Bacteriality

Exploring chronic disease

Category: News Flash

In a recent prospective study appearing in Neurology, researchers at various scientific institutions including many in Korea set out to examine the relation between milk and calcium intake in midlife and the risk of Parkinson’s disease. The team analyzed data based on records of dietary intake observed from 1965 to 1968 in 7,504 men enrolled in a cohort called the Honolulu Heart Program. The men ranged from 45 to 68 years of age.

Parkinson’s disease (PD) is a degenerative condition affecting movement and balance in more than one million Americans each year: its prevalence is expected to rise in aging populations.

The men were followed for three decades. At that point, 128 men had developed Parkinson’s. But… cue drum roll… the risk of Parkinson’s disease increased as the amount of milk consumed each day rose. Heavy milk drinkers, who drank more than 16 oz a day, were 2.3 times more likely to develop Parkinson’s disease than those men who didn’t drink any milk. Milk was related to PD whether it was whole or skim.

One may ask, “Why?” The beautiful person with the milk mustache in the latest magazine add told me milk was good for me!


Perhaps it’s the calcium? Nope. The team, under Dr. Park, used careful statistical analysis to rule out the possibility that calcium could have caused the increased disease incidence. “In addition, calcium intake from non-dietary sources was not related to PD, further suggesting that a role for calcium in altering PD risk is absent,” states the paper, which was published in the March issue of the Journal of Neurology.

Total fat and protein also had no relation with the risk of PD. Park and team suggest that neurotoxins such as organochlorine, tetrahydroisoquinoline, and heptachlor may be to blame, but even they would concede that this explanation is speculative at best. In fact, according to the study’s authors, “Unfortunately, there are no clear explanations for the relation between milk intake and the risk of PD.”

What the researchers fail to even consider is that since the 1930′s, milk suppliers have been fortifying milk with vitamin D. According to, A. W. Norman in the book, Vitamin D: The calcium homeostatic steroid hormone, “There developed in the 1940′s, and continues to the present, a large business of industrial production of vitamin D3 used for the supplementation of foods for human consumption: milk (both homogenized and evaporated), some margarine and breads. Since the 1960′s vitamin D3 has been used also for the supplementation of farm animal and poultry food. In 1973 in the United States some 290 trillion (290 x 1012) International Units of vitamin D3 was manufactured and sold for over 3 million dollars. This vitamin D3 is the equivalent of approximately 8 tons.”

This strongly suggests that the men in the Honolulu heart study were drinking vitamin D fortified milk. With this in mind, the powerful secosteroid incorrectly labelled “vitamin” D seems like an extremely logical culprit for the rise in PD amongst subjects drinking higher amounts of milk. As described in this recent paper, vitamin D’s steroidal properties allow it slow the innate immune response. While this allows for palliation and symptom reduction in the short-term, it causes chronic bacteria that very likely contribute to the progression of PD to proliferate more easily.

When writing previously about vitamin D, I’ve argued that, “One of the abiding weaknesses of studies on vitamin D is that researchers do not follow subjects consuming the secosteroid for a sufficient period of time. Instead they track subjects over the course of weeks, months, or one or two years, during the period of time when study participants are usually feeling the palliative effects of the secosteroid. Researchers will rarely, if ever, track subjects over the course of decades, the length of time needed to begin to note the negative changes that chronic bacteria cause later in life.”

So hooray for the authors of the Honolulu Heart Study who spent the time and money to monitor subjects for 30 years after their dietary intake was reported. Clearly, when it comes to vitamin D, patience is needed for the negative impact of consuming the secosteroid to be noted.

Another clue that vitamin D likely caused the increase in PD risk among men drinking more milk in the Honolulu study was that consumption of cheese and ice-cream did not affect PD risk. The explanation? Although these products are made from milk, they are generally made from milk before it has been fortified with vitamin D.

That Park and team did not even consider the vitamin D in milk as a possible cause for the increase PD among men consuming more of the substance speaks to the incredible strength of the current consensus that fails to recognize the immunosuppresive properties of vitamin D. This is bound to change, but in the meantime, vitamin D fortified milk should at least come with the message, “Immunosuppressive steroid included at no extra charge!!”

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  • Filed under: medical research, News Flash, vitamin D
  • Excuse me, my what?!

    Duh, Kineosphaeram, one of the over 600 bacterial species that may be living in your mouth or other areas of your body. If you don’t harbor Kineosphaeram, then perhaps your mouth is home to Bergeriella, Buttiauxella, Cedecea, Derxia, Faecalibacterium, Hallella, Mannheimia, Paludibacterm, Ruminococcus, Thermovirga, or Wolinella. The list goes on….

    Looks like a few bacteria have visited this mouth.

    If these bacterial species sound new to you, it’s because many of them are. Several of the species were just recently named after researchers led by Dr. Mark Stoneking of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany conducted the first in-depth study of global diversity in the human mouth.[1] The team sequenced and analyzed variations in the bacterial gene encoding 16S rRNA, a component of the bacterial ribosome, in the salivary metagenome (bacterial population) of 120 healthy subjects from six geographic areas. The researchers proceeded to compare the sequences they found with a database of previously categorized 16S rRNA sequences to categorize the types of bacteria present.

    These sequences could be assigned to 101 known bacterial genera, of which 39 were not previously reported from the human oral cavity; phylogenetic analysis suggests that an additional 64 unknown genera are present. The results suggest great diversity in the salivary microbiome within and between individuals that until this point had never been realized.

    “The healthy human mouth is home to a tremendous variety of microbes including viruses, fungi, protozoa and bacteria,” said Professor William Wade from King’s College London Dental Institute. “The bacteria are the most numerous: there are 100 million in every millilitre of saliva and more than 600 different species in the mouth. Around half of these have yet to be named and we are trying to describe and name the new species.”

    Are these bacteria helpful or up to no good? While some may not impact dental health, disease causing bacteria in the mouth are rampant – ranging from species that cause the dental plaque that leads to cavities to forms that weaken the gums or cause bad breath. For decades scientists have advised patients to brush their teeth (don’t forget to scrub for a full three minutes!), floss, and often use a variety of mouthwashes to rid the mouth of as many bacteria as possible. There is little worry that such procedures might kill commensal or “helpful” bacteria in the mouth, probably because most dental bacteria are seen as a menace to to salivary and dental health.

    Three of the bacteria identified in the “healthy” subjects in Stoneking’s study are certainly not bacteria anyone wants to be carrying around – Neisseria. Treponema neisseria and Yersinia. Treponema and Neisseria can cause gonorrhea and syphilis respectively. Infection with Yersinia leads to a variety of symptoms including fever, abdominal pain, and diarrhea, which is often bloody. It has also been implicated in Reactive Arthritis.

    At my last appointment, my dentist showed me an awesome video of biofilm (bacterial colonies) on the surface of normal teeth. The images were so cool that I asked him for permission to put the video up on this site, but, alas, it is copyrighted. My dentist proceeded to laud the virtues of regular flossing, a practice which I do regularly. (I swear!) In his opinion, flossing helps break up these biofilms and is critical to preventing tooth decay.

    Interestingly, the Marshall Protocol does just that – although it uses pulsed, low-dose antibiotics – which have been shown to effectively destroy biofilms – and Benicar to get the job done with more vigor than a flossing addict could ever achieve. Take a certain MP patient (to protect her anonymity, I will call her “Mom”), who has been seeing the dentist for years due to tooth decay. I am told there is a ski home somewhere in Vail funded in large part by “Mom’s” regular dental work. She started the MP two years ago and now her dentist is more than a little surprised. At her last appointment, he said that he simply could not fathom the lack of plaque or tooth decay in any area of her mouth. Boy, does “Mom” wish she had started the MP earlier!

    What intrigues me about bacteria in the mouth is that scientists regard most of them as harmful to our health and have no problem with procedures that would seek to sterilize the mouth. But when one mentions other parts of the body – let’s say the gut – and points out that perhaps the majority of bacteria in that area are also causing inflammation and disease, the same researchers often strongly disagree. Currently bacteria in the gut are largely assumed to be “helpful”, although in many cases such thinking is based only on speculation. Perhaps some gut bacteria may help with metabolic breakdown, but it is quite possible that the environment in the gut more closely resembles that of the mouth – an environment that can easily be overtaken by pathogens. Under such circumstances, a treatment like the MP that kills bacteria in the gut is therapeutic against inflammatory diseases such as Crohn’s, colitis and myriad other bowel ailments. This is especially true since patients on the MP are reporting improvement and recovery from bowel diseases that have never previously been reversed.

    Also interesting is that many bacteria in the mouth seem able to migrate down the esophagus and reach the interior organs of the body. For example,Porphyromonas gingivalis[2] and A. actinomycetemcomitans,[3] both of which cause decay in the mouth, have been repeatedly identified in artherosclerotic plaque. This strongly suggests that these bacteria may be wreaking havoc on the blood vessels and contributing to heart disease. In fact, biomedical research Trevor Marshall believes that arterial plaque is a result of chronic bacterial infection. Indeed, where arterial plaque was once thought to be made of cholesterol and lipids it is now known that it is largely composed of dead macrophages. Since bacteria can infect and kill macrophages the death of such cells and their accumulation in patients with heart conditions seems logically tied to bacterial infection. With the above in mind, it’s not surprising that patients on the MP have reported improvement and recovery from various cardiac conditions. Some have tests showing that after years on the MP the plaque in their arteries is greatly reduced.

    So keep on brushing people, but I recommend doing the MP too. In a theoretical sense the MP “brushes” our insides – the places we can’t reach to kill pathogenic bacteria physically. For most MP patients doing so is proving to be quite rewarding.

    REFERENCES

    1. Nasidze, I., Li, J., Quinque, D., Tang, K., & Stoneking, M. (2009). Global diversity in the human salivary microbiome. Genome Research. []
    2. Dorn, B. R., Dunn, W. A., & Progulske-Fox, A. (2001). Porphyromonas gingivalis traffics to autophagosomes in human coronary artery endothelial cells. Infection and Immunity, 69(9), 5698-708. []
    3. Kozarov, E. V., Dorn, B. R., Shelburne, C. E., Dunn, W. A., & Progulske-Fox, A. (2005). Human atherosclerotic plaque contains viable invasive Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis. Arteriosclerosis, Thrombosis, and Vascular Biology, 25(3), e17-8. []
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  • Filed under: biofilms, microbiome, News Flash
  • Not long ago I reported on the results of multiple studies, the results of which indicate that the class of medications known as Angiotensin Receptor Blockers or ARBs have the potential to ameliorate a variety of cardiovascular conditions.

    Today another study joins the list – this one conducted by Atsushi Hirohata, M.D, Ph.D and his team at the the Sakakibara Heart Institute of Okayama in Japan. Hirohata, who presented his findings at last week’s 20th annual Transcatheter Cardiovascular Therapeutics (TCT) scientific symposium, presented study data, which strongly suggests that Olmesartan may play a role in reducing coronary plaque.

    The trial, “Impact of olmesartan on progression of coronary atherosclerosis; evaluation by IVUS [OLIVUS],” was performed on 247 angina patients with native coronary artery lesions. Angina is chest pain or discomfort that occurs when the heart muscle does not get enough blood. Patients were randomly assigned to receive 20-40mg/day of Olmesartan or a placebo. Then, depending on the guidance of their individual physicians, they were treated with a combination of beta blockers, calcium channel blockers, diuretics, nitrates, glycemic control agents and/or statins.

    Subjects underwent examination by a technique know as Serial Intravenous Ultrasound (IVUS) which allowed the research team to assess the amount of coronary plaque before and 14 months after the start of Olmesartan administration. At the trial’s onset, patient characteristics and all IVUS measurements were identical between the two groups. However, after 14 months of treatment, IVUS showed significant decreases in measurements of plaque volume in the Olmesartan group, despite the fact that subjects displayed similar blood pressure readings. In addition, a multivariate analysis ruled out the other forms as treatment (the beta blockers, statins, etc.) as the source of the decrease in plaque, confirming that Olmesartan administration was indeed one of the factors responsible for the decrease in plaque volume.

    “Management of plaque is a key front in the war on sudden heart attack,” states Hirohata. “These results suggest a positive role in potential plaque regression through the administration of Olmesartan, an angiotension-II receptor blocking agent, for patients with stable angina pectoris.”

    Hirohata’s results are welcome news for patients on the Marshall Protocol (MP) – a novel treatment that uses Olmesartan in concert with carefully chosen pulsed, low-dose antibiotics to eliminate chronic pathogens that are increasingly implicated in inflammatory disease. Cardiovascular diseases are included in this category. “Many years ago, atherosclerosis was thought to be related to lipids and to the excessive deposit of cholesterol in the arteries,” states Luigi Fontan, MD, PhD, assistant professor of medicine at Washington University in St. Louis and an investigator at the Instituto Superiore di Sanita, Rome, Italy. “Nowadays, it’s clear that atherosclerosis is an inflammatory disease.

    But why the reduction in plaque formation? According to biomedical researcher Trevor Marshall, macrophages begin to clump together at injured areas along the blood vessel wall in people with heart disease. Since macrophages are meant to be extremely active immune cells that engulf and kill invading pathogens, Marshall views aggregation of these listless white blood cells in individuals with cardiovascular disease as a sign that the immune system is not functioning optimally. In his opinion, the reason that the white blood cells are weakened in the first place is because they are infected by chronic bacteria. If these bacteria kill their host cells, dead macrophages may eventually accumulate and form part of the plaque that perpetuates cardiac disease – a perspective supported by the fact that Streptococcus was recently identified in arterial plaque. If the immune system were able to function correctly, it might be able to clear away developing plaque, but “When the immune system is compromised, it simply can’t clear away the obstruction,” states Marshall.

    Enter Olmesartan. MP patients take 40 mg of Olmesartan four times a daily. Molecular modeling data shows that Olmesartan is a potent Vitamin D Receptor (VDR) agonist, meaning that it binds and activates the receptor. Because the VDR controls expression of the bulk of the body’s antimicrobial peptides – proteins that serve as natural antibiotics- VDR activation greatly stimulates the innate immune response. This means that the innate immune systems of people taking Olmesartan may regain the ability to recruit active monocytes and other white blood cells to areas where they can clear away dead or dying macrophages, keeping them from becoming part of arterial plaque.

    Regardless of whether Marshall’s hypothesis is right or wrong, Hirohata’s study adds yet another benefit to what’s become a laundry list of positive outcomes associated with Olmesartan administration. Let’s hope that the medical community takes notice!

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  • Filed under: News Flash
  • It seems only a matter of time before “the days of the Petri dish” will be used to refer to an era when culturing bacteria had an air of simplicity that unfortunately is incapable of representing the full glory of the microbial world. With great numbers of scientists pushing the Petri dish aside and using advanced bacterial detection techniques in its place, it’s becoming increasingly clear that while the number of bacteria that inhabit the human body were once considered to be a moderately-sized group, they actually colonize the human body with an abundance that might rival the creatures of the rainforest (many of which, like the human microbiota, have yet to be characterized).

    A study led by Dr. Noah Fierer and team of the University of Colorado at Boulder recently reinforced this reality by using PCR and a high-throughput method called pyrosequencing to identify the number and species of bacteria present on the hands of 51 undergraduate students leaving an exam room. When the students’ genetic material was sequenced, results revealed 332,000 genetically distinct bacteria belonging to 4,742 different species on their hands. This marked a hundred-fold increase in the number of bacteria detected in previous studies that had relied on purely culture-based methods (such as the Petri dish) to characterize the human hand microbiota. Each student carried on average 3200 bacteria from 150 species on their hands.

    The results caused the team to conclude that the average person’s hands probably carry at least 3,000 different bacteria belonging to more than 100 species. According to Fierer, each student’s bacterial “fingerprint” was unique. All students carried known skin “old timers” such as Streptococcus, Staphylococcusand Lactobacillus. But 45% of the species detected were considered rare. Only five species were found on all the students’ hands, while any two hands – even belonging to the same person – had only 13% of their bacterial species in common. Certain bacteria were more frequent on the dominant hand (right for a right-hander), others on the non-dominant hand.

    Fierer is excited by the possibility that the diversity of bacteria on any given human hand may make it possible to tell if an object has been touched by someone, just by looking at the bacteria left behind. Will “bacterial fingerprinting” be added to the cornucopia of techniques used by the modern-day detective? Will it be used to solve crime on the next episode of CSI Miami? It seems that for such a technique to prove accurate, the bacteria on an individual’s hands and the potential object they have touched would have to be characterized rather quickly. Think about it – if the individual ends up in a bacteria-filled arena such as a McDonald’s restroom, the composition of microbes on their hands may change quite rapidly.

    Consider people who go to wash their hands after using the toilet. They have to turn on the sink, and will likely do so with their dominant hand. Then, although both hands are bathed with soap and water, one hand has to turn off the faucet, meaning that it is re-exposed to the pre-hand washing bacteria on the faucet handle. On the way out of the bathroom one is offered little choice but to grasp the door handle, which contains the bacterial species of people who ended up washing only one hand as well as the bacteria of those who flat out chose to skip the sink. With Fierer’s study showing that microbial populations differ so greatly from individual to individual, it seems entirely possible that many of the bacterial species on a particular person’s hands at a particular time of day may simply be due to what railings were recently touched or if one has taken out the garbage.

    But Fierer’s data also raises other questions. To the team’s surprise, women harbored different bacteria from men and significantly more kinds, even though women reported washing hands more often. In a follow-up experiment, the team tracked eight people after they washed their hands. While some species of bacteria took a while to repopulate on the freshly-washed hands, others actually preferred the “clean” environment. But the results were consistent in the sense that men always had fewer types of bacteria on their hands.

    “We were pretty surprised to see such clear differences between men and women,” says Fierer. “We don’t know the causes.” Differences in sweat and sebum production, hormones, and even the use of cosmetics might be involved, but it could simply be that men’s skin is more acidic – acid environments tend to have less microbial diversity.

    Those people familiar with the Marshall Pathogenesis, which implicates latent bacteria in the etiology of inflammatory disease, may not be entirely flabbergasted by Fierer’s results. As described in a recent speech I gave at the 2008 International Congress on Autoimmunity in Portugal, as they age, women may find it harder to fend off invading microbes. In silico data makes for a compelling case that microbe-induced dysregulation of nuclear receptor expression among women may decrease their ability to express certain antimicrobial peptides – natural antibiotics that the body uses to keep microbes under control.

    An increasing number of researchers implicate bacteria rather than an overactive immune system in autoimmune disease – illnesses that, like the bacteria found on the hands of Fierer’s study subjects, also favor women. Biomedical researcher Trevor Marshall has shown that some of the pathogens implicated in autoimmune disease have developed ways of slowing the innate immune response. For example, certain species of gliding biofilm bacteria have been shown to create ligands that dysregulate the Vitamin D Receptor – a receptor that has been called the “gatekeeper to the innate immune response,” The bottom line is that, over their lifetimes, women may accumulate higher pathogenic bacterial loads and become more immunocompromised than their male counterparts. Does this possible discrepancy influence the number and species of bacteria on their hands? Only time and further research will tell.

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  • Filed under: News Flash
  • The year was 2005. Under the guidance of Mary H. Schweitzer, researchers from North Carolina State University reported a groundbreaking finding.[1] The team had, according to its members, discovered bona-fide dinosaur tissue inside a femur bone that had once belonged to Tyrannosaurus Rex. The discovery was reported after Schweitzer’s team, working at a remote dig site in Montana, was forced to break the femur into chunks small enough to be transported by helicopter. Inside were pieces of rubbery material that looked like blood vessels and bone marrow. Eureka?

    Although several scientists voiced skepticism of the possibility that what appeared to be soft, organic matter could have survived intact for over 70 million years, such concerns were set aside and the find was received as one of the year’s most stunning scientific discoveries.

    Schweitzer and team continued to receive accolades from the scientific community until a team of scientists at the Burke Museum of Natural History and Culture at the University of Washington decided to examine a fossilized turtle toe in the hopes of finding even more dinosaur tissue.

    They cracked open the bone, put it under an electron microscope, and within minutes saw spheres reminiscent of blood cells, like those reported by Schweitzer’s group.

    “We did the happy dance,” said Thomas Kaye, an associate researcher at the museum and the leader of the group.

    At first, the findings were similar to those of Schweitzer’s group. Subsequent analysis showed that proteins in the material resembled those found in birds, long thought to be close relatives of dinosaurs. Furthermore, when the team proceeded to dissolve the bone in mild acid, hidden tissue that resembled vessels and bone-forming cells seemed to form.

    But as Kaye examined more fossils, he was puzzled to find similar materials in nearly every bone. Unable to reconcile the notion that so much tissue could have survived for millions of years, he turned to Zbigniew Sawlowicz of Jagiellonian University in Poland. Sawlowicz identified the small spheres resembling blood cells as framboids, or iron-containing structures known to form in the presence of bacteria. The researchers also reported the presence of pockets of microbe-like shapes and tiny furrows that seemed to have been bacteria-blazed trails through the slimy substance.

    At that point Kaye realized that evidence — and common sense — clearly pointed to the fact that he was not examining dinosaur tissue but rather simple bacterial leftovers. In fact, examination with light and electron microscopy led the team to conclude that the substances were most likely remnants of biofilms, or a structured community of bacteria contained within a self-made matrix. According to Kaye, bacterial biofilm colonies infiltrating tiny cavities in the bones long after the dinosaurs died may have naturally molded into shapes resembling the tissues they replaced. His theory is also backed by evidence derived from carbon dating which showed that the tissue-like material in one of the samples had formed around 1960 rather than during prehistoric times. Kaye published his findings in the online journal PLoS ONE two weeks ago.[2]

    The finding sparked a strong response from the researchers who originally claimed to have found ancient dinosaur tissue. Schweitzer argues that there are significant holes in Kaye’s study, namely an explanation for why the protein in the tissue looks like that expected for a dinosaur. She added that her group has considered biofilms but has found no evidence for their presence. Errors in the current study “seem to underlie a fundamental misunderstanding of our work, our data and our interpretations,” Schweitzer commented to the press.

    Kaye disagrees, claiming that between the carbon dating and electron microscopy there is little doubt that the “tissue” is nothing but biofilm sludge. “Believe me, I didn’t want it to be this explanation,” he said. “I would much rather have it be dinosaurian tissue.”

    Other researchers seem hesitant to make a definitive statement about the controversy. “It’s actually quite common to find biofilms in areas where fossils would be formed,” said Frank Corsetti, an earth scientist at USC who was not involved in the research. “It’s an interesting idea, but the jury is still out.”

    Is the jury still out? If it is, I’m not sure it should be. Consider the fact that Kaye found tissue-like substances in a number of fossilized bones. Now consider that biofilms and their remnants are being found in an increasing number of remote places, ranging from the human body, to oceans, even volcanic rock and glaciers. I think it’s pretty clear that Kaye’s explanation has the ring of truth.

    This may be a case of Schweitzer letting her scientific judgment be clouded by the esteem accorded her. If so, this wouldn’t be the first time a researcher regarded as an expert has failed to admit error. There is a whole camp of researchers, including Dr. Michael Holick and Dr. Reinhold Vieth, who have built their reputations on a spurious premise: vitamin D is a near-miracle substance capable of curbing the incidence of an array of chronic diseases. Does this really make sense that a steroid-like substance could reduce chronic disease over the long term?

    That vitamin D can only help chronic disease is one theory which hasn’t aged well. In fact, a growing balance of evidence says the opposite is true. Ingested vitamin D has been shown to deactivate the vitamin D receptor and suppress the innate immune system, and rates of chronic diseases are increasing even as we consume historically high levels of vitamin D. How has the pro-vitamin D camp responded to such contrary evidence?

    Certainly not as well as one might hope. We continue to see papers, which go to extraordinary lengths to distort the evidence. Stephen Strauss deconstructs one such paper – Exhibit A in a long and uninterrupted pattern of denial.

    The next time you are asked how the Marshall Protocol can hold water when the world’s top vitamin D “experts” still clamor for vitamin D supplementation, you may want to think of Dr. Schweitzer. Some things are simply too good to be true, and that goes for dinosaur tissue and vitamin D.

    REFERENCES

    1. Schweitzer, M. H., Wittmeyer, J. L., Horner, J. R., & Toporski, J. K. (2005). Soft-Tissue Vessels and Cellular Preservation in Tyrannosaurus rex. Science, 307(5717), 1952. []
    2. Kaye, T. G., Gaugler, G., & Sawlowicz, Z. (2008). Dinosaurian Soft Tissues Interpreted as Bacterial Biofilms. PLoS ONE, 3(7), e2808. []
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  • Filed under: News Flash
  • The actor and comedian Bernie Mac died today, and it was because of sarcoidosis. Preliminary news reports say otherwise. A statement by Mac’s publicist, who very likely got it on authority from his doctors, said that it was the “complications due to pneumonia” which ended his life. Mac had suffered from the disease sarcoidosis for 20 some years.

    Pneumonia is a lung disease, and the lungs of a patient with sarcoidosis are greatly weakened by the chronic intraphagocytic metagenomic bacteria that cause the illness. Though it is truly a deadly disease, Mac expressed little concern, publicly at least, about sarcoidosis. Mac was likely convinced by his doctors that sarcoidosis could be successfully kept at bay by high doses of immunosuppressants. In one statement, Mac said his sarcoidosis had “gone into remission” around 2005.

    The evidence says that sarcoidosis doesn’t go away. The 2003 NIH ACCESS study followed 215 sarcoidosis patients for two years. Two years is the period during which it is sometimes mistakenly thought that the disease can go into remission. NIH ACCESS found that measures of sarcoidosis severity remained unchanged over the two-year period, despite the fact that many patients were using corticosteroids and other immunosuppressive drugs– and despite the fact that the study’s authors went to great lengths to equivocate about what their data really meant.

    In fact, in the NIH ACCESS study there were no documented cases of spontaneous remission. Even in the positive-sounding “improved” category for clinical markers, the percentages described were at best “improved”, not “better” and certainly not “cured.” The study also concluded that most patients with persistent sarcoidosis at two years were “unlikely to have resolution of the illness” and that “end-stage pulmonary sarcoidosis usually develops over one or two decades.”

    In simple terms, the study found that not one patient recovered over a two year period, and that any patient to remain ill with sarcoidosis for two years is likely to die from the disease over the following ten to twenty years.

    When asked, Mac’s publicist indicated his pneumonia was unrelated to his sarcoidosis, but those of us who know better realize that the opposite is true. Many of the chronic bacterial species that cause sarcoidosis create substances that block the Vitamin D Receptor – a fundamental receptor that controls many components of the innate immune response including transcription of the bulk of the body’s antimicrobial peptides.

    Mac’s choice to be treated with the “first-line treatment” for sarcoidosis – immunosuppressants including prednisone no doubt – was doubly unfortunate. Doing so inactivates the innate immune system, which allows a heavier load of VDR-dysregulating bacteria to accumulate… which, in turn, further inactivates the innate immune system. In such a state of disrepair, the immune system has little recourse in its fight against an otherwise easily dispatched strain of pneumonia.

    Clearly, Mac’s doctors incorrectly faulted an overactive immune response for the disease. Without being too dramatic, it’s also clear their ignorance had deadly repercussions.

    Mac’s story is Exhibit A that sarcoidosis is deadly. Also, it is an apt example of how mortality associated with sarcoidosis goes underreported in cases where opportunistic infections are erroneously attributed to be the cause of death. According to much of the medical community, Mac’s sarcoidosis was in remission and an unrelated case of pneumonia was the cause of death. No wonder statistics on sarcoidosis and death are inaccurate. If a patient succumbs to a co-infection directly related to the sarcoidosis disease process the co-infection is blamed rather than sarcoidosis itself.

    A look back to Mac’s comments about sarcoidosis in 2005 show just how uninformed he was about his disease.

    Four years ago, Mac announced to the public that he had sarcoidosis, communicating through his publicist that he had been dealing with the disease since his 20s.

    Yet, he contended, “I’ve had sarcoidosis since 1983, and it has not altered or limited my lifestyle. No one knows where sarcoidosis comes from or where it starts, and there’s no known cause for this condition that affects primarily minorities.”

    Despite this blithe statement, the actor was promptly hospitalized after completing work on Ocean’s Twelve and filming on the fourth season of The Bernie Mac Show was subsequently delayed.

    Initially, a Fox representative said Mac was merely taking a self-imposed hiatus because he was suffering from exhaustion, brought on by a heavy work schedule. But the network later said Mac was suffering from pneumonia. In fact, his publicist finally admitted that he “had double pneumonia which weakened his lungs and his entire immune system, and the sarcoidosis symptoms became pronounced.”

    The same publicist was quick to point out that sarcoidosis is a “treatable illness and not deadly.” In his statement, Mac says, “I still walk, play basketball and do normal things…. Since sarcoidosis hasn’t slowed me down, then it shouldn’t be a concern for others.”

    While Mac’s death is certainly tragic, a second tragedy is the misinformation he and his publicists repeated. Perhaps he was forced to pretend that he was feeling well despite his sarcoidosis symptoms so that he would not be asked to give up any movie roles or sitcom appearances.

    But anyone familiar with sarcoidosis knows that Mac must have been suffering greatly from the illness, and his case of “double pneumonia” in 2005 makes it obvious how ill he really was. Mac could have done a service to the community by communicating the actual seriousness of his disease to the public, but instead he made the mistake of accepting the statements of his doctors as an accurate depiction of sarcoidosis.

    How long will it take before sarcoidosis is given full credit for the deadly disease that it is? More importantly though, how long will it take for the breadth of the medical world to finally acknowledge that the cure for sarcoidosis exists and has already cured people? It’s disturbing that ever since biomedical researcher Trevor Marshall published the landmark papers “Sarcoidosis and Antibiotics: Reflections on the First Year” in 2003 and “Sarcoidosis Succumbs to Antibiotics” in 2004, physicians and the FDA have been privy to the scientific knowledge that allows sarcoidosis to be treated correctly. Yet, as in Mac’s case, they continue to turn to conventional dogma when treating the disease in place of embracing the paradigm shifts necessary to understand the illness at the molecular level. One thing is for sure – if Bernie Mac had been treated with the Marshall Protocol he would be alive and well today.

    Even those people who have yet to understand the potential of the Marshall Protocol should at least be forced to admit that the standard treatment for sarcoidosis – the ample use of corticosteroids that weaken immune function – puts patients in a place where they can easily succumb to infections. So Mac’s death makes it clear that conventional treatment for sarcoidosis is not only ineffective but also quite dangerous and even life threatening.

    We also can hope that while tragic, Mac’s death may at least cause the medical community and the public to raise an eyebrow about the fact that attempts to deny the seriousness of sarcoidosis do little to stop the disease from taking lives.

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  • How are the pathogens that cause Th1 disease passed from parent to child? For one thing, it’s quite probable that the pathogens are able to survive in the sperm and egg. It’s equally true that the pathogens are simply passed among people in close contact, and infants and their parents are together quite often.

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

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

    HPV attacking a cell

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

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

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

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

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

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

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  • By this point, people familiar with the Marshall pathogenesis realize that the Vitamin D Receptor plays an extremely important role in activating immune function and keeping the chronic, intraphagocytic bacteria that cause inflammatory disease under control.

    But when the vitamin D feedback pathways fleshed out by Marshall in a recentBioEssays paper are examined, another important receptor enters the picture.[1]It goes by the name of the Pregane X Receptor (PXR), and like the VDR, the PXR is also a nuclear receptor. Mainstream researchers generally understand that the PXR plays an important role in regulating the metabolism, transport, and excretion of exogenous compounds, steroid hormones, vitamins, bile salts, and xenobiotics (chemicals that are foreign to the body). However, they are only recently beginning to understand that the receptor is also intricately connected to VDR function, vitamin D metabolism, and proper regulation of the vitamin D metabolites.

    The PXR is unique in the sense that its ligand binding pocket (the place where other molecules can dock into the receptor) enlarges to allow for activation by large molecules or shrinks to accommodate smaller molecules such as the steroids.

    The PXR molecule

    Marshall’s model of vitamin D metabolism predicts that blockage of the VDR will cause problems with the feedback pathways that keep levels of the vitamin D metabolites 25-D and 1,25-D in the correct range. To be more specific, when the VDR is blocked by bacterial substances and 25-D, it can not longer transcribe an important gene that under normal circumstances allows for the transcription of CYP24A1, an enzyme whose role is to inactivate excess 1,25-D. However, while it is the VDR’s job to transcribe the gene for CYP24A1, the PXR actually induces transcription, or actual creation, of the enzyme. This means that any molecule capable of slowing the activity of the PXR also allows for less production of CYP24A1.

    The consequences of the above are two-fold. If the VDR is blocked, it will transcribe the gene for CYP24A1 at a greatly reduced rate. If the PXR is blocked, the actual creation of the enzyme will be thwarted as well. Under such circumstances, the amount of CYP24A1 in the tissues drops significantly, meaning that 1,25-D is able to reach unnaturally high levels without any system to keep it in check.

    But what blocks the PXR? After deriving data from a structural model of the PXR that has just been published, Marshall used nuclear receptor modeling to show that 1,25-D binds the PXR and slows its activity, acting as a strong antagonist. According to Marshall, “[1,25-D] almost certainly will competitively displaces the native ligand(s) [of the PXR] at physiologic concentrations.” This means that high levels of 1,25-D slow PXR activity, blocking production of the CYP24A1 that would otherwise cause 1,25-D to be broken down to other forms of vitamin D.

    Still, a skeptic might ask, “Besides Marshall’s in silico data, how do we know that 1,25-D inactivates the PXR causing a drop in the production of CYP24A1?”

    In a study recently published in BMC Evolutionary Biology researchers performed a detailed analysis of molecules that activate the PXR. They ended up detecting numerous compounds that activate (serve as agonists) of the receptor. Interestingly, 25-D and 1,25-D were not among the compounds that they found to be PXR agonists. This strongly suggests that, as Marshall puts forth, the vitamins D do indeed serve as antagonists of the PXR.

    “Of interest is that they found that 1,25-D and 25-D were not agonists. Since my in-silico work has identified the very high affinity they have for the PXR, it follows that they must be antagonists, which is what I had deduced and published in figures 1 and 2 of my paper [BioEssays 2008],” states Marshall.

    One of the PXR agonists detected by the team was Hyperforin, or St John’s Wort. Now that it is confirmed as a PXR target, Marshall warns against its use, essentially because any molecule that interferes with the receptors that control the vitamin D receptors is likely to dysregulate immune function.The team also noted that another primary target of the PXR is rifampicin. Since rifampicin (a drug often used to treat infections) is derived from streptococcal bacteria, one could say that the PXR is essentially activated by a pathogen, a reality compatible with the fact that pathogens themselves can directly affect the body’s receptors and feedback pathways. Furthermore, the PXR is also strongly activated by dioxin, a compound that has been linked to an increased risk of cancer. According to Marshall, the fact that dioxin binds the PXR with such a high affinity provides a possible pathway for how the substance causes damage to the immune system.

    The VDR and PXR work in such a symbiotic fashion that the two receptors likely evolved from the same base structures. Such PXR/VDR homology fits nicely with Marshall’s view of the immune system. When asked about the immune system, Marshall emphasizes that it was not designed in order to accomplish specific tasks – its creation was never planned. Rather, it simply evolved. Because evolutionary processes are ruled by chance, not everything a particular receptor or cell type does is necessarily beneficial. Yet, it can be assumed that those components of the immune system that remain with us today exist because the bulk of what they do is useful. Certainly the majority of functions performed by the VDR and the PXR are critical to our well being.

    REFERENCES

    1. Ekins, S., Reschly, E., Hagey, L., & Krasowski, M. (2008). Evolution of pharmacologic specificity in the pregnane X receptor. BMC Evolutionary Biology, 8(1), 103. doi: 10.1186/1471-2148-8-103. []
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  • 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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  • 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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  • 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.