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Medical Forum / Diseases and Disorders / Prostatitis / October 2005Nanobacteria Theory disproven
From http://drcranton.com/nanobacteria.htm Alleged Nanobacteria do not Cause Calcification of Arterial Plaque by 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 To Townsend Letter Response to November 2002 issue and Elmer M. Cranton's letter 'Alleged Nanobacteria Do Not Cause Calcification of Arterial Plaque' Nanobacteria Do Exist and Actively Participate in the Calcification of Arterial Plaque By E. Olavi Kajander, MD Department of Biochemistry, University of Kuopio, Kuopio, Finland Email olavi.kajander@uku.fi Dear Editor; Jonathan Collin, MD: The cause of pathological calcification, including atherosclerosis, dental pulp stones and kidney stones, used to be an enigma, but our science is rapidly clarifying the relationship between nanobacterial infections and disease. The life-long incidence of kidney stones appears to have increased throughout the whole 20th century, and now occurs in up to 15% of the population.1 Nanobacteria have been linked to human kidney stone and preliminary studies showed Koch's postulates to be fulfilled.1, 2, 3, 4 Calcified hard plaques is now a common form of coronary heart disease but were surprisingly a clinical rarity 100 years ago5. Calcified plaques can lead to acute myocardial infarct, because apatite (calcium phosphate mineral) exposed to blood activates a thrombotic cascade. Nanobacteria were the first (may still be the only) calcium-phosphate mineral containing particles isolated from human blood. Radioactively labelled nanobacteria were shown to accumulate in rabbit aorta and aortic valve, although their main elimination route was excretion via kidneys into urine6. This study pointed to the potential role that nanobacteria could have in atherosclerosis, heart valve calcification and kidney stone formation. Nanobacteria were present and actively involved in the processes: 1. Nanobacteria were shown to be active nidi forming the right type of calcified mineral. Active nidus means a center of calcification that can mediate calcium-phosphate mineral formation under non-saturating calcium and phosphate concentrations. In fact, nanobacteria are so good in utilizing these minerals that they consume all free calcium and/or phosphate from their culture medium, whichever is first consumed to zero2. 2. Nanobacteria have and release endotoxin7 and thereby stimulate and mediate chronic local inflammatory reactions in atherosclerotic plaque. 3. Nanobacteria have been shown to infect humans and infections last possibly life-long. 4. Almost 100% of atherosclerotic patients in USA and in Finland have antinanobacteria antibodies in their serum, whereas in healthy blood donors antinanobacteria antibodies are present in about 15% (see web pages of Nanobacteria Minisymposium held at Kuopio last year). 5. Nanobacteria have been shown to be susceptible to several antibiotics and sequestering agents8. Since nanobacteria form calcific biofilm it is clear that their eradication needs combination chemotherapy directed at the biofilm, the calcified deposits and the agent. Such chemotherapy can be very demanding since nanobacteria grow very slowly. Thus lessons learned from the treatment of tuberculosis or leprosy should be remembered. Dr. Cranton has not personally studied nanobacteria but has pointed out that nanobacteria do not exist and cannot cause atherosclerosis. His motivation seems to be to stop ongoing combination drug trials that aim at verifying whether nanobacteria cause atherosclerosis and how to cure this infectious process. These studies use the same principles that vindicated Helicobacter pylori in peptic ulcer disease: curative therapy was the evidence for the causative role of the agent. That approach lead into a revolution in the therapy of Helicobacter pylori-mediated diseases. This was a good thing. Nanobacteria form calcific biofilms and replicate under blood/serum conditions, as was first published by Kajander and Ciftctioglu9, a fact that has been reproduced and published by many research groups, e.g., NASA, Mayo Clinic, McGill University, Exeter University, University of Illinois, Alcala University and University of Ulm. Dr. Cranton refers only to one NIH researcher, Cisar10, who could also culture similar particles from serum and human saliva sources. Cisar had no positive or negative controlled controls and did not use valid published immunological control methods. Cisar verified our findings, and also confirmed the extreme difficulties in performing PCR, but finally suggested his opinion that the culturable particles cannot be bacteria, since they were too small, were not inhibited with a respiratory poison, nucleic acids could not be detected with standard procedures and their protein patterns revealed only few proteins, much less than one would expect from a common bacterium. Cisar did not sequence any proteins. He did not do any DNA work besides staining with Hoechst 33258, where he got the same weakly positive result than we did. To the contrary of Dr. Cranton's claims, Cisar did not do a PCR phylogenetic analysis using 16S rDNA sequences simply because he did not get any: all his samples, including negative controls, were contaminated with Pseudomonas sp. This fact is clearly stated in his paper and means that he did not have any data on the bacterial status of nanobacteria. We do totally agree with Cisar that nanobacteria are not common bacteria. Nanobacterial samples may contain pieces of DNA from common bacteria, which makes phylogenetic PCR analysis using universal primers practically impossible and worthless. PCR analysis assumes that the ribosomal gene has 'universial' sequences detectable by the primers, but this is not true for nanobacteria and other organisms. When we originally named nanobacteria in 1990, we wanted to separate them from common bacteria. Unfortunately, the "bacteria" part of the name still lures less-well informed scientists to compare nanobacteria with E. coli and other common bacteria, which are 100-fold bigger and produce biomass 10,000-fold faster than nanobacteria. As pointed out by Dr. Cranton, apatite can be formed under super-saturating concentrations of calcium and phosphate via several mechanisms. To our knowledge, nanobacteria-mediated calcification is the only mechanism to make apatite at non-saturating levels of calcium and phosphate. Cisar did not follow saturation degree analysis in his studies although saliva is known to be highly super-saturated with calcium and phosphate. Yet Cisar suggested as an alternative explanation nanobacteria to be replicating apatite mineral particles. Naming an agent as particles or nanobacteria, living or non-living but self-replicating, has relatively little meaning with respect to causing disease, e.g., the atherosclerotic process. The fundamental importance is that these self-replicating special particles that we call Nanobacterium sanguineum are found in blood and in atheroslerotic plaques. This fact was initially presented by Laszlo Puskas at Nanobacteria Minisymposium held at Kuopio last year, detected by us (unpublished data) and finally now has been verified by Mayo Clinic and University of Texas11. Macrophages in the aorta and other arteries internalise nanobacteria and stimulate a local chronic inflammatory cascade, that eventually proceeds to nanobacteria-mediated calcification. In fact, according to Dr. Cranton, Cisar10 also verified the medical importance of the nanobacteria phenomenon: he stated that submicroscopic crystals of calcium apatite, as occur in plasma, were shown to be nucleators of biomineralization. However, the presence of apatite crystals had earlier been shown only by us, but the role of apatite biofilms in blood clotting and blood vessels is well known. Thus the described presence of apatite particles could be potentially deadly, in fact a mechanism initiating myocardial infarction. Dr. Cranton is putting forward ungrounded claims on nanobacteria and on therapy trials aiming at eradicating them. The claims need short comments: 1. Nanobacteria have been shown to be unique calcifying agents. They can be cultured and passaged in cell culture media mimicking serum in composition. Atherosclerotic plaques contain nanobacteria as detected by researchers from Mayo Clinic and the University of Texas11. 2. The administration strategy of EDTA must maintain drug blood levels on a sustained therapeutically effective level. I have personally conducted serum-EDTA levels on patients treated with NanobacTX, and this prescription combination is effective. 3. Many drugs are successfully administered rectally. In most cases rectal administration is highly effective. The efficacy of NanobacTX to deliver sustained therapeutic levels of EDTA has been determined using analytical methods developed at Kuopio University. 4. In antimicrobial therapy, administration route, dose and frequency has to be carefully considered in order to maintain high enough drug levels. In most infectious diseases, it would be unwise to administer a drug intravenously once or twice a week while knowing that the therapeutic concentrations are retained only for a short period after the administration. 5. Dr. Cranton states:'It makes little sense to assume that calcification of artery walls are an important indicator of clinical significance of the disease state'. This statement is ungrounded and against the perspectives how myocardial infarcts develop. Additionally, the clinical & scientific literature is heavily replete with evidence substantiating the pivotal importance of calcification processes in the development of atherosclerotic disease and contrary to Dr. Cranton's statement. 6. The purpose of NanobacTX treatment is to be effective. This means that it must decrease calcification in atherosclerotic plaques. It is obvious that EDTA alone is not sufficient to reach this goal, because under in vitro tests8 EDTA alone has no inhibitory action on nanobacteria at clinically achievable EDTA concentrations. Dr. Cranton has also stated that intravenous EDTA therapy does not decrease calcification scores. A combination therapy is required to reach this aim. NanobacTX is uniquely effective in decreasing coronary artery calcification12. 7. James Roberts, MD, FACC, has reported significant reduction in EBCT scores. This is an objective way to measure the effect of therapy. Benedict Maniscalco, MD, FACC, will publish a formal study on NanobacTX therapy in Circulation12. 8. It is unknown at this point how nanobacteria infection affects homocysteine levels. There is new published evidence that nanobacteria do exist8,11.12 and are biological entities reacting, e.g., to light13, cause kidney stones and are found in human atherosclerotic plaques. As discussed earlier, new evidence also indicates that several drugs are effective in-vitro against nanobacteria, but in-vivo eradication of nanobacterial biofilms and calcification requires combination therapy. Administration of EDTA alone is ineffective towards this goal, since it will not kill nanobacteria at the blood concentrations achievable and has been shown, by itself, to be ineffective in reducing coronary artery calcification scores. NanobacTX, a unique prescription combinatory nanobiotic is specifically formulated to eradicate nanobacterial biofilm, calcification and the nanobacteria themselves and has been shown in validated IRB-monitored clinical cardiology studies to be uniquely effective in doing so as measured by significant decreases in coronary artery atherosclerotic plaque burden, and other measurement parameters soon to be announced12. E. Olavi Kajander, MD Email olavi.kajander@uku.fi References 1. Kajander, EO, Ciftcioglu, N, Miller-Hjelle, MA, Hjelle, JT. Nanobacteria: controversial pathogens in nephrolithiasis and polycystic kidney disease. Curr Opin Nephrol Hypertens 2001:445-451. 2. Ciftcioglu N, Bjorklund M, Kuorikoski K, et al. Nanobacteria: an infectious cause for kidney stone formation. Kidney Int 1999; 56:1893-1898. 3. Garcia Cuerpo E, Kajander EO, Ciftcioglu N, et al. Nanobacteria. Un modelo de neo-litogenesis experimental. Arch. Esp. Urol 2000; 53:291-303. 4. Sommer, AP, Kajander, EO. Nanobacteria-induced kidney stone formation: novel paradigm based on the FERMIC model. Crystal Growth & Design 2002, in press. 5. Meade, TW. Cardiovascular disease - linking pathology and epidemiology. Int J Epidemiol 2001, 30:1179-1183. 6. Akerman KK, Kuikka JT, Ciftcioglu N, et al. Radiolabeling and in vivo distribution of nanobacteria in rabbit. Proc SPIE Int Soc Opt Eng 1997;3111:436-442. 7. Hjelle JT, Miller-Hjelle MA, Poxton IR, et al. Endotoxin and nanobacteria in polycystic kidney disease. Kidney Int 2000; 57:2360-2374. 8. Ciftcioglu, N, Miller-Hjelle, MA, Hjelle, JT, Kajander, EO. Inhibition of nanobacteria by antimicrobial drugs as measured by a modified microdilution method. Antimicrob Agents Chemother 2002, 46:2077-2086. 9. Kajander EO, Ciftcioglu N. Nanobacteria: An alternative mechanism for pathogenic intra- and extracellular calcification and stone formation. Proc Natl Acad Sci USA 1998; 95:8274-8279. 10. Cisar JO, Xu D-Q, Thompson J, Swaim W, Hu L, Kopecko DJ. An alternative explanation of nanobacteria-induced biomineralization. Proc Natl Acad Sci USA 2000; 97:11511-11515. 11. Rasmussen, TE, Kirkland, BL, Chalesworth, J et al. Electron microscopic and immunological evidence of nanobacterial-like structures in calcified carotid arteries, aortic aneurysms, and cardiac valves. JACC 2002, 39 (Suppl 1):206A. 12. Maniscalco, BS. Letter to the editor. Circulation 2002, in press. 13. Sommer, AP, Hassinen, HI, Kajander, EO. Light-induced replication of nanobacteria: a preliminary report. J Clin Laser Med Surg 2002, 20:241-244. > To Townsend Letter Response to November 2002 issue and Elmer > Cranton's letter 'Alleged Nanobacteria Do Not Cause Calcification of [quoted text clipped - 4 lines] > Biochemistry, University of Kuopio, Kuopio, Finland Email > olavi.kajander@uku.fi Note: article is written by one of the world's foremost proponents of the nanobacteria hypothesis. > Dear Editor; Jonathan Collin, MD: The cause of pathological > calcification, including atherosclerosis, dental pulp stones and [quoted text clipped - 3 lines] > increased throughout the whole 20th century, and now occurs in up to > 15% of the population. So we must believe that these "infections" increased dramatically during the same period that humanity discovered antibiotics? Seems illogical. Far more sensible would be to blame diet and lifestyle changes. > 1 Nanobacteria have been linked to human kidney stone and preliminary > studies showed Koch's postulates to be fulfilled.1, 2, 3, 4 As the excellent study published by National Academy of Sciences points out, fulfilling Koch's postulates does not necessarily mean we are dealing with a living organism. http://www.pnas.org/cgi/content/full/97/21/11511 Prions, which are not alive, also self-propagate. > Calcified hard plaques is now a common form of coronary heart disease > but were surprisingly a clinical rarity 100 years ago5. Which strongly suggest we are not dealing with novel infections. "Nanobacteria", or as I called them "self-propagating macromolecules" or SPMs, are even found on the surface of meteorites. They are not new by any means. See "Nanobacteria-like calcite single crystals at the surface of the Tataouine meteorite." Benzerara K et al. Proc Natl Acad Sci U S A. 2003 Jun. 24;100(13):7438-42. Epub 2003 Jun 5. > Calcified plaques can lead to acute myocardial infarct, because > apatite (calcium phosphate mineral) exposed to blood activates a [quoted text clipped - 15 lines] > release endotoxin7 and thereby stimulate and mediate chronic local > inflammatory reactions in atherosclerotic plaque. The study cited in fact concludes, in the abstract, that "CONCLUSION: Nanobacteria or its antigens were present in PKD kidney, liver, and urine. The identification of candidate microbial pathogens is the first step in ascertaining their contribution, if any, to human disease." which is a long way from the claim made by Kajander. > 3. Nanobacteria have been shown to infect humans and infections last > possibly life-long. So do prions "infect" humans, for life. But they are not bacteria, simply misfolded proteins. > 4. Almost 100% of atherosclerotic patients in USA and in Finland have > antinanobacteria antibodies in their serum, whereas in healthy blood > donors antinanobacteria antibodies are present in about 15% (see web > pages of Nanobacteria Minisymposium held at Kuopio last year). Proving that SPMs (aka nanobacteria) are associated in some way with disease is one thing, but saying that they are bacteria because their inflammatory sequelae can be reversed with strongly antiinflammatory and calcium-binding antibiotics like doxy is quite another. > 5. Nanobacteria have been shown to be susceptible to several > antibiotics and sequestering agents (8). Yes, agents like bisphosphonates (a family of drugs used to prevent and treat osteoporosis) and other agents not used to kill bacteria, but which change the chemistry surrounding the SPMs so that they can no longer self-propagate. Many antibiotics also change this chemistry, specifically DOXYCYCLINE, which is famous for BINDING WITH CALCIUM thus staining teeth, and is contraindicated in pregnant women due to the formation of nonabsorbable complexes with breast-milk calcium, enamel hypoplasia, and inhibition of linear skeletal growth. The whole claim that "nanobacteria" are in fact bacteria is a very shaky hypothesis. > Since nanobacteria form calcific biofilm it is clear that their > eradication needs combination chemotherapy directed at the biofilm, [quoted text clipped - 7 lines] > that aim at verifying whether nanobacteria cause atherosclerosis and > how to cure this infectious process. Very unscientific personal attack! And where's the proof for that claim? > These studies use the same principles that vindicated Helicobacter > pylori in peptic ulcer disease: curative therapy was the evidence for > the causative role of the agent. That approach lead into a revolution > in the therapy of Helicobacter pylori-mediated diseases. This was a > good thing. Oh god, the H. pylori thing again! This has become the reason behind so much bad science. Barry Marshall, you have a lot to answer for! > Nanobacteria form calcific biofilms and replicate under blood/serum > conditions, as was first published by Kajander and Ciftctioglu9, a [quoted text clipped - 24 lines] > bacteria, which makes phylogenetic PCR analysis using universal > primers practically impossible and worthless. So PCR does not support the nanobacteria hypothesis, but instead supports the SPM (self-propagating macromolecule) hypothesis. > PCR analysis assumes that the ribosomal gene has 'universial' > sequences detectable by the primers, but this is not true for [quoted text clipped - 14 lines] > alternative explanation nanobacteria to be replicating apatite > mineral particles. Cisar is probably correct. > Naming an agent as particles or nanobacteria, living or non-living > but self-replicating, has relatively little meaning with respect to > causing disease, e.g., the atherosclerotic process. Whoa! Now he's conceding these may not be bacteria after all! > The fundamental importance is that these self-replicating special > particles ^^^ self-propagating macromolecules? .. hehe > that we call Nanobacterium sanguineum are found in blood and in > atheroslerotic plaques. The rest of the letter is simply a plug for NanobacTX treatment. I wonder if Kajander is a shareholder of the company? Mr Nanobiotech, care to tell us? |
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