Critics on H2S theory

Discussion in 'Fibromyalgia Main Forum' started by SpiroSpero, May 31, 2009.

  1. SpiroSpero

    SpiroSpero New Member

    Although I'm a patient of Prof De Meirleir I want to share these critics with you since at the moment I doubt too that he made a breakthrough.
    There is one thing that disappoints me when thinking about his theory.

    If H2S is responsible for CFS then where is it produced and how do we get rid of it? It can't be that hard to find a way to stop the production of a simple gas. Take some antibiotics that eradicate H2S producing bacteria. Starve them. Use compounds that bind to H2S and transport them out. Use compounds that deactivate H2S. There should be a ton of possibilities. Unfortunately Prof De Meirleir didn't say much about the cause nor what he thinks can be done against it. He claims it a breakthrough but he claimed R-Nase L to be a breakthrough too. He stopped testing for it entirely now. I really hope that Prof De Meirleir is onto something but I can name you several doctors who calimed to have found sth. but still have no wokring treatment and still did not publish in well known scientific journals, e.g. Myhill, Cheney, Pall.



    So here the the two blog entries:

    http://aboutmecfs.org/blog/?p=539

    The Big Breakthrough?
    by cort on May 30, 2009

    Some bloggers have jumped all over the announcement by Dr. De Meirleir that an important cause of ME/CFS has been found. This is, they say, the ‘big breakthrough’. But is it? With just the abstract in hand let’s take a look at what little we know.

    The Announcement - Dr. De Meirleir has been in this business awhile. He was the foremost proponent and investigator of the idea that RNase L was’ it’ in ME/CFS. While RNase L does not appear to be ‘it’ in ME/CFS it was an important contribution to the field. Dr. De Meirleir publishes frequently in the scientific literature and has treated many chronic fatigue syndrome (ME/CFS) patients.

    By holding a press conference - something researchers rarely do - Dr. De Meirleir is putting his reputation on the line. This suggests, of course, that he strongly believes he has found something of great importance.

    One might have wished that the press release title “Research on Extremely Disabled Patients Reveals the True Nature of the Disorder” had been less over the top. Many researchers would shirk from such a blanket statement at this point of the game. Still given Dr. De Meirleir’s contributions from the past we’ll score 1 for the Big Breakthrough.

    Hydrogen Sulfide Producing Bacteria Found in the Gut - In order to have H2S in the gut you to have a means of getting it there. The press release did not indicate, however, that the bacteria were more prevalent in the more severely ill patients than in the less ill patients or even in the controls - sloppy work! Score 0 for the Big Breakthrough.
    More H2S Metabolites Found in the Urine of More Ill Patients - Using a fairly primitive test De Meirlier shows evidence that more H2S is likely being produced in the more severely ill patients - Score another for the Big Breakthrough

    H2S in Excess Causes Many of the Symptoms in ME/CFS - H2S can cause all sorts of problems in the body: photophobia, oxidative stress, increased mercury levels, depressed immune functioning, etc. Oddly enough here is where the theory lets us down a bit. Any type of oxidative stress can cause a multitude of problems. Dr. Pall with nitric oxide and Rich Von Konynenburg with glutathione depletion can all chart an intricate and widespread cycle of dysfunction much like Dr. De Meirleir is. Dr. Cheney has done the same thing with his energy metabolism theories.

    We actually have too many intricate theories in ME/CFS - and not enough testing. The fact that H2S can cause these problems is intriguing. The fact that De Meirlier has found evidence of high H2S levels in ME/CFS patients adds an extra layer to it. One wonders though, how accurate a simple color test really is. Score ½ point.

    Correlation is not Causation: Simply finding high levels of H2S metabolites in ME/CFS doesn’t mean that they cause the disease. High levels of oxidative stress are found in many diseases including ME/CFS but few people believe they cause those diseases. ME/CFS patients have high levels of the ciguatoxin epitope but so do cancer and other patient - ciguatoxin doesn’t cause either disease. Ditto with low cortisol readings and Fibromyalgia, asthma, PTSD and RA.

    Finding higher H2S levels does not necessarily mean that it is causing this disorder. In order for it to cause ME/CFS Dr. De Meirlier has to show that it’s only present in ME/CFS patients, is not found in other diseases, and that removing it from ME/CFS cures the disease. Score ½ point.

    Conclusion: What does this theory - as much as we know of it - have going for it? The word of a well respected researcher, a model that appears (at least to a laymen) to make sense and a finding that illness severity appears to correlated with the level of the agent. (All of these could have been said about RNase L several years ago).

    What does it need for ME/CFS patients to really start clapping? A means to bring down H2S and evidence that doing so erases ME/CFS. A coherent reason why the H2S is present in the first place, independent verification of the results and findings indicating that H2S is not present in other diseases.

    Whether or not H2S actually causes or is an important cause of this disorder a substantial contribution to the field appears to have been made. H2S wasn’t even a blip on the research community’s radar screen until Marian Lemle, the mother of a daugther with ME/CFS/FM, earlier this year published a paper suggesting it played a role. Now De Meirleir has created a test that suggests it’s present. Whatever the final outcome of the H2S saga he and Marian Lemle have added a new layer to the ME/CFS equation and opened up a new arena for research and treatment - always a welcome sight.

    http://blog.blueribboncampaignforme.org/

    Medical tests for a specific disease need to be an accurate and reproducible
    means of establishing the unique pathophysiology of the disease concerned

    I have a scientific background and I have studied the contents of the
    presentation made by Professor Kenny de Meirleir. His hypothesis is that
    high levels of hydrogen sulphate in the urine may possibly be diagnostic of
    the presence and or overgrowth of relatively certain common microbes living
    within the gut. This he then claims produces the symptoms of Myalgic
    Encephalomyelitis.

    This is not a new idea; it is a new variant on the "leaky gut" hypothesis
    that has been around for some time and has been associated with the Candida
    overgrowth hypothesis of ME which produces the same kind of "leaky Gut" in
    which candida travels through the gut and invades the body through the gut
    walls. This hypothesis has been largely discredited although it still has
    its supporters.

    The current hypothesis follows much the same lines, that the micro organisms
    that ought to be contained within the gut are somehow able to penetrate the
    walls of the gut and end up just about everywhere in the body including the
    brain.

    There are a number of problems and issues here which can be summarised but
    are not limited to :-

    1] How can such organisms penetrate the gut wall and invade the
    body in the manner claimed, as this was the Achilles Heel of the previous
    Candida hypothesis?

    2] Assuming that it is possible for these micro organisms to
    invade the body in the way Prof. Kenny de Meirleir hypothesises, then the
    person would be suffering from a very nasty case of infection by one of the
    micro organism concerned, and not ME, since all the micro organisms cited by
    Prof. Kenny de Meirleir are already known to medicine and medical science,
    and this would be picked up by a battery of microbiological tests which
    would confirm the presence of a bacterium as being the cause of the
    infection suffered by the patient. Not all the organisms concerned are not
    that easy to treat and some can be resistant to antibiotics, but diagnosis
    and treatment are relatively strait forward. This leads to the academic
    scientific question as to whether certain levels of some of these microbes
    live in the gut anyway, and speculation as to what would lead them to cause
    an infection.

    3] That in order for a given specific disease to be produced
    through the invasion of the body by a specific microbe, there must be an
    equation made between the microbe responsible and the disease. One cannot
    have the same disease produced by an unspecified number of certain specified
    and also by other un-named and or un-specified microbes because this would
    simply be termed a general bacterial infection. It would not be ME.

    4] That in order for a diagnostic test to detect the presence of
    a given single microbe or family of microbes a given test must detect the
    microbes concerned in the presence of other microbes which may be harmless,
    or not the subject of the test, and therefore the test will not produce
    false positives results when applied to samples taken from patients. There
    is no indication that the proposed test will do this.

    5] That in order for a diagnostic test to detect the presence of
    a given microbe or family of microbes it is necessary for the test to have a
    given provable and reliable sensitivity to the organism it is intended to be
    a test for so that medics and researchers can have confidence that if the
    test says that there is nothing there, then that is indeed the case. This is
    to avoid the problem of false negatives. There is no information whatsoever
    from Prof. Kenny de Meirleir on this subject, so I can only assume that the
    proposed test does not meet the stringent standards of any national or
    international Health Board. This is presumably why the test is not being
    marketed to doctors or to governments or Health Boards, but only to
    individuals.

    6] That in order that for a diagnostic test to be accepted as the
    means of diagnosing a given disease it must be accurate, and it must be
    reliably accurate to a very high standard so that again medics and
    researchers can have confidence that the test really does do what it claims
    it can. Again, there is no information whatsoever from Prof. Kenny de
    Meirleir on this subject, so I can only assume that the proposed test does
    not meet the stringent standards of any national or international Health
    Board. This is presumably also why the test is not being marketed to doctors
    or to governments or Health Boards, but only to individuals.

    Lastly but by no means least, the theory behind the test must be based on a
    unique aspect of the pathophysiology of the disease because only then can
    the equation between a given specific microbe and a given specific disease
    be made. In order to be in a position to make this equation the theory which
    underpins the use and application of any diagnostic test must account
    directly for the disease process itself and not be a consequence or artefact
    of that disease process that could be produced in other ways.

    I consider that Prof. Kenny de Meirleir's hypothesis and Hydrogen Sulphide
    diagnostic test based upon it fails this test on the grounds listed above
    and for the simple reason that he has not accounted for the well known fact
    that patients with ME/CFS/CFIDS are known to have compromised immune
    systems. This would mean that as with HIV/AIDS patients who also have
    compromised immune systems that there is very considerable likelihood that
    in ME/CFS/CFIDS patients the presence of the microbes that Prof. Kenny de
    Meirleir observes and the numbers in which he observes them are simply due
    to the secondary consequences of having ME/CFS/CFIDS as a result of
    opportunistic infections by microbes that would largely be kept at bay by
    the body's immune system in a healthy person.

    I note that Prof. Kenny de Meirleir has been a controversial figure when he
    served as a 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 and that the Board of The National CFIDS
    Foundation, Inc. (NCF), in America, called for his resignation as the result
    of his previous research activities

    I also note that Prof. Kenny de Meirleir's recent work on this matter is not
    published in a Peer Reviewed Journal, and that he does not appear to have
    any plans to publish his work in such a journal, possibly because his work
    on this matter may not reach the standards required by such journals.

    I further note that Prof. Kenny de Meirleir is one of the Editorial Panel of
    the proposed new Journal of Fatigue where presumably he would be able to
    publish this work as presumably this journal does not have the same status
    and standing as a regular Peer Reviewed journal, and he would be standing in
    favourable judgement over his own work.

    In view of the entirety of the above, my advice would be to think long and
    hard before committing £13 or any other sum of money to buy the home testing
    kit proposed by Prof. Kenny de Meirleir or on whether to have the test
    performed in any other way, and I would be very wary indeed of any treatment
    options that may be advanced by Prof. Kenny de Meirleir on the basis of a
    positive test result, or the consequences of a negative test result.

    Ciaran Farrell

  2. Rafiki

    Rafiki New Member

    SpiroSpero, for this terrific contribution to the exciting dialogue now ongoing.

    I find both of these posters very credible. I also suspect, as does Cort, that DeMerileir's findings do point at something relevant. There are many fingers pointing at relevant findings at this time.

    I was a bit taken aback, I must say, by the way in which Friday's press release was worded. It seemed a bit too good to be true while also offering little in the way of specifics. Nevertheless, it does seem to have, perhaps limited but important, implications for our ongoing efforts to understand ME/CFS.

    Again, SpiroSpero, many thanks!
    Rafiki
  3. TigerLilea

    TigerLilea Active Member

    Thanks for posting this, SpiroSpero. Both Cort's and Ciaran's articles were very well written and very informative. As I mentioned in a previous post, I am very doubtful that this is the "big" breakthrough that H2S is being touted as being.
  4. gapsych

    gapsych New Member


    Thanks for posting this. I have had the same doubts that it sounded too good to be true.

    It seems that there are many people, with many different theories how CFS starts.

    Why can't they all work together and exchange information.

    Wait, weren't they suppose to do that in Nevada?

    While I am an advocate for true scientific research, a drawback can be that the researchers are so focused on their theory they are not looking elsewhere or think that theirs is the only theory.

    Too bad.

    gap

    Interesting about the leaky gut.

    ETA I forgot about the conference that was just held in London. One day is not enough time. Sigh.[This Message was Edited on 05/31/2009]
  5. Catseye

    Catseye Member

    I agree with the blogger's conclusion and think he's full of crap, too. Typical doctor, can't see what's BEHIND the door. How did H2S become a problem in the first place? This is so typical of the medical profession, trying to pin the cause on what is simply another symptom.

    But despite reaching the right conclusion, the blogger makes a couple of inaccurate assumptions of his own.

    From the blog entry:

    "This is not a new idea; it is a new variant on the "leaky gut" hypothesis
    that has been around for some time and has been associated with the Candida
    overgrowth hypothesis of ME which produces the same kind of "leaky Gut" in
    which candida travels through the gut and invades the body through the gut
    walls. This hypothesis has been largely discredited although it still has
    its supporters.

    The current hypothesis follows much the same lines, that the micro organisms
    that ought to be contained within the gut are somehow able to penetrate the
    walls of the gut and end up just about everywhere in the body including the
    brain."


    my comment on above; This is quite amusing - he says "the micro organisms that ought (what a funny word to use!) to be contained within the gut are somehow able to penetrate the walls of the gut . . ." But they also say they have a scientific background. In what? Astronomy? Maybe he should have paid a wee bit more attention to Uranus! And his "largely discredited" comment is obviously just from a lack of diligent homework.

    Then shortly after:

    "How can such organisms penetrate the gut wall and invade the
    body in the manner claimed, as this was the Achilles Heel of the previous
    Candida hypothesis?" - it's like this person thinks the gut lining is immortal and cannot be damaged. Even the World Trade Center came down! How is a mucousal lining going to be "undamageable"? It is just another organ!!

    For Pete's sake, 5 seconds worth of googling turned up the following. I guess believing in "leaky gut", aka "intestinal hyperpermeability" is a real stretch for some. Maybe they read quackwatch too much, the idiot's guide to staying sick forever. On quackwatch, the dope lists "leaky gut syndrome" as "Not Scientifically Defined or Recognized". Maybe "intestinal hyperpermeability" were just a couple of words that are too big for him and it threw off his googling!



    below is from:

    http://www.ncbi.nlm.nih.gov/pubmed/19273235?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=3&log$=relatedreviews&logdbfrom=pubmed


    "Department of Internal Medicine, University of New Mexico School of Medicine, Albuquerque, NM 87131, USA.

    Cytokines play a crucial role in the modulation of inflammatory response in the gastrointestinal tract. Pro-inflammatory cytokines including tumor necrosis factor-alpha, interferon-gamma, interleukin-1beta?IL-1beta?, and interleukin-12 are essential in mediating the inflammatory response, while anti-inflammatory cytokines including interleukin-10 and transforming growth factor-beta are important in the attenuation or containment of inflammatory process. It is increasingly recognized that cytokines have an important physiological and pathological effect on intestinal tight junction (TJ) barrier. Consistent with their known pro-inflammatory activities, pro-inflammatory cytokines cause a disturbance in intestinal TJ barrier, allowing increased tissue penetration of luminal antigens. Recent studies indicate that the inhibition of cytokine induced increase in intestinal TJ permeability has an important protective effect against intestinal mucosal damage and development of intestinal inflammation. In this review, the effects of various pro-inflammatory and anti-inflammatory cytokines on intestinal TJ barrier and the progress into the mechanisms that mediate the cytokine modulation of intestinal TJ barrier are reviewed."

    below is from:

    http://www.ncbi.nlm.nih.gov/pubmed/14767487?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=2&log$=relatedreviews&logdbfrom=pubmed

    "Department of Pathology, The University of Chicago, Chicago, IL 60637, USA.

    A critical function of the intestinal mucosa is to form a barrier that separates luminal contents from the interstitium. This intestinal barrier is compromised in a number of intestinal diseases, most notably inflammatory bowel disease. In vitro studies have demonstrated that cytokines elaborated by immune cells can cause the mucosal barrier to become leaky; these cytokines are known to be increased in intestinal mucosa involved in inflammatory bowel disease. Detailed information describing the mechanisms by which altered cytokine signaling occurs is not available, but recent data implicate the cytoskeleton within epithelial cells as a critical regulator of the mucosal barrier under physiological and pathophysiological conditions. Using available data, we describe a model of intestinal disease where an initial insult to the epithelial barrier may trigger a self-amplifying cycle of immune activation, cytokine release, and further barrier dysfunction. This model is supported by the observation that pharmacological abrogation of cytokine signaling corrects both barrier defects and clinical disease in animal models and human patients, although such therapy clearly has multiple mechanisms. Other therapeutic targets that represent strategies to prevent or reverse disease processes are also considered. The overarching hypothesis is that modulation of the mucosal epithelial barrier plays a critical role in the initiation and propogation of inflammatory intestinal diseases."




    There's more . . .

    http://www.ncbi.nlm.nih.gov/pubmed/12657978

    http://www.rush.edu/rumc/page-1203344429947.html


    below is the title for this one:

    http://molecular.biosciences.wsu.edu/Faculty/old%20files/pall/pall_main.htm

    Novel Disease Paradigm Produces Explanations for a Whole Group of Illnesses

    A Common Causal (Etiologic) Mechanism for Chronic Fatigue Syndrome, Multiple Chemical Sensitivity, Fibromyalgia and Posttraumatic Stress Disorder



    This was a brief search. If you don't believe in hyperpermeabilty and you have it, you won't be able to find somebody to help you with it. Not believing in it and the catastrophic effects it can have on health is just like doctors not believing in CFS and fibro. Pretty sad when we have to print out pubmed articles and bring them to the doctor. And pretty embarrassing for the doctor who obviously doesn't do his homework. I guess as long as the money keeps rolling in, he has no incentive to.
    [This Message was Edited on 06/01/2009]