Exploring chronic disease
Biomedical researcher Trevor Marshall is currently at the “Understanding Aging” conference in UCLA where, in his talk, he will bring up an increasingly plausible possibility – namely that our stem cells can become infected with bacteria that contribute to the aging process. Serendipitously, a study released this week by a group of researchers at Ohio State University College of Medicine in Columbus provides evidence that Marshall may be on the right track. At a June 2nd meeting of the American Society of Clinical Oncology the team, under the direction of Sanford Barsky PhD, reported that data obtained from a study on organ transplant donors/recipients supports the hypothesis that many, if not all cancers, are caused when stem cells somehow go bad.
Stem cells allow our organs renew themselves over the course of time. As described by a recent article in the Economist, every organ and tissue in the body has its own collection of stem cells. When these cells divide, they produce two very different daughter cells. One resembles the parent stem cell and thus allows the process of regeneration in the same organ to continue. The progeny of the other differentiate into mature cells within the skin, kidney, lung or what have you. In a healthy organ, the stem cells divide only when needed—usually in response to injury or when other cells have died.
Because dividing cells have been associated with tumors, so have stem cells. The association is commonly explained by the hypothesis that under certain conditions, stem cells somehow lose control and begin to divide endlessly, causing a tumor to form. Based on this hypothesis, Barsky set out to use a registry of US government health data in order to track the fate of stem cells in organ transplant recipients.
His goal was to track the fate of stem cells after they have been implanted, via an organ transplant, into a new host. To this end, he created a clever method to keep track of donor and recipient stem cells. He realized that, in many cases, his team could determine the origin of a transplanted stem cell based on its sex. Cells derived from males carry an X and a Y chromosome, while the cells of females cells carry two X chromosomes.
This means that if a woman develops cancerous cells containing a Y chromosome after transplant surgery, the cells are derived from a male organ donor. Similarly, if a male develops a tumor after a transplant operation, and the cells contain only X chromosomes, they undoubtedly came from a female donor. In order to determine the sex of the stem cells examined, Barsky’s team labeled slices of recipient tumors with green fluorescent tags that bind to the X chromosome and red tags that bind to the Y. When tagged in this manner, cells of each sex glowed brightly in different colors when viewed using specific tools.
Barsky and team sifted through a patient registry of transplant recipients and identified 280 people who had undergone an organ transplant and later developed a solid tumor. In nearly half the cases, donor and recipient were of different sexes. In fact, the results turned up an abundant number of transplant-derived cancers: in 12% of cases, the sex of the tumor matched the donor rather than the recipient. For example, a 62-year-old man developed colon cancer ten years after receiving a kidney transplant from a female donor. The colon-cancer cells lacked a Y chromosome, meaning they had to be female in origin. In a separate instance, a 48-year-old woman developed skin cancer nine months after receiving a bone-marrow transplant from a man. Her tumor cells had a Y chromosome, making it clear that the cancer had arisen from donated bone marrow cells.
Closer examination of the DNA in the tumor cells and surrounding tissue showed that the tumors definitely did originate from the donor organs rather than those of the recipients. Dr. Barsky also found that if a tumor formed in the transplanted organ, it could be derived from either recipient or donor cells. In each of these cases, the tumor that formed resembled any other tumor that would form in that site. The 48-year-old woman’s looked like skin cancer, not cancer of the bone marrow. The 62-year-old man’s looked like colon cancer and not like a kidney tumor.
Naturally, Barsky came up with a hypothesis to explain his observations. He postulated that if donor stem cells migrate to a new site in an organ recipient, the cells can take on the behavior and appearance appropriate to that location—losing the identity they had once held in the donor’s body. Having reached a new location, they somehow “go awry”, leading to the formation of a tumor. The assumption that stem cells can migrate to new organs isn’t far fetched, as biologists have confirmed that stem cells in the bone marrow move into the blood stream.
And yet, the probability reigns high that Barsky’s hypothesis fails to include a major component of tumor formation and cancer pathogenesis in stem cell recipients and cancer patients in general. What’s the missing puzzle piece? You guessed it! Bacteria. The knowledge that the cells of cancer patients are likely teeming with chronic, intraphagocytic, metagenomic bacteria (often referred to as the Th1 pathogens) allows for other, likely more accurate, interpretations of Barsky’s data.
First off, it’s important to note that the presence of bacteria in cancer studies run high. For example, in 2006, D.L. Mager and team published a review article in the Journal of Translational Medicine called, “Bacteria and Cancer: Cause, or Cure?” According to Mager, “An overwhelming body of evidence has determined that relationships among certain bacteria and cancers exist.” In the paper, Mager details how research teams around the world have implicated Salmonella typhi in gallbladder cancer, Streptococcus bovis and E.coli in colon cancer, andChlamydia pneumoniae in lung cancer. According to Mager, the mechanisms by which bacterial agents may induce carcinogenesis include “chronic infection, immune evasion, and immune suppression.”
Not to mention the fact that numerous researchers have actually detected bacteria inside the cells of cancer patients, including Dr. Alan Cantwell, who used acid-fast staining to identify bacteria in patients with Hodgkin’s Disease, lymphoma, prostate cancer and other immunological diseases.
If the Th1 pathogens can infect the stem cells – and growing evidence indicates that they do – then in many cases, transplant recipients may simply be given organs in which the stem cells are infected with chronic bacterial forms. Under such circumstances, the stem cells themselves don’t contribute to tumors and the pathogenesis of cancer. Rather, the bacteria inside the stem cells spread from an infected donor organ to other areas of the body, where, after infecting the stem cells of the new organ, they proceed to cause the development of tumors and cancer in the new area of the body. Rather than the stem cells dividing rapidly, the bacteria spread rapidly, leading to a large number of infected cells.
Or, in a similar scenario, infected stem cells from a donor organ migrate to other areas of the body. Once at a new location, the stem cells transform into cells of the new organ. Meanwhile, the bacteria inside them spread to other cells of the organ, causing a clump of infected cells to develop that eventually turns into a tumor.
“In this second scenario, the donor tissues (containing infected stem cells) spread themselves, via the bloodstream, to the area which becomes cancerous,” argues Marshall.
So while Barsky argues that the new data support the idea that tumors arise from stem cells that have gone wrong, those familiar with the Marshall Pathogenesis realize that the reason the cells have “gone wrong” is almost certainly because they are infected with bacteria.
So there we have it. More evidence which suggests that the Th1 pathogens may infect the stem cells just as easily as they infect other cells types. And since the resiliency of the stem cells strongly contributes to the aging process, the possibility opens up a Pandora’s Box of possible aging-related phenomena. Thus, Barsky’s research not only allows for a better understanding of tumor development, it also brings us one step closer to understanding the processes that may hamper longevity and resiliency.
The Indian sub-continent is situated between 8.4 degree N and 37.6 degree N latitude and has adequate sunshine throughout the year. So say researchers at the Apollo Hospital in New Delhi India. In fact, in their introduction to a recent study on vitamin D, the team postulated further, stating that “it has been presumed that Indians have ‘sufficient’ levels of vitamin D.”
And who wouldn’t presume such a thing? Considering that the average temperature in India is quite high, it’s doubtful that natives would be deficient in a substance that is easily obtained from the sun. Nevertheless, with growing concerns of what mainstream medicine calls vitamin D “deficiency” at hand, the team set out to confirm that the staff from a hospital in north India did indeed possess levels of vitamin D (25-D) that the medical community has deemed healthy – specifically 25-D level between 35-50 ng/ml. Using a machine called dual energy X-ray absorptiometer, the Apollo Hospital team were able to measure the staff’s serum 25-D and 1, 25-D levels.
In the end, the team was unnerved by their results. To their dismay, only 33.7 percent of subjects had 25-D concentrations above 15 ng/ml. And they were probably even more confused that 20.6% of subjects had 25-D levels < 5 ng/ml, 27.2% of subjects had 25-D levels between 5-9.9 ng/ml and 18.5% demonstrated 25-D levels in the range of 10-14.9 ng/ml. Rather than consider any possible alternate hypotheses for the fact that essentially all of their subjects displayed 25-D levels below the “normal range” – after all, the researchers themselves had once described the subjects as healthy – the team leapt to a sobering conclusion. Despite the reality that the subjects were getting adequate amounts of sunlight, they argued that vitamin D “deficiency” was rampant among the staff.
The ease with which the Apollo team jumped to the conclusion that their subjects are vitamin D “deficient” goes a long way towards explaining why incorrect assumptions about vitamin D remain the norm among mainstream researchers. Few seem to truly consider the implications of the fact that 25-D is a secosteroid rather than a vitamin, or the consequences of altering levels of a substance that is controlled by myriad delicate feedback pathways. One would think that with such counterintuitive results at hand, the Apollo team would strive to consider alternate explanations. There are at least two rational alternate hypotheses for the low levels of 25-D observed among the hospital staff.
First off, who’s to say that the current range used to determine what is considered to be a “healthy” level of 25-D is correct? Since the vast majority of the public whose data are used to create such a range consume large amounts of vitamin D fortified products, few people have a truly natural level of vitamin D in their bodies. Consequently, it’s only logical that over the past few decades, the “healthy” range for 25-D obtained from bloodwork has been adjusted upward to accommodate the rise in 25-D levels that results from the consumption of fortified products. The result is that the 25-D levels of people eating a diet without fortified foods – as is probably the case among the hospital staff – are inevitably considered to be too low, out of range, and ultimately a menace to their health.
The possibility that the current “healthy” range for 25-D incorrectly tags people not consuming fortified products as vitamin D “defiecient” is strengthened by other studies including a study by researcher at who tested the level of 25-D in 90 “healthy, ambulatory Chilean women”. Testing revealed that 27% of the premenopausal and 60% of the postmenopausal women had 25-D levels under 20 ng/ml. Similarly, a study on healthy Bangladeshi women found that approximately 80% of the women had a level of 25-D under 16 ng/ml.
The stark reality is that considering all the extra vitamin D we have added to the food chain, we no longer know what amount of 25-D the body would maintain under natural circumstances. Could it be that the people we call “Vitamin D deficient” actually have a normal level of 25-D and actually are, as the Apollo researchers first postulated of their subjects, vitamin D “sufficient?”
Furthermore, among those familiar with the complexities of vitamin D metabolism, the concept of vitamin D “deficiency” is rapidly becoming obsolete. Armed with the knowledge that 25-D actually blocks, rather than activates, the VDR, it has become clear that people – particularly those suffering from chronic disease – are better off with low levels of the secosteroid. In a recent BioEssay, biomedical researcher Trevor Marshall details feedback pathways which show that among patients with chronic disease, 25-D levels are naturally downregulated by the disease process itself – a process driven by the ability of chronic, intracellular metagenomic pathogens to created VDR-blocking ligands.
Although slow growing, these chronic pathogens can easily spread from person to person, particularly among people in close contact. So when one considers that the hospital staff examined by the Apollo research team are in constant contact with patients suffering from a plethora of illness caused by these bacteria, there is little doubt that each staff member has acquired at least some chronic pathogens from their patients.
Perhaps then, the low 25-D observed in many of the staff members reflects the fact that they too are infected with the chronic bacteria that dysregulate vitamin D metabolism and cause 25-D levels to drop.
Unfortunately, although discussed repeatedly on Bacteriality, such alternate hypotheses remain largely foreign to the mainstream medical community. So the concept of vitamin D “deficiency” continues to be spoon fed to the public, who, of course, proceed to supplement with vitamin D in order to keep their 25-D levels in an artificially high range. It’s clear that this trend can only be remedied by a rise in independent thinking. Surely when the results of a study fail to make sense in the light of a current model, it’s time to re-examine the model rather than rationalize the data. So go for it, vitamin D researchers– dare to consider alternate hypotheses for your observations. After all, the health of essentially the entire population is at stake.
This week’s pharmaceutical fiasco? Federal regulators are investigating whether a group of best-selling arthritis drugs made by Abbott Laboratories, Schering-Plough Corp. and other companies heighten the risk of cancer in youngsters.
The drugs under review are called tumor necrosis factor blockers (TNF-alpha blockers) and include Enbrel, Humira, and Remicade. The currentuproar over the medications began after the Food and Drug Administration received 30 reports of children and young adults developing cancer while taking the drugs over the last 10 years. Roughly half the cases were lymphomas, a type of immune system cancer. Others reported were leukemia, melanoma and cancers of various organs. The fact that a possible association between TNF-alpha blockers and some cancers has been recognized for years in adults has only heightened the FDA’s concern.
Since increased cancer risk marks just one of the many side effects associated with TNF-alpha blocking drugs, why are children and teenagers taking them in the first place? Sadly, TNF-alpha blockers are currently considered to be the most popular class of medications used to treat children with rheumatoid arthritis, Crohn’s disease, and other autoimmune conditions.
The link between TNF-alpha blockers and cancer has everything to do with the fact that inflammatory diseases such as rheumatoid arthritis and Crohn’s are actually caused by a chronic intraphagocytic microbiota of pathogens. The immune system constantly releases cytokines – proteins that cause pain and fatigue – in response to these pathogens, and TNF-alpha is one of the main cytokines released as part of the response. But since mainstream medicine still incorrectly considers arthritis, Crohn’s and other inflammatory diseases to be “autoimmune” in nature, most researchers have naturally concluded that TNF-alpha medications provide an optimal way in which to palliate what they incorrectly consider to be an over-active immune system response.
In reality, blocking the production of TNF-alpha requires slowing many components of innate immunity, meaning that the drugs are actually just another class of immunosuppressants. Armed with the understanding that “autoimmune diseases” are are actually caused by bacteria, it’s easy to see that while palliative over the short-term, TNF-alpha blocking drugs allow disease-causing pathogens to spread more easily over the long-run.
“Blocking TNF-alpha allows the bacteria to proliferate and produce lots of capnine-like stuff which blocks the Vitamin D Receptor [the receptor that controls innate immune function] and allows cancers to form and metastasize”, explains Marshall.
Consider the fact that cancers including lymphomas are also, almost certainly, the result of infection with a large microbiota of bacteria. It suddenly becomes clear that the increased rate of cancer seen among youngsters or adults taking TNF-alpha blocking drugs is not due to mysterious side effects of the medications, but rather the fact that any person taking a TNF-alpha blocking medication suffers from a decrease in immune function that allows cancer-causing bacteria to spread with greater ease.
In fact, the deleterious effects of TNF-alpha blockers on the innate immune response mean that the latest findings showing increased cancer rates among youngsters taking the drugs are far from the first reports of “side effects” associated with the class of medications. In 2005 Marcel Flendrie and colleagues, from Radboud University Nijmegen Medical Centre in the Netherlands, followed a population of 289 patients who had been undergoing treatment for rheumatoid arthritis with TNF-alpha blocking drugs for a period of one to ten years. The drugs the patients had been taking included two anti-TNF-alpha antibodies, infliximab and adalimumab, and the TNF-alpha receptors etanercept and lenercept.
The results of the study show that 25% of patients on the therapy suffered from a dermatological condition that led them to visit a skin specialist. In a control group of patients who were not undergoing TNF-alpha blocking therapy and had less severe disease only 13% visited a dermatologist during the same period of time.
The most frequent conditions that patients on therapy suffered from were: skin infections – 33 infections were recorded; eczema, which was diagnosed 20 times; and drug eruptions, which occurred mainly at the beginning of the treatment and were important enough for 7 patients to stop therapy. In addition, 12 patients were diagnosed with skin tumour and 9 with an ulcer. In total, 26% of the patients who developed a dermatological condition ceased their treatment due to the condition.
“Dermatological conditions are a significant and clinically important problem in rheumatoid arthritis patients on TNF-alpha blocking therapy” conclude the authors.
This is not to mention the fact that as noted on the CDC website, the FDA has determined that tuberculosis (TB) is a “potential adverse reaction” from treatment with TNF-alpha blockers. The association makes it abundantly clear that TNF-alpha blockers foster the spread of bacteria.
In fact, according to About.com, it turns out that patients taking TNF-alpha blockers are also at greater risk for developing MS and increasingly prone to develop congestive heart failure, as well as “autoimmune and lupus-like problems.” The drugs have been linked to blood problems like pancytopenia (a decrease in production of all blood cell types) and aplastic anemia (complete loss of production of red blood cells). Again, one must wonder: do TNF-alpha blockers mysteriously cause these other diseases, or do they simply facilitate the spread of the bacteria that drive their progression?
While it’s abundantly clear to those who understand the Marshall Pathogenesis – which implicates bacteria in inflammatory disease – that TNF-alpha blockers elicit “side effects” by nothing more than facilitating the spread of bacteria, the FDA is far from grasping this reality.
Instead, the government body plans to spend our tax dollars on several long-term studies to definitively assess the drugs’ potential to cause cancerous “side effects”, particularly in children. The agency has asked drug makers to provide all information about children who developed cancer while taking the medications, and regulators will report the findings of their review by November. The product of such time consuming and costly investigations will result in the following – a potential label on TNF-alpha medications saying the drugs may increase the risk of cancer. A true step forward for the medical community? Sadly not.
Meanwhile, the TNF-alpha blockers continue to generate large profits for the companies that make and market them. Considering that Abbott’s Humira was the company’s best-selling product last year with over $3 billion in sales, and Remicade also topped Schering-Plough’s portfolio with sales of $1.65 billion, there is little hope that such companies will be willing to embrace a true understanding of how their drugs foster the development of chronic disease.
Note: While Olmesartan reduces levels of TNF-alpha, it does so by blocking the generation of the substance in the first place rather than blocking its release after it has been produced. So Olmesartan is effective at palliating immunopathology, but does not cause the immunosuppression generated by TNF-alpha blockers.
For the last century, the medical community has largely assumed that the bacteria that inhabit our bodies and natural surroundings have been accurately characterized and documented.
Yet according to Penn State researcher Jennifer Loveland-Curtze, “Microbes comprise up to one-third or more of the Earth’s biomass, yet fewer than 8,000 microbes have been described out of the approximately 3,000,000 that are presumed to exist,”
The statistic may be mind-boggling to some, yet, in reality, should come as no surprise. Considering the fact that bacteria are notoriously adept at evolving crafty survival mechanisms and have had eons in which to do so, the amount of research over the previous decades aimed at characterizing new bacteria and their survival adaptations has actually been minimal.
This week, one more of the potential 3,000,000 bacterial species that inhabit our planet was discovered by Loveland-Curtze and team, who released the results of a study in which they document the discovery of a new ultra-small species of bacteria that has survived for more than 120,000 years within the ice of a Greenland glacier at a depth of nearly two miles. The microorganism’s ability to persist in this low-temperature, high-pressure, reduced-oxygen and nutrient-poor habitat makes it particularly useful for studying how life, in general, can survive in a variety of extreme environments on Earth and possibly elsewhere in the solar system.
Called Chryseobacterium greenlandensis, the organism is one of only about 10 scientifically described new species originating from polar ice and glaciers. To study the bacterium in the laboratory, the research team filtered the cells from melted ice and incubated them in the cold in low-nutrient, oxygen-free solutions. The scientists then characterized the genetic, physiological, biochemical and structural features of the species. According to the team, the ultra-small size of the new species could be one explanation for why it was able to survive for so long in the Greenland glacier.
Thus, like many L-forms, Chryseobacterium is among the ubiquitous and tiny bacterial which, because of their minuscule size, are able to pass through microbiological filters. They have even been found living in the ultra-purified water used for dialysis. “Ultra-small cells could be unknown contaminants in media and medical solutions that are thought to have been sterilized using filters,” said Loveland-Curtze.
“Filterable forms” of bacteria have been known for a century — these are the kind of bacteria involved in cancer and certain other inflammatory diseases, states retired Kaiser-Permanente clinician Alan Cantwell. “One suspects these buggers are in vaccines and also in “sterile solutions.”
And so another bacterium joins the list of pathogens previously unknown to man, pathogens that have evolved to survive under the most challenging of circumstances. It’s discovery serves as a stark reminder of the number of chronic pathogens yet to be detected in the human body, many or most of which contribute to inflammatory disease. After all, if bacteria can proliferate in the depths of a glacier, it’s no wonder they have evolved so many ingenious ways to remain alive inside our myriad tissues and cell types.
In fact, the hardiness of Chryseobacterium brings to mind the recent study by researchers at the Glasgow Infection and Immunity Group who used molecular technology to sequence the bacteria present on the surface of prosthetic hip joints. The team discovered that some of their human subjects harbored bacteria previously considered capable of surviving only on hydrothermal heat vents. The fact that such bacteria can clearly remain alive despite the process of boiling or other high-temperature treatments should serve as another eye opener to those who underestimate the capability of bacteria to survive in the human body.
A century ago, Alois Alzheimer and his colleagues suggested that microorganisms likely contribute to the generation of senile plaques in patients with the disease that now bears his name. Apparently few people listened, as over the past decades, research on Alzheimer’s disease has focused almost soley on searching for a genetic cause of the illness. As reported by Science Daily, “The fact that pathogens may suppress, subvert or evade host defenses and establish chronic or latent infection [in Alzheimer’s] has received little attention in the past, despite the fact that during infection, active oxygen and nitrogen species generated by inflammatory cells may cause DNA damage, induce apoptosis, and modulate enzyme activities and gene expression.”
However, since those scientists fixated on finding a genetic cause for Alzheimer’s have yet to correlate particular genes with the disease, an increasing number of other research teams are beginning to search for alternative causes of the illness. Happily, this new streak of research focuses on the role of bacteria in causing the Alzheimer’s.
For example, In a special issue of the Journal of Alzheimer’s Disease published May 2008, guest editors Judith Miklossy, from The University of British Columbia, and Ralph N. Martins, from Edith Cowan University and Hollywood Private Hospital, Perth, Western Australia, explore the role of bacteria in causing Alzheimer’s.
The issue, which consists of a series of reviews, draws attention to both historic and recent observations related to this emerging field of Alzheimer’s research. Although the teams do implicate bacteria as possible causal agents of Alzheimer’s, they still focus on a “one pathogen, one disease” hypothesis. However, those people familiar with the work of biomedical researcher Trevor Marshall understand that Alzheimer’s is not caused by a single pathogen. Rather, Marshall’s in silico and clinical data has made it clear that inflammatory diseases like Alzheimer’s result from infection with an wide array of chronic intraphagocytic bacteria that persist inside biofilms as well as inside the nuclei of the cells they infect.
Yet, it’s still a breath of fresh air that more Alzheimer’s research teams are at least headed down the right path. The first review article accurately stresses the importance of chronic inflammation in Alzheimer’s. A second review is also on the right track in the sense that it discusses a possible correlation between higher levels of pathogenic bacteria in the mouth and the prevalence of Alzheimer’s. Since chronic intraphagocytic bacteria in the mouth likely create substances that block the VItamin D Receptor and subsequently the innate immune response, the team is correct in concluding that the presence of chronic pathogens in one area of the body can facilitate the spread of different chronic pathogens in other areas of the body, such as the brain.
Also, few MP-minded individuals would disagree with Miklossy and Martins statement that, “The historic and new observations reviewed in this special issue clearly show that high priority should be given for further research in this field as it may have major implications for public health, treatment, and prevention as adequate anti-bacterial and anti-viral drugs are available. The impact on reducing healthcare costs would be substantial.”
Yes, it would. That’s why it will be exciting when Miklossy and Martins become acquainted with the Marshall Protocol. Although no patient with Alzheimer’s has completed the treatment, patients with a range of other inflammatory mental illnesses such as ADD, OCD, bipolar disorder, depression, and general brain fog and memory loss are reporting improvement and recovery. It hard to image that Alzheimer’s won’t follow the same trend.
This month, researchers from several institutions including the University of Oulu in Finland and the Imperial College in London reported the results of a study which found an association between high-dose vitamin D supplementation in infancy and an increased risk of atopy, allergic rhinitis, and asthma later in life. Atopy, or atopic syndrome, is an allergic hypersensitivity affecting parts of the body not in direct contact with an allergen. It may involve eczema (inflammation of the upper skin layers), allergic conjunctivitis, allergic rhinitis and asthma.
The team started collecting data in 1967. That year, every mother in the two most northern provinces of Finland – a group of mothers referred to as the Northern Finland Birth Cohort (NFBC) – who had given birth to a child during the previous year was required to report the level of vitamin D they were giving their infant. At the time, Finnish government recommendations stated that mothers should supplement their infants with 50 ug of vitamin D. Mothers were asked to report if they were giving their infant the recommended dose of vitamin D, no vitamin D, or an irregular dose of vitamin D. An irregular dose of vitamin D usually reflected the fact that the infant was given high levels of vitamin D rich cod liver oil.
The infants were then tracked over the next 31 years of their lives. The exact age at which the study participants started to develop allergies and asthma was not specifically documented. However, the team did check in with subjects when they were 14 years old. At that point, subjects who had been taking the requisite 50 µg of vitamin D as infants were found to suffer from a higher prevalence of asthma and allergies. When the researchers checked in with the subjects at 31 years of age – the presence of atopy was determined by skin-prick test – the trend persisted. Prevalence of asthma and allergic rhinitis was greater in participants who had received vitamin D supplementation regularly than in those who had received it irregularly or not at all.
Although the team did not keep track of specific levels of vitamin D supplementation higher than 50 µg, their data did suggest increases in the occurrence of allergic rhinitis and asthma among those participants who had taken the highest doses of vitamin D.
The researchers believe that the NFBC population lends itself to a highly accurate study on the effects of vitamin D. Since during the Northern Finnish winter, daylight last for only 2 hours a day, the infants analyzed may have produced less vitamin D from sunlight. Also, during 1966, infant formula in Finland was not yet supplemented with vitamin D, meaning that lack of information on infant feeding was not likely to have affected estimates of vitamin D intake.
Compliance to vitamin D supplementation recommendations (i.e., child received 50 µg regularly) was associated with several social and behavioral characteristics of the mother. It turns out that mothers who were more proactive, better educated, and of higher social class were most likely to correctly follow the government specified vitamin D supplementation guidelines for their infants. Ironically, the children born to such mothers were found to suffer from higher levels of asthma, atopy, and rhinitis by age 31. This means that, ironically, those children born to mothers who did not correctly comply with the supplementation guidelines were actually healthier 31 years later. As the team states, “Many of the same characteristics that were predictive of worse compliance to vitamin D recommendations were associated with reduced risk of allergies.”
Of course, those of us familiar with the work of biomedical researcher Trevor Marshall understand why those infants given extra vitamin D during the first years of life were more likely to develop asthma and allergies as adults. Molecular and clinical data support the fact that the vitamin D derived from diet and supplements in a secosteroid that, at high levels, blocks the activity of the vitamin D Receptor – a fundamental receptor of the body that controls the activity of the innate immune system. A wide body of research has also confirmed that asthma and allergies are caused by chronic intraphagocytic biofilm-like bacteria. Thus, the innate immune function of those infants given extra vitamin D was depressed at an early age. The subsequent immunosuppression almost certainly made it easier for the infants to acquire the pathogens that cause asthma and allergies. Since L-form and biofilm bacteria grow very slowly, it took many years before the symptoms of their diseases became overt and problematic.
When Dr. S.O. Shaheen of the National Heart and Lung Institute at the Imperial College London was alerted to the results of the above study, he wrote a letter to two researchers (A.A. Litonjua and S.T. Weiss of the Brigham and Women’s Hospital in Boston) who, unaware of the long-term immunosuppressive effects of vitamin D, are urging researchers to conduct more trials in which infants are administered high doses of vitamin D.
“I would argue… that the vitamin D story is, at present, rather more confused than Weiss and Litonjua suggest, and that before rushing into prenatal nutrient supplementation trials, we need more convincing data to support their hypothesis, and greater confidence that such an intervention would be safe, states Shaheen. “Given the failure to translate observational associations between antioxidant deficiency and asthma into beneficial interventions in adults, we need to be more sure that observational links with prenatal nutrition are not confounded, and that longer term follow-up of birth cohorts does not reveal a positive relation between prenatal vitamin D status and [asthma].”
There is little doubt about it: blockage of the Vitamin D Receptor severely impairs human health. Since the Th1 pathogens create substances that block the receptor, they are easily able to create an environment that is conducive to their survival but quite detrimental to the host. If a person acquires enough of the Th1 pathogens, their VDRs likely become blocked by so many bacterial substances that the activity of the receptor decreases to a point where it is essentially off.
Since having a Vitamin D Receptor with no activity is analogous to having no VDR at all, studies on VDR knockout mice can be extremely informative. VDR knockout mice are rodents that have been grown in the lab under conditions that cause them to develop without Vitamin D Receptors. Their receptors are missing, or have been “knocked out.”
This week, a team of researchers at the University of Chicago examined the effects of inducing colitis on VDR knockout mice. Their goal: to investigate the role of the VDR in mucosal barrier homeostasis. The mucosal barrier allows the intestines to retain the proper pH and structure. The team used a substance called dextran sulfate sodium (DSS) in order to create an environment in the rodents’ intestines that resembles that of people with bowel disease.
The team found that while healthy mice did not develop colitis after exposure to 2.5% DSS, mice without VDRs developed severe diarrhea, rectal bleeding, and marked body weight loss, leading to death in two weeks. Examination of the intestines of the dead mice also revealed extensive ulceration and impaired wound healing among cells that had been impacted by DSS. When the researchers examined the intestines of the VDR knockout mice under an electron microscope, they also found “severe disruption” of the junctions that keep the skins of the intestines connected.
The results reveal quite a difference between how healthy mice and VDR knockout mice are affected by DSS! While DSS didn’t even impact the mice with active VDRs it’s obvious how much havoc the substance was able to render on the rodents without the receptor. With the Chicago team’s data in mind, it’s easy to see how someone with a VDR blocked by bacterial substances and/or high levels of 25-D is primed to suffer greatly when the bacteria that cause IBS and colitis infect the tissues of the intestines. Whereas the intestines of a person without VDR blockage might remain stable enough to survive much of the inflammatory damage generated by the Th1 pathogens, the intestines of patients without VDRs are likely so weak that they are literally at the mercy of numerous chronic bacterial forms.
It follows that if patients with severe VDR blockage take a medication such as Olmesartan that is able to push bacterial substances and 25-D out of the VDR and activate the receptor, their intestines should gradually become more resilient to the effects of the Th1 pathogens. Indeed, the Chicago team found when cell cultures of damaged rodent bowel tissue were administered 1,25-D – the vitamin D metabolite that, like Olmesartan, also activates the VDR – subsequent activation of the VDR markedly enhanced the strength of the junctions in the intestines, and preserved their integrity in the presence of DSS. Patients on the Marshall Protocol also find that once on Olmesartan and the MP antibiotics, their intestines are gradually able to recover from the damage caused by the Th1 pathogens.
In another sign pointing to the fact that autism is almost certainly a Th1 disease, a study released on last week found that having a schizophrenic parent or a mother with psychiatric problems roughly doubled a child’s risk of becoming autistic.
“Our research shows that mothers and fathers diagnosed with schizophrenia were about twice as likely to have a child diagnosed with autism,” said Julie Daniels of the University of North Carolina, Chapel Hill, who worked on the study. The teams research has also been confirmed by earlier studies on the same topic.
“We also saw higher rates of depression and personality disorders among mothers, but not fathers,” she said in a statement.
The study of families in Sweden with children born between 1977 and 2003 involved 1,227 children diagnosed with autism. They were compared with families of nearly 31,000 children who did not have autism. Sweden’s detailed health registry provides a wealth of data for such studies.
The association between a child’s autism and mental illness in the parent was strongest with schizophrenia, and was less powerful when the mother suffered from depression or personality disorders. There was little association between autism and parental addiction to alcohol or drugs or certain other types of mental illness.
It is now increasingly recognized that a large microbiota of chronic intraphagocytic biofilm-like and L-form bacteria (the Th1 pathogens) cause mental disorders such as schizophrenia and depression. There are a great number of patients on the Marshall Protocol who suffer from depression and their symptoms, as would be expected if the disease has a bacterial cause, fluctuate in response to antibiotic type and dosage. Many patients are reporting recovery from depression after several years of using the MP to kill the pathogens at the heart of their disease. Patients with OCD, bipolar disorder, and other mental afflictions are also reporting similar patterns.
The Chapel Hill team’s research makes it quite clear that the pathogens that cause mental illness can easily be passed down the maternal line. For one thing, the chronic bacterial forms that cause these diseases can easily survive in the egg that eventually becomes a new child. The child may also inherit bacterial-induced genetic mutations from the mother that create an environment inside the infant’s cells that is more hospitable to the Th1 pathogens. Furthermore, mothers generally pass a great deal of the bacteria they harbor to their infants during the first weeks of life – weeks when the infants’ adaptive immune systems are not yet up and running, but cuddling and close contact are common.
The fact that mothers with mental diseases known to be caused by the Th1 pathogens are in some cases twice as likely to have an autistic child confirms the fact that autism is almost surely a Th1 disease as well.
Unfortunately mainstream medicine remains largely oblivious to this reality. Daniels and team, as well as most other autism researchers, are unfortunately trying to find a connection between various genes they believe might cause mental diseases in order to come up with a hypothesis to explain the above research. Not surprisingly, no genetic connections have turned up.
The fact that the mothers of autistic children tend to suffer from a high degree of mental illness unfortunately poses a problem for many autistic children who can potentially reverse their disease by doing the Marshall Protocol – a treatment that kills the Th1 pathogens over the course of several years. Children on the MP need a strong support network and constant guidance. If the mother of an autistic child is sick with a Th1 condition herself, she will be less able to create the stable environment that an autistic child needs in order to succeed on the MP. Consequently, mothers of autistic children are prime candidates for the MP. Their circumstances enforce the reality that often, an entire family must make the effort to rid themselves of Th1 disease and successfully conquer their illnesses together.
According to The Independent, a mood of deep pessimism has spread among the international community of AIDS scientists after the trial of a promising vaccine failed at the end of last year. It was the latest in a series of setbacks in a 25-year struggle to develop an HIV vaccine.
In fact, according to a poll conducted by the The Independent, most scientists involved in AIDS research believe that a vaccine against HIV is further away than ever and some have admitted that effective immunization against the virus may never be possible.
What went wrong?
It turns out that one of the major realizations to emerge from the failed clinical trial – which involved the most promising prototype HIV vaccine – was that an important animal model used for more than a decade does not work. The model involves testing possible vaccines on monkeys before they are used on humans.
The prototype HIV vaccine appeared to work well when tested on monkeys infected with an artificial virus, but failed to have any effect on human volunteers at risk of HIV. In fact, the vaccine, which was created by the drug company Merck and Co, may have actually increased the incidence of AIDS among those people to receive it.
Anthony Fauci, the director of the US National Institute of Allergy and Infectious Diseases (NIAID), near Washington, told The Independent that the animal model – which uses genetically engineered simian and human immunodeficiency viruses in a combination, known as SHIV – failed to predict what will happen when a prototype vaccine is moved from laboratory monkeys to people. “We’ve learnt a few important things [from the clinical trial]. We’ve learnt that one of the animal models, the SHIV model, really doesn’t predict very well at all,” he said.
“At least we now know that you can get a situation where it looks like you are protecting against SHIV and you’re not protecting at all in the human model – that’s important,” he said.
Robert Gallo, a prominent Aids researcher in the US who is credited with co-discovering the virus in the early 1980s, likened the vaccine’s failure to the Challenger disaster, which forced Nasa to ground the space shuttle fleet for years.
After reading about this fiasco, I wish I could tell the international AIDS community “we could have told you so!” For years now, Dr. Marshall has been writing and lecturing about the fact that trials on animals can seldom be effectively applied to humans. His reasoning: even primates, a species considered to be evolutionarily similar to man, have Vitamin D Receptors that differ greatly from those of humans.
The Vitamin D Receptor is a fundamental receptor of the body that serves as a gatekeeper to the innate immune system. Particularly in a disease such as HIV, where the innate immune system and the receptors that control its activity are front and center in determining progression of the disease, the fact that properties of the Vitamin D Receptor differs substantially between primates and humans must be given great consideration before any experiment is performed using monkeys as models.
Unfortunately, because they arn’t familiar with the Marshall Pathogenesis or the importance of the VDR, AIDS researchers have wasted an estimated 500 million dollars on the failed prototype vaccine.
Now, Merck and Co are now at a loss for how to proceed when it comes towards developing a potential AIDS vaccine. Apparently, in the coming months, Fauci and team will be refocusing the vaccine effort away from expensive clinical trials towards more fundamental research to understand the basic biology of the virus and its effects on the human immune system.
Several scientists polled by The Independent admitted that an HIV vaccine may never be developed, and even those who believe that one could appear within the next 10 years added caveats saying that such a vaccine would be unlikely to work as a truly effective prophylactic against infection by the virus.
They are correct. It’s doubtful that an effective AIDS vaccine can by developed when scientists are still not considering how infection with the TH1 pathogens predisposes the public to HIV. Surely any useful vaccine will have to manage the Th1 pathogens as well as the HIV virus.
But perhaps the most disheartening thought to emerge from the realization that the ape immune system cannot be counted on to mimic that of humans is that of the billions of dollars currently being spent on researching inflammatory disease in mice. While the human and primate VDRs differ to a certain extent, the rat VDR is vastly different from the human VDR. If trials on primates are failing to yield results, then how many studies on mice, whose VDRs barely resemble those of man, are headed or have already led to failure?
With this in mind it’s easy to understand how each year billions of dollars are pumped into research on chronic disease, yet Marshall Protocol aside, no curative treatment options have been found for even a single inflammatory illness.
Last week biologists announced that several studies have solidified that fact that most cases of bad breath are caused by bacteria. Shocking? Not for anyone who understands the Marshall pathogenesis for chronic disease in which nearly all conditions can be attributed to the presence of L-form bacteria, biofilm bacteria, or other persistent forms of bacteria (collectively called the Th1 pathogens).
The culprit behind bad breath – Solobacterium moorei, which uses the tongue as a base on which to brew its halitosis-provoking fatty acids and malodorous compounds.
Two studies helped researchers confirm the findings. One, by the Buffalo School of Dental Medicine, probed 21 people with chronic bad breath and 36 without and found S. moorei in every patient that had halitosis. S. moorei was found in four of the comparison group, and while they were not yet polluting the air with foul emissions, all had periodontitis, an infection of the gums that can also lead to chronically bad breath. The biologists presented their findings at the annual meeting of the American Association for Dental Research in Dallas.
A previous study of of eight subjects with halitosis and five without found that S. moorei was “always found in patients with halitosis and never in patients who did not have the problem”. Dr. Violet I. Haraszthy, who participated in both studies, told Reuters Health “A number of other studies have also found this bacterium in halitosis patients.”
Haraszthy admits that “not much is known about this particular organism”, although Buffalo School of Dental Medicine student Betsy Clark concluded, “As we identify and find out more about the bacteria that cause bad breath, we can develop treatments to reduce their numbers in the mouth.”
Little does she know that such a treatment already exists. Patients on the Marshall Protocol report bad breath as a symptom of immunopathology. Odds are they effectively kill S. moorei and probably other bacteria yet to be detected that contribute to a foul smell from the mouth. After all, while the Buffalo researchers are content with the popular “one bacteria causes one condition” hypotheses, biomedical researcher Trevor Marshall’s work has confirmed that a diverse microbiota of bacteria are generally behind one affliction. When horizontal gene transfer is factored into the equation, it becomes increasingly obvious that an illness or condition is rarely caused by a single pathogen. Biofilms, which are often made up of over 30 or 40 species of bacteria, are common in the mouth, and can no doubt harbor pathogens besides S. mooreithat also contribute to bad breath.
I find it interesting that mainstream researchers have little problem implicating bacteria in conditions that affect the mouth. Perhaps it’s because of the fact that bacteria have been recognized as a cause of cavities for decades. Also, companies intent on creating products that might endow people with brighter smiles have spent enough money on research to realize that the “goo” that often covers teeth is made up of bacterial biofilms. But tell the same researchers that bacterial biofilms and persistent pathogens may also be causing infections in other areas of the body and they often respond with skepticism.
Amy Proal graduated from Georgetown University in 2005 with a degree in biology. While at Georgetown, she wrote her senior thesis on Chronic Fatigue Syndrome and the Marshall Protocol.