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M.E. and Chronic Fatigue Syndrome vitamins, herbs and supplements
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What Causes Chronic Fatigue Syndrome & Myalgic Encephalomyelitis?

Chronic Fatigue Syndrome & Myalgic Encephalomyelitis Causes Although ME/CFS has inspired thousands of scientific and popular publications, its cause remains, as yet, unidentified. The debate surrounding the pathogenesis of ME/CFS has raged for decades. Some support the idea that a single pathogen (e.g a virus) produces the illness, while others adhere to the idea that ME/CFS is environmental, the result of exposure to a number of toxins that damage the nervous and immune systems. Each of these theories generates its own research, its own spate of tests, and its own treatment protocols.

ME/CFS is a complex illness, which makes the search for a cause laden with difficulties. However, enough is known of the illness to establish some basic parameters. Any etiological model for ME/CFS must take into account the following: 1) multisystem symptoms, 2) chronic illness, and 3) outbreaks.

While most researchers tend to focus on 1 and 2, they often forget the infectious aspect of ME/CFS. Ultimately, any theory attempting to explain how ME/CFS occurs in an individual must also account for why it occurs in groups.

Dr. Bell describes the pathogenesis of ME/CFS as the "1-2 punch." The first punch would be the cause, which can eventually become an occult, or hidden infection, the second is the "trigger." The first exposure to a pathogen weakens the host, the second actually makes the person ill. There is considerable support for the idea of occult infection in many disease processes, particularly in persistent viral and bacterial infections (such as Lyme).

The predominant theory in the U.S. is that ME/CFS is caused by a virus. This theory is supported by history (ME/CFS epidemics have often followed polio epidemics), incidence (correlation with a triggering viral illness), flu-like symptoms (swollen lymph nodes, malaise, sore throat), and similarities to other ailments with viral etiologies, notably mononucleosis and post-polio syndrome.

A viral cause is supported by a substantial body of primary research. In the mid-1980s, Dr. Cheney and Dr. Peterson, the two clinicians who reported the 1984 outbreak in Incline Village, Nevada, found high titers of Epstein-Barr virus (EBV) in their patients. At the time, they believed the illness was caused by chronic activation of this virus alone. However, the presence of EBV titers in most of the healthy population, as well as high titers of many other viruses in the ME/CFS population, eliminated EBV as the primary culprit. Nevertheless, the idea that a herpesvirus was at the root of the illness has persisted, primarily because the herpesviruses are known to establish latency - that is, they are never completely eradicated by the immune system.

Dr. Martin Lerner's research has shown that multiple herpesvirus strains can affect what appear to be healthy cells, altering their function. In these cases, the host cells are considered "non-permissive," meaning they don't permit viral replication. However, what Dr. Lerner found in ME/CFS patients was evidence of cell dysregulation eventually leading to cell apoptosis (death) in non-permissive cells. In short, the damage to these healthy cells was just as profound as the damage to those destroyed by viral replication. (Dr. Richardson also observed this phenomenon in Coxsackie virus infections, in which the function of healthy cells was altered due to nearby viral activity.) Dr. Lerner has supported his position with the evidence of successful treatment. In his practice, he has found that antiviral medications which control herpesviruses (e.g., Valcyte) also eradicate ME/CFS symptoms.

Some researchers believe that because herpesviruses are ubiquitous, their replication is a consequence rather than a cause. These scientists have turned their attention to those viruses that are known to have direct effects on the immune system as well as the ability to use the host's own DNA to replicate. In 1986 Dr. Michael Holmes, a researcher in New Zealand, found evidence of a retrovirus in ME/CFS patients. This finding was validated by research conducted in 1990 by Dr. Elaine De Freitas of the Wistar Institute in Philadelphia. She found viral fragments of HTLV (human T-lymphotropic virus) in the mitochondria of cells from 30 patients with ME/CFS. None of the 20 controls tested positive for the virus. Dr. De Freitas concluded that her research supported an association between an HTLV-II-like virus and ME/CFS.

Dr. De Freitas' research was not replicated by the CDC, so her theory of a retroviral etiology was abandoned. However, nearly twenty years later, another retrovirus was discovered in ME/CFS patients. In 2009 the Whittemore Peterson Institute (WPI) announced that a team of researchers had found definitive proof of a retrovirus in ME/CFS patients. The researchers, who hailed from several prestigious labs, including the National Cancer Institute, the Lerner Institute, the Cleveland Clinic, and the Laboratory of Cancer Prevention, identified DNA from a human gammaretrovirus, xenotropic murine leukemia virus-related virus (XMRV) in 68 of 101 patients (67%). The group concluded that their findings "raise the possibility that XMRV may be a contributing factor in the pathogenesis of CFS." Like the work of De Freitas, the study could not be replicated. In September 2011, the researchers were compelled to publish a retraction of the original study, which effectively put a halt to XMRV research, as well as any other significant research into a retroviral cause for ME/CFS.

Retroviruses and herpesviruses are not the only viruses that can cause lasting damage. The late Dr. John Richardson, a British physician who treated patients with post-viral syndromes for more than four decades, believed an enterovirus much like the one which causes polio might be at the root of the ME.

Enteroviruses are highly infectious viruses that enter the body through the gastrointestinal (GI) tract and gravitate to the central nervous system, heart and muscle tissues. They are resistant to both stomach acid and bile, which enables them to persist in the GI tract for long periods of time.

To make his case for an enteroviral etiology, Dr. Richardson pointed to the remarkable similarity and incidence of polio-related symptoms and those produced by ME. Dr. Peter Behan and his team of researchers in Glasgow, Scotland, also found indications of a persistent enteroviral infection in about 60% of the ME/CFS patients they tested. Dr. Behan speculated that the virus is a mutated form of poliovirus that attacks the brain rather than the spinal cord, causing a "cascade effect." This theory fits in well with the historical evidence, as well as epidemiology. (The early outbreaks of ME followed polio epidemics.)

Dr. Chia has also discovered enteroviral infections in ME/CFS patients. Stomach biopsies taken from a group of 165 ME/CFS patients showed persistent active enteroviral infections, in some cases several years after the initial infection was first noted. The degree of viral load matched symptoms to such an extent that the researchers concluded that enteroviral infections might be causal. Dr. Chia tested his hypothesis several years later by following a group of patients who had been admitted to the hospital with acute enteroviral infections. Three of those patients went on to develop ME/CFS.

Other less well-known viruses have also been implicated. In the early 1990s, W. John Martin found evidence of atypical viral infection in the cerebrospinal fluid and brains of several patients who had previously been diagnosed with ME/CFS. The infection was thought to be due to a stealth virus, a class of neurotoxic virus that cause very little inflammation.

Parvovirus B19, a virus that targets red blood cell precursors in bone marrow, has been implicated as well. Follow-up studies of patients with acute parvovirus B19 infections conducted by J.R. Kerr in Great Britain showed that a significant proportion of patients went on to develop both arthritis and ME/CFS. Kerr proposed a genetic flaw that would allow for persistent immune activation - a mechanism which has been explored by many other researchers.

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