Re: Different Treatments with different doctors (GI issues/cholestyramine/mycoto

[Guest guest]

--- In , LiveSimply <quackadillian@...>

wrote:

>

> Thinking about it, I think your doctor probably didn't understand that

> cholestyramine was being used to pull toxins out of enterohepatic

> recirculation. Mycotoxins enter a loop between the liver and small

> intestine and that becomes a point where they can get sent back into

> the bloodstream again and again.. if cholestyramine doesnt intercept

> them.

There is one big problem with the theory that CSM binds the mycotoxins

which cause our illness. Namely, CSM cannot bind trichothecenes (see

the study below).

CSM is added to animal food to bind fumonisins and zearalenone. It's

effective only against these two mycotoxins. And these mycotoxins are

hardly the cause of the Sick Building Syndrome - just take a look at

their properties and effects. They wouldn't be able to cause the

classic mold symptoms that we usually associate with the exposure to

mycotoxins.

http://cat.inist.fr/?aModele=afficheN & cpsidt=16795728

Recent advances on the use of adsorbent materials for detoxification

of Fusarium mycotoxins

Auteur(s) / Author(s)

AVANTAGGIATO G. (1) ; SOLFRIZZO M. (1) ; VISCONTI A. (1) ;

Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)

(1) Institute of Sciences of Food Production (ISPA), National Research

Council (CNR), Via Amendola 122/O, 70126 Bari, ITALIE

Résumé / Abstract

The extensive use of adsorbents in the livestock industry has led to

the introduction of a wide range of new products on the market, most

of them claiming high in vitro mycotoxin adsorption capacity. However,

adsorbents that may appear effective in vitro do not necessarily

retain their efficacy when tested in vivo. Studies performed in our

laboratory during the past few years aiming to evaluate the efficacy

of various adsorbent materials in binding Fusarium mycotoxins are

reported. Adsorption experiments were performed in in vitro screening

tests for Fusarium mycotoxins at different pHs; by in vivo tests using

the increase of the sphinganine to sphingosine ratio in rat urine and

tissues as a biomarker of fumonisin exposure; and by a dynamic,

computer-controlled, gastrointestinal model simulating the

gastrointestinal tract of healthy pigs. Most of the commercially

available mycotoxin-binders failed in sequestering in vitro Fusarium

mycotoxins. Only for a small number of adsorbent materials was the

ability to bind more than one mycotoxin demonstrated. Cholestyramine

was proven to be an effective binder for fumonisins and zearalenone in

vitro, which was confirmed for zearalenone in experiments using a

dynamic gastrointestinal model and for fumonisins in in vivo

experiments. No adsorbent materials, with the exception of activated

carbon, showed relevant ability in binding deoxynivalenol and

nivalenol. The in vitro efficacy of activated carbon toward fumonisins

was not confirmed in vivo by the biomarker assay. The dynamic

gastrointestinal model was a reliable tool to study the effectiveness

of adsorbent materials in reducing the bioaccessibility of Fusarium

mycotoxins, as an alternative to the more difficult and time-consuming

studies with domestic livestock.

[Guest guest]

I'm thought that trichothecene toxins are a hit and run, meaning they

hit and do their damage and don't stay in your system very long.

unless your still exposed. ?

[Guest guest]

Did Dr. Shoemaker ever say the csm was solely for the purpose of

binding mycotoxins? because I thought it was more for just dealing

with the toxic body load in general because those with liver damage

don't detox like they should. and the high cholesterol many of us are

left with. mycotoxins are not the only toxins getting stored in our

omentum which is where they go when reabsorbed before not only go

back to the liver but also some amount can go back into the blood

stream along with the cholesterol and cause more damage. I don't know

about anyone else but I had exposure to other toxins besides just

mycotoxins.

[Guest guest]

Did Dr. Shoemaker ever say the csm was solely for the purpose of

> binding mycotoxins? Live, maybe you should answer this sence you are

the one that gives the impression that csm is only for binding

mycotoxins.

[Guest guest]

yes, good find Branislav, however I disagree that these mycotoxins

cannot be part of our exposure. there may be less of a chance in non-

farming areas, but the molds/myco's useually come from surrounding

areas so liveing close and up wind to farming..crop's,feed lot's ect.

mught be a little different than intercity mold types. maybe.. still

a chance there.

> There is one big problem with the theory that CSM binds the

mycotoxins

> which cause our illness. Namely, CSM cannot bind trichothecenes (see

> the study below).

>

> CSM is added to animal food to bind fumonisins and zearalenone. It's

> effective only against these two mycotoxins. And these mycotoxins

are

> hardly the cause of the Sick Building Syndrome - just take a look at

> their properties and effects. They wouldn't be able to cause the

> classic mold symptoms that we usually associate with the exposure to

> mycotoxins.

>

>

> http://cat.inist.fr/?aModele=afficheN & cpsidt=16795728

>

> Recent advances on the use of adsorbent materials for detoxification

> of Fusarium mycotoxins

> Auteur(s) / Author(s)

> AVANTAGGIATO G. (1) ; SOLFRIZZO M. (1) ; VISCONTI A. (1) ;

> Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)

> (1) Institute of Sciences of Food Production (ISPA), National

Research

> Council (CNR), Via Amendola 122/O, 70126 Bari, ITALIE

>

> Résumé / Abstract

>

> The extensive use of adsorbents in the livestock industry has led to

> the introduction of a wide range of new products on the market, most

> of them claiming high in vitro mycotoxin adsorption capacity.

However,

> adsorbents that may appear effective in vitro do not necessarily

> retain their efficacy when tested in vivo. Studies performed in our

> laboratory during the past few years aiming to evaluate the efficacy

> of various adsorbent materials in binding Fusarium mycotoxins are

> reported. Adsorption experiments were performed in in vitro

screening

> tests for Fusarium mycotoxins at different pHs; by in vivo tests

using

> the increase of the sphinganine to sphingosine ratio in rat urine

and

> tissues as a biomarker of fumonisin exposure; and by a dynamic,

> computer-controlled, gastrointestinal model simulating the

> gastrointestinal tract of healthy pigs. Most of the commercially

> available mycotoxin-binders failed in sequestering in vitro Fusarium

> mycotoxins. Only for a small number of adsorbent materials was the

> ability to bind more than one mycotoxin demonstrated. Cholestyramine

> was proven to be an effective binder for fumonisins and zearalenone

in

> vitro, which was confirmed for zearalenone in experiments using a

> dynamic gastrointestinal model and for fumonisins in in vivo

> experiments. No adsorbent materials, with the exception of activated

> carbon, showed relevant ability in binding deoxynivalenol and

> nivalenol. The in vitro efficacy of activated carbon toward

fumonisins

> was not confirmed in vivo by the biomarker assay. The dynamic

> gastrointestinal model was a reliable tool to study the

effectiveness

> of adsorbent materials in reducing the bioaccessibility of Fusarium

> mycotoxins, as an alternative to the more difficult and time-

consuming

> studies with domestic livestock.

>

[Guest guest]

PS, fumonisins have been found in drinking water, that same water

that leaks out of pipes in houses.

>

> yes, good find Branislav, however I disagree that these mycotoxins

> cannot be part of our exposure. there may be less of a chance in

non-

> farming areas, but the molds/myco's useually come from surrounding

> areas so liveing close and up wind to farming..crop's,feed lot's

ect.

> mught be a little different than intercity mold types. maybe..

still

> a chance there.

>

> > There is one big problem with the theory that CSM binds the

> mycotoxins

> > which cause our illness. Namely, CSM cannot bind trichothecenes

(see

> > the study below).

> >

> > CSM is added to animal food to bind fumonisins and zearalenone.

It's

> > effective only against these two mycotoxins. And these mycotoxins

> are

> > hardly the cause of the Sick Building Syndrome - just take a look

at

> > their properties and effects. They wouldn't be able to cause the

> > classic mold symptoms that we usually associate with the exposure

to

> > mycotoxins.

> >

> >

> > http://cat.inist.fr/?aModele=afficheN & cpsidt=16795728

> >

> > Recent advances on the use of adsorbent materials for

detoxification

> > of Fusarium mycotoxins

> > Auteur(s) / Author(s)

> > AVANTAGGIATO G. (1) ; SOLFRIZZO M. (1) ; VISCONTI A. (1) ;

> > Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)

> > (1) Institute of Sciences of Food Production (ISPA), National

> Research

> > Council (CNR), Via Amendola 122/O, 70126 Bari, ITALIE

> >

> > Résumé / Abstract

> >

> > The extensive use of adsorbents in the livestock industry has led

to

> > the introduction of a wide range of new products on the market,

most

> > of them claiming high in vitro mycotoxin adsorption capacity.

> However,

> > adsorbents that may appear effective in vitro do not necessarily

> > retain their efficacy when tested in vivo. Studies performed in

our

> > laboratory during the past few years aiming to evaluate the

efficacy

> > of various adsorbent materials in binding Fusarium mycotoxins are

> > reported. Adsorption experiments were performed in in vitro

> screening

> > tests for Fusarium mycotoxins at different pHs; by in vivo tests

> using

> > the increase of the sphinganine to sphingosine ratio in rat urine

> and

> > tissues as a biomarker of fumonisin exposure; and by a dynamic,

> > computer-controlled, gastrointestinal model simulating the

> > gastrointestinal tract of healthy pigs. Most of the commercially

> > available mycotoxin-binders failed in sequestering in vitro

Fusarium

> > mycotoxins. Only for a small number of adsorbent materials was the

> > ability to bind more than one mycotoxin demonstrated.

Cholestyramine

> > was proven to be an effective binder for fumonisins and

zearalenone

> in

> > vitro, which was confirmed for zearalenone in experiments using a

> > dynamic gastrointestinal model and for fumonisins in in vivo

> > experiments. No adsorbent materials, with the exception of

activated

> > carbon, showed relevant ability in binding deoxynivalenol and

> > nivalenol. The in vitro efficacy of activated carbon toward

> fumonisins

> > was not confirmed in vivo by the biomarker assay. The dynamic

> > gastrointestinal model was a reliable tool to study the

> effectiveness

> > of adsorbent materials in reducing the bioaccessibility of

Fusarium

> > mycotoxins, as an alternative to the more difficult and time-

> consuming

> > studies with domestic livestock.

> >

>

[Guest guest]

It used to be common practice to ammoniate animal feed to detoxify

grains, etc. Treating the grains with ammonia does neutralize the feed

enough so that the animals were healthy again. They do not reply on

CSM, I doubt. -

> >

> > Thinking about it, I think your doctor probably didn't understand that

> > cholestyramine was being used to pull toxins out of enterohepatic

> > recirculation. Mycotoxins enter a loop between the liver and small

> > intestine and that becomes a point where they can get sent back into

> > the bloodstream again and again.. if cholestyramine doesnt intercept

> > them.

>

>

> There is one big problem with the theory that CSM binds the mycotoxins

> which cause our illness. Namely, CSM cannot bind trichothecenes (see

> the study below).

>

> CSM is added to animal food to bind fumonisins and zearalenone. It's

> effective only against these two mycotoxins. And these mycotoxins are

> hardly the cause of the Sick Building Syndrome - just take a look at

> their properties and effects. They wouldn't be able to cause the

> classic mold symptoms that we usually associate with the exposure to

> mycotoxins.

>

>

> http://cat.inist.fr/?aModele=afficheN & cpsidt=16795728

>

> Recent advances on the use of adsorbent materials for detoxification

> of Fusarium mycotoxins

> Auteur(s) / Author(s)

> AVANTAGGIATO G. (1) ; SOLFRIZZO M. (1) ; VISCONTI A. (1) ;

> Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)

> (1) Institute of Sciences of Food Production (ISPA), National Research

> Council (CNR), Via Amendola 122/O, 70126 Bari, ITALIE

>

> Résumé / Abstract

>

> The extensive use of adsorbents in the livestock industry has led to

> the introduction of a wide range of new products on the market, most

> of them claiming high in vitro mycotoxin adsorption capacity. However,

> adsorbents that may appear effective in vitro do not necessarily

> retain their efficacy when tested in vivo. Studies performed in our

> laboratory during the past few years aiming to evaluate the efficacy

> of various adsorbent materials in binding Fusarium mycotoxins are

> reported. Adsorption experiments were performed in in vitro screening

> tests for Fusarium mycotoxins at different pHs; by in vivo tests using

> the increase of the sphinganine to sphingosine ratio in rat urine and

> tissues as a biomarker of fumonisin exposure; and by a dynamic,

> computer-controlled, gastrointestinal model simulating the

> gastrointestinal tract of healthy pigs. Most of the commercially

> available mycotoxin-binders failed in sequestering in vitro Fusarium

> mycotoxins. Only for a small number of adsorbent materials was the

> ability to bind more than one mycotoxin demonstrated. Cholestyramine

> was proven to be an effective binder for fumonisins and zearalenone in

> vitro, which was confirmed for zearalenone in experiments using a

> dynamic gastrointestinal model and for fumonisins in in vivo

> experiments. No adsorbent materials, with the exception of activated

> carbon, showed relevant ability in binding deoxynivalenol and

> nivalenol. The in vitro efficacy of activated carbon toward fumonisins

> was not confirmed in vivo by the biomarker assay. The dynamic

> gastrointestinal model was a reliable tool to study the effectiveness

> of adsorbent materials in reducing the bioaccessibility of Fusarium

> mycotoxins, as an alternative to the more difficult and time-consuming

> studies with domestic livestock.

>

[Guest guest]

--- In , LiveSimply <quackadillian@...>

wrote:

>

> Branislav,

>

> Its my understanding that cholestyramine is too expensive to be used

> in animal feed.

>

> So the term " commercially available preparations " I think probably

> refers to something else, like some kind of other additive.

No, you are wrong. " Commercially available preparations " here does

refer to CSM also.

CSM IS used as an additive in animal feed, and as far as I know it has

been used for that purpose long before Dr Shoemaker started using it

on mold sensitive patients.

The problem remains - CSM does not bind trichothecenes. If we're

getting better when we take CSM, it's because it binds something else,

not trichothecenes!

> Ive seen studies that used cholestyramine on trichothecenes..

Can you please cite those studies? Because I have been searching now

for more than 3 years and haven't found ONE study which could confirm

that CSM can bind trichothecenes.

What's worse, apart from activated charcoal which apparently can bind

trichothecenes in vivo to some extent, no other substance can bind

trichothecenes either in vivo or in vitro. Therefore now for animal

food biotransformation through enzymes is used to detoxify

trichothecenes, not to bind them.

-Branislav

[Guest guest]

>

> yes, good find Branislav, however I disagree that these mycotoxins

> cannot be part of our exposure. there may be less of a chance in non-

> farming areas, but the molds/myco's useually come from surrounding

> areas so liveing close and up wind to farming..crop's,feed lot's ect.

> mught be a little different than intercity mold types. maybe.. still

> a chance there.

Wouldn't you like to know what exactly causes your illness, or would

you rather just suppose that anything with the name " mycotoxin " is the

culprit of your illness, even though the chances that it can really

cause your symptoms are virtually zero?

Why don't you Google or do a Pubmed search on fumonisins and

zearalenone, see their effects and the routes of exposure. Their

effects don't resemble what we as moldies experience on a daily basis.

Here are the properties for fumonisins:

--------------------------------------------

http://revmedvet.com/artdes-us.php?id=239

Fumonisins are toxic metabolites of the fungus Fusarium moniliforme,

which is a worlwide contaminant of corn. Since the occurence of the

fongus and toxins are often symptomeless and fumonisins are heat

stable, they are frequently found in corn, corn- based animal feed,

and commercial corn based foods. Among the seven fumonisins isolated,

fumonisin B 1 is the most abundant. Though experimentally induced

mycotoxicosis are varied, equine leukoencephalomalacia and porcine

pulmonary edema are the best charactecized in farm animals. ln rats,

fumonisin B1 causes liver cancer.In humans, fumonisins exposure may be

lmplicated in esophageal cancer and atherosclerotic plaques formation.

These mycotoxins are structurally related to sphingosine, and may

exert their biological activity through their ability to block enzymes

involved in sphingolipid biosynthesis. However, much more research is

needed to define the role of sphingolipid disruption in the diseases,

and fumonisins total acceptable daily intake in animals and humans.

-------------------------------------------------

Notice this - " toxins are often symptomless " . That's NOT what we can

say for our toxins while we're exposed.

Properties for zearalenone:

---------------------------------------------------

http://www.oardc.ohio-state.edu/ohiofieldcropdisease/Mycotoxins/mycopagezearalen\

one.htm

Impact on Animal Health

Zearalenone is the primary toxin causing infertility, abortion or

other breeding problems, especially in swine.

When contaminated rations are consumed by animals, they develop a

condition known as hyperestrogenism.

Swine are most sensitive to zearalenone.

As a general rule, rations exceeding 0.5 ppm of zearalenone should not

be fed to swine.

Prepuberal gilts are more susceptible than mature swine.

Abortions and uterine prolapse may occur as a result of consumption of

zearalenone-contaminated feeds.

Zearalenone has been associated with infertility and abortion problems

in dairy cattle in the Midwestern U.S.

Conception rates may be reduced in dairy heifers when fed greater than

12.5 ppm zearalenone.

Poultry in general are more tolerant than swine to zearalenone.

--------------------------------------------------------------

Again, this doesn't resemble the typical exposure to mold toxins that

we experience. Out symptoms are almost immediate and include skin

itching and burning, nausea, diarrhea or constipation, memory

problems, chronic fatigue, pain in joints etc.

Oddly enough, of all mycotoxins only trichothecenes can potentially

produce these classic Sick Building Syndrome symptoms, but CSM does

not bind trichothecenes. That's something to think about.

Btw. I now think that most of us are NOT affected by real

trichothecenes, but that we've become hypersensitive to a small group

of exotic MVOCs (Mirobial Volatile Organic Compounds) that can mimic

trichothecene mycotoxicosis almost perfectly. So in essence, our

illness is a type of extreme chemical sensitivity to mold MVOCs.

There's a lot of data and evidence that speaks in favor of this

theory, but I can't go into the details right now (too tired).

-Branislav

[Guest guest]

Braniskav, I had menstral problems and ended up haveing a

hisderictimy because of endermetreosis, I'm fully aware of what Zear.

can do.I have researched it and the estrogen effects it causes.

I also am one of very few that is very sensitive to any corn products

and anything fermented both inhaled and orally.

and had fusarium in my blood. dont try to put us all in the same box,

we won't fit in there.

I do understand my illness quite well.

[Guest guest]

PS Branislav, it's obvious from your past posts and this one that you

consentrait way to much on myco's and no other part of these

exposures, during and afterwards. I sujest you look at the big

picture of exposure in a WDB. it's not only about mycotoxins. however

sence I had to completely different exposures I can tell you that

mycotoxins can and do cause symptoms, and those are fairly well

documented and while during exposure in most cases your not going to

be able to seperate the effects with the cause, after exposure with

time you may be ab;e to reconize the difference between a allergic

reaction, a chemical reaction, and a mold/vpc reaction vs. a

mold/myco reaction, ect. however if you were exposed to many

molds/myco's at the same time along with man made

chemicals,bacterias,ect. it may be nearly imposable to seperate those

and many mistake that every thing that causes a reaction is myco's

and thats just not true.

a good hint to deturmine if youve been re-exposed to a mycotoxin is

to jnow about how long it takes to to leave your system, than if you

suffered considerable liver damage you might times that by two.

everyone talks about 3 or 4 days of felling ill again with re-

exposure to what they think is myco's,

some myco's take longer to leave your system and the effects well be

much more severe and last much longer.

now I am talking about the myco's I can reconize when I get exposed

to them because of their effects. and not even all myco's can set you

back for months some may cause effects very simular to other

chemicals so it's not easy to seperate and I dont even fell it's all

that important in the big picture here. the big picture here is based

on organ and system damage and that many things, some not even toxic

can aggervate you condition and make life in the real world very

miserable. to some extent I believe we only become hyperreactive to

what we were exposed to in high doses but with organ and system

damage many other things can act as irritants.

[Guest guest]

>PS Branislav, it's obvious from your past posts and this one that you

>consentrait way to much on myco's and no other part of these

>exposures, during and afterwards.

Who,

What other exposures? In my previous post I tried to refute the notion

that in most cases our illness is caused by real mycotoxins. I

suggested that our illness is in fact caused by mold MVOCs in most

cases. MVOCs are primary metabolites of mold, and although they are

not called mycotoxins they do have strong irritative effects and most

of them are neurotoxic. The trick is, we've become hypersensitive to

them in the similar way MCS people become hypersensitive to perfumes.

Dr Shoemaker and all others have led us to believe that real

mycotoxins (secondary metabolites of mold) are the main cause of our

illness. That may prove not to be true for most cases.

Ever wondered why people get sick even if non-toxic molds such as

Cladosporium or Alternaria grow in badly maintained AC units? These

fungi don't give off trichotheces, yet people can get very sick. How?

-Branislav

[Guest guest]

I don't think Shoemaker or anyone else has tried to say this is only

about mycotoxins. Dr. Shoemaker refers to WDB's because he knows it

all a combined exposure/effect. these things are not seperated when

we breath them in, why try to seperate them at all? even in reading

medical articles on fungal infections, there was no seperation of

cause and affect between MVOC's or mycotoxin s or fungal fragments or

spores.

what mold does to protect itself,grow and eat in the envitonment,

chances are it does the same thing in our systems or trys. take away

any part of that and it might not act the same. as for exposures to

molds not known to produce mycotoxins, theres quite a bit to be said

about high dose acute exposures and the effects on the immune system

as I have been trying to get people to realize. with acute exposures

weither it's toxins from the environment or from our own cells

because of reaction it's still toxic to our system. however not

everyones exposure is acute, some are chronic and yes, it's important

to have it realized that mycotoxins can play a role in exposures in

WDB's right along with everything else. but no, I dont fell there

should have to be a need to prove it as there's so much going on

there that just knowning that toxic molds were detected and even non-

toxic ones too and given the right tests and diagnoses should play a

bigger role in deturmineing how bad someone was injured. but it has

to be reconized that these exposures do cause injury even at lower

chronic doses. even sometimes with no high moisture and bacteria's or

anything else but the mold and it's toxins that can get through

mucosae and cause organ damage and brain barriors with seepage and

cause cns/spinal effects. what may be to big to get to your brain

from going up your nose doesn't mean things attached or inside of it

if it's soluable wont. dont you understand that not everyone shows

positive on allery to molds and theres need to document their

exposures in other ways, like mycotoxins? why? because not everything

we are exposed to in these environments can be documented or show a

proven cause and effect. now if our illness was getting proper

testing and diagnoses and treatment it might be a different story.

--- In , " Branislav " <arealis@...>

wrote:

>

> >PS Branislav, it's obvious from your past posts and this one that

you

> >consentrait way to much on myco's and no other part of these

> >exposures, during and afterwards.

>

> Who,

>

> What other exposures? In my previous post I tried to refute the

notion

> that in most cases our illness is caused by real mycotoxins. I

> suggested that our illness is in fact caused by mold MVOCs in most

> cases. MVOCs are primary metabolites of mold, and although they are

> not called mycotoxins they do have strong irritative effects and

most

> of them are neurotoxic. The trick is, we've become hypersensitive to

> them in the similar way MCS people become hypersensitive to

perfumes.

>

>

> Dr Shoemaker and all others have led us to believe that real

> mycotoxins (secondary metabolites of mold) are the main cause of our

> illness. That may prove not to be true for most cases.

>

> Ever wondered why people get sick even if non-toxic molds such as

> Cladosporium or Alternaria grow in badly maintained AC units? These

> fungi don't give off trichotheces, yet people can get very sick.

How?

>

>

> -Branislav

>

[Guest guest]

PS branislav, I am a MCSer also and I posted not long ago that I

don't have the same exact reaction to myco exposure that I do with

most chemicals. so you may be right in that sence that MVOC's may

cause reactions much like other chemicals and voc's.

but I do also know that mycotoxins do play a role in WDB exposures.

I also have a felling that certain mycotoxins may play a role in at

least one type of breast cancer. I hope I don't have to find out the

answer to this.

[Guest guest]

not a farm boy,hey? The farm thing is a pretty easy concept,

documentd too, example: I think it was at 100 yards up wind, a house

by a corn field, found in the house was the dust from the cornfield

and what was in that dust. just add water.

same goes for feed lots but that dust is stirred up constantly and

may travel long distances in the wind. during corm harvest that dust

may travek long distances.

drive by either after a rain and you might not smell anything or have

a reaction if the particles are wet and weighed down. dry and flying

is a different story. and a corn field thats had to much stress from

either to much or to little rain and once it begans to tossle(grow

corn ears) can be hard to drive by for those sensitized as corn has

lots of liquid in those kurnels and fungi really like that.

cutting grasses for hay and even cutting the grass in your yard when

it's fairly dry can stir up alot of whats in them on on the ground in

the top soil thats dry.

I've been tested to being highly allergic/sensitive to dust. when

people talk about felling better outside they must not live in a

farming community type setting.

I have taken mold/myco's slams while being outside, sometimes during

hay bailing season and corn harvest I cant go out my door without

suffering for it big time. every summer when it gets dty my legs

swell from my knees down and it is pretty persistant until late in

the winter.

things normal people may claim as hay fever they may reconize for

what they really are if they become hyperreactive. from exposure in a

WDB. more than just a allergy substance there. unless you consider it

all a allergy substance than I'm just allergic to something in any of

it and if it's not a allergic it's reactive, it all sucks either

way.

kind of throws dirt in that whole theory of exposure to these things

while your young makes you immune to them.WRONG! just heard that

crap being toutted again on the news. WRONG! just goes to show the

differences in dose and occasional exposure vs. chronic exposure and

acute exposure.

--- In , <unitedstatesvet@...>

wrote:

>

> I dont know anything about a farm but I have tricothesimes from

stackybotryous from my house and I want to get rid of these buggers

so and the mycotoxins that are doing whatever they do. I am like lost

in the whole farm thing.

>

>

>  

>  

>  

>  

>  

>

[Guest guest]

Just a thought for all those interested in MVOCs. It might be useful in

researching the action of MVOCs on TRP receptors as well as the other

numerous cell receptors, protein kinases, also the long term effects of

lipid peroxidation including the generation of endogenous aldehydes,

oxidative stress and effects of peroxynitrite on the mitochondria and

endoplasmic reticulum, P38MAPK and the production of inflammatory

cytokines, toxicity of stress hormone metabolites, mast cells

modulation on epithelial permeability and degranulation and

transduction of TRPs that cause increased sensitivity to exogenous as

well as endogenous irritants and how increases and decreases of

serotonin and estrogen modulates inflammatory processes.

HEIRS Abstract Library: http://www.citeulike.org/user/HEIRS

HEIRS Online Weblog: http://www.heirsonline.wordpress.com

HEIRS Blogroll: http://www.bloglines.com/blog/HEIRS

HEIRS Online: http://www.heirs-online.com

Kim Kramer

Health Educator and Researcher

Health Education Information and Resource Services

kkramer@...

--- In , " kl_clayton " <kl_clayton@...>

wrote:

>

> It used to be common practice to ammoniate animal feed to detoxify

> grains, etc. Treating the grains with ammonia does neutralize the feed

[Guest guest]

>

> It used to be common practice to ammoniate animal feed to detoxify

> grains, etc. Treating the grains with ammonia does neutralize the feed

> enough so that the animals were healthy again. They do not reply on

> CSM, I doubt. -

>

Ammonia is effective only against aflatoxins. Other mycotoxins cannot

be detoxified with ammonia.

Btw. I know that Dr Croft claims trichothecenes can be

destroyed with ammonia, but several good chemists told me that was

just impossible. Ammonia does not destroy trichothecenes. Only bleach

with added sodium hydroxide can destroy trhichothecenes and it takes

about 48 hours for the reaction to complete.

Incidentally, maybe some will remember here that last year I had great

problems with the AC units from the building nearby. It poisoned me

terrribly and I was almost sure the offending substance was a

trichothecene mycotoxin. I had all the classic mold symptoms (GI

problems, severe chronic fatigue, disturbed vision, skin burning,

terrible headaches, tooth loss etc.).

I even went so far to suspect it was one particular trichothecene

mycotoxin - Satratoxin - because the effects of satratoxin matched my

symptoms almost 100%. After about one year I discovered that ammonia

is very effective against that contamination. It literally wiped it

out. I talked with a chemist and he told me there was no way it could

have been a trichothecene mycotoxin. The only possibility is that it

was a MVOC (such as a hydrocarbon, aldehyde, ketone etc.) that was

susceptible to ammonia.

Also, it was definitely volatile to some extent, while trichothecenes

are NONvolatile and could become airborne only if mechanically

disturbed and thus aerosolised as fine particles. On the contrary, the

last year's contamination could offgas from contaminated objects even

if there was no air current or wind in the room.

The details are very important if we want to understand what exactly

is affecting us.

I don't mean to say that nobody is affected by real mycotoxins. It

probably happens in WDBs. However, in my opinion we often mistake

MVOCs for mycotoxins. MVOCs shouldn't be underestimated, that's all I

wanted to say in the recent messages. They should be studied more

dilligently since I'm sure they can cause many serious health

problems. At the present time there's not much info about their

effects on people. Even on the EPA site you'll find something like:

" The health effects of inhaling mVOCs are largely unknown, although

exposure to mVOCs has been linked to symptoms such as headaches, nasal

irritation, dizziness, fatigue, and nausea. More research is needed to

determine whether there are any human health effects from

non-occupational indoor exposures to mVOCs. "

or

" Exposure to mVOCs from molds has been linked to symptoms such as

headaches, nasal irritation, dizziness, fatigue, and nausea. Research

on MVOCs is still in the early phase. "

That sounds rather vague. It's as if they didn't want to waste their

time with MVOCs lol. If it turns out that MVOCs are the most common

cause of classic mold symptoms, then this would be one of the best

examples of underestimating a class of chemicals for their potential

to cause illnesses.

[Guest guest]

what Croft said to me is that ammonia temperary neutrolizes trich's

not distoys them. big difference there.

>

> --- In , " kl_clayton " <kl_clayton@>

wrote:

> >

> > It used to be common practice to ammoniate animal feed to detoxify

> > grains, etc. Treating the grains with ammonia does neutralize the

feed

> > enough so that the animals were healthy again. They do not reply

on

> > CSM, I doubt. -

> >

>

>

> Ammonia is effective only against aflatoxins. Other mycotoxins

cannot

> be detoxified with ammonia.

>

> Btw. I know that Dr Croft claims trichothecenes can be

> destroyed with ammonia, but several good chemists told me that was

> just impossible. Ammonia does not destroy trichothecenes. Only

bleach

> with added sodium hydroxide can destroy trhichothecenes and it takes

> about 48 hours for the reaction to complete.

>

> Incidentally, maybe some will remember here that last year I had

great

> problems with the AC units from the building nearby. It poisoned me

> terrribly and I was almost sure the offending substance was a

> trichothecene mycotoxin. I had all the classic mold symptoms (GI

> problems, severe chronic fatigue, disturbed vision, skin burning,

> terrible headaches, tooth loss etc.).

>

> I even went so far to suspect it was one particular trichothecene

> mycotoxin - Satratoxin - because the effects of satratoxin matched

my

> symptoms almost 100%. After about one year I discovered that ammonia

> is very effective against that contamination. It literally wiped it

> out. I talked with a chemist and he told me there was no way it

could

> have been a trichothecene mycotoxin. The only possibility is that it

> was a MVOC (such as a hydrocarbon, aldehyde, ketone etc.) that was

> susceptible to ammonia.

>

> Also, it was definitely volatile to some extent, while

trichothecenes

> are NONvolatile and could become airborne only if mechanically

> disturbed and thus aerosolised as fine particles. On the contrary,

the

> last year's contamination could offgas from contaminated objects

even

> if there was no air current or wind in the room.

>

> The details are very important if we want to understand what exactly

> is affecting us.

>

> I don't mean to say that nobody is affected by real mycotoxins. It

> probably happens in WDBs. However, in my opinion we often mistake

> MVOCs for mycotoxins. MVOCs shouldn't be underestimated, that's all

I

> wanted to say in the recent messages. They should be studied more

> dilligently since I'm sure they can cause many serious health

> problems. At the present time there's not much info about their

> effects on people. Even on the EPA site you'll find something like:

>

> " The health effects of inhaling mVOCs are largely unknown, although

> exposure to mVOCs has been linked to symptoms such as headaches,

nasal

> irritation, dizziness, fatigue, and nausea. More research is needed

to

> determine whether there are any human health effects from

> non-occupational indoor exposures to mVOCs. "

>

> or

>

> " Exposure to mVOCs from molds has been linked to symptoms such as

> headaches, nasal irritation, dizziness, fatigue, and nausea.

Research

> on MVOCs is still in the early phase. "

>

> That sounds rather vague. It's as if they didn't want to waste their

> time with MVOCs lol. If it turns out that MVOCs are the most common

> cause of classic mold symptoms, then this would be one of the best

> examples of underestimating a class of chemicals for their potential

> to cause illnesses.

>

[Guest guest]

sure makes you wonder how much some people that had MCS symptoms that

ran around for 20 years tring to get everyone to believe that

mycotoxins was what caused it and touting great abilitys of detection

to mycotoxins and experts that talk of seeing volatile mycotoxins in

the air has hurt the cause of getting this illness reaconized.what a

travisty to those really severely injured from their exposures.

kind of makes you wonder, with all their self proclaims of extreme

knowledge just what side of this they are really on. and those that

knownly go along when reliable documentation says otherwise over and

over again for the sake of who their beholding to doesn't when no

prizes in my book. in fact it answers quite a few questions. even

stranger is when their beholden but state that they wouldn't use this

expert if they had a case but set back knowing that very sick people

are and doesn't say a damn word. no excuse for that. none at all.

[Guest guest]

oh, please,I didn't even mention yellow rain so quit trying to inply

that that I was. you are forgeting that I had two seperate exposures.

I have talked about that green(not yellow,gold or browm)green resin

many times, THAT WAS IN MY SECOND HOME WITH HIGH MOISTURE PROBLEMS

AND MANY TOXIC MOLDS.this is were I got MCS, not in my first home

with several years exposure. I have also talked about my first home

were mainly stachy was found and someone has even seen pictures of. I

have talked about the black DUST there. did I ever once say that

there was a problem there all those years with a resin type coating?

NO!

> > sure makes you wonder how much some people that had MCS symptoms

that

> > ran around for 20 years tring to get everyone to believe that

> > mycotoxins was what caused it and touting great abilitys of

detection

> > to mycotoxins and experts that talk of seeing volatile mycotoxins

in

> > the air has hurt the cause of getting this illness

reaconized.what a

> > travisty to those really severely injured from their exposures.

> > kind of makes you wonder, with all their self proclaims of extreme

> > knowledge just what side of this they are really on. and those

that

> > knownly go along when reliable documentation says otherwise over

and

> > over again for the sake of who their beholding to doesn't when no

> > prizes in my book. in fact it answers quite a few questions. even

> > stranger is when their beholden but state that they wouldn't use

this

> > expert if they had a case but set back knowing that very sick

people

> > are and doesn't say a damn word. no excuse for that. none at all.

> >

>