Nanobacteria Theory disproven
- From: HubbaBubba <HubbaBubba@xxxxxxxxxxxx>
- Date: Sat, 29 Oct 2005 06:52:48 +0800
From http://drcranton.com/nanobacteria.htm
Alleged Nanobacteria do not Cause
Calcification of Arterial Plaqueby Elmer M. Cranton, M.D.
Copyright © 2005 Elmer M Cranton, M.D.
Pathologic calcification of atherosclerotic plaque, dental plaque and kidney stones has been attributed to a previously unreported and putative bacterial species, Nanobacterium sanguineum, by Finnish researchers, Kajander and Ciftcioglu.(1) That work has since been duplicated by scientists at NIH, who made identical observations, but concluded that biomineralization was caused by the nonliving, nucleating activities of self-propagating microcrystalline centers (nidi), which form crystaloid macromolecules of calcium carbonate phosphate apatite.(2)
These submicroscopic (submicron) crystals could be transferred in a deceptively life-like manner through serial dilutions using techniques similar to those used for subcultures, while retaining their crystalline ability to grow into calcific concretions at physiologic pH. Six serial 1:10 dilutions were transferred to fresh culture media, and were observed to repeatedly propagate as tiny coccoid appearing or dome-shaped crystals. Photographs of these non-living structures taken under electron microscopy were identical in appearance to those previously published by the Finnish researchers and mistakenly labeled as “Nanobacteria.”
The 16S rDNA sequences attributed by Kajander and Ciftcioglu to Nanobacteria sanguineum were identified as belonging instead to an environmental microorganism, Phyllobacterium mysinacearum, previously described and a known contaminant of culture media and laboratory reagents—not associated with calcification. Although reagents and culture media are sterilized before use, traces of DNA sequences remain, which are greatly amplified using the described detection techniques. Those same 16S rDNA sequences were found in controls that had no potential source of Nanobacteria present. No controls were reported by the Finnish researchers, who unknowingly assigned these 16S rDNA sequences to a new genus.(1)
Examination of calcific biofilms identical to those previously described by Kajander and Ciftcioglu revealed no nucleic acids or proteins, of the type that would be present in bacteria. Progressive crystalline propagation was not inhibited by sodium azide, an extremely potent cellular and bacterial toxin.
High-dose gamma radiation and ultra filtration to the submicron level did prevent propagation, but that is not evidence for living bacteria. Those two procedures can both alter macromolecular and crystalline properties, thus blocking further growth of calcific crystals.
Calcium and phosphate ions, when added to sterile solutions of culture media, also resulted in progressive calcific mineralization. Phospholipids, lipid-protein complexes, and submicroscopic crystals of calcium apatite, as occur in plasma, were all shown to be nucleators of biomineralization.
Cell cultures of fibroblasts grown in the presence of calcific biofilms showed evidence of cytotoxicity and were observed to take up microcrystals of calcium apatite. The fact that intracellular calcification is poorly tolerated is not new information and that observation cannot be interpreted as evidence for the presence of Nanobacteria.
Antibodies can be produced to react with surface structures of such nonliving crystalline macromolecules using monoclonal techniques. Chelating agents such as EDTA, citrate, and tetracycline (an antibiotic that also has calcium binding properties) can alter the surface properties of nonliving calcific and crystalline nucleators—both halting calcific propagation and blocking immunologic reactivity to previously reactive antibodies. Diagnostic testing based on immunologic properties could thus become non-reactive following exposure to calcium chelators. That change therefore does not indicate that a bacterial infection has been eliminated, as claimed by one laboratory.
There has been a recent flurry of marketing activity attempting to sell EDTA suppositories to unwary medical practitioners―and even by health food stores to the general public. Proponents of those products base their sales pitch on the unproven suppositions that Nanobacteria cause arterial plaque and that EDTA suppositories will remove the alleged "calcific shields" supposedly produced by Nanobacteria as protection. Proponents of EDTA suppositories further claim that a powder must be taken by mouth to delay the renal excretion of EDTA, resulting in higher blood levels. None of those claims are credible for the following reasons:
1. Nanobacteria (if they even exist) have not been shown to have any relationship to pathologic calcification as found in atherosclerotic plaque.
2. EDTA is 100% filtered by renal glomeruli. The filtration rate of EDTA equals the glomerular filtration rate (GFR). EDTA is not subject to tubular secretion or reabsorption. The only way to delay excretion of EDTA would be to poison the kidneys sufficiently to reduce creatinine clearance (GFR)—not a wise thing to do.
3. No drug is better absorbed rectally than by mouth (although enteric coating against stomach acid is sometimes helpful, which does not apply to EDTA). Suppositories are used in cases of persistent vomiting, in uncooperative patients who refuse to take oral medicines, and in pediatric patients who will not swallow medicines by mouth. Passive absorptive properties of the colon and rectum are similar to the upper G/I tract. It is well documented that orally administered EDTA is not absorbed in significant amounts—approximately five percent. Oral EDTA therefore ends up in the rectum, right where a suppository would be inserted. If rectal or colon uptake of EDTA were greater than in the upper G/I tract, then total absorption by mouth would be greater than 5%. It has been scientifically demonstrated that both rectal and oral absorption of EDTA is at most seven percent.
4. The "secret formula" powder recommended to be administered by mouth to enhance rectal EDTA also contains additional oral EDTA. It may therefore add somewhat to total absorption, but not by delaying renal excretion, as asserted by the marketers of this product. Blood levels of EDTA that were reported using this combination of oral and rectal EDTA are less than one sixth that achieved by intravenous infusion. It is true that 12 hours later the small amount of EDTA continuing to be absorbed from the gut will produce blood levels at that time which exceed what would remain from a rapidly-excreted intravenous infusion. It is untrue, however, to state that the EDTA suppositories combined with oral EDTA result in a higher blood level of EDTA using this type of deceptive data.
5. Eighty-five percent of patients have consistently responded well to intravenous EDTA, administered according to the protocol developed and widely accepted over almost 50 years. Electron beam CT (EBCT) scores of coronary artery calcium usually remain unchanged while patients improve dramatically. Many published studies have presented objective evidence of increased blood flow and improvement in symptoms and function, with no change in EBCT calcium scores. It therefore makes little sense to assume that change in calcification of artery walls is an important indicator of clinical improvement. Arterial plaque is a proliferative and inflammatory disease, involving soft tissue cell replication during most of its course. Any experienced chelation doctor can produce large numbers of case histories showing dramatic improvement following the well-established protocol of intravenous EDTA. Do proponents of EDTA suppositories and oral EDTA believe that intravenous treatment is not effective, despite these proven benefits reported in dozens of published studies? If another party proposes an innovative method to produce similar results, they should publish data from a series of consecutively treated patients with tabulated, objective and statistically significant evidence to document both effectiveness and safety of their position.
6. While EBCT calcium scores do correlate with presence of plaque, they do not correlate well with degree of occlusion. Exaggerating to make a point, wearing a skirt correlates very highly with the incidence of breast cancer. Using this same type of reasoning, it might seem that if women stopped wearing skirts and wore only slacks, they would not get breast cancer. In other words, correlation does not mean cause and effect. Other more important variables are clearly involved. It is known that prolonged administration of EDTA, 50 to 100 infusions, can reduce pathologic calcification and even dissolve kidney stones. But EDTA has other profound effects in the body, not just on undesirable calcium. It also binds a spectrum of essential nutritional trace elements. There is no reason to assume that pharmacologic blood levels of EDTA sustained continuously for prolonged periods of time are safe (as implied by proponents of both oral and rectal EDTA). In fact, it seems logical to believe that eventual disruptions will occur to vital metalloenzyme systems. If EDTA is continually present in the digestive tract it will bind to nutrients, and should interfere with nutritional uptake of essential trace metals, leading to deficiencies.
7. Dr. James Roberts, a cardiologist, recently reported his own results using EDTA suppositories in coronary heart disease patients, while also administering the recommended powder by mouth. At the May, 2002, ACAM conference, Dr. Roberts wrote in his printed handout: “My EBCT scores are not dropping by 58% [as claimed by suppository proponents] . . . my patients are dropping their scores in the 15% to 25% range.” The 15% to 25% range does not mean much using this technique. The electron beam can only measure discrete slices, and does not cut through exactly the same location on repeat measurement. Variability between examinations of EBCT calcium scores ranges as high as plus or minus 38%, depending on the test site and equipment calibration.(3)
8. The Nanobacteria hypothesis ignores the well-established relationship of plaque to homocysteine levels.
There may be reason to suspect that an infective organism plays some role in the course of atherosclerosis―Chlamydia, for example. Whether it is a late stage and secondary factor or a causative agent has yet to be determined. Recent studies have failed to show benefit from a variety of antibiotics.
In the absence of new evidence to the contrary, Nanobacterium sanguineum now seems now to be a myth. What we are left with is a clever and deceptive marketing scheme.
1. Kajander EO, Ciftcioglu N. Nanobacteria: an alternative mechanism for pathogenic intra- and extracellular calcification and stone formation. Proc Natl Acad Sci USA. 1998 Jul 7;95(14):8274-9.
2. Cisar JO, Xu DQ, Thompson J, Swaim W, Hu L, Kopecko DJ. An alternative interpretation of nanobacteria-induced biomineralization. Proc Natl Acad Sci USA. 2000 Oct 10;97(21):11511-5.
3. Nieman K, van Geuns J, Wielopolski P, et al. Noninvasive coronary imaging in the new millennium: A comparison of computed tomography and magnetic resonance techniques. Rev Cardiovasc Med 2002 3(2):77-84.)
Last modified: May 26, 2005 .
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