NANOBACTERIAL CALCIFICATION is REVERSIBLE

 

Growing in cell culture media, Nanobacteria will generate biofilm, and then aggregate to form up carbonate apatite shelters, but only in a serum free environment.  If serum is present, shelters will not form.  If serum is introduced, within twenty-four hours the shelters automatically break down, releasing coccoid shaped live and active Nanobacteria back into the blood or growth media, along with (A) D-shaped Nanobacteria, (B) fruiting bodies, and (C) elementary particles.  16 S rRNA analysis demonstrates that all of these forms are N. sanguineum.  They are truly pleomorphic.

Why does this occur?  Serum contains anti-ossification factors that prevent bone from growing in blood (seems like a good idea), and they also prevent Nanobacteria from forming carbonate apatite shelters.  This is why the shelters form up only within organs and within the walls of blood vessels. 

Serum can dissolve Nanobacterial shelters; so what else can?  In the kidney stone study, to be abstracted in a latter section, Kajander used HCL to dissolve Nanobacterial shelters recovered from human kidney stones.  Decalcification with HCL amplified the binding of anti-Nanobacterial monoclonal antibodies to the ground up stone material (Antibodies, host generated or diagnostic, can’t bind to calcium; they bind only to their target antigen.).  Puskas found that the binding of fluorescent anti-Nanobacterial monoclonal antibodies to human calcified atherosclerotic plaque was greatly enhanced by pre-treatment with EDTA.  Mezo, Ciftcioglu, and Kajander have confirmed Puskas’ work in clinical studies. 

Nanobacterial biology is not about causing cardiovascular disease; it’s about perpetuating Nanobacterial survival.  Human tissue, arteries, kidneys, kidney stones, dental pulp stones, etc, are simply niches that lend themselves well to Nanobacterial proliferation in their calcific form. 

Once encased in calcium, the Nanobacteria are semi-dormant and grow slowly. Once in their calcific structures, Nanobacteria enter a dormant, slow growth phase, doubling only every six days.  This is good for humans with vascular wall Nanobacterial infection; slow, steady growth, is obviously better than rapid growth.  CT measured coronary calcification progresses steadily in untreated persons by 20-52% per year, similar to that of kidney stone calcium, but it can speed up to 82%. We can therefore expect a person’s HeartScan score to go up at the rate of 5-20% every 4 months or 20-82% per year (more on the HeartScan in a later section).

Once Nanobacteria is unroofed from its carbonate apatite shelters, it speeds up its growth rate, now dividing every three days.  If you add pure EDTA to a beaker containing calcified Nanobacterial colonies, the shelters will dissolve, and out will come individual Nanobacteria – “pissed off”, dividing rapidly and eager to embark on a new cellular search, destroy, or calcify mission.

IV EDTA has been used in the treatment of cardiovascular disease for over 50 years.  The mechanisms of action of IV EDTA are:

 

a)      Removal of heavy metals, improving cellular biochemistry, and

 

b)      Parathyroid stimulation, hopefully promoting the transfer of metastatic coronary calcium back into bone.

 

One cannot say exactly why patients get better, but they do for the most part.   Orthodox medicine does not "believe in" IV EDTA, and some studies of EDTA in stable angina have shown no effect, but with my own eyes I have seen human train wrecks regain their health following a course of treatment (years ago, pre-EECP, several of my patients with refractory angina underwent IV EDTA chelation "behind my back" and got better - this opened up my mind) of my patients .  But not all patients respond well to IV EDTA, and some need 60+, not 20 treatments.  Experience has shown that monthly maintenance therapy is important.  Hancke, surveying his long-term experience, found that Danish coronary patients who continued with maintenance EDTA treatments on a monthly basis did much better over the long run; they “maintained their gain” better than did patients who quit after an initial 30 sessions. 

 

Why should this be?  If the goal is to remove lead and cadmium, and the patient doesn’t smoke, and he quit driving truck 20 years ago, then why do we need to keep going after his heavy metals?  Periodic boosting of parathyroid function makes sense, but could it be that EDTA has another mechanism of benefit?  Could it be that EDTA is working by punching nano-sized holes in accessible vascular wall Nanobacterial shelters, those closest to a capillary, or any other route by which EDTA can attach to it, and then relying on the immune system to finish the job?  Could it be that EDTA alone is not getting the job done, and that we need strong immune function to kill the Nanobacteria, now “pissed off” and in their rapid growth phase after being unroofed by EDTA calcium chelation?  Experienced chelating physicians tell me that 30 treatments given over 10 weeks works much better than 30 treatments given over 30 weeks.  Carlos Lamar admitted his patients for a weekend of chelation, giving a low but steady dose from Friday night to Monday morning, and his patients did great.  If Nanobacteria double every three days, and we give EDTA every seven days, could it be that maintenance chelation is necessary because weekly EDTA “didn’t get the job done”.  Maybe we need to add in an antibiotic or other immune stimulant. 

 

The concept underlying the anti-Nanobacterial approach to atherosclerosis is that:

  a) Nanobacterial infection causes vascular calcification and soft fibrous plaque.

  b) A frustrated immune response generates short and long-term inflammatory responses.

  c) To resolve the problem we must unroof the Nanobacteria with EDTA, and then kill  them with Tetracycline, the one antibiotic that has activity against Nanobacterium sanguineum. 

 

Studies carried out by Mezo, Ciftcioglu, Kajander, and other Nanobacterial researchers show that EDTA as a monotherapy closed in on, but did not reach, the scientific (eradicating Nanobacteria) and clinical outcome (reversing calcific atherosclerosis) targets common to all physicians.

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