Nanobacteria Do Exist and Actively Participate in the Calcification of Arterial Plaque
E. Olavi Kajander, MD
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 labeled 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
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.
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
Dr. Cranton is putting forward ungrounded claims on nanobacteria and on therapy trials aiming at eradicating them. The claims need short comments:
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.
Olavi Kajander, MD