“Men who have excessive faith in their theories or ideas are not only ill prepared for making discoveries; they also make very poor observations. Of necessity, they observe with a preconceived idea, and when they devise an experiment, they can see, in its results, only a confirmation of their theory. In this way they distort observation and often neglect very important facts because they do not further their aim…”
–Claude Bernard, An Introduction to the Study of Experimental Medicine

 

I’ve been on the Marshall Protocol since May of 2005. Before I began the MP, I remember reading through the documentation and thinking, “You know, this makes a lot of sense to me. I could really see how this could work.”

What follows are ten reasons why the MP made sense to me. Those of you who have other thoughts about why the MP “just makes sense” are encouraged to share your insights by posting a comment at the end of this piece. You must click on the title of the piece for the comment box to appear.

Bacteria are everywhere, probably causing more harm than good.

Every major disease to befall mankind has, in the end, been linked to a pathogen. Whereas centuries ago doctors who treated patients with leeches and bloodletting wondered about the cause of tuberculosis, polio, syphilis, leprosy, even the plague - it wasn’t long before these diseases were linked to bacteria.

Now, we find ourselves in the midst of a new epidemic of chronic disease in which millions of people are suffering from ailments that mainstream medicine still insists to be of unknown cause. Is it possible that this community has underestimated the ability of bacteria to cause other diseases? That, would be an understatement.

Just a month ago, NASA announced that the results of a study which demonstrated that the so-called sterile clean rooms in which they assemble spacecraft and prepare them for launch are actually filled with a diversity of hardy bacteria.[1]

In the human body, bacterial cells outnumber human cells.

Why were the bacteria not previously detected? Because according to Dr. Venkateswaran who ran the study, the bacterial species had never before been cultivated in a medium in which they were actually able to grow.

It was only after Venkateswaran and team used a powerful molecular detection mechanism known as ribosomal RNA gene sequence analysis, that they were able to detect myriad bacterial species in the rooms previously touted as “sterile.”

In fact, according to the study, samples taken from clean rooms at the Jet Propulsion Laboratory, the Kennedy Space Flight Center in Florida, and the Johnson Space Center in Houston revealed the presence of almost 100 types of bacteria, about 45 percent of which were previously unknown to science. The findings were a major wake-up call for NASA, an agency now forced to wonder exactly how many unknown pathogens have been taken to the moon and Mars.

Similarly, it’s clearly overreaching for doctors and researchers to think that we have come to appreciate the full extent to which bacteria drive illness. How could any physician actually believe that the discovery of penicillin and other antibiotics has forever stopped bacteria in their tracks? Especially when an increasing number of studies are showing that most of the bacteria in our environment have yet to be named and detected?

“It has been estimated that only 0.4% of all extant bacterial species have been identified. Does this remarkable lack of knowledge pertain to the subset of microorganisms both capable and accomplished in causing human disease?” asks Dave Relman, PhD, of Stanford University.[2] Yes, argues the assistant professor of medicine and of microbiology and immunology, and those of us familiar with the Marshall Protocol know that he is absolutely right.

The bacteria we harbor are likely causing more harm than good.

Of course every physician will admit that a virtually endless number of bacteria thrive in the human body. Yet few of them pause to wonder what all these pathogens are capable of doing. “Most of the cells in your body are not your own, nor are they even human,” argues Rowan Hooper of Wired Magazine. “They are bacterial. From the invisible strands of fungi waiting to sprout between our toes, to the kilogram of bacterial matter in our guts, we are best viewed as walking ‘superorganisms,’ highly complex conglomerations of human cells, bacteria, fungi and viruses.”

But for decades, the medical community has sloughed off the implication that these trillions of pathogens we harbor can affect our health by assuring us that these bacteria are commensal, sharing our food but doing no real harm. It’s wishful thinking. In a world where predators dominate the circle of life, isn’t it rather odd to assume that the trillions of bacteria that invade and persist in our bodies are all microscopic Buddhas, intent on living harmoniously inside their host? Surely as people begin to age and the species of bacteria in the body begin to shift, many, if not the majority, of these bacteria have their own interest in mind.

L-form bacteria have been detected, studied, and photographed for decades.

In 1895, scientists first observed that classical forms of bacteria are capable of transforming into smaller forms that lack cell walls. Since that time, these pathogens have been repeatedly grown under specific laboratory conditions and at the moment are easily visualized under the electron microscope.

Lida Mattman’s displays hundreds of pictures of L-form bacteria.

So much information has been gathered about these pathogens– the way they grow, reproduce, move, change shape, how they can be cultured– that researchers such as Lida Mattman and Gerald Domingue have published entire textbooks that detail how L-form bacteria persist in the tissues and change form during different stages of their lifecycles. These textbooks and as well as many of the hundreds of papers published on L-form are filled with pictures clearly showing the persistent pathogens in the tissues of people with nearly every disease that the MP can potentially treat. If seeing is believing, then what more proof do we need?

L-form bacteria would get more scholarly ink were it not for a single factor: they don’t grow in a standard Petri dish using the usual culture methods. L-form bacteria must be grown at different temperatures than classical bacterial forms and in mediums such as blood agar. Since the vast majority of mainstream researchers have failed to familiarize themselves with these laboratory techniques it’s no wonder that most doctors are oblivious to the bacteria making their patients sick.

“Features of a number of important but poorly explained human clinical syndromes strongly indicate a microbial etiology,” states Relman. “In these syndromes, the failure of cultivation-dependent microbial detection methods reveals our ignorance of microbial growth requirements.”

The concept of autoimmune disease makes little sense.

At the beginning of the 20th century German scientist Paul Ehrlich proposed the concept of “horror autotoxicus”, wherein a “normal” body does not mount an immune response against its own tissues. Soon, researchers began to hypothesize that inflammatory disease might stem from the failure of an organism to recognize its own constituent parts as “self”, resulting in an immune response against its own cells and tissues.

The “autoimmune disease” article on Wikipedia lists seven different theories that try to explain what might cause the immune system to supposedly lose control - all of which are quite complicated, and all of which are supported by little evidence at the molecular level.

Some researchers favor the Clonal Deletion Theory, in which self-reactive lymphoid cells are destroyed during the development of the immune system. Others back the Clonal Anergy Theory, insisting that self-reactive T- or B-cells become inactivated in the normal individual and thus cannot amplify the immune response. Then, there is the Idiotype Network theory, wherein a network of antibodies capable of neutralizing self-reactive antibodies exists naturally within the body. And don’t forget the Clonal Ignorance theory, the Supressor Population theory, or the Regulatory T-cell theory.

These and other suspiciously complex explanations can’t help but invoke Occam’s Razor which states that in the absence of other factors the simplest explanation is usually the right one. Why then, is it so hard to appreciate that inflammatory diseases are the result of infection?

“Why would the human body, which has evolved so elegantly over the course of millions of years retain such a debilitating flaw?”Surely the actual mechanisms behind “autoimmune disease” also remain elusive because when it comes down to it, the concept makes little sense. Could it really be possible that the millions of people who suffer from “autoimmune disease” all have immune systems that have turned against them? Why would the human body, which has evolved so elegantly over the course of millions of years retain such a debilitating flaw? Evolutionarily speaking, since the immune system is such a vitally important part of survival, the genes of those people who lost the ability to differentiate “self” from “non-self” should have been eliminated by natural selection long ago. There is simply no parallel for a long-standing trait that puts humans at such a profound reproductive disadvantage.

Central to the concept of autoimmune disease is the presence of an inflammatory response that results when the immune system secretes cytokines, or proteins that cause pain and fatigue. But what triggers this cytokine release? Doesn’t it make sense that something is provoking the immune system? Perhaps….a pathogen? Since it’s universally accepted that bacteria cause the release of cytokines during acute infection, why wouldn’t they cause the inflammation seen in patients with chronic disease? “The epidemiologic, clinical, and pathologic features of many chronic inflammatory diseases are consistent with a microbial cause,” states the CDC.[3]

Symptom presentation in patients with chronic disease suggests an infectious cause.

Modern medicine’s understanding of the body as a series of discrete systems blinds the profession to the nature of bacterial infections, which care nothing of such categories. If doctors were ever to fully embrace the overlap of symptoms and diagnoses - the fact that sarcoidosis patients have dyslexia, and fibromyalgia patients have gastrointestinal problems - it would be all too clear that chronically ill patients are suffering from system wide dysfunction which is best explained by infection.

“But specialists have trouble recognizing the systemic nature of chronic symptoms.”But specialists have trouble recognizing the systemic nature of chronic symptoms. Most pulmonologists will tell you that sarcoidosis is only a lung disease, when in fact, many patients with the illness actually find other symptoms to be more of a problem than those in the lungs. “Funnily enough, I never had much in the way of lung symptoms, yet most doctors think of sarcoidosis just as a lung disease,” states Julia Greer, an MP patient with sarcoidosis.

It’s almost as if, as the classic analogy goes, these doctors are all blindfolded, yet still trying to figure out the nature of something that’s right in front of their faces. One feels a tusk, another rough skin. Others large toenails or giant ears – yet each of them remains focused only on the small area they can physically examine. Take off your blindfolds, doctors – it’s an elephant, and by that I mean an infection.

This analogy essentially applies to most diseases of “unknown cause” which the medical community has labeled with an array of different names, but, in reality, all result from the same pathogenesis - namely infection with different species of L-form bacteria, biofilm bacteria, and other treatment resistant, hard-to-detect “persisters”. Once the immune system is weakened by these bacteria, viruses, fungi, and protozoa can also thrive.

Each person’s symptoms arise from the unique mix of pathogens they collect over a lifetime, meaning that no two people are alike. Surely this explains why most people who end up at the doctor’s office have symptoms that could be attributed to multiple conditions. What name you give these symptoms doesn’t really matter. “The fact that some conditions are not currently diagnosed as illness doesn’t matter either,” says Marshall.

Marshall’s molecular modeling research has revealed the most logical of bacterial survival mechanisms.

Researchers at McGill University have compiled two lists of genes transcribed by the Vitamin D Receptor including 913 genes on the confirmed list and over 20,000 on the putative list. As this list implies, the VDR plays an undeniably fundamental role in the body.

But the role of the VDR doesn’t stop at gene transcription. It also controls the activity of the innate immune system and the production of many of the antimicrobial peptides - peptides that kill bacteria, viruses, and fungae by a variety of mechanisms including disrupting membranes, interfering with metabolism, and targeting components of the machinery inside the cell.

Thus, if the Vitamin D Receptor is not functioning correctly, it’s no stretch to think that dysfunction will occur. First, the expression of thousands of genes is thwarted. Then, the innate immune system slows down. And finally, production of the AMPs decreases – meaning that bacteria in the body find it exceptionally easy to spread.

Marshall points to a 2007 paper showing that a species of gliding bacteria creates a substance that is able to bind the VDR and slow its activity. Eureka! This discovery strongly suggests that other pathogens can create similar substances, each of which can potentially block the VDR and diminish its ability keep bacteria in check. “There is now proof of concept that bacterial genomes are capable of producing at least one ligand which acts as a strong VDR antagonist,” says Marshall.

“What an exceptionally logical survival mechanism for any form of pathogen.”What an exceptionally logical survival mechanism for any form of pathogen. By creating one single substance to block the VDR, they can, in a knockout blow, disable the receptor that would otherwise activate numerous pathways to interfere with their ability to persist in the body.

“Think about it for a minute,” says Marshall. “If you were a persistent pathogen, wouldn’t it seem a good idea to disable your host’s ability to produce the antimicrobial peptides? And if you discovered that disabling just one receptor, the VDR, would get rid of [many types of AMPs], wouldn’t you try to evolve a mechanism for doing that?”

Thus, many of the bacteria we harbor have hit the nail on the head. Take control of the VDR and other vital receptors and it’s suddenly easy to disrupt the body’s delicate state of homeostasis.

One would also look at the ability of L-form bacteria to live inside the cells of the immune system that are supposed to render them dead, or persist inside biofilms – protective protein matrixes that once again protect them from the effects of standard antibiotic therapy as exceptionally logical survival mechnisms. According to the Centers for Disease Contol and Prevention, ”Biofilms, or microbial communities that behave like biofilms, represent potential, unrecognized stages in the pathways from infectious agent exposure to chronic disease.”[3]

Mainstream medicine is clearly caught up in a cascade of mistaken consensus.

The contradicting studies released year after year about autoimmune disease, the failure of researchers in the field of genetics, who have been given billions of dollars in grant money, to create even one effective form of gene therapy, the ever greater number of patients who are referred from doctor to doctor without receiving an accurate diagnosis, the fact that patients given vitamin D fail to show long-term improvement – all suggest that most members of the medical community are caught in a cascade of mistaken consensus.

“We like to think that people improve their judgment by putting their minds together, and sometimes they do,” says John Tierney of the New York Times. “The studio audience at ‘Who Wants to Be a Millionaire’ usually votes for the right answer. But suppose, instead of the audience members voting silently in unison, they voted out loud one after another. And suppose the first person gets it wrong.”

If the second person isn’t sure of the answer, he’s liable to go along with the first person’s guess. By then, even if the third person suspects another answer is right, she’s more liable to go along just because she assumes the first two together know more than she does. Thus begins an “informational cascade” as one person after another assumes that the rest can’t all be wrong.

“Cascades are especially common in medicine.”“Cascades are especially common in medicine”, explains Tierney. Doctors unable to keep up with the volume of research take their cues from others and look for guidance from experts — or at least someone who sounds confident.This happens more than one might think.

One recent example is the cascade that led researchers to conclude that a relationship exists between dietary fat and heart disease when in reality, as Pulitzer prize winning author Gary Taubes explains in his book “Good Calories, Bad Calories”, the theory that low-fat diets afford protection against coronary heart disease has been repeatedly overturned in clinical trials.

Taubes describes how, in the case of dietary fat and heart disease, the NIH hosted a series of “consensus conferences” that officially put an end to decades of debate on the issue. Researchers who did not agree with the theory were simply not invited and ostracized to the sidelines. “The NIH Conference officially gave the appearance of unanimity where no unanimity existed,” states Taubes. “After all, if there had been a true consensus, you wouldn’t have had to have a consensus conference.”

This brings to mind the recent 2007 NIH conference “Vitamin D and Health in the 21st Century” where the only people invited to speak at the gathering were those who have spoken favorably about Vitamin D supplementation. Rather than inviting Dr. Marshall to chair the session “Potential Adverse Outcomes of Vitamin D”, the slot was given to Professor Reinhold Vieth, one of the most zealous and outspoken proponents of the notion that the public should consume huge amounts of extra vitamin D.

“The presence of the immunopathological reaction is proof positive that the body is indeed killing bacteria.”Naturally, other doctors and researchers are taking their cues from Vieth and the other “consensus” conference participants, rendering them oblivious to the actual controversy surrounding vitamin D. These and other similar accounts are proof positive that when researchers and doctors get caught up in cascades even large groups of intelligent people can turn out to be wrong.

It’s also only natural that those researchers caught up in the cascades surrounding autoimmune disease, genetic predisposition, and vitamin D are reluctant to take note of the novel concepts put forth by Marshall and other researchers stressing the importance of bacteria and the VDR in chronic disease. As Atle Selberg, winner of the 1950 Fields Medal in mathematics once stated, “The thing is, it’s very dangerous to have a fixed idea. A person with a fixed idea will always find some way of convincing himself in the end that he is right.”

The idea of psychosomatic illness doesn’t make sense.

When patients with CFS, fibromyalgia, Lyme disease and some other chronic conditions complain of pain and fatigue they are all too often told their illness is psychosomatic. This diagnosis has no greater explanatory power than saying such a person is a witch and inhabited by sinister spirits. Is it not the height of ridiculousness that the mind would ever conspire to simulate a real illness?

Has the psychosomatic diagnosis ever made any sense? It’s against human nature and contrary to the survival of the species for the mind to create the sensation of symptoms in instances where there is apparently nothing wrong with the body. Yet, over and over again, we hear stories of people who are repeatedly diagnosed with psychosomatic illness after seeing multiple doctors.

People with fibromyalgia and CFS suffer from real physical symptoms.

Greatly ironic is the fact that those researchers who truly understand fibromyalgia, CFS and Lyme disease argue that patients with these illnesses often experience more physical debilitation than patients with diseases consistently recognized as real.

A study published recently in the International Journal of Clinical Practice found that patients with fibromyalgia had an overall health status burden that was greater in magnitude compared to people with other specific pain conditions that are widely accepted as impairing.[4]

Similarly, according to Dr. William Reeves, the lead expert on CFS at the Center for Disease Control and Prevention, “People with CFS are as sick and as functionally impaired as someone with AIDS, with breast cancer, with chronic obstructive pulmonary disease.”[5] In fact, researchers at DePaul University in Chicago found that the mean age at which patients with CFS die from cancer is considerably younger than that of the general population.[6]

It’s time to accept the obvious. Nobody would go to a doctor unless they were feeling real physical symptoms. Nobody would pay the extravagant fees for multiple doctor visits unless they were seriously sick. And few people would complain of symptoms to their friends and family unless something was seriously wrong. Nobody wants to be seen as the person who never feels like doing anything. Attention is great, but only when it comes from your Dad, or your sister, or your co-workers – not from a dubious doctor. Who needs that kind of abuse?

The psychosomatic diagnosis is the perfect group hug of laziness, ignorance, and hubris. Patients on the receiving end of the diagnosis are essentially being told, “I cannot explain your symptoms, so I’m blaming you for them.”It’s only logical that those unfortunate people who are told that severe physical symptoms are “all in their heads” are suffering from chronic bacterial infections. Infections with pathogens that their doctors have no idea how to culture or identify.

So called vitamin D “experts” are missing vital information about the substance they study.

Vitamin D is not a vitamin. Any molecular biologist will state with confidence that it is actually a potent secosteroid and transcriptional activator that controls the activity of the Vitamin D Receptor. This understanding has been seemingly lost to all those clinicians who, picturing vitamin D as a nutrient, unreservedly recommend the addition of the substance to our diets, from pre-natal vitamins right through to the end of life – adhering to a model no more sophisticated than “vitamin in, benefit out.”

In fact, the actions of the various forms of vitamin D are so complex that the vast majority of vitamin D “experts” are missing important chunks of the actual picture. These “experts” incorrectly attribute grandiose healing properties to vitamin D. Yet one must ask, in their view, what exactly is “vitamin” D doing in the body?

Most understand that the activated form of vitamin D (1,25-D) controls the transcription of thousands of genes. Yet these researchers still remain completely unaware of the molecular models showing that high levels of the precursor form of vitamin D (25-D) obtained from supplements and excess sun exposure (which is an immunosuppressive secosteroid) thwarts the entire transcription process.

In an article on a Canadian health website John Jacob Cannell, head of the Vitamin D Council, an agency that advocates high levels of vitamin D supplementation states, “There is no better anti-cancer agent than activated vitamin D. I mean, it does everything you’d want.” Everything you’d want? Does he have a model to support that statement?

Marshall’s molecular models reveal exactly what vitamin D does in the body.

The reality is that these “experts” will never be able to put forth an accurate model of vitamin D’s purely “beneficial” actions because they don’t appreciate the fundamental properties of the substance they are dealing with, nor the underlying bacterial cause of symptoms in patients with chronic disease. In contrast, Marshall has precise molecular models detailing exactly what receptors and substances vitamin D affects in the body – models now backed up by a substantial amount of clinical evidence. Hmm…who to believe?

Of course uttering a collective “whoops” will not come easily to these “experts.” After all, as Mark Nathan Cohen states in Health and the Rise of Civilization, “A colleague once defined an academic discipline as a group of scholars who had agreed not to ask certain embarrassing questions about key assumptions.”

The rate of chronic disease continues to go up, despite the fact that people are taking more vitamin D supplements and taking more immunosuppressive drugs

If the claims made by vitamin D “experts” are correct, and the idea of “autoimmune disease” is correct, then why is the rate of chronic disease increasing as we add an ever-greater amount of vitamin D to the food supply and doctors continue to treat their patients with immunosuppressive drugs?

A team of researchers at John Hopkins University released a statement saying that if people keep gaining weight at the current rate, 75 percent of U.S. adults and 24 percent of U.S. children will be overweight or obese by 2015. Similarly, according to the CDC, seven of every 10 Americans who die each year, or more than 1.7 million people, die of a chronic disease.

“The difference is that over the past few decades the rate of chronic disease has escalated to the point where we are now in the midst of a literal epidemic.”Researchers at the University of Cincinnati College of Medicine in Ohio found that almost 9% of American Children meet DSM-IV criteria for ADHD. The Center for Disease Control and prevention now estimates that 2.54% of persons 18 to 59 years of age suffer from CFS. The number of American children and adolescents treated for bipolar disorder increased 40-fold from 1994 to 2003. The list goes on and on….

Chronic diseases have been around for centuries. Shakespeare and Beethoven are rumored to have suffered from chronic symptoms resembling those of sarcoidosis or CFS. Even the neolithic Iceman, who, a decade ago was found embedded in ice, is thought to have suffered from arteriosclerosis, a stroke, and arthritis. The difference is that over the past few decades the rate of chronic disease has escalated to the point where we are now in the midst of a literal epidemic.

Is it merely a coincidence that during the 20th century we have:

1. Added vitamin D to the food chain – to the point where today not just milk but butters, orange juice, cereals, grain and pasta products, cheeses and soy milk are all fortified with the secosteroid.

2. Started to routinely give patients anti-inflammatory drugs, ranging from over the counter anti-pyretics and anti-histamines, to prescription steroids, such as prednisone, in order to suppress what is incorrectly regarded as inflammatory response by an immune system that has lost control (e.g autoimmune disease).

3. Have started to equate tanned skin with beauty – meaning that excessive sun exposure at the beach and the use of tanning beds has become commonplace.

4. >Frequently administered the beta-lactam antibiotics such as penicillin, which kill most classical forms of bacteria during acute infection but cause the formation of L-form bacteria in the process.

Surely these factors offer a plausible explanation for why the rate of chronic disease has skyrocketed.

There is no other explanation for immunopathology then bacterial death.

Since a boatload of evidence suggests that diseases of “unknown cause” are infectious, any effective treatment would kill the microbes causing such an illness. In sufficient numbers, bacteria that die generate an immunopathological reaction. This reaction is unavoidable, and it is the hallmark of the MP.

Immunopathology occurs because after bacteria die, the associated release of toxins and cellular debris occurs faster than the body can process them via the kidneys and liver. Bacterial death is also accompanied by the release of cytokines – proteins that cause pain and fatigue. All of the above cause a temporary rise in diseases symptoms.

The existence of this reaction has been noted decades before the creation of the MP. Both Adolf Jarisch, an Austrian dermatologist, and Karl Herxheimer, a German dermatologist, are credited with the discovery of how the immune system reacts to bacterial death.

Jarisch noticed that patients with syphilis experienced unexpected worsening of skin lesions after being treated with mercury (which has antibacterial properties). His patients also experienced fever, nausea, and vomiting. The reaction lasted several days, but was almost always followed by resolution of the skin lesions.

Patients on the MP use a combination of Benicar and pulsed, low-dose antibiotics to elicit bacterial death. Because, like Jarisch’s syphilis patients, people on the MP note an increase in symptoms once they have started medication, the presence of the immunopathological reaction is proof positive that the body is indeed killing bacteria – which in turn means that bacteria are undoubtedly driving the disease process in the first place.

A devil’s advocate would be hard-pressed to explain MP patients’ consistent immunopathology in any other way. After all, both Benicar and the antibiotics used by the MP have excellent safety profiles, so rises in symptoms can seldom, if ever, be attributed to the side effects of these medications.

Just as one might suspect, patients who increase their antibiotics find that their symptoms return with increased severity. Similarly, taking lower doses of antibiotics, which decreases the number of bacteria being killed, results in a reduction in symptoms.

In fact, since each MP antibiotic targets different species of bacteria, patients can often switch from one antibiotic to the next in order to elicit different symptoms.

Nothing but calculated and controllable bacterial death can explain the above reactions. And, nothing but the absence of bacterial death can explain why when patients who complete the MP - who are taking just as much Benicar as the day they started, along with the highest dose of antibiotics allowed by the treatment - find that the medications no longer elicit immunopathology. Why? Because all their bacteria have been killed - a reality backed up by the fact that their symptoms have resolved.

Why does the MP make sense to you? Post a comment! And don’t forget to click on the title of the piece for the comment box to appear

 

REFERENCES

  1. Leary, W. E. (2007). In NASA’s Sterile Areas, Plenty of Robust Bacteria. The New York Times. [↩]
  2. Relman, D. A. (1998). Detection and Identification of Previously Unrecognized Microbial Pathogens. Emerging Infectious Diseases, 4(3). [↩]
  3. O’Connor SM, Taylor CE, Hughes JM. (2006). Emerging infectious determinants of chronic diseases. Emerging Infectious Diseases. [↩] [↩]
  4. Hoffman, D. L., & Dukes, E. M. (2007). The health status burden of people with fibromyalgia: a review of studies that assessed health status with the SF-36 or the SF-12. Int J Clin Pract. [↩]
  5. Tuller, D. (2007). Chronic Fatigue No Longer Seen as ‘Yuppie Flu’. The New York Times. [↩]
  6. Jason, L. A., Corradi, K., Gress, S., Williams, S., & Torres-Harding, S. (2006). Causes of death among patients with chronic fatigue syndrome. Health care for women international, 27(7), 615-26. [↩]