Nanobacteria -- The New Thing In Heart Disease
Click HERE for Dr. Elmer Cranton's comments on Nanobacteria
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Source:
Chelation Therapy On Line Web Site
Contact_FirstName: Gary
Contact_LastName: Mezo
Contact_MiddleInitial:
Contact_Title: Dr./Pres/CEO
Contact_Organization: NanobacLabs
Contact_WorkPhone: Tollfree
1-877-676-2241
Contact_HomePhone:
Contact_FAX: Tollfree 1-866-Nanobac
Contact_Email:
gmezo@nanobaclabs.com
Contact_URL:
www.nanobaclabs.com
Dear Karl,
I have noted that you are using my copyrighted material on your website.
[Karl Note: Copyrighted material is subject to the "fair use" doctrine, covered here. My use of this material is fully covered by this doctrine.]
Please call me to discuss this.
This research is too important to be misconstrued in any way.
We have proof that we are indeed eradicating nanobacteria, the calcification they cause and the atherosclerotic plaque they cause: meaning that we are reversing heart disease.
[Karl Note: I continue to find, based on all my research and study, that heart disease is caused by free radical damage, and that the "plaque" being talked about so casually in the popular press is NOT a coating on the inside of an artery, but excessive calcium INSIDE individual cells. If "nanobacteria" can be shown to exist, and be alive, I would be further interested, but they would still have to fit into a "free radical theory of disease" that is well established, by Dr. Harmon, originally, and now accepted by many others, including me.]
Please do not distort or imply that free-radicals can cause nanobacteria....that inference is destructive.
You really must report only the facts....many read your website.
If they are led to believe that oral supplements can help nanobacterial infections in any way, they may resort to all kinds of supplements that will not help.
[Karl Note: This, of course, goes against 17+ years of fantastic success with my formula -- using various chelating agents to remove metals, thus reducing free radical activity, thus allowing cells to be revitalized, and blood circulation to improve. There may or may not be actual nanobacteria that exist, but their existence does not need to be a part of successful treatment of metal toxicity, free radical proliferation, and resultant cell damage.]
Please, we all have a moral imperative here. Heart Disease is largely resultant from a nanobacterial infection.
[Karl Note; I disagree. That is what the "fair use" doctrine of the copyright law is intended for.]
Nanobacteria are the toughest of all earthly pathogens....we have spent millions on our research and its just the beginning.
[Karl Note: To the man with a hammer, all the world looks like a nail! If I had spent millions on research into something, I might well be inclined to want to sell the idea, too. I have, myself, fallen for false information at times in the past. Fortunately, not having any great amount of money invested, but only pride, it has been easy for me to admit I was wrong.]
Supplements will help to boost our immune system if it is impaired, but FACT: ! no supplements will kill nanobacteria.
[Karl Note: I would never claim to be able to kill something that is not alive! See my article on the subject of the AIDS virus. Literally billions of dollars of supposed research money has been spent to figure out how to "kill" the AIDS virus when, in truth, the AIDS virus is not a living thing. Click here to read my full expose of this scandal in "medical research."
Nanobacteria seem to have some origin in interstellar rock dust -- or life on other planets -- or whatever mysterious origin you care to read about. Click here, or here to read articles about nanobacteria.]
Our bodies have absolutely NO defenses against nanobacteria.
[Karl Note: The real truth here is that our bodies have no defense against free radicals. We have lots of defense against REAL bacteria. Our immune system is well designed to handle living bacteria. Our immune system can do NOTHING against free radicals.]
They even kill our lymphocytes and NK cells. We make antibodies against the nanobacterial biofilm so that our bodies will rush to the area to kill nanobacteria, but when they arrive to the scene to kill....they cannot detect any nanobacterial presence (nanobacteria are too small).
[Karl Note: Here is the first internal inconsistency. The originator of this process claims that nanobacteria are alive! I dispute that. In this paragraph, above, he claims that antibodies rush to kill nanobacteria but can't find them -- they being too small to detect. Is that not an oxymoron! If they are too small to detect, how can the immune system recognize that some anti-bodies are needed?]
...it's like fighting against the invisible man.
Meanwhile, when our defense system arrives, the nanobacteria invade our lymphocytes and NK and kill them.
[Definitely, like those who spread the AIDS hoax, this man has given the attributes of LIFE to a nanobacteria -- saying that it "invades" the lymphocytes, etc. How can something which is NOT ALIVE do any invading. It is the same fruitless argument used about AIDS -- the claim that the AIDS virus invades a cell and causes damage. Something which is NOT alive does not invade anything.]
Please, I beg of you, if you want to display our pages....please do so without commentary unless we talk about it.
[Karl Note: I have made "fair comment" on this subject, and have published their complaint. I will be pleased to publish any continuing dialogue on this matter -- hoping that the truth will be the victor!]
This is too big to be distorted.
If you don't believe me, just wait until our prelim results of the cardiology study are published in April....it is huge. '
My mission is pure: educate the world about nanobacterial infections, R & D on nanobacterial infections, diagnosis & treatment of nanobacterial infections and reversal of the effects of pre-existing nanobacterial infections.
We are a Christian organization and conduct ourselves accordingly.
[Karl Note: Christianity has no lock on the truth, nor does the Bible on Science. Have there been no Christian criminals?]
We know what we are up against, and it is huge as well.
I really appreciate that you find our work important, but it is extremely important not to color or distort the findings.
I look forward to your phone call.....
God Bless,
Gary
Dear Gary,
My mind is still open to your thesis, but I view "new science" as having to meet the obligation of having links to traditional science. I am far beyond the usual cardiologist in my explanation of heart disease, but I am not so far beyond that I cannot link my concept with well established science, including the activity of free radicals and the results of having heavy metals in the body.
When some "new science" is so far beyond the current scene, it is almost by definition, not capable of being proven or disproved.
It seems to me that you are denying the role that free radicals and metals play in the progress of heart disease.
Whether a nanobacteria is "alive" within the traditional definition of "life" is not demonstrated for me, at least.
I'm ready to review other materials, but like any layman looking for hope from current killers, including heart disease, I am not a biochemist -- I may be very intelligent, but I can only apply simple logic and a demand for definitions of terms == definitions that come out of traditional medical dictionaries.
I would be pleased to have your comments on my remarks, here, and to publish them.
Karl Loren
February
25, 2002
Dear Karl,
1) There are Scientific researchers all over the world studying nanobacterial infections and disease....there is no question that they have RNA and DNA and they are the smallest self-replicating organisms.
Even the well-respected Mayo Clinic Rochester is conducting in-depth research as to how (not if) nanobacteria cause atherosclerosis, kidney stones and Polycystic Kidney Disease.
They are involved in a plethora of degenerative human diseases. You can read more at www.nanobaclabs.com.
2) Free-radical processes are indeed problematic for all humans. But free-radical disorders have NOTHING to do with nanobacterial infections.
Karl, you're doing a great job of educating people about free-radical disease and how your product helps. Please don't be so myopic about nanobacterial infections, they have nothing to do with free-radical disease.
By the way, our bodies develop antibodies to the nanobacterial BIOFILM that they secrete, the BIOFILM is the endotoxin that causes our bodies to develop antibodies.
God Bless,
Gary
Dear Gary,
The Mayo Clinic would be a very negative endorsement in my book, but that would not be conclusive.
My interest in nanobacteria started when I became interested in EDTA suppositories. I have a page on that subject at: http://www.chelationtherapyonline.com/articles/p20.htm .
On that page I wrote:
It is interesting to note that the big promotion is on EDTA suppositories, but all the descriptions of their use seem to make reference, also, to an antibiotic called tetracycline, used, it is claimed, to kill "nanobacteria" that have been found associated with heart disease. Source:
To whatever extent people are getting good results with heart disease, using EDTA suppositories, the claim seems confused by the additional statement that nanobacteria are also involved.
Gary, do I understand that YOUR success rate with killing nanobacteria and "handling" heart disease never involves, also, the use of EDTA, or of EDTA suppositories?
I'd like to know.
Cordially,
Karl
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Alleged Nanobacteria do not Cause by Elmer M. Cranton, M.D. Copyright © 2002 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.)
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