[extropy-chat] Hello Fellow Extropians, Just found out about this addition to diet... heard of this?

Robert Bradbury robert.bradbury at gmail.com
Mon Mar 13 19:46:31 UTC 2006

On 3/12/06, Mark Lyons <mark at mark-lyons.com> wrote about nanobacteria and
Nanobacteria Life Sciences (http://www.nanobac.com):

Since we are all into the latest good health discoveries, [snip]

Yes particularly those which do not have the faint odor of "snake oil" [1].

The major problem is that there are a small number of people who have great
> LDL/HDL levels but still have calcification (hardening) of the arteries.
> The medical community simply explains this away by saying this is due to
> genetic factors, but they have yet to produce any genetic assay that ties
> any specific gene to this anomaly!

There are thousands of diseases which have been described but which
currently still lack information regarding the specific gene(s) which cause
them.  See the OMIM database [2,3].  If you do not have a specific gene
which causes a specific biophysical condition you cannot produce a "genetic
assay" for it.  Connecting specific biochemical conditions to specific
genetic mutations is like looking for a needle in a haystack and can be a
very difficult, time consuming and expensive process.  The two diseases of
accelerated aging, Werner's Syndrome [4] and Hutchinson-Guilford Syndrome
(Progeria) [5] are two classic examples of diseases for which the
researchers (and the people having those diseases) *really* wanted to know
the genetic basis (for decades).  It wasn't however until 1996 and 2003
respectively that the phenotype-genotype linkages were pinned down.  This is
still a complex and ongoing process for common conditions which may involve
dozens of underlying genes such as diabetes or asthma and of course cancer
and heart disease.

Here's where it gets interesting.  These folks have discovered a new form of
> life that has characteristics of both bacteria and viruses, but lies
> somewhere in between the two: http://www.nanobac.com/

Directly from their web site...
"Nanobacteria are Calcifying Nano-Particles (CNPs), which are known for
their ability to create and propagate calcium phosphate coated vesicles."

If they studying "calcifying nanoparticles" then why not name the company
"CalcNanoPart" or something similar?  We have a *very* good working
understanding of "bacteria" which includes such features as the fact that
they are complex nanosystems based upon a DNA information carrier which
require a minimum of ~250 genes/proteins for self-replication.  Their
minimal size is 250+/-50 nm [6].  If one uses the standard definitions of
"nano-" as meaning 10^-9, or the extended NSF definition of anything less
than 100nm, when combined with the word "bacteria" yielding 'nanobacteria"
one has a term which comes close to being an oxymoron. One cannot physically
have a nano-anything where by definition to be "anything" requires a
complete "anything".  At least for me, considering the word "nanobacteria"
and a company based around it, such terms as "disingenuous" or perhaps
"specious" come to mind.

If you investigate the history of nanobacteria [briefly in 7] one finds it
is controversial to say the least.  At first they were treated with great
interest, but when the curtain started to be pulled back [8, 6 and refs
therein] it became clear that there were significant problems.  Indeed [8],
points out the problems with Kajander's initial work identifying nucleic
acids in the samples and finds the probable cause of previous observations
to be "nonliving macromolecules and transferred on 'subculture' by
self-propagating microcrystalline apatite".  So concepts involving "life"
(and the term "bacteria") are not required.  I.e. we are not dealing with a
pathogen (bacteria or virus) in calcification, at least in kidney stones,
but instead simple biophysical processes.

Now, returning to "Nanobac Life Sciences", we discover that their testing
services are from "Nanobac Oy Clinical Laboratory, under the direction of
Olavi Kajander, M.D., Ph.D. The laboratory is fully accredited by the Social
Health Ministry of Finland."  Dr. Kajander played a key role in attempting
to link nanobacteria and human disease [9] though he is not the source of
the term [10].

Looking at the string of Nanobac press releases (which span several years)
one finds it is an OTC BB stock (Symbol: NNBP) [11] which if I'm reading the
5 year chart correctly would seem to suggest the company could serve as a
front and center player on a "Penny Stocks -- How to lose your shirt"
poster.  The final icing on the cake appears to be their product list which
includes (1) a book "The Calcium Bomb: The Nanobacteria Link to Heart
Disease" (published in 2004, long after [8] pretty much 'dissed the
"bacteria" idea); (2) An oral supplement (ingredients undisclosed); and (3)
an EDTA suppository.

EDTA [12] is a chelating agent designed to bind to and remove metals from
solutions (including calcium) -- though EGTA [13] is a better calcium
chelating agent and so one has to wonder why they aren't using that
instead?  Chelation therapy, using EDTA, is a controversial medical therapy
at this time, in part because it is non-specific -- i.e. it will tend to
bind and remove metals important in many biological processes.  I suspect
there are diseases involving excessive metal accumulation, such as
Hemochromatosis [14] (excess iron) and Wilson Disease [15] (excess copper)
where chelation therapy could be useful.  [In both of these cases there are
other therapies which are preferred because they can target specific metal
excesses.]  It may be the case that Nanobac is attempting to remove excess
calcium which may contribute to the microcrystalline apatite [16] using EDTA
and perhaps uses oral (mineral) supplements to restore any Mg & Cu (or other
elements) that may be removed by the EDTA.  However I would consider this a
questionable strategy for the general population.

Further PubMed investigation shows that a lot of research has been done on
hydroxyapatite, calcium phosphate, and carboxy apatite.  This leads such
disease terms as "chondrocalcinosis" and "hypocalciuric hypercalcemia" which
turn out to be diseases involving improper calcium metabolism.  These are
associated with the loci CCAL1, #CCAL2 and #HHC1, HHC2, HHC3 [17-21].  Those
two loci with #'s have been determined to be specific gene mutations.  So it
simply isn't true that we don't at least some of the causes of calcium
metabolic disorders.  Whether we know all of the specific genes involved in
such metabolic disorders, particularly those that might contribute to
calcification of the arteries I do not know.  Even if we did know them all,
I am sure that at this time testing for them at the clinical level would be
prohibitively expensive.

They believe these organisms explain the mystery of the underling cause of
> calcification (Hardening) of the arteries.  Their treatment consists of
> destroying the organism's calcium walls, and then killing it with
> antibiotics.

This is silly.  If there is no "organism" one cannot destroy it with
antiboiotics, particularly if it is a "new" form of "life" and common
antibiotics that are extremely specific towards inhibiting *known*
bacterial  processes such as bacterial cell wall formation or bacterial
ribosome translation.

If one has a genetic defect in the regulation of hydroxyapatite, or poorly
evolved genetic system dictating where and/or how much hydroxyapatite is
deposited, one gets a simplified atherosclosis  paradigm [22] as part of the
problem of aging along the lines of:

   1. Circulating cholesterol becomes oxidized.
   2. Macrophages go after OxChol and form foam cells in arterial
   3. The foam cells alter the biochemical environment contributing to
   calcification (esp. in those with genetic susceptibilities).
   4. Peridontal disease (or even aggressive brushing of teeth) allows
   bacteria normally attached to the hydroxyapatite in the teeth to enter the
   bloodstream and become attached to hydroxyapatite accumulating in the
   5. The macrophages get even more upset over the new invading bacteria
   than they did over the oxidized cholesterol and contribute to greater
   inflammation in the body (with a host of side effects a.k.a.
   collateral damage).
   6. The process continues (accumulating foam cells, hydroxyapatite,
   bacteria, inflammation, etc.) until such time as the arteries become
   completely blocked or burst (heart attacks & strokes).

The EDTA chelation therapy is probably of little help in reducing already
calcified arteries with accumulated hydroxyapatite, at best it may slow down
the rate of accumulation while creating significant risks of disrupting
other biochemical processes.  The antibiotic therapy isn't impacting the so
called "nanobacteria" but may be diminishing the oral bacterial load
contributing to peridontal disease and subsequent blood stream
dissemination.  Antibiotics may as well minimize subsequent replication of
the bacteria in the arteries reducing inflammation and/or calcification.  Of
course long term antibiotic treatment will likely produce antibiotic
resistant bacteria which simply ignore such therapies.

If the above model is reasonable it leads to some interesting questions
regarding lifespan increases during the 20th century because there are are
at least 3 different factors providing different contributions to the
primary causes of death in different population groups at different periods
of time:

   1. dental hygeine;
   2. antibiotic consumption;
   3. calcium consumption (esp. from milk).

The net of this is that we should all not run off and start using chelators
to decrease our calcium levels or antibiotics to reduce bacterial load
because there are nontrivial downsides to such approaches.  The type of
therapy that Nanobac is promoting (for those who still believe nanobacteria
are "real") should only be considered by people after ultrasound diagnosis
(or other tests) indicate that calcification is indeed taking place and in
those people whose family history or personal symptoms place them at greater
risk from heart attack or stroke compared with osteoporosis.

For those who really do want to "believe" in ultra-small bacteria (< 200nm
in size), I would offer [23].


1. Though to be fair, given the recent health benefits associated with the
EPA & DHA found in fish oil and the fact that snakes must remain reasonably
active at low temperatures (similar to the cold water fish species with high
levels of EPA & DHA), one might suspect that a reexamination of the health
benefits of "snake oil" derived from specific species could be of interest.
2. http://www.ncbi.nlm.nih.gov/Omim/omimfaq.html
3. http://www.ncbi.nlm.nih.gov/Omim/mimstats.html
4. Werner's Syndrome:
5. HGS/Progeria: http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=176670
6. Size Limits of Very Small Microorganisms: Proceedings of a Workshop
    National Academies Press
discusses the gene/size limits
7. Discussed in "Nanobacteria: not a life-form?"
8. Cisar, J. O. et al, PNAS (Oct 2000):
9. Kajander, E. O. et al, PNAS (Jul 1998):
10. "Nannobacteria" appears in Sillitoe, Folk & Saric in Science in May

11. http://www.otcbb.com/
12. http://en.wikipedia.org/wiki/Calcium_disodium_EDTA
13. http://en.wikipedia.org/wiki/EGTA
14. Hemochromatosis
15. Wilson Disease:
16. http://en.wikipedia.org/wiki/Apatite - apatite in the body is typically
Ca <http://en.wikipedia.org/wiki/Calcium>5(PO4<http://en.wikipedia.org/wiki/Phosphate>
17. CCAL1: http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=600668
18. CCAL2: http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=118600;
      ANKH: http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=605145
19. HHC1: http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=145980;
      CASR: http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=601199
20. HHC2: http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=145981
21: HHC3: http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=600740
22. http://en.wikipedia.org/wiki/Atherosclerosis
23. There was one portion of the Size Limits document [6] which would have
allowed the information density (genome packing) limits to be transcended
allowing "nanobacteria" collectives to exist.  That required that the
"bacteria" exist as multi-celled collectives where each individual cell only
contained as much DNA as was required to produce part of the collective
organism's proteome.  The cell colony/cluster would be required to export
(pass around) the DNA, RNA or proteins required for a fully functional
system.  This seemed highly improbable result of natural evolution although
one could imagine constructing such a system using "intelligent design".
(Your local car garage doesn't have to have a duplicate set of tools for
each mechanic.) If one steps very far back, one can kind of view species
which require sex to reproduce as being based on such a system because
certain essential sex-specific material (e.g. the SRY gene [22]) which is
required for complete species self-replication  is being carried around by a
specific subset of the genome copying agents.
24. http://en.wikipedia.org/wiki/SRY
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