Mold, Dr. Cheney and ME/CFS

[Gerwyn]

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: http://www.safeencasement.com/mold_timeline.htm

Best regards,

Rich

I agree that a particular mold infection can lead to glutathione depletion.so can any other chronic infection.I would prefer an objective diagnosis of ME.I am talking about the CCC definition.Anecdotes are not evidence Rich however convincing they are subjective interpretations.I genuinely hope that there is a study that will test the hypothesisTthe sequence of events you describe are more akin to an allergy.Anyone living in these conditions would experience trouble.Mycotoxicity<as you know, would mimic most of the FUKUDA presentations quite easily as would clinical depression and a number of other things.

Mold(just for argument I will reduce the number to just one) can cause symptoms very similar to CFS(Fukuda) but not ME/cfs(CCC) or anything like them.

Sick building syndrome and Fukuda symptoms are identical without the PEM.

Most fukuda presentations dont make pem mandatory.people in water damaged buildings can have severe problems.

That i think is beyond dispute especially if the Aw raises above 0.9.That does not mean that this exposure causes CFS the neuroimmume endocrine disorder.there is no convincing evidence that glutathione depletion on its own could cause the symptom spectrum seen in CCC Me/cfs.

A retrovirus could via insertional mutagenesis into regulatory genes NFAC and CREB.I do think that glutathione depletion is important but can see no plausible mechanism how it cause the multsystemic presentations seen in ME or the gene regulation patterns seen in kerrs work.

There always remains the possibility however that there are seperate illnesses within the cfs banner.CFS is simply a metaphor and does not referr to any mind independent characteristics of the illness.There are many ways to damage mitochondria, for example some mycotoxins would do this at a high enough dosage for long enough

 

[Forbin]

Although I stand second to no one in my low regard for the "Failure to Detect..." study published in PLoS ONE last January, unless I am mistaken Silverman and DeRisi's original paper on the discovery of XMRV (originally found in prostate tumors) was published in PLoS Pathogens in March 2006.

http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.0020025

PLoS Pathogens, however, took three months to review the Silverman/DeResi paper, whereas PLoS ONE only took 3 or 4 days to review the Wessely/Cleare paper. Still, this strikes me as something to be aware of when talking about PLoS.

 

[Gerwyn]

Although I stand second to no one in my low regard for the "Failure to Detect..." study published in PLoS ONE last January, unless I am mistaken Silverman and De Risi's original paper on the discovery of XMRV (originally found in prostate tumors) was published in PLoS Pathogens in March 2006.

http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.0020025

PLoS Pathogens, however, took three months to review the Silverman/De Resi paper, whereas PLoS ONE only took 3 or 4 days to review the Wessely/Cleare paper. Still, this strikes me as something to be aware of when talking about PLoS.

yes it is strange because given the category Mclures work should have been in plos pathogen.why was it in plos one i wonder.Are the peer review systems different.Mclure said that her work took two weeks. That is interesting considering the following


A clinical trial is any research study that prospectively assigns human participants or groups of humans to one or more health-related interventions to evaluate the effects on health outcomes. Interventions include but are not restricted to drugs, cells and other biological products, surgical procedures, radiologic procedures, devices, behavioural treatments, process-of-care changes, preventive care, etc"

PLoS supports the position of the International Committee of Medical Journal Editors (ICMJE) on trial registration. All trials initiated after 1 July 2005 must be registered prospectively in a publicly accessible registry (i.e., before patient recruitment has begun), or they will not be considered for publication. For trials initiated before 1 July 2005, all trials must be registered before submission to our journals. See the ICMJE faq on trial registration for further details. The WHO's list of approved registries is listed here.

Was this done if it was where was it posted? did the study comply with the preamble.Anyone know?

 

[richvank]

Hi, Gerwyn.

My responses are at the asterisks:

I agree that a particular mold infection can lead to glutathione depletion.so can any other chronic infection.

***I'm in agreement with you on this. Glutathione depletion alone does not bring about CFS, in my hypothesis. There must be a genetic predisposition toward developing a partial methylation cycle block if glutathione goes low enough. This explains why not everyone develops CFS when they are subject to stressors that deplete their glutathione. It also explains why when you get detailed histories from a large number of people who have CFS, you find a wide variety of pre-onset stressors. The common factor is that all these stressors place demands on glutathione, and thus they channel all these genetically predisposed people toward onset of the same condition.

I would prefer an objective diagnosis of ME.I am talking about the CCC definition.

***I think that's a pretty good definition, too. In our study, we used the Fukuda definition, but also required the presence of post-exertional fatigue. I think that captured the essence of the Canadian definition.

Anecdotes are not evidence Rich however convincing they are subjective interpretations.

***I might differ with you a little there. As Dr. Myhill essentially said in her defense, when you have a lot of independent anecdotal accounts that are telling you the same thing, it might not be evidence to which one can assign a p-value, but it most assuredly is evidence to which one should pay attention.

I genuinely hope that there is a study that will test the hypothesis

***I hope so, too. Getting it funded and done and published are the challenges.

Tthe sequence of events you describe are more akin to an allergy.Anyone living in these conditions would experience trouble.

***I don't think this is the case. People do appear to have very different susceptibilities. Somewhat related to this is the condition multiple chemical sensitivity. I can be standing right next to a person with MCS, and they can suffer mightily from some exposure that I hardly even notice. This has happened to me numerous times, as someone in my family has MCS.

Mycotoxicity<as you know, would mimic most of the FUKUDA presentations quite easily as would clinical depression and a number of other things.

***If the Fukuda criteria are properly applied by someone who is familiar with CFS, I think these things can be separated, though I am not a fan of the Fukuda criteria, and as I mentioned above, in our clinical study we included post-exertional fatigue as a criterion.

Mold(just for argument I will reduce the number to just one) can cause symptoms very similar to CFS(Fukuda) but not ME/cfs(CCC) or anything like them.

***I'm not sure I can agree with this statement. As you have said, I think we need more data. The Canadian criteria are still pretty fuzzy criteria, though they are an improvement over the Fukuda criteria, in my opinion.

Sick building syndrome and Fukuda symptoms are identical without the PEM.

***Again, I would need more data to agree with a statement this categorical.

Most fukuda presentations dont make pem mandatory.

***I think this is true.

people in water damaged buildings can have severe problems.

***We agree on this.

That i think is beyond dispute especially if the Aw raises above 0.9.That does not mean that this exposure causes CFS the neuroimmume endocrine disorder.

***I think that in people who are genetically predisposed to developing toxic mold illness, it does. Again, proof of this is needed.

there is no convincing evidence that glutathione depletion on its own could cause the symptom spectrum seen in CCC Me/cfs.

***I agree. I believe that a genetic predisposition toward developing a partial methylation cycle block when glutathione becomes sufficiently depleted is also necessary for a case of CFS to develop. With regard to whether there is convincing evidence for this, I will agree that it is not yet in the peer-reviewed literature, but from my point of view, the evidence for this combination being at the crux of the biochemical dysfunction in CFS is becoming overwhelming. I spend a good part of my time consulting on cases with a lot of biochemical testing data, and I see glutathione depletion and partial methylation cycle block over and over. And when these issues are treated, good things happen to a lot of the people. Are they all completely recovered? No, I wish they were, and I'm hoping to see improvement in outcomes as we learn more about effective treatment for these conditions. A few people have been able to return to full-time work, but there are many who experience partial recovery, and others who don't experience benefit. I continue to study these cases.

A retrovirus could via insertional mutagenesis into regulatory genes NFAC and CREB.

***I think this is fascinating. It sounds as though XMRV can insert into a variety of locations in the human DNA, and if so, it would seem that it could have a variety of effects. Maybe that's why it is implicated in both prostate cancer and CFS. What effect it has may depend on where it inserts.

I do think that glutathione depletion is important but can see no plausible mechanism how it cause the multsystemic presentations seen in ME

***I discussed this in detail in my 2007 poster paper, which can be found at www.cfsresearch.org

or the gene regulation patterns seen in kerrs work.

***Methylation has major effects on gene expression. Kerr found that something like 85 out of 88 genes that were expressed differently in CFS were overexpressed. That would be the direction expected if there were a methylation deficit, which is the case when there is a partial methylation cycle block.

There always remains the possibility however that there are seperate illnesses within the cfs banner.CFS is simply a metaphor and does not referr to any mind independent characteristics of the illness.

***I agree. It's a very heterogeneous population. I don't think I have studied two casese that were alike in nearly every respect. There is a commonality, but each one has its own wrinkles.

There are many ways to damage mitochondria, for example some mycotoxins would do this at a high enough dosage for long enough

***I agree. I do think that in CFS the mito dysfunction is well-explained by the GD-MCB hypothesis. Glutathione depletion allows oxidizing free radicals to block the Krebs cycle and the respiratory chain, and it also allows the buildup of toxins. The oxidizing free radicals also damage the mito membranes. The partial methylation cycle block leads to depletion of Co Q-10 and carnitine, both of which require methylation for their synthesis. When the Krebs cycle and the respiratory chain are blocked, ATP production goes down, and the membrane ion pumps have an energy crisis, which accounts for the low magnesium and the high calcium. The presence of viral DNA in the mitochondria can be accounted for the shift away from Th1, which is needed to combat viruses, and which can be caused by gltutathione depletion. I think all the things that Sarah and John McLaren Howard have found in the brilliant mito testing they have done are readily accounted for by the GD-MCB model.

***Best regards,

***Rich

 

[Gerwyn]

Hi, Gerwyn.

My responses are at the asterisks:

I agree that a particular mold infection can lead to glutathione depletion.so can any other chronic infection.

***I'm in agreement with you on this. Glutathione depletion alone does not bring about CFS, in my hypothesis. There must be a genetic predisposition toward developing a partial methylation cycle block if glutathione goes low enough. This explains why not everyone develops CFS when they are subject to stressors that deplete their glutathione. It also explains why when you get detailed histories from a large number of people who have CFS, you find a wide variety of pre-onset stressors. The common factor is that all these stressors place demands on glutathione, and thus they channel all these genetically predisposed people toward onset of the same condition.

I would prefer an objective diagnosis of ME.I am talking about the CCC definition.

***I think that's a pretty good definition, too. In our study, we used the Fukuda definition, but also required the presence of post-exertional fatigue. I think that captured the essence of the Canadian definition.

Anecdotes are not evidence Rich however convincing they are subjective interpretations.

***I might differ with you a little there. As Dr. Myhill essentially said in her defense, when you have a lot of independent anecdotal accounts that are telling you the same thing, it might not be evidence to which one can assign a p-value, but it most assuredly is evidence to which one should pay attention.

I genuinely hope that there is a study that will test the hypothesis

***I hope so, too. Getting it funded and done and published are the challenges.

Tthe sequence of events you describe are more akin to an allergy.Anyone living in these conditions would experience trouble.

***I don't think this is the case. People do appear to have very different susceptibilities. Somewhat related to this is the condition multiple chemical sensitivity. I can be standing right next to a person with MCS, and they can suffer mightily from some exposure that I hardly even notice. This has happened to me numerous times, as someone in my family has MCS.

Mycotoxicity<as you know, would mimic most of the FUKUDA presentations quite easily as would clinical depression and a number of other things.

***If the Fukuda criteria are properly applied by someone who is familiar with CFS, I think these things can be separated, though I am not a fan of the Fukuda criteria, and as I mentioned above, in our clinical study we included post-exertional fatigue as a criterion.

Mold(just for argument I will reduce the number to just one) can cause symptoms very similar to CFS(Fukuda) but not ME/cfs(CCC) or anything like them.

***I'm not sure I can agree with this statement. As you have said, I think we need more data. The Canadian criteria are still pretty fuzzy criteria, though they are an improvement over the Fukuda criteria, in my opinion.

Sick building syndrome and Fukuda symptoms are identical without the PEM.

***Again, I would need more data to agree with a statement this categorical.

Most fukuda presentations dont make pem mandatory.

***I think this is true.

people in water damaged buildings can have severe problems.

***We agree on this.

That i think is beyond dispute especially if the Aw raises above 0.9.That does not mean that this exposure causes CFS the neuroimmume endocrine disorder.

***I think that in people who are genetically predisposed to developing toxic mold illness, it does. Again, proof of this is needed.

there is no convincing evidence that glutathione depletion on its own could cause the symptom spectrum seen in CCC Me/cfs.

***I agree. I believe that a genetic predisposition toward developing a partial methylation cycle block when glutathione becomes sufficiently depleted is also necessary for a case of CFS to develop. With regard to whether there is convincing evidence for this, I will agree that it is not yet in the peer-reviewed literature, but from my point of view, the evidence for this combination being at the crux of the biochemical dysfunction in CFS is becoming overwhelming. I spend a good part of my time consulting on cases with a lot of biochemical testing data, and I see glutathione depletion and partial methylation cycle block over and over. And when these issues are treated, good things happen to a lot of the people. Are they all completely recovered? No, I wish they were, and I'm hoping to see improvement in outcomes as we learn more about effective treatment for these conditions. A few people have been able to return to full-time work, but there are many who experience partial recovery, and others who don't experience benefit. I continue to study these cases.

A retrovirus could via insertional mutagenesis into regulatory genes NFAC and CREB.

***I think this is fascinating. It sounds as though XMRV can insert into a variety of locations in the human DNA, and if so, it would seem that it could have a variety of effects. Maybe that's why it is implicated in both prostate cancer and CFS. What effect it has may depend on where it inserts.

I do think that glutathione depletion is important but can see no plausible mechanism how it cause the multsystemic presentations seen in ME

***I discussed this in detail in my 2007 poster paper, which can be found at www.cfsresearch.org

or the gene regulation patterns seen in kerrs work.

***Methylation has major effects on gene expression. Kerr found that something like 85 out of 88 genes that were expressed differently in CFS were overexpressed. That would be the direction expected if there were a methylation deficit, which is the case when there is a partial methylation cycle block.

There always remains the possibility however that there are seperate illnesses within the cfs banner.CFS is simply a metaphor and does not referr to any mind independent characteristics of the illness.

***I agree. It's a very heterogeneous population. I don't think I have studied two casese that were alike in nearly every respect. There is a commonality, but each one has its own wrinkles.

There are many ways to damage mitochondria, for example some mycotoxins would do this at a high enough dosage for long enough

***I agree. I do think that in CFS the mito dysfunction is well-explained by the GD-MCB hypothesis. Glutathione depletion allows oxidizing free radicals to block the Krebs cycle and the respiratory chain, and it also allows the buildup of toxins. The oxidizing free radicals also damage the mito membranes. The partial methylation cycle block leads to depletion of Co Q-10 and carnitine, both of which require methylation for their synthesis. When the Krebs cycle and the respiratory chain are blocked, ATP production goes down, and the membrane ion pumps have an energy crisis, which accounts for the low magnesium and the high calcium. The presence of viral DNA in the mitochondria can be accounted for the shift away from Th1, which is needed to combat viruses, and which can be caused by gltutathione depletion. I think all the things that Sarah and John McLaren Howard have found in the brilliant mito testing they have done are readily accounted for by the GD-MCB model.

***Best regards,

***Rich

the genetic susceptibility to mold is unproven.Glutathione depletion can certainly contribute to mito dysfunction as can raised NO levels which can also cause a block in the methylation cycle.Both can occur asa result of upregulated TNF alpha as a result of upregulated NFAC.A progesterone analogue binding to xpr-1 could also cause a shift to TH2.Gammaretroviruses have been found in mito dna and can directly reduce function.I have some data somewhere that a very small base sequence mutation(deletion or substitution) can dramatically reduce function.The XMRV hypothesis could account for your observations and Sarahs brilliant work NFAC upregulation would also explain the dysregulated HPA acis via upregulated interferon alpha.Downregulation of CREB can and does lead to severe neurocognitive symptoms anxiety depression and potentiate the tendancy to neoplasmia. I am trying to put a model together can I send it to you when or if it is finished.it would be interesting to kick it around

all the best

Gerwyn

 

[Gerwyn]

The symptoms of sick building syndrome

The symptoms particularly associated with the proposed chemical sub-syndrome include fatigue, headache, and dry and irritated eyes, nose and throat sometimes with nausea or dizziness. Those most common to the proposed microbial sub-syndrome include itchy, congested or runny nose, itchy watering eyes, sometimes with wheezing, tight chest or flu-like symptoms...These symptoms fit with a presumed trigeminal nerve irritation mechanism in the case of chemicals, and an infective or allergic mechanism in the case of microbes.'

pretty close to fukuda

 

[richvank]

The symptoms of sick building syndrome

The symptoms particularly associated with the proposed chemical sub-syndrome include fatigue, headache, and dry and irritated eyes, nose and throat sometimes with nausea or dizziness. Those most common to the proposed microbial sub-syndrome include itchy, congested or runny nose, itchy watering eyes, sometimes with wheezing, tight chest or flu-like symptoms...These symptoms fit with a presumed trigeminal nerve irritation mechanism in the case of chemicals, and an infective or allergic mechanism in the case of microbes.'

pretty close to fukuda

Hi, Gerwyn.

I guess so, but I don't see anything about cognitive dysfunction. However, if the stuff in the "sick building" lowered glutathione enough in a person genetically susceptible to developing a partial methylation cycle block, I could understand how cognitive dysfunction could develop, also. If the person was not genetically predisposed, I suspect that they might develop some of these symptoms, but not have CFS.

Best regards,

Rich

 

[richvank]

the genetic susceptibility to mold is unproven.Glutathione depletion can certainly contribute to mito dysfunction as can raised NO levels which can also cause a block in the methylation cycle.Both can occur asa result of upregulated TNF alpha as a result of upregulated NFAC.A progesterone analogue binding to xpr-1 could also cause a shift to TH2.Gammaretroviruses have been found in mito dna and can directly reduce function.I have some data somewhere that a very small base sequence mutation(deletion or substitution) can dramatically reduce function.The XMRV hypothesis could account for your observations and Sarahs brilliant work NFAC upregulation would also explain the dysregulated HPA acis via upregulated interferon alpha.Downregulation of CREB can and does lead to severe neurocognitive symptoms anxiety depression and potentiate the tendancy to neoplasmia. I am trying to put a model together can I send it to you when or if it is finished.it would be interesting to kick it around

all the best

Gerwyn

Hi, Gerwyn.

I'm glad you are doing this, and I think that's just the type of thing that needs to be done. If you can get these various pieces fitted into a cause and effect "tree" that agrees with accepted genetics, biochemistry, immunology, endocrinology and physiology and also explains observed features of this disorder, you will have a hypothesis that can be tested.

Best regards,

Rich

 

[slayadragon]

Gerwyn and Rich, thanks so much for your comments. This is turning into a stimulating discussion.

For those who are reading this thread more casually or who are just tuning in, I thought Id try putting together a little summary of some of the topics that have been recently discussed.

I trust that if I misrepresent a viewpoint, folks will let me know.


1. Mold is not just an allergen or a pathogen. Some molds also make toxins that serve to poison people.

More than 26 years ago, Erik walked into Dr. Cheneys office stating that mold was making him sick and, no, it wasnt just a runny nose or asthma.

At the time, the only literature about mold toxicity was a few studies related to aspergillus in animal feed. Stachybotrys (black mold) wasnt even on the radar screen.


Today, even the most casual search uncovers ample literature to show easily to even the most doubtful that mold indeed has the potential of making people sick in non-allergy ways.

So thats progress.

A question I have is why it is that such literature didnt exist prior to the mid-1980s. Was it because such illness did exist but nobody noticed? Or is this a problem thats worse now than in the past?

Considering my own experience at controlling my own CFS through mold avoidance, I also would like to know whether the emergence of both Sick Building Syndrome and Chronic Fatigue Syndrome (which clearly are not the same thing) in the mid-1980s are in any way connected.

Im not saying they are connected, just that I think it would be interesting to explore whether that might be.


2. Mold is a term so broad as to be ridiculously useless.

Suggesting that mold has anything to do with my illness or anybodys illness is inherently misleading.

Just as there are lots of different kinds of bacteria (some good, some bad, some neither), there are lots of different kinds of mold.

My own interest is not related to pathogenic molds that colonize the body, nor to molds that cause only allergic responses. Although people can suffer as a result of those molds, they do not seem to me specifically related to CFS.

The molds that Im particularly focusing on are a few species of toxin producers. Stachybotrys, described earlier in this thread, is foremost.

Often when I mention Stachybotrys, people say, But sometimes Aspergillus makes toxins that are just as bad, so you cant leave that out.

Unfortunately, because mixed colonies in buildings are normal, its sometimes hard to pick out exactly what toxic species is causing a problem even if you send in samples to a laboratory.


However, an initial evaluation makes it seem that Stachy tends to be associated with CFS - in terms of the exposures that CFS sufferers have experienced, their subjective impressions of what molds do bother them, and the symptoms of the mold. 

I thus am going to try to focus on this one.


3. Dr. Shoemaker holds the belief that certain genotypes are associated with a propensity to be made ill by mold.

The genes that Dr. Shoemaker has identified actually do exist. They can be ascertained from LabCorp tests.

The question is whether Dr. Shoemaker is correct in his assessment of the correlation with mold illness.

Until such time as his work is published, the formal wording should be, the genes that Dr. Shoemaker believes to be associated with mold susceptibility and/or multi susceptibility.

If someone (hopefully not me) slips and calls them the mold susceptible gene or multi susceptible gene, perhaps others reading the thread will jump in and remind them that this is just Dr. Shoemakers contention rather than something that has been shown to be true through peer review.


4. Mold illness is not equivalent to CFS.

The effects of Sick Building Syndrome have been detailed in the literature. The effects are not the same as have been demonstrated to be present in ME/CFS (according to the Canadian Criteria). They are more similar to the Fukuda Criteria for CFS.

This, by the way, is consistent with Eriks description of what happened to him during the Incline Village epidemic. He says that when he was just being influenced by the mold, his illness was more like chronic fatigue (e.g. Fukua). It only was after getting a pathogen of some sort that it turned into classic ME/CFS.

*

I was a patient of Dr. Cheney's before the "Yuppie Flu" went through and dropped a bunch of us in our tracks.

Guess what my complaint was?

"Chronic Fatigue."

I told Dr. Cheney, "I have an inexorably increasing reactivity to mold that gets progressively worse no matter where I live or how well I take care of myself.

This is what brought me to Dr. Cheney's office in Carnelian Bay in early 1984.

So I was reactive to mold prior to CFS.

Afterwards my reactivity was absolutely life threatening.

Prior to the weird flu, my problems would have been adequately described as inexplicable fatigue, but after the "?" happened, the sensation turned into life-destroying godawful drop-dead neurological living death illness that was nothing like fatigue.

My susceptibility to mold was prior, not later as is automatically assumed, just as it was for the Truckee teachers and various other CFSers I have questioned about this phenomenon.

I thought that it was more than coincidental that this same mold that has such an effect on me showed up so often in clusters of CFS - especially the one that started it all, at my old high school, Truckee HS.

Interesting how Dr. Shoemakers "24%" HLA genotype is suggestive of the "25% ME group.

-Erik (2006)


5. Dr. Mikovits states: 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.

Im of the understanding that Gerwyn is inclined to agree with Dr. Mikovits on this statement.

As a non-virologist, Im willing to accept this as a tentative conclusion for the purposes of this discussion.

Ive not heard Rich weigh in.


6. Dr. Mikovits also states: 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.

Here she is going out of her way to state that while it could be that XMRV is both necessary and sufficient, it has not been shown to be sufficient in itself.

She thus is suggesting the possibility that something else could be necessary in order to allow the XMRV to cause CFS or other similar illnesses.

Dr. Mikovits does not speculate (at least not here) on what additional factor(s) might be necessary in order to allow XMRV to create CFS. Perhaps an additional pathogen. Perhaps some systemic problem. Perhaps even a toxin. We just dont know.

Insofar as Dr. Mikovits is leaving the door open on this point, it seems to me that no one else should be closing it for her until they have studied the virus and published their results in a peer-reviewed journal.


7. Dr. Mikovits also suggests that certain factors may serve as triggers for XMRV to become active:

> Q: If XMRV is present but inactive, are there any suggestion as to what could be a trigger for (re)-activation?

> A: Estrogens, androgens, cortisol (stress) and inflammation.

As I understand this, XMRV may flare like (say) a genital herpes infection. Insofar as those things that Dr. Mikovits mentions are present, the virus may become more problematic.

The interesting thing to me is that both cortisol and inflammation are strongly associated with exposures to certain strains of toxic mold, and in particular to Stachybotrys exposures.

When she states stress, it may mean emotional stress. But it could also mean stress to the system through any sort of event (and in particular, an inflammation-inducing event).

Its my hypothesis that one of the reasons that mold avoidance has been successful in promoting my own wellness is because doing so reduces both cortisol levels and inflammation in my system.


Lowering cortisol and inflammation is good for anybody, but it seems that if you have XMRV, its especially good.

This is what I mean by addressing the virus using a control point.

Getting the virus to be inactive is not as good as getting rid of it, but it seems to me that its still better than letting it be active.

In addition, I suspect (and someone who knows more about virology than I do can correct me if Im wrong) that a virus thats already partially under control is going to be a lot less stressful for the body to address using antivirals than one that is not under control at all.

If this is true, it would be consistent with my contention that using antivirals in conjunction with even a minimal amount of mold avoidance might be a good strategy.

I do not have any peer reviewed studies to support these hypotheses. They are based on logical analysis of the information that is available to me. Hopefully (perhaps as a result of reading our discussion) someone will decide to do a controlled double blind study and then publish the results.

I am open to other ideas of how to reduce cortisol levels and inflammation, or to safely addressing the estrogens and androgens that Dr. Mikovits mentions. Suggestions would be appreciated.


8. Different types of people tend to focus on different parts of the process of the scientific method of gathering knowledge.

According to Wikipedia, Science (from the Latin scientia, meaning "knowledge") is a systematic enterprise of gathering knowledge about the world and organizing and condensing that knowledge into testable laws and theories.[1] As knowledge has increased, some methods have proved more reliable than others, and today the scientific method is the standard for science. It includes the use of careful observation, experiment, measurement, mathematics, and replication -- to be considered a science, a body of knowledge must stand up to repeated testing by independent observers.

Until a theory gets through all the stages (from observation to experiment to measurement to mathematics to replication), it is not considered to have been shown to have validity. It is still a hypothesis.

In order to get to the end of the process, all the stages are important. This includes the first stage--careful observation.

This stage is particularly important with a new discipline that is not very well understood. In that case, researchers may use inductive reasoning to look at the cases that they find and to try to come up with plausible hypotheses to test.

In that case, neither the observations nor the hypotheses will have been shown to have validity when they are first discussed. That wont happen until they get all the way to the end--the replication stage.

The goal at this first stage is to generate ideas that can be tested, and to make a case for why they merit testing.

Generating these ideas and making this case is my goal, both in my journey down the rabbit hole of looking at the world through the no mold here lens and in my bringing this topic up on this board.

The goal of this discussion is not to prove anything to anybody. Its to share observations and think through the issues.

There is no reason for anyone to feel the need to participate if they are not interested in this part of the scientific process. We all have our own interests and contributions to make.

I certainly appreciate the thoughts of anyone who would like to join me in this discussion though.

On a related note, I have recently obtained a flurry of messages and e-mails from people who state that they have become too intimidated to post on this thread. One of them called me a brave woman for persisting in doing so myself.

I find that rather peculiar.

Having CFS requires us to have vast amounts of bravery every day, as we face the many challenges in our lives.

Posting on a message board about how we might consider trying to recover our health should not be an activity in which such bravery is required.

I thus invite everyone to post freely on this thread.

Best, Lisa

 

[Gerwyn]

Gerwyn and Rich, thanks so much for your comments. This is turning into a stimulating discussion.

For those who are reading this thread more casually or who are just tuning in, I thought I’d try putting together a little summary of some of the topics that have been recently discussed.

I trust that if I misrepresent a viewpoint, folks will let me know.


1. Mold is not just an allergen or a pathogen. Some molds also make toxins that serve to poison people.

More than 26 years ago, Erik walked into Dr. Cheney’s office stating that mold was making him sick and, no, it wasn’t just a runny nose or asthma.

At the time, the only literature about mold toxicity was a few studies related to aspergillus in animal feed. Stachybotrys (“black mold”) wasn’t even on the radar screen.


Today, even the most casual search uncovers ample literature to show easily to even the most doubtful that mold indeed has the potential of making people sick in “non-allergy” ways.

So that’s progress.

A question I have is why it is that such literature didn’t exist prior to the mid-1980s. Was it because such illness did exist but nobody noticed? Or is this a problem that’s worse now than in the past?

Considering my own experience at controlling my own CFS through mold avoidance, I also would like to know whether the emergence of both Sick Building Syndrome and Chronic Fatigue Syndrome (which clearly are not the same thing) in the mid-1980s are in any way connected.

I’m not saying they are connected, just that I think it would be interesting to explore whether that might be.


2. “Mold” is a term so broad as to be ridiculously useless.

Suggesting that “mold” has anything to do with my illness or anybody’s illness is inherently misleading.

Just as there are lots of different kinds of bacteria (some “good,” some “bad,” some neither), there are lots of different kinds of mold.

My own interest is not related to pathogenic molds that colonize the body, nor to molds that cause only allergic responses. Although people can suffer as a result of those molds, they do not seem to me specifically related to CFS.

The molds that I’m particularly focusing on are a few species of toxin producers. Stachybotrys, described earlier in this thread, is foremost.

Often when I mention Stachybotrys, people say, “But sometimes Aspergillus makes toxins that are just as bad, so you can’t leave that out.”

Unfortunately, because mixed colonies in buildings are normal, it’s sometimes hard to pick out exactly what toxic species is causing a problem even if you send in samples to a laboratory.


However, an initial evaluation makes it seem that Stachy tends to be associated with CFS - in terms of the exposures that CFS sufferers have experienced, their subjective impressions of what molds do bother them, and the symptoms of the mold. 

I thus am going to try to focus on this one.


3. Dr. Shoemaker holds the belief that certain genotypes are associated with a propensity to be made ill by mold.

The genes that Dr. Shoemaker has identified actually do exist. They can be ascertained from LabCorp tests.

The question is whether Dr. Shoemaker is correct in his assessment of the correlation with mold illness.

Until such time as his work is published, the formal wording should be, “the genes that Dr. Shoemaker believes to be associated with mold susceptibility and/or multi susceptibility.”

If someone (hopefully not me) slips and calls them the “mold susceptible gene” or “multi susceptible gene,” perhaps others reading the thread will jump in and remind them that this is just Dr. Shoemaker’s contention rather than something that has been shown to be true through peer review.


4. Mold illness is not equivalent to CFS.

The effects of Sick Building Syndrome have been detailed in the literature. The effects are not the same as have been demonstrated to be present in ME/CFS (according to the Canadian Criteria). They are more similar to the Fukuda Criteria for CFS.

This, by the way, is consistent with Erik’s description of what happened to him during the Incline Village epidemic. He says that when he was just being influenced by the mold, his illness was more like “chronic fatigue” (e.g. Fukua). It only was after getting a pathogen of some sort that it turned into classic ME/CFS.

*

I was a patient of Dr. Cheney's before the "Yuppie Flu" went through and dropped a bunch of us in our tracks.

Guess what my complaint was?

"Chronic Fatigue."

I told Dr. Cheney, "I have an inexorably increasing reactivity to mold that gets progressively worse no matter where I live or how well I take care of myself.”

This is what brought me to Dr. Cheney's office in Carnelian Bay in early 1984.

So I was reactive to mold prior to CFS.

Afterwards my reactivity was absolutely life threatening.

Prior to the weird flu, my problems would have been adequately described as inexplicable fatigue, but after the "?" happened, the sensation turned into life-destroying godawful drop-dead neurological living death illness that was nothing like fatigue.

My susceptibility to mold was prior, not later as is automatically assumed, just as it was for the Truckee teachers and various other CFSers I have questioned about this phenomenon.

I thought that it was more than coincidental that this same mold that has such an effect on me showed up so often in clusters of CFS - especially the one that started it all, at my old high school, Truckee HS.

Interesting how Dr. Shoemaker’s "24%" HLA genotype is suggestive of the "25% ME group.”

-Erik (2006)


5. Dr. Mikovits states: “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.”

I’m of the understanding that Gerwyn is inclined to agree with Dr. Mikovits on this statement.

As a non-virologist, I’m willing to accept this as a tentative conclusion for the purposes of this discussion.

I’ve not heard Rich weigh in.


6. Dr. Mikovits also states: “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.”

Here she is going out of her way to state that while it could be that XMRV is both necessary and sufficient, it has not been shown to be sufficient in itself.

She thus is suggesting the possibility that something else could be necessary in order to allow the XMRV to cause CFS or other similar illnesses.

Dr. Mikovits does not speculate (at least not here) on what additional factor(s) might be necessary in order to allow XMRV to create CFS. Perhaps an additional pathogen. Perhaps some systemic problem. Perhaps even a toxin. We just don’t know.

Insofar as Dr. Mikovits is leaving the door open on this point, it seems to me that no one else should be closing it for her until they have studied the virus and published their results in a peer-reviewed journal.


7. Dr. Mikovits also suggests that certain factors may serve as “triggers” for XMRV to become active:

> Q: If XMRV is present but inactive, are there any suggestion as to what could be a trigger for (re)-activation?

> A: Estrogens, androgens, cortisol (stress) and inflammation.

As I understand this, XMRV may flare like (say) a genital herpes infection. Insofar as those things that Dr. Mikovits mentions are present, the virus may become more problematic.

The interesting thing to me is that both cortisol and inflammation are strongly associated with exposures to certain strains of toxic mold, and in particular to Stachybotrys exposures.

When she states “stress,” it may mean “emotional stress.” But it could also mean “stress to the system” through any sort of event (and in particular, an inflammation-inducing event).

It’s my hypothesis that one of the reasons that mold avoidance has been successful in promoting my own wellness is because doing so reduces both cortisol levels and inflammation in my system.


Lowering cortisol and inflammation is good for anybody, but it seems that if you have XMRV, it’s especially good.

This is what I mean by addressing the virus using a “control point.”

Getting the virus to be inactive is not as good as getting rid of it, but it seems to me that it’s still better than letting it be active.

In addition, I suspect (and someone who knows more about virology than I do can correct me if I’m wrong) that a virus that’s already partially under control is going to be a lot less stressful for the body to address using antivirals than one that is not under control at all.

If this is true, it would be consistent with my contention that using antivirals in conjunction with even a minimal amount of mold avoidance might be a good strategy.

I do not have any peer reviewed studies to support these hypotheses. They are based on logical analysis of the information that is available to me. Hopefully (perhaps as a result of reading our discussion) someone will decide to do a controlled double blind study and then publish the results.

I am open to other ideas of how to reduce cortisol levels and inflammation, or to safely addressing the estrogens and androgens that Dr. Mikovits mentions. Suggestions would be appreciated.


8. Different types of people tend to focus on different parts of the process of the “scientific method” of gathering knowledge.

According to Wikipedia, “Science (from the Latin scientia, meaning "knowledge") is a systematic enterprise of gathering knowledge about the world and organizing and condensing that knowledge into testable laws and theories.[1] As knowledge has increased, some methods have proved more reliable than others, and today the scientific method is the standard for science. It includes the use of careful observation, experiment, measurement, mathematics, and replication -- to be considered a science, a body of knowledge must stand up to repeated testing by independent observers.”

Until a theory gets through all the stages (from observation to experiment to measurement to mathematics to replication), it is not considered to have been shown to have validity. It is still a hypothesis.

In order to get to the end of the process, all the stages are important. This includes the first stage--careful observation.

This stage is particularly important with a new discipline that is not very well understood. In that case, researchers may use “inductive reasoning” to look at the cases that they find and to try to come up with plausible hypotheses to test.

In that case, neither the observations nor the hypotheses will have been shown to have validity when they are first discussed. That won’t happen until they get all the way to the end--the replication stage.

The goal at this first stage is to generate ideas that can be tested, and to make a case for why they merit testing.

Generating these ideas and making this case is my goal, both in my journey down the “rabbit hole” of looking at the world through the “no mold here” lens and in my bringing this topic up on this board.

The goal of this discussion is not to prove anything to anybody. It’s to share observations and think through the issues.

There is no reason for anyone to feel the need to participate if they are not interested in this part of the scientific process. We all have our own interests and contributions to make.

I certainly appreciate the thoughts of anyone who would like to join me in this discussion though.

On a related note, I have recently obtained a flurry of messages and e-mails from people who state that they have become too intimidated to post on this thread. One of them called me a “brave woman” for persisting in doing so myself.

I find that rather peculiar.

Having CFS requires us to have vast amounts of bravery every day, as we face the many challenges in our lives.

Posting on a message board about how we might consider trying to recover our health should not be an activity in which such bravery is required.

I thus invite everyone to post freely on this thread.

Best, Lisa

There is no evidence that mold causes ME at all.just forthe record dr Judy said that a retrovirus alone was sufficient to cause ME.\that is the statement I agree with.Please dont try to redefine science to support your argument.it is a well known ploy and gets very tiresome.A hypothesis is based on objective measurable observations.Mold causation is pure speculation.your argument has nothing at all to do with the scientific process.Logical analysis has nothing to do with science either.The observations come first they must be objectively measurable.If you want to discuss treatments then there is a section for that purpose this is nothing to do with XMRV.people can do what they wish of course.My conversation with Rich was to do with scientific issues.Your idea of keeping a psuedogene latent is a classic example of that.

This is the section from wikepedia which is relevant

Although procedures vary from one field of inquiry to another, identifiable features distinguish scientific inquiry from other methodologies of knowledge. Scientific researchers propose hypotheses as explanations of phenomena, and design experimental studies to test these hypotheses. These steps must be repeatable in order to dependably predict any future results. Theories that encompass wider domains of inquiry may bind many independently-derived hypotheses together in a coherent, supportive structure. This in turn may help form new hypotheses or place groups of hypotheses into context.

If people don,t adhere to the scientific method then they are not scientists.A number of disciplines within the social"sciences" erroneously claim that title when they dont use the scientific method at all

Just as a final point mold is pathogenic because of the mycotoxins they produce not that they also produce toxins that poison people.Your mold sensitivity was not measured in any way so you have noway of knowing when it began or even if it exists inany objective sense.

i am quite happy to discuss science.you originally offered to provide scientific evidence regarding your claims.You are perfectly entitled to express your beliefs wherever and whenever you like.They do not however have any scientific evidence in support of them. Scientific reasoning by the way has adifferent meaning to the word as used in everyday language.A lot of people confuse that issue

 

[slayadragon]

There is no evidence that mold causes ME at all.just forthe record dr Judy said that a retrovirus alone was sufficient to cause ME.\that is the statement I agree with.Please dont try to redefine science to support your argument.it is a well known ploy and gets very tiresome.A hypothesis is based on objective measurable observations.Mold causation is pure speculation.your argument has nothing at all to do with the scientific process.Logical analysis has nothing to do with science either.The observations come first they must be objectively measurable.If you want to discuss treatments then there is a section for that purpose this is nothing to do with XMRV.people can do what they wish of course.My conversation with Rich was to do with scientific issues.Your idea of keeping a psuedogene latent is a classic example of that.

This is the section from wikepedia which is relevant

Although procedures vary from one field of inquiry to another, identifiable features distinguish scientific inquiry from other methodologies of knowledge. Scientific researchers propose hypotheses as explanations of phenomena, and design experimental studies to test these hypotheses. These steps must be repeatable in order to dependably predict any future results. Theories that encompass wider domains of inquiry may bind many independently-derived hypotheses together in a coherent, supportive structure. This in turn may help form new hypotheses or place groups of hypotheses into context.

If people don,t adhere to the scientific method then they are not scientists.A number of disciplines within the social"sciences" erroneously claim that title when they dont use the scientific method at all

Just as a final point mold is pathogenic because of the mycotoxins they produce not that they also produce toxins that poison people.Your mold sensitivity was not measured in any way so you have noway of knowing when it began or even if it exists inany objective sense.

i am quite happy to discuss science.you originally offered to provide scientific evidence regarding your claims.You are perfectly entitled to express your beliefs wherever and whenever you like.They do not however have any scientific evidence in support of them. Scientific reasoning by the way has adifferent meaning to the word as used in everyday language.A lot of people confuse that issue

Hi Gerwyn,

The Wikipedia quote that you mention states the following: "Scientific researchers propose hypotheses as explanations of phenomena, and design experimental studies to test these hypotheses."

I am doing the first part: proposing hypotheses as explanations of phenomena. I am doing this specifically because my goal is to get researchers to test those hypotheses through the use of the scientific method, not because I want people to believe what I am saying based on the observations of the phenomena and the hypotheses themselves.

As the two Wikipedia quotes state, the careful observations of phenomena that have not yet been scientifically proved/disproved and the creation of hypotheses that can be proved/disproved via experiments are part of the scientific method. They are not the entire process of the scientific method. All I have to offer is my observations of what I have seen, and my layman's attempts to tie it to other work that has been done in this field. I am offering this knowledge freely and openly, to all who choose to consider it. What they do with it is up to them.

Hopefully it will lead to scientific studies of the sort that you mention. If that comes about, then it will feel like everything that has happened to me so far - getting sick with CFS to begin with and then this journey down the rabbit hole of mold avoidance - will have been worth something.

At no time have I used the word "cause" with regard to the relationship between mold and CFS.

The quotes that I mentioned offer evidence that Dr. Mikovits believes that certain factors can cause XMRV to become latent or to flare, and that she is leaving the door open to XMRV being necessary but not sufficient for XMRV to lead to CFS. Until I am provided with evidence that, in her scientific view, this is not the case, or until someone else provides me with scientific evidence to the contrary, I personally am inclined to give tentative acceptance to what she has said.

Others are welcome to make their own conclusions, of course.

Thanks much for all your comments on this thread so far. They actually been really helpful in my attempts to think through the topic.

Best, Lisa

 

[Gerwyn]

MOLDS the science

Molds (also spelled "moulds") are ubiquitous in the biosphere, and mold spores are a common component of household and workplace dust. However, when mold spores are present in unspecified quantities, they can present a health hazard to humans, potentially causing allergic reactions and when present in large quantities, other types of respiratory problems. Mold allergies have always been a serious problem for many people. Research in the field of environmental health has yielded tests such as the MELISA assay, which can identify whether a person is allergic to specific epitopes associated with any particular mold.

A common mycotoxin known to the general population of most western societies is penicillin. Extreme exposure to very high levels of mycotoxins can lead to neurological problems and in some cases death; fortunately, such exposures rarely to never occur in normal exposure scenarios, even in residences with serious mold problems.

Trichothecenes are a very large family of chemically related mycotoxins produced by various species of Fusarium, Myrothecium, Trichoderma, Trichothecium, Cephalosporium, Verticimonosporium, and Stachybotrys.

Trichothecenes are powerful inhibitors of protein synthesis. They do this by reacting with components of the ribosomes: the structure within the cell where proteins are made. The specific site of action of T-2 toxin, which is a reaction with a critical site on the ribosomal RNA (rRNA) is known. Protein synthesis is an essential function in all tissues, but tissues where cells are actively and rapidly growing and dividing are very susceptible to the toxins.[3] Trichothecenes are different from most other potential weapons toxins because they can act through the skin.


satratoxin-H, a trichothecene mycotoxin, is a naturally occurring mold byproduct of Stachybotrys chartarum which is toxic to humans and animals. The clinical condition it causes is known as Stachybotrotoxicosis. It is related to the mycotoxin T-2, but unlike T-2 has not been reported to have been used as a biological weapon.

all molds may produce mycotoxins and thus all molds may be potentially toxic if large enough quantities are ingested, or the human becomes exposed to extreme quantities of mold. Mycotoxins are not produced all the time, but only under specific growing conditions. Mycotoxins are harmful or lethal to humans and animals only when exposure is high enough. Some of the most deadly chemicals on the planet are similarly harmless at the concentrations normally encountered in ambient air.

Originally, toxic effects from mold were thought to be the result of exposure to the mycotoxins of some mold species, such as Stachybotrys chartarum. However, studies are suggesting that the so-called toxic effects are actually the result of chronic activation of the immune system, leading to chronic inflammation.[citation needed] Studies indicate that up to 25% of the population have the genetic capability of experiencing chronic inflammation to mold exposure, but only 2% actually experience such symptoms. A 199394 case study based on cases of pulmonary hemorrhage in infants in Cleveland, Ohio originally concluded there was causal relationship between the exposure and the disease. The investigators revisited the cases and established that there was no link to the exposure to S. chartrum and the infants in their homes.


Satratoxin-H, a trichothecene mycotoxin, is a naturally occurring mold byproduct of Stachybotrys chartarum which is toxic to humans and animals. The clinical condition it causes is known as Stachybotrotoxicosis. It is related to the mycotoxin T-2, but unlike T-2 has not been reported to have been used as a biological weapon.

The presence of black mold can be detected using a simple blood test and can be cleared using a simple antifungal antibiotic.If someone feels that they are having a health problem due to mold exposure.A blood test will confirm it and an antibiotic will clear it

 

[Gerwyn]

Hi Gerwyn,

The Wikipedia quote that you mention states the following: "Scientific researchers propose hypotheses as explanations of phenomena, and design experimental studies to test these hypotheses."

I am doing the first part: proposing hypotheses as explanations of phenomena. I am doing this specifically because my goal is to get researchers to test those hypotheses through the use of the scientific method, not because I want people to believe what I am saying based on the observations of the phenomena and the hypotheses themselves.

As the two Wikipedia quotes state, the careful observations of phenomena that have not yet been scientifically proved/disproved and the creation of hypotheses that can be proved/disproved via experiments are part of the scientific method. They are not the entire process of the scientific method. All I have to offer is my observations of what I have seen, and my layman's attempts to tie it to other work that has been done in this field. I am offering this knowledge freely and openly, to all who choose to consider it. What they do with it is up to them.

Hopefully it will lead to scientific studies of the sort that you mention. If that comes about, then it will feel like everything that has happened to me so far - getting sick with CFS to begin with and then this journey down the rabbit hole of mold avoidance - will have been worth something.

At no time have I used the word "cause" with regard to the relationship between mold and CFS.

The quotes that I mentioned offer evidence that Dr. Mikovits believes that certain factors can cause XMRV to become latent or to flare, and that she is leaving the door open to XMRV being necessary but not sufficient for XMRV to lead to CFS. Until I am provided with evidence that, in her scientific view, this is not the case, or until someone else provides me with scientific evidence to the contrary, I personally am inclined to give tentative acceptance to what she has said.

Others are welcome to make their own conclusions, of course.

Thanks much for all your comments on this thread so far. They actually been really helpful in my attempts to think through the topic.

I am doing the first part: proposing hypotheses as explanations of phenomena. I am doing this specifically because my goal is to get researchers to test those hypotheses through the use of the scientific method, not because I want people to believe what I am saying based on the observations of the phenomena and the hypotheses themselves.

what you are actually doing Lisa is basing an idea based on your assumption of what your experience means.Phenomena in science have a specific meaning.Subjective interpretation is not a phenomenon.you are assuming that mold exposure is the cause of your problem without testing that assumption.You are then developing a theory based on an assumption and not an observation.A retrovirologist like Dr M knows precisely the conditions which make a latent virus activate.

The quotes that I mentioned offer evidence that Dr. Mikovits believes that certain factors can cause XMRV to become latent or to flare, and that she is leaving the door open to XMRV being necessary but not sufficient for XMRV to lead to CFS. Until I am provided with evidence that, in her scientific view, this is not the case, or until someone else provides me with scientific evidence to the contrary, I personally am inclined to give tentative acceptance to what she has said.

Quotes are not evidence Lisa.You have once again made assumptions about her meaning which suits your preconceived ideas.She clearly said that retroviruses are able to produce the symptoms of ME unaided. You are happy to accept the quotes you agree with but want scientific evidence to change your mind when someone else gives a different interpretation of what she said! Interpretations are not fact scientific hypotheses are constructed on the basis of observed facts




Best, Lisa

No you are basing an idea on what you assume

 

[slayadragon]

Hi Gerwyn,

I don't know where you got this article, but it's important to point out a couple of things.

There are blood tests to determine the presence of Stachy toxin in the system, but their accuracy has been disputed.

More importantly, unlike Aspergillus, Stachybotrys does not live in the body. The negative effects on people are a result of the toxic chemicals that are inhaled or that are otherwise taken into the system, not a result of colonization.

Unfortunately, antifungals, antivirals or antibiotics will have no direct effect on any toxic chemicals already in the system. (I personally am interested in the idea that eliminating pathogens in the body will increase its overall health and thus its ability to deal effectively with toxic exposures, but there is as of yet to my knowledge no scientific evidence to support this concept.)

In some cases, the presence of mold toxicity causes immune system problems that make candida more likely to flourish. If that is the case, antifungal drugs may provide some health benefits. But these have nothing to do with addressing the Stachybotrys problem.

The studies regarding the Cleveland problem and the dose of the toxin required to create illness are generally not thought to be substantive enough to be held to be conclusive scientific "truth." For example, different Stachybotrys strains make different types of toxins, and molds vary in the amounts of toxins they make depending on factors such as competition with other molds in the environment. It thus is possible that in some circumstances, people are getting much more exposure to particularly problematic toxins than some researchers have assumed. In addition, some studies have shown that different mold toxins exercise a synergistic effect, meaning that two or more working together are much more damaging than single ones alone. It thus would be necessary to do lab experiments involving combinations of toxins (plus other "Sick Building Syndrome" components such as the presence of bacteria or various chemicals) to ascertain precisely how much damage may be taking place. The studies also do not take into consideration what the cumulative effects of a toxin might be if an individual were exposed to it on a continuous basis over many years, as occurs with people who have toxic mold in their homes.

As is the point of this thread, the simultaneous presence in the system of whatever sort of pathogen also could lead to a synergistic effect that would increase the damage done by a particular type of toxin.

The "chronic inflammation" mentioned as the method by which Stachy exercises its toxic effects is one reason that it has relevance to this discussion of "control points," since (as Dr. Mikovits states) inflammation is thought to have the potential of activating or re-activating XMRV.

The studies citing the 25% genetic susceptibility are consistent with Dr. Shoemaker's statements of 24% having what he calls the "mold susceptible genotype" or "multi susceptible genotype." I don't know if the studies mentioned in that article are his or someone else's.

I'm not sure what the comment that "only 2% actually experience such symptoms" means. If this means that 25% have the potential to get sick from mold, but only 2% do because the rest do not get enough mold exposure to be made sick by it, I accept that this may indeed be the case. Encouraging people to look into whether their homes are really moldy and to take care of any mold problems (not just for their own sake but for the sake of others living in the home) in order to prevent illness from occurring is one of my goals in discussing this topic in public.

The rest of the article looks good to me. Thanks much for posting it on the board.

Best, Lisa

 

[Gerwyn]

Hi Gerwyn,

I don't know where you got this article, but it's important to point out a couple of things.

There are blood tests to determine the presence of Stachy toxin in the system, but their accuracy has been disputed.

there is no scientific dispute about their accuracy at al

More importantly, unlike Aspergillus, Stachybotrys does not live in the body. The negative effects on people are a result of the toxic chemicals that are inhaled or that are otherwise taken into the system, not a result of colonization.

no the toxic chemicals are released by the spores after inhalation Exposure to the mycotoxins present in Stachybotrys chartarum or Stachybotrys atra can have a wide range of effects. Depending on the length of exposure and volume of spores inhaled or ingested, (wikepedia)

Unfortunately, antifungals, antivirals or antibiotics will have no direct effect on any toxic chemicals already in the system. (I personally am interested in the idea that eliminating pathogens in the body will increase its overall health and thus its ability to deal effectively with toxic exposures, but there is as of yet to my knowledge no scientific evidence to support this concept.)

Antifungal antibiotics are mycotoxins and will clear the source of production so unfortunately you are wrong

In some cases, the presence of mold toxicity causes immune system problems that make candida more likely to flourish. If that is the case, antifungal drugs may provide some health benefits. But these have nothing to do with addressing the Stachybotrys problem.

Antifungal drugs also treat stachybotyris--any mycology text book will tell you that

The studies regarding the Cleveland problem and the dose of the toxin required to create illness are generally not thought to be substantive enough to be held to be conclusive scientific "truth."

It was enough objective truth for the scientist who reviewed the paper.generally not thoght to be conclusive for who exactly?

For example, different Stachybotrys strains make different types of toxins, and molds vary in the amounts of toxins they make depending on factors such as competition with other molds in the environment.

No the chemical formula for the toxin is the same.The rest is also incorrect


In addition, some studies have shown that different mold toxins exercise a synergistic effect, meaning that two or more working together are much more damaging than single ones alone.

NOT in VIVO they haven,t


It thus would be necessary to do lab experiments involving combinations of toxins (plus other "Sick Building Syndrome" components such as the presence of bacteria or various chemicals) to ascertain precisely how much damage may be taking place. The studies also do not take into consideration what the cumulative effects of a toxin might be if an individual were exposed to it on a continuous basis over many years, as occurs with people who have toxic mold in their homes.

they dont have to take into consideration what might be just what has been observed



As is the point of this thread, the simultaneous presence in the system of whatever sort of pathogen also could lead to a synergistic effect that would increase the damage done by a particular type of toxin.

Never been observed what do you mean by synergistic

The "chronic inflammation" mentioned as the method by which Stachy exercises its toxic effects is one reason that it has relevance to this discussion of "control points," since (as Dr. Mikovits states) inflammation is thought to have the potential of activating or re-activating XMRV.

No the study clearly showed that the chronic inflammation was nothing to do with the mold

The studies citing the 25% genetic susceptibility are consistent with Dr. Shoemaker's statements of 24% having what he calls the "mold susceptible genotype" or "multi susceptible genotype." I don't know if the studies mentioned in that article are his or someone else's.

I'm not sure what the comment that "only 2% actually experience such symptoms" means. If this means that 25% have the potential to get sick from mold, but only 2% do because the rest do not get enough mold exposure to be made sick by it, I accept that this may indeed be the case. Encouraging people to look into whether their homes are really moldy and to take care of any mold problems (not just for their own sake but for the sake of others living in the home) in order to prevent illness from occurring is one of my goals in discussing this topic in public.

What the study means is that of 25% ofpeople have theoretical susceptibility to mold infection.When such people are actually exposed to mold only 2% actually get symptoms.The theory of gene susceptibility is disproved


It wasn,t an article by the way

 

[Dreambirdie]

Hi Lisa--

I have a few questions for you.

Is there a place to have mold tested, and how much does it cost?
I have some growing around the window ledge in my computer room and I really want to check it out.

Also, are there special instructions on how to treat and remove moldy wood, that you can recommend?

thanks

 

[slayadragon]

Hi Gerwyn,

A couple of comments.

Dormant stachybotrys spores are released from the colony into the air. Most of these immediately sink the ground, where they almost immediately fragment and turn into poison "dust." This dust is just as poisonous as the intact spores. Recent research makes it clear the the spores or spore fragments do not have to be inhaled in order to cause damage; the poison gases released from the spores is sufficient. (Erik has been saying this for more than a decade, based on his own experiments with the molds, btw.)

Conceivably, an intact spore could land in the body and turn into live mold. It is extremely rare to have Stachybotrys growing in the body, however. Aspergillus infections occur much more frequently, but these are mostly in people whose immune systems are already problematic.

(The idea that molds like Stachybotrys damage the immune system, allowing molds like Aspergillus to colonize, in Sick Building Syndrome environments is one that is worthy of scientific testing, in my view.)

Stachbotrys produces a wide variety of mycotoxins, all of which have different effects. Here's an article:

“Mycotoxins and Other Biologically Active Metabolites,” from Eckhardt Johanning and Chin Yang’s book on bioaerosols.

The mycotoxins and other biologically active compounds produced by S. chartarum are of concern to human health (23,32,33,57). Mycotoxin poisoning by this fungus is referred to as stachybotryotoxicosis.

S. chartarum produces a variety of macrocylic trichothecenes and related trichoverroids: roridin E and L-2; satratoxins F, G, and H; isosatratoxins F, G, and H; verrucarins B and J; and the trichoverroids, trichoverrols A and B and trichoverrins A and B. The satratoxins are generally produced in greater amounts than the other trichothecenes, but all compounds are produced in low quantities. They apparently occur in all parts of the fungus (53). The difficulty in obtaining, identifying, and purifying these toxins has slowed extensive studies on their biological activity. Hinkley and Jarvis (23) recently published analytical methods for the identification and quantification of bioactive compounds produced by this fungus. These methods were designed to quantitate individual compounds in culture extracts and detect low levels of trichothecenes in samples.

Macrocyclic trichothecenes are highly toxic compounds with a potent ability to inhibit protein synthesis (32). Numerous studies have demonstrated the toxicity of toxins from S. chartarum on animals and animal and human cells (42,45,49,51). Yang et al. (62) reported that satratoxin G was the most cytotoxic of eight trichothecenes tested on mammalian cells, even more toxic than the well known T-2 toxin associated with alimentary toxic aleukia. Other researchers have also reported the high toxicity of satratoxins compared to other trichothecenes (18). The LD50 in mice for satratoxins is ~1 mg/kg (32).

In addition, the fungus produces nine phenylspirodrimanes (spirolactones and spirolactams) and cyclosporin, which are potent immunosuppressive agents (33). Jarvis et al. (33) suggested that the combination of trichothecenes and these immunosuppressive agents may be responsible for the observed high toxicity of this fungus. New biologically active compounds are still being discovered in cultures of S. chartarum. Hinkley et al. (24,25) recently described the metabolites atranones A-G and two dolabellane diterpenes, but the complete biological activity of these compounds is unknown. Vesper and colleagues (57,59,60) reported some isolates produce Stachylysin, a hemolysin (compounds that lyse erythrocytes), and a hydroxamate siderophore. They suggest these compounds could be pathogenicity factors involved in pulmonary hemorrhage in infants exposed to S. chartarum.

There is considerable variation among isolates of S. chartarum in the production of mycotoxins and other metabolites (2,24,27,34,40). Indeed, Hinkley et al. (25) suggest there are two chemotypes of the fungus: the atranone and the macrocyclic trichothecene producers.

http://www.apsnet.org/online/feature/Stachybotrys/


Unfortunately, I can't respond to the rest of your comments without the cites.

Best, Lisa

 

[slayadragon]

Hi Dreambirdie,

Your post reminded me that there are some comments earlier in the thread that i need to address.

Sorry about that!

I will do that soon.

Best, Lisa

 

[Gerwyn]

Test Name
Sample Type(s) Description Uses Time for Results
Susceptibility testing
Sample of fungus isolated in culture Follow-up to fungal culture. When a pathogenic fungus has been identified, susceptibility is sometimes ordered to determine the most effective antifungal agent(s) to use. Guide treatment Days to weeks after culture
Antigen testing
Blood, CSF, body fluids Detects proteins associated with a specific fungus. This type of test available for a variety of fungi. Diagnose infection by specific fungus Day(s)
Antibody testing
Blood, CSF, body fluids Detects immune response to a specific fungus. May be ordered as a single sample or as acute and convalescent samples collected 2 to 3 weeks apart. Diagnose current or recent infection by specific fungus; monitor treatment Day(s) or Weeks
Molecular tests for DNA, RNA Sample of fungus isolated in culture, blood, CSF, body fluids Detects genetic material of a specific fungus. Detects some fungi; not yet widely available, some in research settings only Days to weeks

If fungal elements are identified in a KOH prep or Calcofluor white stain, then a fungus is present in the sample and may be causing the symptoms a patient is experiencing or be present as a harmless colonizer of the skin. The presence of multiple organisms in a fungal culture may indicate multiple pathogens or a mixture of pathogens and normal flora. If there is only normal flora present in the culture, then the infection may be due to an opportunistic fungus (part of the normal flora), the pathogen may have been missed in the sample, or the condition may be due to another cause.

If an antigen test is positive, then it is likely that the fungus identified is the cause of the person’s infection. A positive antibody test result in a single serum sample may indicate exposure to a specific fungus, but it does not indicate when the exposure occurred. Rising levels of antibodies in two serum samples, measured as acute and convalescent tests, can indicate an active or recent fungal infection. Some infected patients with compromised immune systems may have lower than expected antibody levels.

 

[Gerwyn]

Hi Gerwyn,

A couple of comments.

Dormant stachybotrys spores are released from the colony into the air. Most of these immediately sink the ground, where they almost immediately fragment and turn into poison "dust." This dust is just as poisonous as the intact spores. Recent research makes it clear the the spores or spore fragments do not have to be inhaled in order to cause damage; the poison gases released from the spores is sufficient. (Erik has been saying this for more than a decade, based on his own experiments with the molds, btw.)

Conceivably, an intact spore could land in the body and turn into live mold. It is extremely rare to have Stachybotrys growing in the body, however. Aspergillus infections occur much more frequently, but these are mostly in people whose immune systems are already problematic.

(The idea that molds like Stachybotrys damage the immune system, allowing molds like Aspergillus to colonize, in Sick Building Syndrome environments is one that is worthy of scientific testing, in my view.)

Stachbotrys produces a wide variety of mycotoxins, all of which have different effects. Here's an article:

“Mycotoxins and Other Biologically Active Metabolites,” from Eckhardt Johanning and Chin Yang’s book on bioaerosols.

The mycotoxins and other biologically active compounds produced by S. chartarum are of concern to human health (23,32,33,57). Mycotoxin poisoning by this fungus is referred to as stachybotryotoxicosis.

S. chartarum produces a variety of macrocylic trichothecenes and related trichoverroids: roridin E and L-2; satratoxins F, G, and H; isosatratoxins F, G, and H; verrucarins B and J; and the trichoverroids, trichoverrols A and B and trichoverrins A and B. The satratoxins are generally produced in greater amounts than the other trichothecenes, but all compounds are produced in low quantities. They apparently occur in all parts of the fungus (53). The difficulty in obtaining, identifying, and purifying these toxins has slowed extensive studies on their biological activity. Hinkley and Jarvis (23) recently published analytical methods for the identification and quantification of bioactive compounds produced by this fungus. These methods were designed to quantitate individual compounds in culture extracts and detect low levels of trichothecenes in samples.

Macrocyclic trichothecenes are highly toxic compounds with a potent ability to inhibit protein synthesis (32). Numerous studies have demonstrated the toxicity of toxins from S. chartarum on animals and animal and human cells (42,45,49,51). Yang et al. (62) reported that satratoxin G was the most cytotoxic of eight trichothecenes tested on mammalian cells, even more toxic than the well known T-2 toxin associated with alimentary toxic aleukia. Other researchers have also reported the high toxicity of satratoxins compared to other trichothecenes (18). The LD50 in mice for satratoxins is ~1 mg/kg (32).

In addition, the fungus produces nine phenylspirodrimanes (spirolactones and spirolactams) and cyclosporin, which are potent immunosuppressive agents (33). Jarvis et al. (33) suggested that the combination of trichothecenes and these immunosuppressive agents may be responsible for the observed high toxicity of this fungus. New biologically active compounds are still being discovered in cultures of S. chartarum. Hinkley et al. (24,25) recently described the metabolites atranones A-G and two dolabellane diterpenes, but the complete biological activity of these compounds is unknown. Vesper and colleagues (57,59,60) reported some isolates produce Stachylysin, a hemolysin (compounds that lyse erythrocytes), and a hydroxamate siderophore. They suggest these compounds could be pathogenicity factors involved in pulmonary hemorrhage in infants exposed to S. chartarum.

There is considerable variation among isolates of S. chartarum in the production of mycotoxins and other metabolites (2,24,27,34,40). Indeed, Hinkley et al. (25) suggest there are two chemotypes of the fungus: the atranone and the macrocyclic trichothecene producers.

http://www.apsnet.org/online/feature/Stachybotrys/


Unfortunately, I can't respond to the rest of your comments without the cites.

Best, Lisa

yet again a book ok

The mycotoxins and other biologically active compounds produced by S. chartarum are of concern to human health (23,32,33,57). Mycotoxin poisoning by this fungus is referred to as stachybotryotoxicosis.

would you like to tell me what the symptoms are.? Then tell me how this would not be immediately apparent?

This is from the same article

The spores are therefore not readily disseminated in the air compared to other fungi such as Aspergillus. However, when the fungus and substrate dries and is disturbed by mechanical means or air movement, conidia can become bioaerosols.

there is no evidence whatsoever of toxic dust

no mention of the spores falling to the floor

The idea that molds like Stachybotrys damage the immune system,

An idea is not a hypothesis there is no evidence to support it as the author concedes

your initial point was that different species produced different toxins.They do not

this is also from the same article

There is considerable controversy, however, about the role of S. chartarum in pulmonary hemorrhage in the Cleveland incident and in human health in the indoor environment (15,16,19,30,36,50,54). Some members of the scientific-medical community believe there is insufficient evidence to prove a solid causal relationship between S. chartarum and these health problems. Indeed, in 2000 the Centers for Disease Control and Prevention in Atlanta (3) published two reports critical of the study conducted in Cleveland and concluded that the association between S. chartarum and acute pulmonary hemorrhage/hemosiderosis was not proven.

The specific site of action of T-2 toxin, which is a reaction with a critical site on the ribosomal RNA (rRNA) is known

Is there evidence of any such abnormality in patients with ME or any evidence of inhibited protein synthesis?