Re: Potential role played by mycotoxins in human intestinal inflammatory diseases.

[Guest guest]

If one was to have mycotoxins in the intestinal track, how do you get the

mycotoxins out? Anybody??

From: KC <tigerpaw2c@...>

Subject: [] Potential role played by mycotoxins in human intestinal

inflammatory diseases.

Date: Monday, October 25, 2010, 6:13 PM

 

Potential role played by mycotoxins in human intestinal inflammatory

diseases.

Give feedback

Dr Marc Maresca

Université Cézanne

Published on 25 October 2010

http://www.scitopics.com/Potential_role_played_by_mycotoxins_in_human_intestinal\

_inflammatory_diseases.html

Human intestinal inflammatory diseases or inflammatory bowel diseases (IBD) are

caracterized by chronic inflammation of the gut, leading to pain, malabsorption,

malnutrition, diarrhea and eventually to lethal complications such as cancers.

Among IBD, Crohn's and celiac diseases are the best know and caracterized. In

both cases, exacerbated immunity and auto-immunity reactions lead to persistent

intestinal inflammation. Although IBD depend primary on genetic predispositions

(associated with mutations in various genes involved in the intestinal immunity

and epithelial integrity) such genetic back-ground is not suffisant. Like in

many other diseases, the induction and the progression of IBD also critically

depend on environmental factors, such as food allergen (i.e. gluten) or bacteria

in celiac and Crohn's diseases, respectively.

Although many publications reported that some mycotoxins, described as

enterotoxic, are able to affect gut integrity and to cause intestinal

inflammation, a link between chronic exposure to mycotoxins and the induction

and/or persistance of IBD in predisposed patients was not proposed until

recently.

Mycotoxins are secondary metabolites produced by different fungal species,

mainly Penicillium, Aspergillus and Fusarium. Due to their antibiotic

activities, it is admitted that molds produce mycotoxins in their natural

environment (i.e. crops and plants) to kill others micro-organisms (bacteria,

others fungi) colonizing the same niche.

In addition to possess antibiotic activities, mycotoxins are known to affect the

cell functions in animals, including humans. Thus, mycotoxins are able to affect

the functions of numerious tissus and systems, including: i) renal, hepatic,

respiratory and intestinal epithelia and ii) the immune, reproductive and

nervous systems. In addition, exposure to certain mycotoxins have been related

to cancerigenic and teratogenic effects in humans and animals.

The impact of some mycotoxins on the intestinal physiology is well known. In

addition to animal experiments, the recent use of cell lines mimicking human

intestinal epithelial cells (hIEC), demonstrated that many food-associated

mycotoxins (mainly aflatoxins, ochratoxins, patulin, fumonisin, trichothecenes,

zearalenone) are able to perturbate key intestinal functions such as: the

barrier function, the absorption of nutriments or the intestinal immunity. Based

on these publications, we recently critically analysed the potential role of

certain mycotoxins as etiologic agents in patients predisposed to IBD [Maresca

and Fantini, 2010].

Based on scientific publications reporting the action of single mycotoxin on

human intestinal epithelial cells and/or animals, we found that many mycotoxins

could be considered as at risk for this particular population based on: i) the

similarity existing between the pathophysiological process involved in the

on-set / the progression of IBD and in mycotoxicosis and ii) on the low security

factor existing in many cases between the doses of mycotoxin causing the

intestinal perturbations and the tolerable daily intact doses (TDI) fixed by

health and agricultural administrations.

Situtation could be even more dramatic if we consider that humans are not

exposed to single mycotoxin but rather to cocktail of mycotoxins and to mixture

of mycotoxins with others toxicans (such as phytotoxins, pesticides, heavy

metals) also able to perturbate the gut function [Mattsson, 2007]. In vitro

experiments on hIEC have already demonstrated that mixture of mycotoxins results

in addive and/or synergistic toxicity eventually leading to a decrease in the

efficient toxic dose of each compound of the mixture [Creppy et al., 2004;

Kouadio et al., 2007]. If such potentiation due to mixture of contaminants also

happens in vivo, it will have major consequence on the safety values of the the

tolerable daily intact doses (TDI).

Although epidemiologic studies are required to confirm our hypothesis, it seems

that certain food-associated mycotoxins have to be added to the list of

molecules and environmental factors potentially involved in the etiology of IBD

in predisposed patients. Effort must be made to limit further the exposure of

this particular population to mycotoxin-contaminated food.

We hope our hypothesis will stimulate discussions and will leads to an

epidemiologic evaluation of a link between food-associated mycotoxins and IBD.

Human intestinal inflammatory diseases or inflammatory bowel diseases (IBD) are

caracterized by chronic inflammation of the gut, leading to pain, malabsorption,

malnutrition, diarrhea and eventually to lethal complications such as cancers.

Among IBD, Crohn's and celiac diseases are the best know and caracterized. In

both cases, exacerbated immunity and auto-immunity reactions lead to persistent

intestinal inflammation. Although IBD depend primary on genetic predispositions

(associated with mutations in various genes involved in the intestinal immunity

and epithelial integrity) such genetic back-ground is not suffisant. Like in

many other diseases, the induction and the progression of IBD also critically

depend on environmental factors, such as food allergen (i.e. gluten) or bacteria

in celiac and Crohn's diseases, respectively.

Although many publications reported that some mycotoxins, described as

enterotoxic, are able to affect gut integrity and to cause intestinal

inflammation, a link between chronic exposure to mycotoxins and the induction

and/or persistance of IBD in predisposed patients was not proposed until

recently.

Mycotoxins are secondary metabolites produced by different fungal species,

mainly Penicillium, Aspergillus and Fusarium. Due to their antibiotic

activities, it is admitted that molds produce mycotoxins in their natural

environment (i.e. crops and plants) to kill others micro-organisms (bacteria,

others fungi) colonizing the same niche.

In addition to possess antibiotic activities, mycotoxins are known to affect the

cell functions in animals, including humans. Thus, mycotoxins are able to affect

the functions of numerious tissus and systems, including: i) renal, hepatic,

respiratory and intestinal epithelia and ii) the immune, reproductive and

nervous systems. In addition, exposure to certain mycotoxins have been related

to cancerigenic and teratogenic effects in humans and animals.

The impact of some mycotoxins on the intestinal physiology is well known. In

addition to animal experiments, the recent use of cell lines mimicking human

intestinal epithelial cells (hIEC), demonstrated that many food-associated

mycotoxins (mainly aflatoxins, ochratoxins, patulin, fumonisin, trichothecenes,

zearalenone) are able to perturbate key intestinal functions such as: the

barrier function, the absorption of nutriments or the intestinal immunity. Based

on these publications, we recently critically analysed the potential role of

certain mycotoxins as etiologic agents in patients predisposed to IBD [Maresca

and Fantini, 2010].

Based on scientific publications reporting the action of single mycotoxin on

human intestinal epithelial cells and/or animals, we found that many mycotoxins

could be considered as at risk for this particular population based on: i) the

similarity existing between the pathophysiological process involved in the

on-set / the progression of IBD and in mycotoxicosis and ii) on the low security

factor existing in many cases between the doses of mycotoxin causing the

intestinal perturbations and the tolerable daily intact doses (TDI) fixed by

health and agricultural administrations.

Situtation could be even more dramatic if we consider that humans are not

exposed to single mycotoxin but rather to cocktail of mycotoxins and to mixture

of mycotoxins with others toxicans (such as phytotoxins, pesticides, heavy

metals) also able to perturbate the gut function [Mattsson, 2007]. In vitro

experiments on hIEC have already demonstrated that mixture of mycotoxins results

in addive and/or synergistic toxicity eventually leading to a decrease in the

efficient toxic dose of each compound of the mixture [Creppy et al., 2004;

Kouadio et al., 2007]. If such potentiation due to mixture of contaminants also

happens in vivo, it will have major consequence on the safety values of the the

tolerable daily intact doses (TDI).

Although epidemiologic studies are required to confirm our hypothesis, it seems

that certain food-associated mycotoxins have to be added to the list of

molecules and environmental factors potentially involved in the etiology of IBD

in predisposed patients. Effort must be made to limit further the exposure of

this particular population to mycotoxin-contaminated food.

We hope our hypothesis will stimulate discussions and will leads to an

epidemiologic evaluation of a link between food-associated mycotoxins and IBD.

continue reading

Further reading

Abid-Essefi et al., (2009). Comparative study of toxic effects of zearalenone

and its two major metabolites alpha- zearalenol and beta-zearalenol on cultured

human Caco-2 cells. J Biochem Mol Toxicol. 23(4):233-43.

Bouhet S, Oswald IP. (2005). The effects of mycotoxins, fungal food

contaminants, on the intestinal epithelial cell-derived innate immune response.

Vet Immunol Immunopathol. 108(1-2):199-209.

Bouhet S, Oswald IP. (2007). The intestine as a possible target for fumonisin

toxicity. Mol Nutr Food Res. 51(8):925-31.

Caloni et al., (2002). Evaluation of Fumonisin B(1) and its metabolites

absorption and toxicity on intestinal cells line Caco- 2. Toxicon.

40(8):1181-188.

Caloni et al., (2006). Aflatoxin M1 absorption and cytotoxicity on human

intestinal in vitro model. Toxicon. 47(4):409-15.

Creppy et al., (2004). Synergistic effects of fumonisin B1 and ochratoxin A: are

in vitro cytotoxicity data predictive of in vivo acute toxicity? Toxicology.

201(1-3):115-23.

Diesing et al., (2010). Mycotoxin deoxynivalenol (DON) mediates biphasic

cellular response in intestinal porcine epithelial cell lines IPEC- 1 and

IPEC-J2. Toxicol Lett. In press.

Kasuga et al., (1998). In vitro effect of deoxynivalenol on the differentiation

of human colonic cell lines Caco- 2 and T84. Mycopathologia. 142(3):161-7.

Kouadio et al., (2005). Comparative study of cytotoxicity and oxidative stress

induced by deoxynivalenol, zearalenone or fumonisin B1 in human intestinal cell

line Caco-2. Toxicology. 213(1-2):56-65.

Kouadio et al., (2007). Effects of combinations of Fusarium mycotoxins on the

inhibition of macromolecular synthesis, malondialdehyde levels, DNA methylation

and fragmentation, and viability in Caco- 2 cells. Toxicon. 49(3):306-17.

Lambert et al., (2007). Ochratoxin A displaces claudins from detergent resistant

membrane microdomains. Biochem Biophys Res Commun. 358(2):632-6.

Mahfoud et al., (2002). pH-dependent interaction of fumonisin B1 with

cholesterol: physicochemical and molecular modeling studies at the air-water

interface. J Agric Food Chem. 50(2):327-31.

Mahfoud et al., (2002). The mycotoxin patulin alters the barrier function of the

intestinal epithelium: mechanism of action of the toxin and protective effects

of glutathione. Toxicol Appl Pharmacol. 181(3):209-18.

Maresca et al., (2001). The mycotoxin ochratoxin A alters intestinal barrier and

absorption functions but has no effect on chloride secretion. Toxicol Appl

Pharmacol. 176(1):54-63.

Maresca et al., (2002). The mycotoxin deoxynivalenol affects nutrient absorption

in human intestinal epithelial cells. J Nutr. 132(9):2723-31.

Maresca et al., (2008). Both direct and indirect effects account for the pro-

inflammatory activity of enteropathogenic mycotoxins on the human intestinal

epithelium: stimulation of interleukin-8 secretion, potentiation of interleukin-

1beta effect and increase in the transepithelial passage of commensal bacteria.

Toxicol Appl Pharmacol.228(1):84-92.

Maresca M, Fantini J. (2010) Some food-associated mycotoxins as potential risk

factors in humans predisposed to chronic intestinal inflammatory diseases.

Toxicon. 56(3):282-94.

Mattsson (2007). Mixtures in the real world: the importance of plant

McLaughlin et al., (2004). Ochratoxin A increases permeability through tight

junctions by removal of specific claudin isoforms. Am J Physiol Cell Physiol.

287(5):C1412-7.

McLaughlin et al., (2009). The mycotoxin patulin, modulates tight junctions in

caco- 2 cells. Toxicol In Vitro. 23(1):83-9.

Pestka (2010). Deoxynivalenol: mechanisms of action, human exposure, and

toxicological relevance. Arch Toxicol. 84(9):663-79.

Pinton et al., (2009). The food contaminant deoxynivalenol, decreases intestinal

barrier permeability and reduces claudin expression. Toxicol Appl Pharmacol.

237(1):41-8.

Pinton et al., (2010). Deoxynivalenol Impairs Porcine Intestinal Barrier

Function and Decreases the Protein Expression of Claudin- 4 through a

Mitogen-Activated Protein Kinase-Dependent Mechanism. J Nutr. 140(11):1956-62.

Razafimanjato et al. (2010). The food-associated fungal neurotoxin ochratoxin A

inhibits the absorption of glutamate by astrocytes through a decrease in cell

surface expression of the excitatory amino- acid transporters GLAST and

GLT-1.Neurotoxicology. 31(5):475-84.

[Guest guest]

Probabl_ CSM, charcoal, fiber rich diet, etc, detox st_ff.

>

> From: KC <tigerpaw2c@...>

> Subject: [] Potential role played by mycotoxins in human

intestinal inflammatory diseases.

>

> Date: Monday, October 25, 2010, 6:13 PM

>

>

> Potential role played by mycotoxins in human intestinal inflammatory

diseases.

>

>

> Dr Marc Maresca

>

> Université Cézanne

>

> Published on 25 October 2010

>

>

>

http://www.scitopics.com/Potential_role_played_by_mycotoxins_in_human_intestinal\

_inflammatory_diseases.html

>

[Guest guest]

I had IBS  for years the funny thing is I think I got it from processed

foods. 

When I stopped eating processed foods it resolved on it's own. 

  

God Bless !!

dragonflymcs

Mayleen

________________________________

From: KC <tigerpaw2c@...>

Sent: Mon, October 25, 2010 9:13:56 PM

Subject: [] Potential role played by mycotoxins in human intestinal

inflammatory diseases.

 

Potential role played by mycotoxins in human intestinal inflammatory diseases.

Give feedback

Dr Marc Maresca

Université Cézanne

Published on 25 October 2010

http://www.scitopics.com/Potential_role_played_by_mycotoxins_in_human_intestinal\

_inflammatory_diseases.html

Human intestinal inflammatory diseases or inflammatory bowel diseases (IBD) are

caracterized by chronic inflammation of the gut, leading to pain, malabsorption,

malnutrition, diarrhea and eventually to lethal complications such as cancers.

Among IBD, Crohn's and celiac diseases are the best know and caracterized. In

both cases, exacerbated immunity and auto-immunity reactions lead to persistent

intestinal inflammation. Although IBD depend primary on genetic predispositions

(associated with mutations in various genes involved in the intestinal immunity

and epithelial integrity) such genetic back-ground is not suffisant. Like in

many other diseases, the induction and the progression of IBD also critically

depend on environmental factors, such as food allergen (i.e. gluten) or bacteria

in celiac and Crohn's diseases, respectively.

Although many publications reported that some mycotoxins, described as

enterotoxic, are able to affect gut integrity and to cause intestinal

inflammation, a link between chronic exposure to mycotoxins and the induction

and/or persistance of IBD in predisposed patients was not proposed until

recently.

Mycotoxins are secondary metabolites produced by different fungal species,

mainly Penicillium, Aspergillus and Fusarium. Due to their antibiotic

activities, it is admitted that molds produce mycotoxins in their natural

environment (i.e. crops and plants) to kill others micro-organisms (bacteria,

others fungi) colonizing the same niche.

In addition to possess antibiotic activities, mycotoxins are known to affect the

cell functions in animals, including humans. Thus, mycotoxins are able to affect

the functions of numerious tissus and systems, including: i) renal, hepatic,

respiratory and intestinal epithelia and ii) the immune, reproductive and

nervous systems. In addition, exposure to certain mycotoxins have been related

to cancerigenic and teratogenic effects in humans and animals.

The impact of some mycotoxins on the intestinal physiology is well known. In

addition to animal experiments, the recent use of cell lines mimicking human

intestinal epithelial cells (hIEC), demonstrated that many food-associated

mycotoxins (mainly aflatoxins, ochratoxins, patulin, fumonisin, trichothecenes,

zearalenone) are able to perturbate key intestinal functions such as: the

barrier function, the absorption of nutriments or the intestinal immunity. Based

on these publications, we recently critically analysed the potential role of

certain mycotoxins as etiologic agents in patients predisposed to IBD [Maresca

and Fantini, 2010].

Based on scientific publications reporting the action of single mycotoxin on

human intestinal epithelial cells and/or animals, we found that many mycotoxins

could be considered as at risk for this particular population based on: i) the

similarity existing between the pathophysiological process involved in the

on-set / the progression of IBD and in mycotoxicosis and ii) on the low security

factor existing in many cases between the doses of mycotoxin causing the

intestinal perturbations and the tolerable daily intact doses (TDI) fixed by

health and agricultural administrations.

Situtation could be even more dramatic if we consider that humans are not

exposed to single mycotoxin but rather to cocktail of mycotoxins and to mixture

of mycotoxins with others toxicans (such as phytotoxins, pesticides, heavy

metals) also able to perturbate the gut function [Mattsson, 2007]. In vitro

experiments on hIEC have already demonstrated that mixture of mycotoxins results

in addive and/or synergistic toxicity eventually leading to a decrease in the

efficient toxic dose of each compound of the mixture [Creppy et al., 2004;

Kouadio et al., 2007]. If such potentiation due to mixture of contaminants also

happens in vivo, it will have major consequence on the safety values of the the

tolerable daily intact doses (TDI).

Although epidemiologic studies are required to confirm our hypothesis, it seems

that certain food-associated mycotoxins have to be added to the list of

molecules and environmental factors potentially involved in the etiology of IBD

in predisposed patients. Effort must be made to limit further the exposure of

this particular population to mycotoxin-contaminated food.

We hope our hypothesis will stimulate discussions and will leads to an

epidemiologic evaluation of a link between food-associated mycotoxins and IBD.

Human intestinal inflammatory diseases or inflammatory bowel diseases (IBD) are

caracterized by chronic inflammation of the gut, leading to pain, malabsorption,

malnutrition, diarrhea and eventually to lethal complications such as cancers.

Among IBD, Crohn's and celiac diseases are the best know and caracterized. In

both cases, exacerbated immunity and auto-immunity reactions lead to persistent

intestinal inflammation. Although IBD depend primary on genetic predispositions

(associated with mutations in various genes involved in the intestinal immunity

and epithelial integrity) such genetic back-ground is not suffisant. Like in

many other diseases, the induction and the progression of IBD also critically

depend on environmental factors, such as food allergen (i.e. gluten) or bacteria

in celiac and Crohn's diseases, respectively.

Although many publications reported that some mycotoxins, described as

enterotoxic, are able to affect gut integrity and to cause intestinal

inflammation, a link between chronic exposure to mycotoxins and the induction

and/or persistance of IBD in predisposed patients was not proposed until

recently.

Mycotoxins are secondary metabolites produced by different fungal species,

mainly Penicillium, Aspergillus and Fusarium. Due to their antibiotic

activities, it is admitted that molds produce mycotoxins in their natural

environment (i.e. crops and plants) to kill others micro-organisms (bacteria,

others fungi) colonizing the same niche.

In addition to possess antibiotic activities, mycotoxins are known to affect the

cell functions in animals, including humans. Thus, mycotoxins are able to affect

the functions of numerious tissus and systems, including: i) renal, hepatic,

respiratory and intestinal epithelia and ii) the immune, reproductive and

nervous systems. In addition, exposure to certain mycotoxins have been related

to cancerigenic and teratogenic effects in humans and animals.

The impact of some mycotoxins on the intestinal physiology is well known. In

addition to animal experiments, the recent use of cell lines mimicking human

intestinal epithelial cells (hIEC), demonstrated that many food-associated

mycotoxins (mainly aflatoxins, ochratoxins, patulin, fumonisin, trichothecenes,

zearalenone) are able to perturbate key intestinal functions such as: the

barrier function, the absorption of nutriments or the intestinal immunity. Based

on these publications, we recently critically analysed the potential role of

certain mycotoxins as etiologic agents in patients predisposed to IBD [Maresca

and Fantini, 2010].

Based on scientific publications reporting the action of single mycotoxin on

human intestinal epithelial cells and/or animals, we found that many mycotoxins

could be considered as at risk for this particular population based on: i) the

similarity existing between the pathophysiological process involved in the

on-set / the progression of IBD and in mycotoxicosis and ii) on the low security

factor existing in many cases between the doses of mycotoxin causing the

intestinal perturbations and the tolerable daily intact doses (TDI) fixed by

health and agricultural administrations.

Situtation could be even more dramatic if we consider that humans are not

exposed to single mycotoxin but rather to cocktail of mycotoxins and to mixture

of mycotoxins with others toxicans (such as phytotoxins, pesticides, heavy

metals) also able to perturbate the gut function [Mattsson, 2007]. In vitro

experiments on hIEC have already demonstrated that mixture of mycotoxins results

in addive and/or synergistic toxicity eventually leading to a decrease in the

efficient toxic dose of each compound of the mixture [Creppy et al., 2004;

Kouadio et al., 2007]. If such potentiation due to mixture of contaminants also

happens in vivo, it will have major consequence on the safety values of the the

tolerable daily intact doses (TDI).

Although epidemiologic studies are required to confirm our hypothesis, it seems

that certain food-associated mycotoxins have to be added to the list of

molecules and environmental factors potentially involved in the etiology of IBD

in predisposed patients. Effort must be made to limit further the exposure of

this particular population to mycotoxin-contaminated food.

We hope our hypothesis will stimulate discussions and will leads to an

epidemiologic evaluation of a link between food-associated mycotoxins and IBD.

continue reading

Further reading

Abid-Essefi et al., (2009). Comparative study of toxic effects of zearalenone

and its two major metabolites alpha- zearalenol and beta-zearalenol on cultured

human Caco-2 cells. J Biochem Mol Toxicol. 23(4):233-43.

Bouhet S, Oswald IP. (2005). The effects of mycotoxins, fungal food

contaminants, on the intestinal epithelial cell-derived innate immune response.

Vet Immunol Immunopathol. 108(1-2):199-209.

Bouhet S, Oswald IP. (2007). The intestine as a possible target for fumonisin

toxicity. Mol Nutr Food Res. 51(8):925-31.

Caloni et al., (2002). Evaluation of Fumonisin B(1) and its metabolites

absorption and toxicity on intestinal cells line Caco- 2. Toxicon.

40(8):1181-188.

Caloni et al., (2006). Aflatoxin M1 absorption and cytotoxicity on human

intestinal in vitro model. Toxicon. 47(4):409-15.

Creppy et al., (2004). Synergistic effects of fumonisin B1 and ochratoxin A: are

in vitro cytotoxicity data predictive of in vivo acute toxicity? Toxicology.

201(1-3):115-23.

Diesing et al., (2010). Mycotoxin deoxynivalenol (DON) mediates biphasic

cellular response in intestinal porcine epithelial cell lines IPEC- 1 and

IPEC-J2. Toxicol Lett. In press.

Kasuga et al., (1998). In vitro effect of deoxynivalenol on the differentiation

of human colonic cell lines Caco- 2 and T84. Mycopathologia. 142(3):161-7.

Kouadio et al., (2005). Comparative study of cytotoxicity and oxidative stress

induced by deoxynivalenol, zearalenone or fumonisin B1 in human intestinal cell

line Caco-2. Toxicology. 213(1-2):56-65.

Kouadio et al., (2007). Effects of combinations of Fusarium mycotoxins on the

inhibition of macromolecular synthesis, malondialdehyde levels, DNA methylation

and fragmentation, and viability in Caco- 2 cells. Toxicon. 49(3):306-17.

Lambert et al., (2007). Ochratoxin A displaces claudins from detergent resistant

membrane microdomains. Biochem Biophys Res Commun. 358(2):632-6.

Mahfoud et al., (2002). pH-dependent interaction of fumonisin B1 with

cholesterol: physicochemical and molecular modeling studies at the air-water

interface. J Agric Food Chem. 50(2):327-31.

Mahfoud et al., (2002). The mycotoxin patulin alters the barrier function of the

intestinal epithelium: mechanism of action of the toxin and protective effects

of glutathione. Toxicol Appl Pharmacol. 181(3):209-18.

Maresca et al., (2001). The mycotoxin ochratoxin A alters intestinal barrier and

absorption functions but has no effect on chloride secretion. Toxicol Appl

Pharmacol. 176(1):54-63.

Maresca et al., (2002). The mycotoxin deoxynivalenol affects nutrient absorption

in human intestinal epithelial cells. J Nutr. 132(9):2723-31.

Maresca et al., (2008). Both direct and indirect effects account for the pro-

inflammatory activity of enteropathogenic mycotoxins on the human intestinal

epithelium: stimulation of interleukin-8 secretion, potentiation of interleukin-

1beta effect and increase in the transepithelial passage of commensal bacteria.

Toxicol Appl Pharmacol.228(1):84-92.

Maresca M, Fantini J. (2010) Some food-associated mycotoxins as potential risk

factors in humans predisposed to chronic intestinal inflammatory diseases.

Toxicon. 56(3):282-94.

Mattsson (2007). Mixtures in the real world: the importance of plant

McLaughlin et al., (2004). Ochratoxin A increases permeability through tight

junctions by removal of specific claudin isoforms. Am J Physiol Cell Physiol.

287(5):C1412-7.

McLaughlin et al., (2009). The mycotoxin patulin, modulates tight junctions in

caco- 2 cells. Toxicol In Vitro. 23(1):83-9.

Pestka (2010). Deoxynivalenol: mechanisms of action, human exposure, and

toxicological relevance. Arch Toxicol. 84(9):663-79.

Pinton et al., (2009). The food contaminant deoxynivalenol, decreases intestinal

barrier permeability and reduces claudin expression. Toxicol Appl Pharmacol.

237(1):41-8.

Pinton et al., (2010). Deoxynivalenol Impairs Porcine Intestinal Barrier

Function and Decreases the Protein Expression of Claudin- 4 through a

Mitogen-Activated Protein Kinase-Dependent Mechanism. J Nutr. 140(11):1956-62.

Razafimanjato et al. (2010). The food-associated fungal neurotoxin ochratoxin A

inhibits the absorption of glutamate by astrocytes through a decrease in cell

surface expression of the excitatory amino- acid transporters GLAST and

GLT-1.Neurotoxicology. 31(5):475-84.

[Guest guest]

I never had this problem until I was exposed in a WDB.

what you breath,you also eat.

and no, it hasn't gone away, and yes, my stomach and bowels are just as reactive

as the rest of my body and when the inflamation gets going it's painful.

a process of discovering what than caused flareups after my WDB exposure and

what I had to avoid became very important. first it was elimanating yeast foods,

corn,dairy,flour, than on to vinigar, can goods, eating only very fresh,actually

unripe fruits if any, than I just went for a year liveing only on greens and

white meat. took along time for the constant dierrhea to become not constant and

the blood that came along with it. some foods I can now tolerate that I couldn't

before.

I still get flareups. haveing this made CSM not tolerable for me,

and probably no other binders, getting constapated by toxin binders is not a

option when you have IBD. haveing that happen once will greatly detur you from

trying that again.

actually, it may be that constapation or not, toxin binders and IBD

just are not going to work well together, exspecially if the toxins you are

binding are the ones that caused the problem.

I have re-exposures cause immediate flareups in my stomach followed shortly by

running to the bathroom, and I not talking about re-exposure meaning something I

ate, I talking about breathing, still happens sometimes, smells, smelling

something I am reactive to

can bring this on just like eating something I'm reactive to.

same way it happened to me, still the same way it can happen now.

it's not just about what you eat.

>

> I had IBS  for years the funny thing is I think I got it from processed

foods. 

> When I stopped eating processed foods it resolved on it's own. 

>   

> God Bless !!

> dragonflymcs

> Mayleen

> >

> ________________________________

> From: KC <tigerpaw2c@...>

>

> Sent: Mon, October 25, 2010 9:13:56 PM

> Subject: [] Potential role played by mycotoxins in human

intestinal

> inflammatory diseases.

>

>  

> Potential role played by mycotoxins in human intestinal inflammatory diseases.

> Give feedback

>

> Dr Marc Maresca

> Université Cézanne

> Published on 25 October 2010

>

>

http://www.scitopics.com/Potential_role_played_by_mycotoxins_in_human_intestinal\

_inflammatory_diseases.html

>

>

> Human intestinal inflammatory diseases or inflammatory bowel diseases (IBD)

are

> caracterized by chronic inflammation of the gut, leading to pain,

malabsorption,

> malnutrition, diarrhea and eventually to lethal complications such as cancers.

> Among IBD, Crohn's and celiac diseases are the best know and caracterized. In

> both cases, exacerbated immunity and auto-immunity reactions lead to

persistent

> intestinal inflammation.

[Guest guest]

photoguy, have you had a colonopsy? just wondering.

it seems to me that unless your mucosal lineings are damaged where mycotoxins

may than get stuck in the tissues, maybe causeing polops or cysts that re-accure

that may be hard to catch at the right time with a colonopsy, the mycotoxins in

the intestines should pass on through. the liver is supposed to nutralize toxins

but I dont think

it does when mycotoxins are cerserned. ? just my thoughts.

I think it might be a better idea to have one of those camera pills swallowed

while your stomach and bowels are in a uproar to get the effects of whats going

on there documented, maybe, dont know.

I had a colonopsy,they did see one sore/cyst type thing in my stomach

but reports says the intestinal lineings are fine. I know better, but this is

what happens when doctors are not experts on this illness and dont know what to

look for and when. I dont think the one cyst in my stomach is the only one, I

think theres some in my bowels, no, they didn't find any hemeroids up in there

to blame the blood on.

I know for a fact that there is something in my bowels that when aggervated

swells with blood.

something they missed because it wasn't doing it's thing when the colonopsy was

done. and you dont get hemeroids from WDB exposure, you get polops,cysts. I

probably got all the hemeroids I was going to get with child birth, that was

along time ago.

from what I've read, it really takes a expert to see the slight change on color

from healthy pink /mucosal lineing in tact, from a damaged mucosal lineing and

raw tissue. of corse if I would have had the colonopsy done right after my

exposure it may have been better.

maybe if done while the inflammation is in action.

>

> Ok so how do i solve this problem? Thanks

>

>

>

[Guest guest]

Okay, so this is what I was wondering about.

My GI problems (inability to keep food down and malabsorption) have so far

caused me to lose over 30 pounds and 6-8 dress sizes. I am now a size zero and

keep losing. It turns out I don't have GERD and I only have mild gastroparesis.

My GI specialists are concerned because I am whittling down to nothing but so

far there isn't a reason why. More tests are in the works

Sent from my iPhone

On Oct 25, 2010, at 8:13 PM, " KC " <tigerpaw2c@...> wrote:

Potential role played by mycotoxins in human intestinal inflammatory diseases.

Give feedback

Dr Marc Maresca

Université Cézanne

Published on 25 October 2010

http://www.scitopics.com/Potential_role_played_by_mycotoxins_in_human_intestinal\

_inflammatory_diseases.html

Human intestinal inflammatory diseases or inflammatory bowel diseases (IBD) are

caracterized by chronic inflammation of the gut, leading to pain, malabsorption,

malnutrition, diarrhea and eventually to lethal complications such as cancers.

Among IBD, Crohn's and celiac diseases are the best know and caracterized. In

both cases, exacerbated immunity and auto-immunity reactions lead to persistent

intestinal inflammation. Although IBD depend primary on genetic predispositions

(associated with mutations in various genes involved in the intestinal immunity

and epithelial integrity) such genetic back-ground is not suffisant. Like in

many other diseases, the induction and the progression of IBD also critically

depend on environmental factors, such as food allergen (i.e. gluten) or bacteria

in celiac and Crohn's diseases, respectively.

Although many publications reported that some mycotoxins, described as

enterotoxic, are able to affect gut integrity and to cause intestinal

inflammation, a link between chronic exposure to mycotoxins and the induction

and/or persistance of IBD in predisposed patients was not proposed until

recently.

Mycotoxins are secondary metabolites produced by different fungal species,

mainly Penicillium, Aspergillus and Fusarium. Due to their antibiotic

activities, it is admitted that molds produce mycotoxins in their natural

environment (i.e. crops and plants) to kill others micro-organisms (bacteria,

others fungi) colonizing the same niche.

In addition to possess antibiotic activities, mycotoxins are known to affect the

cell functions in animals, including humans. Thus, mycotoxins are able to affect

the functions of numerious tissus and systems, including: i) renal, hepatic,

respiratory and intestinal epithelia and ii) the immune, reproductive and

nervous systems. In addition, exposure to certain mycotoxins have been related

to cancerigenic and teratogenic effects in humans and animals.

The impact of some mycotoxins on the intestinal physiology is well known. In

addition to animal experiments, the recent use of cell lines mimicking human

intestinal epithelial cells (hIEC), demonstrated that many food-associated

mycotoxins (mainly aflatoxins, ochratoxins, patulin, fumonisin, trichothecenes,

zearalenone) are able to perturbate key intestinal functions such as: the

barrier

[Guest guest]

I dont know why you would still be throwing up, did you get out of the WDB? I

lost alot of weight too. now, with practiceing advoidance I've gained it

back,plus. I'm still not getting the nutreints from my food I guess,I think my

body wants to store up fat cells now.

metabolism disorders probably doesn't help things.

hard to exercise with fatigue and fibromyalgia.

I used to walk alot, hard to do that with the chemical sensitivity and throat

always wanting to close up, constant thirst.

>

> Okay, so this is what I was wondering about.

>

> My GI problems (inability to keep food down and malabsorption) have so far

caused me to lose over 30 pounds and 6-8 dress sizes. I am now a size zero and

keep losing. It turns out I don't have GERD and I only have mild gastroparesis.

My GI specialists are concerned because I am whittling down to nothing but so

far there isn't a reason why. More tests are in the works

>

> Sent from my iPhone

>

>

[Guest guest]

My MD uses Doctor's Data Comprehensive Stool Analysis with Parasitology and

Genova GI panel. Genova is dna based and finds critters that DD might not but DD

has its own benefits. Either way.. good tests. A lab I think called Parasitology

is very good for detecting parasites.. better than labs above.

Metabolic Analysis Panel by Genova or the OAT (Organic Acids Test) are good

screeners for gut issues as well as many other issues.. cant remember

specificaly without looking at one.

An MD or ND who uses these tools and can integrate allopathic med with

alternative has been for me, a good way to go.

Entero labs has a very good set of tests for antibodies and other reactiosn to

gluten, milk, soy, egg.. gluten and milk being most important to us so the ones

we check.

Anyone can order a test from them. Most likely a good idea to go gluten free no

matter and to test dairy out of diet and see what happens.

The Specific Carbohydrate Diet and the GAPS diet are extreme and interesting

diets to consider. Both have support groups. Bee also has an interesting

candida diet.. extreme.. interesting.. (Healing Naturally with Bee.. I think)

Mercola and others have interesting perspectives on NO GRAINS.. this includes

the SCD as well as GAPS perspectives.

Dr Usman has the gut biofilm protocol.. google will find all of the above.. she

uses biofilm busters before the herb or abx. then clean up with a binder.

Digestive enzymes helped me quite a bit. Also addressing clostridia and strep

with vancomycin, though a way to go still .. much better. We tried other drugs

before the vanco and that one seemed to help me the most.

Robin

>

> You need professional medical help, not layman opinion. That said, I realize

it is difficult to find.

>

> But even worse is to try to continue to rely on those physicians who don't

know. We can't force them to believe or to treat contrary to their knowledge. If

they don't believe and aren't open to learning, stop seeing them.

>

>

[Guest guest]

Wm Croft, pathologist, sa_s that mold mcotoxins can destro_ the cilia in

digestive tract and the cilia is how the gi tract absorbs n_trients. He said he

has seen some where people didn't have an_ cilia left in gi tract so co_ldn't

get an_ benefit from food. If gi iss_es are a concern, I wo_ld think the mold

free diet AT LEAST, so _o_ don't swallow an_ m_cos. He also said the_ don't

grow back so be caref_l.

>

> I dont know why you would still be throwing up, did you get out of the WDB? I

lost alot of weight too. now, with practiceing advoidance I've gained it

back,plus. I'm still not getting the nutreints from my food I guess,I think my

body wants to store up fat cells now.

> metabolism disorders probably doesn't help things.

> hard to exercise with fatigue and fibromyalgia.

> I used to walk alot, hard to do that with the chemical sensitivity and throat

always wanting to close up, constant thirst.

>

>