Study: Calcification in coronary artery disease can be reversed

[JimChicago]

My surgeon said my valve problems were due to calcification - that makes mw wonder if treatments like this will be able to reverse such calcification -

From:
http://www.ncbi.nlm.nih.gov/entrez/...ve&db=pubmed&dopt=Abstract&list_uids=15364120
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Pathophysiology. 2004 Oct;11(2):95-101. Related Articles, Links


Calcification in coronary artery disease can be reversed by EDTA-tetracycline long-term chemotherapy.

Maniscalco BS, Taylor KA.

4730 N. Habana Avenue, Suite 201, Tampa, FL 33614, USA.

Atherosclerosis is a complex process with multiple mechanisms and factors contributing to its initiation and progression. Detection and quantification of coronary artery calcium (CAC) scores with electron beam tomography has been shown to correlate with obstructive and nonobstructive coronary artery disease (CAD). Pathogen-triggered calcification could play a role in CAD. Recent reports suggest that infectious blood nanobacteria (NB) emerge to be such a trigger. So far, minimal or no reversal of atherosclerosis has been claimed by therapies with iv ethylenediaminetetraacetic acid disodium salt (EDTA), antibiotics, or other regimens, and therapies for atherosclerosis remain non-curative. We have now combined EDTA with antibiotic tetracycline (comET), an in vitro proven nanobacteriocidal treatment, and tested comET therapy in patients with documented CAD. Three hypotheses were probed: (1) Are NB present in patients with CAD?; (2) Does treatment with comET affect blood NB antigen and serology?; (3) Does a comET decrease CAC scores? One hundred patients with stable CAD and positive CAC scores were enrolled into a 4 month study of comET therapy. ComET therapy is composed of (1) Nutraceutical Powder (Vitamin C, Vitamin B6, Niacin, Folic Acid, Selenium, EDTA, l-Arginine, l-Lysine, l-Ornithine, Bromelain, Trypsin, CoQ10, Grapeseed Extract, Hawthorn Berry, Papain) 5cm(3) taken orally every evening; (2) Tetracycline HCl 500mg taken orally every evening; (3) EDTA 1500mg taken in a rectal suppository base every evening. CAC scoring was repeated at 4 months and serum samples were analyzed for NB antigen and serology at baseline, 2 and 4 months. Complete blood count, metabolic panel, liver function, C-reactive protein (hs-CRP) and lipids were analyzed at baseline and 4 months. Seventy-seven patients completed the study and all patients were positive for NB serology, antigen or both. Responders (n = 44; 57%) had significant decreases in total CAC scores (P = 0.001), the average decrease being 14%. Non-responders (n = 33; 44%) had no change or had increases in CAC scores. Angina was decreased or ablated in 16 of 19 patients (84%). Lipid profiles improved to non-atherogenic direction significantly (P = 0.001), a remarkable finding in a patient group where 86% were on continuous statin medication already before the trial. No adverse physiologic effects were seen in renal, hepatic, or hematopoetic systems. In conclusion, CAC scores decreased during ComET therapy trial in most CAD patients inferring regression of calcified coronary artery plaque volume. The patients tolerated the therapy well and their angina and lipid profiles improved. Further treatment trials for long term therapy with matched controls are warranted.
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[Marguerite53]

a good question

a good question

can we have some more discussion about this? The calcificatiion issue is so puzzling. That is the nature of the stenosis, the nature of the disease, yes? Is it something that attacks compromised areas somewhat like a bacteria does?? Is the term calcification just a general term. It doesn't actually have much to do with calcium, does it?

Thanks, Jim.

Marguerite

 

[JimChicago]

Hi Marguerite,
I agree with you - it seems like an interesting development - I came across this issue by hearing a book author on a radio show - his website is:
http://www.calcify.com/

He has a new book out about this. I'm going to try to obtain a copy of his book. It is a "cutting edge" issue since the nanobacteria involved are 1/1000 the size of the regular old bacteria critters that are well known. Apparently until recently scientists said such things as nanobacteria were impossible - but I guess that's what they said about flying machines 150 years ago too.

The implications are extrmely interesting like this report:

From:
http://www.noaw.com/Nanobacteria/nanobacteria.htm
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NanobacLabs in conjunction with Dr. Mezo have developed blood and urine tests to identify persons infected with the nanobacteria. Once identified, he has formulated a therapy to treat the infection. In one of his studies, of the 91 participating patients, the mean decrease in their coronary artery calcification scores was 58.5 percent after treatment with NanobacTX therapy for three months. Interestingly, in 19 of those 91 patients 100 percent of coronary artery calcification was eradicated.
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The research on this came in part from NASA -

From:
http://www.medicalnewstoday.com/medicalnews.php?newsid=20076
>>>>
NASA researchers announce a potential cause of rapid kidney stone formation in astronauts on space travels. The authors of a study published in Kidney International call for a "Major Initiative" to investigate nanobacteria.

Nanobacteria (NB), a novel self-replicating, mineralizing agent, has been identified by National Aeronautics and Space Administration (NASA) scientists as a potential culprit in kidney stone formation among astronauts. With the potential for future exploratory space missions to the moon and Mars, longer missions, and exposure to the elements of outer space, health is a major concern for astronauts.
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Notice that NASA describes nanobacteria as "a novel self-replicating, mineralizing agent" - I wish I knew about this research before I had my heart surgery - I would rather have gotten that treatment descibed in the article I posted at the beginning of this thread.

 

[tobagotwo]

It's certainly not impossible that nanobacteria, or even "regular-sized" bacteria are involved in the formation of calcium deposits in at least some cases of valve disease. Perhaps viruses as well. The difficulty may lie in timing. Once we've calcified to the point that it is noticeable to our doctors, will the antibiotics still be effective? The bacteria could be well-encrusted into the stone, and relatively impervious to antibiotic treatment.

Of course, every possible answer comes with new questions. If existing calcification did disintegrate, how would we control its dissolution, to avoid larger pieces drifting into the bloodstream to do unknown damage? Finding an approach to that would be one of the next steps. It would certainly have to be better than replacement.

One thing that might not fit this theory is the understanding that younger people calcify things at a much more rapid rate, which seems an unlikely response to bacteria alone. That certainly doesn't mean that there can't be multiple causations, though. Perhaps so-called "senile" calcification is a more likely candidate for bacterial causation.

There was a revelation only a few years ago that helicobacter pylorii bacteria were responsible for most ulcers, and many other intestinal ills. You'd think that we'd have figured out about bacteria by now, but I guess there are a lot of possible venues.

It makes me want to try to talk my cardiologist into something like this, just to be sure. I would have to think that the replacement wouldn't have removed all of the vermin, if they were there. I would like to avoid further calcifications elsewhere, where there may not be fixes at all.

Best wishes,

 

[KimC]

Jim, thanks for pointing out this fascinating study. I plan to speak to my doc about it and will share his thoughts.

Bob, you bring up a very interesting point, i.e., the GI connection. They've linked ulcerative colitis to aortic valve disease, did you know that? Inflammation definitely plays a role in atherosclerosis.

Although I don't like to talk about it, I have lymphocytic colitis. I lived with it for years before seeking treatment. For whatever reason, the ACE I take has stopped my GI symptoms.

Best,

 

[Phyllis]

" younger people calcify things at a much more rapid rate"

Bob,
This is something **** and I were discussing last night and we're not sure of the answer. Maybe you have the answer. Do bovine and porcine vlaves in younger people calcify at a much more rapid rate because younger people are more physically active or is it a biological fact? Naturally, we are curious as **** at 71 is as active as many in their 50's.

 

[JimChicago]

That's also interesting Kim and Bob about the link with ulcers, colitis and inflamation.

Here's another article on it:

From:
http://adsabs.harvard.edu/cgi-bin/nph-bib_query?bibcode=1998SPIE.3441..105C&db_key=AST
>>>>
Title:
Stone formation and calcification by nanobacteria in the human body
Authors:
Ciftcioglu, Neva; Bjorklund, Michael; Kajander, E. Olavi
[excerpt of abstract]
Previously, only struvite kidney stones composed of magnesium ammonium phosphate and small amounts of apatite have been regarded as bacteria related. 90 percent of demineralized human kidney stones now screened, contained nanobacteria. At least three different distribution patterns of nanobacteria were conditions, and human kidney stones that are formed from small apatite units. Prerequisites for the formation of kidney stones are the supersaturation of urine and presence of nidi for crystallization. Nanobacteria are important nidi and their presence might be of special interest in space flights where supersaturation of urine is present due to the loss of bone. Furthermore, we bring evidence that nanobacteria may act as crystallization nidi for the formation of biogenic apatite structures in tissue calcification found in e.g., atherosclerotic plaques, extensive metastatic and tumoral calcification, acute periarthritis, malacoplakia, and malignant diseases. In nanaobacteria-infected fibroblasts, electron microscopy revealed intra- and extra-cellular needle-like crystal deposits, which were stainable with von Kossa stain and resemble calcospherules found in pathological calcification. Thus bacteria-mediated apatite formation takes place in aqueous environments, in humans and in geological sediments.
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One possible vector some speculate can lead to the nanobacteria infestation might be inadverently contaminated vaccine batches -

From:
http://www.pnas.org/cgi/content/full/95/14/7846
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Proteobacterial infections are common in cows, and fetal bovine serum is the presumed origin of the tissue culture contaminants. Kajander and Çiftçioglu (5) have found that more than 80% of fetal bovine serum batches, each pooled from several thousand animals, have nanobacteria, as determined by immunoassay with monoclonal antibodies and by direct culture. Because nanobacteria are relatively resistant to the antibiotics commonly added to tissue culture media, it seems likely that many established cell lines might have a superimposed nanobacterial contaminant. Just as problems with mycoplasma and simian virus 40 infection have confounded tissue culture experiments in the past, so nanobacterial infestation could perversely influence the immunologic, metabolic, and growth properties of normal and malignant cells propagated in vitro. Such effects have already been reported, and the necessary technology to detect nanobacteria in tissue culture is emerging (6).
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I guess some vaccines are grown in monkey or bovine serum - since the technology to identify nanobateria in them is its infancy some speculate some of those batches my be contaminated with nb. Could younger people who are required to get some 25-35 vaccines be more susceptible? I was told the calcification in my heart valves was due to radiation treatments for Hodgkins. Could it be that tissues burned by radiation are less resistance to nb infection?

 

[KimC]

Here's my doctor's reply to the original post by Jim:

"Tetracycline has not yet been proven to be efficacious. Chelation has
not been shown to be beneficial in treating coronary heart disease if one
takes an end point of heart attack, death, or need for surgery or
angioplasty, but there is a big, very scientific study now goiing on at the
NIH which should definitively answer the question. The key to understanding
the article is to note their conclusion " Further treatment trials for long
term therapy with matched controls are warranted". We'll see."


Thanks again for sharing the research! I hope we hear more when the NIH study is complete.

Best,

 

[JimChicago]

Thanks for giving us the update Kim.

Appparently a researcher from Mayo is looking into this too -

From:
http://www.ncbi.nlm.nih.gov/entrez/...t=Abstract&list_uids=15142839&itool=iconabstr
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Am J Physiol Heart Circ Physiol. 2004 Sep;287(3):H1115-24. Epub 2004 May 13. Related Articles, Links


Evidence of nanobacterial-like structures in calcified human arteries and cardiac valves.

Miller VM, Rodgers G, Charlesworth JA, Kirkland B, Severson SR, Rasmussen TE, Yagubyan M, Rodgers JC, Cockerill FR 3rd, Folk RL, Rzewuska-Lech E, Kumar V, Farell-Baril G, Lieske JC.

Department of Surgery, Mayo Clinic, Rochester, Minnesota 55905, USA. [email protected]

Mechanisms mediating vascular calcification remain incompletely understood. Nanometer scale objects hypothesized to be a type of bacteria (nanobacteria) are associated with calcified geological specimens, human kidney stones, and psammona bodies in ovarian cancer. Experiments were designed to evaluate human vascular tissue for the presence of similar nanometer-scale objects

......

Therefore, nanometer-scale particles similar to those described as nanobacteria isolated from geological specimens and human kidney stones can be visualized in and cultured from calcified human cardiovascular tissue.
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I have to wonder though if there needs to be some sort of insult/injury to tissue before the nb critters can begin to colonize in them. Why is that the calcification is more prevalent in areas around the heart than in the rest of the circulation system?