rate-limiters and booster proteins for Cpni reproduction... So make sure your abxi are full dose today!
My daughter does not have Lyme, although it was first suspected. Both of us were significantly anemic at the beginning of treatment and required iron supplementation. The clinical question is a dicey one, as iron sequestering is a natural immunei (macrophage) response to an iron-consuming bacteria like Cpn, but low iron also reduces oxygen carrying functions leaving your body less functional in other ways. I was iron supplemented by a doc who did not know about anemia as Cpn caused. Dr. Powell did reams of research when looking at the choices for my daughter, and talked to one of the worlds's experts on iron and infectionsi at UCLA (it really helps that Dr. Powell did a post-doc at Stanford!) and consulted with Dr. Stratton. His conclusion: that there are neuroi-developmental considerations which warranted iron supplementation even if it might crank up the Cpn.
It actually took injectable iron, a nightmare I don't recommend, to finally get her iron up to normal range as the oral form was not cutting it. My impression overall is that if you are treating the Cpn actively, then supplementing iron if it is needed is probably not going to make much difference. This was Dr. Stratton's take on it. You drive the Cpn more into replication, but the anti-replicant abxi (doxyi, roxyi, zithi, rifampin, INHi) are dampening that down. I think this was true for me. In my daughters case, I think the antireplicant abx were not full enough in dosage, and we possibly worsened her Cpn and resulting porphyriai. But we may have prevented developmental damage from lack of iron which is not recoverable, whereas an increase in Cpn and porphyria is with a bit more time and suffering. Choices, choices.
As Sarah noted, there are far better choices for preventing or limiting Cpn than iron depletion, as this is such an important element for our functioning. Better to just plain kill the buggers! I know a doc who takes daily Flagyli as a prophalaxis for Cpn. He has no, repeat no side effects from it, and argues that his regular exposure to the bug from hospital work, and his unwillingness to get Cpn again after clearing it from his system, warrants this preventative. Just repeat to yourself, "Flagyl is my friend, Flagyl is my friend, Flagyl is my friend, Flagyl is my friend..."
Combined Antibiotic Protocol for Chlamydia pneumonia in Chronic Fatigue Syndromei & Fibromyalgiai- Currently: 150mg INH, Doxycycline/Zithromycin, 300mg Rifampin, 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
 I had iron injections
I had iron injections after the birth of my second daughter and wasn't taking any antibioticsi at the time, that must have given the bugs a nice boost, it wasn't a question of choices as I didn't know anything about Cpni.
But come to think of it ....the hemorrhaging continued until the injections stopped, was my body trying to protect itself from the onslaught to come?
Elinor from England, UK..... on Wheldon protocol for ME/lyme borreliosis , positive for borrelia and Cpn. Started Aug 05, stopped Jan06, started again Sept 06.
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Elinor ..... from England on CAPi, doxyi/roxi/tini for ME/CFSi/lyme borreliosis, positive Cpni and borrelia. Started Aug05, stopped Jan06, started again Sept 06.
Elinor, please don't get
Elinor, please don't get yourself too twisted up in knots about this. If you were given iron injections, you must have needed them because of the haemorrhaging. With all the chelated iron I took, I was still borderline anaemic. If I had stopped, I would still have been losing as much blood but I would have become seriously anaemic, which isn't the same as being kept in a carefully monitored iron depleted state........Sarah
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I was also borderline
I was also borderline anamic half my life and was shocked to find so many others here with the same problem but now it all makes sense. I am off to take my abxi before going to my family's house for Turkey. I am glad flagyli is my friend and I do not have to swallow that friend today. I holding off until next weekend :).
Happy Thankgiving!
On Wheldon protocol for MSi since April, 2006. doxyi 200 mgs daily, zithromax 250 mgs 3x/ week , Flagyl Pulses start end Sept., LDNi 2004
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On Wheldon protocol for MSi since April, 2006. doxyi 200 mgs daily, zithromax 250 mgs 3x/ week , Flagyli Pulses start end Sept., LDNi 2004. Gad-enhanced MRI of brain and spine shows NO NEW DISEASE ACTIVITY and one lesion diminishing in size on 9/30. Ma
Joyce, all excellent
Joyce, all excellent questions. I too read the posted paper about Cpni and iron, and pursued that whole issue quite a bit as well.
Several questions occured to me as well. One was perhaps that the liver is a frequent site of infection by Cpn because it provides a unique iron-rich environment. The other is that perhaps porphyriai is not merely a side-effect of Cpn's metabolism, but is a normal metabolic function of Cpn metabolism that Cpn uses to make iron more availabe for its own use. That is, I wondered if hemei iron was less available to Cpn than the iron transported to the mitochnondria by transferrin for incorporation into heme as the last step.
In point of fact, I found a paper (see link) describing the increase of Cpn transferrin receptors in Cpn grown in iron-starved cultures. This would indicate 1) Cpn needs iron, and 2) obtains its iron directly from transferrin, thereby directly competing with cellular process for said iron-bearing transferrin.
http://www.blackwell-synergy.com/doi/abs/10.1046/j.1462-5822.2001.00125....
Incorporation of iron is the last step of heme synthesis, so by preventing heme biosynthesis from completing, the transferrin transporting iron to the mitochondria would be prevented from giving up its iron to heme biosynthesis, and alternatively may be available to Cpn tansferrin receptors on Cpn, which are located near the mitochondria. This easy availability of iron may be another reason Cpn are found near mitochnodria.
Thus, disruption of heme biosynthesis and consequent porphyria may not simply be a side-effect of Cpn infection, but an essential part of Cpn metabolism and survival.
Finally, tissues with well-developed iron-based functions, such as the liver's hepatocytes, other tissues with heavy cytochrome (particularly cytochrome P450) activity, and ertheyroid cells may therefore be special targets of Cpn infection, or at least provide an environment that is exceptionally well suited for Cpn functioning.
Treatment implications are more difficult to assess. Removal of sufficient iron to impact Cpn behavior may be so large as to negatively impact host function. Furthermore, iron removal might simply result in formation of cryptic bodies.
Furthermore, currently, the most favored way to reduce iron in cases of iron-overload, such as hemochromtosis, is via phlebotomy (blood removal).
Also, note that the human body does not have an effective mechanism for removing excessive iron accumulation resulting from the failure of iron-absorption regulation. As a consequence, I've never been a fan of iron supplmentation unless indicated by testing and under medical supervision.
Since red meat is a major source of iron, and given the apparent role of iron and Cpn in CAD and numerous other diseasesi, perhaps that's another good reason to avoid excessive read meat consumption as well.
basil
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If cats are outlawed, only outlaws will have cats.
Basil- I'll throw in
Basil- I'll throw in another one, just in brief as I don't fully understand the mechanisms involved. One of the drugs used to treat porphyriai, which also happens to have a direct anti-chlamydial effect according to Dr. Stratton, is the antimalarial drug Plaquinil (hydroxychloroquine). This reference (http://www.emedicine.com/DERM/topic344.htm) states:
http://www.liebertonline.com/doi/abs/10.1089/088318703320910106
Another reference here
Dr. Powell tried it briefly with my daughter in treating her anemia with the idea that it might help redistribute iron bound into cells (by the natural immunei response) and make it more available for functioning. Her anemia was too severe to respond to this, but it is an interesting strategy.
Combined Antibiotic Protocol for Chlamydia pneumonia in Chronic Fatigue Syndromei & Fibromyalgiai- Currently: 150mg INHi, Doxycycline/Zithromycin, 300mg Rifampin, 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
 I'm not a fan of
I'm not a fan of supplementing anything at all without having tested to find out whether it is needed or not. More is not always better and its so easy to upset the delicate balance of essential vitaminsi and minerals in sick, infected, compromised bodies such as many of us have. Certain substances are easily excreted but there are many that can build up to toxic levels. It must be an enormous stress to a very sick body to have to deal with excess substances poured into it all day long, how do we know we are not unwittingly upsetting the complicated chemical reactions in all the different cycles involved in keeping us going? And which cycles are we upsetting? Under-supplying can cause as much stress.
Reasonably healthy bodies might be able to deal with these imbalances for quite some time before starting to break down but I don't think mine can, things keep going wrong. In an earlier post Sarah said I shouldn't tie myself in knots about iron....... don't worry Sarah I'm not doing that but I'm trying to work out what might be happening so that I can stay on the CAPi, I was just thinking aloud. I wish I could let my body's innate wisdom deal with it but it isn't coping too well. You won't need me to tell you how lucky you are to have your own doctor in house but the only one I can trust is hundreds of miles away and very busy with thousands of other patients, I can't go to see him and it takes weeks to get a telephone appointment, it helps to work out what to ask well in advance.
This question of supplementing is occupying other minds as well, there is a post about it today in the Vitamin Di thread, even getting a test result is no guarantee that supplementing will be the right thing to do, there are too many unknown variables of pathogens, host reactions and shortages or excesses.
You're right Sarah, I am in knots, Joyce has stirred the pot a bit with this question and there probably won't be a definite answer or at least there will be different answers for different people, reading what everyone thinks is helping me untangle the knots.
Elinor from England, UK..... on Wheldon protocol for ME/lyme borreliosis , positive for borrelia and Cpni. Started Aug 05, stopped Jan06, started again Sept 06.
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Elinor ..... from England on CAPi, doxyi/roxi/tini for ME/CFSi/lyme borreliosis, positive Cpni and borrelia. Started Aug05, stopped Jan06, started again Sept 06.
I wandered into
I wandered into investigating this same subject matter again today and rediscovered the same links. Wish I could remember everything I've read since becoming a bug investigator. Anyway, it's interesting stuff, and it's a good chance to celebrate the wonderful difference in Elinor's condition since November '06 and now.
Joyce~caregiver-advocate in Dallas for Steve J (SPMSi). CAPi since August 06, Cpni, Mpn, B. burgdorferi, systemic candidiasis, EBVi, CMV & other herpes family viral infectionsi, elevated heavy metals, gluten+casein sensitivity.
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Joyce~caregiver-advocate in Dallas for Steve J (SPMSi). CAPi since August 06, Cpni, Mpn, B. burgdorferi, systemic candidiasis, EBVi, CMV & other herpes family viral infectionsi, elevated heavy metals, gluten+casein sensitivity.