Enterohepatic recirculation, cholestyramine. toxin elimination rate?

[Guest guest]

Haley,

No, this is very wrong.. Its never 'before they make trouble'

They do make trouble, but, especially when we are in our 20s and early 30s,

some of us are well enough to not notice it,

while others are sick from cumulative exposure AND bio-accumulation.

Genetics do matter

but its in cases of chronic exposure where they matter the most.

Yes, genetics do matter.. But the genetics dont come into play until

the toxins

get inside the body and even under the best of genetic conditions,

they do damge at the point of contact, in the bloodstream,

and liver, brain still linger

doing damage.. the genetic question is how long.. Other things effect

that factor too.

>

>

> My recollection from reading Mold Warriors is that it isn't a pre-

disposition to get sick, exactly, it's that some of *us* (I haven't

been tested, but believe I'm in this group) don't make vital

antibodies that address and remove biotoxins. What happens when

we're exposed is that these toxins get in us and keep running around

wreaking havoc, whereas for others they would be eliminated from the

body before they make trouble... hence some of us get sick while

others can have limited or no ill effects under certain

circumstances...

I think it's pretty clear that mycotoxins, pretty much all of the

toxins like the trichothecenes, aflatoxin, ochratoxin, and many

others, are frequently toxic to every living thing. They have yeast

assay methods that can quantitatively measure direct toxicity and

several important kinds of toxic effect are not effected by genetics

at all.

Where genetics does matter is, as Dr. Shoemaker explained in Mold

Warriors and lots of other science shows too, is in a specific thing

called enterohepatic recirculation of mold toxins.

Cytotoxic mycotoxins, for example, damage everything they touch, on

the surface of the body, they can damage the eyes, the nasal passages,

the lungs, the throat, the gut (much of what you breathe that doesn't

get absorbed ends up in the stomach if the cillia manage to remove it

) then it gets absorbed into the bloodstream where it goes into the

brain, the liver, the kidne and other organs, the fate of different

mycotoxins varies, depending on a lot of different things. But the

liver does eventually try to remove them, and if it succeeds they go

into the bile which is manufactured in the liver and then stored in

the gall bladder, and its released when you need to digest food.

That is where " enterohepatic recirculation " of the mold toxins and

cholestyramine comes in.

Nutritive status, (especially glutathione) and indirecty, age matters

too. Malnourished and older people are much more prone to damage from

mycotoxins.

Youth does too. Babies and children are particularly vulnerable to

lifelong damage from inhibition of protein synthesis because it

prevents their brains, lungs, etc, from growing and repairing

themselves.

Everything I have seen and experienced screams to me that cumulative

damage from mold is additive. The more you have been exposed, the more

they make you ill.

Mold TOXICITY causes 'mold allergy'

There is another situation too, In VERY high dose situations, these

toxins are able to kill, rapidly.

THEN, the cumulative effect that might have caused a massive allergic

reaction or genetics don't matter much at all because they would have

happened hours after the exposure. In the meantime the animal or

person has died from direct toxicity.

Dr. Shoemaker says that 24% of us have one of the genotypes.

A good way to look at that is that for half of all the couples in

America, for example, AT LEAST one member of the partner has one of

the HLA-DR types that Dr. Shoemaker mentions.

For families of three people or more, the odds are MUCH more than 50%

that they will have a family member whose health is threatened.

Children might not be good at articulating why or how they are getting

sick, but its still dangerous for them.

For older people, also, any source of inflammation can hit

particularly hard too.

These factors really come into play in chronic, repeated exposure

situations. A short exposure at a mall might not effect most people,

but it would effect us.

Longer term exposures can be really dangerous.

Neurotoxicol Teratol. 2005 Sep-Oct;27(5):733-43. Epub 2005 Aug 15.

Related Articles, Links

Click here to read

Chronic biotoxin-associated illness: multiple-system symptoms, a

vision deficit, and effective treatment.

Hudnell HK.

U.S. Environmental Protection Agency, Office of Research and

Development, National Health and Environmental Effects Research

Laboratory, Neurotoxicology Division, MD:B105-05, Research Triangle

Park, NC 27711, USA. hundell.ken@...

Blooms of toxigenic organisms have increased in spatial and

temporal extent due to human activities and natural forces that alter

ecologic habitats and pollute the environment. In aquatic

environments, harmful algal blooms pose a risk for human health, the

viability of organisms, and the sustainability of ecosystems. The

estuarine dinoflagellate, Pfiesteria piscicida, was discovered in the

late 1980s at North Carolina State University as a contaminant in fish

cultures. P. piscicida was associated with fish death in laboratory

aquaria, and illness among laboratory workers who inhaled the mist

above aquaria. Both the fish and humans exhibited signs of toxicity.

During the 1990s, large-scale mortality among fish and other aquatic

organisms was associated with high concentrations of Pfiesteria sp. in

estuaries on the eastern seaboard of North America from New York to

Texas. Illness among humans was associated with direct exposure to

estuaries and exposures to estuarine aerosols around the time of

Pfiesteria-related fish kills. This review of the scientific

literature on associations between Pfiesteria and human illness

identified some of the possible mechanisms of action by which putative

Pfiesteria toxins may have caused morbidity. Particular attention was

given to the Pfiesteria-associated, human-illness syndrome known as

Possible Estuary Associated Syndrome (PEAS). PEAS was characterized by

multiple-system symptoms, deficits in neuropsychological tests of

cognitive function, and rapid and severe decrements in visual contrast

sensitivity (VCS), an indicator of neurologic function in the visual

system. PEAS was diagnosed in acute and chronic illness cases, and was

reacquired during re-exposure. Rapid normalization of PEAS signs and

symptoms was achieved through the use of cholestyramine therapy.

Cholestyramine, a non-absorbable polymer, has been used by humans to

lower cholesterol levels since it was approved for that use by the

U.S. Food and Drug Administration in 1958. When dissolved in water or

juice and taken orally, cholestyramine binds with cholesterol, bile

acids, and salts in the intestines, causing them to be eliminated

rather than reabsorbed with bile during enterohepatic recirculation.

Cholestyramine also has been reported to bind and eliminate a variety

of toxic substances. The efficacy of cholestyramine therapy in

treatment of PEAS supported the hypothesis that PEAS is a

biotoxin-associated illness.

Publication Types:

* Review

PMID: 16102938 [PubMed - indexed for MEDLINE]