Sam is a 32-year-old patient who is using the Marshall Protocol to treat CFS and depression (and doing extremely well). But Sam is certainly not the only person in his family suffering from Th1 disease – the name given to inflammatory illness caused by bacteria that reside undetected inside biofilms and the cells of the immune system. These bacteria, which are often in a cell-wall-deficient form (the L-form), are collectively referred to as the Th1 pathogens.

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.[1] 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.[2] 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.[3]

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.[4] 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.[5]

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.[6]

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.[7]

“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.[8] One study reported three cases of sarcoidosis among ten firefighters who apprenticed together.[9]

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.[10]

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.[11]

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.[12] 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.[13]

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.

REFERENCES

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  2. Machin, G. A., Honoré, L. H., Fanning, E. A., & Molesky, M. Perinatally acquired neonatal tuberculosis: report of two cases. Pediatric pathology / affiliated with the International Paediatric Pathology Association, 12(5), 707-16. [↩]
  3. Xu, Y., Xie, J., Li, Y., Yue, J., Chen, J., Chunyu, L., et al. (2003). Using a cDNA microarray to study cellular gene expression altered by Mycobacterium tuberculosis. Chinese medical journal, 116(7), 1070-3. [↩]
  4. Bukholm, G., Modalsli, K., & Degré, M. (1986). Effect of measles-virus infection and interferon treatment on invasiveness of Shigella flexneri in HEp2-cell cultures. Journal of medical microbiology, 22(4), 335-41. [↩]
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  8. Gribbin, J., Hubbard, R. B., Le Jeune, I., Smith, C. J. P., West, J., Tata, L. J., et al. (2006). Incidence and mortality of idiopathic pulmonary fibrosis and sarcoidosis in the UK. Thorax, 61(11), 980-5. [↩]
  9. Kern, D. G., Neill, M. A., Wrenn, D. S., & Varone, J. C. (1993). Investigation of a unique time-space cluster of sarcoidosis in firefighters. The American review of respiratory disease, 148(4 Pt 1), 974-80. [↩]
  10. Hippisley-Cox, J., & Pringle, M. (1998). Are spouses of patients with hypertension at increased risk of having hypertension? A population-based case-control study. The British journal of general practice : the journal of the Royal College of General Practitioners, 48(434), 1580-3. [↩]
  11. Scheeren, A., & Stauder, J. (2007). Broader Autism Phenotype in Parents of Autistic Children: Reality or Myth? J Autism Dev Disord. [↩]
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  13. Osterling, J., & Dawson, G. (1994). Early recognition of children with autism: a study of first birthday home videotapes. Journal of autism and developmental disorders, 24(3), 247-57. [↩]