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Mold, Dr. Cheney and ME/CFS

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

  1. slayadragon

    slayadragon Senior Member

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    Gerwyn, thank you for your comments. I will get back to them and to other comments related to the "control points" concept shortly.

    Dreambirdie, here is my own perspective on mold testing. However, please note that this is not scientifically proven to be the optimal approach and also is not what professionals in the remediation industry will tell you to do.

    There are several challenges with regard to finding out if a home has a mold problem. This is why most CFSers who are affected by mold don't know it. And insofar as people don't know if mold is an issue for them, it has the potential of undermining any other treatments (including use of antiviral drugs) that they may choose to pursue.

    Mold professionals usually recommend air tests. These take photos of the air in the home. Someone then looks at the pictures to see how many of various mold spores are present.

    One problem with this is that Stachybotrys (which is generally considered a particularly dangerous mold and the one that I think is especially relevant to CFSers) almost never shows up on air tests. It releases a heavy, sticky spore that falls to the ground within at most an hour or two. At that point, the majority of the spores immediately disintegrate into "spore fragments" that look like dust. These fragments (which are just as poisonous as the whole spores) are blown around or are carried around the environment.

    In addition, Stachy releases its spores in waves. Some observers have found homes showing no Stachy problems on air tests for 23 hours per day, but horrific problems during the remaining hour.

    Air tests attempt to "control" for the issue of whether a house is moldy by doing a comparison with the outdoor air. Unfortunately, some of us with CFS have found that it doesn't matter if it's the outside air vs. the inside air that's giving us mold exposure. It still makes us sick.

    Air tests are expensive. Professionals usually want to test multiple rooms in the house as well as the outside air. The total can run to $1000 or more.

    The ERMI is another test that can be used. It looks at household dust to create an estimation of how likely the home is to have a mold problem compared to other homes. The results are given in quartiles, with the top 25% said to have "the greatest likelihood of having a mold problem."

    I have not used the ERMI or read its enclosed materials, and I'm not certain how Stachy is weighted compared to other molds. The cost is a bit over $300.

    This is a DNA test, and so does take into consideration mold that has fallen from the air and spore fragments. I suspect that it's fine with regard to identifying buildings that are so bad that they are making ordinary people sick.

    However, knowing that a home has "passed" the ERMI doesn't mean that CFSers are not being affected by mold. Being in the top 25% of homes is not generally "good enough" for really reactive people to make a lot of progress. Those of us who have partially or fully recovered from CFS just as a result of attending to mold have needed to be looking at mold in the outside air and on our possessions (and on our own hair) in order to maintain that wellness. These sources of exposure will not be measured in an ERMI test.

    It's my own belief that getting the ERMI test done is useful as a basic evaluative step for CFSers though. Moving to a home that passes the ERMI won't necessarily improve wellness in itself, but it's my suspicion that living in a home that's very moldy will prevent other treatments from working as well as they could. This hypothesis wouldn't be very hard to test, so hopefully this can be done in conjunction with other CFS treatment studies soon.

    The test that you are requesting looks at a particular obvious mold and gets an identification of it. This type of test is readily available. However, regardless of what comes up on the test, it shouldn't be considered to be useful in providing information on whether an environment is problematic. Stachy grows almost wholly within walls, and most moldy homes have more than one type of mold growing. If Stachy actually can be seen (in many cases, it looks more like smears of dirt than mold), that's a suggestion that the problem is really horrific.

    There's a company called MouldWorks that does a very nice job of giving a description of what samples of mold include. Regardless of what they say, their analysis shouldn't be thought to be very helpful in CFSers' decision making.

    Those CFSers who have realized that mold is a problem for them have mostly done so as a result of leaving their home for a while and then returning. Dr. Sarah Myhill actually recommends this, suggesting that "you'll have to go on holiday" in order to find out whether mold is an issue for you since "mould allergy" does not show up on conventional allergy testing. (That's because it's a toxicity problem rather than an allergy problem, of course.)

    This is an excellent suggestion, but it only works if the "holiday" actually reduces toxic mold exposure. If people bring their contaminated clothing and other belongings with them, they may not get to a low enough level to make much difference. If they stay in a moldy building (most hotels are quite moldy) or happen upon a place with a lot of outdoor mold, this also will negate the experiment. I've heard that Dr. Myhill recommends that people in England try going to another country, like Greece, for the experiment.

    In addition, this does not work like a mold allergy. Getting away from the mold for a short period of time does not necessarily create much improved wellness. If people are poisoned by pesticides, getting away from new pesticide exposures wouldn't be expected to provide immediate relief. This is the same principle. It takes time for the system to detoxify previous exposures and to repair itself from downstream problems. And since mold is just one part of the equation, other treatments (such as antivirals) may be needed. This is just a stepping stone.

    If a person who's getting a lot of mold exposures does go to a clear environment, they do usually feel a bit different. They may be more able to "exercise," whatever that means. They may have less agitated exhaustion, more falling into a deep heavy sleep that promotes detox.

    Most importantly, they may find that they feel particularly bad when they return to their usual environment. In some cases, the downturn is so dramatic that they have a difficult time remaining in their homes.

    Erik has written a lot more extensive information on this kind of "mold test," which I can supply to people if they want it. Please write and ask.

    CFSers who try to do their own remediation often get much more ill as a result of the process. In many cases, they do not recover to their previous baseline. Some patients have died or become bedridden as a result of doing this.

    I write more about this topic on this thread (currently post #26):

    http://www.forums.aboutmecfs.org/sh...XMRV-activated-via-mold-and-Lyme-toxins/page3

    Anything to do with windows makes me especially nervous, because Stachy tends to grow in places where it can get lots of water on a regular basis (which happens when a window has a leak).

    I therefore STRONGLY urge you not to remove that wood yourself. Please don't do that. It's too dangerous.

    I strongly urge others reading this thread not to go looking for or repairing mold in their own homes either. It could prove to be really harmful or deadly.

    Please be safe!!!

    Best, Lisa
  2. Dreambirdie

    Dreambirdie work in progress

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    Hi Lisa--

    So if you do have mold, you're recommending to just LEAVE IT there? That doesn't sound like a good idea to me.

    I know a TCM practitioner in L.A. who works with a lot CFS and MCS patients, and has dealt with mold issues. In fact his own wife became ill with mold toxicity from mold (stachybotrys) growing in their own house. She moved out for a while while they did the mold removal, and then she was able to live in the house again. I think I need to find out how he did it. I'm not satisfied just letting the mold to continue to fester, but I want to think it out carefully before I jump into any mold removal project.

    Thanks for all your info.
  3. slayadragon

    slayadragon Senior Member

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    Hi Dreambirdie,

    Mold certainly should be removed. I just want to be sure that CFSers don't do it themselves.

    The safe way to do this is to have a mold professional take care of it. They should seal the surrounding area off with plastic so that the spores do not disseminate all over the environment when they are exposed. The professionals should be wearing protective clothing and masks for their own health.

    Obviously this costs money.

    I'm reluctant to suggest to people that they have non-professionals help them to remove the mold. Depending on the extent of the problem, they may risk long-term damage to their own health even from one exposure. In addition, if the area is not sealed off properly, the spores may disseminate into the area and make it more problematic long-term for CFS sufferers.

    All of this, like everything else about the topic of toxic mold, sounds ridiculous. But people used to think that asbestos, lead paint and mercury fillings/vaccines were perfectly innocuous too.

    I wish I had better answers for people.

    Best, Lisa
  4. Gerwyn

    Gerwyn Guest

    So are you talking about mold or molds again now
  5. Gerwyn

    Gerwyn Guest

    One problem with this is that Stachybotrys (which is generally considered a particularly dangerous mold and the one that I think is especially relevant to CFSers) almost never shows up on air tests. It releases a heavy, sticky spore that falls to the ground within at most an hour or two. At that point, the majority of the spores immediately disintegrate into "spore fragments" that look like dust. These fragments (which are just as poisonous as the whole spores) are blown around or are carried around the environment.

    In addition, Stachy releases its spores in waves. Some observers have found homes showing no Stachy problems on air tests for 23 hours per day, but horrific problems during the remaining hour.

    Air tests attempt to "control" for the issue of whether a house is moldy by doing a comparison with the outdoor air. Unfortunately, some of us with CFS have found that it doesn't matter if it's the outside air vs. the inside air that's giving us mold exposure. It still makes us sick.

    NO Lisa that is either not true or there is no objective evidence to support it
  6. Dreambirdie

    Dreambirdie work in progress

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    Okay Lisa. I would not dream of removing the mold myself. I have dealt with construction people a lot in the past, and I think the most important thing is to find someone who you can trust to do what you instruct them to do. I would NOT trust someone I didn't know. Have learned my lesson with that! I am going to have to research exactly how it's all done, and give him the directions on how to proceed.

    I am even thinking that I want my worker to come in and out of the room through the window, because I don't want him walking through my house after he's been exposing moldy wood in there. There's not a lot of people who will go that far for you, but I think I know just the one.

    Thanks again for bringing all this to my attention.
  7. slayadragon

    slayadragon Senior Member

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    OK, Gerwyn. Using language that is wholly precise is a bit cumbersome, but I will try.

    From now on, when I say "Mold" or "Molds," what I mean is, "Toxic molds that have been shown in research studies to cause negative effects in humans."

    I am especially concerned about Stachybotrys, but other toxic molds that have been shown to be damaging in peer-reviewed published research studies are also included.

    Hopefully folks will accept this as shorthand.

    I accept your contention that until I write a paper on my own health history and have it published in a peer-reviewed journal, I do not have evidence that mold is making me sick.

    It's just my opinion.

    Thanks for your comments.

    Best, Lisa
  8. slayadragon

    slayadragon Senior Member

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    Hi Dreambirdie,

    I wish I had a good book on remediation to offer you. There are a few on the market, but I'm not sure how to evaluate them.

    What you might consider doing is going to a Yahoo group called SickBuildings. There are a couple of professional remediators on that board that offer information to people. Usually they will offer some basic suggestions for free, and then provide more extensive consultation for a flat fee by telephone.

    A lot of the people on that board are pretty sick with CFS or mold illness, so they're accustomed to discussing the matter in the context of people who may need to take special care with the removal process.

    Lots of CFSers actually DO start off thinking that they should remove mold themselves or participate in the process, unfortunately. So thanks much for bringing this topic up.

    If you like, please let me know your progress.

    Best, Lisa
  9. Gerwyn

    Gerwyn Guest

    Thankyou Lisa. all you need to do for said paper is to run some longitudinal blood tests.You obviously said that mold did not cause your ME,cfs or at least that is my understanding.If you can work out some symptoms that the mold is exacerbating or even creating De Novo and measure them in some objective manner you could provide some correlative evidence.That although a case study would be a major advance over what we have now.

    I wish you all the best with it
  10. Dreambirdie

    Dreambirdie work in progress

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  11. slayadragon

    slayadragon Senior Member

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    Gerwyn, I have a question I'd like to ask you.

    This is not a question in order to offer an argument in response. I really would like your opinion.

    Many times, we hear reports of things like, "Red dye #2 causes cancer" (according to either prevalence studies in humans or laboratory studies with animals).

    Clearly, this substance is not the ONLY cause of cancer. People are still getting cancer even though this stuff was removed from the market. And lots of people consumed this stuff without getting cancer.

    That means that there have to be other underlying causes for the disease. For instance, my impression that cancer researchers think that viral issues underlie many or all cancers, even though specific viruses (e.g. Hepatitis B in liver cancer) have been identified in only a few kinds of cancers so far.

    People don't seem to hesitate about using the word "causes" with regard to the red dye though.

    I ask this because of some comments that Erik made regarding his observations about what was happening during the Incline Village epidemic.

    Prior to the epidemic (as I mentioned earlier on this thread), Erik was aware that toxic mold bothered him somewhat. He thus paid attention to where it was in his surroundings.

    It is his contention that people who already were living or working in "Sick Buildings" (e.g. the ones that bothered him) were more likely to come down with the "Yuppie Flu" and much more likely not to recover from it after a few weeks than those people who were living in environments that he found to be "good" with regard to the apparent absence of toxic mold.

    Obviously we should not trust Erik's observations on this. Any hypotheses that we make about this topic need to be scientifically verified before we can give any credibility to them.

    Even if Erik is right and this can be proven, that still wouldn't mean that previous toxic mold exposure is necessary in order for people to come down with CFS. As with the red dye, it only would mean that the toxic mold exposure makes it more likely that people will get the disease.

    And obviously, it also wouldn't mean that toxic mold exposure makes people get CFS all by itself. Lots of people work or live in sick buildings and don't get sick at all, much less get CFS. Just like lots of people consumed Red Dye #2 and didn't get any sort of illness (to our knowledge) as a result.

    I think that Erik's observation is worth considering as a hypothesis for research. Regardless of how the study came out, I'd like to know the answer.

    But I'm having a hard time framing this.

    Every time he or I mentions the words "toxic mold" and "CFS" in the same sentence, people respond by saying, "Mold doesn't cause CFS" and then dismiss the whole idea.

    Do you have any suggestions on how to phrase it in a way that will make people with scientific mindsets give it more consideration?

    In general, I want to extend my appreciation for your comments here. You're absolutely right that I need to put together a really solid literature review to support everything that I'm saying, and to make it more clear whether things are my opinion, other people's opinions, informal observations, generally accepted "industry norms" or scientific demonstrations. That will take some effort, but I've realized through this discussion that it's going to be necessary to get credibility.

    Best, Lisa
  12. Gerwyn

    Gerwyn Guest

  13. Gerwyn

    Gerwyn Guest

    You have really got me thinking Lisa

    If I look at things from another perspective CFS as an objective entity does not exist.it is merely a subjective label of convenience.In essence it is an illness created by the definition used.If you change your recruitment parameters you end up with a different cohort of patients. We are accepting that CFS is somehow real in a mind independent sense.It is likely that we are talking about different illnesses.Plausibly we share mitochondrial damage of different aetiologies.if then the question becomes can mycotoxins cause mitochondrial damage I think the answer must be yes. Mitochondrial damage could account for the symptom complex of "CFS" but have different causes.I dont know if that approach helps.If you dont mind me being cheeky do you have PEM--that seems to be key in mito dysfunction. My suggestion would be to measure mito function perhaps with a few people who experience "cfs" symptoms with mold exposure which alieviate when the environmental insult is removed. I think that it is well worth developing a discussion but to be taken seriously we need some kind of objective correlation and or a plausible causative theory.A literature search would be a great start
  14. Gerwyn

    Gerwyn Guest

    How is this for a first contribution

    Article
    Novel Mycotoxin from Acremonium exuviarum Is a Powerful Inhibitor of the Mitochondrial Respiratory Chain Complex III

    * Abstract
    * HTMLFull Text HTML
    * PDFHi-Res PDF[597 KB]
    * PDFPDF w/ Links[212 KB]

    Alexey G. Kruglov†‡, Maria A. Andersson†, Raimo Mikkola†, Merja Roivainen, Laszlo Kredics, Nils-Erik L. Saris† and Mirja S. Salkinoja-Salonen*†
    Department of Applied Chemistry and Microbiology, University of Helsinki, P.O. Box 56, FIN-00014 Helsinki, Finland, Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Institutskaya 3, Pushchino, Moscow Region, 142290 Russia, Department of Viral Diseases and Immunology, National Public Health Institute, Mannerheimintie 166, FI-00300 Helsinki, Finland, and Department of Microbiology, Faculty of Science and Informatics, University of Szeged, Kozep fasor 52, H-6726 Szeged, Hungary
    Chem. Res. Toxicol., 2009, 22 (3), pp 565–573
    DOI: 10.1021/tx800317z
    Publication Date (Web): February 5, 2009
    Copyright 2009 American Chemical Society
    * To whom correspondence should be addressed. Tel: +358(0)40 5739049. Fax: 358(0)9 19159301. E-mail: mirja.salkinoja-salonen@helsinki.fi., †

    University of Helsinki.
    , ‡

    Russian Academy of Sciences.
    ,

    National Public Health Institute.
    ,

    University of Szeged.
    Abstract
    Abstract Image

    A novel mycotoxin named acrebol, consisting of two closely similar peptaibols (1726 and 1740 Da), was isolated from an indoor strain of the mitosporic ascomycete fungus Acremonium exuviarum. This paper describes the unique mitochondrial toxicity of acrebol, not earlier described for any peptaibol. Acrebol inhibited complex III of the respiratory chain of isolated rat liver mitochondria (1 mg of protein mL−1) with an IC50 of 80 ng mL−1 (50 nM) after a short preincubation, and 350 ng mL−1 caused immediate and complete inhibition. Acrebol thus is a complex III inhibitor almost as potent as antimycin A and myxothiazol but completely different in structure. Similarly to myxothiazol but in contrast to antimycin A, acrebol decreased the level of mitochondrial superoxide anion detectable by chemiluminescent probe 3,7-dihydro-2-methyl-6-(4-methoxyphenyl)imidazol[1,2-a]pyrazine-3-one. Unlike other peptaibols, acrebol in toxic concentrations did not increase the ionic and solute permeability of membranes of isolated rat liver mitochondria, did not induce disturbance of the ionic homeostasis or the osmotic balance of mitochondria, and did not release apoptogenic proteins like cytochrome c from the intermembrane space of mitochondria. In boar spermatozoa, acrebol inhibited the respiratory chain and caused ATP depletion by activation of the oligomycin-sensitive F0F1-ATPase, which resulted in the inhibition of the progressive movement. In mouse insulinoma MIN-6 cells, whose energy supply solely depends on oxidative phosphorylation, acrebol induced necrosis-like death. The pathophysiological relevance of these findings is discussed.
  15. slayadragon

    slayadragon Senior Member

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    You've gotten precisely to the point of what Erik has been trying to communicate to people for more than 25 years. (And you're amongst the first half-dozen or so people anywhere to have wholly grasped the point.)

    When Erik first got sick during the Incline Village epidemic, he had not just "post-exertional malaise" but what he calls "no-exertional malaise." Just trying to crawl to the bathroom or open a can of soup (to eat cold because heating it was too hard) made him relapse.

    What he eventually found was that if he could get free enough of all traces of toxic mold contamination (or, at least, what he identified subjectively as toxic mold contamination), his post-exertional malaise and exercise intolerance went away.

    However, this only worked insofar as he made this special effort. He only could exercise in areas with "good" outside air (since, in his subjective opinion, the substance that he identified as toxic mold can be outside as well as inside). And he only could do it insofar as he was thoroughly decontaminated (e.g. after he washed his hair and changed into clothes that hadn't been exposed to toxic mold). Otherwise, both the PEM and exercise inability came back.

    Insofar as he made this special effort, he was able to exercise without any problems. His exercise intolerance and PEM went totally away.

    If he didn't make this special effort, he stopped being able to exercise. The exercise intolerance and PEM returned at full force.

    It's not just that the exercise intolerance and PEM improved. It went totally away, enough so that he was able to climb to the top of Mt. Whitney (14,000 feet; half of all people making the attempt don't finish) every summer for 10 years in a row.

    The first time he did it was six months after being approved for Ampligen from Dr. Peterson, so he obviously was pretty sick.

    I found the same thing to be true. My own PEM used to be marked. Now, if (and only if) I follow Erik's "protocols," I am able to exercise without negative consequence as well (though I haven't gotten to the top of Mt. Whitney yet....just the "difficult" hikes in the Frommer's books).

    Other people with CFS report their exercise intolerance and PEM going away as long as they attend closely enough to mold avoidance as well.

    That's an interesting article. I need to look up a few of the terms and think through the concepts before I comment on it.

    Thanks much for your help.

    Best, Lisa
  16. slayadragon

    slayadragon Senior Member

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    Medical Testing Related to Toxic Mold

    I'm going to go back and answer a few questions from earlier in this thread. Hopefully folks are still reading this!

    Jewel, here is some information about various kinds of tests related to whether individuals are being affected by mold illness.

    1. One kind of test panel is the one that Dr. Shoemaker has developed. It includes a number of measurements related to inflammation and immune responses. This includes measurements of various cytokines (such as MMP-9 and TNF), since that kind of inflammation seems to be related to toxic mold illness. It also includes measurements of various hormones (such as MSH, cortisol, leptin and ACTH), since those are thought to be affected by the presence of the inflammation and other negative effects brought about by toxic mold. Measurements of complement elevations (C3a and C4a) also are included, since those are thought to be related to current acute toxic mold exposures. VEGF, which is a chemical signal directing growth of new blood vessels, is also part of the panel. The HLA-DR genetic testing, which Dr. Shoemaker says that he has observed to be strongly correlated with toxic mold illness, also is included on the panel.

    These tests still are unfamiliar to many practitioners, but seem to be gaining acceptance. To my knowledge, Dr. Shoemaker has not published any papers verifying their reliability or usefulness. They are described in detail in Dr. Shoemaker's book "Mold Warriors" and on his website at www.biotoxins.info.

    2. Also on his website, Dr. Shoemaker makes available a test that he calls variously the VCS (visual contrast sensitivity) and the BIRS (biotoxin illness risk score). This is an eye test of visual contrast, which he states is a good detector of the presence of neurotoxins of whatever sort (not just biotoxins) in the brain. It can be completed online and serves as an initial screening device.

    My own personal experience and observations suggest that this is a useful screening device, but that it doesn't necessarily do a good job in ruling out mold illness in CFS sufferers. When I was living in my moldy house, I indeed did terribly on the VCS. At that point, my vision has declined to the point that everything looked dim and I could barely see anything to read inside. This was scary!

    During the couple of months after I moved out of my moldy house, my vision improved to the point where I could pass the VCS. I felt a bit better, but was not even close to being well. It only was after I visited Erik for a week and got really clear (and then started this ridiculous "extreme mold avoidance" thing) that my health really recovered.

    Most of the time now, I can pass the VCS. Sometimes, especially after I've had a good bit of mold exposure, I fail it.

    Dr. Shoemaker says although people who aren't suffering from biotoxin illnesses (which also can include things like chronic Lyme, dinoflagelites and brown recluse spider bites) shouldn't fail the test, those people who are having problems sometimes can pass it.

    The idea that I can pass the test even though I'm being affected by small amounts of mold toxin is consistent with one hypothesis about the role that toxic mold plays in this illness. Certainly, significant amounts of the neurotoxin itself (enough to affect the vision) can be present in CFSers who are suffering from mold illness. However, a hyperreactivity of the complement component (C3a and C4a) seems to be a more fundamental part of the problem, just as it is in people who suffer from peanut "allergies." This is more related to what the body does to itself when it senses the mold toxin than to the direct effects of the toxin. Why the body is going nuts when it senses tiny bits of this stuff is, in my mind, a key question that we need to answer about the disease.

    Interestingly, the C4a responses has been mentioned in other research related to CFS. I'm going to post an abstract related to that topic below.

    I certainly think that it's a good idea for CFSers to take the VCS. On its own or in combination with the ERMI, it can provide substantial information on whether people are living or working in really moldy buildings.

    That's important to know, so that the problem can be addressed if so. No one should be living in a sick building. That's especially the case for anyone with an illness that affects the immune system, regardless of whether we think that mold might be a "cause" of that illness.

    However, passing the VCS should not be taken to provide conclusive evidence that mold toxicity is not a factor in an individual's illness. It is only a first step.

    3. Another kind of test is an allergy test panel. Here we are talking about allergic reactions to toxins, not to their poisonous effects. Still, I have heard of people using them for cases of mold toxicity illness, so I will discuss them.

    One measure is the IgE tests to different species of mold. These measure allergic reactions, which result in symptoms such as watery eyes, runny nose and asthma.

    This is not useful for the purpose of measuring mold toxicity, because this is not an allergy. In my case, even though I appear to be suffering from the negative effects of toxic mold, I do not have any allergic symptoms of mold at all.

    A second component of this test is the IgG. This apparently measures the extent to which people have been recently exposed to various species of mold.

    As it was explained to me, the rationale for the use of this test is to try to determine the extent to which various molds are present in the person's usual environment. If the IgG to Stachybotrys comes up high, it is thought to mean that the person's home (or other area where s/he spends time) has a Stachybotrys problem.

    This does not mean that the person is being affected by the particular mold, though. Some people appear to be able to get a very large amount of exposure to these molds and not suffer from any apparent ill effects at all.

    Having a low IgG does not mean that the person is not being affected either. Again, it is our contention that for some of us, even small amounts of exposure (apparently triggering complement to go ballistic) are enough to keep us sick.

    The potential usefulness of the IgG is to serve as an environmental test, since the tests that remediators use (air tests, ERMI, tape lists) are so unreliable. I don't have enough data on the accuracy of the IgG for this purpose to say whether it actually provides good information.

    4. Another type of test is the one that Gerwyn mentions in this thread (May 5, currently post #99). This is a test that shows whether various molds, including toxic species such as Aspergillus, have colonized the body. In this case, the molds are serving as pathogens (like a bacteria would). Insofar as the molds continue to produce toxins while living in the body, this would be contributing to any toxicity problem present.

    It's my impression that this sort of test is reliable. However, the colonization of individuals' systems with these pathogens is only one part of the problem. We also are affected by the toxins that we take in just by breathing them in. One toxicologist (Dr. Jack Thrasher) told me recently that these toxins appear to have the ability to go straight up the olfactory nerve and into the brain, totally bypassing the lungs or bloodstream.

    Stachybotrys, which is possibly the most problematic toxic mold for CFS sufferers, very rarely can get any sort of a foothold in the body. Aspergillus does so more frequently, especially in people who are already immune compromised. It tends to cause sinus infections and lung problems. These types of problems often are attributed in CFS sufferers to infections with candida, bacteria (such as chlamydia pnemoniae) or mycoplasma. Considering the idea that they might be related to Aspergillosis or other mold colonization, especially if mold in the home is suspected, may be warranted.

    I actually had a lung problem, with mild-ish pneumonia-like coughing, during the couple of months before I found out about the mold in my house. It went away within a couple of weeks after I moved out. One hypothesis is that immune defects resulting from mold toxicity make Aspergillosis more likely to occur. Of course, other immune problems from CFS also could contribute to its presence.

    5. There also is a panel of tests that measure the presence of various chemicals, including various mycotoxins, in the bloodstream. These tests are used frequently by various environmental specialists, such as Dr. William Rea.

    This kind of test was originally designed to assess the presence of manmade chemicals, as might occur from industrial exposures to solvents or pesticides. They then were extended to measure mycotoxins.

    One issue here is that toxic molds make a whole variety of chemicals. We don't have enough knowledge yet to be able to say for sure which ones are particularly bad.

    Another issue is that the body tends to sequester mold toxins and other chemicals in the fat cells rather than in the bloodstream. The amounts in the blood thus may be misleading.

    I don't have enough information about these tests to gauge their accuracy. From what I've heard, people who have environmental exposures to most chemicals tend to see their blood levels gradually go down if they get away from the environmental exposures and engage in active detox. The levels of the mycotoxins seem more likely to stay stubbornly elevated.

    Everything I run into suggests that there's something weird going on with the mold compared to all other substances. I wish I understood better what it is.

    6. The test that Dr. Myhill suggests ("you'll have to go on holiday") and that Erik has long advocated ("the Godforsaken wilderness" sabbatical) discussed above are designed to help individuals determine how much of an impact small amounts of toxic mold are having on them.

    The test needs to be done carefully in order to yield a useful result though. Because CFSers are affected by such small amounts of mold, staying in a bad building, a bad region or amidst bad belongings (or other objects) can make it seem that toxic mold is not a problem even when it actually is.

    If the test is done right though, it provides much more convincing results than any of the lab tests. Only two weeks after moving out of my moldy house and four days after putting aside my belongings from the house, I found that I couldn't go back into close proximity with those items without feeling ill. Washed clothing made my heart beat fast. Putting my hand inside my purse caused a painful burn that lasted for a week. Putting on my heavy coat made me have to stop by the side of the road to repeatedly vomit.

    This is what Dr. Rea calls "unmasking." Interestingly, CFSers talk about it with regard to food allergens all the time---e.g. needing to stop eating wheat in order to figure out that small amounts of it cause a problem. Considering that toxic mold is inherently a "worse" substance for people than is "wheat" (consumed by the majority of the population with only positive results), the idea that the former may be causing problems that are at least as bad as the latter at low levels does not seem that unfathomable of a concept. Just an unfamiliar one.

    In general, practitioners seem to be moving more toward using Dr. Shoemaker's panel of tests (including the VCS) to assess mold illness. For CFSers, the "Godforsaken wilderness" one (perhaps in combination with Dr. Shoemaker's panel) seems to work best. The others seem to be more useful for particular situations rather than for the diagnosis and monitoring of mold illness in general.

    If you have any other questions, please let me know.

    Best, Lisa
  17. slayadragon

    slayadragon Senior Member

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    Here's an article on the measurement of mycotoxins in tissues and body fluids (as mentioned above in #5).

    *

    Int J Mol Sci. 2009 Apr 1;10(4):1465-75.
    Mycotoxin detection in human samples from patients exposed to environmental molds.

    Hooper DG, Bolton VE, Guilford FT, Straus DC.

    RealTime Laboratories, LLC, 13016 Bee Street #203, Dallas, TX 79234, USA.
    Abstract

    The goal of this study was to determine if selected mycotoxins (trichothecenes, aflatoxins, and ochratoxins) could be extracted and identified in human tissue and body fluids from patients exposed to toxin producing molds in their environment. Human urine and methanol extracted tissues and sputum were examined. Trichothecenes were tested using competitive ELISA techniques. Aflatoxins B1, B2, G1, and G2, and ochratoxin A were tested by using immunoaffinity columns and fluorometry. Test sensitivity and specificity were determined. Levels of detection for the various mycotoxins varied from 0.2 ppb for trichothecenes, 1.0 ppb for aflatoxins, and 2.0 ppb for ochratoxins. Trichothecene levels varied in urine, sputum, and tissue biopsies (lung, liver, brain) from undetectable (<0.2 ppb) to levels up to 18 ppb. Aflatoxin levels from the same types of tissues varied from 1.0 to 5.0 ppb. Ochratoxins isolated in the same type of tissues varied from 2.0 ppb to > 10.0 ppb. Negative control patients had no detectable mycotoxins in their tissues or fluids. These data show that mycotoxins can be detected in body fluids and human tissue from patients exposed to mycotoxin producing molds in the environment, and demonstrate which human tissues or fluids are the most likely to yield positive results.

    http://www.ncbi.nlm.nih.gov/pubmed/19468319'
  18. slayadragon

    slayadragon Senior Member

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    Continued from my post on testing above (#2):

    Transcriptional Control of Complement Activation in an Exercise Model of Chronic Fatigue Syndrome.

    Journal: Mol Med. 2008 Nov 16.

    Authors: Sorensen B, Jones JF, Vernon SD, Rajeevan MS.

    Affiliation: Division of Viral and Rickettsial Diseases, National Center for Zoonotic, Vector-borne and Enteric Diseases, Centers for Disease Control and Prevention, Atlanta, GA, USA 30333;

    NLM Citation: PMID: 19015737

    Complement activation resulting in significant increase of C4a split product may be a marker of post-exertional malaise in chronic fatigue syndrome (CFS) subjects. This study was focused to identify the transcriptional control that may contribute to the increased C4a in CFS subjects post-exercise.

    Differential expression of genes in the classical and lectin pathways were evaluated in peripheral blood mononuclear cells (PBMCs) using quantitative reverse transcription PCR. Calibrated expression values were normalized to internal (peptidylpropyl isomerase B [PPIB]) or external (ribulose-1,5-bisphosphate carboxylase/oxygenase large subunit [rbcL]) reference genes or geometric mean (GM) of genes ribosomal protein, large, P0 (RPLP0) and phosphoglycerate kinase 1 (PGK1).

    All nine genes tested, except mannose-binding lectin 2 (MBL2), were expressed in PBMCs. At 1 hr post-exercise, C4, mannan-binding lectin serine protease 2 (MASP2) and ficolin 1(FCN1 ) transcripts were detected at higher levels (>/= 2-fold) in at least 50% (4 out of 8) of CFS subjects that increased to 88% (7 out of 8) CFS subjects when subjects with over-expression of either C4 or MASP2 were combined.

    Only increase in MASP2 transcript was statistically significant [PPIB, p=0.001; GM, p=0.047; rbcL, p=0.045]). This may be due to the significant but transient down-regulation of MASP2 in control subjects (PPIB, p = 0.023; rbcL, p = 0.027). By 6 hrs post-exercise, MASP2 expression was similar in both groups.

    In conclusion, lectin pathway responded to exercise differentially between CFS and controls subjects. MASP2 down-regulation may act as an anti-inflammatory acute-phase response in healthy subjects, whereas its elevated level may account for increased C4a and inflammation mediated post-exertional malaise in CFS subjects.

    *

    And here is a further comment made to Erik and me by Keith Berndtson, M.D.:

    The conclusion to the study whose abstract Erik provided above:

    “In conclusion, this study detected expression of both classical and lectin pathways in PBMCs of normal healthy and CFS subjects, but transcripts for components of the lectin pathway (C4 and MASP2) were observed at higher level in CFS subjects 1 hr post-exercise. Higher expression of C4 and MASP2 may contribute to the increased C4a split product in CFS subjects 6 hr post exercise. MASP2 expression was significantly down-regulated in control subjects 1 hr post-exercise, and this down-regulation may be mediated by the anti-inflammatory effect of cortisol in response to exercise. Further studies are needed to replicate the differential expression of complement genes and its potential link with inflammation and cortisol secretion in response to exercise.”

    Notice the possible connection with hypocortisolism, in which decreased cortisol release post-exercise may be what allows transcription of C4a splitters to proceed at a higher rate than in healthy controls, who produce enough cortisol within 1 hour after exertion to contain the complement system.

    Such a dynamic could apply to toxic mold responses where high C4a levels are also seen. Perhaps the same CDC group would be interested enough to compare the time vs. C4a level curves in post-exertional CFS with post-acute toxic mold exposure CFS, and then correlate any differences with HLA typing.

    This might allow subtyping of CFS patients using HLA typing and post-challenge C4a levels as biomarkers.

    More of this kind of research could make the disinterest response too conspicuous to ignore. Then again, it may be the kind of bias that only fades one funeral at a time.

    -Keith
  19. lono

    lono

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    I wanted to add some additional info in relation to C4a and the Sorensen article (Transcriptional Control of Complement Activation in an Exercise Model of Chronic Fatigue Syndrome) referenced by Lisa in #118.

    A recently published research article has added to our understanding of C4a in relation to PEM and CFS/ME. The recent paper is:

    Unravelling the nature of postexertional malaise in myalgic encephalomyelitis/chronic fatigue syndrome: the role of elastase, complement C4a and interleukin-1β
    Journal of Internal Medicine, Volume 267, Number 4, April 2010 , pp. 418-435(18)
    Nijs, J.; Van Oosterwijck, J.; Meeus, M.; Lambrecht, L.; Metzger, Frmont, Paul,


    It was posted to the forum here.

    A couple of interesting things they found in this recent paper (from Nijs et al) regarding C4a:

    1. Sorensen tested patients 6 hours after exercise and found a steep rise in C4a that corresponded with PEM. In the Nijs paper they tested participants 1 hour after exercise (for whatever reason) and didn't find an increase of C4a. However, they explicitly state in the paper that they didn't test after 6 hours so there's no evidence in their findings that C4a won't rise 6 hours after exercise. What makes their findings most interesting is that -

    2. They tracked C4a levels over time and they found that an increase in "complement C4a level was strongly related to the increase in pain and
    fatigue 24 hours following the [exercise]." Additionally (and most interestingly) they found, "The level of complement C4a following submaximal exercise was identified as a clinically important biomarker in people with ME/CFS."

    We need all the biomarkers we can get in the CFS/ME world, so bravo.
  20. jewel

    jewel Senior Member

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    Thank you for slayadragon and lono for this wonderfully detailed information. J.

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