Detection of Mycotoxins in Patients with CFS

[Ifish]

soulfeast,
I have not discussed this with him specifically, so the correct answer is to say, "I don't know". But I can say that it has now been two years since my family first did the mycotoxin tests and at no time along the way did he ever suggest we do the HLA typing. As I have indicated before, Brewer's cfs patients almost uniformly test positive for mycotoxins, therefore all patients excrete mycotoxins, so these patients are all detoxing. At our last meeting I did ask about detox and he indicated that some patients might detox mycotoxins faster than others, but they will all get the job done if we can stop the input of myctoxins into the body.
I was a patients of Dr. Shoemaker about 15 years ago and I was told I had the worst possible HLA type. Of course, my genetics have not changed, yet many years later I was excreting massive amounts of mycotoxins. (I was the record holder among Brewer's patients for the highest trichothecene level, but perhaps it has now been broken). So if mycotoxin testing is valid this would seem to be an absolute repudiation of the idea the HLA typing has any validity at all. I have read that Shoemaker takes the position that urine mycotoxin testing is not valid, but I have not seen an explanation as to why. Indeed, this really seems to paint him in a corner. To admit the test is valid would amount to an admission that the cornerstone of his whole mold theory has been wrong this whole time.

Ifish, do you know what Brewer thinks of Shoemaker's HLA typing? I am curious especially because my husband has a multisuseptable 11-12-53b and is fine. He is sure he has had many exposures with moldy homes in the past. He also has lyme and did not "herx" while on a year of abx. I have my mother's multisuseptable 4-3-53 and was in what would be considered a level 5 sick building (her home with over 20,000 spore count.. not sure what was in there) and mold behind half the walls and all plumbing (very very bad builder-this was a new home and 3 years old when remediated). She seems fine, though has chronic pain issues. I am sure she has been exposed many times over her 74 year life time. Makes me question. I don't know how Shoemaker came to this conclusion.. the science behind it.

 

[acer2000]

Is it that shoemaker thinks that mycotoxin testing in the urine is invalid in that its inaccurate or is it just that he prefers his testing more because he feels it accurately predicts response to treatment by looking at the actual inflammation that may or may not be caused by the mycotoxin exposure?

 

[Ifish]

lfish, can I ask how you're doing now with Dr. Brewer's protocol? Are you being exposed to mold at all or are you in a mold-free environment? My son and I started the protocol a week ago and we both feel pretty crappy, but I'm curious when people start feeling better. It doesn't seem like there are many of us doing this protocol yet, so it's hard to compare notes. Oddly enough, I felt really good the first day I was on the nasal sprays but went downhill from there... Hope you're doing better.

gailw,
I received our ERMI results and I thought I should clarify my previous answer.
Our original ERMI was done in March, 2012. This is a test developed by the EPA. It is explained at their website http://www.epa.gov/microbes/moldtech.htm The scale ranges from -10 to 20. Our score was 8.61 and showed the presence of some of the worst molds, including stochybotrys. I believe Shoemaker wants all his patients to live in an environment that is 2.0 or below. After many, many consultations, months of research and a failed remediation attempt I hired a company that does an elaborate remediation that centers around the use of an enzyme based product called TM-100. It was expensive, but a better alternative than selling our house and attempting extreme mold avoidance.

A subsequent ERMI in February 2013 showed a score of -3.5.

Our repeat follow up ERMI in April 2014 showed a further drop to -6.7. There are no traces of stochybotrys. The only thing we have done since the remediation is to continually keep our humidity below 45% with a dehumidifier. So it appears the remediation has had a continuing effect. Given that some bad molds are present in outdoor air and will inevitably blow into a home it would seem this result is as good as it gets.

 

[Ifish]

Is it that shoemaker thinks that mycotoxin testing in the urine is invalid in that its inaccurate or is it just that he prefers his testing more because he feels it accurately predicts response to treatment by looking at the actual inflammation that may or may not be caused by the mycotoxin exposure?

I have not seen anything written by Shoemaker online. I have been advised that he has addressed this in one of his books, available for purchase:

"86. Urinary testing for mycotoxins
What does a measurement of urinary levels of mycotoxins tell me?

I do not use mycotoxin testing. I am aware of a recent paper published by Dr. Brewer
suggesting presence of mycotoxins in the urine in people with Chronic Fatigue
Syndrome. I am aware of several labs selling urinary tests and blood tests for
mycotoxins. The far greater injury from mycotoxins is from activators of innate immune response. This is an evolving field in diagnosis. Some physicians find the tests useful. I await careful clinical confirmation. See the CSM video for more information."
source: Surviving Mold FAQ Vol. 2 question 86

 

[acer2000]

I have not seen anything written by Shoemaker online. I have been advised that he has addressed this in one of his books, available for purchase:

"86. Urinary testing for mycotoxins
What does a measurement of urinary levels of mycotoxins tell me?

I do not use mycotoxin testing. I am aware of a recent paper published by Dr. Brewer
suggesting presence of mycotoxins in the urine in people with Chronic Fatigue
Syndrome. I am aware of several labs selling urinary tests and blood tests for
mycotoxins. The far greater injury from mycotoxins is from activators of innate immune response. This is an evolving field in diagnosis. Some physicians find the tests useful. I await careful clinical confirmation. See the CSM video for more information."
source: Surviving Mold FAQ Vol. 2 question 86

Yeah pretty much as I thought. Also, if you look at the big picture that Shoemaker is looking at, the urine tests only test for a small and specific subset of known mycotoxins. So it is conceivable that you could test negative on the urine test but still have the problem he's looking for, I suppose.

 

[Forebearance]

Do you suppose that a person's genetics may tell us more about how inflamed they will get from mycotoxins in the body, rather than how quickly they may be able to detox them? I guess time and more data will help sort these questions out.

 

[soulfeast]

The claim has consistantly been that certain HLA types don't produce antibodies (some say enzymes) to tag mycotoxins thus they are reabsorbed. How accurate this claim is, I don't know. It's confounded me for a few years now. If the RTL and other mycotoxin urine tests are accurate, then I think Ifish is saying that Shoemaker's theory that certain HLA don't detox (if that's the theory) or don't detox well enough may not hold up to all those positive test results that Brewer is getting.. these people are detoxing. I have not read Shoemaker linking HLA type strictly to immune response to mycos rather to immune response to "stuck" undetoxed mycos. Maybe we all have been reading Shoemaker wrong? Or that's what he's been saying.

 

[soulfeast]

Another possibility: I know of some doctors specializing in mold/mycotoxin illness who are warning people not to use glutathione without a binder (like CSM, charcoal, clay) because mycos will be released and some excreted in urine but some (much? most?) will be reabsorbed in the intestines due to this inability to tag and destroy?? So ends up being a state of constant retox. I have never gotten the specifics with the HLA can't detox theory and am really growing weary of taking info on faith. Esp given I have relatives with "dreaded" HLA types who were exposed with me or in situations seemingly worse and also seemingly fine.

 

[Ifish]

The claim has consistantly been that certain HLA types don't produce antibodies (some say enzymes) to tag mycotoxins thus they are reabsorbed. How accurate this claim is, I don't know. It's confounded me for a few years now. If the RTL and other mycotoxin urine tests are accurate, then I think Ifish is saying that Shoemaker's theory that certain HLA don't detox (if that's the theory) or don't detox well enough may not hold up to all those positive test results that Brewer is getting.. these people are detoxing. I have not read Shoemaker linking HLA type strictly to immune response to mycos rather to immune response to "stuck" undetoxed mycos. Maybe we all have been reading Shoemaker wrong? Or that's what he's been saying.

The good thing here is that at least some of this may be answered in the upcomming months. If Brewer has a high level of success by treating nasal fungi without the aid of binders it will point increasingly away from Shoemaker's way of thinking and increasingly toward a more successful approach. I have the advantage of knowing Brewer over many years. The fact that he has already had a significant number of patients get well or nearly well resonates with me in a way that I can't expect with other people. I have discussed research and treatment options with him many many times. Everything from HHV-6, to XMRV, to mitrochondrial disfunction. He has never overstated anything in the past.

 

[acer2000]

I'm curious. What can throw the RTL test? Many foods contain trace levels of mold/mycotoxins. Several popular enzyme preparations (i.e. Beano) also contain them. If one were to do this test, are there things that should be avoided and for how long?

 

[cigana]

I have not read Shoemaker linking HLA type strictly to immune response to mycos rather to immune response to "stuck" undetoxed mycos..

Hi Soulfeast, could you explain this a little more, I don't get what you are saying...are you saying there's a different immune response to "stuck mycos" than there is to standard "mycos"?

 

[cigana]

The good thing here is that at least some of this may be answered in the upcomming months. If Brewer has a high level of success by treating nasal fungi without the aid of binders it will point increasingly away from Shoemaker's way of thinking and increasingly toward a more successful approach. I have the advantage of knowing Brewer over many years. The fact that he has already had a significant number of patients get well or nearly well resonates with me in a way that I can't expect with other people. I have discussed research and treatment options with him many many times. Everything from HHV-6, to XMRV, to mitrochondrial disfunction. He has never overstated anything in the past.

Hi lfish, thankyou for posting all of your experiences and thoughts, I find it very interesting.
One thing at the back of my mind though...how is Brewer's view consistent with the very positive results seen by people doing extreme avoidance? In theory, if the fungus is internal, avoidance would not help. Unless, of course, the situation is more complicated, and it is the interaction between something in the air (a pollutant say) and the mycotoxins that actually causes the illness.

 

[N.A.Wright]

I'm curious. What can throw the RTL test? Many foods contain trace levels of mold/mycotoxins. Several popular enzyme preparations (i.e. Beano) also contain them. If one were to do this test, are there things that should be avoided and for how long?

A point I made much earlier in this thread: http://forums.phoenixrising.me/inde...n-patients-with-cfs.22743/page-10#post-447761 Excluding all exterior sources of mycotoxin is a Sisyphaen task, and with such tiny amounts credited as clinically significant (just 4% of what is considered safe as part of human food) and with animal studies* showing that a third of daily ingested aflotoxin is excreted in urine, it seems impossible to know whether what is measured in human urine could have come from an endemic source or from inhaled and ingested sources.

* http://pub.epsilon.slu.se/1886/1/Thieu_Thesis.pdf

 

[cigana]

A point I made much earlier in this thread: http://forums.phoenixrising.me/inde...n-patients-with-cfs.22743/page-10#post-447761 Excluding all exterior sources of mycotoxin is a Sisyphaen task, and with such tiny amounts credited as clinically significant (just 4% of what is considered safe as part of human food) and with animal studies* showing that a third of daily ingested aflotoxin is excreted in urine, it seems impossible to know whether what is measured in human urine could have come from an endemic source or from inhaled and ingested sources.

* http://pub.epsilon.slu.se/1886/1/Thieu_Thesis.pdf

But isn't it the case that the controls that were used to establish the reference range would also be eating a similar diet (on average), meaning that those that excrete more are more likely to either (a) be exposed to mycotoxins other than those in their food, or (b) somehow be more efficient at excretion?

 

[Ifish]

But isn't it the case that the controls that were used to establish the reference range would also be eating a similar diet (on average), meaning that those that excrete more are more likely to either (a) be exposed to mycotoxins other than those in their food, or (b) somehow be more efficient at excretion?

I would also argue:
1. A thesis paper written about pig feed does not establish an international standard for human mycotoxin consumption.
2. Ingested mycotoxins are likely absorbed differently than inhaled myctoxins.
3. Only some mycotoxins can be tested.
4. Mycotoxins represent only a part of the substances causing illness in mold exposed patients.
5. The volume of mycotoxins being excreted would naturally be far greater than the amount shown in a single urine sample. Myoctoxins are also excreted in stool and, of course, people urinate multiple times per day.
6. Brewer's clinical experience is showing a direct correlation between mycotoxin levels and illness. As his patients are improving their levels are decreasing. The patients with very minimal levels of mycotoxins are either well or nearly well.

 

[Ifish]

Hi lfish, thankyou for posting all of your experiences and thoughts, I find it very interesting.
One thing at the back of my mind though...how is Brewer's view consistent with the very positive results seen by people doing extreme avoidance? In theory, if the fungus is internal, avoidance would not help. Unless, of course, the situation is more complicated, and it is the interaction between something in the air (a pollutant say) and the mycotoxins that actually causes the illness.

I don't see this as being inconsistent. Brewer thinks that if a mold exposed patient that has not been colonized leaves a moldy environment and detoxes, the patient will get well. This is the result Shoemaker achieved with some of his briefly exposed patients. Then there are patients that improve with extreme avoidance but don't get completely well . Remember sick or not, all people have a daily load of contaminants that must be detoxed daily - chemicals, natural mold etc. If the amount of toxins being produced internally is relatively static then it would make sense that decreasing input of external mold and other environmental contaminants plus promoting increased detox capacity would result in a better ability of the body to process the daily burden of colonized mold toxins. This would result in feeling better but not completely well.

 

[N.A.Wright]

But isn't it the case that the controls that were used to establish the reference range would also be eating a similar diet (on average), meaning that those that excrete more are more likely to either (a) be exposed to mycotoxins other than those in their food, or (b) somehow be more efficient at excretion?

There was a paper, but not the paper that started off this thread, that arbitrarily concluded that a rate – not a range, of one part per billion in urine was a cut off point, the excess of which was deemed evidence of clinical significance.
The shortcomings of the cohorts used were discussed earlier in this thread I think, as far as I recall there was no exterior reference to to the significance of the cut off points.

There seems to be no published evidence at all that a measure equivalent to between one and two micrograms of aflatoxin being present in an average daily human urinary output represents clinical significance. These measures are tiny when compared to the known levels of acute aflatoxicity which are in the milligram range. Aflatoxins are certainly nasty but for humans the known threat is largely from long term high volume exposure causing explicit organ damage. If tiny levels of widely spread environmental factors are source of disabling chronic disease, then every human faces a lifetime of ill helth..

Also there’s also the question of what the source of the mycotoxin is. As I understand it , some people are arguing in this thread that the toxins are originating from mycoses growing in the nasal tract and sinuses, but is it realistic to believe that a pretty low level infection (many untreated mycoses produce really nasty localised effects) could produce mycotoxins at levels which outstrip background exposure ?

 

[cigana]

There was a paper, but not the paper that started off this thread, that arbitrarily concluded that a rate – not a range, of one part per billion in urine was a cut off point, the excess of which was deemed evidence of clinical significance.

I see, so you're not talking about Brewer's paper on detection of mycotoxins.

There seems to be no published evidence at all that a measure equivalent to between one and two micrograms of aflatoxin being present in an average daily human urinary output represents clinical significance. These measures are tiny when compared to the known levels of acute aflatoxicity which are in the milligram range.

So we know the effects of large exposure, but we don't know the effects of smaller exposures. Specifically, we don't know the effects of smaller exposures on people genetically susceptible to MECFS who may also be undergoing another biological stress.

If tiny levels of widely spread environmental factors are source of disabling chronic disease, then every human faces a lifetime of ill helth..

Wouldn't this be like saying the presence of tiny levels of grass pollen in the air would lead to an allergic reaction in every human if some humans are disabled by them?

but is it realistic to believe that a pretty low level infection (many untreated mycoses produce really nasty localised effects) could produce mycotoxins at levels which outstrip background exposure ?

Good question, I don't know.

I suppose it is also possible that the infection produces multiple types of mycotoxin, and the urine tests simply act as a marker, so it could be that small levels of particularly potent mycotoxins are more the problem than the known (eg. aflatoxin) mycotoxins.

I am curious as to how you would explain Brewer's results - that reduction of mycotoxins in urine corresponds to symptom improvement? Or perhaps you think he's made a mistake? (sorry if this is repeating earlier discussion )

 

[waiting]

Does anyone know if Dr. Brewer does phone consults?

 

[soulfeast]

Hi Soulfeast, could you explain this a little more, I don't get what you are saying...are you saying there's a different immune response to "stuck mycos" than there is to standard "mycos"?

Cigana, this is my basic understanding.. what I mean by stuck mycos are ones recirculating in the body triggering the immune response Shoemaker calls CIRS. I think CIRS develops (partial at least) from prolonged toxin exposure (some markers like c4a and maybe tgf-b1?) or from mycos not leaving the body (eventually full blown CIRS)... they keep triggering the immune system. That is how I understand it. People who do not have Shoemaker's HLA types can "get well" (at least fairy easily) once they leave a bad environment where they are constantly exposed. People who have his HLA types don't because the toxins are "stuck" for lack of a better word. They like fat, lipid. I'm curious if someone who does not have one of the HLA types and is constantly exposed could develop full blown CIRS that is difficult to recover from. I am understanding, not. I have problems with the HLA type = inevitable CIRS = CFS-ME paragidm since I know people with "dreadeds" who have been very exposed and are fine.