The 12th Invest in ME Research Conference June, 2017, Part 2
MEMum presents the second article in a series of three about the recent 12th Invest In ME International Conference (IIMEC12) in London.
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Mold, Dr. Cheney and ME/CFS

Discussion in 'Addressing Biotoxin, Chemical & Food Sensitivities' started by slayadragon, Apr 27, 2010.

  1. Forbin

    Forbin Senior Member

    Well, since I became ill in 1983 and had largely recovered before there was a CFS definition, I cannot claim to have had confirmed CFS. However, my symptoms from '83-'87 were completely consistent with CFS.

    In my first post,, I went into some detail about how the start of my recovery, 3.5 years after sudden onset, was, at the very least, cotemporaneous with a trial of treatment for a supposed overgrowth of the yeast Candida albicans in the GI tract. I do not mean to suggest that this is a treatment that would meet with broad success, merely that it seems to have tipped the balance for me and I was quite ill.

    For what its worth, yeasts and molds are both fungi, but I suspect that that is probably just a coincidence as far as how they might be related to CFS is concerned.

    However, it certainly seems as though something (XMRV is certainly a good candidate) is disrupting the normal function of the immune system causing both an inability to deal with existing pathogens and a weird hypersensitivity to some things that the body previously found innocuous. [In my case, I also developed a nearly-anaphylactic reaction to a fairly ubiquitous food additive (HFCS)].

    My laymans impression is that there is some sort of a tipping point at which the immune systems gets into a feedback loop (possibly with XMRV) creating a chronic state of activation because it can no longer deal with some co-pathogen. In some cases (perhaps only a small number), it might be possible to break that loop by reducing the exposure to whatever the immune system is responding to such as to yeast overgrowth or, perhaps, to mold exposure.

    It would be more difficult if your immune system was fighting something such as another virus, like EBV, which, as I understand it, can never be completely cleared. Maybe this is why some people get only a measure of temporary relief when they go on antivirals. Its possible that my recovery was only possible because I was negative for EBV (and all the other viruses they tested me for), and so yeast overgrowth was the only "fire" to put out, so to speak.

    Anyway, since I am layman (a software developer), I dont know if this really adds to the conversation. These are just some conjectures that Ive formed in the 27 years since the onset of my symptoms.

  2. slayadragon

    slayadragon Senior Member

    Thank you to everyone for your comments thus far.

    Following are some brief responses to the issues raised. This is a very complex topic, and so I hope that you will view this just as a starting point for more discussion.


    A common reason for ruling mold out as a factor of particular relevance to this disease is that “mold is just an allergy.”

    Indeed, mold can cause allergies. However, certain species of mold also contain chemical poisons that can cause severe illness or death in all manner of species, including humans.

    These poisons are made by molds as “secondary metabolites” to kill off other fungi and bacteria in an environment, so that they themselves can grow unchecked. Some of these toxins are strong enough that they also cause illness and death in humans.

    Trichothecene is the main class of chemicals that is known to be of concern and have been classified by the U.S. government as bioweapons. T-2 toxin is generally considered to have been used as a bioweapon. Satratoxin, the chemical made by Stachybotrys (commonly known as “black mold”) is said to be several times stronger than T-2.

    An allergy is the misidentification by the body of a benign substance as problematic. Any species of mold can cause allergies.

    A toxicity reaction is the poisoning of the body by a particular chemical substance. Examples include rattlesnake and brown recluse spider venom. (The latter substance is particularly relevant here because that poison is similar in chemical structure to ionophore mycotoxins.)

    Typical allergic symptoms to mold include sneezing and runny nose, watery or itching eyes, and asthmatic symptoms such as wheezing and coughing.

    Toxic mold symptoms are largely neurological, including memory loss, attention deficit/concentration problems, personality changes such as irritability/depression, tremors, tingling or burning of nose and mouth, chronic fatigue, dizziness, nausea/vomiting, bleeding or fluid in the lungs, suppression of the immune system, headache, flu-like symptoms, incoordination, muscle spasms and cramps, and damage to various internal organs (especially the gall bladder and liver). They are cytotoxic, disrupting various cellular structures such as membranes and interfering with various cellular processes such as protein, RNA and DNA synthesis. Decreased Natural Killer Cell function has been cited as a particularly common effect of mold toxicity.

    Many people have mold allergies but have not been poisoned to any significant extent by mold. On the other hand, many victims of mold toxicity (including myself) do not have any mold allergy symptoms at all.

    Substantial academic research on the effects of mycotoxins can easily be accessed. Keywords include mycotoxins, satratoxins, T-2, DON, aflatoxin and Stachybotrys.


    The leading clinical researcher in the area of the effects of mycotoxins on humans is Dr. Ritchie Shoemaker. Dr. Shoemaker presented some of his work at the 2009 CFS conference in Reno. He was one of the members of the Ratna Ling/Sonoma Working Group (which also included CFS researchers Paul Cheney, Jose Montoya, Kenny de Meirleir, Martin Pall, Richard Deth, Jacob Teitelbaum and Rich van Konynenberg). His M.D. is from Duke University.

    Dr. Shoemaker’s book “Mold Warriors” was published in 2005. He also has published numerous academic papers on the topic. His web site is here:

    Dr. Shoemaker has developed a number of laboratory tests measuring the propensity for and presence of mold illness in patients. He states on his web site that this is based on looking at approximately 6000 individuals.

    The genetic tests referenced in some of the posts above are standard HLA DR tests that can be obtained through LabCorp. Dr. Shoemaker’s observation is that specific genetics are correlated with mold illness, with about 24% of the population susceptible. About 2% of the population has at least a multisusceptible gene (causing susceptibility to being affected by various biotoxins such as mycotoxins, Lyme toxins, dinoflagellates and brown recluse spider toxin). About 24% of the population is susceptible to being affected by various mycotoxins.

    The multisusceptible genes are 4-3-53, 11/12-3-52B and 14-5-52B. The mold susceptible genes are 7-2/3-53, 13-6-52A/B/C, 17-2-52A, and 18-4-52A.

    Dr. Shoemaker states that CFS patients are vastly more likely than the population as a whole to have the mold susceptible genotypes and (especially) the multisusceptible genotypes. While correlation is not causation, Dr. Shoemaker speculates that people with mold susceptible and multi susceptible genotypes do not have the antibodies to remove mold toxins from the body through the immune system that the rest of the population does.


    Although a wide variety of mycotoxins can cause damaging symptoms in humans, satratoxins seem to be especially worth consideration with regard to CFS. An excellent review of the academic work along with several laboratory studies is this dissertation, which has the particular merit of being available for free on the Web.

    (ADDENDUM: This paper was published in 7/2010. The cite and abstract are below.)

    David Straus, the committee chair for this Texas A&M doctoral graduate, has been a leading researcher in the study of mycotoxins. Numerous papers by him are readily accessed.

    The dissertation has the following conclusion:

    “These experiments demonstrate that the macrocyclic trichothecenes produced by Stachybotrys chartarum are able to induce apoptotic and inflammatory cascades in endothelial cells, astrocytes, and neurons. These studies suggest that exposure to low to moderate doses of satratoxin could activate cellular pathways that induce a series of events leading to neurological tissue damage, which may induce the symptoms observed in individuals exposed to Stachybotrys chartarum.

    The experiments also demonstrate that Stachybotrys is able to induce perforations in the blood-brain barrier, allowing various substances that should not be there to enter. Although other chemicals such as formaldehyde can pass the blood-brain barrier themselves, I have been unable to locate research that suggests that other chemicals are able to create these perforations.

    In addition, satratoxin was shown in this study and in others to increase the presence of NF-kappa-beta in cells such as astrocytes.

    Substantial research easily accessible suggests demonstrates that Satratoxin H generates reactive oxygen species and lipid peroxidases. Research findings demonstrate that this occurs at least in part due to the decreased presence of reduced glutathione in the cells.

    Those who are familiar with very recent developments in the field of CFS will immediately understand why these particular findings are of relevance.

    This addresses only a portion of the comments and questions thus posed on this thread. I will respond to the others (as well as whatever new ones emerge) shortly.

    Best, Lisa


    Karunasena E, Larraaga MD, Simoni JS, Douglas DR, Straus DC. Building-Associated Neurological Damage Modeled in Human Cells: A Mechanism of Neurotoxic Effects by Exposure to Mycotoxins in the Indoor Environment. Mycopathologia. 2010 Jun 13. PMID: 20549560.

    Damage to human neurological system cells resulting from exposure to mycotoxins confirms a previously controversial public health threat for occupants of water-damaged buildings. Leading scientific organizations disagree about the ability of inhaled mycotoxins in the indoor environment to cause adverse human health effects. Damage to the neurological system can result from exposure to trichothecene mycotoxins in the indoor environment. This study demonstrates that neurological system cell damage can occur from satratoxin H exposure to neurological cells at exposure levels that can be found in water-damaged buildings contaminated with fungal growth. The constant activation of inflammatory and apoptotic pathways at low levels of exposure in human brain capillary endothelial cells, astrocytes, and neural progenitor cells may amplify devastation to neurological tissues and lead to neurological system cell damage from indirect events triggered by the presence of trichothecenes.
  3. Gerwyn

    Gerwyn Guest

    none of this is scientific evidence of any kind Stachybotrotoxicosis is a clinical condition the mycotoxin concerned is a biochemical weapon if treated in aparticular way at a very high concentration.this has nothing to do with ME.I

    A dissertation is not scientific evidence.Scientific evidence is peer reviewed and published.this remains a hypothesis untill the weight of corroborating evidence enables it to take a the status of a theory with a grater than 95% probability of being the correct explanation of the initial observations

    Any alien toxin will activate the immune response which will activate TNF alpha which will inturn activate Nf -kappa -beta via the up regulation of the NFAT gene. the same goes for glutathione depletion.The dissertation was obviouly not published.

    Multiple genes are activated in every immune response.One mans opinion is not scientific fact.Dr shioemakerss work is not published ina scientific journal of any kind and is not peer reviewd whatever he says.he is entitled to his opinion but that is all it is.

    "Mold Warriors " this has nothing to do with science.If you have any SCIENTIFIC evidence in support of his subjective opinions then I would be pleased to read it. I,m afraid that none of this is in that category

    This is scientific evidence

    Fungal Genetics and Biology
    Volume 39, Issue 2, July 2003, Pages 103-117
    doi:10.1016/S1087-1845(03)00026-4 | How to Cite or Link Using DOI
    Copyright 2003 Elsevier Science (USA). All rights reserved. Cited By in Scopus (78)
    Permissions & Reprints
    Mycotoxin production by indoor molds
    Purchase the full-text article

    References and further reading may be available for this article. To view references and further reading you must purchase this article.

    Kristian Fog NielsenCorresponding Author Contact Information, E-mail The Corresponding Author, E-mail The Corresponding Author

    The Mycology Group, BioCentrum-DTU, Building 221, Technical University of Denmark, DK-2800, Kgs. Lyngby, Denmark
    Received 2 January 2003;
    accepted 6 March 2003. ;
    Available online 29 April 2003.


    Fungal growth in buildings starts at a water activity (aw) near 0.8, but significant quantities of mycotoxins are not produced unless aw reaches 0.95. Stachybotrys generates particularly high quantities of many chemically distinct metabolites in water-damaged buildings. These metabolites are carried by spores, and can be detected in air samples at high spore concentrations. Very little attention has been paid to major metabolites of Stachybotrys called spirocyclic drimanes, and the precise structures of the most abundant of these compounds are unknown. Species of Aspergillus and Penicillium prevalent in the indoor environment produce relatively low concentrations of mycotoxins, with the exception of sterigmatocystins that can represent up to 1% of the biomass of A. versicolor at aw’s close to 1. The worst-case scenario for homeowners is produced by consecutive episodes of water damage that promote fungal growth and mycotoxin synthesis, followed by drier conditions that facilitate the liberation of spores and hyphal fragments.
  4. slayadragon

    slayadragon Senior Member

    Forbin’s comment gets to the heart of why this topic is related to XMRV.

    Marty Pall has done a wonderful job in laying out some of the ways in which these feedback loops may occur. I think it’s clear that what he says has relevance to what’s going on in this disease.

    The problem that I have with his theory is his speculation that once the cycle gets going, it keeps going on of its own accord for all eternity. While this is possible, it seems to me more likely that there are some trigger mechanisms that are keeping it going. One way of treating this disease is thus to identify what those triggers are and intercede.

    One trigger mechanism seems to be XMRV. Still, as the WPI studies suggest, not everyone with XMRV has CFS. And some people with CFS have “spontaneous” remissions or substantial decreases in the severity of the disease. It thus seems worthwhile to look for other trigger mechanisms, especially insofar as we are still in the process of learning to how to address the virus directly through the use of available drugs and waiting for new drugs to be developed.

    I agree with the idea that a wide variety of “stressors” might serve as triggering mechanisms to keep the feedback cycles going. The question is whether we can find ones that 1) are especially good at doing that and 2) can be addressed.

    Candida seems to me to be a good place to start, and indeed it has gotten plenty of attention in this disease. Interestingly (but not surprisingly), candida produces a toxin that is similar to that produced by toxic molds. This type of toxin seems to be especially good at contributing to oxidative stress. And, as I understand Cheney, this leads to another feedback loop, with the oxidative stress leading to a comparatively anaerobic environment of the system, and the anaerobic environment making it easier for yeast to proliferate.

    Certainly, candida is not the cause of CFS. But the topic of this thread was not to suggest a “cause.” It was to suggest how we can intercede at control points in order to a) make it easier to treat the virus(es) and b) work toward achieving a remission in the context of what researchers now know or suspect about XMRV.

    As Forbin suggests, there are a variety of stressors that have the potential of being relevant here. My focus here is on mold because a) the little research that we have about it suggests that the particular ways in which it exerts its toxicity seems consistent with the problems in CFS, b) it is a toxin to which many “average” people (e.g. not farm or industrial workers) are exposed to (in most cases unknowingly) on a continuous long-term basis, c) I myself and a number of others with classic documented CFS (including Erik Johnson, one of the original Incline Village prototypes for the disease) have achieved close to full remission by systematically addressing mold and doing nothing else, d) my recent experience with Valcyte suggests that addressing mold reduced the die-off and other problematic symptoms associated with the drug to basically nil and allowed me to benefit from it in ways that very few CFS patients have reported doing, and e) unlike just about every other stressor imaginable, mold (apart from Dr. Shoemaker’s and Erik Johnson’s work) has received almost no attention in CFS thus far.

    A couple of elaborative comments.

    Considering the extent to which toxins are increasingly present in the environment, research into any kinds of toxins has been extremely limited. Part of this is another “feedback loop”: if most medical researchers study viruses, their students also are going to be studying viruses and they are more likely to be receptive to papers from other virologists when deciding what to include in medical journals. In addition, it’s hard to get funding for toxicity issues. Drug companies are happy to fund work into viruses (e.g. Jose Montoya’s $1 million grant for the Valcyte study), since this has the potential to lead to profitability for them. Toxicity research seems less likely (at least on the surface) to lead to more drug sales; indeed, insofar as people focus on toxicity, they may be less inclined to consider any drugs at all. This does not mean that we should ignore the need for scientific research in the area; rather, it suggests the idea to develop hypotheses based on the information that we do have so that they can be tested with whatever moneys and researchers can be solicited.

    One area in which toxicity actually has been studied is in agriculture, since farmers have the needs to a) keep livestock healthy and b) kill bugs and other pests. I thus spent some time looking into various chemicals to see if I could find ones that might serve as models for what might be going on with the mold.

    One that seemed close was phosphine, which is used to kill insects in grain as well as rodents. Unlike most other toxins, phosphine exercises its mechanism primarily through oxidative stress. Interestingly, large doses of phosphine are not particularly effective at killing insects; rather, they actually can induce resistance. The thing that is particularly effective at killing insects is small doses of phosphine administered over very long periods of time.

    This seemed relevant to me because it is analogous to the conditions under which people are exposed to toxic mold. Probably it is true that a very large dose of satratoxin is effective at causing damage. But it may also be that a very low level of satratoxin administered over a period of years (as would occur if people live or work for a long time in one moldy building or in a series of moldy buildings) may have an equal or greater effect.

    It would be terrific to have such actual studies to prove that this hypothesis has merit, but since they would be expensive and would take a long time to be completed (e.g. 20 years of exposure), likely that will not occur soon. The hypothesis does seem consistent with the anecdotal evidence of large numbers of people (most of whom have no financial motivation for doing so) reporting far worse symptoms as a result of exposure to various molds than research studies suggest that they should be.

    CFS sufferers do on occasion experience “spontaneous” remissions, and so it is important to consider whether the ones that those of us who are attributing our recoveries to mold avoidance are misguided. The strongest argument is that staying well is contingent upon maintaining a high avoidance level. Insofar as this level of avoidance is not attended to extraordinarily carefully by those using such a strategy, health immediately plummets. Renewing mold avoidance is immediately followed by a restoration in health (with the time period needed for the restoration varying from an hour to several months depending on the extent to which and length of time mold avoidance was not pursued successfully).

    This results in a “quasi-experimental deisgn” (see the book of this name by a former professor of mine, Thomas Cook) that those who are pursuing mold avoidance cannot help but repeat over and over again as they encounter small amounts of mold in the environment. For instance, at the time that I was most reactive, the amount of mold spores in my hair as a result of a 30-second visit to a moldy building would cause me to become increasingly sick until I washed them out. Mold toxin (or the toxins on the spores) caused this reaction regardless of whether it was growing in a building, cross-contaminating objects, or present in the outside air.

    Clearly, getting to this level of mold avoidance is not something that would occur by chance. This seems to explain why “moving” is not generally successful in allowing CFS sufferers who have mold issues to recover their wellness. It also suggests (at least to me) that this is not a placebo effect: as placebos go, this is the last one I would choose! Neither I nor the others who have achieved partial or full remission as a result of this strategy have anything to gain as a result of pursuing it except for renewed health and the possibility of helping others to achieve the same thing. There are much easier ways to get attention.

    Certainly this could be a case of mass hysteria. But that’s what’s said about the entire disease of CFS, so what else is new?

    I’ve put off talking about mold in recent months because I wanted to observe what would happen as a result of my Valcyte trial. Back when I was living unknowingly in my moldy house, I was unable to take even a small dose (250 mg) of Famvir without getting more ill than what most people were reporting on full doses of Valcyte. After an extended period of what Erik calls “extreme mold avoidance,” I was able to take a full dose (1000 mg) of Famvir with no symptoms whatsoever. I then added a full dose of Valcyte (900 mg) with few die-off symptoms.

    The Famvir caused my mold reactivity (the extent to which mold makes me sick) to go up for three days and then go down below baseline. The Valcyte caused my mold reactivity to go up for about three months and then go down below baseline. At this point it is down to the point that no objects and relatively few buildings have an effect on me, which means that (insofar as this continues) I will be able to move back towards having a much more normal life.

    In addition, after just a month or so on Valcyte, my cognitive functioning started to “flicker” on at a level that I had not experienced since getting sick in 1996. This has occurred increasingly frequently since then, and now is at that level the majority of the time. Apart from continuing hangover-like detox symptoms every morning, remaining reactions to mold toxins and (recently, perhaps as a result of increased detox as a result of P450 restoration?) pollution, and an odd recent case of TMJ, I have no symptoms whatsoever of any disease at this time.

    My CFS was classic and increasingly severe (low NKC function, low suppressors, high Rnase-L and LMW Rnase-L, high apoptosis, extremely high interferon alpha, HHV6 titres sufficient to qualify for Montoya’s study, reactivated EBV, CMV, mycoplasma, chlamydia pneumoniae, post-exertional malaise, cognitive issues described in Osler’s Web, exercise intolerance, agitated exhaustion, sleep difficulties, need to stay within an “energy envelope," candida, food sensivities, gut problems, hormonal dysregulation, extreme die-off to doxycycline as well as Famvir, huge detox reaction to the supplements on Rich’s methylation protocol, gradual-then-sudden onset apparently triggered by high stress level, a series of Hepatitis B vaccines, a head injury, a pregnancy and a bad flu, ill for 12 years, bedridden 18-22 hours a day for the last year). As an Incline Village prototype, Erik’s illness was even more severe and obviously classic. Others who have recovered as a result of using this strategy report similar histories.

    An interesting question to me is the fact that Valcyte had such a positive effect on my health when it targets herpes viruses rather than retroviruses. One conclusion is that HHV6a is established in the body opportunistically, secondarily to the XMRV, but directly caused symptoms such as cognitive problems and inflammation. (That would make XMRV an interesting "cause," if HHV6a were also needed and provoked all the symptoms that weren't addressed fully by getting away from the mold). It also seems possible that HHV6 or one of the other herpes viruses serves as a helper virus to XMRV and that a one-two punch is needed for the XMRV to exert its effects, as Jen mentioned. Or perhaps the reduction in overall stress on my system as a result of lowering the mold exposures, pursuing two year’s worth of intensive detox, and getting the herpes viruses under control allowed my body to regain enough of its immune system functioning to get the XMRV under control naturally.

    The “one-two punch” conceivably could apply to the XMRV and mold combination as well. Judy Mikovits and Paul Cheney have acknowledged that there may be some sort of “terrain” issue that is allowing the virus to lodge itself into the system and/or not be kept in check. Considering how much health I and others have been able to regain just by avoiding the mold, it does not seem to be inconceivable that the mold is a factor (or the factor) causing this terrain issue. It even is conceivable (and to my understanding this has not been disproved) that XMRV is not a new virus at all, and instead is exerting itself as a result of the changed terrain that results as a result of people’s increased exposure to more mold (e.g. as a result of the emergence of drywall in the early 1970s) or the emergence of a new particularly damaging “super mold” (similar to the “super bacteria” that are known to have emerged recently). If that’s the case, then XMRV would be considered opportunistic, just as (say) toxoplasmosis is in AIDS.

    That mold is a “terrain” issue is wholly consistent with Erik’s observations that those individuals who were being exposed to large amounts of mold during the Incline Village epidemic were the ones who were more likely to get the “Yuppie Flu” to begin with and then to remain really sick after catching it. Obviously, his is just one observation. However, ALL science starts with one observation. Neither he nor I is a medical researcher. Our goal in bringing this up is not to prove anything. It is to supply professional medical researchers with our observations and experiences so that they will have a starting point to pursue testing what may be useful channels of inquiry in terms of better understanding and then treating this disease.

    In the meantime, regardless of whether researchers decide to pursue this line of research, my own experience that I was able to take and benefit from Valcyte only after addressing the mold seems that it has the potential of having value for people. As LadyBugMandy’s experience suggests, taking antiretrovirals seems to have the potential of proving as difficult and unproductive for CFS patients as does taking Valcyte. To the extent that addressing mold can be used as a leverage point to allow people to be more likely to be able to take and benefit from any of these drugs, the topic seems worth discussing in the context of XMRV.

    I will address some other the other questions on this thread in my next post.

    Best, Lisa
  5. Gerwyn

    Gerwyn Guest

    there is no science here have not addressed any questions whatsoever.It is total speculation when you promised scientific evidence to back up your claims.this has nothing to do with XMRV have used a lot of words but have provided no scientific information whatsoever.Qualitative speculation is nothing to do with science.this is a section set aside for XMRV and this does not belong here
  6. BEG

    BEG Senior Member

    Southeast US
    Thank you, slayadragon, for one of the most informative posts on the forum. This approach is definately worth investigating and pursuing. A treatment that relies on hypervigilance by the individual can't be easy, however. As you aptly put it, our environment today is producing super viruses, why not super toxins/molds? We must be surrounded and bombarded. This is just fascinating.

    You mentioned that you moved because of mold. May I ask, what was different about the next building you moved into? Besides no leaks, what other perpetuating factors were you avoiding?

    Really looking forward to your future posts --- Brown-eyed Girl.
  7. Navid

    Navid Senior Member

    Gerwyn please discuss this more

    gerwyn can you please expand on your stmt above.......some cfid's pts are going to start experimenting w/haart...why could the treatment prove fatal in 3 years.

    and if haart is inadvisable for cfid's pts testing xmrv+, what do you think will be the treatment?

    what do you think abt GFmac?

    thanks for your advice.
  8. Gerwyn

    Gerwyn Guest

    We almost certainly have mitochondrial damage. Haart will likelymake that damage much worse.

    If 30% of patients without mitochondrial damage suffer serious side effects after three years the likelyhood is high that people with mitochondrial damage will suffer much worse outcomes and in all probability death. An integrase inhibitor should be ok because it is not chemically similar to a chemical in DNA so wont insert into Mitochondrial DNA and cause chaos
  9. Gerwyn

    Gerwyn Guest


    Aspergillus species are ubiquitous moulds with worldwide
    distribution. Exposure most commonly occurs when airborne
    spores are inhaled into the lungs or sinuses. Once inhaled,
    spores reach distal areas of the lung by virtue of their small
    size. The most common infecting species is A. fumigatus,
    followed by A. flavus and A. niger (Marr et al, 2002; Husain
    et al, 2003). In normal hosts, isolation of Aspergillus generally
    reflects colonization and not infection (Uffredi et al, 2003).
    The clinical manifestations of aspergillosis vary depending
    upon the nature of the host. In atopic individuals with an
    allergic or hypersensitivity response, the fungus triggers
    immune phenomena including allergic rhinitis, asthma, hypersensitivity
    pneumonitis and allergic bronchoplumonary aspergillosis
    (ABPA) (Horner et al, 1995). In patients with cavitary
    pulmonary lesions, saprophytic colonization by Aspergillus
    leads to aspergillomas. Finally, immunocompromised patients
    may develop invasive aspergillosis (IA). This article will focus
    on the latter group of patients. The degree of fungal invasion,
    response to therapy and clinical outcome of IA depends upon
    the type and depth of immune suppression. In susceptible
    hosts, Aspergillus conidia germinate to form hyphae, the
    Table I. Defects in host defences that predispose patients to infections
    with specific fungi.
    Fungal pathogen Host factor
    Candida (mucosal) Impaired cell mediated immunity
    Candida (disseminated) Impaired mucosa or integument,
    Aspergillus Neutropenia, high-dose corticosteroids
    Cryptococcus Impaired cell mediated immunity,
    Zygomycetes Neutropenia, deferoxamine treatment,
    corticosteroids, diabetic ketoacidosis
    Fusarium Neutropenia, impaired integument,
    Scedosporium Neutropenia
    Trichosporon Neutropenia, impaired integument
    570 2005 Blackwell Publishing Ltd, British Journal of Haematology, 129, 569–582
    invasive form of the organism. An essential aspect of the
    immune response to Aspergillus is recognition and killing of
    conidia and activation of appropriate host defences to confront
    fungi that have escaped killing and transitioned to the hyphal
    form. In highly compromised patients, early detection of IA,
    institution of antifungal therapy and improvement in host
    immune status are crucial determinants in the outcome of
    infection (von Eiff et al, 1995).
    Qualitative and quantitative disorders of phagocyte function
    are the most important host factors predisposing patients to
    IA. In patients with neoplasms, virtually all cases are due to the
    therapy used to treat the malignancy, rather than the
    underlying disease itself. The major risk factor for IA is
    chemotherapy-induced neutropenia, with the risk being
    directly proportional to both the severity and the duration of
    the neutropenia (Gerson et al, 1984). Treatment with high
    doses of corticosteroids, which depresses neutrophil and
    macrophage function, also predisposes patients to IA. Other
    risk factors include chronic granulomatous disease, advanced
    AIDS and chronic graft-versus-host disease. The incidence of
    invasive fungal infections occurring after resolution of neutropenia
    is also increasing with the widespread use of highly
    immunosuppressive regimens, such as CAMPATH1-H or
    fludarabine for low intensity transplantation. The most
    frequent sites of involvement are the lungs followed by the
    sinuses. Infection may disseminate from the respiratory tract
    to other sites including the eyes, brain, liver, spleen, kidney,
    skin and bone (Stevens et al, 2000). Occasionally, direct
    inoculation of the fungus during invasive procedures or
    injection drug use can lead to soft tissue and even disseminated
    infection. IA in neutropenic hosts is characterized by extensive
    hyphal infiltration, angioinvasion, coagulative necrosis, intraalveolar
    haemorrhage, extra-pulmonary dissemination and
    high mortality (Berenguer et al, 1995). In hosts that are less
    severely compromised, such as transplant recipients receiving
    corticosteroids and calcineurin inhibitors, IA tends to be more
    indolent and is associated with a relatively higher survival rate.
    Inhaled Aspergillus conidia that are not repelled by respiratory
    tract mucociliary defences are mostly phagocytosed by
    macrophages and dendritic cells. These cells constitute the
    initial line of defence and have a dual role as antifungal
    effectors and as activators of the immune response (Kan &
    Bennett, 1988). Resident and monocyte-derived macrophages
    ingest and kill conidia, thus preventing transition into the
    invasive hyphal form (Schaffner et al, 1982, 1983; Waldorf
    et al, 1984a; Levitz et al, 1986; Philippe et al, 2003). After
    recognition and binding of conidia, actin-dependent pseudopodia
    capture and internalize the fungal particles. Swelling of
    the conidia inside the macrophage appears to be a prerequisite
    for fungal killing (Philippe et al, 2003). Aspergillus containing
    phagosomes mature by fusion with endocytic compartments.
    Conidial killing proceeds with acidification of the phagolysosome
    (Ibrahim-Granet et al, 2003). Production of reactive
    oxidant intermediates within alveolar macrophages is important
    for conidial killing, although non-oxidative killing mechanisms
    also play a role. In mice, impairment of NADPH
    oxidase inhibits killing without impairing phagocytosis. Corticosteroids
    inhibit production of reactive oxidant intermediates
    and killing of phagocytosed fungi, which may help to
    explain the elevated rates of IA in steroid recipients (Philippe
    et al, 2003). Cyclosporin A exerts only a modest effect on
    phagocytic defences and in the absence of corticosteroids does
    not increase the progression of IA (Roilides et al, 1994;
    Berenguer et al, 1995). Experimental models, as well as reports
    of IA in patients receiving anti-TNF-a antibodies, suggest
    cytokine networks are essential for the activation of leucocyte
    antifungal activity (Warris et al, 2001).
    Humoral factors participate in the host response to Aspergillus.
    Resting conidia, germinating conidia and hyphae are
    potent activators of the complement cascade and induce
    deposition of complement components upon the fungal
    surface. Resting conidia activate the alternative pathway and
    induce neutrophil chemotaxis. As the fungus matures into
    swollen conidia and then hyphae there is progressive dependence
    on the classical pathway (Kozel et al, 1989). In alveolar
    fluid, surfactant proteins A (SP-A) and D (SP-D) enhance
    chemotaxis, binding, phagocytosis and oxidative killing (Madan
    et al, 1997). These C-type lectins also agglutinate Aspergillus
    conidia, thereby immobilizing the pathogen. However,
    despite the importance of these humoral factors in experimental
    systems, the predisposing factor for the vast majority of
    patients with IA is phagocytic dysfunction and not defects in
    the humoral immunity.
    Macrophages and dendritic cells activate host defences in
    response to Aspergillus. At the surface of these cells are TLRs
    that identify microbial products (Akira et al, 2001). Signalling
    pathways associated with each TLR vary and activation of
    different receptors may result in dissimilar biological responses.
    For example, TLR 2 and TLR 4 differentially mediate
    the release of specific cytokines in response to the fungus
    (Braedel et al, 2004). When stimulated by Aspergillus conidia,
    macrophages produce proinflammatory cytokines, including
    TNF-a, IL-1a and IL-1b through TLR 4-dependent mechanisms.
    Aspergillus hyphae, on the other hand, stimulate
    production of the anti-inflammatory cytokine IL-10 through
    TLR 2-dependent mechanisms. Thus, activation of specific cell
    surface receptors during germination may allow Aspergillus to
    counteract host defences (Netea et al, 2003). TNF-a release,
    initially by resident macrophages and later by recruited
    immune cells, is associated with chemokine production
    [including Macrophage Inflammatory Protein (MIP)-1a and
    MIP-2] and influx of neutrophils and monocytes into infected
    tissues (Mehrad et al, 1999). Mice lacking functional CC
    chemokine receptor 1(CCR1) are much less efficient at
    blocking tissue invasion from the blood and have increased
    susceptibility to infection (Gao et al, 1997). Aspergillus conidia
    and hyphae induce nuclear factor (NF)-jB translocation, and
    release of TNF-a and MIP-2 in a TLR 2- and TLR 4-dependent
    manner. Neutrophil recruitment is severely impaired in mice
    lacking both functional TLR 2 and TLR 4, but is less impaired
    2005 Blackwell Publishing Ltd, British Journal of Haematology, 129, 569–582 571
    in single TLR 2 or TLR4 deficient mice, suggesting that both
    receptors are required for an optimal immune response to
    Aspergillus (Meier et al, 2003). In humans, optimal TNF-a
    signalling in response to the various morphotypes of Aspergillus
    requires TLR 2, CD14 and MyD88 (Mambula et al, 2002;
    Levitz, 2004). Administration of corticosteroids suppresses
    macrophage production of IL-1a, TNF-a, and MIP-1a, all of
    which are protective against aspergillosis (Brummer et al,
    Dendritic cells modulate the antifungal host response.
    Aspergillus antigens induce activation and maturation of these
    cells. Ingestion of Aspergillus conidia and hyphae proceeds
    through distinct phagocytic mechanisms and elicited responses
    differ depending upon the morphotype encountered. Following
    exposure to Aspergillus, dendritic cells migrate to the spleen
    and draining lymph nodes and induce local and peripheral Th
    cell reactivity to the fungus (Bozza et al, 2002). The development
    of specific Th responses is an essential determinant of the
    host’s susceptibility or resistance to IA. As with other fungi,
    production of Th1 cytokines appears to be protective, whereas
    Th2 responses are not (Cenci et al, 1998; Cenci et al, 1999,
    2001; Del Sero et al, 1999). In that regard, proinflammatory
    signals, including granulocyte-macrophage colony-stimulating
    factor (GM-CSF), TNF-a, IFN-c, IL-1, IL-6, and IL-12, IL-18
    as well as the chemokines MIP-1, monocyte chemoattractant
    protein (MCP)-1, and MIP-2, are associated with protection,
    and IL-4 and IL-10 with invasion. Cell surface and secreted
    pattern recognition receptors mediate the development of Th
    responses. TLR-associated MyD88-dependent signalling is
    crucial for priming antifungal Th1 responses (Bellocchio et al,
    2004). The secreted pattern recognition receptor PTX3 binds
    to select microbial products, including Aspergillus conidia, and
    has a non-redundant role in resistance to the fungus. PTX3-
    deficient mice are susceptible to invasive pulmonary aspergillosis
    with impaired recognition of the fungus by alveolar
    macrophages and dendritic cells and inappropriate induction
    of a Th2 response (Garlanda et al, 2002).
    When bronchoalveolar macrophages fail to control the
    fungus, conidia germinate into hyphae, pierce through the cell
    and grow extracellularly. Neutrophils and monocytes recruited
    from the circulation phagocytose and damage fungi that have
    escaped killing and are transitioning (or have transitioned)
    into hyphae. As described above, proinflammatory signals,
    including TNF-a, complement, chemokines, and surfactant
    proteins, recruit neutrophils into sites of infection. Since
    hyphae are too large to be completely phagocytosed, hyphal
    damage is achieved via extracellular means. Non-oxidative
    mechanisms include release of lysozyme and neutrophil
    cationic peptides. Oxidative killing is mediated by myeloperoxidase
    (MPO)-dependent and MPO-independent oxidative
    systems (Washburn et al, 1987). The importance of oxidative
    killing is demonstrated in chronic granulomatous disease. This
    hereditary disease is characterized by impaired production of
    oxidative intermediates and elevated rates of invasive infections
    due to several catalase positive pathogens, including
    Aspergillus (Cohen et al, 1981; Diamond & Clark, 1982).
    Phagocytosis of Aspergillus is enhanced by opsonization and
    proinflammatory molecules (Marr et al, 2001). TNF-a augments
    the capacity of neutrophils to damage hyphae, possibly
    through enhanced oxidative mechanisms, and increases anticonidial
    phagocytic activity of resident macrophages (Roilides
    et al, 1998a). Granulocyte colony-stimulating factor (G-CSF),
    GM-CSF and especially IFN-c enhance monocyte and neutrophil
    activity against hyphae (Gaviria et al, 1999). IL-15
    enhances hyphal damage and IL-8 release by neutrophils
    challenged with Aspergillus (Winn et al, 2003a). IL-8 recruits
    neutrophils to sites of inflammation and mediates release of
    antimicrobial peptides. By contrast, production of IL-4 by
    CD4+ T lymphocytes impairs neutrophil antifungal activity
    (Cenci et al, 1997). IL-10 suppresses oxidative burst and
    antifungal activity of mononuclear cells against hyphae, while
    increasing their phagocytic activity (Roilides et al, 1997).
    Corticosteroids reduce oxidative burst and superoxide anion
    release by neutrophils, thereby inhibiting hyphal killing
    (Roilides et al, 1993; Brummer et al, 2003). Treatment with
    G-CSF and IFN-c may prevent this impairment.
    A variety of factors that may augment virulence by immune
    evasion have been described in Aspergillus, but their contribution
    in vivo is difficult to gauge. Gliotoxin inhibits ciliary,
    macrophage, neutrophil, and lymphocyte function and induces
    apoptosis in immune cells (Mullbacher & Eichner, 1984; Pahl
    et al, 1996; Tsunawaki et al, 2004). Other Aspergillus-derived
    factors inhibit oxidative killing, interfere with ciliary function,
    inactivate complement, disrupt production of proinflammatory
    cytokines and promote adhesion to endothelium (Washburn
    et al, 1986; Jahn et al, 2001
  10. Forbin

    Forbin Senior Member

    Attachment to IACFS/ME Newsletter
    Volume 3, Issue 1 April 2010

    Questions and Answer Session with:
    Dr. Judy Mikovits: Principal Investigator, Whittemore-Peterson Institute.

    Q: Do you feel that XMRV is necessary and sufficient or necessary but not sufficient or not necessary or sufficient to cause chronic illnesses like CFS?

    Mikovits: Our hypothesis is that chronic XMRV infection creates results in an immune deficiency that is necessary but not necessarily sufficient to result in chronic illnesses like CFS. As with HIV/AIDS copathogens define AIDS, CMV retinitis, kaposis sarcoma are AIDS defining co-pathogens. That said XMRV is a type C retrovirus and Type C retroviruses are associated with neurovirulence in a range of host species, including humans, cats,rodents and birds with or without concurrent immunological disease suggesting XMRV can be Necessary and sufficient to cause CFS.

    Q: How might the finding of the XMRV virus relate to Lyme Disease?

    Mikovits: We are seeing XMRV in Chronic Lyme patients sent to us from several physicians. The hypothesis that chronic XMRV infection creates an underlying immune deficiency is consistent with many co-pathogens including Lyme.

    [Italics added]


    I take that to mean that it is Dr. Mikovits hypothesis that a co-pathogen in addition to XMRV may be necessary to cause a chronic illness like CFS.

    Based on that, is it unreasonable to speculate that dealing with the co-pathogen(s) might be of some benefit?
  11. Gerwyn

    Gerwyn Guest

    I think that is the key

    That said XMRV is a type C retrovirus and Type C retroviruses are associated with neurovirulence in a range of host species, including humans, cats,rodents and birds with or without concurrent immunological disease suggesting XMRV can be Necessary and sufficient to cause CFS.

    having said that as I have said before avoiding any pathogen would be a good idea.XMRV could make people susceptible to other infections.The jury is still out on that and the persistent high levels of NO and the shift to T2 indicates that the innate response may be compromised.That is nothing even remotely close to what Lisa was claiming.all this has happened as aresult of XMRV and mold(which does not exist scientifically-there are different molds) is no more causative of the immune problems than any other pathogen the immune system is already compromised.Mold could not come even close to explaining the biochemical abnormalities seen in ME or the symptom spectrum.
  12. lansbergen

    lansbergen Senior Member

    One of the things I did was lower infectionpressure. I avoided crowds and places with mechanic circulating air systems as much as possible. I also did not shake hands, I said it hurt and that was not a lie.
  13. richvank

    richvank Senior Member

    Hi, Gerwyn.

    Here's the abstract of a published paper that discusses the susceptibility of people to mold toxicity as a function of their HLA genotypes.

    Best regards,


    Int J Environ Res Public Health. 2005 Apr;2(1):186-93.
    How much should we involve genetic and environmental factors in the risk assessment of mycotoxins in humans?

    Creppy EE, Moukha S, Bacha H, Carratu MR.

    Dept of Toxicology, University of Bordeaux 2, 146, rue Lo-Saignat, 33076 Bordeaux, France.

    Despite consented efforts in prevention, mycotoxins remain a problem of human health concern in several parts of the world including developed countries. Within the same range of toxins concentrations in the blood some people develop a disease while others do not. Could this inequality in front of mycotoxins effects be explained by environment factors and/or genetic predisposition? Among recent advances in environmental health research Correlation between chronic diseases and mycotoxins in humans deserves attention through several questions: Are genetic factors involved in disease causation of mycotoxins? How much are these factors currently taken into account for mycotoxins risk assessment and how much should we involve them? Answers are still to come. Genetic and environment factors deserve therefore more attention when dealing with regulatory limits, since among the general population, those who are at risk and will develop specific diseases are likely those bearing genetic predispositions. We have addressed these questions for the specific case of ochratoxin A in humans by investigating in Tunisia, county of Jelma, in four rural families forming a household of 21 persons all exposed to ochratoxin A in diet. Our results confirm that ochratoxin A induces chronic tubular nephropathy in humans and mainly point at those having the HLA haplotype A3, B27/35, DR7 to be more sensitive to the disease for quantitatively similar or lower exposure. Persons with such haplotype were found to bear chronic interstitial nephropathy with tubular karyomegalic cells while others were apparently healthy. Godin et al. (1996) in France have also found in sibling (a sister and her brother from urban area) that have similar HLA haplotype B35-patern, OTA-related renal tubulopathy with mild proteinuria including beta2-microglobulinuria. Several mechanisms are discussed that could be put ahead to explain how the HLA haplotype could lead to tubular cells lyses and renal failure. In the mean time it is urgent to search for mass screening biomarkers for mycotoxins in humans and related genetic factors to set-up more appropriate regulation.

    PMID: 16705817 [PubMed - indexed for MEDLINE]
  14. richvank

    richvank Senior Member

    Comments on mold illness and CFS

    Hi, all.

    Lisa has asked me to make some comments on this thread. Here they are, for what they are worth.

    As I understand the situation, there are three types of reactions humans can have to mold:

    1. Type 1 sensitivity, also called allergy, which involves IgE and histamine.

    2. Infection of the human body by a mold, such as an aspergillosis infection of the lung.

    3. Mold toxicity, due to response to a toxin produced by a mold.

    I believe that Lisa is referring to the third of these reactions.

    My impression is that there is a larger published literature on the first two types of reactions, but there is also a literature on the third.

    I agree that the standard of peer-reviewed publication is the cornerstone of our system of trying to arrive at scientific truth. However, in my view it is somewhat like what I think Winston Churchill said about democracy. Basically, it has a lot of problems, but we haven't found anything better. It's a human system, and it has all the frailties we humans have. Publishers, editors and reviewers are under a variety of pressures, sometimes economic and political pressures, and none of these people are omniscient. Some of them are motivated to defend the status quo. Some of them are in competition with the authors of submitted papers for the same funding. Some derive part of their financial support from economic interests that would prefer not to see published papers that could be used against them in court. The result of all this is that a lot of good papers are not published, and some of what is published is later found not to be true. The best we can do as scientists is to try to improve the performance of this system as much as we can. But I don't think we should be naive as to what actually goes on in unfortunately, too many cases. From time to time this comes out in the open and efforts are made at reform, but ultimately the system relies on the integrity and competence of the people involved. I have been a peer reviewer for scientific journals, and I have submitted papers for peer review, so I have a little experience on both ends of this system.

    I think that one of the things that happens in science education, particularly at the beginning of this process, is that people study from textbooks in which fairly well established products of scientific research are presented in an organized way. Coming through this system, it's easy to get the impression that the scientific process is black and white, and that it's very clear what is scientific truth and what is not. However, I've found that at the frontiers of the process of using the scientific method, things are much murkier. In a field in which not much is known yet, it's more akin to groping in the dark than to applying very clear criteria for what is true and what is not.

    In the case of mold toxicity, we are not yet dealing with a mature science. For a lot of it, we are still in the pre-hypothesis stage, dealing with anecdotal evidence. If we apply the standards of mature science at this stage, I think we run the risk of staunching consideration of something very important. My view is that we should keep open minds at this stage, recognizing that we don't have much hard scientific evidence, but also recognizing that there is something here that is worthy of study and is actually vital to the health of a large number of people.

    With regard to CFS, based on my experience over the past 14 years in studying this disorder, my view is that mold toxicity is one route into CFS. Not everyone with CFS suffers from mold toxicity, but there is a significant subset who do. Do we have hard numbers in the peer-reviewed literature for the extent of this problem? Not yet. But as is always true in human endeavors, we have to start from where we are, and I believe that this work needs to be done.

    Best regards,

  15. Gerwyn

    Gerwyn Guest

    thanks Rich

    isnt ochratoxin A mutagenic in its own right and damages DNA.Establishing cause and effect would be rather problematic given that aspergillus oracheous is probably the most common food borne mycotoxin.there would seem to be a number of confounding variables involved here.the best here would be correlation.I can,t really comment without seeing the methodology.diseases progress at different rates and so did they quantify the degree of exposure.Do you have any access to the full article.I get fed up with people talking about mold<not talking about you, there are a myriad of different molds all with different mycotoxins with different effects. avoiding all of those would be somee achievement.

    all the best

  16. Dreambirdie

    Dreambirdie work in progress

    N. California
    Thanks Rich, for elucidating these very important points.

    And thanks Lisa. I am really grateful for the info on this thread pertaining to the mold toxicity issue.

    Since no one has the CURE for CFS yet, I'm more than willing to keep my mind open to options that might be helpful at remedying my situation.
  17. Gerwyn

    Gerwyn Guest

    I have to disagree Rich.

    There is no data to support the idea of subsets or any plausible mechanism by which MOLDS can cause multi systemic disease

    .The problem we face now, in my view, is that people are assuming subsets based on different people reporting a different symptom pattern.

    While it may be a useful metaphor there is no evidence that this is true in any mind independent sense.

    Without the construction of explanatory hypotheses to test a cure would seem remote

    We interpret our observations in line with our cognitive biases.This ,as you well know, is why the often ignored part of the scientific method is so important.Namely the active attempt to disprove an explanatory model.

    I agree completely about the politics and published papers turning out to be false.We have the example of the Dutch study at the moment

    Scientific evidence provides the probability of truth and that "truth" will probably change with time such is the nature of the discipline.

    I have long cautioned about the naive acceptance of politically motivated studies.

    I am all for creating an explanatory hypothesis of how a myriad of different mycotoxins could be causative of a neuroimmune endocrine disorder based on measurable observations and then testing that hypothesis.

    Is there any hard evidence of mycological toxicity in patients with Me/cfs sufferers.Either we apply the standards of hard science or we do not.

    If we don't then we can hardly complain when our opponents do not.We have to apply the same standards or we have no consistent defence against the pseudoscience of the opposition

    At the moment there is no evidence on which even to base that hypothesis on
  18. Dreambirdie

    Dreambirdie work in progress

    N. California
    Peer reviewed studies are not what they are cracked up to be.

    "Dr. Drummond Rennie, who relies on review as deputy editor of JAMA, the Journal of the American Medical Association, said of the process, ''The more we look into it, the harder it is to prove whether it does good or bad."

    Rennie has called for greater study of whether peer review improves research, and he has a personal policy of disclosing his name when he reviews articles.

    ''It would be lovely to start anew and to set up a trial of peer review against no peer review," Rennie said. ''But no journal is willing to risk it."

    Rennie's journal published the study, which said that subsequent research had found that almost one-third of the top papers that appeared in top journals over a 13-year period from 1990 to 2003, had been either contradicted or found to have potentially exaggerated results. All the articles had undergone vigorous peer review, leading to questions about whether problems should have been caught by reviewers."

    "Under the system of peer review, a researcher submits findings to a journal for publication. Along with a review by editors, the article is sent to several specialists in the field.

    These reviewers are not paid for their time, their names are usually not published, and their comments usually remain secret. They are usually not allowed to contact the researchers directly to ask questions, and they do not try to replicate the research.

    The system has often had successes; many journal editors say peer review has saved countless prominent scientists from publishing seriously flawed work, and has spared the public from following mistaken medical advice.

    But peer review also lacks consistent standards. Procedures vary among the world's 10,000 or so journals. A peer reviewer often spends about four hours reviewing research that may have taken months or years to complete, but the amount of time spent on a review and the expertise of the reviewer can differ greatly, especially at lesser-known journals.

    ''It has been bandied about as a sort of 'Good Housekeeping Seal of Approval,' " said Marcia Angell, former editor of the New England Journal of Medicine. ''It is only as good as the peer reviewers and editors."

    Ioannidis, the author of the study on flawed research, said he had examined articles from top journals published from 1990 to 2003, and had found that 16 percent of those studies were later contradicted, and that another 16 percent were not found to have had as strong a result in subsequent research.

    Many factors led to the conflicting results, he said, including the fact that scientific research is often updated when larger or better-controlled trials are conducted. But flaws in the initial studies, including integrity and methodology, could not be ruled out."
  19. Gerwyn

    Gerwyn Guest

    It isn,t the peer review process.there are different processes in different journals and excercised with different degrees of vigour.Science for example has probably the most stringent peer review system in the world.The peer reviewer must ok the paper before the editor can decide whether to publish it or not.In other journals like Plos one for example the decision to publish is ultimately the editors decision irrespective of the peer reviewers comments.It is therefore not the principle of peer review at fault but the presence of bad journals whose main focus is commercial gain.SCientists in my experience give more weight to evidence printed in certain journals compared to others.
  20. richvank

    richvank Senior Member

    Hi, Gerwin.

    My responses are at the asterisks below:

    I have to disagree Rich.

    ***Fair enough.

    There is no data to support the idea of subsets or any plausible mechanism by which MOLDS can cause multi systemic disease

    .The problem we face now, in my view, is that people are assuming subsets based on different people reporting a different symptom pattern.

    While it may be a useful metaphor there is no evidence that this is true in any mind independent sense.

    Without the construction of explanatory hypotheses to test a cure would seem remote

    ***I think we actually have quite a bit of agreement on most of this (but see below regarding your first point). I agree that subsets have not been successfully delineated in the published literature. I agree that trying to define subsets of CFS by symptoms is not productive. I agree that the process needs to be hypothesis-driven. In fact, this is the very point I tried to make during the open-mike session that was held at the AACFS conference in Madison, Wisconsin in 2004. The audience of patients applauded, but I don't think the "powers-that-were" in the AACFS accepted my point. What I said at that time, and what I've tried to do since, is that we need to start developing hypotheses that will account for at least some of the patients in the CFS "bucket." When we have one that seems to fit some of them, we take them out of the bucket and then work on developing a hypothesis for another group of them, and so on. Sort of a divide-and-conquer approach. I was fortunately able to develop the GD-MCB hypothesis a few years later, based on research that was done in autism. This is primarily a pathogenesis hypothesis, which allows for a variety of etiologies, and in that sense, I think it takes in the majority of cases of CFS, at least based on the lab testing we have been able to do thus far. Is this in the peer-reviewed literature? Not yet. Is it valid? Well, I believe it is, and I continue to study cases in detail that this hypothesis appears to fit. Of course, everyone is free to make up their own mind about it.

    We interpret our observations in line with our cognitive biases.This ,as you well know, is why the often ignored part of the scientific method is so important.Namely the active attempt to disprove an explanatory model.

    ***I agree with these statements, too. Once in a while, though, someone changes their cognitive bias based on evidence. I like to think that I do that from time to time. :)-)

    I agree completely about the politics and published papers turning out to be false.We have the example of the Dutch study at the moment

    Scientific evidence provides the probability of truth and that "truth" will probably change with time such is the nature of the discipline.

    I have long cautioned about the naive acceptance of politically motivated studies.

    ***I think we generally agree on these issues. I'm not sure I have all the facts concerning the Dutch study, so I will reserve judgment on that.

    I am all for creating an explanatory hypothesis of how a myriad of different mycotoxins could be causative of a neuroimmune endocrine disorder based on measurable observations and then testing that hypothesis.

    ***O.K. Me, too. I suspect that a basis for it could be the mechanism or mechanisms by which some mycotoxins have been found to deplete glutathione in cells, as has been reported in the peer-reviewed literature, not only in the thesis that Lisa cited. If this is coupled with an HLA genotype based inability to remove mycotoxins that some people have inherited, so that the mycotoxins build up enough in these people to have a significant impact on their glutathione stores, and if in addition these people are genetically predisposed to developing a partial methylation cycle block if their glutathione drops down enough, then I think we have the makings of a hypothesis that could account for many of the observations, while at the same time being compatible with accepted biochemistry and immunology. Yes, there are several unproven steps in this chain of cause and effect, and yes, a lot of hard work would need to be done to test it, but where there currently is information that can be used to test it, I think it stands up to the test.

    Is there any hard evidence of mycological toxicity in patients with Me/cfs sufferers.Either we apply the standards of hard science or we do not.

    ***I'm not sure what your criteria are for "hard evidence." I've heard from several people whose symptoms would qualify them for CFS who have reported experiences that are pretty convincing to me. Namely, they have the symptoms of CFS, they begin to suspect that their living environment is hosting toxic molds, based on a long-standing water leak, observation of mold growing on a wall, the smell of mold, and sometimes an ERMI test of their home. Some have reported that they feel better if they are out of their home for a while. Some have gone through Dr. Shoemaker's test program where they are tested, move out, are treated and recover, are tested again, then move back in, get sick again, and are tested again. Dr. Shoemaker is careful to note that there can be other components involved in these homes beside molds, but there is pretty good evidence that mold is a major contributor in many cases. I agree that quantitative studies are needed. Dr. Shoemaker has published a couple of papers about his work involving people exposed to water-damaged buildings. The PubMed I.D. numbers are 15681119 and 17010568.

    If we don't then we can hardly complain when our opponents do not.We have to apply the same standards or we have no consistent defence against the pseudoscience of the opposition

    ***I agree with this, too.

    At the moment there is no evidence on which even to base that hypothesis on

    ***If you mean in peer-reviewed publications, I agree that more is needed. From my point of view, though, there is plenty of evidence on which to base more than one hypothesis. I might add that Dr. Shoemaker does not accept my hypothesis, and in fact has his own, but there is a clinical study in the works now that may shed light on this. I might add that it is not easy to get funding for research in this area. Owners of very large buildings are vulnerable to expensive lawsuits if a convincing connection can be made between conditions in a building and the health of its occupants. Dr. Shoemaker has participated in several of these court proceedings on the side of the plaintiffs, and getting research funded and papers published in peer-reviewed journals that would support such a connection is a high-stakes effort. It's also interesting to note that the headquarters buildings of the U.S. Environmental Protection Agency in Washington, D.C. a few years ago had a serious mold problem, and a lawsuit was brought against them by their own employees. Here's a site that reviews some of the history of "sick building syndrome," particularly in the U.S., including mold-related issues:

    Best regards,


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