But the results of a recent study show it’s also likely that some of the chronic bacterial species that cause inflammatory disease can remain alive in breast milk and thus be passed from mother to child by breast feeding. While the study, conducted by researchers at the University of Turku in Finland, indicates that a virus can be passed in breast milk during feeding, the fact that the Th1 pathogens have evolved so many survival mechanisms and are such persistent pathogens strongly suggests that at least some of them possess the same capability.

More specifically, the Finnish research team found that Human papillomavirus type 16 (also called high-risk HPV-16), which has been linked to cervical cancer, can be detected in human breast milk collected during the early period after a woman delivers her baby. According to the team, the fact that viral particles survive in breast milk greatly implies that infants can acquire oral HPV infection via breast feeding.

HPV attacking a cell

The findings are supported by previous research in which Syrjanen, a pathologist at the University of Turku, and colleagues found evidence of transmission of HPV from an infected mother to her newborn infant. The discovery led them to initiate the Finnish HPV Family Study, the goal of which is to elucidate the transmission modes of HPV between family members.

For their current report, Syrjanen’s team looked for HPV in cervical scrapings obtained from 223 mothers and in oral scrapings from 87 fathers. Then, they performed HPV testing of the breast milk samples 3 days postpartum. High-risk HPV DNA was detected in 10 milk samples (4.5 percent) and DNA sequencing from nine samples confirmed that the virus was indeed high-risk HPV-16.

Interestingly, a statistically significant correlation was also found between HPV in milk and the presence of high risk-HPV in oral scrapings obtained from the father.

According to Syrjanen, this means transmission could have occurred by the spouse, from the mouth to the nipple and then to the breast, or it could have occurred from the mother’s hands. If HPV and other pathogens can remain alive in the sperm, it could also be hypothesized that some fathers simply pass their infants HPV while they are in the womb. Since chances are high that the father has also passed the virus to the mother (or it could have been the other way around!) HPV could end up in her breast milk as well.

So why are so many adults infected with HPV in the first place? It boils down to the reality that many of them also harbor high levels of the Th1 pathogens. Since the Th1 pathogens are able to create ligands that slow the activity of the Vitamin D Receptor and subsequently the innate immune response, their presence creates an atmosphere in which it’s also easy for co-infectious agents like HPV to survive.

One thing’s for sure. Pathogens are stealthy. The conventional belief that washing hands and covering the mouth after sneezing largely prevents their spread will almost certainly be replaced by the knowledge that they can be passed much more easily among family members. So it’s not defective genes we’re sharing…it’s crafty pathogens!

Just this month, researchers led by John H. Werren at the University of Rochester in New York elucidated yet another way that bacterial DNA is likely passed from person to person. This demonstrates just how easy it is for bacterial DNA to become incorporated into human DNA – a reality that is central to biomedical researcher Trevor Marshall’s model of chronic disease in which pathogens are constantly swapping genetic material with each other and their host.

The study describes how due to horizontal gene transfer – or the reality that once inside the body, organisms swap genetic material with each other, and also with the host – bacterial DNA often ends up integrated into human DNA. This integrated genetic material is then passed from generation to generation, and it is very likely that many of these acquired segments of DNA may help bacteria survive more easily in the body. “Our data are indicating that [DNA transfer] is going on all the time,” says Werren.

“The mechanism therefore provides an alternative to mutation of existing DNA as a way for the species to acquire new genetic traits,” states Patrick Barry of Science News. “The transfer of DNA from bacteria means that an individual could acquire and pass on genes that it had not inherited.”

Warren’s team looked at several species of insects and roundworms infected by a parasitic bacterium called Wolbachia pipientis. The bacterium lives inside the animals’ cells, including their egg cells, giving it ready access to the chromosomes that are passed on to the animals’ offspring.

When the researchers compared the genetic code of the bacterium with the code of 11 other species: four roundworms, four fruit flies, and three wasps, they found that all but three of the fruit fly species had segments of the bacterium’s genetic code embedded in their DNA.

The team also scanned an archive of published genomes for 21 other invertebrate species and found bacterial genes in nine of them – proving that bacterial DNA can indeed be passed from mother to child. Whether this occurs in humans has not yet been demonstrated, but in principle, seems quite possible.

But this process has been taking place for centuries. Why hasn’t it been analyzed sooner?

“Such bacterial genetic code is routinely ignored during the sequencing of animals’ genomes because most scientists have assumed that the foreign DNA is a sign of contamination, Werren says. However, the new research rules out the possibility of contamination, says the scientist.

Sam’s mother suffers from fibromyalgia, accompanied by insomnia, fatigue, and irritable bowel disorder. His father recently had a stroke, and deals with substantial fatigue and depression. His older brother has debilitating back pain and is hard of hearing. His youngest sister suffers from alopecia, brain fog, depression, excessive fatigue, and mild attention deficit disorder. The youngest brother in the family has a severe case of bipolar disorder, as well as irritable bowel syndrome.

It’s obvious that every member of Sam’s immediate family harbors a substantial load of the Th1 pathogens and that these bacteria have, over time, spread from person to person. Clearly, just like other forms of bacteria, the Th1 pathogens can be passed around. Although Th1 diseases are not obviously contagious, they are communicable – meaning that transmission of chornic bacteria requires close contact and is seen often within the family unit. The pathogens can also be transmitted from person to person through bodily fluids released during coughing, sneezing and other intimate contact.

L-form bacteria can survive in sperm cells.

People whose parents harbor high loads of the Th1 pathogens are much more likely to fall ill with a Th1 disease earlier in life. Research indicates that L-form bacteria are able to survive in sperm, so a father can pass these pathogens to his child at the moment of conception. Evidence is also growing that L-form bacteria and other pathogens are able to cross the placental barrier – meaning they can be passed from a pregnant woman to her fetus.

Researchers at Peking University in Beijing recently discovered that the H5N1 bird flu virus can pass through a pregnant woman’s placenta to infect her fetus. Other studies have revealed that other bacterial species such as Borrelia burgdorferi and Mycobacterium tuberculosis are also capable of crossing the placental barrier during pregnancy. If these pathogens can be passed from mother to child during gestation, then why not other forms of bacteria that are capable of transforming into the L-form?

Successive infection

Infants born into families whose members harbor high loads of the Th1 pathogens are also more likely to pick up these bacteria after birth. As described here, it takes an infant several weeks to develop a fully functional innate immune system, meaning that during the first few weeks of life, infants are particularly vulnerable to bacteria passed around by other members of the family unit. But in order to fully understand what eventually causes an infant to develop a full-fledged Th1 disease, one must understand the concept of successive infection.

Inside every cell in the body are sequences of DNA that make up our genes. Over thousands of years, bacteria, viruses, bacteriophages, and other pathogens have evolved mechanisms that allow them to mutate and alter the expression of the genes inside the cells they infect. Researchers at the Institute of Genetics in China found that when the bacterial species Mycobacterium tuberculosis infects immune cells called macrophages, it causes mutations in about 70 genes and affects the expression of another 366.

The genes affected by pathogens inside a cell are active in regulating the activity of cytokines, coding for receptors on the surface of cells, regulating cell signaling pathways, monitoring cell death (apoptosis), controlling cell mediated immunity, regulating the production of proteins, creating enzymes, and many other essential processes.

Unfortunately, as pathogens gradually gain control over the genes that regulate the above processes, many of the mutations or changes in gene expression they produce can manipulate the host cell in order to aid their survival and reproduction. These changes also create an environment inside the cell that makes it easier for new pathogens to invade and persist. For example, Bukholm and team found that Measles virus infection of cell cultures makes the cells more susceptible to a secondary bacterial invasion. Quite a few species of bacteria have even developed the ability to use the Beta-lactams antibiotics in order to increase the likelihood of DNA sharing as they transform into the L-form.

“When one of the nasty bugs arrives, does it find your DNA intact in the cell it invades, or has the DNA already been altered by a previous pathogen?” asks Marshall. “If it tries to act on an altered gene, then the result will be different from if it acts on a ‘clean’ gene.”

Thus, as each subsequent pathogen that people encounter proceeds to make even more changes to their cellular DNA, eventually these mutations create a snowball effect where, as a person acquires an increasing number of pathogens, it becomes even easier for them to pick up a diverse array of other infectious agents.

In addition to the genetic changes that accumulate as a person encounters an increasing number of pathogens, some bacteria also alter the activity of the immune system by creating substances that bind and block the Vitamin D Receptor (VDR) – a fundamental receptor of the body that controls the activity of the innate immune system and the expression of the antimicrobial peptides (AMPs) – proteins that kill bacteria, viruses, and fungi by a variety of mechanisms including disrupting membranes, interfering with metabolism, and targeting components of the machinery inside the cell. As a person acquires more and more Th1 pathogens, the activity of their innate immune system decreases, and less antimicrobial peptides are produced, making it even easier for these pathogens to survive in the body and continue to alter human cellular DNA.

Inside every cell of the body are sequences of DNA that form genes.

But why do different members of a family develop different forms of Th1 disease? The key is that every person eventually encounters different pathogens and thus develops a unique infectious history. Maybe someone picks up various species of L-form bacteria from a roommate at college. Another person eats a contaminated piece of meat on their trip to Mexico, and on and on. The distinct mix of pathogens that each individual collects is sometimes referred to as their “pea-soup.”

Once a plethora of pathogens find themselves inside the same cell, there is no end to the number of interactions that may allow some species to develop a survival advantage. For example, researchers at the University of Washington found that when the bacterial species P. aeruginosa and S. aureus were incubated together, a protein created by P. aeruginos protected S. aureus from being killed by various forms of antibiotics. When the two pathogens were kept together for a longer period of time, P. aeruginos actually caused S. aureus to develop into small-colony variants, which are more difficult for the immune system to identify and kill.

Bacteria are very competitive, so some species have evolved mechanisms that allow them to gain dominance over other strains of bacteria. The final disease state that a person develops and the population structure of bacterial communities is also influenced by the sequence in which pathogens infect the body and their respective virulence.

It doesn’t help that the world teems with the Th1 pathogens. Because they cannot be killed by pasteurization or chlorination, they are found in food, milk, and water. Since they are too small to be filtered during the “purification” process used in pharmaceutical manufacturing procedures, they can also be found in injectable medicines. Whereas people with little previous exposure to the Th1 pathogens are often able to fend off a greater number of these bacteria in their immediate environment, those whose DNA has been altered since birth and whose innate immune system and AMPs are less active, can pick up chronic disease-causing bacteria much more easily.

It’s worth nothing that people taking high levels of vitamin D are at an even greater disadvantage, since, according to biomedical research Trevor Marshall, the precursor form of vitamin D is actually a secosteroid that also binds and blocks the VDR. “The epidemic of imbalance we are facing now, where the genomes of the microbiota which I call the ‘Th1 pathogens’ have started to gain dominance over the genome of their host, is due to mistakes made during the 20th century, particularly the decision to call “vitamin D” a vitamin,” says Marshall.

Marshall’s insight can also be applied to people who pass their partners the Th1 pathogens. As evidenced by progress reports on the Marshall Protocol study site, there are a substantial number of spouses who both suffer from Th1 disease. There are also entire families on the MP – with each member is using the treatment to eliminate his or her own pea-soup.

Thus, what changes between family members is the mix of species acquired, the sequence in which the pathogens are acquired, the subsequent mutations and changes in gene expression caused by the pathogens, and the profound changes to the body’s proteins, enzymes and metabolites caused by these factors. In most people these alterations develop slowly until they become obvious and diagnosable as a disease.

According to the Marshall Protocol study site, “What disease you develop and how quickly you develop it is determined by factors such as exposure (some species are acquired before birth), route of transmission (health care workers have a higher incidence of sarcoidosis), L-form species, virulence of the species and external stimuli.”

Horizontal DNA transfer also causes bacterial DNA to be passed from generation to generation

Just this month, researchers led by John H. Werren at the University of Rochester in New York elucidated yet another way that bacterial DNA is likely passed from person to person.

Due to horizontal gene transfer – or the reality that once inside the body, organisms swap genetic material with each other, and also with the host – bacterial DNA often ends up integrated into human DNA. This integrated genetic material is then passed from generation to generation, and it is very likely that many of these acquired segments of DNA may help bacteria survive more easily in the body. “Our data are indicating that [DNA transfer] is going on all the time,” says Werren.

“The mechanism therefore provides an alternative to mutation of existing DNA as a way for the species to acquire new genetic traits,” states Patrick Barry of Science News. “The transfer of DNA from bacteria means that an individual could acquire and pass on genes that it had not inherited.”

Warren’s team looked at several species of insects and roundworms infected by a parasitic bacterium called Wolbachia pipientis. The bacterium lives inside the animals’ cells, including their egg cells, giving it ready access to the chromosomes that are passed on to the animals’ offspring.

When the researchers compared the genetic code of the bacterium with the code of 11 other species: four roundworms, four fruit flies, and three wasps, they found that all but three of the fruit fly species had segments of the bacterium’s genetic code embedded in their DNA.

The team also scanned an archive of published genomes for 21 other invertebrate species and found bacterial genes in nine of them – proving that bacterial DNA can indeed be passed from mother to child. Whether this occurs in humans has not yet been demonstrated, but in principle, seems quite possible.

But this process has been taking place for centuries. Why hasn’t it been analyzed sooner?

“Such bacterial genetic code is routinely ignored during the sequencing of animals’ genomes because most scientists have assumed that the foreign DNA is a sign of contamination, Werren says. However, the new research rules out the possibility of contamination, says the scientist.

Moving away from the hypothesis of genetic predisposition

It’s obvious then, that most researchers are making a big mistake in assuming that the correlation between disease symptoms and mutated genes implies that genes (rather than the pathogens creating the genetic mutations) are responsible for the progression of an illness.

Clearly, humans accumulate a plethora of infections during their lifetimes, and it is the genetic mutations which result from active infection that play a major role in what is commonly thought of as “genetic susceptibility.” In the vast majority of diseases, parents do not pass on defective genes to their children. Instead, they often pass on the Th1 pathogens, which are the real underlying factor responsible for causing the symptoms of Th1 disease. Not that inherited genetic variations don’t have an effect in some very rare illnesses, but the vast majority of diseases result from successive infection.

Consider the fact that there is only a 20% chance that identical twins will both develop breast cancer. Geneticists attempt to explain this fact by saying that a person’s environment and upbringing can cause their genes to be expressed differently. These speculations have developed into a prominent “nature vs. nurture” debate.

But an understanding of successive infection should put a damper on these discussions as more researchers start to understand that the main environmental factor affecting the expression of genes is actually the unique mix of pathogens in any given place. Not that nurture won’t play a role – a good upbringing can help ensure that people learn to avoid high levels of vitamin D as well as immunosuppressive drugs that can hamper the activity of the immune system.

It’s true that twins are often more likely to develop the same illness. However it is quite likely that this is not because they share the same genes passed along through generations. Rather, disease correlation may result because twins are in the womb at the same time, and are exposed to the same Th1 pathogens through the mother’s placenta. Identical twins may have the highest risk of developing similar illnesses because they develop from the same sperm and egg, and thus carry the same Th1 pathogens as the sperm and egg. The genes inside the sperm and egg cells have also been mutated and consequently have the same influence on gene expression.

It comes as no surprise then, that after billions of dollars spent on research, not one gene therapy, not even research on the classic genes implicated in causing cystic fibrosis, has proven effective.

In fact, the statistical correlation in most gene studies is very low. “Part of the problem is that the folks computing the statistics are not the physicians who collected the data, and so there is a disconnect, and two disparate sets of knowledge are not quite meeting when discussing the meaning of statistical certainty,” says Marshall.

“The reason for this failure-to-perform is that the hypothesis is incorrect,” he continues. “What the researchers are seeing as changes on genes are indeed changes, but they only correlate at low levels of significance because they are due to pathogens. They are due to mutations from chronic infection. Consequently there is no causal effect – only an associative observation.”

Consider the fact that it takes most patients on the Marshall Protocol study site, who are killing intracellular bacteria at the fastest rate possible, over three years to completely recover their health. This hints at the huge amount of pathogen-altered DNA that many people, even those who are not yet displaying the hallmarks of Th1 disease, are carrying.

Surely this explains why, despite abundant research efforts, researchers have been unable to isolate any specific sequences of DNA that might make a person susceptible to a certain disease. They fail to consider that the predisposition for any Th1 illness is likely not genetic but acquired.

It is quite likely that in the coming years, medicine will move away from the hypothesis of genetic predisposition and towards the concept of successive infection. As this new understanding of the role that bacteria play in chronic disease spreads, the concept of inheritance may no longer refer to parents passing on a defective genes, but may instead be superseded by the notion that bacteria themselves are acquired from the mother during pregnancy, and through a father’s sperm.

Changing the definition of inheritance

No small number of researchers continue to cling to the idea that parents pass their children faulty genes. But if this is so, then why do multiple studies show that spouses – whose genetic backgrounds are not connected – have a higher risk of developing the same Th1 diseases that their partners have?

Pathogens such as Mycobacterium tuberculosis (seen here under electron microscope) can directly alter the expression of genes.

A six-year study of the Th1 disease sarcoidosis, conducted by the National Heart, Lung and Blood Institute at the National Institutes of Health (NIH) in Maryland found that among the 215 study participants who had been diagnosed with sarcoidosis, there were five husband-and-wife couples that both had the disease. Yet sarcoidosis is such a rare disease that based on statistics there should have been none. They also noted that the risk for sarcoidosis increased nearly five-fold in parents and siblings with the disease.

“It seems that the ‘germs’ [L-form bacteria] are passed around families pretty easily,” says biomedical researcher Trevor Marshall of Autoimmunity Research Foundation. “The NIH study found an incidence of sarcoidosis in spouses 1,000 times higher than could be expected.”

There have been other case reports of familial clustering of sarcoidosis. A case-controlled study of residents of the Isle of Man found that 40 percent of people with sarcoidosis had been in contact with a person known to have the disease, compared with 1 to 2 percent of the control subjects. One study reported three cases of sarcoidosis among ten firefighters who apprenticed together.

Dr. Garth Nicholson, a researcher at The Institute of Molecular Medicine in California has also conducted several studies on the communicability of diseases such as Chronic Fatigue Syndrome, autism and Gulf War Syndrome (a disease with symptoms very similar to those of CFS). He noted that among soldiers who developed Gulf War Syndrome during the war in Iraq, 70% or more of family members showed symptoms of the same disease within 10 years after the soldier had returned from the war.

Similarly, researchers at Queens Medical School in England found that men whose spouses had hypertension had a two-fold increased risk of hypertension. Similarly, women whose spouses had hypertension also doubled their risk of developing the disease. The risk for both male and female subjects persisted after adjustment for other variables such as diet.

Further evidence for communicability of Th1 disease among spouses was confirmed by British clinician and Chronic Fatigue Syndrome researcher Dr. Andy Wright, who at the 2006 Marshall Protocol Conference in Chicago, stated that he very rarely sees a family in which the spouses do not both have the L-form bacteria in their blood.

Scientists at the University of Maastricht in the Netherlands also found that relatives of individuals with autism often begin to show mild autistic traits, a phenomenon known as the broader autism phenotype (BAP). In one study conducted by the group, fathers with an autistic child demonstrated a different reaction time pattern and responded slower on the social cues than control fathers.

Spouses can pass each other bacteria.

Since recent research has suggested bacteria are also involved in causing obesity, it’s not surprising that a study recently published in the New England Journal of Medicine found that a person’s risk of becoming obese increases by 57% if they have a friend who becomes obese, and by 37% if their spouse becomes obese. The researchers attributed the results to social factors, but the spread of bacteria is a more logical explanation.

And none of the above studies even take into consideration the fact that spouses and siblings very often develop different forms of Th1 disease. If researchers were to look for the incidence of Th1 disease among family members and take into account all possible Th1 diagnoses, all of the above numbers would be notably higher.

Now think of all the Th1 diseases that are known to “run in families”– heart disease, arthritis, bipolar disorder, breast cancer, inflammatory bowel disease, Alzheimer’s disease – and it becomes increasingly plausible that nearly all inflammatory diseases are communicable, not genetic.

“The spread of Th1 disease in families is undeniable,” says Marshall. “Some members come down with rheumatoid arthritis, some with CFS, as well as a mix of the other Th1 diseases.”

Th1 disease develops as part of a gradual process

Since Th1 diseases result from a gradual accumulation of pathogens who alter the host’s genetic material over the course of decades, each Th1 disease is due to a spectrum of symptoms that gradually accumulate into a recognizable condition.

“I recognize that most people identify a date as the point at which the disease became manifest, but I believe they are mistaken in their understanding of the insidious progression of the Th1 syndromes,” says Marshall.

As they age, some people suffer from aches and pains yet don’t make the connection between these symptoms and exposure to the Th1 pathognes. Others become so used to living with a certain level of symptoms that they are convinced that what they feel everyday is “normal.”

At first, Th1 disease may not be very pronounced. It may manifest as a little arthritic pain in the joints, slow healing of wounds, inability to maintain a healthy weight, added brain fog, or mild fatigue. Some people fail to realize that mental symptoms such as irrational aggression, paranoia, depression, obsession are also signs of Th1 disease. “These symptoms stand out like beacons once one is attuned to them,” says Marshall.

Take, for example, the following case study taken from the Marshall Protocol study site. When the patient was first diagnosed with sarcoidosis, he was convinced that an insect bite he had received during military training – which caused a six-week bout of continuous coughing, was probably what had given him the disease. But, twenty years later, when he reviewed chest X-rays taken well before that incident, the disease was clearly apparent even then. “I was clinically sick, but didn’t know it,” the patient later reported. “Nobody around me noticed, including the person who read those initial X-rays. However, hindsight is 20:20, and nobody could review the early X-rays, knowing what happened to me later, without noting the significance of the adenopathy present on them.”

Similarly, a recent study by researchers at the University of Washington found that children with autism displayed signs of the disease at birth that were not recognized by their parents at the time. The team analyzed coded home videotapes of 11 autistic and 11 normally developing children’s first year birthday parties for social, affective, joint attention, and communicative behaviors and for specific autistic symptoms. Autistic children displayed significantly fewer social and joint attention behaviors and significantly more autistic symptoms, despite the fact that their parents had considered them to be “normal” at the party.

The group went on to show that parents’ recollections of when their child “became autistic” were completely unreliable, and that behavioral traits could instead be accurately recognized by third parties from videos of early life.

The Marshall Protocol can stop the spread of the Th1 pathogens among family members

Fortunately, the Marshall Protocol is finally a way to stop the spread of pathogens among families that has occurred for centuries – giving the next generation a fresh start.

Information gathered from the Marshall Protocol study site suggests that once a person is taking over the minimum inhibitory concentration (MIC) of minocycline, along with Benicar, they will kill any opportunistic blood-borne bacteria that try to leave the body. At this point, there is little chance of them passing L-form bacteria to another person, as the bacteria will be killed within 48 hours of leaving the cells and entering the bloodstream.

Since the Th1 pathogens grow very slowly, it is not very difficult to kill them before they overcome the immune system, as long as a person starts the Marshall Protocol before symptoms become severe. Thus, it is important that people whose parents and siblings suffer from Th1 disease start the Marshall Protocol as soon as possible, in order to kill disease-causing bacteria that have surely been passed among the family. “The less ill a family member is, the less difficulty they will have throwing off the infection,” says Marshall.

Once on minocycline, Marshall Protocol patients usually kill any Th1 pathogens that try to leave the body.

It is also important to remember that when L-form bacteria and other pathogens alter a person’s genetic material, they are only affecting the DNA in the nucleus of infected cells, not the DNA/chromosomes that remain with the person throughout life. This means that every time a cell dies, the genetic mutations in that cell are gone for good. When the immune system has killed all infected cells, the genetic mutations once caused by the Th1 pathogens will no longer be passed from parent to child.

It also seems that once the Th1 pathogens have been killed, and the cells they infected have died, the body is usually able to recover completely. “We are seeing very few signs of permanent damage, except for structural damage (fibrosis, scarring), and the body is showing a remarkable ability to even work around the collagen, in any case,” says Marshall.

1. How did you become interested in looking for bacteria, first in diseases like scleroderma and later in cancer?

It all started when I was a second year resident in dermatology. I was in the medical library and I came across a paper in the Southern Medical Journal describing a group of people who had been given allergy injections and who subsequently developed deep skin infection with tuberculosis-like germs. It was thought the allergy injection bottles were contaminated with these bacteria.

At the time, I had a mentally disturbed patient who had been given multiple injections of medications into her buttocks. She later developed deep painful skin nodules in the same areas. No one knew what was causing these nodules that were diagnosed as “panniculitis,” an inflammation of the fat layers of the skin. I thought, “Let’s culture a skin biopsy from one of these deep nodules and see if I can find any TB-like germs.” I was amazed when Eugenia Craggs, the technician at the TB lab, reported that “acid-fast” bacteria were discovered in the skin tissue. I thought “Hey this is just like the article!”

We also had three other patients with “panniculitis” of the fatty portion of the skin, all of unknown cause. I took biopsy samples and TB-like bacteria were found in all four. These cases were later reported in the Archives of Dermatology in 1966. At the time my dermatology professor was J. Walter Wilson, who was also a world famous mycologist, an expert in fungal diseases. He was somewhat skeptical about my findings of acid-fast bacteria in all these four patients and he suggested I use a scleroderma patient as a “control.” Scleroderma is a so-called “collagen disease” where the skin becomes hardened. The disease can affect the internal organs and is sometimes fatal. The cause is unknown, and bacteria were never thought to cause this disease. Dr. Wilson said I should check a scleroderma skin biopsy because that would serve as a negative “control” case. I was astonished when Eugenia Craggs called me from the TB lab and told me the skin tissue grindings of the scleroderma sample were positive for acid-fast bacteria, the kind of bacteria found in tuberculosis. She would try and grow the germ in a TB culture. After much searching I was also able to find a few acid-fast rod forms of bacteria in the scleroderma skin biopsy microscopic sections prepared by the pathologist.

The scleroderma bacterial took a long time to grow and could not be diagnosed as a TB germ or other definite “atypical” mycobacteria. The microbe was highly pleomorphic (various forms). There were round staphylococccal forms, as well as typical acid-fast rod forms. Eventually this isolate became fungal-like and “actinomycete- like.” Despite expert opinion, it was impossible to classify the microbe into a specific species. This case of scleroderma was reported in The Archives of Dermatology in 1966.

Some time later, Roy Averill, one of the dermatology residents, told me he heard a woman physician being interviewed on a San Diego radio talk show. She was explaining how she found TB-like bacteria in scleroderma in the late 1940s. That woman was Virginia Livingston M.D. She quickly became a dear friend and mentor in my scleroderma research. She told me that scientists at the Pasteur Institute in Belgium also reported finding acid-fast bacteria in scleroderma in 1953, thus confirming her own research.

I naturally thought all these reports in the medical journals would be recognized by other dermatologists and scientists, and that scleroderma would be recognized as an infectious disease caused by acid-fast bacteria. But after more than a half-century, I’m sad to say that scleroderma is still considered a disease “of unknown etiology” and the bacteria we found are simply ignored. After discovering acid-fast bacteria in scleroderma, Livingston found similar bacteria in cancer. This made her one of the most controversial physicians in America, as detailed in my book, “The Cancer Microbe.”

2. How did you identify the bacteria in your samples?

I began my dermatology practice at Kaiser in Hollywood in 1965. Virginia Livingston introduced me to Dan Kelso, a Los Angeles microbiologist who thereafter cultured my skin biopsy samples from scleroderma, and later from lupus erythematosus and a variety of cancers. Depending on the case, sometimes he cultured Staphylococcus epidermidis, or corynebacteria, more rarely streptococci, and pleomorphic bacteria that appeared sporadically as acid-fast bacteria similar to Mycobacterium tuberculosis.

Naturally I attempted to find acid-fast rod forms in my specially-stained skin biopsy sections, because these forms are the typical forms signifying infection with Mycobacterium tuberculosis or other species of mycobacteria. “Acid-fast” refers to red-stained mycobacteria that can be observed after staining tissue samples with a special procedure and a special dye. At first, I didn’t see the L-form bacteria since they react differently to acid staining. Instead of rod-forms, they appeared as round forms which were only partially acid-fast, staining purple or magenta with the acid-fast stain. It took me many years to finally realize that these partially acid-fast and round forms were bona fide growth forms of mycobacteria. The typical bright red-stained acid-fast rod forms of mycobacteria are unique and easily recognized by pathologists, but unfortunately the non-acid-fast round forms are not recognized and accepted by pathologists. For a long time I passed over these granular and “dusty” tiny forms as meaningless, not realizing that they were, in actuality, what L-forms look like!

I knew basically nothing about the microscopic appearance of L-form bacteria (also known as cell wall deficient bacteria and “mycoplasma”) until I carefully read the published papers of microbiologist Lida Mattman. Then I realized all the guises that bacteria can undergo, including transformation into “large bodies.” At that point, I went back and looked at my first case of scleroderma and realized that one skin biopsy sample contained large L-form bodies that appeared as yeast and fungal-like forms! These forms, in 1966, were dismissed as “fat degeneration” by one pathologist; and the biologist thought they looked like yeast cells.

These large L-forms are compatible with what pathologists recognize as Russell Bodies. William Russell (1852-1940) was a well-known Scottish pathologist who first discovered “the parasite of cancer” in 1890. His view of an infectious agent in cancer was dismissed in the early part of the twentieth century. However, I believe Russell bodies are actually large growth forms of cell wall deficient bacteria — and that Russell was indeed recognizing an infectious agent in cancer. More than a half-century later, Lida Mattman was able to transform mycobacteria into “large bodies” by exposing them to antibiotics. For more information on Russell and pictures of Russell bodies, Google my paper “The Russell Body” in the Journal of Independent Medical Research (joimr.org).

The fact that L-form bacteria have a “life cycle” and can appear in so many different shapes and sizes (pleomorphism) may be why they are so hard to eradicate and why the immune system cannot cope with them. Maybe the large Russell bodies are harder to kill. Or maybe they are easier to kill. I don’t know.

3. You found bacteria in the tissues of people who died of certain cancers and AIDS and scleroderma at autopsy. What gave you the idea to look for bacteria in autopsies?

I got that idea from Florence Seibert, a world famous biochemist who developed the tuberculin skin test for tuberculosis, which is still used worldwide. When Seibert heard about the TB-like bacteria discovered in cancer by Virginia Livingston and her colleagues, which included microbiologist Eleanor Alexander-Jackson and cell cytologist Irene Diller, she decided to come out of retirement and help with the women’s cancer research. Seibert advised me to search for bacteria in autopsy specimens and to determine if I could also find them in the internal organs and connective tissue of people who died of scleroderma. She believed this would make my skin research more credible. For the full story of these four remarkable women scientists, read my book Four Women Against Cancer, published in 2005, and available through Internet book sources.

Alan Cantwell with Eleanor Alexander-Jackson and Irene Corey Diller

After I decided to look for bacteria in autopsy material, I contacted colleagues in the Pathology department at Kaiser and asked them to provide me with stored tissue autopsy samples, which they did graciously. I was very fortunate to have them assist me in doing this. One of the great things about Kaiser-Permanente is that everything is under one roof. Few private dermatologists would have the easy access to autopsy material that I did at Kaiser.

4. When did you begin to look for bacteria in people with cancer?

Never in my wildest dreams did I think I would ever find bacteria in patients with cancer. Before I started my cancer research (which was totally instigated by my friendship with Livingston), it seemed inconceivable that scientists could have failed to recognize a microscopically visible infectious bacterial agent in cancer.

For a decade I avoided the cancer controversy because I worked for an HMO and I didn’t want to be regarded as a “quack.” Tragically, Virginia Livingston, because of her outspokenness that cancer was caused by bacteria, was widely regarded as a “quack doctor.” However, in the mid-1970s, I found pleomorphic bacteria in patients with sarcoidosis, and also in a patient with lymphoma. I was amazed at how easy it was to detect bacteria in sarcoidosis and lymphoma when the tissue sections were properly stained with an acid-fast staining technique.

Once I saw for myself that Virginia Livingston was correct about acid-fast bacteria in cancer, I became very enthusiastic about studying bacteria in other forms of cancer, as well as in immune diseases, like lupus. At that point, I finally had enough conviction in my findings, and had the courage to take a stand along with Virginia.

5. How did you colleagues react to your research?

Over the years there were very few doctors interested in seeing the bacteria I found in tissue sections. Some would tentatively acknowledge that there were bacteria present. Most were non-committal. With a little arm twisting I convinced several pathologists, who helped supply the autopsy specimens, to put their name on my published papers. But for the most part they didn’t want to get involved. They would say, “Oh Alan, it’s your research…” “Oh Alan, you’ll win the Nobel Prize someday.” Nobody ever wanted to sit down with me and seriously look at the material. I think it’s because finding bacteria in illnesses that are not attributed to infection is highly controversial, and most doctors shy away from controversy. The finding of bacteria in cancer is like opening Pandora’s Box. Once it’s open, a lot of stuff flies out, and pisses off a lot of people. The bacteria aren’t supposed to be there, they are in closet and not supposed to come out.

Even after I was retired for almost a decade, I never lost interest in trying to uncover bacteria in cancer. In 2003, my partner was diagnosed with prostate cancer. He underwent a prostatectomy, the total removal of the prostate gland. I decided to see if bacteria could be found in his prostate cancer tissue sections after surgery. Prostate cancer is every older man’s worst nightmare, just as breast cancer is every woman’s worst nightmare. I asked the Kaiser pathologist to cut me a section of my partner’s cancerous prostate and to stain it with an acid-fast stain so that I could study it. Sure enough, there were bacteria in the samples. I had a private microscopist photograph the bacteria. One can view the bacteria in prostate cancer I discovered by reading my paper published at the www.joimr.org website.

6. What’s going on? Why aren’t doctors and researchers taking the idea that bacteria cause cancer seriously?

As I see it, the identification of simple-to-see cancer microbes would cause havoc in the scientific world and in the cancer treatment industry. It would be the biggest embarrassment to befall modern medicine. Can you imagine the furor resurrecting Russell’s “cancer parasite” — the “parasite” that was thrown out of medical science a century ago?

It is rare to find a scientist interested in “cancer microbes.” Most physicians are repelled by the idea that bacteria cause cancer. How do you prod scientists to become interested? I’m still not sure.

A century ago, doctors stopped looking for bacteria in cancer. It’s weird because around that time major diseases like syphilis, tuberculosis, and leprosy were proved to be caused by bacteria. I suppose researchers think, “Well, we looked for bacteria 100 years ago, so there’s no need to look for them now.” But a lot has changed in bacteriology in 100 years. A century ago there was no such thing as an “L-form.” Even now most scientists don’t realize that regular bacteria can change into L-form bacteria, or cell wall bacteria, or mycoplasma, or pleomorphic bacteria, or nanobacteria, or whatever you choose to call these peculiar and little-known growth forms.

Microbiologists still have a hard time dealing with the fact that bacteria can change so widely in shape and size. How do you get scientists to understand that the tiniest L-forms have the potential to enlarge into a form the size of a red blood cell (or even bigger!). But if you think about it, all human beings were once a microscopic bunch of dividing cells, hardly visible to the naked eye. And we know that these tiny cells can evolve into seven foot tall basketball players. Why then, do we take such a simple view of what bacteria are supposed to do and what they are supposed to look like?

And the strange part is that using a light microscope you can easily see L-form bacteria. Every scientific paper that I have had published shows pictures of these bacteria. But even when doctors are shown photographs or see these bacteria via a light microscope, they still have a hard time accepting them. It’s bizarre because doctors believe viruses exist, even though most have never seen one. You can’t see viruses. They are too small to be seen with a microscope.

7. When doctors and researchers claim that there are no bacteria in your samples what explanations do they give?

When doctors or other researchers try to deny that there are bacteria in scleroderma and cancerous samples their explanations are pretty lame. Maybe something like, “Those aren’t bacteria, those are enlarged red blood cells.” Those “bacteria” are really cell debris, or stain material, or nuclear dust, of mast cell granules, or fat granules— anything but true bacteria. It’s impossible to convince a pathologist, for example, that a “tiny” bacteria can transform into a giant-sized form hundreds of times larger.

8. Who’s to blame for the fact that bacteria have not been recognized as part of the pathogenesis of cancer?

Pathologists, dermatologists, infectious disease specialists, oncologists, virologists, microbiologists, and basically all medical scientists who have ignored a century of cancer research pointing to cancer microbes. They have collectively let us down. Unfortunately, pathologists and microbiologists seem to be on two different planets. Pathologists pay little attention to germs in a laboratory, and microbiologists pay little attention to what bacteria do when they infect human tissues that are subsequently examined by pathologists.

9. What keeps other researchers from finding L-form bacteria in patients with cancer?

Unfortunately, most microbiologists who have worked with L-form bacteria have not demonstrated how these same forms appear in tissue in human disease when viewed in the light microscope. It’s one thing to describe a microbe in a lab, but what does it look like when it infects the human body? It’s one thing to show these L-forms in pictures taken with an electron microscope that magnifies objects thousands of times. But what do these bacteria look like when view with a “regular” light microscope that magnifies only 1,000 times? As a result, these pleomorphic forms go undetected in diseased tissue. Another reason, of course, is that the pathologist uses a routine stain (the H&E stain) that does not detect these forms. One needs to use an acid-fast stain. This was one of Livingston’s and Eleanor Alexander-Jackson’s most brilliant discovery— the idea that the “cancer microbe” is intermittently “acid-fast” at one or more stages of its growth.

10. What are some of your concerns about the current medical climate?

It saddens me greatly that all this great research has been ignored. That is why I wrote The Cancer Microbe (1990), and AIDS: The Mystery and the Solution (1984) and Four Women Against Cancer (2005).

Every first year med student knows that until you know what’s causing a disease it’s very hard to treat it. In my opinion, hunting for the exact cause of an illness is the most exciting part about being a doctor. The scientists who clued us into the cause of tuberculosis and syphilis, for example, were medical greats because they gave us an idea of what exactly is making the patient ill.

In my 30 years as a doctor and researcher I’ve never convinced one doctor, not even one, that bacteria cause cancer. My own younger brother is a physician — and I don’t even think he believes me entirely. Two years ago, his daughter-in-law died at age 39 of Hodgkin’s Disease, leaving two small children. I told him, “I wrote about Hodgkin’s Disease!” But he wouldn’t comment. If I can’t convince my own brother — or even interest him in the subject —I feel there is little hope.

11. What concerns did Kaiser Permanente have about your research?

A problem with my research was that over a period of years I was finding acid-fast bacteria in patients with a wide array of different illnesses. Some skeptics would say “OK, maybe I can accept that you found bacteria in scleroderma, but come on, in all these diseases?” After several years of productive cancer microbe research, the research committee insisted I be interviewed by a statistician. The committee was concerned because I was discovering bacteria in too many diseases. The statistician insisted that I attempt a statistical study of these bacteria with suitable “controls.” I explained that previous researchers had already determined that all human beings harbor such bacteria, and that these bacteria needed further study as pathogens. It might be impossible to find “negative” controls. At that point I thought, “I’m doomed.” There was no way I could do a statistical analysis of my observations. My research was terminated.

12. Did anyone try to censor your work?

In 1984 Virginia Livingston wrote a second book about bacteria in cancer called The Conquest of Cancer. She asked me to write a blurb for the back cover of her book. Her publisher took out an ad for her book in the Los Angeles Times Book Review, which included my blurb. Unfortunately, my quote mentioned my association with the Southern California Permanente Medical Group. When the top brass at Kaiser discovered this they were furious. “You can’t do this! You can’t associate our name with a quack like Livingston!”

At the time I had also discovered that cancer bacteria play a role in the development of Kaposi’s sarcoma, the most common cancer in the newly discovered disease called AIDS. I explained that I had also written a book about AIDS and the bacteria involved in this disease, and that the book was in press and was to be published soon. The Kaiser officials were aghast and told me I was simply not allowed to publish this book. This was at a time shortly before the discovery of HIV and during the period when the precise cause of the immune deficiency was “a mystery.” I had always been well-respected at Kaiser, but I was fearful the Livingston brouhaha and the impending publication of my book might threaten my job.

Finally my literary lawyer stepped in and worked out a deal with Kaiser whereby I could publish AIDS: The Mystery & The Solution as long as I didn’t mention Kaiser in the book. I had to make sure the printer deleted all references to where I had done my cancer and AIDS research. The thing I had tried to avoid for so long had become a reality: I had inadvertently become a threat to the medical establishment, just like Virginia Livingston.

13. Tell me about your role model and colleague Virginia Livingston.

Alan Cantwell with Virginia Livingston

Virginia was a dear friend whose research formed the foundation of my scleroderma research and subsequent cancer microbe studies. My association with her and Irene Diller and Eleanor Alexander-Jackson and Florence Seibert, changed my life forever. Although she died in 1990 at the age of 84, Virginia still influences me. She is my “scientific soulmate.” These four women are my four greatest heroines in medical science. In Four Women Against Cancer, I describe their amazing cancer research. I knew them all personally, and sadly all of them are now gone.

14. What do you think about the Marshall Protocol?

When I heard about the Marshall Protocol I was taken aback. I never thought that a possible cure for chronic disease would happen in my lifetime. I used to tell people that there was no way known to kill L-form bacteria in the body.

In mid-life Trevor Marshall set out to figure out a good treatment or a cure sarcoidosis because he had the disease himself. That is how — via his own research — that he discovered me and I was made aware of his own admittedly controversial ideas on how chronic diseases might be successfully treated. He certainly, almost single-handedly, revived my scientific career and I am exceedingly grateful to him for his interest and support of the cancer microbe work.

Having a disease is unfortunate, but it can serve as a great consciousness-raiser. Illness can also bring people together who would have never been brought together otherwise. This interview is a good example of that! From Trevor I am learning about the importance of the “vitamin D receptor” and that Benicar, along with long-term antibiotics can help rev up the immune system and apparently diminish L-form bacteria in patients who are trying his ideas. It’s interesting because Livingston always said that the key to curing chronic disease and cancer is to improve the function of the immune system. In my opinion, the proof is in the pudding. Some people with chronic disease are reporting benefit from the MP.

Trevor’s not a medical doctor but he obviously is an avid researcher and well-versed and well-trained in biochemistry, pharmacology, molecular biology, subjects that are way beyond my ken. Plus, I went to medical school a half century ago.

The MP has revealed that the healing process of certain chronic disease needs to go slowly, which in many ways goes against scientific dogma with its “quick cure with a round of antibiotics.” Both Trevor and I believe bacteria are implicated in sarcoid, even though this is still denied by many physicians who consider sarcoid a “disease of unknown etiology” — and all the research pointing to bacteria in sarcoid is ignored. Trevor obviously believes bacterial infection also plays a role in certain other chronic diseases. If you think about it, diseases like tuberculosis, leprosy and cancer all take years to treat. You don’t necessarily expect to get well in one month, one week, or even one year. Similarly, one shouldn’t expect a quick cure in chronic disease, even though bacteria play a big role in these diseases.

15. What do you feel lies ahead in terms of cancer research?

I feel that the treatment of cancer will remain dismal until these bacteria are recognized as cancer-causing agents by the scientific and cancer establishments. Only then can better treatment methods be employed that actually are specifically directed against the buildup of these L-forms or are directed towards strengthening the immune system against them, or both.

IMAGES OF L-FORM BACTERIA BY ALAN CANTWELL

Click to enlarge and see descriptions.