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Infectious Microorganisms: the Real Culprits Behind Today's Most Debilitating Chronic Degenerative Diseases?

A number of cutting edge medical doctors, researchers and scientists have slowly been coming to a startling conclusion: Many of today's most debilitating and sometimes deadly chronic degenerative diseases for which medical science cannot find an underlying cause, are actually being caused by hidden, long-term infections, or are otherwise being triggered by the long-term deleterious effects of pathogenic microorganisms on the human body.

This includes but is not limited to diseases such as cancer, heart disease and stroke, arthritis, multiple sclerosis (MS), lupus, fibromyalgia, chronic fatigue syndrome, Lou Gehrig's disease (ALS), diabetes, Alzheimer's, schizophrenia and other mental disorders, and many others.

You're Their Favorite Host
Pathogens always require a host. And the human body is one of the most convenient hosts of them all. And when pathogens `set up shop,' so to speak, in the human body, their #1 goal is to survive. To do so, they have a number of sneaky tricks in their survival repertoire. Some can crawl right into the cells of the human body and hide. Some can ``hibernate'' for decades, only to ``awaken'' when the body is weak and less able to defend itself. Some are pleomorphic, meaning they can literally change from one form into another and back again, as the situation for their survival requires. Some can even attach a piece of the human body to their own DNA much like putting on a mask or disguise -- so that the immune system overlooks them even as they wreak havoc on the body.

Many of these insidious ``stealth pathogens'' work just below the level of immune system ``awareness,'' ever so slowly and stealthily wearing down the body's defenses over long periods of time…hiding when the immune system is triggered…and coming out to conquer more ground when the immune system has been weakened.

Well Worth Reading

Though it is unlikely you will ever hear about it from your doctor, the truth is, a great number of books have already been written on this fascinating subject. Many of the authors of these books have been reviled by the orthodox medical establishment for claiming that most, if not all, of the chronic degenerative diseases currently said to be rooted purely in genetics, environment or lifestyle, are actually being caused by bacterial, viral or fungal infections, and that much of what passes for “incurable” chronic degenerative disease can indeed now be cured or at least mitigated by either long-term antibiotic, anti-viral or anti-fungal treatments.

Fortunately, a small handful of these authors are now gaining a certain amount of notoriety even within orthodox medical circles, as the research behind their painstaking documentation becomes more widely known, and the power of their arguments becomes more widely accepted. Writers such as Professor Paul Ewald, Ph.D., a professor of biology at The University of Kentucky, and author of the controversial book Plague Time: How Stealth Infections Cause Cancers, Heart Disease and Many Other Ailments, have helped bring the concept of a microbial cause for most chronic degenerative diseases out of the darkness of medical disdain and into the spotlight. Ewald’s impeccable scholarly credentials (he was the first recipient of the George E. Burch Fellowship in Theoretic Medicine and Affiliated Sciences), coupled with his persuasive documentation, has helped open the eyes of many other medical researchers who are now following his lead and blazing new trails in medical research.

Similarly, books like The Virus Within: How Medical Detectives Are Tracking a Terrifying Virus that Hides in Almost All of Us by long-time ABC World News Tonight and Nightline correspondent Nicholas Regush have helped bring mass public attention to the idea that hidden pathogens are in many cases wreaking havoc on our bodies, and that many of the diseases and disease complexes once thought to have “no known cause” are indeed being caused by microbial infections.

These popular works have in turn helped pave the way for new attention to be paid to some of the other outstanding books which have been published on this same subject over the course of the past two decades, but which were either ridiculed by the medical establishment, or completely overlooked when they first came out. Our favorites among the books on this subject published over the past few decades include:


These are just a few of the many great books which, taken together, help document the key role played by infectious microorganisms in almost every form of chronic degenerative disease known to man. We urge you to read these books, and see for yourself the clear evidence set forth within them.

In the meantime, here is a series of excerpts from articles that have been published in major medical publications, news sources, or on web sites around the world, discussing the vital topic of microbial infections and their direct relationship to chronic degenerative diseases such as cancer, heart disease, arthritis, diabetes, Alzheimer’s, Multiple Sclerosis, lupus, Crohn’s disease, Lou Gehrig’s disease (ALS) and many others. Simply click on the links below to be taken directly to the article excerpts of your choice, or scroll down to view the articles one by one.

Click on a link below to go to the article of your choice...

Are Cancer, Heart Disease, Arthritis and Many Other Killer Diseases Secretly Being Caused by Hidden Infections?

Does Alzheimer's Disease Have a Bacterial Link?

Could Amyloid-Producing Bacteria Be Causing Alzheimer's?

Are Killer Microbes Causing Breast Cancer?

Are Bacterial and Viruses Playing a Hidden Role in Just About Every Chronic Degenerative Disease Known to Man?

Are Bacteria Playing a Major Role in Heart Disease?

Have Bacteria Been Linked Medically to Heart Disease and Stroke?

Can Arthritis Be Caused by Hidden Infections?

Is Antibiotic Treatment for Rheumatoid Arthritis Effective?

Are Mycoplasmas Bacterial Infections a Cause of Asthma?

Are Bacteria from Root Canals Secretly Causing Degenerative Diseases of the Heart, Eyes, Lungs, Kidneys, and other Organs?

Are Nanobacteria Making Us Ill?

Do Clouds Harbor Infectious Nanobacteria?

Is There Any Real Medical Evidence of Nanobacteria as a Cause of Chronic Disease?

Can Hidden Infections Be a Major Cause of Mental Illness?

What Does Medical Science Know About the Infectious Basis of Mental Illness?

Is The ``Russell Body'' the Forgotten Clue to the Bacterial Cause of Cancer?

Are Chronic Hidden Infections Causing Clogged Arteries?

Is Heart Disease Caused by a Virus?

Is the Human Papillomavirus Causing Cancers of the Head and Neck?

Is a Cancer-Causing Virus Injected Into Millions of Americans in the 1950's and '60's Now Quietly Wreaking Havoc On Our Bodies?

Can a Common Bacteria Found in Ticks Cause Cancer in Humans?

Are 1.2 Million New Cases of Cancer a Year Being Caused by Infections?

Does This Common Virus Explain the High Rates of Breast Cancer in Europe and America?

Is Coxsackievirus B a Secret Cause of Insulin-dependent Diabetes Mellitus?

Is Cytomegalovirus Infection Causing Post-Surgical Diabetes in Transplant Patients?

Is More Than 52% of Stomach Cancer Being Caused by H. Pyloria Bacterial Infection?

Can Mosquitoes and Biting Flies Be Passing Infectious Microorganisms to Humans and Causing Chronic Disease?

Can Urinary Tract Infections Cause Kidney Stones?

Is a Herpes Virus Triggering Multiple Sclerosis in Many People?

Interferon Is An Anti-Virul Drug. So Why Does It Work Against Multiple Sclerosis?

Is There Even More Evidence Linking Viral Infection With Risk of MS?

Is Anti-Biotic Resistant E. Coli Slowly Infecting Humans Through the Food Chain?

Is a Retro-Virus Causing Schizophrenia?

Can Psychiatric Illnesses Be Caused by Hidden Infections?

Are Slow Acting Bacteria and Viruses Simply Wearing Us Down?

Is a Bacteria in Milk Causing Some Forms of Crohn's Disease?

Is a Mycobacterium Causing Other Forms of Crohn's Disease?

Can a Virus Make You Fat?

Is It Really Possible All of These Degenerative Diseases Are Caused, Triggered or Exaserbated by Infectious Microorganisms?

Why Are Germs from Hospitals Now the Fourth Leading Cause of Death Among Americans?

Why Are Drug-Resistant Germs From Hospitals Now Spreading Into the General Population?




Are Cancer, Heart Disease, Arthritis and Many Other Killer Diseases Secretly Being Caused by Hidden Infections?

What Makes You Sick? It Isn't What You Think

(Feature article from Popular Science magazine, 4-01; subscribe to Popular Science at 75% off the cover price: http://www.popsci.com/popsci/)

By Gunjan Sinha

Infectious microbes are to blame for cancer, heart disease, and most other ailments, says controversial biologist Paul Ewald.

On a blustery and frigid evening in early December, Professor Paul Ewald is huddled inside an auditorium with a group of 30 Amherst College students.

It's the last day of classes, and as part of their final project for "Seminar in Evolution," the students are presenting data suggesting that almost every disease under the sun -- including common killers such as heart disease and cancer -- might be caused by bacteria, viruses, or other infectious organisms.

Ewald, an evolutionary biologist whose book "Plague Time" about this very subject had recently been released, sits attentively in the front row with his legs casually crossed...

One student points to the clustering of multiple sclerosis cases as evidence that the disease might be caused by something infectious. Another suggests the seasonal variation in births of autistic children is a reason to suspect that an infection during pregnancy induces the disease.

If I hadn't just spent the entire day with Ewald, I would have found the presentations almost laughable. Like most students of science, I was taught that statistical associations are soft science: They can't prove cause and effect. But that's exactly the kind of thinking that Ewald is out to dispel.

In "Plague Time," Ewald argues that the majority of chronic diseases -- any disease that progresses gradually over time -- are caused by infections. Just because you haven't proven cause and effect is no reason to ignore the data, he says.

To back up his arguments, Ewald goes beyond curious associations such as those found for multiple sclerosis and autism, and argues his case from an evolutionary point of view: Diseases such as cancer, heart disease, and even schizophrenia and obsessive-compulsive disorder are too common to be caused primarily by bad genes, Ewald claims.

Natural selection, he says, should have weeded those genes out of the population long ago. Instead, some genes might merely be making people more susceptible to infectious organisms, which are the true culprits of chronic disease ...

But Ewald is more like a lone wolf than the leader of a pack. While some scientists, such as famed virologist Robert Gallo (the co-discoverer of the AIDS virus), agree in part with some of Ewald's ideas, others of equal stature are downright dismissive…

"Much of it is flagrant nonsense," says Robert Weinberg...a cancer researcher at the Whitehead Institute of Biomedical Research in Cambridge, Massachusetts...

As Weinberg points out, the average life expectancy of humans today is much higher than in the past. Until recently, most people didn't live long enough to get diseases like cancer and Alzheimer's. "Traditionally, human life was 30 or 40 years," Weinberg argues," and there was not any selective pressure against a genetic defect that manifested itself at the age of 60 or 70."

Ewald counters that there is no evidence proving that at least some of our ancestors didn't live to be old. "One must not look at average ages but rather at whether a substantial part of the population lived to be 60 or 70."

Besides, Ewald adds, similar skepticism was leveled against the now-famous Barry Marshall -- an Australian doctor who finally, despite much guffawing and finger-pointing from his peers, proved in 1984 that a bacterium called Helicobacter pylori causes most peptic ulcers.

Marshall's theory challenged widely held and seemingly unassailable notions that ulcers were primarily caused by stress.

[Worse than ridicule is the autoimmune disease disinformation campaign -- perhaps sponsored by organizations who want to cut costs by denying treatment with antibiotics.

Any mammal would have a selective disadvantage if it tended to destroy itself when invaded by micro-organisms. The increasing number of people who are color blind to various degrees can be pointed to as an example of the survival of defects, but this does not apply to our response to parasites:

Humans have substantially reduced their chances of coming in contact with macro - predators such as tigers; and this security has been with us for at least 10,000 years -- plenty of time for the effect to show itself of no penalty for not being able to distinguish green from yellow.

This is not the case with micro - predators. Polio, diphtheria, syphillis, tuberculosis, and HIV have wrecked havoc on us within the last hundred years. For every smallpox we put down, it seems that ten more species of pathogens rise in its place.

It was only in the 19th century that the germ theory of disease began to be accepted; and, even today, genetic tendencies and environmental stresses are the preferred explanations. In the 19th century, for example, doctors at the University of Vienna hospital had their collegue Semmelweis fired because he cut the maternity death rate of one mother for every eight admissions to one in thirty by having the staff on his ward wash their hands. (See "Plague Time" p. 17)]

However controversial, Ewald's ideas do have scientific legs to stand on. In the past few decades, a handful of cancers have been unquestionably linked to infections.

Take the case of cervical cancer and the human papilloma virus (HPV), for example. The Centers for Disease Control reports that the sexually transmitted virus is responsible for as much as 93 percent of all cases of cervical cancer.

But because most women infected with HPV never develop cervical cancer (the CDC estimates that 20 million Americans carry the virus), and the cancer takes years to kick in -- characteristics very uncharacteristic of infectious disease -- figuring out the connection took years.

"Over 100 years ago," Ewald explains, "people noticed that the frequency of cervical cancer was higher in prostitutes, and also that there were couples with penile and cervical cancer. But people didn't accept an infectious cause until the organism was identified over a century later."

Also pegged as cancer culprits are a herpes virus that causes Kaposi's sarcoma, a human T-cell leukemia virus (HTLV 1) responsible for a rare form of leukemia, and hepatitis viruses that cause liver cancer.

These and other viruses are responsible for between 15 and 20 percent of all cancers. The rest, say most scientists, can be blamed on rogue genes and non-infectious environmental factors such as diet and smoking.

Ewald, however, is convinced that evidence from other cancers, including those of the breast, will soon tip the scales in favor of infectious causes ...

Despite the lack of data proving a cause-and-effect relationship, scientists shouldn't disregard the possibility of an infectious cause, says Ewald.

Take the case of HTLV 1, which causes a rare form of leukemia prevalent in western Japan. The virus can be transmitted sexually or via mother's milk. People typically don't develop the cancer until 50 or 60 years after they've been infected, and some infected people never develop leukemia.

"It's not like chicken pox or some other organism that follows the established rules of infection," says Ewald, "and because it's transmitted in families, people could mistakenly assume it's hereditary."

Like HTLV 1, an infectious organism may be causing breast cancer but operating too cryptically to be detected with the tools available.

AIDS researcher Gallo, who also discovered HTLV 1, agrees: "Sure, there may be a breast cancer microbe, difficult to find, present rarely or occasionally, which in the right circumstances contributes to breast cancer, but that's still a very open issue."

Ewald argues that, from an evolutionary perspective, breast cancer is simply too common in the population for it to be caused by rogue genes.

His reasoning, backed up by mathematical calculations, goes something like this: Older people are still subject to natural selection after they stop reproducing because they pass on their care and wisdom to their children and grandchildren (as in some societies where grandmothers are responsible for preparing food). So a child without a grandparent will presumably be less "fit" than a child with a grandparent.

Over many generations, children with grandparents will prevail over children without grandparents (whose genes presumably made them more vulnerable to disease).

Ewald applies the same rationale to Alzheimer's and cardiovascular disease. Studies have shown that people with a gene called APO E4 appear to be more susceptible to both diseases.

But Ewald argues that a faulty gene is too prevalent (between 10 and 50 percent of a given population carries APO E4) to have been conserved through evolution, and that it is merely making people more susceptible to infection.

An airborne bacterium that infects the respiratory system, Chlamydia pneumoniae, may be one of the real culprits.

People with E4 are much more likely to be infected by Chlamydia, and several studies have confirmed the bug's presence in the fatty lesions associated with coronary artery disease.

But it's difficult to discern whether the organism initiates the disease, exacerbates the disease, or is even contributing at all.

[In "Plague Time", Professor Ewald, p. 109, writes concerning a Finnish study: "... 70 percent of the samples from heart attack patients had antibodies to Chlamydia [pneumoniae]. This percentage was significantly higher than the percentage in the control serums from people who had not had heart attacks."

Is it possible that all the deaths in recorded history from bubonic plague are miniscule compared to the people who are dying right now from heart disease due to chronic bacterial infection?]

Chlamydia's role in Alzheimer's disease is much more tenuous. In 1998, microbiologist Alan Hudson reported that he had found the bug in 22 out of 23 brains of Alzheimer's patients, whereas only one out of 25 normal brains tested positive.

"I couldn't believe my eyes, so I spent three years using every tool known to man confirming that the organism was really there, before going public with it," recalls Hudson.

Although Hudson and Ewald have become close collaborators, one can't help but wonder whether it was mutual professional interest that truly drew them together, or their shared experience of being treated like pariahs by the medical establishment.

A self-described "gene jockey," Hudson has spent his career studying how genes enable organisms to do what they do. He stumbled onto the Alzheimer's research through a former colleague when he was at the Philadelphia College of Osteopathic Medicine.

When Hudson submitted his Alzheimer's work to a journal for publication, the editors sent it out for peer review, as is standard practice among all journals. "The Chlamydia reviewers said `publish the thing,' the Alzheimer's people hated it," he says.

The journal initially rejected the paper, and it was only after some reviewers pressured the journal that they finally published it.

Hudson's experience is all too common in a field where arguments over scientific ideas can devolve into something akin to turf war ...

Just as the medical establishment ridiculed Barry Marshall and his germ theory of ulcers, says Ewald, scientists who have spent a lifetime studying the genetic basis of disease are of course going to reject alternative explanations. "They've simply got too much invested in existing theories," he argues.

Nevertheless, researchers are working to confirm Hudson's findings. As of this writing, a group based in the Netherlands has also found an association between Alzheimer's and C. pneumoniae, as has Chlamydia expert James Mahoney at McMaster University in Hamilton, Ontario.

One of the problems, says Hudson, is that identifying the organism is very difficult and the slightest deviation in established protocol can throw off results.

As for Ewald's evolutionary argument, most scientists agree that grandparents do contribute to fitness -- the question is how much. Evolutionary arguments don't prove cause and effect.

To this, Ewald responds: "We always have to keep on the table the various hypotheses, even though we don't see direct evidence of them. One can never jump to the conclusion that infection is not important just because we find genes and environment are important."

"In most cases there's little evidence to exclude infectious causation of chronic disease. That kind of thinking has been responsible for a lot of death over the past 40 years."

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Does Alzheimer's Disease Have a Bacterial Link?
Alzheimer's Disease Related to Common Stomach Bacteria Disorder

Posted by: Dr. Kalish
www.mercola.com
  
September 26, 2006

Helicobacter pylori is a bacteria long associated with gastritis (inflammation of the stomach) and ulcers. Now scientists have further linked this common bacterial infection of the stomach to the development of Alzheimer's disease. Using histological analysis, the gold standard test for h. pylori infection, researchers determined:

46.7% of control group had h. pylori

88% of those subjects with Alzheimer's had h. pylori

In other words, h. pylori infection rates were nearly double in the group with Alzheimer's disease vs. their non-Alzheimer counterparts suggesting a relationship between this common stomach infection and the development of Alzheimer's disease.

Neurology. 2006 Mar 28;66(6):938-40.

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Could Amyloid-Producing Bacteria Be Causing Alzheimer's?
Bacteria produce fibers similar to those in Alzheimer's disease
   
By Edward R. Winstead

February 15, 2002
 
Common bacteria produce proteins that are remarkably similar to those found in the brains of Alzheimer's patients, according to a new study. Scientists found that E. coli bacteria generate protein fibers with the characteristics of amyloidsthe proteins that accumulate in the brain during debilitating human ailments such as Alzheimer's and prion diseases.

Bacteria use extracellular fibers, called curli, to colonize surfaces and mediate interactions with proteins in host cells. The discovery of bacterial amyloids gives researchers a new tool for investigating the details of how amyloids form in humans and for developing drugs to block their formation.

The discovery "also raises the intriguing possibility that bacterial amyloids could play a role in certain human neurodegenerative and amyloid-related diseases," the researchers write in Science. Scott J. Hultgren, of Washington University School of Medicine, St. Louis, Missouri, led the study.

The researchers used biochemical, biophysical, and imaging analyses to determine that the curli fibers produced by E. coli were in fact amyloid. They found differences as well as similarities between bacterial fibers and those associated with human disease. Amyloids in humans, for example, seem to assemble spontaneously, while bacteria have a specific machinery designed to assemble curli fibers.

[Chapman, M.R. et al. Role of Escherichia coli curli operons in directing amyloid fiber formation. Science 295, 851-855 (February 1, 2002).]

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Are Killer Microbes Causing Breast Cancer?
Suppressed and Forgotten Research Could Hold the Key to a Cure for this Dread Disease

© 2003, by Alan Cantwell, Jr. M.D.

Despite a century of cancer research the cause of breast cancer remains unknown. Age, diet, stress, hormone factors, genetic predisposition, and cancer viruses are all suspected as possible causative factors, but totally ignored are infectious bacteria which have been implicated in breast cancer and other forms of cancer.

A century ago when major diseases like tuberculosis, leprosy, and syphilis were discovered to be bacterial (not viral) infections, many physicians suspected bacteria might also cause cancer. At the close of the nineteenth century (when the science of microbiology was in its infancy), many different microbes were cultured from cancer. Variously called "cancer coccidia," "sporozoons" and "cancer parasites," a few of these microbes produced cancer tumours when injected into animals. But many did not, and most doctors finally assessed these cancer germs as laboratory "contaminants" or as "secondary invader microbes" that infect the tissue after the cancer is already formed.

The idea of a cancer parasite was finally dismissed in 1919 by noted American pathologist James Ewing. In his popular textbook, Neoplastic Diseases, he declared: "Few competent observers consider it (the parasitic theory) as a possible explanation in cancer." In Ewing's opinion, cancer did not act like an infection. Therefore, he concluded that microbes couldn't possibly cause it. He wrote: "The general facts of the genesis of tumours are strongly against the possibility of a parasitic origin."1 Subsequently, few doctors dared to contradict Ewing by investigating bacteria in cancer.

Nevertheless, during the 1920s a few persistent physicians like pathologist John Nuzum of the University of Illinois College of Medicine; surgeon Michael Scott from Butte, Montana; and obstetrician James Young of Edinburgh, Scotland, continued to publish research showing that bacteria were implicated in breast cancer and other forms of cancer.

Working independently of one another, all three researchers cultured unusual bacteria from breast cancer, as well as from breast cancer tumours in mice. The peculiar growth of the "pleomorphic" cancer germ defied the established laws of microbiology by its ability to change shape and form, depending on how it was cultured in the laboratory, as well as the amount of oxygen supplied for growth and the age of the culture.

At first, the germ was barely visible as tiny round coccal forms. Later, these cocci enlarged into rod-shaped bacteria, which could connect together to form chains resembling a fungus. Small cocci could also enlarge into larger yeast and fungal-like spore forms.

Nuzum grew his "micrococcus" from 38 of 41 early breast cancers, and from the cancerous lymph nodes and metastatic tumours resulting from spread of the cancer to other parts of the body.2,3 During his 6 years of intensive bacteriological study, he learned the microbe could pass through a filter designed to hold back bacteria, indicating that some forms of the microbe were as small as the size of some viruses. With special stains he detected these small round coccoid forms within the breast cancer tumour cells. Although Nuzum couldn't produce cancer tumours in mice, he was able to induce breast cancer tumours in 2 of 5 dogs injected with the microbe.

In a dangerous human experiment he injected the groin of a 70-year-old man with the bacteria he cultured from breast cancer. After 62 injections over an 18-week period, a skin cancer formed in the man's groin. This experiment showed that breast cancer microbes were also capable of producing a different kind of cancer, such as skin cancer.

Young found his microbe in 16 cases of breast cancer, and in two mice with breast cancer. He identified "spore forms" and clumped "spore balls" in microscopic sections prepared from the mouse tumours.

Scott described three stages in the life cycle of his parasite: rod forms, spore or coccus-like forms, and large spore-sacs resembling a fungus.6,7 He treated cancer patients with an effective antiserum against these microbes, and spent the rest of his life trying to alert his colleagues to the infectious cause of cancer. But the antagonism of the medical profession to Scott's cancer parasites and his antiserum was overwhelming, and he died a forgotten man.

During the last half of this century cancer microbe research was barely kept alive by a quartet of women, now all dead. The published research of Virginia Wuerthele-Caspe Livingston-Wheeler (a physician), Eleanor Alexander-Jackson (a microbiologist), Irene Diller (a cellular biologist) and Florence Seibert (a chemist) provides indisputable evidence that bacteria are implicated in cancer.

Livingston, who never let the male-dominated medical profession intimidate her, independently discovered the cancer microbe in the late 1940s and never stopped talking about it until her death in 1990, at the age of 84. Aided by Alexander-Jackson, who supplied the bacteriologic expertise, they became an unstoppable research team.8-12 The two women found a special stain (the acid-fast stain) that allowed the microbe to be recognised in culture and within the cancer tumour. Like the researchers back in the 1920s, they confirmed the microbe was filterable; and electron microscopic photos provided further proof that the filterable forms were indeed viral-size. Livingston named the microbe "Progenitor cryptocides" (Greek for the hidden-killer), which angered cancer experts, microbiologists, and American Cancer Society spokespersons, all of whom insisted the cancer microbe did not exist!

In the 1950s Irene Diller of the Institute for Cancer Research at Fox Chase, Philadelphia, discovered fungus-like microbes in cancer cells. Joining forces with the Livingston team, Diller worked with specially bred mice with a proven cancer incidence. By injecting them with microbes cultured from breast cancer and other tumours, she was able to more than double the cancer incidence of the mice.

She injected healthy animals with cancer bacteria. When cancer tumours developed she successfully cultured the microbe from the tumours - thus proving that these bacteria were implicated in the production of cancer. Utilising Livingston's methods, Diller also grew the microbe from the blood of cancer patients.

In the early 1960s Florence Seibert became so impressed with Diller's research that she quit retirement to help prove that bacteria cause cancer. Back in the 1920s Seibert devised a method to make intravenous transfusions safe by eliminating contaminating ubiquitous bacteria. Later, as one of the foremost authorities investigating the chemistry and immunology of the acid-fast bacteria that cause tuberculosis, she perfected the skin test for tuberculosis that has been used worldwide ever since. In 1938, she was awarded the famed Trudeau Medal, the highest prize given to tuberculosis research.

Experiments conducted by Seibert and her research team showed these acid-fast and TB-like cancer microbes were not laboratory contaminants because they were able to isolate bacteria from every piece of tumour (and every acute leukemic blood) they studied.

In her autobiography, Pebbles on the Hill of a Scientist, published privately in 1968, she wrote: "One of the most interesting properties of these bacteria is their great pleomorphism. For example, they readily change their shape from round cocci, to elongated rods, and even to thread-like filaments depending upon what medium they grow on and how long they grow. This may be one of the reasons why they have been overlooked or considered to be heterogenous contaminants... And even more interesting than this is the fact that these bacteria have a filterable form in their life cycle; that is, that they can become so small that they pass through bacterial filters which hold back bacteria. This is what viruses do, and is one of the main criteria of a virus, separating them from bacteria. But the viruses also will not live on artificial media like these bacteria do. They need body tissue to grow on. Our filterable form, however, can be recovered again on ordinary artificial bacterial media and will grow on these. This should interest the virus workers very much and should cause them to ask themselves how many of the viruses may not be filterable forms of our bacteria."

Seibert's provocative papers, some emanating from the prestigious Annals of the New York Academy of Sciences, should have caused a stir. But with the quartet slowly closing in on the infectious cause of cancer, funds from previous supporters (like the American Cancer Society) suddenly dried up. All cancer microbe researchers eventually discovered that studying cancer bacteria was the kiss of death as far as funding was concerned. And without adequate funding, this type of cancer research was made more difficult.

But coming from thirty years of research into the acid-fast bacteria that cause tuberculosis, Seibert knew that the discovery of a pleomorphic and acid-fast microbe in cancer was tremendously important. She fervently believed that knowledge of this microbe would be instrumental in developing a possible vaccine and more effective antibiotic therapy against cancer. In Pebbles she confided: "It is very difficult to understand the lack of interest, instead of great enthusiasm, that should follow such results, a lack of certainty not in the tradition of good science. The contrast between the progress made in tuberculosis where we know the cause, where we have good general diagnostic tests, where we have a vaccine and effective antibiotic controls, and that made in cancer with the millions invested, is very striking. Some dedicated scientists should indeed find it rewarding to confirm or deny these painstaking and time-consuming experiments, for the sake of establishing the first necessary step in the important problem of the etiology of cancer."

Like the other women, Seibert observed the virus-like forms of the cancer microbe within the nucleus of the cancer cells. She theorised this infection could disrupt and transform nuclear genetic material that could lead to malignant change. Even though cancer microbes might appear to be simple and common microbes, their ability to infiltrate the nucleus of cells meant they were far from harmless.

In 1990, at the age of 92, Florence Seibert was inducted into the National Women's Hall of Fame, along with Barbara Jordan (Government), Billie Jean King (Athletics) and Margaret Bourke-White (Arts). When she died the following year her passage was noted in Time and People magazines, and in major newspapers like The Los Angeles Times. All the obituaries mentioned her contributions to the safety of intravenous fluids and her great achievement with the TB skin test. But not a word was written about her cancer microbe research, to which she devoted the last thirty years of her life.

Each year 190,000 American women are diagnosed with breast cancer. And the prognosis is still dismal for women whose breast cancer has spread to the lymph nodes and beyond. Yet the medical establishment remains adamantly and irrationally opposed to cancer microbe research. It is perhaps understandable from an economic viewpoint that the medical profession would not welcome a proposed infectious cause of cancer that would challenge the highly lucrative multibillion-dollar cancer industry.

Physicians confidently ignore cancer bacteria because they have been carefully taught in medical school that there are no significant bacteria detectible in cancer. They still believe that cancer microbes represent contaminant bacteria or bacteria of no significance. Thus, published reports of cancer microbe research are rarely cited and the subject remains virtually unknown.

The idea of a microbe with virus, bacteria, and fungal-like stages is also anathema to most doctors. However, over the past several decades the study of cell-wall deficient bacteria and "mycoplasma-like" bacteria (which are both bacterial and viral-like) indicates that microbes indeed have a complex life cycle. In 1919, when Ewing offered his damning opinion of cancer parasites, none of these microbiologic peculiarities were even recognised!

In some instances, cancer microbe research appears to be deliberately suppressed. For example, the National Cancer Institute on its "cancer Facts" web page (http://oncolink.upenn.edu/pdg/600911.html) informs viewers about Virginia Livingston and states: "There is no scientific evidence to confirm her theories of cancer causation or to justify her treatments." Obviously, this official judgement is a blatant lie because, as we have noted, Livingston's discoveries have been confirmed by many competent scientists.

In addition, Livingston has written three books on the cancer microbe: Cancer: A New Breakthrough (1972), The Microbiology of Cancer (1977), and The Conquest of Cancer (1984).15-17 More recent books on bacteria in cancer include Alan Cantwell's The Cancer Microbe (1990) and Can Bacteria Cause Cancer? (1997) by David J Hess.

Using acid-fast staining techniques, bacteria have been identified in breast cancer, lymphoma, Kaposi's sarcoma (the so-called "gay cancer" of AIDS) and other forms of cancer.20-22 Figure 1 shows bacteria identified in breast cancer, indicating that such microbes are already present within the tumour and are not laboratory contaminants. Microbes have also been identified in "normal" and cancer-free breast tissue removed at the time of surgery. This suggests that the bacteria are not "secondary invaders" because they are identifiable in areas before the tissue has been invaded by cancer.20 Figure 2 shows the appearance of a microbe cultured from the same breast cancer. Note how the size and shape and appearance of the microbes within the tumour (Fig. 1) approximates the appearance of the bacteria cultured from the metatastic spread of the tumour to the skin (Fig. 2).

The current lack of knowledge about the cause of advanced breast cancer has resulted in the recommendation of some very expensive and death-defying treatments for this horrendous disease. Bone marrow transplants, which carry a 5% death rate, are being proposed as a routine treatment, at a minimal cost of $100,000 per patient.

As described in Karen Stabiner's To Dance With the Devil: The New War on Breast Cancer (1997), the procedure is not pretty.23 First, a catheter is placed in a woman's chest to deliver the drugs. A surgical treatment is then performed to scrape out bone marrow from her pelvis, followed by 7 days of growth hormone injections. Then starts days of intravenous chemotherapy that can cause kidney and bladder damage. A catheter is placed in the bladder, followed by a round of intravenous BCNU, or carmustine, a drug that makes a woman feel like she is falling down drunk. Patients become sleepy, sullen, disoriented, agitated, and angry. Loss of bowel control and vomiting are common. After all this, women are put into isolation because the white count drops precipitously, making her vulnerable to all sorts of infections. There may be inexplicable spiking fevers and rashes, and the inevitable loss of hair. After three weeks, patients are allowed to go home where they are told to watch for, "interstitial pneumonitis," a potentially fatal after-effect if not diagnosed and treated early.

Bone marrow transplant for breast cancer is not guaranteed, nor is it considered a cure. Women have been known to die of cancer three months after the procedure, proving that some patients do not respond to chemotherapy no matter how high the dose.

Even with radiation, chemotherapy and surgery, the cost of dying of cancer is not cheap. At the price patients are paying, physicians should not have the luxury of being ignorant about cancer microbe research, particularly when these microbes can be identified in cancer tumours.

With 40,000 American women dying annually from breast cancer, it is time medical science re-evaluated the parasite of cancer that James Ewing so casually dismissed in 1919. Perhaps if he hadn't been so adamant about cancer microbe research, his colleagues might have been able to do more to save him when he himself eventually died of "the Big C."

REFERENCES

Ewing J: The parasitic theory. In, Ewing J (Ed): Neoplastic Diseases (Ed1). Saunders, Philadelphia, 1919, pp 114-126

Nuzum JW: A critical study of an organism associated with a transplantable carcinoma of the white mouse. Surg Gynecol Obstet 33:167-175, 1921.

Nuzum JW: The experimental production of metastasizing carcinoma in the breast of the dog and primary epithelioma in man by repeated inoculation of a micrococcus isolated from human breast cancer. Surg Gynecol Obstet 11:343-352, 1925.

Young J: Description of an organism obtained from carcinomatous growths. Edinburgh MedJ (New Series) 27:212-221, 1921.

Young J: An address on a new outlook on cancer: Irritiation and infection. Brit Med J, Jan 10, 1925, pp 60-64.

Scott MJ: The parasitic origin of carcinoma. Northwest Med 24:162-166, 1925.

Scott MJ: More about the parasitic origin of malignant epithelial growths. Northwest Med 25:492-498, 1925.

Wuerthele Caspe (Livingston) V, Alexander-Jackson E, Anderson JA, et al: Cultural properties and pathogenicity of certain microorganisms obtained from various proliferative and neoplastic diseases. Amer J Med Sci 220:628-646, 1950.

Wuerthele-Caspe Livingston V, Alexander-Jackson E: An experimental biologic approach to the treatment of neoplastic disease. J Amer Med Women's Asssn 20:858-866, 1965.

Wuerthele Caspe Livingston V, Livingston AM: Demonstration of Progenitor Cryptocides in the blood of patients with collagen and neoplastic diseases. Trans NY Acad Sci 34(5):433-453, 1972.

Wuerthele Caspe Livingston V, Livingston AM: Some cultural, immunological, and biochemical properties of Progenitor cyptocides. Trans NY Acad Sci 36(6):569-582, 1974.

Alexander-Jackson E: A specific type of microorganism isolated from animal and human cancer: Bacteriology of the organism. Growth 18:37-51, 1954.

Diller IC: Growth and morphologic variability of pleomorphic, intermittently acid-fast organisms isolated from mouse, rat, and human malignant tissues. Growth 26:181-209, 1962.

Seibert FB, Yeomans F, Baker JA, et al: Bacteria in tumors. Trans NY Acad Sci 34(6):504-533, 1972.

Wuerthele Caspe Livingston V: Cancer, A New Breakthrough. Nash Publishing Corp, Los Angeles, 1972.

Livingston-Wheeler VWC, Wheeler OW: The Microbiology of Cancer. Livingston Wheeler Medical Clinic Publication, San Diego, 1977.

Livingston-Wheeler VWC, Addeo EG: The Conquest of Cancer. Franklin-Watts, New York, 1984.

Cantwell AR Jr: The Cancer Microbe: The Hidden Killer in Cancer, AIDS, and Other Immune Diseases. Aries Rising Press, Los Angeles, 1990.

Hess DJ: Can Bacteria Cause Cancer? Alternative Medicine Confronts Big Science. New York University Press, New York, 1997.

Cantwell AR Jr, Kelso DW: Microbial findings in cancer of the breast and in their metastases to the skin. J Dermatol Surg Oncol 7:483-491, 1981.

Cantwell AR Jr: Histologic observations of variably acid-fast coccoid forms suggestive of cell wall deficient bacteria in Hodgkin's disease. A report of four cases. Growth 45:168-187, 1981.

Cantwell AR Jr: Kaposi's sarcoma and variably acid-fast bacteria in vivo in two homosexual men. Cutis 32:58-64,68, 1983.

Stabiner K: To Dance with the Devil: The New War on Breast Cancer. Delacourt Press, New York, 1997.


Dr. Cantwell is a dermatologist, and an AIDS and cancer researcher. He is the author of The Cancer Microbe, and AIDS and the Doctors of Death (both published by Aries Rising Press, Los Angeles). Correspondence address: PO Box 29532, Los Angeles, CA 90029, USA. Dr. Cantwell's books, including The Cancer Microbe, are available at: http://ariesrisingpress.com/books/


(New Dawn No. 48 May-June 1998)

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Are Bacterial and Viruses Playing a Hidden Role in Just About Every Chronic Degenerative Disease Known to Man?

In a bold new book, evolutionist Paul Ewald argues that viruses and bacteria play a huge, hidden role in heart disease, cancer and other modern plagues

By Geoffrey Cowley, NEWSWEEK, 11-27-00

`` Back in the 1880s, before tuberculosis had a known cause, experts attributed it to a combination of risk factors -- things like depression, bad ventilation, insufficient food and "family predisposition". One standard textbook noted expansively that "the idea of infection being a cause... still prevails in the South of Europe".

FAST-FORWARD TO the 1980s, and you hear similar accounts of peptic ulcers. The highly touted risk factors were stress, smoking, alcohol and, of course, "genetic predisposition." Never mind that an Australian researcher named Barry Marshall was successfully giving himself ulcers by swilling beakers of bacteria -- and curing them with antibiotics. The textbooks didn't even mention his work.

We now know that TB and ulcers are infectious conditions, caused by specific microbes and treatable with anti microbial drugs. Yet we're still laboring to explain most of our leading scourges -- cancer, heart disease, mental illness, Alzheimer's-- with long lists of risk factors.

In a compelling new book titled "Plague Time" (282 pages. Free Press $25), Amherst College biologist Paul Ewald argues that we're missing an obvious lesson here. Roughly translated: "It's the germs, stupid."

Though genes and lifestyle are no doubt important, Ewald says, the primary causes of today's "slow-burning plagues" are parasites --viruses, bacteria and other infectious microbes --whose long-term effects we have simply failed to recognize.

Ewald is not a virologist but a bold-minded evolutionist who, in past work, has created a whole new framework for thinking about infectious disease. To understand why microbes behave as they do, he considers their ecological incentives.

Cold viruses can't afford to be too virulent because they require mobile hosts. (A dying cold sufferer wouldn't get around enough to infect other people.)

Parasites that can survive outside their hosts don't have to be so considerate -- especially if they can travel from host to host via mosquitoes or drinking water. A dying malaria sufferer is, if anything, preferable to a healthy one from the parasite's perspective. All the person has to do to spread infection is lie still and get bit.

In "Plague Time" he takes a similar approach. By his reasoning, our genes shouldn't cause much heart disease, Genes that impede our survival tend to die out over time, as their owners fail to reproduce.

By contrast, the parasites with the best tricks for exploiting us are the most likely to stay in the game. THERE IS NO QUESTION THAT VIRUSES AND BACTERIA CAN TAKE UP LONG-TERM RESIDENCE IN OUR BODIES. Some hide deep within our cells to avoid detection by the immune system, while others disguise themselves to resemble our own tissues.

We know the consequences can be serious. Suppose the immune system catches sight of a streptococcal bug that normally evades detection by masking itself as a heart cell. As the body attacks the invader, it may demolish the organ as well.

The question is whether these chronic infections are as pervasive as Ewald suspects. Some experts would scoff at the notion, but the recent findings are impressive. "Until the 1980s," he writes, "it was generally not appreciated that women who were suffering and dying from cervical cancer were the victims of a venereal disease epidemic".

Today it's undeniable. Epidemiologists have puzzled for more than a century over the link between sexual promiscuity and cervical cancer. But over the past 15 years, studies have revealed that human papillomaviruses, America's most common sexually transmitted pathogens, are present in some 93 percent of cervical tumors. Scientists have even identified the proteins that HPVs use to release the brakes on normal cell division.

TIP OF THE ICEBERG

Cervical cancer may be the tip of an iceberg. Less definitive studies have linked childhood strep infection to obsessive-compulsive disorder and Tourette's syndrome.

Traces of a virus that causes mammary cancer in mice have been recovered from human breast tumors.

Researchers in Japan and Germany have linked borna virus --a brain infection seen in horses, sheep and cats-- to schizophrenia and bipolar disorder in people.

A growing body of evidence suggests that Chlamydia pneumoniae, a common respiratory bug, may play a key role in coronary artery disease, the leading cause of death throughout the Western world. Since 1988, researchers have consistently found the bacterium in clogged vessels but not in healthy ones. They've caused arterial lesions in rabbits by infecting them with the germ. They have even found hints that antibiotics can slow the progression of heart disease in infected patients.

As these connections are borne out, they could change medicine as profoundly during the 21st century as germ theory did in the 20th. The question is whether they'll get the attention they deserve.

As Ewald observes, "Those who control access to funding and the channels of scientific communication tend to be believers in the established views."

When Edward Jenner hit upon the notion of a smallpox vaccine in 1797, the Royal Society of London scolded him for risking his reputation on something "so much at variance with established knowledge, and withal so incredible."

When the Hungarian physician Ignaz Semmelweis figured out that physicians' unwashed hands were causing fatal infections among new mothers at the University of Vienna in the 1850s, he lost his own position there.

Though Barry Marshall first reported his findings on the infectious cause of ulcers in 1983, his peers ignored the discovery until 1990, when the National Enquirer got hold of the story and told the world. Let's hope the scientific community is less slow to notice this book. ''

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Are Bacteria Playing a Major Role in Heart Disease?
Bacteria's Role in Heart Disease Discovered
  
Scientists believe they have discovered how a common bacterial infection can trigger heart disease - a controversial hypothesis that is generating enormous interest among heart researchers. The key finding, reported in this week's Science, is that chlamydia bacteria, which cause lung and eye infections and a sexually transmitted disease, have a protein on their outer coat that mimics a protein found in the heart muscle of mammals. Normally this molecular mimicry allows the bacterium to evade the chlamydia-infected individual's immune system. But sometimes the immune cells are not fooled; they mount an attack against the chlamydia germs that gets misdirected against heart cells as if they were the enemy. What we now see is that we don't have to have bacterial damage to the heart in order for bacteria to cause heart disease.

Chlamydia infections are very common; at least two out of three adults have antibody evidence of a past infection. Since heart disease is also common, it has been impossible to know from epidemiology alone if the two diseases were really linked. Boston University researchers reported earlier this month that British patients who had been treated with certain antibiotics were less likely to develop heart disease. Two large human studies are underway to see if antibiotic treatment will prevent heart attacks among individuals who have already survived one.

DR. MERCOLA COMMENT: It does appear that there is a strong link between heart disease and these infections. Antibiotic treatment would be one way to address the issue. I suspect the situation is very similar to the issue with rheumatoid arthritis. I have treated more than 2,500 patients with this illness over the last ten years. (You can find my protocol at ) However, I believe it is far better to boost the immune system with nutritional interventions. I believe that is why people who follow my diet recommendations seem to do better with the antibiotics. They do not generally experience a severe worsening of their symptoms and usually respond dramatically well to the treatment. I suspect that the situation is open to a more aggressive intervention of heart disease by screening individuals for antibodies to chlamydia and treating them with a low dose pulsed regimens similar to the one we use in rheumatoid arthritis. The Minocin in the protocol works wonderfully well for chlamydia.

(http://www.mercola.com Simply the best health newsletter on the internet. ED)

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Have Bacterial Been Linked Medically to Heart Disease And Stroke?
Bacterial Infections Linked to Heart Disease and Stroke
  
Common, chronic bacterial infections, including lung and urinary tract infections, as well as gum disease, may increase the risk of atherosclerosis, a build-up of fatty plaques in the arteries that could lead to heart attack, study findings suggest.

During the 5-year study, people with chronic bacterial infections were nearly three times more likely to develop new plaques in carotid arteries, which are the large arteries in the neck that deliver blood to the brain.

A buildup of fat in the neck arteries can increase the risk of stroke, and is a sign that heart arteries may be clogged as well.

But the researchers cautioned that widespread use of antibiotics to fight chronic infections -- and hopefully prevent atherosclerosis -- is not justified.

Previous research has suggested a link between infections and heart attacks, but few studies have examined the relationship between infections and atherosclerosis, which can lead to heart attack and stroke.

During the study, 41% of participants developed new plaques in their carotid arteries. People who had chronic infections were 2.78 times more likely to develop new plaques than people who did not have any infections.

But not all infections were linked to an increased risk of atherosclerosis. The study found that only bacterial infections, not infections caused by viruses like cytomegalovirus, the herpes zoster virus or hepatitis B or C, increased the risk of artery disease.

Researchers suspect that infection-related inflammation may play a role in the increased risk. Patients with infections who had high levels of inflammation tended to have a greater risk of atherosclerosis. Another possible explanation, according to the authors, is that bacterial infections may trigger the immune system to turn against itself. This so-called autoimmune response may damage vessels, making it easier for fatty deposits to accumulate.

(Circulation February 27, 2001;103:1064-1070)

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Can Arthritis Be Caused by Hidden Infections?
Bacteria, Viruses Can Cause Infectious Arthritis

Most people are familiar with osteoarthritis the common ``wear and tear'' arthritis that occurs over years of musculoskeletal stress and injury, and the source of many of the aches and pains we attribute to aging. Another well-known ailment is rheumatoid arthritis, an autoimmune disease that usually affects several joints in the body at once. But there are actually about 100 types of arthritis and related disorders, many of which are caused by bacteria or viruses.

Arthritis is a condition in which the joints of the body become swollen, tender and inflamed. ``With infectious arthritis, a bacterium, virus or other infection directly invades the joint and causes pus to form there,'' says James J. Nocton, MD, Associate Professor of Pediatrics at the Medical College of Wisconsin. ``While infectious arthritis itself is not contagious, the cause of the infection can be.'' Dr. Nocton practices in the Division of Pediatric Rheumatology, Department of Pediatrics, at Children's Hospital of Wisconsin, a Medical College affiliate.

Bacteria such as staphylococcus aureus (``staph'') and streptococcus (``strep'') are the most common causes of infectious arthritis. These bacteria can gain access to the body in various ways, for example through a cut or break in the skin or via an ear infection. The infectious agent travels through the bloodstream and settles in a joint, where the body's own defense system the immune response fights against the intruder. The end result is inflammation.

Untreated Lyme disease, caused by a bacterium carried by the deer tick, can lead to infectious arthritis, as can untreated sexually transmitted diseases, particularly gonorrhea.

In addition to certain common bacteria, some viruses can also initiate arthritic disorders. Parvovirus, which causes the common childhood infection known as ``fifth disease,'' can cause infectious arthritis in children or adults. While illness from parvovirus generally resolves without treatment, anti-inflammatory medications may be prescribed to treat joint swelling and pain if infectious arthritis develops.

People whose immune systems are already compromised by health conditions such as diabetes or sickle cell anemia may be at even greater-than-average risk of developing infectious arthritis.

This article includes information from:
Medical College of Wisconsin Department of Pediatrics
Children's Hospital of Wisconsin, Pediatric Rheumatology
© 2003 Medical College of Wisconsin

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Is Antibiotic Treatment for Rheumatoid Arthritis Effective?
From Carol & Richard Eustice, Your Guide to Arthritis
www.About.com

The History Of The Search For Cause And Cure

With no known cure for the more than 100 types of arthritis, treating and coping with the painful symptoms have become the core of concern for patients and physicians.

In the 1930's, a bacterial cause for rheumatoid arthritis was investigated but the research was short-lived except for distinct cases of acute infectious or septic arthritis. In 1939, the first real lead regarding an infectious cause for rheumatoid arthritis arose when mycoplasma, an atypical viral-like bacteria, was isolated from the exudate and tissue of rheumatic patients.

Investigators had already shown that mycoplasmas cause arthritis in mice, rats, chickens, goats, and cows.

They had found mycoplasmas in the genitourinary tracts of humans too, especially females.
In 1949 at the International Congress on Rheumatic Diseases the possible relationship between mycoplasmas and joint disease was reported. After obtaining one of the first National Institutes of Health (NIH) research grants in 1950, Thomas McPherson Brown, M.D. and colleagues at the arthritis research unit reported the following year that the rheumatoid disease mechanism was more of an immunologic reaction of antigen and antibody (with mycoplasma as the suspected antigen) rather than the infectious and transmissible type.

In 1955, the research unit reported that mycoplasmas, unlike bacteria and viruses could live in tissue cell cultures without destroying the tissue cells. To further support mycoplasmas as a causative agent/antigen, in 1964 a high incidence of mycoplasma antibodies in the blood of rheumatoid arthritis patients and lupus patients was found, indicating current or previous infection. Also recognized was a 4:1 higher incidence of mycoplasma antibodies in females suggesting a correlation with the higher incidences of rheumatoid arthritis in females.


Antibiotic Therapy

Efforts to demonstrate the effectiveness of tetracycline therapy were initiated and first reported over 40 years ago by Thomas McPherson Brown, M.D. Two weeks after Brown's death in 1989, NIH requested grant applications for the controlled clinical trials of tetracycline therapy for rheumatoid arthritis which he had been seeking. The preliminary results of the clinical trials, known now as MIRA or Minocycline in Rheumatoid Arthritis, were promising and the NIH requested grant applications for studies of mycoplasma and other infectious agents as causes for rheumatoid diseases in 1993, and a pilot study for intravenous antibiotics for rheumatoid arthritis in 1994.

The result of the MIRA clinical trial stated, "Patients who suffer from mild to moderate RA now have the choice of another therapeutic agent. Not only did the antibiotic significantly reduce symptoms, but side effects were minimal and less severe than observed for most other common rheumatoid treatments".

"Why Arthritis?"

Throughout the years, the theories that focus on mycoplasma as the responsible infectious agent and on tetracycline as the antibiotic treatment of choice have been hampered by lack of adequate funding for more research and from politics. "Why Arthritis?" by Harold W. Clark, Ph.D., one of Brown's colleagues, assesses the rheumatoid diseases, decades of research, the search for a cure, and the frustration of researchers whose case for anti-mycoplasma therapy was overlooked for 40 years by the government and various arthritis organizations. Clark believes efforts were impeded because a safe, simple treatment threatens the medical establishment since patients would then require less medical intervention.

Many physicians remain skeptical and still do not suggest antibiotic treatment to their patients. The Arthritis Foundation was seemingly unimpressed even after antibiotic therapy was deemed as safe and effective. The foundation's medical director reportedly said he did not view the treatment as a breakthrough and more study of dosages and long-term use of minocycline is needed.

According to the American College of Rheumatology, "Minocycline is prescribed for patients with symptoms of mild rheumatoid arthritis. It is sometimes combined with other medications to treat patients with persistent symptoms of this form of arthritis."

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Are Mycoplasmas Bacterial Infections a Cause of Asthma?
ASTHMA ASSOCIATED WITH BACTERIAL INFECTION
From: Respiratory Reviews.com

The latest clinical information on respiratory medicine

Vol. 6 No. 7 July, 2001

DENVER Increasingly, microbes appear to be involved in the etiology of some cases of asthma. In addition to previous findings indicating that viral infection may exacerbate acute asthma, emerging evidence now implicates bacterial infection as a cause of chronic asthma. Richard Martin, MD, and colleagues report detecting infection with Mycoplasma pneumoniae or Chlamydia pneumoniae in 31 of 55 asthma patients using a combination of polymerase chain reaction (PCR), serology, and culture.[1] By contrast, PCR revealed mycoplasma infection in only one of 11 normal controls.

``Given that we detected infection in 56% of asthma patients [vs one in 11 control subjects], there may indeed be a link between bacteria in the airways and asthma in some patients,'' said Dr. Martin, head of the Pulmonary Division and Vice Chair of the Department of Medicine at National Jewish Medical and Research Center (NJMRC) in Denver. The researchers did not, however, find an association between chronic stable asthma and viral infection.

``We were surprised to find these bacteria in the lower airways of a subset of stable asthmatics,'' said coauthor Monica Kraft, MD, Associate Professor in the Department of Medicine and Division of Pulmonary Medicine at NJMRC. ``The association raises an interesting `chicken versus egg' issuedid the asthma allow microorganisms to `set up shop,' or do the microorganisms actually cause chronic asthma?'' Dr. Kraft told RESPIRATORY REVIEWS. If the latter is true, then antibiotics would be expected to help some patients with asthma.

LONG-TERM ANTIBIOTIC THERAPY?

The authors have garnered support for this idea from both clinical experience and research. ``Using an empirical approach, we've tried clarithromycin with some of our clinical patients. Anecdotally speaking, we have steroid-dependent asthmatics who improved with clarithromycin,'' said Dr. Kraft. ``Initially, we tried a six-week course, but we found that respiratory function continued to improve in many patients [if the antibiotic was administered] over three to six months.''

Dr. Martin explained the reason for the lengthy course: ``Unfortunately, mycoplasma is difficult to eradicate from the airways. In true pneumonias, even after chest X-rays show that mycoplasma infection is largely cleared from the lungs, some residual infection lingers.''

Dr. Martin and colleagues also back up their clinical experience with experimental evidence. ``We're submitting a manuscript shortly, describing a study demonstrating that asthmatics who are PCR-positive for chlamydia or mycoplasma infection show a 12% to 13% improvement in airway function following clarithromycin treatment,'' he reported. Said Dr. Kraft, ``Most antibiotics do have some anti-inflammatory quality, so it's not clear how this works. Hopefully, animal studies will answer this question.''

While the researchers are encouraged by clinical and experimental success with antibiotic therapy in a subset of asthma patients, Dr. Kraft recognizes that long-term antibiotic treatment for asthma may be controversial. In light of concerns regarding general overuse of antibiotics and need to justify long-term administration under managed health care, this approach might be questioned. However, in the absence of a practical means of establishing the diagnosis, she said, ``We haven't found any other way.''

Reference
1. Martin RJ, Kraft M, Chu HW, et al. A link between chronic asthma and chronic infection. J Allergy Clin Immunol. 2001;107:595-601.

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Are Bacteria from Root Canals Secretly Causing Degenerative Diseases of the Heart, Eyes, Lungs, Kidneys, and other Organs?
 
An Interview with George Meinig, D.D.S.

Dr. Meinig brings a most curious perspective to an expose of latent dangers of root canal therapy - fifty years ago he was one of the founders of the American Association of Endodontists (root canal specialists)! So he's filled his share of root canals. And when he wasn't filling canals himself, he was teaching the technique to dentists across the country at weekend seminars and clinics.

About two years ago, having recently retired, he decided to read all 1174 pages of the detailed research of Dr. Weston Price, (D.D.S). Dr. Meinig was startled and shocked. Here was valid documentation of systemic illnesses resulting from latent infections lingering in filled roots. He has since written a book, Root Canal Cover Up Exposed - Many Illnesses Result", and is devoting himself to radio, TV, and personal appearances before groups in an attempt to blow the whistle and alert the public.

MJ Please explain what the problem is with root canal therapy.

GM First, let me note that my book is based on Dr. Weston Price's twenty-five years of careful, impeccable research. He led a 60-man team of researchers whose findings - suppressed until now rank right up there with the greatest medical discoveries of all time. This is not the usual medical story of a prolonged search for the difficult-to-find causative agent of some devastating disease. Rather, it's the story of how a "cast of millions" (of bacteria) become entrenched inside the structure of teeth and end up causing the largest number of diseases ever traced to a single source.

MJ What diseases? Can you give us some examples?

GM Yes, a high percentage of chronic degenerative diseases can originate from root filled teeth. The most frequent were heart and circulatory diseases and he found 16 different causative agents for these. The next most common diseases were those of the joints, arthritis and rheumatism. In third place - but almost tied for second - were diseases of the brain and nervous system. After that, any disease you can name might (and in some cases has) come from root filled teeth.

Let me tell you about the research itself. Dr. Price undertook his investigations in 1900. He continued until 1925, and published his work in two volumes in 1923. In 1915 the National Dental Association (which changed its name a few years later to The American Dental Association) was so impressed with his work that they appointed Dr. Price their first Research Director. His Advisory Board read like a Who's Who in medicine and dentistry for that era. They represented the fields of bacteriology, pathology, rheumatology, surgery, chemistry, and cardiology.

At one point in his writings Dr. Price made this observation: "Dr. Frank Billings (M.D.), probably more than any other American internist, is due credit for the early recognition of the importance of streptococcal focal infections in systemic involvements."

What's really unfortunate here is that very valuable information was covered up and totally buried some 70 years ago by a minority group of autocratic doctors who just didn't believe or couldn't grasp - the focal infection theory.

MJ What is the "focal infection" theory?

GM This states that germs from a central focal infection - such as teeth, teeth roots, inflamed gum tissues, or maybe tonsils - metastasize to hearts, eyes, lungs, kidneys, or other organs, glands and tissues, establishing new areas of the same infection. Hardly theory any more, this has been proven and demonstrated many times over. It's 100% accepted today. But it was revolutionary thinking during World War I days, and the early 1920's!

Today, both patients and physicians have been "brain washed" to think that infections are less serious because we now have antibiotics. Well, yes and no. In the case of root-filled teeth, the no longer-living tooth lacks a blood supply to its interior. So circulating antibiotics don't faze the bacteria living there because they can't get at them.

MJ You're assuming that ALL root-filled teeth harbor bacteria and/or other infective agents?

GM Yes. No matter what material or technique is used - and this is just as true today - the root filling shrinks minutely, perhaps microscopically. Further and this is key - the bulk of solid appearing teeth, called the dentin, actually consists of miles of tiny tubules. Microscopic organisms lurking in the maze of tubules simply migrate into the interior of the tooth and set up housekeeping. A filled root seems to be a favorite spot to start a new colony.

One of the things that makes this difficult to understand is that large, relatively harmless bacteria common to the mouth, change and adapt to new conditions. They shrink in size to fit the cramped quarters and even learn how to exist (and thrive!) on very little food. Those that need oxygen mutate and become able to get along without it. In the process of adaptation these formerly friendly "normal" organisms become pathogenic (capable of producing disease) and more virulent (stronger) and they produce much more potent toxins.

Today's bacteriologists are confirming the discoveries of the Price team of bacteriologists. Both isolated in root canals the same strains of streptococcus, staphylococcus and spirochetes.

MJ Is everyone who has ever had a root canal filled made ill by it?

GM No. We believe now that every root canal filling does leak and bacteria do invade the structure. But the variable factor is the strength of the person's immune system. Some healthy people are able to control the germs that escape from their teeth into other areas of the body. We think this happens because their immune system lymphocytes (white blood cells) and other disease fighters aren't constantly compromised by other ailments. In other words, they are able to prevent those new colonies from taking hold in other tissues throughout the body. But over time, most people with root filled teeth do seem to develop some kinds of systemic symptoms they didn't have before.

MJ It's really difficult to grasp that bacteria are imbedded deep in the structure of seemingly-hard, solid looking teeth.

GM I know. Physicians and dentists have that same problem, too. You really have to visualize the tooth structure - all of those microscopic tubules running through the dentin. In a healthy tooth, those tubules transport a fluid that carries nourishment to the inside. For perspective, if the tubules of a front single-root tooth, were stretched out on the ground they'd stretch for three miles!

A root filled tooth no longer has any fluid circulating through it, but the maze of tubules remains. The anaerobic bacteria that live there seem remarkably safe from antibiotics. The bacteria can migrate out into surrounding tissue where they can "hitch hike" to other locations in the body via the bloodstream. The new location can be any organ or gland or tissue, and the new colony will be the next focus of infection in a body plagued by recurrent or chronic infections.

All of the "building up" done to try to enhance the patient's ability to fight infections - to strengthen their immune system - is only a holding action. Many patients won't be well until the source of infection - the root canal tooth - is removed.

MJ I don't doubt what you're saying, but can you tell us more about how Dr. Price could be sure that arthritis or other systemic conditions and illnesses really originated in the teeth - or in a single tooth?

GM Yes. Many investigations start with the researcher just being curious about something - and then being scientifically careful enough to discover an answer, and then prove it's so, many times over. Dr. Price's first case is very well documented. He removed an infected tooth from a woman who suffered from severe arthritis. As soon as he finished with the patient, he implanted the tooth beneath the skin of a healthy rabbit. Within 48 hours the rabbit was crippled with arthritis!

Further, once the tooth was removed the patient's arthritis improved dramatically. This clearly suggested that the presence of the infected tooth was a causative agent for both that patient's and the rabbit's - arthritis.

[Editor's Note - Here's the story of that first patient from Dr. Meinig's book: "(Dr. Price) had a sense that, even when (root canal therapy) appeared successful, teeth containing root fillings remained infected. That thought kept prying on his mind, haunting him each time a patient consulted him for relief from some severe debilitating disease for which the medical profession could find no answer. Then one day while treating a woman who had been confined to a wheelchair for six years from severe arthritis, he recalled how bacterial cultures were taken from patients who were ill and then inoculated into animals in an effort to reproduce the disease and test the effectiveness of drugs on the disease.

With this thought in mind, although her (root filled) tooth looked fine, he advised this arthritic patient, to have it extracted. He told her he was going to find out what it was about this root filled tooth that was responsible for her suffering. "All dentists know that sometimes arthritis and other illnesses clear up if bad teeth are extracted. However, in this case, all of her teeth appeared in satisfactory condition and the one containing this root canal filling showed no evidence or symptoms of infection. Besides, it looked normal on x-ray pictures.

"Immediately after Dr. Price extracted the tooth he dismissed the patient and embedded her tooth under the skin of a rabbit. In two days the rabbit developed the same kind of crippling arthritis as the patient - and in ten days it died.

"..The patient made a successful recovery after the tooth's removal! She could then walk without a cane and could even do fine needlework again. That success led Dr. Price to advise other patients, afflicted with a wide variety of treatment defying illnesses, to have any root filled teeth out."]

In the years that followed, he repeated this procedure many hundreds of times. He later implanted only a portion of the tooth to see if that produced the same results. It did. He then dried the tooth, ground it into powder and injected a tiny bit into several rabbits. Same results, this time producing the same symptoms in multiple animals.

Dr. Price eventually grew cultures of the bacteria and injected them into the animals. Then he went a step further. He put the solution containing the bacteria through a filter small enough to catch the bacteria. So when he injected the resulting liquid it was free of any infecting bacteria. Did the test animals develop the illness? Yes. The only explanation was that the liquid had to contain toxins from the bacteria, and the toxins were also capable of causing disease.

Dr. Price became curious about which was the more potent infective agent, the bacteria or the toxin. He repeated that last experiment, injecting half the animals with the toxin-containing liquid and half of them with the bacteria from the filter. Both groups became ill, but the group injected with the toxins got sicker and died sooner than the bacteria injected animals.

MJ That's amazing. Did the rabbits always develop the same disease the patient had?

GM Mostly, yes. If the patient had heart disease the rabbit got heart disease. If the patient had kidney disease the rabbit got kidney disease, and so on. Only occasionally did a rabbit develop a different disease - and then the pathology would be quite similar, in a different location.

MJ If extraction proves necessary for anyone reading this, do you want to summarize what's special about the extraction technique?

GM Just pulling the tooth is not enough when removal proves necessary. Dr. Price found bacteria in the tissues and bone just adjacent to the tooth's root. So we now recommend slow-speed drilling with a burr, to remove one millimeter of the entire bony socket. The purpose is to remove the periodontal ligament (which is always infected with toxins produced by streptococcus bacteria living in the dentin tubules) and the first millimeter of bone that lines the socket (which is usually infected).

There's a whole protocol involved, including irrigating with sterile saline to assure removal of the contaminated bone chips, and treating the socket to stimulate and encourage infection-free healing. I describe the procedure in detail, step by step, in my book [pages 185 and 186].

MJ Perhaps we should back up and talk about oral health - to PREVENT needing an extraction. Caries or inflamed gums seem much more common than root canals. Do they pose any threat?

GM Yes, they absolutely do. But let me point out that we can't talk about oral health apart from total health. The problem is that patients and dentists alike haven't come around to seeing that dental caries reflect systemic - meaning "whole body" - illness. Dentists have learned to restore teeth so expertly that both they and their patients have come to regard tooth decay as a trivial matter. It isn't.

Small cavities too often become big cavities. Big cavities too often lead to further destruction and the eventual need for root canal treatment.

MJ Then talk to us about prevention.

GM The only scientific way to prevent tooth decay is through diet and nutrition. Dr. Ralph Steinman did some outstanding, landmark research at Loma Linda University. He injected a glucose solutioninto mice - into their bodies, so the glucose didn't even touch their teeth. Then he observed the teeth for any changes. What he found was truly astonishing. The glucose reversed the normal flow of fluid in the dentin tubules, resulting in all of the test animals developing severe tooth decay! Dr. Steinman demonstrated dramatically what I said a minute ago: Dental caries reflect systemic illness.

Let's take a closer look to see how this might happen. Once a tooth gets infected and the cavity gets into the nerve and blood vessels, bacteria find their way into those tiny tubules of the dentin. Then no matter what we do by way of treatment, we're never going to completely eradicate the bacteria hiding in the miles of tubules. In time the bacteria can migrate through lateral canals into the surrounding bony socket that supports the tooth. Now the host not only has a cavity in a tooth, plus an underlying infection of supporting tissue to deal with, but the bacteria also exude potent systemic toxins. These toxins circulate throughout the body triggering activity by the immune system - and probably causing the host to feel less well. This host response can vary from just dragging around and feeling less energetic, to overt illness - of almost any kind. Certainly, such a person will be more vulnerable to whatever "bugs" are going around, because his/her body is already under constant challenge and the immune system continues to be "turned on" by either the infective agent or its toxins - or both.

MJ What a fascinating concept. Can you tell us more about the protective nutrition you mentioned?

GM Yes. Dr. Price traveled all over the world doing his research on primitive peoples who still lived in their native ways. He found fourteen cultural pockets scattered all over the globe where the natives had no access to "civilization" - and ate no refined foods.

Dr. Price studied their diets carefully. He found they varied greatly, but the one thing they had in common was that they ate whole, unrefined foods. With absolutely no access to tooth brushes, floss, fluoridated water or tooth paste, the primitive peoples studied were almost 100% free of tooth decay. Further - and not unrelated - they were also almost 100% free of all the degenerative diseases we suffer - problems with the heart, lungs, kidneys, liver, joints, skin (allergies), and the whole gamut of illnesses that plague Mankind. No one food proved to be magic as a preventive food. I believe we can thrive best by eating a wide variety of whole foods.

MJ Amazing. So by "diet and nutrition" for oral (and total) health you meant eating a pretty basic diet of whole foods?

GM Exactly. And no sugar or white flour. These are (and always have been) the first culprits. Tragically, when the primitives were introduced to sugar and white flour their superior level of health deteriorated rapidly. This has been demonstrated time and again. During the last sixty or more years we have added in increasing amounts, highly refined and fabricated cereals and boxed mixes of all kinds, soft drinks, refined vegetable oils and a whole host of other foodless "foods". It is also during those same years that we as a nation have installed more and more root canal fillings - and degenerative diseases have become rampant. I believe - and Dr. Price certainly proved to my satisfaction - that these simultaneous factors are NOT coincidences.

MJ I certainly understand what you are saying. But I'm still a little shocked to talk with a dentist who doesn't stress oral hygiene.

GM Well, I'm not against oral hygiene. Of course, hygiene practices are preventive, and help minimize the destructive effect of our "civilized", refined diet. But the real issue is still diet. The natives Dr. Price tracked down and studied weren't free of cavities, inflamed gums, and degenerative diseases because they had better tooth brushes!

It's so easy to lose sight of the significance of what Dr. Price discovered. We tend to sweep it under the rug - we'd actually prefer to hear that if we would just brush better, longer, or more often, we too could be free of dental problems.

Certainly, part of the purpose of my book is to stimulate dental research into finding a way to sterilize dentin tubules. Only then can dentists really learn to save teeth for a lifetime. But the bottom line remains: A primitive diet of whole unrefined foods is the only thing that has been found to actually prevent both tooth decay and degenerative diseases.

(This article was excerpted from http://www.mercola.com, the best health newsletter on the interent. Dr. Meinig's book, The Root Canal Cover Up, is available on Amazon.com)

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Are Nanobacteria Making Us Ill?
www.Wired.com
By Amit Asaravala|
02:00 AM Mar, 14, 2005

Olavi Kajander didn't mean to discover the mysterious particles that have been called the most primitive organisms on Earth and that could be responsible for a series of painful and sometimes fatal illnesses.

He was simply trying to find out why certain cultures of mammalian cells in his lab would die no matter how carefully he prepared them.

So the Finnish biochemist and his colleagues slipped some of their old cultures under an electron microscope one day in 1988 and took a closer look. That's when they saw the particles. Like bacteria but an astonishing 100 times smaller, they seemed to be thriving inside the dying cells.

Believing them to be a possible new form of life, Kajander named the particles "nanobacteria," published a paper outlining his findings and spurred one of the biggest controversies in modern microbiology.

At the heart of the debate is the question of whether nanobacteria could actually be a new form of life. To this day, critics argue that a particle just 20 to 200 nanometers in diameter can't possibly harbor the components necessary to sustain life. The particles are also incredibly resistant to heat and other methods that would normally kill bacteria, which makes some scientists wonder if they might be an unusual form of crystal rather than organisms.

In 1998, Kajander tried to prove the skeptics wrong by turning up what he believed to be an example of nanobacteria's ribosomal RNA, something that only organisms have. But the claim was squashed two years later by a National Institutes of Health study, which found that the RNA was actually a remnant from a type of bacteria that often contaminates lab equipment.

The debate would have ended there, except for a steadily increasing number of studies linking nanobacteria to serious health problems, including kidney stones, aneurysms and ovarian cancer. The studies show that nanobacteria can infect humans, a find that has helped push nanobacteria back into the limelight. Now the pressure is on to resolve the controversy and expose how nanobacteria works -- no matter what it is.

"It's all pretty exciting stuff," said David McKay, chief scientist for astrobiology at NASA's Johnson Space Center. "Whether these are bacteria or not -- it doesn't matter at this point. What matters is if we can figure out the association between nanobacteria and kidney stones and develop some kind of countermeasure."

The link between nanobacteria and human diseases was first noticed by Kajander and microbiologist Neva Çiftçioglu in 1998. The researchers had observed, through an electron microscope, nanobacteria particles building shells of calcium phosphate around themselves. They began to investigate whether such particles played a role in causing kidney stones, which are also made of calcium compounds. Sure enough, at the center of several stones was a nanobacteria particle.

Another breakthrough came in 2003 when a team from the University of Vienna Medical Center discovered nanobacteria in the calcified debris found in tissue samples from ovarian cancer patients. Meanwhile, several other studies revealed nanobacteria in samples of calcified arteries.

Sensing a growing need for tools to detect and study nanobacteria, Kajander and Çiftçioglu formed a company called NanoBac in 1998. The decision was greatly criticized as a conflict of interest and is still brought up whenever either of the two publishes a new paper.

Fortunately for the researchers, a 2004 study by the esteemed Mayo Clinic supported many of their key findings and helped them regain some of their support. The Mayo study found that nanobacteria do indeed self-replicate, as Kajander had noticed, and endorsed the idea that the particles are life forms.

Kajander and Çiftçioglu were further vindicated this February when patients with chronic pelvic pain -- thought to be linked to urinary stones and prostate calcification -- reported "significant improvement" after using an experimental treatment provided by Nanobac Life Sciences, which now owns NanoBac. The study was conducted by a team at Cleveland Clinic Florida.

There's a lot riding on studies like these. Roughly 177,500 patients were discharged from U.S. hospitals with kidney stones and related problems in 2001, according to the NIH. More than 25,000 women in the United States are diagnosed with ovarian cancer each year. In the same period, 14,000 Americans die from complications caused by calcified arteries.

"It brings up a lot of questions," said John Lieske, who led the 2004 Mayo Clinic study. "How many kidney stones are caused by this? Are there other calcification-related diseases that are caused by nanobacteria? Is it infectious?"

Surprisingly, few groups are actually working on answering these questions. One would be hard-pressed to find more than a half-dozen research teams around the globe studying nanobacteria full time.

Lieske suggests it's because the field is still relatively young. But it's clear that there's an additional culprit: the often heated controversy over whether nanobacteria particles are, in fact, alive.

"There's a reluctance to get into controversial areas. It's hard to get proposals funded," said McKay. "Most people are waiting until there's a little more meat on the bones."

Even John Cisar, who led the 2000 NIH study that contradicted Kajander's initial findings, agrees that the issue has become muddled. Though he maintains his stance that nanobacteria are not alive, he said in a phone interview that he is not against further research.

"I'm not saying there's nothing there," said Cisar. "It's just that we were looking at it from a microbiologist's perspective. And when we didn't find any signs of life, we moved on."

Kajander stands by his original assertion that nanobacteria are life forms. However, he blames himself for getting researchers hung up on the life question by using the name "nanobacteria."

"Calcifying self-propagating nanoparticles would have been much better," he wrote in an e-mail to Wired News.

But he added that his regrets about the name don't change the fact that nanobacteria have "miraculous" properties. Those include a growth cycle that closely matches typical biological cycles, the ability to form a shell and the "presence of both mammalian and bacterial components."

It's these properties -- and the potential to save lives -- that keep researchers focused on nanobacteria.

In February, NASA's McKay and Nanobac's Çiftçioglu announced that they had observed nanobacteria growing at five times its normal rate after they placed it in an incubator that simulates the microgravity conditions of space. The findings mean astronauts may be at an elevated risk for kidney stones on long flights -- something NASA is extremely worried about in light of its new plans to send humans to Mars.

The findings could also add fuel to nanobacteria research by giving scientists a way to grow cultures faster.

"The trouble with studying nanobacteria is that trying to get enough material is very hard," said Lieske. "Trying to culture a lot of it takes time."

Indeed, nanobacteria particles double about once every three days. In comparison, typical bacteria double about every 20 minutes.

Lieske's group has continued to experiment with nanobacteria since its 2004 paper. Though he said the team is looking for evidence of DNA and RNA, he is cautious about saying whether he thinks the particles are alive or just an unknown form of crystal.

As a possibility, he offered a third option: The particles could be a form of archaea, a relatively new category of tiny organisms whose DNA is vastly different from that found in typical bacteria. Over the past two decades, archaea have surprised scientists by turning up in places where life was least expected, like in sulfurous lakes and hydrothermal sea vents.

Whatever the case, the Mayo Clinic team may publish a paper outlining new findings in about six months, according to Lieske.

The world may not be waiting, but a handful of faithful microbiologists certainly will.

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Do Clouds Harbor Infectious Nanobacteria?
Clouds May Harbor Nanobacteria
www.wired.com

By Amit Asaravala
02:00 AM Apr, 11, 2005

Tiny particles linked to a number of painful and sometimes deadly diseases may spread across the globe by hitching a ride in clouds, claim researchers in a recent issue of the Journal of Proteome Research.

The particles, known as nanobacteria, are 100 times smaller than typical bacteria and have been found in kidney stones, arterial plaques and ovarian cancers.

But scientists have yet to agree whether the particles actually cause the diseases or how they infect humans.

Also unknown is whether the particles are life forms or an unknown type of crystal -- a rift that has sparked one of the biggest controversies in modern microbiology.

Now, a new theory by Andrei Sommer, of the University of Ulm, Germany, and N. Chandra Wickramasinghe, of Cardiff University in the United Kingdom, attempts to show how nanobacteria moves from humans to the environment and back.

In a letter in the February issue of the Journal of Proteome Research, the pair describe studies suggesting that nanobacteria exist in the atmosphere -- at least above Hyderabad, India, where the researchers captured samples of the air with a specially designed balloon.

The nanobacteria particles closely resembled those found in humans when compared on seven key criteria, including size and shape -- a finding that suggests humans can be infected through the atmosphere.

In the journal's introduction to the paper, Sommer theorizes that the particles may be introduced to the atmosphere through human urine, which enters waste-water streams and becomes aerosolized.

Once in the atmosphere, the nanobacteria can fall back to Earth in dry or wet form. The researchers think dry forms are relatively harmless, but wet forms, in raindrops, would be more likely to be infectious because the nanobacteria would still be "active."

"Inactive, transiently desiccated microorganisms, transported back from the dry atmosphere to the Earth by gravity, are likely to cause little harm, compared to those returning in rain drops, after having been incorporated for some time in long-lived clouds, where they would encounter better conditions for revitalization," wrote the researchers.

The researchers also suggested that nanobacteria could help clouds develop by clumping together at the perfect size to promote the collection of airborne water droplets.

Attempts to contact Sommer and Wickramasinghe after business hours Friday were unsuccessful.

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Is There Any Real Medical Evidence of Nanobacteria as a Cause of Chronic Disease?

New Evidence on Infection as Chronic Disease Trigger Published, Debated by
World-Class Scientists

Cutting Edge Research Aimed at Redefining the Way Doctors Diagnose and Treat Disease

TAMPA, FL (Dec. 20, 2006) New evidence that may help solve one of the great puzzles of 21stcentury medicine was published today in a special section of the Journal of Investigative Medicine. It features leading scientists in the field brought together by The American Federation for Medical Research and the American Physiological Society.

Is chronic disease triggered by an infection? New evidence comes from scientists at NASA, Mayo Clinic, and Nanobac Pharmaceuticals who pioneered investigations into infectious calcifying particles. A condition known as calcification occurs in most diseases on the leading cause of death list and in illnesses such as kidney, gallbladder and prostate stones. Calcification is also linked to chronic inflammation in atherosclerosis and end-stage renal disease, but it is unclear how this occurs.

Half-a-dozen papers in the Journal resulted from a symposium that assembled, for the first time in medical history, experts from biology, medicine and geology to debate these possible causes of calcification: chemical crystallization; cell-mediated crystallization; and potentially infectious calcifying nanoparticles (CNPs) that generate calcification.

One conclusion by symposium organizers: Although infection is just one of three potential causes of calcification, it deserves focus as a chronic disease trigger, based on new evidence presented. "Increasingly, micro-organisms are being identified as an unexpected cause of disease..." writes symposium co-organizer and Mayo Clinic scientist Dr. Virginia Miller.

The symposium considered works by Dr. Neva Ciftcioglu and Dr. Olavi Kajander, lead scientists with Nanobac Pharmaceuticals, as well as two other works by Mayo researchers, which provide evidence that calcifying nanoparticles might be infectious and spark calcification in disease.

Although Dr. Miller says the idea of infectious nanoparticles is still controversial, she concludes that, "Nanoparticles might serve as an inflammatory stimulus that initiates cell transdifferentiation, stimulate the formation of matrix vesicles, or simply form a nidus for subsequent inorganic calcium accumulation."

Participants in the symposium included scientists from such world-class institutions as UCLA and various institutes in Europe. Scientists from Nanobac Pharmaceuticals are the leading investigators on the issue of infection as a possible cause of calcification, and have published the most papers on this topic.

Participants list:

Neva Ciftcioglu, Ph.D., director of science at Nanobac Pharmaceuticals, is one of the scientists who originally isolated nanoparticles from mammalian blood and, working at NASA's Johnson Space Center, presented concepts of nanoparticles as a nidi for biomineralization.

Neal X. Chen, Ph.D., assistant professor in the Department of Medicine at Indiana University, reviews mechanisms of cell transdifferentiation and crystallization in renal cells.

John C. Lieske, MD, associate professor of Medicine, Mayo Clinic College of Medicine, continued the theme of calcification of renal tissue, in particular Randall's plaques, by presenting evidence for self-replicating, self-calcifying nanoparticles in renal stones.

Linda L. Demer, MD, Ph.D., professor of medicine, Division of Cardiology, The David Geffen School of Medicine at UCLA, reviewed transdifferentiation of vascular smooth muscle cells to a boneassociated phenotype and the importance of RANKL and receptor in that process.

Howard H.T. Hsu, Ph.D., associate professor, Department of Pathology, University of Kansas Medical Center, reviewed data supporting the contribution of matrix vesicles to vascular calcification and presents a provocative theory of the stimuli involved in their formation.

Karim Benzerara, Ph.D., Institut de Mineralogis et de Physique des Milieux Condenses and Institut de Physique du Globe of Paris, France, demonstrates how the state-of-the-art scanning transmission X-ray microscopy and near-edge x-ray absorption fine structure (NEXAFS) can be used to define the biochemical characteristics of nanoparticles isolated from the environment and human tissue.

Virginia M. Miller, PhD., Professor of Surgery, Mayo Clinic College of Medicine, symposium coorganizer.

For more information or to schedule a briefing/interview please contact Carson Chandler (202) 367-1625, cchandler@akerpartners.com or Matt Taylor (202) 367-1631, hyperlink.

About Nanobac Pharmaceuticals: Nanobac Pharmaceuticals Inc. ((OTCBB:NNBP)) is dedicated to the discovery and development of products and services to improve human health through the detection and treatment of calcifying nanoparticles (CNPs). The company's pioneering research is establishing the pathogenic role of CNPs in soft tissue calcification, particularly in coronary artery, prostate and vascular disease. Nanobac's drug discovery and development is focused on new and existing compounds that effectively inhibit, destroy or neutralize CNPs.

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Can Hidden Infections Be a Major Cause of Mental Illness?
The Infection Connection - how infections might be partly responsible for mental illnesses

Psychology Today, July, 1999

by Harriet Washington


PSYCHOLOGY HAS LONG HELD THAT MENTAL ILLNESS IS BORN OF ADVERSE EXPERIENCES. MORE RECENTLY, RESEARCH HAS POINTED THE FINGER AT FLAWED GENES. NOW A THIRD CULPRIT MAY BE EMERGING: INVASION BY BACTERIA AND VIRUSES.

Eight-year-old Seth broke from the grasp of Jane, his harries mother, for the third time in 10 minutes. Tering across the emergency room, he stopped short, transfixed by a piece of paper lying on the floor. His ref-rimed eyes seemed to bulge from their sockets and his mouth twitched violently, as if he were in pain. Indifferent to Jane's pleas to stop, he proceeded to pick up from the floor every piece of paper, no matter how filthy, with hands that were reddened and raw. It was the state of his hands that had precipitated the trip to the hospital: Seth had spent most of the night in the bathroom, washing them over and over.

With his head jerking spasmodically and his fingers pecking at pieces of paper and cigarette butts, the boy resembled some strange overgrown bird. Then, suddenly terrified, he flew back to Jane and began pulling on her arm. "Mommy, Mommy, let's leave!" he whimpered. "They're going to kill us. They're coming!"

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Jane tried her best to calm him, but she too was beginning to panic. Two days before, Seth had been a perfectly normal little boy whose most serious health problems were the occasional cold or sore throat. He had become mentally ill overnight.

What caused Seth's anxiety, his tics, his obsessive-compulsive behavior? Astonishingly, it was probably that minor sore throat, his doctors concluded. Today, scientists are increasingly coming to recognize that the bacteria and viruses that frequently invade our bodies and cause sore throats and other minor ailments may also unleash a host of major mental and emotional illnesses, including anorexia, schizophrenia and obsessive-compulsive disorder.

It is a theory sharply at odds with earlier views of the genesis of psychological illness. Followers of Freud long held that mental and emotional trouble is primarily the result of poor parenting, especially by mothers. Indeed, until about 30 years ago, psychoanalysts frequently placed the blame for schizophrenia on "schizophrenogenic" mothers. Obsessive-compulsive disorder, also, was put at Mom's door. "It was thought to be the result of harsh toilet training," observes Susan Swedo, M.D., chief of pediatrics and developmental neuropsychiatry at the National Institutes of Mental Health. But such theories, which added immeasurable guilt to the burdens of parents with mentally ill offspring, have turned out to have little evidence to back them up, most experts now agree.

Instead, in recent years, the focus has shifted to genes as the main source of mental illness. Faulty DNA is thought to be at least partly responsible for, among other problems, anxiety and panic disorders, schizophrenia, manic depression and antisocial personality disorder, which is characterized by impulsive, excessively emotional and erratic patterns of interpersonal behavior.

Yet genetics doesn't appear to wholly account for the occurrence of major psychiatric ailments. If heredity alone were to blame, identical twins would develop schizophrenia with a high degree of concordance, but in fact in only 40% of cases in which one identical twin has the disease does the other twin have it as well. Autism, though it has been observed to run in families, also strikes five of every 10,000 children apparently arbitrarily Nor can depression and other affective disorders be completely explained by damaged DNA. Says Ian Lipkin, Ph.D., a neuroscientist and microbiologist at the University of California at Irvine: "Genetics doesn't hold the key to understanding how to fit these square pegs into round holes."

Bacteria and viruses may be that key, but scientists have been slow to grasp the idea. Consider the case of syphilis, which is caused by the bacterium Treponema pallidum. In its final, or tertiary, stage, the disease can precipitate psychiatric problems like dementia, mania, depression, delusions and Tourette's like tics. Though some scientists' suspected a connection between infection with the bacterium and the mental disturbances that may take three to live decades to emerge, the link became widely accepted only in the 1940s after the introduction of the antibiotic penicillin as a treatment for syphilis. In the interim, patients with syphilis who later developed psychiatric problems were often institutionalized as crazy But even with the link established, Freud's theories were in ascendance and few scientists were willing to consider that microbes might be a common source of other mental illness.

Now, decades later, infection has emerged as a prime suspect in psychological illnesses. The inadequacy of genetic and experiential explanations has prompted scientists to look elsewhere--and their gaze has come to rest on physical ailments, such as heart disease, cancers and ulcers, that in some cases have an infectious origin. Could the same be true, they wonder, for mental and emotional ills?

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What Does Medical Science Know About the Infectious Basis of Mental Illness?
The Role of Infections in Mental Illness

by Frank Strick, Clinical Research Director

THE RESEARCH INSTITUTE FOR INFECTIOUS MENTAL ILLNESS (RIIMI)

Call 1800 6992466 then press pound (#) 8314255555; E-mail: riimiusa@gmail.com

San Francisco, USA

In considering an infectious etiology to any chronic mental illness there are at least four categories to consider. First are those infections already recognized to induce psychiatric symptoms. These include pneumonia, urinary tract infection, sepsis, malaria, Legionnaire's disease, syphilis, typhoid, diphtheria, HIV, rheumatic fever and herpes. (Ref: Chuang)

While the psychiatric effects of these infections are known to the medical field, they are rarely screened for if the initial presentation is made to a mental health professional. Moreover, the significance of some of these infections may date back to prenatal development. Research done at the John Hopkins Children's Center and published in the Archives of General Psychiatry in 2001 found that mothers with evidence of Herpes Simplex Type 2 infection at the time of pregnancy had children almost six times more likely to later develop schizophrenia. And in the US, Europe and Japan, birth clusters of individuals who develop schizophrenia later in life closely mirror the seasonal distribution of Ixodes ticks at the time of conception (Lyme disease).

Second are those parasitic infections such as neurocysticercosis where the brain is directly invaded by the infective agent through a well-established, imageable (visible on brain scan) mechanism (cysts, lesions, cerebral swelling etc.) Signs of psychiatric disease (depression and psychosis) were found in over 65% of neurocysticercosis cases (caused by a tapeworm whose incidence in the US is rising due to demographic increases in foreign immigrant populations.) [Ref: Forlenza] While the mechanisms for psychiatric manifestations are easy to demonstrate when brain tissue is directly affected, there are also multiple documented reports in the literature of psychiatric symptoms associated with other parasites like giardiasis, ascaris (roundworm), trichinae (cause of trichinosis), and Lyme borrelia and viruses like borna virus. Documentation also exists of these psychiatric symptoms resolving when the underlying hidden infection is treated.

Dr. J. Packman of Yale University wrote over ten years ago that "Patients with parasitic loads are more likely to exhibit mental status changes and there is an improvement in mental status of a subset of psychiatric patients following treatment for parasites." In fact, a review of 1300 human cases of trichinosis in Germany found CNS (central nervous system) involvement in up to 24% of the cases (Menningeal inflamation or encephalitis). [Ref: Froscher]

Clinically, in cases like neurocysticercosis, the problem is not the lack of a well-defined mechanism but the lack of mental health practitioners qualified to make such a diagnosis or even suspect it. Even infectious disease specialists tend to underestimate the scope of the problem, in part due to underreporting (neurocysticercosis is not a reportable condition in most states and the incidence of trichinosis is, we believe, vastly underestimated according to newly developed antibody assays only made available in 2003).

Next are those parasitic, bacterial and viral infections like toxoplasmosis and strep where a strong statistical link to mental illness has been demonstrated but research is underway to establish a causal connection. In humans acute infection with toxoplasmosis gondii can cause brain lesions, changes in personality and symptoms of psychosis including delusions and auditory hallucinations. Researchers at Rockefeller University and NIMH have suggested that after streptococcal infection some children may be at increased risk for Obsessive Compulsive Disorder. Toxoplasma gondii can alter behavior and neurotransmitter function. Since 1953, eighteen out of nineteen studies of T. gondii antibodies in persons with schizophrenia and other severe psychiatric disorders have reported a higher percentage of T. gondii antibodies in the affected persons. (For example, in one large study toxoplasmosis infection was twice as common in mentally handicapped patients as in healthy controls and in a recent German study of "individuals with first episode schizophrenia compared to matched controls, 42% of the former compared to just 11% of the latter had antibodies to toxoplasma").

Two other studies found that exposure to cats (the primary carrier for toxoplasmosis transmission) in childhood is a risk factor for the development of schizophrenia. Furthermore, certain antipsychotic and mood-stabilizer drugs such as Halperidol and Valproic acid inhibited this parasite in vitro at a concentration below that found in the cerebrospinal fluid and blood of individuals being treated with this medication, suggesting that some medications used to treat schizophrenia and bipolar disorder may actually work by inhibiting the replication of toxoplasmosis gondii. (Ref: Jones-Brando, Torrey, Yolken)

Other studies have shown that antipsychotic drugs like Thorazine, Haldol and Clozapine inhibit viral replication and that the cerebrospinal fluid of patients with recent-onset schizophrenia shows a significant increase in reverse transcriptase (an enzyme) activity - which is an important component of infectious retroviruses (a type of virus). Furthermore, when the CSF (cerebral spinal fluid) from these patients was used to inoculate a New World monkey cell line there was a tenfold increase in reverse transcriptase activity which suggests the presence of a replicating virus. Malhotra has demonstrated the absence of CCR5-32 homozygotes (specific matching genetic codes) in over 200 schizophrenic patients - which dramatically increases susceptibility to retroviral infection. (Ref: F.Yee).

It is research like this that has led Johns Hopkins virologist Robert Yolken and psychiatry professor and former special assistant to the Director of the National Institute for Mental Health Dr. E. Fuller Torrey to believe that toxoplasmosis is one of several infectious agents that causes most cases of schizophrenia and bipolar disorder. The idea is not new. In fact, as far back as 1922 the famous psychiatrist Karl Menninger hypothesized that schizophrenia was "in most instances the byproduct of viral encephalitis." Torrey notes that in the late nineteenth century schizophrenia and bipolar disorder went from being rare diseases to relatively common ones at the same time that cat ownership became popular. And Yolken designed a retrospective study of twenty-five hundred families showing that mothers of children who later developed psychoses were 4.5 times more likely to have antibodies to toxoplasmosis than the mothers of healthy controls. Due to the frequency of cat ownership, a large percentage of the US population (up to 50%) has been exposed to toxoplasmosis but most immunocompetent carriers remain asymptomatic until another immunological burden such as HIV or a separate parasite weakens the host defenses and precipitates pathogenic expression. That is what makes interpretation of the chronic state so tricky and at the Research Institute for Infectious Mental Illness we make sure to try to identify any parasitic coinfections before deciding on an appropriate course of treatment.

Finally, while toxoplasmosis gets a lot of attention due to Torrey's and Yolken's pioneering studies and the known mechanism of brain lesions, there are many other infective agents that may not target the brain specifically but can severely affect mental function through the cumulative downstream consequences of chronic infection. While the importance of this link in the etiopathogenesis of mental illness is rarely recognized, these focal and systemic infections are very common and their psychiatric effects often severe. (Parasites are the most common causes of mortality and morbidity in the world.) In this nonspecific category are scores of parasites, protozoa, helminths, bacteria, fungi and viruses which, if not directly invading and disabling brain tissue and neurotransmitter function, do so indirectly by depleting the host of essential nutrients, interfering with enzyme functions, and releasing a massive load of waste products - enteric poisons and toxins which disrupt brain metabolism. (A single mature adult tapeworm can lay a million eggs a day and roundworms, which infect about twenty-five per cent of the world's population, lay 200,000 daily).

Remember, the brain is your body's most energy-intensive organ. It represents only three percent of your body weight but utilizes twenty-five percent of your body's oxygen, nutrients and circulating glucose. Therefore any significant metabolic disruptions can impact brain function first. This link is borne out statistically. Mental patients have much higher rates of parasitic infection than the general population. Between 1995 and 1996 researchers at the University of Ancona did stool tests on 238 residents of four Italian psychiatric institutions and found parasites in 53.8 percent of the residents including all of those residents with behavioral aberrations(Ref: Giacometti). In our experience parasites are often implicated in cognitive dysfunction and chronic emotional stress disorders and, to the untrained eye, classic symptoms like apathy, exhaustion, confusion, appetite and memory loss, "nervous stomach," social withdrawal, lethargy and loss of sex drive and motivation are frequently assumed to signal a depressive disorder without an adequate differential diagnosis being made or even attempted. Adding to the confusion, classic indicators of acute infection such as fever or elevated antibodies often reverse themselves in chronic cases due to secondary hypothyroidism and immunodepression. Unfortunately, until Western psychiatry further recognizes that the mind/body connection goes in both directions patients will continue to suffer from a de facto lack of differential diagnostic criteria in clinically identical syndromes.

Even for those clinicians who recognize the devastating psychological effects that chronic intestinal, focal and even dental infections can have on normal brain function, accurate diagnosis presents formidable challenges. In fact some standard parasite stool test procedures identify less than ten percent of active infections and even the "politically correct" holistic specialty labs miss many infections that are nondetectable in fecal specimens, have inconsistent shedding patterns, are extra intestinal or otherwise hard to identify. For example, according to the World Health Organization, over two billion people are infected with worms, yet rarely will they show up in stool assays.

(These numbers are not surprising once you realize that the exposure vectors are potentially everything you eat, drink, breathe and touch. If you think you have to leave the country to be exposed to exotic parasites, think again. In fact, try walking into the kitchen of your favorite restaurant and see if the cook speaks English.)

At the Research Institute for Infectious Mental Illness we use multiple labs with complementary strengths and a combination of advanced scientific diagnostic procedures including O & P microscopy, multifluid antigen and antibody detection, stool cultures, enzyme immunoassay, mucosal markers, inflammation assays, imaging techniques and other indirect laboratory indicators combined with extensive historical and clinical evaluations to identify chr