Re: Nanobacteria Alive per NASA, Mayo and many others

nanobiotech reviews wrote:
> To Townsend Letter Response to November 2002 issue and Elmer
> 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, PhD Department of
> Biochemistry, University of Kuopio, Kuopio, Finland Email
> olavi.kajander@xxxxxx

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
> 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.

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
> 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.

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,
> 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.

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
> 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.

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
> 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.

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?
.

Relevant Pages

  • Re: Nanobacteria: Kajanders Published Response to the Cranton Idiocy
    ... Cranton's letter 'Alleged Nanobacteria Do Not Cause Calcification of Arterial Plaque' ... Active nidus means a center of calcification that can mediate calcium-phosphate mineral formation under non-saturating calcium and phosphate concentrations. ... 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. ...
    (sci.med.prostate.prostatitis)
  • Re: Nanobacteria Theory disproven
    ... > To Townsend Letter Response to November 2002 issue and Elmer> Cranton's letter 'Alleged Nanobacteria Do Not Cause Calcification of> Arterial Plaque' ... > under non-saturating calcium and phosphate concentrations. ... but saying that they are bacteria because their ...
    (sci.med.prostate.prostatitis)
  • Re: Nanobacteria are "non-living macromolecules"
    ... > To Townsend Letter Response to November 2002 issue and Elmer> Cranton's letter 'Alleged Nanobacteria Do Not Cause Calcification of> Arterial Plaque' ... > under non-saturating calcium and phosphate concentrations. ... but saying that they are bacteria because their ...
    (sci.med.prostate.prostatitis)
  • Nanobacteria Theory disproven
    ... Calcification of Arterial Plaque ... 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. ... Chelating agents such as EDTA, citrate, and tetracycline can alter the surface properties of nonliving calcific and crystalline nucleators—both halting calcific propagation and blocking immunologic reactivity to previously reactive antibodies. ...
    (sci.med.prostate.prostatitis)
  • Re: Nanobacteria Theory disproven
    ... 'Alleged Nanobacteria Do Not Cause Calcification of Arterial ... Calcified plaques can lead to acute myocardial ... atherosclerosis, heart valve calcification and kidney stone formation. ...
    (sci.med.prostate.prostatitis)