Nanobacteria "a deceptive marketing scheme"?

[webslave]

In this May 2005 article, Harvard-educated Dr Cranton, a chelation expert, says:

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.

http://drcranton.com/nanobacteria.htm

[webslave]

Interestingly, the National Academy of Sciences of the United States of America does not seem to support nanobacteria as living organisms. The Academy carries one main article on the subject, which concludes that:

...we provide evidence that biomineralization previously attributed to nanobacteria may be initiated by nonliving macromolecules and transferred on "subculture" by self-propagating microcrystalline apatite.

http://www.pnas.org/cgi/content/full/97/21/11511

[Dj Smitty]

so this kind of thinking would only give more substance to people who still believe that this disease/condition is caused by phantom bacteria? I'm surprised not many doctors talk about some kind of virus being responsible as well.

[alprost]

When I was at the Stanford clinic, one of my fellow patients had been advised to try treatment for nanobacteria as his treating Uro could find no other cause for his symptoms.

When examined by the PT he had multiple trigger points which recreated his symptoms.

Nanobacteria are one in a long list of blind alleys which attempt to explain chronic prostatitis / chronic pelvic pain syndrome IMHO.

[webslave]

A supporter of the NanobacTx product, perhaps an employee, posted this anti-Dr Cranton letter on Usenet:

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 [email protected]

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 [email protected]




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 which the response came:

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 [email protected]

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! The discovery of H. pylori has become
the motivation for 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?

[webslave]

I wonder if Kajander is a shareholder of the company? Mr Nanobiotech, care to tell us?

I can answer that question myself. From the Nanobaclabs website (Nanobac Life Sciences):

Dr. E. Olavi Kajander is the discoverer of Nanobacteria and is the Director of Scientific Research at the NanobacLabs Research Institute (Tampa, Florida) and Nanobac OY (Kuopio, Finland). NanobacLabs Research Institute and Nanobac OY are subsidiaries of Nanobac Pharmaceuticals, Inc. Dr. Kajander is the developer of Nanobac's NanobacTEST-S® blood test for Nanobacteria

[james-d]

Does that mean we discredit Dr. Shoskes too?

Also a supporter with some type of interest in the product?

I disagree with this stance - and while I don't know if there is any connection or not - will remain open minded on the topic until all evidence is in.

Besides - I have yet to see an article publishe in the Journal of Urology to contradict the one by Shoskes on its effectivness (granted - it was a very small sample size and not the most scientific study ever).

But I am not going to question him - his motives - or his treatment plans - his contributions to the cause of our suffering have been too great.

Thats my opinion - I am I sure I will suffer the slings and arrows for it with the replies......

[webslave]

Dr Shoskes found that by helping to eliminate prostatic stones with EDTA suppositories, NanobacTX and doxy he was able to alleviate symptoms in a small minority of carefully chosen men with lower urinary tract symptoms. I have no argument with that finding.

But I do think the whole theory of "infection" with stone-generating bacteria is problematic.

[dshoskes]

It WAS a small study but the patients were not "carefully chosen" (they were patients I saw who had prostatic stones with their chronic prostatitis / chronic pelvic pain syndrome and had failed every other therapy I had to offer) and symptoms were allieviated in the majority, not the minority of the patients.

I really don't understand why the debate over whether these entitities are a novel form of bacteria or a type of replicating particle is being played out so strongly on chronic prostatitis / chronic pelvic pain syndrome discussion boards. Who cares? If this particular therapy is useful for suffering patients does it matter? Currently, this therapy is on equal published clinical scientific footing with physical therapy: useful in an uncontrolled open label study and awaiting a placebo/sham contolled trial to confirm its true effectiveness. Other treatments have been equally efficacious in open label studies and then failed the placebo/sham test in chronic prostatitis / chronic pelvic pain syndrome (eg TUNA, Vioxx, Elmiron, Cipro, levaquin), or passed and been shown effective after placebo/sham control (eg alpha blockers, quercetin). Ultimately the data will prevail.

Dr Shoskes found that by helping to eliminate prostatic stones with EDTA suppositories, NanobacTX and doxy he was able to alleviate symptoms in a small minority of carefully chosen men with lower urinary tract symptoms. I have no argument with that finding.

But I do think the whole theory of "infection" with stone-generating bacteria is problematic.

PS. It was tetracycline, not doxy.

[webslave]

It WAS a small study but the patients were not "carefully chosen" (they were patients I saw who had prostatic stones with their chronic prostatitis / chronic pelvic pain syndrome and had failed every other therapy I had to offer) and symptoms were alleviated in the majority, not the minority of the patients.

Clarification: the fact that the cohort had prostatic stones and had failed other therapy makes them, in my view, a distinct and therefore carefully chosen group. The "minority" I referred to should have read "minority of all pelvic pain patients".

I really don't understand why the debate over whether these entities are a novel form of bacteria or a type of replicating particle is being played out so strongly on chronic prostatitis / chronic pelvic pain syndrome discussion boards. Who cares? If this particular therapy is useful for suffering patients does it matter? Currently, this therapy is on equal published clinical scientific footing with physical therapy: useful in an uncontrolled open label study and awaiting a placebo/sham controlled trial to confirm its true effectiveness. Other treatments have been equally efficacious in open label studies and then failed the placebo/sham test in chronic prostatitis / chronic pelvic pain syndrome (eg TUNA, Vioxx, Elmiron, Cipro, levaquin), or passed and been shown effective after placebo/sham control (eg alpha blockers, quercetin). Ultimately the data will prevail.

The debate is not really about whether a minority of all chronic prostatitis / chronic pelvic pain syndrome patients will be helped by dissolving their stones, but about the packaging and marketing of the solution by the proponents of the therapy. I suspect the whole scientific world would be more friendly to this hypothesis if the idea of these nanoparticles as consisting of living, infecting bacteria had been left as an imponderable and purely theoretical, perhaps one of many alternatives, and the simple self-replicating nature of the particles had been cited as reason enough for treatment with chelation and various other chemicals. After all, calcium deposits in the body are NOT always benign and can cause a lot of pain and inflammation (ask me, I have calcific tendinitis in my shoulders - Ouch!). Moreover, as a patient group we have a long and bitter history of being treated fruitlessly for non-existent "infections", and we're sensitized to that terminology.

PS. It was tetracycline, not doxy.

Same family of antibiotics, not much difference between them, and doxy was used in other studies with nano"bacteria".

[webslave]

Update
http://www.urologytimes.com/urologytime ... ?id=372143

[The Wayfarer]

Sorry, I'm late to this debate but I have a question. In another thread Dr. Shoskes wrote:

"If you want to try the therapy, you need a prescription for tetracycline 500 mg once a day from your doctor. The other 2 components can be bought directly over the counter from Nanobac Labs. A reasonable first try should last 3 months."

I went to the Nanobac web site and couldn't find a links to purchase anything. Can someone post a link? I was also under the impression that EDTA was a medication or chelation therapy and not OTC. No? From what I read this treatment is not on the market yet.

Help would be appreciated. Just interested.

Mike

[gifford]

Unless I missed something, the update article seems to support the treatment to dissolve stones. Isn't it worth a 3 month try for those who have prostate calcifications/stones and other treatment has not worked? Certainly people have tried all sorts of things on this site. In my case, I have a calcification in my prostate. Pressing on my prostate intensifies my discomfort and testicle pain. If this treatment is not effective, what IS done to dissolve or remove prostate stones? My uro seems reluctant do do anything.
gifford