What's up with Dr. De Meirleir and the NCF?

Discussion in 'Fibromyalgia Main Forum' started by swedeboy, Jan 25, 2007.

  1. swedeboy

    swedeboy Member

    I recently found this posted by the National CFIDS Foundation. I read the article but my cognitive dysfunction keeps getting in the way, hehe, can anyone explain why the NCF doesn't like Dr. Meirleir?

    Here's the first paragraph:

    "NCF Board Calls for Researcher's Resignation!"

    "The Board of The National CFIDS Foundation, Inc. (NCF) has called for the resignation of Dr. Kenny L. De Meirleir, Professor of Physiology and Medicine at the Vrige Universiteit (Free University) Brussel, Belgium, Board Member of the American Association for Chronic Fatigue Syndrome, and editor of The Journal of Chronic Fatigue Syndrome put out by The Haworth Medical Press. Dr. DeMeirleir both a Ph.D. and an M.D. (clinician) whom, in the board's opinion, should not be allowed to ever see patients again."

    The rest of the article is at

    Thanks, Peace and Love, Swedeboy
  2. cherylsue

    cherylsue Member

    Here's the article. Sounds like someone got a little greedy. He's an excellent researcher, however.

    NCF Board Calls for Researcher's Resignation!

    The Board of The National CFIDS Foundation, Inc. (NCF) has called for the
    resignation of Dr. Kenny L. De Meirleir, Professor of Physiology and Medicine at
    the Vrige Universiteit (Free University) Brussel, Belgium, Board Member of the
    American Association for Chronic Fatigue Syndrome, and editor of The Journal of
    Chronic Fatigue Syndrome put out by The Haworth Medical Press. Dr. DeMeirleir
    both a Ph.D. and an M.D. (clinician) whom, in the board's opinion, should not be
    allowed to ever see patients again.

    His discovery, fully covered in the preceeding article, is of such huge
    significance that, had he published years ago when it was first discovered, further
    research on this particular discovery could have saved many lives of patients who
    are now deceased as well as many more who are battling for their very lives at this
    very moment.

    The board members of the NCF did not take this vote lightly, but considered
    the ramifications of the work that Dr. De Meirleir neglected to publish in
    peer-reviewed medical journals, although he carefully put his work into patents to
    protect the monetary rewards he would get from his discovery as well as in a book
    he published, Chronic Fatigue Syndrome: A Biological Approach, that was
    published by CRC Press (Florida) in 2002. The book presents his research as well
    as research of others on ME/CFIDS. The small hardcover volume edited by
    Patrick Englebienne, Ph.D. and De Meirleir, has different authorship of each
    chapter but is filled with abbreviations for a variety of molecules and receptors
    that are not easy to remember without frequent reference to the full text. The
    volume is very technical and should never be reviewed by those without a
    moderate knowledge of molecular genetics or biochemistry. However, his
    important discovery is in his own chapter and was discovered by the medical
    director of the NCF. Without publication in a medical journal, it went unnoticed
    and unread by most researchers in the world and did millions of ME/CFIDS
    patients a huge disservice along with many wasted years.

    In its discussion of the ramifications of keeping such important work
    unpublished, the board members related stories of many patients whose very lives
    have been snuffed out by the effects of this research discovery. De Meirleir
    capitalized on the work on Dr. Robert Suhadolnik's important discovery of the
    dysregulation of the antiviral RNase-L pathway that plays a central role in
    ME/CFIDS. Had DeMeirleir published his work in a medical journal, others could
    have combined their own discoveries and related it to this work to further what
    could be a significant therapy for ME/CFIDS. Years have been lost because of
    his failure to share this information freely with the research community.
    Lives have been lost and that continues to this very day.

    The RNase-L is a molecule that, when it is activated, degrades single and
    double-stranded RNA that is both viral and cellular. It is vital to the apoptosis
    (programmed cell death) that is going on in ME/CFIDS. Usually, the RNase L
    molecule is carefully controlled by another molecule, the 37 KDalton, but this
    controlling molecule has been degraded and can no longer control this antiviral
    pathway. The results is the breaking apart (cleavage) or bending of some vital
    intracellular proteins. Indeed, the discoverer of this pathway's upregulation, Dr.
    Suhadolnik, once asked at an international conference on ME/CFIDS, why these
    patients with ME/CFIDS are still alive! (Dr. Suhadolnik works at the School of
    Medicine at Temple University. The medical school sold the patent rights of his
    discovery to both Dr. DeMeirleir and RED Laboratories of Belgium. Both Dr.
    DeMeirleir's co-editor and colleague of his book, Dr. Englebienne, and the owner
    of RED Laboratories, C. V. Herst, Ph.D., worked for Dr. Suhadolnik in the past
    before moving to Belgium.)

    The board of the NCF has found the actions of Dr. DeMeirleir (and his
    collaborators and partners) particularly reprehensible and ask that the AACFS
    dismiss him as a member immediately, that The Haworth Medical Press fire him as
    a co-editor, and that other organizations around the world that have lauded him in
    the past rethink their positions carefully and join our us in our dismay of someone
    who would neglect those suffering in favor of his monetary agenda. The National
    CFIDS Foundation, Inc., upon hearing of this important work that went
    unpublished, immediately asked other researchers to look into doing this work and
    have, since, funded them for the work. It is hoped that the work will be completed
    soon, published in a peer-reviewed medical journal, and we will be able to go on
    and fund work that will show how this damaging activity can be blocked within
    the body to stop the ongoing destruction which is the result of ME/CFIDS.

    [Ed. Note: DeMeirleir also promotes the experimental drug, Ampligen in his book
    as he has for years. He never mentions, however, the money he got for every
    patient he put on the drug from Hemispherx Biopharma. It is known, from patents
    owned by the manufacturer of Ampligen, Hemispherx BioPharma, that Ampligen
    contributes to apoptosis (cell death) causing the road to malignancies to be far
    shorter. DeMeirleir is now promoting Acclydine, another herbal extract that he
    knows will help the patient feel a bit better but will, in no way, stop the process
    that is leading toward ME/CFIDS ending up fatal. By helping just one arena that
    is causing such a vast amount of damage in the body, the others go on unchecked
    and the professor knows this all too well having protected his work in expensive
    patents. Yet he, evidently, feels a compulsion to lighten the wallets of patients
    with fairly useless drugs.]

    The National CFIDS Foundation * 103 Aletha Rd, Needham Ma 02492 * (781) 449-3535 Fax (781) 449-8606
  3. spacee

    spacee Member

    Sure can't tell a book by it's cover really fits here.

    How sad.

  4. Slayadragon

    Slayadragon New Member

    Please see my post called "Rnase and Ampligen."

    I'm trying to figure out what to think of Dr. DeMeirleir in it.

  5. deliarose

    deliarose New Member

    he just happened to come up in conversation.. my doc said he has probably seen more CFS patients than any other physician in the world.

    But it sounds like a conveyor belt system. He sees 100 patients a week!

    It's not particularly relevant .(unless u infer he's making a lot of $$ off his patients). I just throw it in teh mix.

  6. karinaxx

    karinaxx New Member

    has met him several times and i am gonna see him in march.

    apparently he cares very much and does not have any other joice than seeing so many patients, because there are just so many patients who want to see him.

    the disagreement with the NCF was a very strange one: they accused him of witholding important findings:( losss of STAT1 + RLnase)
    i and all of us, dont know what agreement he had with them and what realy happend!
    i find the politics of the NCF in general a bit strange and they use a lot of headlines slogans in their news letter and other presantations.

    the fact that they had a disagreement does not change the fact, that he is one of the most knowledgeable doctors for CFIDS around. he also recently helped to draw up the Cannadian Consensus Document and is widly respected for his work.

    hope that helps to clear up the confusion.

    he is also on the advisery comitee here on the board, i think.
    [This Message was Edited on 01/25/2007]
  7. Slayadragon

    Slayadragon New Member

    My own experience in publishing things in academic journals is that it's a major pain in the butt and takes a huge amount of time ane energy. Usually the reviewer tear apart articles and force you to do a lot more study before they will publish them.

    My best guess is that Dr. DeMeirlier had a few tentative findings as well as a hypothesis about this topic, but not enough to get it published in a good journal. If he was uncertain with regard to how well his work would be received and feared having to spend much of his time getting it published, he may have chosen to work with patients rather than to jump through the hoops of getting it accepted.

    I have no direct experience in getting things published in medical journals, of course. However, it is my impression that this effort to get stuff in those journals requires more effort even than getting stuff in psychology or marketing journals (where I have my experience).

    The idea that huge numbers of patients have been hurt by Dr. DeMeirlier's decision not to publish his probably inconclusive findings as well as tentative theories seems remote. I haven't seen any other findings about issues related to CFS leading to magic treatments, and this one does not seem that outrageously clear and startling that it would have made much difference either.

    I could be wrong, of course. I don't know Dr. DeMeirlier and do not understand exactly what he found out. (Note that the article does not make this clear and purposely advises people not to read the book in which he mentioned his tentative findings because it's purportedly too hard to understand.)

    I don't understand why Dr. DeMeirlier is under such attack at the moment. I will say that academia is a tremendously competitive and political field, and sometimes a very dirty business. (If you've read "And the Band Played on," you will have a bit of an understanding about just how ruthless researchers were with regards to being the first to figure out what was going on with AIDS.)

    I'm not saying that's the reason that Dr. De Meirlier is being attacked. It's merely one plausible explanation, based on my own first-hand observations of how academia can work.

    [This Message was Edited on 01/27/2007]
  8. swedeboy

    swedeboy Member

    I really admire the NFC. I think it's commitment to it's members is great. And the fact that they are not afraid to take a side and voice their opinion is outstanding.

    But it makes me wonder when I read stuff like the above article. And Is everyone aware of the NCF's press release last year? Where they boldly claim that they have discovered the virus that causes CFS. I haven't heard of that claim leading to anything yet.

    I Sure hope the NFC is on the right track here!
  9. karinaxx

    karinaxx New Member

    Dr.Meirleirs research finding could actually (and is) a bio marker he found to be unique in CFIDS patients.
    There is a lot on information on the loss of STAT 1 and the RLnase on the NCF archives and here in the archives.

    STAT 1 is a marker for immune deficiencies like in AIDS and others. it is actually not very difficult to understand , i am just not good at explaining.
    it is one test you can do to support the diagnosis of CFIDS/ME.
    RLnase is the antiviral pathway, which seems to be damaged in us ect.

    its best if you read up on this yourself, as i said , i am no good at explaining.

    take care karina
  10. karinaxx

    karinaxx New Member

    yes, most of us have discussed this findings here on the board and have not heard more anything yet.
    if you go back into their archives you find that they made numerous such claims. and i am more sceptical now of this claims made.
    but who nows, maybe one day the are right, matter of time, at least they are searching.

  11. Lichu3

    Lichu3 New Member

    I have had articles published in medical journals and as Lisa says, it is not an easy process and at times, who reviews your articles has an impact on whether it is published and what you end up putting in the articles.

    However, it is generally a given in academia that if you have an important discovery, that you publish it both for your own gain (recognition,future grants, etc.) as well as for general public knowledge. All research has flaws but if these are discussed in the article, oftentimes it can still be accepted. I would also add a)most respected journals require researchers to disclose the funding sources for the research and whether they have financial ties to the research (this means that the results may need to be taken with a grain of salt) b)some scientists will sign an agreement beforehand with a pharmaceutical-sponsored projects that they (the scientists) have control of what will be published (e.g. both negative and positive results). There's still a lot of behind the scenes politics but these are some safeguards.

    Statements about the impact of him withholding his research are difficult to gauge without long-term studies of patients on Ampligen or the other med.(I haven't gone to NCF site though.)

    It seems the CDC/NIH/?pharma researchers need to get their act together to keep us from being at the mercy of poor research and potential snake oil sellers.

    For all of you interested and not aware of this already, free summaries of published medical research from the major medical journals (here and abroad) are available on www.pubmed.gov. I'm trying to get access to a website which will allow me to read full-text articles without having to pay a fee (can't venture to the library anymore) Anyone with ideas?

  12. swedeboy

    swedeboy Member

    Are you an MD?

    Where in Northern Cali are you. I am in Saratoga. I am looking for a good Doctor. Do you know of any?

    Thanks for the great feedback!

    Peace and Love, Sean
  13. Lichu3

    Lichu3 New Member

    I am located in the Peninsula. Unfortunately, I can't really recommend a good doctor since I've only lived here briefly and didn't really get to know the other doctors yet. My primary doctor wasn't accepting patients at all but accepted me. She was a friend of a friend.

    I would be interested to hear how things go with your appt. with Dr. Montoya. My history is somewhat similar to yours in that I had a couple of strange episodes following a "flu" two years ago before really getting sick this year. I think if it isn't HHV-6 (which I don't have either) that those of us with this history probably do have some yet unknown virus or some known virus with as yet unknown actions.

    Oh, I was a physician but I worked primarily with people in their 80-90s (geriatrics) so I didn't see the group of people covered by this board.

    Have to get to bed!
    [This Message was Edited on 01/25/2007]
  14. karinaxx

    karinaxx New Member

    here you are?
    how are you?

    as you can see, my brain is getting worse day by day, i am not even getting Rnase-L right.
    But i still have some part of the brain left and this is the one to connect information.

    ok, here it is: Two of the enzymes implicated in CFS, RNase L and PKR, are activated by IFN’s (See RNase L in CFS). this IFN is directed by the Hypothalamus (BRAIN;CNS)

    i am blabbl-ing away since some weeks about the Hypothalamus, because i asked myself why we dont get fever anymore? Fever is produced by Pyrogen,Pyrogen needs ACTH,ACTH needs ATP and all this is elicited by the Hypothalamus/thalamus. When i studied the interaction of the Hyppthalamus i realized that ALL the findings yet, including the Rnase-L, congestive heart failure(chenney), metabolism, low NKcells, low blood volume , Interleukins (ergo large part of the Immunesystem)information processing (Aphasia)and so on, leads to the Hypothalamus, brain.
    not to my surprise i found that a few have made this connection before me (dont think i have that much brain left to top all the research allready done, hahah) and i stumbled over several articles on the http://www.phoenix-cfs.org
    there are more, but recently there has been alot of attention on HHV-6, which is a good canditate to make resposnible for all of this, because this virus attacks this part of the brain.
    there are a lot of good articles on the site i got this from, i just paste this one here:


    A Laymen's Guide to Chronic Fatigue Syndrome and the Brain

    Part I: The Fatigue in Chronic Fatigue Syndrome

    Is it Central?

    by Cort Johnson

    Keep Up on CFS Research - Get the Monthly Newsletter!


    Where does the fatigue in CFS originate? Fatigue can either be induced by problems in the periphery (i.e. the muscles) or can have an central (i.e. brain) origin. Chaudhuri and Behan assert the particular type of fatigue found in CFS could only come from the brain. Several studies have shown brain abnormalities in CFS. Not only do CFS patients display impaired motor performance but measurements of the part of the brain devoted to motor activity, the motor cortex, have at times shown reduced motor cortex activity. Other tests indicate CFS patients are unable to activate normal amounts of muscle during exercise. The cause of this inadequate muscle activation appears to lie not in reduced nerve conduction from the motor cortex but in impaired activation of the circuits leading to the motor cortex. Chaudhuri and Behan assert disrupted circuitry in the deep brain structures called the basal ganglia causes the phenomena known as central fatigue. They posit that disrupted informational flows from the basal ganglia to the cerebral cortex interrupt the process of ‘sustained attention’ that is critical to carrying out tasks. This interruption leads to a greater sense of effort, reduced motivation and ultimately to the increased fatigue during both physical and cognitive activities found not only in CFS but in other diseases with prominent fatigue.

    Introduction - In what part of the body does the fatigue in CFS originate? Is it the muscles? The immune system? The mitochondria? The brain?

    There’s more to CFS than the fatigue that its unfortunate name suggests. People with CFS often experience cognitive problems, sleep impairment, allergies and sensitivities, headaches, low grade fever, orthostatic intolerance, etc., etc. For many, however, fatigue – particularly after exercise – is the symptom that most colors their experiences.

    Fatigue, though, is a simple term for rather complex phenomena. This paper looks at the different types of fatigue that occur in diseases, describes which type is found in CFS and suggests a possible origin for it. It is primarily based on a series of papers by Chaudhuri and Behan (Chaudhuri and Behan 2000a, 2000b, 2004a, 2004b, Chaudhuri et. al. 2003)

    Weakness vs. Fatigue - The first thing to note is the difference between weakness and fatigue. Weakness is the ability to mount a specific amount of muscular force. Fatigue, a subjective term, denotes a feeling of tiredness or exhaustion. The distinction between these two terms is confused a bit by the definition of ‘muscular fatigue’ which is the inability to mount a specific a specific amount of force (weakness) over time Many neuromuscular disorders that cause extreme muscle weakness do not leave their victims feeling fatigued; they’re simply weak. Similarly victims of fatigue are not necessarily weak.

    Transitory vs. Chronic Fatigue - Transitory episodes of fatigue occur in healthy people when they are under stress, have poor sleep, during menstruation and during the acute phase of viral infections (Chaudhuri and Behan 2000). Fatigue is part of a constellation of signs and symptoms (lethargy, poor concentration, fever) that make up what is called ‘illness behavior’ which is evoked during the acute phase of viral infections. Illness behavior occurs when pro-inflammatory cytokines such as IL-1b, Il-6 and TNF-a interact with the brain.

    Stress, poor sleep, hormonal abnormalities and viral infections have all been suggested to contribute to the fatigue in CFS but none, as yet, can provide a satisfactory answer for it.

    Peripheral vs Central Fatigue - Pathologic fatigue can originate in the periphery (i.e. muscles) or it can be central (brain - induced) in nature or it can be both. Most often it is the result of one or the other.


    Early muscle fatigability is seen in defects in muscle function, neuromuscular transmission (myasthenic), diseases of the peripheral nerves and low motor neuron syndromes. While some CFS patients do display some muscular weakness it does not reach the level found in those with neuromuscular disorders such as myasthenia gravis or metabolic muscle diseases. The weakness CFS patients display in tests appears to be more the result of inactivity than an underlying pathology affecting the muscles (Chaudhuri and Behan 2000).

    The degree to which a peripheral dysfunction contributes to the fatigue in CFS is unclear. The presence of enteroviruses in the muscles of CFS patients is controversial but suggests peripherally induced fatigue could be a factor for a subset of patients (Lane et. al. 2004, Dalakas 2003). While some abnormalities in muscle histology (structure) were seen in one study, consistent abnormalities in muscle biochemistry and metabolism have not been seen. The evidence thus far suggests peripherally induced fatigue does not appear to play a large role in most CFS patients; i.e.CFS is not primarily a disorder of impaired muscle function.


    Central fatigue is characterized by feelings of constant tiredness or exhaustion. In contrast to peripheral fatigue central fatigue is largely a result of central nervous system (CNS) activity. What makes central (i.e. brain induced) fatigue stand apart from peripheral (i.e. muscle induced) induced fatigue is its extension into cognitive activities. In diseases of central fatigue both physical and mental activities evoke weariness. In diseases of peripheral fatigue only physical activities evoke fatigue.

    Diseases That Induce Central Fatigue - The authors list 22 neurological disorders and CFS that are associated with central fatigue. Some of interest in CFS include cerebral vasculitis, channelopathies (ciguatera, RNase L), hypothalamic disease, post Guillain Barre syndrome, post-infective fatigue states (post-polio, Lyme, Q-fever, viral fatigue) and sleep disorders.

    Narrowing their focus further the author’s list 12 diseases with fatigue symptoms similar to those found in CFS. They are found in the following categories:

    Genetic – mitochondrial cytopathy, myotonic dysfunction

    Viral - HIV induced encephalopathy, post-polio syndrome, chronic hepatitis C (added)

    ‘Diet’ - Vitamin B-12 deficiency, ciguatera poisoning

    Brain/CNS - Parkinson’s Disease, Alzheimer’s disease, multiple sclerosis, motor neuron disease, myotonic dysfunction, migraine, epilepsy, paroxysmal dsykinesia.

    (Editorial additions – Primary biliary cirrhosis (liver) and overtraining syndrome are also diseases with prominent fatigue.)

    Since there doesn’t appear to be a strong genetic component to CFS, the above list strongly suggests the type of fatigue found in CFS has an immune or central nervous system origin (or both).

    Defining Central Fatigue - Chaudhuri and Behan (2000) define central fatigue as the failure to initiate and/or sustain attentional tasks and physical activity. An inability to maintain in central fatigue since ‘focused attention’ is a key liability in central fatigue since ‘focused attention" (an automatic process) is necessary to incorporate the mental, physical and sensory inputs involved in completing a task. That is, if focused attention is impaired then integrating the various types of information needed to complete any task becomes difficult and the task become inordinately effortful.

    Where in the brain might this centrally induced fatigue arise? Some observations by Chaudhuri and Behan give us a starting place.

    The Central Motor System and Fatigue - Three of the five observations Chaudhuri and Behan use to support their claim that the fatigue in CFS is largely central concern decreased central motor activation or drive. Some are quite complex, they will be explained later.

    CFS patients have delayed central motor conduction similar to that seen in multiple sclerosis (MS) patients
    The delayed facilitation of central motor evoked potential (MEP) seen post-exercise CFS suggests depressed cortical excitability
    CFS patients display increased perception of effort that is associated with reduced central motor drive during exercise
    CFS patients are unable to fully activate their muscles during intense exercise despite having muscle activity (muscle metabolism, contraction)
    There is insufficient histological evidence of muscle injury to suggest structural muscle problems in CFS. Histology is the science of the minute structures of cells, tissues and organs.
    Motor Performance in CFS – Numerous studies indicate CFS patients exhibit impaired motor performance (Starr et. al. 2000. Davey et. al. 2001, Davey et. al. 2003). Motor performance tests usually involve doing a simple task like flexing a finger or limb. While these tests may seem simple almost to the point of banality the mental activity needed to repeatedly tap a finger or flex a muscle is actually quite complex These tests often show reduced repetitive movements over time and reduced reaction time to a stimulus.

    Reduced motor performance can be due to a disruption in the nerve conduction pathways leading from the motor cortex to the muscles, to a problem with the motor cortex itself, or with the circuits providing information to the motor cortex. Normal sensory nerve conduction times suggest the motor performance problems do not lie downstream of the motor cortex. Several studies, however, have found reduced motor cortex excitability in CFS patients during the performance of simple motor tasks.

    The Motor Cortex – Part of the cerebral cortex, the motor cortex activates the motor neurons that innervate the skeletal musculature. Motor cortex activity is particularly important in fine movements. The motor cortex is not only involved in the mechanistic propagation of muscle activity, however, it is also involved in the preparation for movement and in thinking about movement. Functional MRI’s (fMRI’s) have found that simply reading words referring to movement increases blood flows to the motor cortex.

    Motor Cortex Excitability refers to the activation of the motor cortex as measured by transcranial magnetic stimulation (TMS). In TMS a magnetic coil placed on ones head activates the ‘cortico-spinal tract’. (The cortico-spinal tract runs from the motor cortex via cortico-spinal fibers to the motor neurons. Motor neurons are nerves in the spinal cord whose axons connect with the skeletal muscles). If I have this right researchers vary the power of the magnetic field produced by TMS in order to determine the amplitude or range of the signals produced by the motor cortex. This amplitude, which is called the motor evoked potential (MEP) High MEP's during an activity such as moving a finger suggests the brain is sending sufficient amounts of information to properly activate the muscles needed to move that finger. Low motor cortex activity suggests reduced information flows may impede muscular activity.

    During prolonged exercise MEP's usually rise as the brain works to activate more and more motor units of the muscles. (A motor unit consists of a single motor neuron and the group of muscle fibers innervated by it.) Following exercise MEP's usually remain high for a period of time called the facilitation phase probably in order to maintain muscle readiness (contraction) or simply to keep the brain primed for more muscular activity. In the last or depression phase motor cortex excitability drops below baseline for a time.

    Ever increasing MEP during exercise is probably due to the motor cortex’s need to recruit more and more motor units of a muscle as it becomes become fatigued. High MEP’s in the post-exercise facilitation phase is believed to either be an attempt to maintain muscle contraction in the face of fatigue or to keep the muscles or brain primed for more muscle activity. During the depression phase following the facilitation phase motor cortex excitability drops down to below baseline for a time..

    Several studies have found abnormalities in MEP amplitude during exercise or the facilitation period in CFS. MEP immediately after exercise was significantly lower in CFS and depressed patients than controls and MEP facilitation 30 minutes after exercise was significantly less in CFS patients than other control groups in one study (Samii et.al. 1996). MEP's were lower both during exercise and in the facilitation period in another (Starr et. al. 2000). MEP was normal in another but a larger than normal ‘twitch response’ (see below) during exercise suggested an abnormality in the ‘electromechanical response’ to exercise was present. Interestingly given the feeling of always contracted muscles some CFS patients evidence, the authors noted background levels of muscle contraction effect the twitch/MEP relationship (Sacco et. al. 1999). Is resting muscle contraction in CFS increased? Corticospinal excitability or inhibition were normal in two other studies (Davey et. al. 2001, Zaman et. al 2001).

    The Twitch Response – (It was difficult to get background information on this subject – hopefully it’s correct). Another way to examine how effective motor cortex activity is is to examine the ‘twitch response’. As muscles fatigue during exercise the motor cortex activates more and more ‘motor units’ of the muscles. By stimulating the motor cortex and simultaneously determining through an electromyograph (EMG) reading the ‘twitch response’ evoked in the muscle TMS can be used to determine how fully muscles are activated by the motor cortex during exercise. If a muscle is fully activated by the motor cortex it will not respond to TMS. A less than fully activated muscle, however, will respond with a ‘twitch’. Larger than normal twitch responses suggest inadequate muscle recruitment by the motor cortex has occurred..

    The gold standard for measuring motor drive to the muscles involves stimulating the motor nerve and measuring the magnitude of the ‘muscle twitch’ that ensues. That has not been done in CFS but a substitute test involving interpolating the twitch force evoked during TMS suggested that CFS patients not only were not activating normal amounts of muscles during exercise but that the reduced muscle activation seen was due central inactivation; i.e. it was due to problems in the brain (Sacco et. al .1999).

    Stimulation of the motor cortex at the beginning of exercise involving a maximal effort should have no effect on the twitch response – one should be able to voluntarily recruit all the muscles needed. As fatigue progresses, however, apparently the brain is either not capable or is unwilling to recruit all the motor units it can. During this period TMS is able to evoke a strong twitch response. As all the motor unit of a muscle become recruited during exhaustive exercise, however, the twitch response fades. An early study (Kent-Braun 1993) found that even at the beginning of exercise before fatigue had a chance to occur electric stimulation could increase the maximum voluntary contraction elicited in CFS patients. A later study found the twitch force in CFS continued to increase in CFS patients during exercise far longer than it did in healthy controls (Sacco 1999). This in concert with decreased muscle rmsEMG levels suggested CFS patients were less able to activate their muscles during exercise than normal.

    Electromyography (EMS) - Another way to examine motor drive is to measure how much electrical activity is present in the muscles during exercise. The electrical activity a muscle is producing can be measured by an electromyography (EMG). Several studies have indicated CFS patients display greater reductions in rmsEMG activity during exercise than do controls and that the gap between the two groups becomes greater and greater as the exercise gets more and more fatiguing (Sacco et. al. 1999). This also suggests that as exercise progresses CFS patients are less and less able to recruit normal amounts of muscle.

    But is the problem with the motor cortex itself or with the information it is receiving? A 1991 study concluded that the fatigue in CFS is due to a dysfunction upstream of the primary motor cortex. Starr suggested the impairments seen are due to reduced premovement potentials because of impaired drive to the motor cortex (Starr et. al. 2000). Increased reaction and movement times in both visual and motor imaging tasks suggest that, instead of deficiencies in informational processing, CFS patients have a disrupted ‘motor response’ associated with response preparation (Davey et. al. 2003, de Lange et. al. 2004). That a measure believed to reflect cortical inhibition, SP duration, was prolonged in CFS patients suggested increased motor cortex inhibition (Sacco et. al. 1999) The brain is a maze of inhibitory and activating circuits. The overactivation of an inhibitory circuit could cause reduced motor cortex activity.

    A recent study also found strongly diminished central activation during exercise in CFS patients (Schillings et. al. 2004). Although electrical stimulation tests before exercise indicated CFS patients had the same muscle capacity as controls, CFS patients exerted a much (much) smaller maximum voluntary contraction of their biceps muscle (87-144) than did the control group. Significantly greater muscle activation by electrical stimulation during maximal muscle contraction indicated once again CFS patients were activating fewer of their muscles than were controls. The researchers concluded this was due to a ‘failure of central activation’, i.e. a failure of the brain to fully recruit all the muscles (Schillings et. al 2004).

    The authors put the reduced muscle activation seen in CFS patients in perspective by noting it was similar in magnitude to that measured in some stroke victims and ALS patients (Schillings et. al. 2004). Is this not a remarkable fact? CFS patients may be fatigued simply because they don’t use all their muscles. In fact their brains put into operation about as much of their muscles as some stroke victims.

    Possible Causes of Reduced Central Activation in CFS - The authors posited several possible causes for the reduced central activation found;

    Increased perception of pain or effort could lead to negative internal feedback and impaired muscle activation. This theory posits negative feedback suggesting imminent damage prompted the brain to refuse to employ all the muscles.
    Impaired concentration and effort prevented CFS patients from fully exerting themselves. This explanation was largely discarded by the authors.
    Disrupted processing in the motor or premotor areas possibly due to altered neurotransmitter concentrations prevented proper motor cortex activation (Shillings et al. 2004).
    The Location of the Problem - That many progressive neurodegenerative diseases that produce central fatigue involve injury to the pathways descending from the hypothalamus (basal ganglia, reticular, autonomic) suggests this part of the brain is involved in the genesis of centrally induced fatigue.

    The hypothalamus is ‘prominently involved in the functions of the autonomic (visceral motor), nervous system and in endocrine mechanisms; it also appears to play a role in neural mechanisms underlying moods and motivational states’ (Stedman’s Electronic Medical Dictionary 2004).

    Central fatigue is also often seen in people with lesions in the pathways in the brain associated with arousal and attention. A lesion is simply a wound or injury. These include the reticular and limbic systems and the basal ganglia.

    The reticular activating system denotes that part of the brainstem (which extends into the thalamus) that plays a central role in the organism's bodily and behavorial alertness. Through its ascending connections it affects the function of the cerebral cortex in modulating behavioral responsiveness; its descending (reticulospinal) connections effect body posture and reflexes.

    The limbic system is a collective term that denotes an array of interconnected brain structures (hippocampus, amygdala, fornicate gyrus) at or near the edge (limbus) of the cerebral hemisphere that connects with the hypothalamus. By way of these connections, the limbic system exerts an important influence upon the endocrine and autonomic motor systems; its functions also appear to affect motivational and mood states.

    Note that most of these systems interact either directly or are one step removed from interacting with the basal ganglia.

    THE BASAL GANGLIA – Chaudhuri and Behan believe the genesis of central fatigue begins in one of deepest parts of the brain, the basal ganglia. Sitting in the interior of the brain, the basal ganglia consists of six interconnected nuclei (caudate nucleus and putamen (striatum), globus pallidus, substantia nigra, subthalamic nucleus, amygdala that provide a link with the limbic system and the hypothalamus.

    The basal ganglia (and cerebellum) gets information from the cerebral (i.e. motor cortex), bounces it around its nuclei (processes it) and then sends it back to the cerebral cortex via the thalamus. Two circuits, a motor circuit and an ‘association’ or complex loop, connect the basal ganglia with the cerebral cortex. Chaudhuri and Behan believe the key disruption in central fatigue occurs in the non-motor or complex circuit (Chaudhuri and Behan 2000a). Why the non-motor circuit when we have been taking about reduced motor performance? Perhaps because lesions in the motor circuit are known to cause spectacular (and horrifying) symptoms not found in CFS. The continuous writhing movements of Huntington’s disease and the violent limb flinging of Ballismus are caused by damage to the subthalamic nucleus of the basal ganglia. The odd combination of rigidity and tremor seen in Parkinson’s disease are due to damage to the substantia nigra of the basal ganglia. Instead of having problems with circuits devoted specifically to movement Chaudhuri and Behan believe CFS patients have problems with circuits involved in information processing

    (Lets not forget the cerebellum - An extremely neuron rich organ, the cerebellum processes information involving movement, balance, cognition, language, etc. The inability of many CFS patients to pass the Romberg Test, appears to indicate damage to the cerebellum has occurred. Just like the basal ganglia the cerebellum sends its information to the cerebral cortex through the thalamus.)

    Based on current models of how the basal ganglia works Chaudhuri and Behan posit three disruptions that could be responsible for the central fatigue seen in CFS and other diseases. (Warning: very complex).

    an interruption in the associated or complex loop of the basal ganglia that provides information from the basal ganglia to the prefrontal cortex. The complex loop is associated with non-motor functions; i.e. information planning and processing.
    an increase in thalamic inhibition that impairs information flow from the basal ganglia to the thalamus and cortex. Remember the increased silent period times in CFS suggested increased motor cortex inhibition. Recent FMS studies finding reduced thalamic blood flow levels and activation suggest this scenario may apply to CFS's sister disease, Fibromyalgia.
    a modification of the cortex’s response to basal ganglia inputs due to altered activity between the thalamic and subthalamic nucleus in the basal ganglia.
    This is all very complex but the factor common to all these theories involves reduced information flows by one means or another (interrupted circuit, increased inhibition) from the basal ganglia to the rest of the brain.

    The authors note that interrupted signaling in the thalamic cortical loop is often found in diseases that induce central fatigue. They suggest reduced information flow through this circuit inhibits activation of the frontal lobe. Since the frontal lobe is involved in a very wide array of activities, frontal lobe impairment could cause a wide array of problems. Interestingly, given the similarities between post-polio syndrome and CFS, autopsies of polio patients showed damage to a number of deep brain structures including four of the six nuclei of basal ganglia (Chaudhuri and Behan 2000b).

    Based on their clinical experiences Chaudhuri and Behan assert that reduced self-motivation seen in people with central fatigue is at least partly due to the increased effort perceived by them. In order to initiate and perform any task sets of emotive, motor and sensory cues need to be integrated in such a manner as to propel one onto the series of actions needed to accomplish it. An inability to efficiently process these cues could cause an apparently easy activity to appear highly effortful. Since the basal ganglia are highly involved in processing the cues needed for task performance they are a logical place for a disruption that causes central fatigue to occur. One section of the basal ganglia, for instance, the caudate nuclei, connects motivational values to visual information.

    Chaudhuri and Behan suspect that disrupted ion channel/neurotransmitter activity in the basal ganglia alters the 'neuronal excitability of the cortical, limbic and brainstem areas. The disruptions in these deep brain areas could be responsible for the wide variety of symptoms seen in CFS. They believe the down regulated HPA axis activity (hypocortisolism) in CFS is probably an adaptive response to alterations in neurotransmitter activity rather than the primary cause of the fatigue in CFS. The immunological aberrations seen in CFS, in turn, reflect the disrupted HPA axis activity (Chaudhuri and Behan 2000b).

    Support for the Theory - Several studies have provided support for Chaudhuri and Behan’s model since it was published in 2001. Reduced activity during task activity was found in the caudate nuclei of the basal ganglia of CFS patients relative to controls (de Lange et. al. 2004). Three small magnetic resonance spectroscopy (MRS) studies have found increased choline peaks in the basal ganglia of CFS patients that are possibly indicative of increased reparative gliosis (membrane turnover perhaps due to infection) (Tomoda et. al. 2001, Puri et. al. 2002, Chaudhuri et. al. 2003) (See Choline on the Brain?). Another study found increased thalamic activation in CFS patients. Thalamic overactivation in CFS may indicate the need for increased attention to previously non-effortful tasks, a common finding for disorders characterized by reduced prefrontal perfusion (McHale et. al. 2000).

    Remember that all information from the basal ganglia (and the cerebellum) goes through the thalamus on the way to the cerebral cortex. The thalamus, formerly thought to be simply a sensory relay station for signals leading to the brain, is now believed to participate in motor function and planning and motor and cognitive coordination. Intriguingly the thalamus receives information regarding the ‘motor state’ from both the muscles and the cerebrum. Chaudhuri and Behan, however, suggested thalamic inhibition may occur in central fatigue. As noted earlier thalamic inhibition has recently been found in Fibromyalgia.

    Research into the origin of other fatiguing illnesses such as multiple sclerosis (MS) may provide clues to the fatigue experienced in CFS. MS patients with fatigue exhibit significantly lower activation of the cortical and subcortical areas of the brain devoted to motor planning and execution than do MS patients without fatigue. Several studies have indicated dysfunction in the subcortical circuits linking the basal ganglia, thalamus and frontal cortex occurs in MS. Just as in CFS patients fatigued MS patients display increased thalamic activation. The brain, a very malleable organ, does not sit still when one part of it is disturbed - it adjusts to the disturbance by routing information around the damaged area and ramping up activity elsewhere. In what may also be a compensatory reaction to impaired brain activity elsewhere, both fatigued MS and CFS patients exhibit a marked activation of the anterior cingulate region of the brain (Schmalling et. al. 2003). A part of the frontal lobe, the anterior cingulate is involved in the early stages of motor learning or planning and in ‘attentional tasks’. Interestingly, interferon A treatment, which often causes great fatigue, also results in increased anterior cingulate activation (Capuron et .al. 2005).This, of course, suggests an intriguing neuro-immune connection to fatigue centered in anterior cingulate. Two of the enzymes implicated in CFS, RNase L and PKR, are activated by IFN’s (See RNase L in CFS).

    Update - A recent update on the CDC's CFS webpage reported that a PET scan study examining interferon's effect on patients with malignant melanoma found that interferon treatment resulted in increased basal ganglia activity, particularly in the putamen and globus pallidus nuclei. This ties together increased the increased immune activity (interferon) that may be occurring in CFS with the altered function in the basal ganglia circuitry hypothesized by Chaudhuri and Behan How intriguing this is!

    Summary - These findings suggest the fatigue in CFS, MS and other diseases of central fatigue originates in abnormalities in deep brain circuits involved in motor planning and execution. The problem, then, appears to lie not in a disruption in the brains signal to the muscles but in brains ability to produce the signal in the first place. They suggest that the brains of central fatigue patients are hindered in their ability to integrate the multitude of signals involved in producing muscle activation. Thus this is a 'thinking' problem not a muscle problem. These findings appear to be in agreement with Chaudhuri and Behan’s model positing that disrupted deep brain (cortical-striatal (basal ganglia)-thalamo) circuitry plays an important role in central fatigue seen in CFS and other diseases.

    The Genesis of Central Fatigue – How might such a disruption occur? Both stroke and neurodegenerative disorders are known to destroy the subcortical circuits leading to the frontal cortex. Neither of these occur in CFS but neurotransmitter abnormalities can impair proper nervous system functioning and there is evidence of abnormal neurotransmitter activity. Neuronal channelopathies could alter sensitivities to neurotransmitters and/or cause defects in neurotransmitter transport and delivery that impair the proper transmission of nerve signals. Hypoxia (reduced oxygen levels), viruses, pro-inflammatory cytokines and an altered neurotransmitter balance can all cause central fatigue. The possibilities are explored in Part II of Central Fatigue in CFS - Potential Causes.

    Ongoing Research

    * In July 2005 the NIH opened a new RAF (request for applications) providing $4,000,000 for studies examining the neuro-immune interface in CFS.

    * During the 2004-5 period the CFID Association of America funded Dr. Shungu to examine brain metabolites using H MRS technology. Part of the abstract from the CAA's website is below.

    H MRS Neurometabolites as Diagnostic Markers for Chronic Fatigue Syndrome - During the past 3-4 years, our research group had the opportunity to use a brain imaging technique known as hydrogen magnetic resonance spectroscopic imaging (H MRSI) – an imaging technique that is similar to conventional MRI, except that it can measure levels of certain important brain chemicals or neurometabolites – to record the levels of such chemicals in the brain of 31 individuals suspected with CFS. Comparison of the levels of these neurometabolites with those in normal people, showed about 50% of all CFS patients had abnormal levels of the chemicals.

    This proposal's overall objective will be to develop H MRSI as a tool for evaluating CFS. To accomplish this, we will test the hypotheses that (1) CFS will be associated with specific changes in the levels of certain brain chemicals, and that such changes will be measurable by H MRSI; by refining this technique, these measurable brain chemical changes could serve as diagnostic markers of CFS; and (2) that the profile of these brain chemicals in CFS will be significantly different from that in people with psychiatric diseases, such as generalized anxiety, that are very similar to and often confused with CFS. Therefore, the results of this research will be able to establish not only that CFS has a distinct profile of certain brain chemicals than healthy human brain, but also that its profile is different from that of a very similar psychiatric disorder. This finding can be the basis for using the levels of brain chemicals measured by H MRSI as markers for chronic fatigue syndrome in clinical evaluations as well as in clinical trials of promising treatments.

    * From Dr. de Lange - F.C. Donders Centre for Cognitive Neuroimaging, University of Nijmegen, NL-6500 HB Nijmegen, The Netherlands - Dr. Lange recently published a paper indicating reduced gray matter volume in CFS.

    'The focus of my investigations are functional and structural alterations in the brain of CFS patients. With help of functional magnetic resonance imaging, we have found that CFS patients recruit more visually related structures to solve a motor imagery task, which could point to problems with motor planning. Furthermore, there was a difference between CFS patients and controls in error processing, pointing to differences in emotional/motivational processing. In a recent study, we found that grey matter volume was markedly reduced in CFS patients, w.r.t. healthy controls. This reduction bore a relationship with physical activity: the less physically active the CFS patient, the larger the grey matter reduction. Currently we're following up on this finding, to see whether the gray matter reduction we observed can be reversed with improvements or recovery of CFS over time.'

    *The longtime CFS researcher Dr. Natelson proposed a study to use microarrays to examine gene expression in the spinal fluid of CFS patients. Despite his already having the spinal fluid his request for funding to the NIH was denied and this very worthy project has been, unfortunately, been put on the back shelf.


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    Chaudhuri, A. and P. Behan. 2000b. Neurological dysfunction in Chronic Fatigue Syndrome. Journal of Chronic Fatigue Syndrome 6, 51-68.

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    Chaudhuri, A. and P. Behan. 2004b. Fatigue in neurological disorders. Lancet 363: 978-988.

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    Davey N J, Puri B K, Catley M, Main J, Nowicky A V, Zaman R. 2003. Deficit in motor performance correlates with changed corticospinal excitability in patients with chronic fatigue syndrome. Int J Clin Pract.;57(4):262-4.

    Dalakas MC. 2003. Enteroviruses in chronic fatigue syndrome: "now you see them, now you don't". J Neurol Neurosurg Psychiatry. 74:1361-2

    Dantzer, R. 2001. Cytokine-induced sickness behavior: mechanisms and implications. Ann N Y Acad Sci. 933:222-34.

    DeLange, F., Kalkman, J., Bleijenberg, G., Hagoort, P., Werf, S., van der Meer, J. and I. Toni. 2004. Neural correlates of the chronic fatigue syndrome – an fMRI study. Brain 127. 1948-1957.

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    Lane RJ, Soteriou BA, Zhang H, Archard LC. 2003. Enterovirus related metabolic myopathy: a postviral fatigue syndrome. J Neurol Neurosurg Psychiatry. 74(10):1382-6.

    Filippi, M., Rocca, M., Colomgo, B. Falini, A., Codella, M., Scotti, G. and G. Corni. 2002. Functional magnetic resonance imaging correlates of fatigue in multiple sclerosis. Neuroimage 15: 559-567.

    McHale, S., Lawrie, S., Cavanagh, J., Glabus, M., Murray, C., Goodwin, G. and K. Ebmeier. 2000. Cerebral perfusion in chronic fatigue syndrome. Britixh Journal of Psychiatry 176, 550-556.

    Puri, B., Counsell, S., Zaman, R., Main, J., Collins, A., Hajnal, J. and N. Davey. 2002. Relative increase in choline in the occipital cortex in chronic fatigue syndrome. Acta Psychiatrica Scandanavia 106: 224-226.

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  15. karinaxx

    karinaxx New Member

    actually this is somewhere from this site, just to clear up facts.

    carla was right, it is not only found in cfids, but FM too, others i do not know of. i just remembered from a interview i read, that what is unique, is that cfids patient apparently build up a small version of Rnase-L , seperate of the normal existing one. i hope i explained this one right.

    Dr. Kenny De Meirleir’s Breakthrough Research and Recommendations for CFS Testing & Treatment
    by Editor


    Kenny De Meirleir, MD, PhD, is a member of ProHealth’s Scientific Advisory Board
    As described in the following article, Dr. De Meirleir reports that his research indicates Chronic Fatigue Syndrome patients can be differentiated from healthy people with 99 percent accuracy based on a test for the presence of “low molecular weight” RNase L in the blood. He says the weight of LMW RNase L molecules found in the blood of CFS patients is less than half that of normal RNase L molecules. (And this holds true for individuals with several other illnesses, including Fibromyalgia.) Increased symptom severity correlates directly with increased levels of LMW RNase L.

    Additionally, though Dr. De Meirleir emphasizes that each patient’s profile is unique, he says his research indicates that CFS patients tend to fall into three groups with different test profiles and treatments. Based on the results of six tests, he reports he has been able to predict patients’ symptoms with 95 percent accuracy while the remaining 5 percent had overlap features. (See the footnotes for information about the workshop materials Dr. De Meirleir has developed for physicians and patients, and about his lab – located in Reno, Nevada – which offers diagnostic testing of samples from patients who may be candidates for a diagnosis of ME/CFS.)

    Highlights of Dr. Kenny De Meirleir’s Lecture on “Advances in ME/CFS Testing and Treatment,” presented in Calgary, Alberta, on April 2, 2006

    by Marjorie van de Sande


    Dr. De Meirleir is a world renowned researcher and is professor of Physiology and Internal Medicine at Free University of Brussels in Belgium. Dr. De Meirleir recently published his 600th peer-reviewed paper. He is co-editor of Chronic Fatigue Syndrome: A Biological Approach, co-editor of the Journal of Chronic Fatigue Syndrome, and reviewer for more than 10 other medical journals. Dr. De Meirleir was one of four international experts on the panel that developed the Canadian Consensus Document for ME/CFS. He assesses/treats 3,000 to 4,000 ME/CFS patients annually.

    Normal Response to Infectious Agents

    Numerous infectious agents can trigger ME/CFS. Infectious agents that invade cells release ribonucleic acid (RNA) or deoxyribonucleic acid (DNA) when they reproduce. Normally when a virus infects a cell, an enzyme called Ribonuclease L (RNase L) is activated and cuts the RNA of the infectious agent so it cannot replicate itself. The RNase L molecule also cuts the RNA of the infected cell, which triggers the cell’s death and removal. Then the RNase L molecule “switches off” and remains inactive so that it doesn’t damage healthy cells.

    Abnormal RNase L Molecule Found in ME/CFS Patients

    The normal weight of the RNase L molecule is 80 kilo Daltons (kDa). In ME/CFS patients, the RNase L molecule is being cut and weighs 37 kDa - less than half its normal weight. The low molecular weight (LMW) RNase L molecule can discriminate ME/CFS patients from healthy people, and illnesses such as Fibromyalgia, multiple sclerosis, cancer, AIDS and depression. The Centers for Disease Control and Prevention sent 100 blood samples to Dr. De Meirleir. Using the test for LMW RNase L, Dr. De Meirleir was able to identify which blood samples came from ME/CFS patients with 99 percent accuracy. These findings confirm an organic origin of ME/CFS and validate the diagnosis.

    Abnormal RNase L Molecule Causes Chronic Dysfunction of the Immune System

    The damaged RNase L molecule is not able to kill infectious agents and it keeps damaged cells alive. The body is unable to “switch off” these abnormal RNase L fragments, so they continue to cut the RNA of normal cells. The destructive RNase L fragment is six times more active than normal and consumes approximately 70 percent of the cells’ energy (ATP). RNase L fragments destroy normal protein synthesis, enzyme production, and other vital cellular functions. They inhibit respiratory muscles, and cause hyperventilation, metabolic alkalosis, sleep disturbances, and central fatigue. There is sodium retention, low magnesium levels, and dramatically low levels of potassium. Natural killer cells, which protect against viruses and intracellular infections, are also being damaged. Thus, the immune system is in a state of chronic dysfunction.

    Testing for ME/CFS

    Dr. De Meirleir is co-founder of REDLABS (www.redlabsusa.com), which recently opened a lab in Nevada. This lab offers diagnostic and treatment tests for ME/CFS patients. Although each patient’s profile is unique, patients tend to fall into three groups with different causes and treatments. Based on the results of six tests, Dr. De Meirleir was able to predict patients’ symptoms with 95 percent accuracy while the remaining 5 percent had overlap features. Symptom severity rises in correlation to the rise in the level of LMW RNase L.

    Group Profiles

    Group 1: (15 to 20 percent)

    This group has high levels of LMW RNase L and elastase, low levels of protein kinase (PKR) and uric acid, and low to normal levels of nitric oxide. Spinal taps indicate elevated levels of lymphocytes and proteins in the spinal fluid, and there is increased pressure upon opening the lumbar puncture.

    These patients have a chronic low-grade viral infection and inflammatory reaction in the brain. Many micro-organisms are associated with this profile. Heavy metals, pesticides, and other triggers may also be involved. Approximately 20 percent of this group has low-grade Herpes Virus 6A (HHV6A) encephalitis.

    The prominent feature is neurocognitive problems such as confusion and impaired concentration and memory. Fatigue originates in the brain. Pain is not prominent. Patients exhibit symptoms that have some similarities to multiple sclerosis (MS).

    Group 2: (10 to 15 percent)

    These patients have very high levels of LMW RNase L and elastase, high protein kinase activity, severely low natural killer cell activity, and very low serum uric acid levels.

    This group of severely ill patients has bacterial infections originating from animals such as pets, rodents, ticks, etc. These patients have severe bowel problems. The gut is an important part of the immune system because 70 percent of immune cells are in the digestive tract. When a patient has leaky gut syndrome, the gut has become permeable and foreign proteins enter the blood and tissues and inflammation results. Dr. De Meirleir tests for 12 pathogenic gut bacteria.

    Group 3: (60 to 70 percent)

    The majority of ME/CFS patients are in this group. This profile is basically similar to Group 2, but not as severe. Generalized pain originating from dysfunction in the pain processing areas of the brain and CNS is a prominent feature. These patients have gastrointestinal infections, and bacteria are in the blood.

    Some Other Areas of Investigation


    Part of the immune system is activated and part is suppressed, leaving the patient vulnerable to opportunistic infections. Patients may have one or a number of infections. Serum Immunobilan tests are done to identify which ones are active. Suspect microorganisms include viruses, bacteria, and mycoplasma. A chlamydia pneumonia infection is often found in patients with chronic sinus infections. Approximately 8 to 10 percent of ME/CFS patients have infections of animal origin such as Rickettsiae, Coxiella, Bartonella, and Borrelia. Many of these infections come from pets. A small percentage come from ticks.

    Heavy Metals

    Exposure comes from many sources including food, insulation, air, etc. ME/CFS patients have increased sensitivity to chemicals, environmental pollutants, and heavy metals, particularly mercury and nickel. Toxins can trigger an inflammatory response.

    One of the RNase L fragments has a structure that is almost identical to a protein involved in the removal of heavy metals and toxic chemical from cells. When this protein is blocked by the RNase L fragments, the cells become more sensitive to mercury. Now a tiny amount of mercury that would normally kill 10 percent of the cells can kill 50 to 100 percent of the cells.


    Fungi such as Aspergillus Niger and Candida can contribute to ME/CFS symptoms. Candida is a yeast fungal infection that changes sugars to aldehydes, a toxic form of alcohol.

    Digestive Tract

    Gastrointestinal problems are a serious concern in ME/CFS patients: 70 percent of the body’s immune cells are found in the gastrointestinal tract. These immune cells prevent bacteria and foreign protein from entering the blood stream. When the gut becomes permeable and foreign protein enters the blood stream, elastase is produced. Elastase is the enzyme that is responsible for cutting the RNase L molecule into fragments. Elastase breaks down elastin, which gives elasticity to collagen. As a result, there is pain and a loss of elasticity in ligaments and tendons.

    Peripheral Resistance to Thyroid Hormone

    Most patients have normal results for common thyroid tests. However, ME/CFS patients have a much higher level of a protein that is 98 percent identical to T3, which is the active form of thyroid. Because this foreign protein can bind to T3 receptors, T3 cannot find receptors and is therefore ineffective in its role of activating cellular metabolism.

    Treatment Summary

    Some psychiatrists advocate that no tests or lab work be done on ME/CFS patients because testing will reinforce delusions of physical illness. Given the wealth of confirmed biochemical abnormalities, such a rationale is ludicrous. Dr. De Meirleir stressed that tests must be done in order to determine the origin of the problem. Then treatment can be prescribed to eliminate the cause. A “clean-up” of all the consequences of the problem must also be undertaken. Therapies and the order of treatments vary according to the patient’s unique test profile. Treatment includes:

    Restoring immune competence
    Removing microorganisms
    Restoring hormonal balance
    Restoring intestinal flora
    Decreasing prostaglandins and protein kinase activity
    Removing heavy metals and toxic chemicals.
    This summary of Dr. De Meirleir’s lecture, written by Majorie van de Sande, B Ed, Grad Dip Ed, was reproduced with permission from Quest, the newsletter of Canada’s National ME/FM Action Network. Ms. van de Sande is the Action Network’s Advisor and Webmaster, Conference Planning Committee.

    Dr. De Meirleir describes various treatment therapies in a full-day physicians’ workshop, which is available as a set of four DVDs and a CD. For information about how to order these materials, and a patient workshop in DVD format, visit the National ME/FM Action Network site, at http://www.mefmaction.net/

    For information on the diagnostic testing supplies and services available via Dr. De Meirleir’s lab – REDLABS USA, in Reno, Nevada – visit http://www.redlabsusa.com/. This site also offers a free downloadable PowerPoint presentation for physicians on the interpretation of test results.

    Note: The information provided here is not intended to diagnose, treat, cure, mitigate, or prevent any disease.

  16. u34rb

    u34rb New Member

    So Dr. DeMeirleir sees 100 patients a week? No wonder he has no time to publish his findings!

    So all these patients, 4000 to 5000 per year, are all sworn to secrecy? Really?

    I smell some sour grapes here.

    And pharmaceutical companies don't conceal their intellectual property, do they?

    And the same people who complain about Dr. DeMeirleir are also complaining about the pharmaceutical companies? Right!
  17. Slayadragon

    Slayadragon New Member

    The information about low molecular weight of Rnase-L is interesting.

    However, what I think you're saying is that this means it does not do a good job with regard to getting rid of infections from the body.

    As far as I can tell, this is not consistent with what the NCF is saying in its criticisms of Dr. DeMeirleir, though.

    Their complaint seems to be that Rnase-L is killing off more cells than is optimal. It refers to cell death ("apoptosis") as being too high.

    This thus suggests to me that regardless of the molecular weight of Rnase-L, they they it is "doing its job" adequately or too well.

    Am I right about this.

    As a side note, my Rnase-L is elevated (40, normal range 1-10) as is my apoptosis (10%, normal range 1-5%).

    I don't know if this is optimal, but it doesn't suggest that Rnase-L is broken in the same way that my NK Cell activity is broken (my level is 4, normal range 20-60).

    Swedeboy, I wonder if Rnase-L weight is included in the new ImmunoSciences CFS panel. When will you get your results back?

    I tend to agree that a primary place that is dysfunctional in CFS patients is the brain.

    From an objective assessment of symptoms, the brain seems to be responsible for a high percentage of symptoms, including fatigue.

    Of course, Cheney's research presentations make me believe that the heart is a real problem for many of us too, though. And endocrine dysfunction seems clearly a problem as well.

    As a side note, most of the negative effects I have experienced since going through die-off on Famvir have been brain related (cognitive and emotional). Sleep has become more erratic as well. These symptoms have been far worse that what I experienced before going on the drug.

    If we go by the hypothesis that die-off symptoms tend to occur in the areas of the body where viruses are housed, this makes sense.

    On those occasions when I have stopped taking the antiviral or lowered its dose, I have experienced some increases in functioning compared to before I started it. Specifically, my mood was much better, my cognitive abilities (including concentration and task-switching) were better, my perceptions seemed clearer, and my aversion to noise seemed to have improved.

    I mentioned this to my doctor, stating that I was surprised that the shift in my mood had been so dramatic. He said that this was common, and that my other experiences were typical too.

  18. karinaxx

    karinaxx New Member

    i did not understand your Rnase-L thing, but i can say something to the brain issue. the hypothalamus is a part of the brain which is resposible for the endroctrine system
    (HPAaxis) and the disfunction in this part of the brain can be responible for congestive heartfailure (Dr.Chenney thinks that the heart problems accure because there is not enough ATP,which again leads to the Hypothalamus) and for much more. i suggest you check out the site of wikipedia for more information on the Hypothalamus. its much more complex and there is so much more which connects there, i could never explain it just like this.
    also it is very intresting what Puri and Chaudhuri have to say about that.

    anyway, my brain is realy fried now
    take care karina
  19. Slayadragon

    Slayadragon New Member

    It's an interesting thought that the brain could be responsible for the endocrine system problems (I thought of that) as well as those of the heart (I had focused less on that).

    Do you think it's responsible for muscle pain as well? I don't have that problem much (I did to a small amount in the past), but lots of others obviously do.

  20. cherylsue

    cherylsue Member

    Thanks for sharing that info. Does anyone have the DVD's of Mr. De Meirleir's treatment therapies? Does anyone know what they are in detail? They are summarized in the article, but I want specifics.

    Dr. P. Cheney does not believe CFS is a hypothalamic injury. He mentioned that in his DVD.

    I fit the Group 1 profile. "Fatigue orginiates in the brain. Pain is not prominent."

    I think Dr. DeM's findings are pretty accurate from my experience, and explain things well. I have low potassium, and certainly feel better when I take foods with it.

    How does one "restore immune competence?"