by
Douglas Mulhall
Extracted from Nexus
Magazine
Volume 12, Number 5
(August - September
2005)
from
NexusMagazine Website
Editor’s Note:
This article is based on material in the book
The Calcium Bomb:
The Nanobacteria Link to Heart Disease & Cancer, by
Douglas Mulhall and Katja Hansen (The Writers’ Collective, 2005), which was selected as a Finalist for the
2004 Book of the Year Award for Health by Foreword Magazine.
Nanoparticles are implicated in the harmful calcification
that’s common to
many illnesses.
A simple treatment is now reversing the symptoms, especially in heart
disease,
so why aren’t the health authorities telling patients and doctors about it? |
Millions of seriously ill patients are unaware that heart disease is being
measurably reversed with an approach pioneered by researchers at the
National Aeronautics and Space Administration (NASA) and in Finland, aided
by Mayo Clinic and Washington Hospital Center findings. This approach is now
prescribed by hundreds of doctors for thousands of patients. A similar
approach has been developed with prostate disease at the renowned Cleveland
Clinic in Florida. According to doctors, both approaches are practical
options for those whose other medicines and surgery have failed. So why
aren’t other desperately ill patients whose treatments don’t work being told
about it?
In July 2004, the medical journal Pathophysiology published a peer-reviewed
research paper with the innocuous title:
"Calcification in coronary artery
disease can be reversed by EDTA–tetracycline long-term chemotherapy".1
In
plain terms, it meant that hardening of the arteries was being reversed. Not
only were rock-hard calcium deposits being reduced, but chest pains were
being resolved in most patients and bad cholesterol levels were being cut
beyond what other medicines had achieved. The findings were important for
patients whose other drugs and surgery weren’t working, i.e., the "cardiac
cripples", whose numbers are in the millions and whose doctors have told
them there is nothing more to be done. They were the ones who responded most
favorably to the new approach.
Then, in February 2005, a paper published in the prestigious Journal of
Urology by researchers from the Cleveland Clinic, one of the leading urology
hospitals in America, reported "significant improvement" in chronic prostatitis—a growing problem for millions of men—again, where other
approaches had failed.2
The studies, although otherwise separate, had a compelling link. They used a
cocktail of well-known, inexpensive medicines that have been around for half
a century but were never before used in this combination. Both reports urged
more studies to confirm their conclusions, and emphasized that not every
patient experienced a reversal; only a majority did. Nonetheless, the
results were encouraging. Chronic diseases that had befuddled modern
medicine were being reversed.
To put a human face on this, take the case reported by Dr Manjit Bajwa of
McLean, Virginia, who did not participate in the clinical studies but whose
experience with one patient paralleled study results. Dr Bajwa reported in a
testimonial of 5 May 2005:
"Two years ago I had a patient with severe coronary artery disease with a
75–85% blockage in left coronary and two other arteries. Open heart surgery
was recommended as stents could not be put in. The patient was told he would
probably die within two weeks if surgery was not performed.
"He declined surgery and instead chose
chelation. [Author’s note: chelation
in this case is an intravenous form of heavy metal removal.] After
twenty-five treatments of chelation, his angina worsened [author’s
emphasis]. With [his] heart calcium score of 2600, I started the
nanobacteria protocol. Within two to three weeks his angina abated. He was
able to return to all his normal activities and exercises in two months.
"Nanobacteria protocol helped this patient measurably, when other treatments
had failed. I am quite impressed with his results. With heart calcium scores
of 750 or more, nothing else seems to work."
Bajwa and her patient are far from alone. In Santa Monica, California,
general practitioner Dr Douglas Hopper said he recorded impressive results
with a diabetic patient when he used the treatment to help her recover from
congestive heart failure. Hopper then put his patient on the same treatment
used in the clinical study: a regimen of tetracycline, EDTA and
nutraceuticals,3 administered by the patient at home. Note that this was not
intravenous chelation, which has been broadly analyzed and critiqued, but,
instead, a mix of oral and suppository treatments.
In Toledo, Ohio, cardiologist Dr James C. Roberts, who pioneered early
patient treatment with this approach, has on his website case histories from
dozens of patients who have shown remarkable improvement. In Tampa, Florida,
cardiologist Dr Benedict Maniscalco, who supervised the clinical study [Pathophysiology
study, referenced previous page], reports that patients who stayed on the
treatment after the study was completed showed dramatic reductions in their
heart disease symptoms. There are many more examples.
Normally results such as these, when reinforced by clinical studies, however
preliminary, would be cause for loud celebration. If the findings had been
reported by a major pharmaceuticals company, they could have easily made the
front pages of medical news services because, until then, no one had
reported reversing the symptoms of such diseases to such an extent. More
encouraging still, because the medicines have been around for many years and
their side effects are minimal and well known, the new approach is already
available across the USA and used with thousands of patients. That leaves
thousands more doctors with millions more patients who might benefit right
now. On top of that, a blood test based on the new approach has been used to
identify heart disease early in patients who show no outward symptoms.
Why, then, has the response from government authorities, medical
associations and health experts been cavernous silence?
To understand this requires looking at a scourge that has been with us for
millennia, and which science has been at a loss to explain until now. It is
known as calcification.
CALCIFICATION
Calcification is a rock-hard mix of the most plentiful minerals in the body:
calcium and phosphorus. Normally this calcium phosphate mix is essential for
building bones and teeth. But as we age, and sometimes when we are still
young, some of it goes haywire, stiffening arteries, roughing up skin,
destroying teeth, blocking kidneys and salting cancers.
The arithmetic is frighteningly easy. Calcification doubles in the body
about every three or four years. We can have it as teenagers and not notice,
although it mysteriously accelerates in some athletes. Then as we age and
also live longer, it becomes so endemic that most people over seventy have
it.
For decades, calcification has been growing imperceptibly in tens of
millions of baby boomers. Politicians and pundits are among the high-profile
victims of this slow-motion explosion that is ripping apart healthcare with
skyrocketing treatment costs. In December 2004, doctors diagnosed US
President George W. Bush with one of the more commonly known forms: coronary
artery calcification.
Former President Clinton required emergency surgery
because doctors missed much of his calcification when they used older tests
to track it. Vice President Dick Cheney and many of his Senate colleagues
are calcified. At least three sitting US women governors have had it in
breast cancer as well. And they are not alone. Media types who cover
politics or poke fun at it haven’t escaped. Larry King and David Letterman
are both calcified, as are many ageing news anchors. A much younger CBS
Early Show co-host, Rene Syler, has it too.
As we learn more about it, calcification is competing to be the leading
medical disorder. Although it is nowhere on the "Leading Causes of Death"
list, it contributes to most diseases that kill us, including heart disease,
diabetes and cancer. The numbers are staggering. For the 60 million
Americans who have heart disease, most have calcification. Of the millions
of women who develop breast or ovarian cancer or who have breast implants,
calcification is a warning. Men with prostate disease often have it, as do
kidney-stone sufferers. Athletes with stress injuries like bone spurs and
tendonitis get it frequently.
Most of us don’t know the pervasiveness of calcification because it has a
different name in many diseases, and here are just a few:
Unsuspecting patients aren’t the only ones in the dark. Many doctors are
unaware of new studies that show calcification is toxic, causing acute
inflammation, rapid cell division and joint destruction. Oddly, these nasty
effects are well known to specialists who study calcification in arthritis,
but awareness of them hasn’t translated very well to the cardiovascular
community, with the result that calcification is still misperceived by many
as an innocent bystander instead of an inflammatory devil.
The double-think about calcification is illustrated by how it is treated in
breast cancer. When microcalcification is detected in the breast with
routine scans, it is a warning sign for cancer and the deposits are biopsied
for malignancies. This was the case, for example, with Connecticut Governor
Jody Rell in early 2005. Doctors found cancer in the calcium deposits in her
breast before scans detected a tumour. This let them surgically remove it
before it spread to her lymph nodes.
That typifies one perverse advantage of calcification: it helps doctors
pre-empt more serious disease. In some ways, it is a canary in the mine of
the body. And yet, if cancer is not found in calcium deposits, these are
often declared as "benign" and patients are told there is nothing to worry
about.
The same thing goes for heart disease. Coronary artery calcification is seen
as an excellent predictor of the illness. Tens of billions of dollars are
spent every year on scanning technology to identify the telltale thin white
lines that betray its presence. Yet most doctors see calcification in the
arteries as something that comes along later once the disease takes hold,
despite evidence that calcium phosphate crystals generate the same type of
inflammation that, according to cardiologists, plays a big role in heart
attacks.
Incredibly, with all the advanced detection techniques, there has been no
way to find calcium deposits where they get started in the billions of
capillaries in the human body—so, without being able to see the starting
point, doctors often conclude that what they don’t see isn’t there. But make
no mistake: calcification is there, and it is a medical disorder. It was
registered in 1990 as a disorder under the International Classification of
Diseases list of the World Health Organization and was adopted by WHO member
states as of 1994 (see
http://www.who.int/classifications/icd/en/).
When well established, calcification stares defiantly at radiologists every
day from X-rays as it multiplies incessantly. There has been no proof of
where it comes from, and there is no known way to prevent it or sustainably
get rid of it without removing it surgically. Due to its gestation period of
years before it triggers real trouble, it has just begun sucking the life
out of baby boomers and their healthcare budgets.
Among its more exotic effects, it threatens space exploration when it
disables astronauts with unexpected kidney calcification and it is a
budget-breaker for pro-sport-team owners who lose athletes to its ravages.
At the more mundane level, it complicates root canals and it disrupts the
lives of otherwise healthy young people when it strikes as kidney stones.
Worst of all, it infiltrates plaque in heart disease and stroke and it plugs
bypasses and stents used to fix our internal plumbing.
The US National Library of Medicine holds thousands of research documents
referencing calcification, and various medical journals cover it in depth.
GE Healthcare, Toshiba, Philips and Siemens sell thousands of machines for
detecting it.
TREATMENT A THREAT TO PHARMCO PROFITS
But with all this money being thrown at calcification, there has been
virtually no success at finding the cause. So when researchers such as those
at Mayo Clinic and NASA find something that seems to cause it, and clinical
studies show that a new approach seems to get rid of it, you’d think that
most of the medical establishment would be rapt with attention, right?
Wrong.
Only a few small studies have been co-financed by the National Institutes of
Health (NIH) to look into this, and neither has to do with the treatment.
The only thing the Food and Drug Administration (FDA) seems to have done is
to make rumblings about whether the treatment is legitimate, although the
active ingredients—tetracycline and EDTA—have been FDA approved for other
uses for decades. So far, no government agency has made public note of the
peer-reviewed studies that many physicians say are so promising.
According to doctors familiar with the approach, here are a few reasons why
the treatment has not been given the attention that it seems to merit...
• The most perturbing for patients: the
treatment is relatively inexpensive
and produces poor profits compared to other drugs. It is exponentially
cheaper than open heart surgery. Because it does not have to be taken for
life at full dose—as is the case with most other heart drugs—it does not
provide the steady cash flow that other medicines do. • Although the treatment is initially used alongside other medicines as a
precaution to make sure patients don’t switch prematurely and suffer
problems, evidence suggests that the new approach might replace more
profitable blood thinners and anti-inflammatories that are staples of the
pharmaceuticals industry. • And if the approach continues to reverse coronary artery disease, it will
cut down on expensive surgical procedures that are the financial mainstay of
hospitals.
That’s not to say surgeons don’t want to get rid of calcification. New
stents that go into arteries are specially coated with time-release drugs
that seem to ward off calcification. But that only happens where the stent
is located, not in the other 99.999 per cent of the arteries.
Also, the EDTA–tetracycline–nutraceutical combo that has demonstrated such
promise is not the only treatment shown to work. A group of drugs known as
bisphosphonates, used for example to treat osteoporosis, has been shown to
be effective in the lab against some calcification. But bisphosphonates can
have nasty side effects, especially with the type of regular application
that seems to be necessary to reverse heart disease in seriously ill
patients. Due to these risks, the only present approach that seems to be
safe and effective in reversing heart disease is the one that uses the EDTA–tetracycline–nutraceutical
mix.
Critics claim the reason why the treatment isn’t adopted more broadly has
nothing to do with money but instead with science. They say researchers
can’t show how the treatment works.
NANOBACTERIA DISCOVERED IN OUR BLOOD
It all comes down to a sub-microscopic blood particle known as a nanobacterium, discovered in 1988 by Finnish researcher
Dr Olavi Kajander at
Scripps Research Institute in California.
The particle has a special habit no other blood particle has been known to
possess: it forms a rock-hard calcium phosphate shell that is chemically
identical to the stuff found in hardening of the arteries, prostate disease,
kidney disease, periodontal disease and breast cancer. The problem is, the
particle is so small that it apparently can’t accommodate nucleic acid
strings that, according to commonly accepted wisdom, would let it replicate
on its own and be alive. So scientists are stumped over how it manages to
self-replicate.
For 15 years, microbiologist Dr Neva Ciftcioglu (pronounced "shift-show-lew")
has been peering with an electron microscope at this blood particle that
critics say doesn’t live. But according to NASA colleagues and Mayo Clinic
researchers, the question of whether it lives is less important than what it
does. Despite or perhaps due to its tiny size and genetic elusiveness, this
speck may be the Rosetta stone for a calcified language found in most
diseases on the Leading Causes of Death list.
Like her science, Ciftcioglu’s life is full of unusual turns. Being a woman
microbiologist from Turkey speaks volumes. Throw into that her once-fluent
Finnish, a position at NASA and professorships on both sides of the
Atlantic, and you’ve got a determined character struggling with a stubborn
scientific cryptogram.
Ciftcioglu’s work with nanobacteria began when her PhD scholarship took her
to the University of Kuopio in Finland, where alongside her once mentor,
biochemist Olavi Kajander, she developed the antibodies necessary to find
the particle in the human body. A decade later, her work caught the eye of
NASA chief scientist Dr David McKay and she ended up at the Johnson Space
Center in Houston, gathering science awards that testify to her success.
Now Ciftcioglu and long-time collaborator Kajander, who discovered
the nanoscopic artifact, stand at the eye of a growing storm. They and their
colleagues are garnering praise and scorn because they claim to have
evidence for why most of us are literally petrified by the time we die. More
profoundly, their work may influence how new life is found on Earth and
other planets.
SELF-REPLICATING NANOPARTICLES
An intense dispute has raged for years that connects how we look for
infection in the body with how we look for bio-kingdoms on Earth and
throughout the universe. Researchers have long sought terrestrial extremophiles that tell them what might survive on
Mars, while others doubt
the wisdom of looking for life on Mars at all. The mystery remains: what is
the most effective way to find novel organisms?
Until recently, every life-form was found to have a particular RNA sequence
that can be amplified using a technique known as Polymerase Chain Reaction (PCR).
Nucleic acid sub-sequences named 16S rRNA have been universally found in
life-forms. By making primers against these sub-sequences, scientists
amplify the DNA that codes for the 16S rRNAs. Resulting PCR products, when
sequenced, can characterize a life-form.
One high-powered group persuaded NASA with a "Don’t fix it if it ain’t
broke" line and lobbied successfully to use the same method employed for
years: get a piece of RNA and amplify it. The group—led by scientists such
as Dr Gary Ruvkun at the Department of Genetics in Massachusetts General
Hospital, Boston, and advised by luminaries such as Dr Norman Pace at the
University of Colorado—got money from NASA to build a "PCR machine" that
would automatically seek such clues in harsh environments such as those
found on Mars.
Other scientists known as astrobiologists say the PCR machine approach is a
waste of money because such amplification shows only part of the picture—not
what nature might have done on other planets or, for that matter, in extreme
Earthly environments.
However, their argument always suffered from lack of evidence—that is, until
2003 when scientists associated with the San Diego–based Diversa Corporation
and advised by Professor Karl Stetter, of the University of Regensburg,
Germany, published the genome of an extremophile known as Nanoarchaeum
equitans, which Stetter’s team had discovered in Icelandic volcanic vents.
N. equitans was special because it had the smallest known genome found so
far, but it also had another intriguing trait. With Nanoarchaeae, the
particular 16S rRNA sequence found in other life-forms wasn’t in the place
that it was expected to be and did not respond to conventional PCR tests.
The 16S rRNA sequence was different in areas addressed by the PCR primers
and did not amplify. Stetter noted that the so-called universal probes that
work with humans, animals, plants, eukaryotes, bacteria and archaeae did not
work in this organism.
How, then, was the discovery made if the organism couldn’t be sequenced in
that way? Stetter had found that the organism’s sequence where the
traditional "universal" primers are located was abnormal. This finding let
him use other means to sequence the gene. In reporting their discovery in
the Proceedings of the National Academy of Sciences,4 the Stetter team
observed that the information-processing systems and simplicity of
Nanoarchaeum’s metabolism suggests "an unanticipated world of organisms to
be discovered". In other words, it might be the tip of a nano-lifeberg.
Stetter’s finding gave ammunition to scientists such as Neva Ciftcioglu who
say they have found other extremophiles, including human nanobacteria, that
cannot have their nucleic acids detected with standard PCR amplification.
One of the differences between Stetter’s N. equitans and the
nanobacteria
found by Ciftcioglu and Kajander’s team is that Nanoarchaeae need another
organism to replicate, whereas at least some nanobacteria seem to replicate
by themselves. Another difference is that Nanoarchaeae are slightly wider:
400 nanometres compared to 100–250 for nanobacteria. The greater size allows
for what conventional wisdom says is the smallest allowable space for
life-replicating ribosomes.
Which leads to the question: how do nanobacteria copy themselves? Evidence
for self-replicating nanoparticles has been around for years in everything
from oil wells to heart disease, but failure to sequence them using regular
PCR led some to dismiss them as contamination or mistakes. However,
researchers have found characteristics that make the particles hard to
explain away. They replicate on their own, so are not viruses. They resist
high-level radiation, which suggests they are not bacteria. They respond
well to light, where non-living crystals don’t. So if they aren’t viruses,
regular bacteria or crystals, what are they?
Some supporters of standardized 16S rRNA tests are quick to discount
nanobacteria. That’s not surprising. If a novel nucleic sequence holds true
with other extremophiles as with N. equitans, then a machine that searches
for life using standard PCR tests might miss them and be obsolete. Conscious
of this, the PCR machine team has said that as part of their work, they plan
to "search for the boundaries" of the 16S sequences, but what exactly that
means and how they plan to overcome the problem hasn’t been set out yet.
Reputations, money and perhaps the foundations of life ride on the 16S rRNA
dispute. Resolving it may determine who gets money to find the next great
biological kingdom.
NANOBACTERIAL INFECTION
How relevant is the outcome for human welfare? In 2004, researchers reported
finding nanobacteria in everything from heart disease to cancer and kidney
stones. Medical researchers reported to the American Heart Association’s
Scientific Sessions 2004 that a test for nanobacteria is an accurate
predictor of heart disease risk. But the work that these researchers say may
already have saved lives has been ridiculed by critics who claim that such
nanobes don’t exist, which in turn has made funding for basic research hard
to get.
Who is right? One well-respected astrobiologist observer qualified the
struggle this way:
"Unless we declare [the nano-organism scientists]
incompetent, then the info they have gathered is rather compelling that
something interesting is going on."
That’s why a few intrepid investors have plopped US$7 million and counting
into a Tampa biotech start-up devoted exclusively to Ciftcioglu and
Kajander’s discoveries about the calcifying particle. For the big
pharmaceuticals companies that’s pocket change, but for these entrepreneurs
it’s a pocketful of faith that’s been keeping them on edge for years. And
it’s starting to show some results, as published research from NASA,
Mayo
and various universities indicates. Moreover, despite its relative financial
insignificance, this venture may end up wagging the dog due to a
long-overdue paradigm shift in, of all things, the space program.
After decades of resistance, NASA—provoked by successful upstart private
projects such as the X Prize, which led to the first private foray into
space—is now collaborating with fledgling companies, instead of just
corporate behemoths, on intractable problems: in this case, why perfectly
healthy astronauts come down with kidney and other calcifying disorders. The
result: in March 2005, NASA’s Johnson Space Center put the finishing touches
on a tightly secured lab aimed at decoding nanobacteria found at the core of
kidney stones. After some serious growing pains, the lab is finally
beginning to look into what Ciftcioglu and Kajander began examining so many
years ago: the genetic content of nanobacteria. Meanwhile, Ciftcioglu and
others have published results showing that nanobacteria multiply five times
faster in weightlessness than in Earth gravity,5
which may explain why calcification shows up so suddenly in space.
But while researchers argue over what this nanobacterium is and how it
multiplies, doctors are finding that, when they treat it with a medical
cocktail, their patients improve.
Nor is it unusual that doctors are succeeding before science figures out
why. Antibiotics were used successfully against bacteria long before
scientists deciphered DNA. Doctors stopped infecting patients by washing
their hands long before they were able to identify all the viruses and
bacteria that they inadvertently transported from patient to patient.
Most recently, a vaccine that prevents cervical cancer has been put on the
market. It apparently works by targeting the human papilloma virus. Problem
is, researchers can’t show exactly how the virus causes cancer; they can
only show that when it is stopped, the cancer doesn’t occur. But that hasn’t
prevented the drug from being patented and put on the market. The history of
medicine is full of such examples where patients improve with treatments
whose mechanisms aren’t fully understood at the start.
The idea that infection could be at the heart of chronic illness is
intriguing because it has been around for more than a century but only now
is regaining favour due to discoveries of, for example, a vaccine that
prevents cervical cancer (as mentioned above). The resulting debates over
infection in chronic disease have a novel twist because they are driven by
new diagnostic technologies that give researchers the molecular accuracy
required to confirm older theories about infection. On one hand, clinical
results suggest antibiotics alone do not prevent the rate of heart attacks
among coronary patients. On the other, discoveries that infection is
responsible for most stomach ulcers and some cancers support the long-held
idea that the same might be true in heart disease, if only science could
find the right infection and get rid of it.
Some say that nanobacteria may be one such infection. Yet scientists’
inability to fully explain the genetics of nanobacteria is being used by
high-ranking medical authorities as an excuse to ignore the pathogen and its
treatment. This is especially perplexing because scientists involved in the
discoveries work at some of the highest level institutions in America,
including NASA, Mayo Clinic, Cleveland Clinic, Washington Hospital Center
and many others, and are not only respected in their field but are also
award winners. Other centers of excellence internationally, such as
University Hospital in Vienna, have also isolated the pathogen and observed
it in diseases such as ovarian cancer.
For decades, scientists have shown that disease can be caused by
contaminants that are not "alive" and cannot replicate on their own.
Environmental toxins, many viruses and, most recently, particles known as
prions have all been shown as players in disease processes, although they
cannot self-replicate.
So it seems unusual that nanobacteria would be discounted just because no
one has yet shown how they multiply. Which takes us to the question of where
nanobacteria might come from.
NANOBACTERIA-CONTAMINATED VACCINES
When Dr Olavi Kajander discovered nanobacteria in 1988, he was not looking
for disease at all. He was looking for what was killing the cells that are
used to develop vaccines. Labs everywhere have a vexing and expensive
problem with these widely used cell cultures: they stop reproducing or die
after a few generations and have to be thrown out.
Kajander surmised that something invisible was killing them; and when he
incubated supposedly sterile samples for more than a month under special
conditions, he got a milky biofilm. That biofilm contained particles that he
later named nanobacteria, unaware at the time that some of their
characteristics made them quite distinct from bacteria.
The serum that Kajander used to grow the nanobacteria came from the blood of
cow foetuses. Serum from the UK especially was full of nanobacteria, but a
much later study also concluded they were present in some cow herds in the
eastern US. In other words, nanobacteria are in cows, and cow blood is used
to develop many vaccines. Kajander emphasizes that this should not stop
people from using vaccines, because the immediate risk from diseases that
the vaccines are intended to prevent is relatively higher than the
calcification risk in the short term. Nonetheless, the potentially explosive
implications of contaminated vaccines and cow by-products would be clear to
everyone at government agencies who has examined the issue.
In that context, a series of hotly disputed discussions went back and forth
between Kajander and Ciftcioglu and disease prevention agencies. And it
certainly wasn’t a secret because the Medical Letter on the CDC & FDA (10
June 2001) published an article entitled "Nanobacteria Are Present In
Vaccines; But Any Health Risks Remain Unknown", explaining that nanobacteria
had been discovered in some polio vaccines.
The minutes of a subsequent meeting of the FDA Center for Biologics
Evaluation and Research (CBER) advisory committee in November 2002 reveal an
extraordinary decision by the committee members: they elected not to
investigate the potential contamination. According to the minutes they based
their decision on a lone experiment, suggesting that what Kajander had found
was a contaminant often found in lab experiments and nothing new. In other
words, they maintained that Kajander had made a mistake.
But one of the glaring problems with the NIH-funded experiment performed
around late 1999 or early 2000, as shown in the published paper about the
results,6 is that it did not use a control sample that could have been
provided by Kajander. In other words, the experiment never examined the
particle that Kajander had discovered, but instead relied on growing the
particle independently without knowing if it was the same one Kajander was
referring to. Moreover, the experiment was never repeated after the
preliminary finding. On that very slim basis, according to the CBER
committee minutes, the whole issue of nanobacteria was dismissed as a
potential contamination issue for the time being. Since then, papers have
been published showing that nanobacteria have been grown in labs around the
world and that patients began to improve when the pathogen was targeted in
disease. Nonetheless, neither the FDA nor NIH has indicated much readiness
to re-investigate the vaccine contamination issue or the nanobacteria
treatment.
What might be the price for this delay in researching nanobacteria?
Annually, millions of heart disease patients go through agony or die because
drugs and surgery prescribed for them haven’t worked. For this last-ditch
group, the choices are simple: try something new or die.
The question that the NIH and FDA may one day face is: when such promising
early evidence was being reported and so many patients had exhausted their
other options, why were doctors not advised of this new possibility so that
they could at least tell patients and make some informed decisions?
Researchers like Ciftcioglu and Kajander, along with cardiologists like
Benedict Maniscalco plus experienced general practitioners such as Douglas
Hopper, profess frustration that so many patients and their doctors are not
being given the information that could help them, especially in last-ditch
situations. Meanwhile, calcification continues its relentless march in
millions, and the human and financial costs are mounting.
POSTSCRIPT
In May 2005, Dr Olavi Kajander delivered a sobering message to a joint
meeting of the US FDA and the European Medicines Agency on viral safety when
he presented new evidence to support something first published in 1997: that
vaccines are contaminated with nanobacteria.
Since 1999, government agencies have done virtually nothing to investigate
the claim, due largely to that NIH experiment which failed to use particles
discovered by Kajander as control samples; so now that the vaccine
contamination has been officially reported to authorities, the question is:
what will be done?
Then on 24 June 2005, a "smoking gun" was announced about calcium deposits
in heart disease. British researchers published proof in the leading medical
journal Circulation Research7
that calcium phosphate crystals cause inflammation in the arteries.
Inflammation is a leading cause of heart attacks, but until now most
cardiologists have believed calcification to be an innocent bystander in the
inflammatory process. Because of that, calcium deposits were never targeted
with treatment. If true, the British discovery would force a re-evaluation
of the whole medical approach, not only to inflammation but also to the
foundations of heart disease, looking at calcification as a prime culprit.
Endnotes:
1. Maniscalco et al., "Calcification in Coronary Artery Disease can be
Reversed by EDTA–Tetracycline Long-term Chemotherapy", Pathophysiology, July
28, 2004. 2. Shoskes, Daniel A., Kim D. Thomas and Eyda Gomez, "Anti-nanobacterial
therapy for men with chronic prostatitis/chronic pelvic pain syndrome and
prostatic stones: Preliminary Experience", J. Urology, February 2005.
3.
The ingredients are described in The Calcium Bomb, p. 94; they are: (1) nutraceutical powder (vitamins C and B6, niacin, folic acid, selenium, EDTA,
L-arginine, L-lysine, L-ornithine, bromelain, trypsin, CoQ10, grapeseed
extract, hawthorn berry, papain), 5 cm3 taken orally every evening; (2)
tetracycline HCl, 500 mg taken orally every evening; (3) EDTA, 1500 mg taken
in a rectal suppository base every evening. According to the representatives
of the company that sells the nutraceutical/EDTA combo, the treatment works
this way: the nutraceuticals boost the immune system, accelerate EDTA action
and reduce inflammation; the EDTA strips off the calcium phosphate shell;
and the tetracycline eradicates the nanobacteria. The tetracycline is also a
chelator on its own and helps remove the calcium phosphate.
4. Waters, Elizabeth et al., "The Genome of Nanoarchaeum equitans: Insights
into early archaeal evolution and derived parasitism", PNAS
100(22):12984-12988, October 28, 2003.
5.
Ciftcioglu et al., "A potential cause for kidney stone formation during
space flights: Enhanced growth of nanobacteria in microgravity", Kidney
International 67:1-9, 2005.
6. Cisar, John O. et al., "An alternative interpretation of nanobacteria-induced
biomineralization", PNAS 97(21):11511-11515, October 10, 2000.
7. Nadra, Imad et al., "Proinflammatory Activation of Macrophages by Basic
Calcium Phosphate Crystals via Protein Kinase C and MAP Kinase Pathways – A
Vicious Cycle of Inflammation and Arterial Calcification?", Circulation
Research 96(12):1248-1256, June 24, 2005.
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