Bacteriality

Exploring chronic disease

High tofu intake correlated with memory loss

Chickens beware. Your meat, and that of other animals, may soon be in higher demand. The problem is that tofu, a soy product often used to replace meat, has once again been tied to negative health consequences – in this case, memory loss and dementia.

Researchers at Loughborough University in England recently published two studies — in the journal Dementias and in Geriatric Cognitive Disorders – which found that eating high levels of some soy products may raise the risk of memory loss.

The research team, led by Professor Ef Hogervorst, tracked soy intake and subsequent memory function in 719 elderly Indonesians living in urban and rural regions of the island of Java. They found high tofu consumption – at least once a day – was associated with worse memory, particularly among subjects over 68 years of age.

A variety of compounds are found in soy products, so naturally Hogervorst and other researchers are intent on discovering which specific compounds, or group of compounds found in soy might contribute to impaired health, such as memory loss among the elderly.

Hogervorst and team seem to be leaning towards the hypothesis that phytoestrogens – micronutients found in soy that partially mimic the hormone oestrogen – may be to blame for the mental damage observed in their study subjects. According to Rebecca Wood of the Alzhemier’s Research Trust (which funded the study), oestrogens tend to promote growth among cells. Could there be something about faster growing cells that could be detrimental to the elderly brain?

Without much evidence at hand to prove the above hypothesis correct, Hogervost and team have also considered the possibility that high levels of oestrogens might allow cells to be damaged more frequently by free radicals, yet the mechanisms behind such a hypothesis also remain cloudy.

Finally, the researchers have hypothesized that the observed mental decline in the Indonesian subjects might not have been caused by the tofu, but by formaldehyde, which is sometimes used in Indonesia as a preservative. Yet the fact that previous research has also linked high tofu consumption to an increased risk of dementia in older Japanese American males, and Amercian soy products do not contain formaldehyde, renders the hypothesis rather dubious as well.

So how would one explain this evidence? Hogervost and his research team seem to have their share of hypotheses, but here’s another: the reason why soy is harmful for older adults is that the primary isoflavone found in soy, Genistein, is immunosuppressive. Dr. Marshall has shown that Genistein actually dysregulates the innate immune response by binding and inactivating the vitamin D receptor. Just like exogenous vitamin D (known as 25-D), chlorogenic acid (found especially in coffee), or other compounds that negatively affect VDR activity, high levels of Genistein are able to slow the innate immune response (which is controlled by the VDR). As innate immune system activity decreases, less of the chronic bacteria implicated in causing a plethora of physical and cognitive symptoms are killed. The result is a temporary decrease in the inflammation generated when the pathogens die and a feeling of temporary palliation.

Dr. Hogervost may not know it, but his data is consistent with that of Dr. Martha Payne. In 2007, Payne and her team showed that vitamin D intake in older adults correlated with higher total volume of brain lesions. What’s the common thread between these two studies? In both cases, the elderly subjects are consuming foods (or supplements in the case of vitamin D) that slow the VDR. The resulting immunosuppression allows numerous bacteria-driven chronic diseases, including Alzheimer’s and dementia– to develop with greater ease -and within the time parameters defined by the study. Younger, and presumably healthier subjects, will likely suffer from the same detrimental effects if given a longer window of time.

Dr. Hogervorst has stated that there is some evidence that soy may “protect” the brains of younger and middle-aged people from damage but its effects on the aging brain are less clear. The statement directly supports the hypothesis that soy is immunodulatory. The periods of “protection” Hogervorst refers to are almost certainly periods of immunosuppression which ultimately allow enough bacterial spread in the brain so that elderly patients present as symptomatic.

Since the Th1 pathogens are picked up over the course of a lifetime, elderly people also generally have higher bacterial loads than their younger counterparts. Since many of the Th1 pathogens likely create ligands that also block the VDR, elderly patients are more susceptible to compounds like Genistein that contribute to VDR dysregulation. Because their VDRs have already been rendered largely inactive by the pathogens they harbor, smaller amounts of a compound like soy can more easily push the elderly “over the edge” into a state where they are strongly immunosuppressed.

Unfortunately the great majority of mainstream researchers remain unaware of Genistein’s negative effects on the VDR. And because the same researchers also fail to factor chronic bacteria into the pathogenesis of mental disorders such as Alzheimer’s and dementia, they are continually confused by other anomalies in their study data. For example, a different study recently found that eating tempe, a fermented soy product made from the whole soy bean, is associated with better memory. Huh?

Again, it is only when the new study is viewed through the lens of the Marshall Pathogenesis that the mental “improvements” observed in subjects can be better understood. Tempe is not only high in soy but also high in folic acid – a compound that bacteria use to their advantage. Upon consumption, folic acid is enzymatically converted into a form that the body can use to produce the nucleic acids that make up our DNA. However, if a person consumes extra folic acid, the Th1 pathogens are able to use the substance to generate their own nucleic acids and replicate and create their own DNA.

The result is that the Th1 pathogens find it easier to survive in a folate-rich environment, so high levels of the substance again prevent the immune system from effectively killing the chronic pathogens implicated in causing memory loss and dementia. By temporarily keeping many these pathogens at bay, folic acid also prevents the rise in inflammation associated with their deaths, and mistakenly, at least in the short-term, gives the impression of “wellness.”

When will the difference between palliation and true wellness become commonly understood? We know enough now to realize that the feel good effects of food simply can’t be taken at face value.

In the meantime, there’s no need to be obsessive about avoiding soy or folic acid. Marshall recommends that soy product in the diet be kept to a minimum (particularly among those patients on the MP). And because it’s excess folic acid that tends to most greatly benefit the bacteria we harbor, he recommends eating only those foods which naturally contain the substance. So products with extra folic acid, particularly white bread products, should be avoided.

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  • Filed under: diet, News Flash
  • For several years now, studies have emerged showing that breastfed babies often perform better on standardized tests and display higher overall levels of intelligence than their formula-fed counterparts. And since baby formula possesses, at least according to a number of mainstream researchers, many of the same basic characteristics as breast milk, the reality that breastfed babies tend to display higher levels of intelligence currently presents a conundrum for the medical community.

    Of course, theories have been proposed. One such theory is that women who breastfeed their babies possess different personality traits than those women who chose to feed their infants formula. It’s been postulated that women who take the time to feed their babies from their own breasts are smarter. Perhaps the fact that such women harbor the desire to breastfeed also indicates that they are more invested in the future of their infant. And if they are more invested their baby, then it could be proposed that they interact more closely with the baby and initiate a greater number of activities to foster its intelligence.

    The hypothesis is plausible and may be true to a certain extent. Yet a recent study by researchers at McGill University and conducted at a Belarrussian hospital has poked a serious hole in its accuracy, highly suggesting that other factors govern the level of mental development achieved by breastfed and formula fed babies.

    Key to the Belarussian study is that unlike any of the previous studies conducted on breastfed/formula fed infants, the mothers of the babies were randomly assigned to two different groups. Other studies on the same topic have instead allowed mothers to chose whether or not they want to breastfeed or formula feed their infants. Or, research teams have simply tracked the children of breastfeeding mothers and then compared them to the children of mothers who had independently made the choice to use formula instead. The problem with such study designs is that in each case, the mothers themselves chose how to feed their infant, making it impossible to test whether children’s intelligence levels later in life are due to the milk/ formula or the characteristics of the mother.

    However, in the Belarussian trial, about half the 14,000 babies under study were randomly assigned to a group in which prolonged and exclusive breastfeeding by the mother was encouraged at several hospitals and clinics. The mothers of the other babies received no special encouragement. The result was that those infants in the breastfeeding encouragement group were, on average, breastfed longer than the others and were less likely to have been given formula in a bottle, yet the decision to breastfed was largely influenced by the researchers conducting the study rather than the personalities of the mothers themselves.

    “The design of the study — randomly assigning babies to two groups regardless of the mothers’ characteristics — was intended to eliminate the confusion [of whether breastfed babies are given more attention],” state the team.

    At 3 months, 73 percent of the babies in the breastfeeding encouragement group were breastfed, compared to 60 percent of the other group. At 6 months, it was 50 percent versus 36 percent. In addition, the group given encouragement was far more likely to give their children only breast milk. The rate was seven times higher, for example, at 3 months.

    The children were monitored for about 6 1/2 years, at which point the researchers proceeded to measure the differences between the children in two groups using IQ tests administered by the children’s pediatricians and by ratings by their teachers of their school performance in reading, writing, math and other subjects.

    Interestingly, despite the fact that the study design had largely eliminated the “mothers who breastfeed are more likely to invest in their infants” variable, children who had been breastfed still scored higher on intelligence tests. In fact, the children in the group where breastfeeding was encouraged scored about 5 percent higher in IQ tests and did better academically.

    Although Kramer and team were able to identify a causal relationship between breastfeeding and measured intelligence, they admit to being somewhat flummoxed by exactly how this happens. A number of mechanisms are suggested including the notion that maybe there’s some constituent unique to breast milk, such as polyunsaturated fatty acids, which offers breastfed infants an advantage. However studies that have attempted to add polyunsaturated acids to formula have yielded inconsistent results when tested on infants. Others have proposed that breast milk may superior to formula because it contains more insulin-like growth factor I, but it’s difficult to connect a growth factor to cognitive function.

    One of the old refrains you hear on Bacteriality time and again is “What about the alternate hypothesis?” So, what about it? In this case, the variable which escaped the researchers’ consideration is right under their noses. Whereas natural breast milk is low in vitamin D, infant formula is fortified with the secosteroid,

    So, it’s very likely that the characteristics of the baby formula itself, rather than the characteristics of breastfeeding mothers or possibly even the properties of natural milk, are the driving factor determining intelligence levels among formula-fed children. The vitamin D added to baby formula is in the form of 25-D – the vitamin D metabolite that slows activity of the Vitamin D Receptor. Since the Vitamin D Receptor is key to controlling the activity of the innate immune response, those infants fed formula gradually ingest enough 25-D to slow the activity of the receptor. It follows that the chronic, intraphagocytic bacteria capable of infecting the brain and causing numerous mental deficiencies, learning disorders, and overall mental sluggishness (the very conditions and diseases correctable by removing vitamin D from one’s diet) are able to infect and persist in the heads of the formula fed babies with greater ease.

    Here then is a summary of the McGill study. People add unnatural substance to food for infants. Infants ingest said substance. Infants grow up to have lower intelligence.

    Mothers and their doctors privy to this study will probably opt to breastfeed their babies, albeit for the wrong reason. So at least, even if based on misinformation, most doctors currently recommend breastfeeding over formula feeding. Still, the number of formula fed babies reigns in the millions, compromising their later health and well-being.

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  • Filed under: News Flash, vitamin D
  • Several years ago, this grandmother from Oklahoma was forced to quit her job due to debilitating symptoms including chronic pain, fatigue, and extreme dryness in her eyes and mouth. But today, after 2 1/2 years on Autoimmunity Research Foundation’s Marshall Protocol, she feels like a completely normal person again and is spending much more time with family and friends. Meet Bonnie B.

    Can you describe the progression of your disease?

    I first started to feel symptoms of illness when I was in high school. I suffered from fatigue, weakness and joint pain. Yet, the symptoms were rather vague and only flared periodically.

    In fact, they stabilized for the most part until I had my first child when I was 23. At that point, the same symptoms returned, but this time they were stronger. They were also accompanied by new central nervous symptoms such as blurry vision and dull headaches. An EEG test showed that my brainwave function was off balance.

    But in a few months, the symptoms started to wane again in an on/off fashion. They would either flare or not be much of a problem. During the times when my symptoms weren’t flaring, I would try to push the idea of disease from my mind and considered myself healthy. Yet by the time I reached my late 30s, the pain and symptoms started to become more prominent and started to become constant. The fatigue and weakness were severe.

    At that point I had just stopped attending nursing school. During one of my nursing clinicals, I had treated a woman with lupus. As her caretaker, I was required to do a case study about the disease. As I researched lupus, I was struck by how many of my own symptoms resembled those of my patient. I was also flabbergasted by the fact that her disease history was very similar to mine.

    I had started seeing several doctors in an effort to understand why I was feeling so ill. I mentioned the fact that I might have lupus to my doctor and it turned out that he had also been considering that possibility. He ran an ANA (anti-nuclear antibody) test. Positive results to the test strongly suggest a patient is suffering from lupus. My test results were positive, and since I also displayed essentially all the symptoms of the disease, I was officially diagnosed with lupus.

    Around the same time, I saw an eye doctor. I had gone to see him partly because my eyes and mouth were incredibly dry. It turns out that dry mouth and dry eyes are classic symptoms of Primary Sjogren’s Syndrome. Thus, I was also diagnosed with Sjogren’s.

    My doctors insisted that corticosteroid medications could help my conditions. I started a month of heavy high-dose IVs containing the steroid medication medrol. At the same time, I was also put on another steroid medication called methodextrate. After a month of intensive IV therapy with medrol I began to take it orally, and did so, along with methodextrate, for the next 12 years. I now understand that while these steroids may have temporarily lowered the inflammation generated by the bacteria causing my symptoms, the fact that they slowed by immune system allowed the same pathogens to spread with much greater ease, making me much sicker over the long-term.

    Bonnie along with her daughter (center) and her mother (left)

    So as time wore on I got worse, and in the process, became increasingly cognitively impaired. I suffered from a high level of brain fog. I started to have trouble coming up with the correct word when writing or speaking, and also had problems reading because words didn’t seem to register anymore. This meant I could no longer enjoy reading, which was difficult. I also suffered from short-term memory loss.

    Despite extreme difficulty, I continued to work as a teacher. But during the early 90s I started teaching under very stressful conditions. I began to suffer from extra fatigue and joint pain. I also started to have TIAs or “mini” strokes that can sometimes be followed by an actual stroke. Finally, all my symptoms flared so badly that I had to quit my job and go on disability. The symptoms hit me all at once and harder than ever. I felt really terrible.

    How did you find the Marshall Protocol?

    At the time I was seeing a doctor in Texas who was really knowledgeable about cutting-edge medical treatments for lupus. For a while he had me on an antibiotic therapy called the RoadBack Protocol. Like the MP, the treatment uses pulsed, low-dose minocycline. But without the help of Benicar and the other bacteriostatic antibiotics used by the MP, I was unable to fully target my bacterial load.

    Then, one day, my physician informed me that he had learned about the Marshall Protocol. He was really excited about it and had come across the treatment in an effort to treat scleroderma – a skin condition that he suffered from. He planned to start the Marshall Protocol himself and also prescribed me the medications necessary to begin. I started the MP about 2 1/2 years ago.

    After some time, I was forced to switch physicians, in part because I wanted to see a doctor who practiced closer to Oklahoma, where my husband and I currently live. I found another MP doctor in Oklahoma through the MP study site and he has proven to be extremely helpful and knowledgeable.

    Since I had been taking corticosteroid medications for 12 years, and the medications were slowing the activity of my immune system, I needed to stop them before starting the MP. I was surprised that a few ups and downs aside, I was able to wean off them without too much anguish. I definitely felt an increase in my disease symptoms as I weaned off the steroids, but it was livable and I was able to “hang in there.” I have a strong feeling that the reason I was able to wean off the steroids with such success was that I took Benicar as per the MP guidelines during the weaning process. The anti-inflammatory effects of the medication surely made it easier for me to tolerate the heightened level of symptoms that resulted when my immune system started to “wake up” again and begin to combat the bacteria making me ill. After the weaning process was complete, I spent several months stabilizing on Benicar alone before starting the MP antibiotics.

    Within six months of starting the antibiotics, I felt a bit better in the sense that my fatigue and weakness were not as bad as before. My sense of overall wellness also improved at that point. My immunopathology (bacterial die-off reactions) fluctuated as expected, depending on my antibiotic dose and the combination of antibiotics I was taking at any given period of time.

    How do you feel today?

    I’m on Phase 3 of the MP and almost feel like a completely normal person again. I have resiliency and energy for the first time in years.

    Bonnie is now able to spend much more time with her grandchildren

    For as long as I can remember, I’ve had a housekeeper come to my house to do the cleaning for me. Now, I have started to do all the cleaning on my own again. I do all my own shopping again too. There are many other little things I’m able to do now that I haven’t been able to do for a very long time. I’m able to travel much more easily. I go on more vacations and have been able to visit my children frequently.

    The results of my ANA tests have been negative the last few times when it was checked, strongly suggesting I no longer have lupus. Of course, before I started the MP the test results were positive. My eyes and mouth feel more moist and I doubt that I’d qualify for a Sjogren’s diagnosis anymore either.

    I also feel much more alert and I certainly don’t have the degree of brain fog that I had when I started the MP. Any central nervous system symptoms are minimal if present at all. I can finally enjoy reading again and can spend more time on the computer.

    Tell me about your your ability to tolerate light.

    I was already light-sensitive for years before starting the MP. When I started the MP, I continued to stay out of sunlight and bright lights. It’s hard to judge how much my light sensitivity has improved because I’m still cautious about not getting too much light, but it doesn’t seem that light bothers me as much anymore. There have been several times when I’ve been exposed to sunlight, yet failed to react with the increase in symptoms that I would have expected before the MP. We just got a new puppy. I’ve been taking him on more walks outside during the day and have not been bothered by the light at all.

    How does you doctor feel about your progress?

    Two appointments ago he told me that all my lab work indicates that I’m recovering. He said that the MP is clearly helping me.

    What advice do you have for other patients interested in the MP?

    The MP seems daunting at first, especially because of the dietary and sunlight restrictions. But it’s so worth hanging in there! Right now I can function better than I have in years, better than I could when I was younger! Oh, it’s so worth it! I know the hard part is behind me and I’m enjoying life again.

    What lies ahead?

    I see no limits to my ability to recover and hope to become increasingly active. I also hope to share the story of my success on the MP with as many people as possible since I firmly believe the Marshall Protocol is the answer for illnesses such as lupus, Sjogren’s and other inflammatory diseases.

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  • Filed under: interview (patient), marshall protocol
  • 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.

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  • Filed under: News Flash
  • 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.

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  • Filed under: News Flash, vitamin D
  • 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 drug etanercept binds to TNF-alpha to block its action on the immune system.

    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.

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  • 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.

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  • In 2005, this father of seven could hardly breathe and suffered from intense joint pain. Exhausted and sore, he found it extremely difficult to walk up the stairs. Now, after about 2 1/2 years on Autoimmunity Research Foundation’s Marshall Protocol he’s essentially pain and symptom free and is back to digging trenches in his garden. Roy P. will now take your questions.

    Can you describe the progression of your disease?

    Everything started around Christmas of 2000. I was at work when my legs started to swell down in the area by my ankles. I was also in pain, couldn’t walk, and had a very difficult time breathing. A co-worker called my wife who took me home. We saw a doctor and I was diagnosed with rheumatoid arthritis. However the doctor still wasn’t able to explain why my legs were swollen, or why I was suffering from other severe symptoms. Personally, I thought I was having a heart attack. At that point I asked, “Do you think any of this is related to the lumps I have under the bicep of my right arm?” He paused, and said, “What lumps? Show me.” After examining my arm he said “Wait a minute, I know what else you might have….sarcoidosis!” I proceeded to have a series of lung X-rays done which confirmed that I did indeed have the disease.

    My doctor told me that one of two things would happen to me. Either the disease would fizzle out on its own (something I now realize does not happen) or I would die. His only solution at that point was to put me on prednisone, a corticosteroid medication that works by slowing the activity of the immune system. While this causes short-term palliation by slowing the number of toxins released by the bacteria that cause sarcoidosis, I now realize that the drug actually allowed the bacteria at the heart of the disease to spread.

    Because of its immunosuppressive effects, when I first started prednisone, I felt like a million bucks. But then, not surprisingly, I started to gradually feel worse again. More symptoms appeared and I started to suffer from severe fatigue. I had such a hard time breathing that I literally couldn’t do anything – any form of mild exertion caused my breathing to go totally out of control. My energy level was at a minimum.

    At that point I started to use the Internet in order to research sarcoidosis on my own. I found sarcinfo.com- the precursor website to the Marshall Protocol study site. I learned that Marshall’s molecular modeling research had allowed him to create a new pathogenesis for chronic disease which implicated bacteria as the cause of the illness. The moderators on the site also explained how prednisone was negatively affecting my immune function and based on their advice, and my doctor’s subsequent permission, I stopped taking the medication.

    Three months later, I saw a pulmonologist who tried to convince me that there was no connection between vitamin D and sarcoidosis, and that sarcoidosis has no known cause. He was functioning from the older body of medical knowledge and refused to even review Dr. Marshall’s new discoveries. But at least he didn’t force me to go back on prednisone.

    Over the next few months I continued to feel worse. New body aches appeared and I started to develop headaches after exposure to bright light. I also started to suffer from increasing amounts of brain fog and short-term memory loss.

    How bad was the brain fog?

    It was so bad that at this point I can’t remember very much to tell you about my symptoms at that time….or what my brain fog was like! All I know is that it was bad and I started to have an ever increasingly hard time at work.

    I see…so back to the progression of your disease…

    Well, due to a takeover of my company, I stopped working and decided to go back to school instead. I managed OK because the department chair and secretary knew about my illness and were very accommodating. Some days though, it was extremely hard to get out of bed and go to class. Luckily, I only had classes 2-3 days a week. I did well in spite of my symptoms, but today I have to admit that I don’t remember a single thing I was taught.

    When did you start the Marshall Protocol?

    After I graduated from school, I went back and took another look at sarcinfo.com. This time, the moderators on the site sent me over tomarshallprotocol.com which had evolved into the main study site. After reading even more about the treatment I decided to finally give it a try. I started in September 14th of 2005 when I received my NOIR’s (sunglasses that block UV rays).

    It was tough because around the same time I started the MP I had to go back to work. I worked contract jobs. I had to take a few days off because my immunopathology (bacterial-die off reaction) was very strong, but I managed. One time I accidentally took too high a dose of one of my antibiotics and felt terrible. After that experience, I was extremely careful to make sure I took my antibiotics correctly.

    In fact, my advice to anyone who has to work while on the MP is to very careful and deliberate about taking your antibiotics and Benicar. Write everything down, such as when you need to take a dose of medication and keep track of your antibiotic levels on paper. I keep a weekly pillbox loaded with all the Benicar and antibiotics that I will need and put the drugs into the pillbox during a time when I can work slowly in order to make sure the pills are correct.

    I have a Palm Pilot alarm that alerts me when I need to take a new dose of Benicar. It also alerts me as to where I am in my antibiotic cycle so that I am always on schedule and never forget to take the meds. I’ve found that if my immunopathological reaction is too strong, I can use extra Benicar to tone it down, so I keep extra Benicar handy. I also carry around a big bottle of ibuprofen (which is not an MP medication) because I find that it can help control my swelling (inflammation) in an emergency.

    One of the hardest parts about working while on the MP was the fact that I needed to block light while my co-workers did not. Everybody else wanted the bright lights on, and it was hard to come off as a weird batman type that would prefer them off. But I made sure to communicate my need for light restriction to my boss who did allow me to switch off the lights over the row where I sit. So that’s been a help.

    How light sensitive were you when you first started the MP?

    I was so sensitive that even when I was indoors wearing sunglasses and all the lights were off except one tiny light, I felt as if I could see everything perfectly. At night when driving, I could wear sunglasses and see every detail on the road. It was almost as if I had developed night vision. Today my light sensitivity has improved tremendously to the point where I can’t see anything in the dark if I’m wearing sunglasses. I only need to wear sunglasses when I’m outside in the bright sunshine. Sometimes I garden all day while wearing only long sleeves, a special cap, and gloves and get no sun-related symptoms.

    So how are you feeling these days?

    I’m feeling so much better. I’ve been able to ramp my way up through the highest level of each antibiotic combination on the MP and still manage the immunopathology. Even while on high doses of the antibiotics, I find that my breathing is dramatically better.

    I need to walk up fifteen stairs to reach my bedroom. Before the MP, I couldn’t walk up all the stairs. I would have to stop halfway up, rest, and then continue. Now I go up and down the stairs many times a day without even thinking about it. Sometimes my breathing still gets a little heavy, but it’s nothing like it was before.

    My fatigue is largely gone; literally it is nothing like it was pre-MP. Occasionally I feel mild fatigue but it is always correlated to a difficult time in my cycle of antibiotics. Now, I am always busy. I’m always working and doing something, whether it’s working in the office or working out in the yard. Before the MP I couldn’t garden at all. Now I can dig trenches and put in sprinkler lines.

    My arthritis/joint pain is much, much better. I guess I still might feel it now and then but I’m hardly conscious of it. My brain fog and memory has improved tremendously, although one of the MP antibiotics is still able to elicit occasional moments where I experience episodes of blurry vision. But I know the symptoms are just a result of my body killing bacteria and I’m confident the blurry vision will go away completely in the coming years.

    Overall my quality of life is just so much better. My whole attitude is better. I am more emotionally stable and I can handle much more stress. Things don’t bother me the way they used to – overall, I’m a much calmer person.

    Unless I have a bad day of immunopathology, I am almost pain and ache free. If I do have pain, it’s generally fleeting. Before the MP all I could think about was my pain. That, and what to do about my life and how to support my family. Now I hardly ever think about my symptoms at all.

    I have seven kids, and I’m once again able to be a very active parent.

    Wow! Seven kids. How did you manage seven kids while on the MP?

    My children have actually been a source of help during my time on the treatment. In the beginning it took them a while to get used to the fact that I was very sensitive to light. They would accidentally flick on a bright light and then say, “Oh whoops! Sorry Dad!” But then I actually enlisted their help. The little ones would go around turning lights off. We changed the bulbs in the house to 40-watt bulbs to cut down on brightness.

    Did you try to explain the MP to your children?

    Oh yes, my wife and I sat them down and explained what the treatment entailed. We explained that I would feel worse before I would feel better, and that I would need to avoid bright lights. They were very understanding and accepting of my circumstances.

    Your member name on the Marshall Protocol study site is Bookdad. I get the Dad part, so I’m assuming you really like books as well?

    Oh yes. I love to read. Mostly non-fiction; math, science, religion, the founding fathers are some of my favorite topics.

    What lies ahead?

    I look forward to getting back to the outdoors and going camping, fishing and hunting again. Those were all activities that fell by the wayside when I got sick but I think I can start to enjoy them again now.

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  • 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.

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  • 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].”

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  • Filed under: News Flash, vitamin D
  • About Amy Proal

    Amy and Zeus

    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.