Re: Mold and MCS

[Guest guest]

what about the fact that toxins can and do get to the brain by way of the nose

and olfactory system and that has nothing to do with the BBB.

>

> My understanding is that both Slaya and are chemically sensitive unless

they practice massive mold avoidance. Re-exposure to the mycotoxin(s) that they

are sensitive to brings back chemical sensitivity with a vengeance, as if

someone had flipped a switch.

>

> My theory is that massive avoidance lowers the matrix metalloproteinase (MMP)

enzymes that punch holes in the blood brain barrier and gives it a chance to

heal. For an idea of the time scales involved, PMID: 10663964 says that in rats

given a stroke it takes about 3 days for the blood brain barrier to collapse and

around a month for it to be restored.

>

> With an intact blood brain barrier, many chemicals are kept out of the brain

so they don't hurt even though the brain's NMDA receptors are still sensitized

from previous exposures. The inflammatory response to mycotoxins brings down the

blood brain barrier, chemicals are free to bum rush the brain, and the Dr. Pall

NO/ONOO- cycle spins up to peak fierceness.

>

[Guest guest]

sounds like you need to do some more homework before you write that book.

> >

> > My understanding is that both Slaya and are chemically sensitive unless

they practice massive mold avoidance. Re-exposure to the mycotoxin(s) that they

are sensitive to brings back chemical sensitivity with a vengeance, as if

someone had flipped a switch.

> >

> > My theory is that massive avoidance lowers the matrix metalloproteinase

(MMP) enzymes that punch holes in the blood brain barrier and gives it a chance

to heal. For an idea of the time scales involved, PMID: 10663964 says that in

rats given a stroke it takes about 3 days for the blood brain barrier to

collapse and around a month for it to be restored.

> >

> > With an intact blood brain barrier, many chemicals are kept out of the brain

so they don't hurt even though the brain's NMDA receptors are still sensitized

from previous exposures. The inflammatory response to mycotoxins brings down the

blood brain barrier, chemicals are free to bum rush the brain, and the Dr. Pall

NO/ONOO- cycle spins up to peak fierceness.

> >

>

[Guest guest]

> My understanding is that both Slaya and are chemically sensitive unless

they practice massive mold avoidance. Re-exposure to the mycotoxin(s) that they

are sensitive to brings back chemical sensitivity with a vengeance, as if

someone had flipped a switch.

> My theory is that massive avoidance lowers the matrix metalloproteinase (MMP)

enzymes that punch holes in the blood brain barrier and gives it a chance to

heal. For an idea of the time scales involved, PMID: 10663964 says that in rats

given a stroke it takes about 3 days for the blood brain barrier to collapse and

around a month for it to be restored.

> With an intact blood brain barrier, many chemicals are kept out of the brain

so they don't hurt even though the brain's NMDA receptors are still sensitized

from previous exposures. The inflammatory response to mycotoxins brings down the

blood brain barrier, chemicals are free to bum rush the brain, and the Dr. Pall

NO/ONOO- cycle spins up to peak fierceness.

Krillin, thanks for your response. I'd actually been meaning to ask you about

this.

That's an interesting article. Does it seem to you that this study does provide

pretty strong evidence that the BBB indeed can repair itself? I can't tell very

well just from the abstract how convincing it is.

(I'm going to paste it below in case anyone else wants to look at it.)

I found the following article interesting because it suggests that satratoxins

indeed can " punch holes " in the BBB:

http://etd.lib.ttu.edu/theses/available/etd-05252005-163223/unrestricted/Karunas\

ena_Enusha_Diss.pdf

OR

http://etd.lib.ttu.edu/theses/available/etd-05252005-163223/

Obviously certain other chemicals (such as formaldehyde) can cross the BBB

themselves, but I've yet to hear about any others that can cause perforations

that will allow other chemicals to get in as well. Are you aware of any that

can do that?

My experience with how my MCS is affected has been one of the interesting things

that I've learned from being down in the extreme avoidance " rabbit hole. "

For a while I did think/hope that my BBB had been wholly repaired. But my

experiences with the " switch " being flipped doesn't seem consistent with my

understanding that the BBB repairs itself slowly (as in this rat study) if at

all.

When I get too much mold exposure now, my MCS comes back suddenly and at exactly

the same level that it did before I started avoiding mold. It seems that 's

MCS comes back his pre-avoidance level (much worse than mine) when he gets mold

exposure as well.

For me, it usually takes a day or two of reasonably large mold exposures before

the switch flips. In 's case, when I was visiting, it was about six hours

after his first exposure of the day.

The MCS turns off fairly quickly too....maybe 1-3 days after avoidance is

resumed.

(Note that a similar thing happens with alcohol. I went for years and years not

being able to drink anything. Now I have no problems with any sort of alcohol,

unless I've gotten some mold exposures recently. Are Moldies sensitive to

alcohol because of the MCS or for other reasons, do you think?)

It seems to me reasonable to think that people might have multiple defenses to

keep chemicals from getting into our brains, considering how important that is

with regard to our survival.

So I wonder if we have some kind of protection mechanism that keeps chemicals

from doing us harm even if a) our BBB's are leaky or we're exposed to

toxins that do go in through the olfactory nerve.

Could this be related to Rich van Konynenberg's thoughts regarding the role of

glutathione, for example?

Intuitively it feels to me like my brain is still really vulnerable to stuff

getting inside of it, but that there's some process that's happening that's

keeping it at bay.

I'd love to hear other people's comments as well.

Best,

*

Acta Neuropathol. 2000 Mar;99(3):231-7.

Impairment and restoration of the endothelial blood-brain barrier in the rat

cerebral infarction model assessed by expression of endothelial barrier antigen

immunoreactivity.

Nishigaya K, Yagi S, Sato T, Kanemaru K, Nukui H.

Department of Neurosurgery, Yamanashi Medical University, Nakakoma-gun,

Yamanashi, Japan.

Endothelial barrier antigen (EBA) can be used to detect the blood-brain barrier

in the central nervous system of rats. This study investigated the temporal

profile of antigen expression in cerebral vessels after infarction and assessed

the relationship between re-establishment of this antigen in newly formed

vessels and astrocytes around these vessels. Rats were subjected to cerebral

ischemia for 2 h by the intraluminal thread method, then killed after 1, 3, 7,

14 and 28 days. Perfusion-fixed paraffin-embedded brains were immunostained for

detection of EBA and glial fibrillary acidic protein (GFAP) by the

streptavidin-biotin-peroxidase complex method. EBA immunostaining in vessels in

the infarcted lesion was reduced at day 1 and had almost disappeared by day 3.

Newly formed vessels were found from day 3, but were not stained at day 7.

However, these new vessels were weakly stained at day 14 and definitely stained

at day 28. GFAP immunostaining was completely negative around these

proliferating vessels. The temporal profile of disappearance and re-expression

of EBA in cerebral infarcted lesion may be associated with aggravation and

improvement of brain edema, although barrier permeability was not explored in

this study. The expression of this antigen has no relationship to the formation

of astrocyte/endothelial contacts.

PMID: 10663964 [PubMed - indexed for MEDLINE]

[Guest guest]

well, as many of us here know, those little rat studies just sometimes aren't

very

reliable.  I have a therory that short term studies, like short term thinking

can lack

credability in many areas. kindof like a short term fix to a water leak thats

causeing mold growth in the home, it just wont do.

maybe they should see how long the BBB can suffer the chronic insult of exposure

before it get's to the point of not being able to heal itself.

because a short term insult  by toxins, oxidative stress , ect.  is basically

discribing a short term exposure and/or a exposure not bad enough to cause any

major long term damage and  chances are that you might just recover from that

anyway.

 

 

well, I have more important things to do than rehash old thoughts /therories and

things that have allready been discused in detail in this group.

 

bye bye eric.

> My understanding is that both Slaya and are chemically sensitive unless

they practice massive mold avoidance. Re-exposure to the mycotoxin(s) that they

are sensitive to brings back chemical sensitivity with a vengeance, as if

someone had flipped a switch.

> My theory is that massive avoidance lowers the matrix metalloproteinase (MMP)

enzymes that punch holes in the blood brain barrier and gives it a chance to

heal. For an idea of the time scales involved, PMID: 10663964 says that in rats

given a stroke it takes about 3 days for the blood brain barrier to collapse and

around a month for it to be restored.

> With an intact blood brain barrier, many chemicals are kept out of the brain

so they don't hurt even though the brain's NMDA receptors are still sensitized

from previous exposures. The inflammatory response to mycotoxins brings down the

blood brain barrier, chemicals are free to bum rush the brain, and the Dr. Pall

NO/ONOO- cycle spins up to peak fierceness.

Krillin, thanks for your response.  I'd actually been meaning to ask you about

this.

That's an interesting article.  Does it seem to you that this study does provide

pretty strong evidence that the BBB indeed can repair itself?  I can't tell very

well just from the abstract how convincing it is.

(I'm going to paste it below in case anyone else wants to look at it.)

I found the following article interesting because it suggests that satratoxins

indeed can " punch holes " in the BBB:

http://etd.lib.ttu.edu/theses/available/etd-05252005-163223/unrestricted/Karunas\

ena_Enusha_Diss.pdf

OR

http://etd.lib.ttu.edu/theses/available/etd-05252005-163223/

Obviously certain other chemicals (such as formaldehyde) can cross the BBB

themselves, but I've yet to hear about any others that can cause perforations

that will allow other chemicals to get in as well.  Are you aware of any that

can do that?

My experience with how my MCS is affected has been one of the interesting things

that I've learned from being down in the extreme avoidance " rabbit hole. "

For a while I did think/hope that my BBB had been wholly repaired.  But my

experiences with the " switch " being flipped doesn't seem consistent with my

understanding that the BBB repairs itself slowly (as in this rat study) if at

all.

When I get too much mold exposure now, my MCS comes back suddenly and at exactly

the same level that it did before I started avoiding mold.  It seems that 's

MCS comes back his pre-avoidance level (much worse than mine) when he gets mold

exposure as well.

For me, it usually takes a day or two of reasonably large mold exposures before

the switch flips.  In 's case, when I was visiting, it was about six hours

after his first exposure of the day.

The MCS turns off fairly quickly too....maybe 1-3 days after avoidance is

resumed.

(Note that a similar thing happens with alcohol.  I went for years and years not

being able to drink anything.  Now I have no problems with any sort of alcohol,

unless I've gotten some mold exposures recently.  Are Moldies sensitive to

alcohol because of the MCS or for other reasons, do you think?)

It seems to me reasonable to think that people might have multiple defenses to

keep chemicals from getting into our brains, considering how important that is

with regard to our survival.

So I wonder if we have some kind of protection mechanism that keeps chemicals

from doing us harm even if  a) our BBB's are leaky  or  we're exposed to

toxins that do go in through the olfactory nerve.

Could this be related to Rich van Konynenberg's thoughts regarding the role of

glutathione, for example?

Intuitively it feels to me like my brain is still really vulnerable to stuff

getting inside of it, but that there's some process that's happening that's

keeping it at bay.

I'd love to hear other people's comments as well.

Best,

*

Acta Neuropathol. 2000 Mar;99(3):231-7.

Impairment and restoration of the endothelial blood-brain barrier in the rat

cerebral infarction model assessed by expression of endothelial barrier antigen

immunoreactivity.

Nishigaya K, Yagi S, Sato T, Kanemaru K, Nukui H.

Department of Neurosurgery, Yamanashi Medical University, Nakakoma-gun,

Yamanashi, Japan.

Endothelial barrier antigen (EBA) can be used to detect the blood-brain barrier

in the central nervous system of rats. This study investigated the temporal

profile of antigen expression in cerebral vessels after infarction and assessed

the relationship between re-establishment of this antigen in newly formed

vessels and astrocytes around these vessels. Rats were subjected to cerebral

ischemia for 2 h by the intraluminal thread method, then killed after 1, 3, 7,

14 and 28 days. Perfusion-fixed paraffin-embedded brains were immunostained for

detection of EBA and glial fibrillary acidic protein (GFAP) by the

streptavidin-biotin-peroxidase complex method. EBA immunostaining in vessels in

the infarcted lesion was reduced at day 1 and had almost disappeared by day 3.

Newly formed vessels were found from day 3, but were not stained at day 7.

However, these new vessels were weakly stained at day 14 and definitely stained

at day 28. GFAP immunostaining was

completely negative around these proliferating vessels. The temporal profile of

disappearance and re-expression of EBA in cerebral infarcted lesion may be

associated with aggravation and improvement of brain edema, although barrier

permeability was not explored in this study. The expression of this antigen has

no relationship to the formation of astrocyte/endothelial contacts.

PMID: 10663964 [PubMed - indexed for MEDLINE]

--- End forwarded message ---

[Guest guest]

> >

> > what about the fact that toxins can and do get to the brain by way

> > of the nose and olfactory system and that has nothing to do with

> > the BBB.

Slaya's the one who is composing a document about observations and possible

mechanisms of severe mold reactors, not me. I don't even react to mold that way.

I'm only hypersensitive to the volatile non-persistent mold chemicals

(1,4-dialdehydes are possible suspects) that activate the TRPA1 receptor and are

only released when it's humid.

(Or are you alluding to the ribbing that Stewie frequently gave about his

book-in-progress on " The Family Guy " ?)

http://www.yourdailymedia.com/media/1138015227

The lungs have at least four orders of magnitude more surface area available for

mass transfer than the nose, and they're probably more permeable. So with a

defective BBB, you get massively higher doses to the brain from the lungs than

from the nose. It seems perfectly reasonable to me that someone could shrug off

the trickle of chemicals getting in through the nose, but be devastated by the

flood of chemicals getting in through the lungs. Here are my calculations:

This paper found that human lungs have 24-69 square meters of surface area.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1271180/?page=9

PMID: 15858850 says that the olfactory epithelium is the most probable route of

nasal chemical absorption, PMID: 9772217 says that the olfactory epithelium

comprises less than 5% of the human nasal cavity, and this paper reported human

nasal cavity surfaces areas averaging 20,120 square mm.

http://jap.physiology.org/cgi/content/full/103/3/1082/T1

20,120 square mm * 5% = 1006 square mm = 0.001006 square meters

24/0.001006 = lungs have at least 24,000 times as much surface area as the

olfactory epithelium.

[Guest guest]

The lungs have at least four orders of magnitude more surface area available for

mass transfer than the nose, and they're probably more permeable. So with a

defective BBB, you get massively higher doses to the brain from the lungs than

from the nose. It seems perfectly reasonable to me that someone could shrug off

the trickle of chemicals getting in through the nose, but be devastated by the

flood of chemicals getting in through the lungs. Here are my calculations:

is this based on dose or level or organ damage ?

or are you talking about someone who received little or no organ damage?

you just made my point, maybe it seems reasonable for you to think that way

because you have not live with or researched how the chronic assult of toxins

can damage the olfactory system and beyond.

are you saying that after the damage is done that it still takes large doses to

cause the same reacuuring effects ?

sorry, your message is just to generalized, again , assumpsion that everyone

recieves the same level of damage to all the same organs might leave your theory

lacking and I'm not up thinking or typeing much rught now as my sinuses are

bothering me.

[Guest guest]

> That's an interesting article. Does it seem to you that this study

> does provide pretty strong evidence that the BBB indeed can repair

> itself? I can't tell very well just from the abstract how

> convincing it is.

The peer reviewers let them say in the title that the barrier was restored, so

I'm convinced. I also found some papers about an MS drug currently in clinical

trials (fingolimod) that confirm that the BBB can be repaired. In rats

" Late-stage rescue therapy with FTY720, even up to 1 month after EAE onset,

reversed BBB leakiness and reduced demyelination, along with normalization of

neurologic function. " (PMID: 18540945). In humans, " After 24 months, 79 to 91%

of patients were free from Gd(+) lesions and up to 77% of patients remained

relapse free. " (PMID: 19122034) I think that Gd(+) lesions are those that are

currently inflamed by autoimmune T-cells getting into the brain through a

compromised BBB.

> Obviously certain other chemicals (such as formaldehyde) can cross

> the BBB themselves, but I've yet to hear about any others that can

> cause perforations that will allow other chemicals to get in as

> well. Are you aware of any that can do that?

All I have in my notes is PMID: 12270692 where a cocktail of Gulf War chemicals

(pyridostigmine bromide, DEET, and permethrin) in the presence of stress did it.

> For me, it usually takes a day or two of reasonably large mold

> exposures before the switch flips. In 's case, when I was

> visiting, it was about six hours after his first exposure of the

> day.

>

> The MCS turns off fairly quickly too....maybe 1-3 days after

> avoidance is resumed.

That does complicate things. Your first recovery from MCS took 8 months, so

perhaps the BBB matrix was chewed up then, and perhaps the brief mold exposures

are just interfering with cell adhesion. I wonder if a good analogy would be:

first the window is slid open, and then it gets smashed to bits.

This abstract has just such a two-step process, and gives us one more chemical

that brings down the BBB: phorbol esters, a component of tung oil (which by the

way is associated with CFS). In the short term, cell-cell contacts get

disrupted. Long-term, MMP-9 gets upregulated and (I presume) munches away at the

matrix.

Brain Res. 2005 Nov 30;1063(2):168-79.

Phorbol ester induced short- and long-term permeabilization of the blood-CSF

barrier in vitro.

Angelow S, Zeni P, Höhn B, Galla HJ.

Institut für Biochemie, Westfälische Wilhelms-Universität, Wilhelm-Klemm-Strasse

2, D-48149 Münster, Germany.

Interconnected by tight junctions, the epithelial cells of the choroid plexus

form a barrier separating the cerebrospinal fluid (CSF) from blood. Using an in

vitro model based on porcine choroid plexus epithelial cells (PCPEC), we

investigated the influence of PKC activating phorbol 12-myristate 13-acetate

(PMA) on barrier properties and analyzed mechanisms involved in the regulation

of barrier tightness. Applied in concentrations of 5-25 nM, PMA induced a fast

and lasting decrease of the transepithelial electrical resistance (TER), which

could be blocked by rottlerin, indicating the involvement of PKCdelta in signal

transduction. The immediate impairment of barrier integrity was accompanied by

dephosphorylation of occludin and formation of actin bundles. Moreover, in the

presence of at least 25 nM PMA, changes of cell shape as well as discontinuities

of tight junction strands were observed, suggesting the disruption of cell-cell

contacts. Exposure to PMA for 1-2 days additionally induced down-regulation of

claudin-2 and up-regulation of barrier modulating matrix metalloproteinase

(MMP)-9, respectively. The results show that different interconnected mechanisms

directly and indirectly targeting at the tight junctions are released by PMA

contributing to the short-term and long-term decrease of TER and opening of the

blood-CSF barrier in vitro.

PMID: 16271356

Here's a paper called " Vascular matrix adhesion and the blood–brain barrier " for

more background.

http://www.biochemsoctrans.org/bst/034/1261/bst0341261.htm

I wonder if getting 25-OH vitamin D to 40-50 ng/ml (that's my target) would be

protective, since it induces adhesion proteins in colon and breast cancer

(PMIDs: 11470825 and 17288543) and lowers MMP-9 (PMID: 19615945 etc.).

> (Note that a similar thing happens with alcohol. I went for years

> and years not being able to drink anything. Now I have no problems

> with any sort of alcohol, unless I've gotten some mold exposures

> recently. Are Moldies sensitive to alcohol because of the MCS or

> for other reasons, do you think?)

Goldstein theorized that alcohol depletes an already low level of dopamine

and/or norepinephrine in neurosomatics. (His word for Dr. Pall's 10th Paradigm

diseases.) In parts of the brain involved in attention, whenever NMDA receptors

fire, DA and NE have to be released to get a decent signal to noise ratio. If

the NMDA receptors are overactive a la Dr. Pall's NO/ONOO- cycle, DA and NE get

depleted and the brain's circuits get totally messed up.

http://books.google.com/books?id=7ccB3CCAtYkC & printsec=frontcover & dq=tuning+the+\

brain#v=onepage & q=alcohol & f=false

One final thought: would you characterize your first mold sabbatical experience

as moving from a masking state to the alarm state, in Dr. Rea's MCS terminology?

http://books.google.com/books?id=bWIQWjR_MZEC & pg=PA24 & lpg=PA24 & dq=rea+masking+al\

arm & source=bl & ots=MTw0xCY8Z_ & sig=8SR8iULdRjXX5iJIDM4okkBdYAs & hl=en & ei=SWUkS5S_Go\

uMswO-xp3hDg & sa=X & oi=book_result & ct=result & resnum=1 & ved=0CAgQ6AEwAA#v=onepage & q=\

& f=false

[Guest guest]

first you site a 2000 article that you might want to reed a little closer,

claiming BBB heals itself, next you conclude that you think the effects to the

brain from the nose route are minor, I'm telling you your wrong. you can post

your theories all you want, I'm not reading them, I tell you some facts that you

could go spend some time researching but I not helping anyone write their book.

>

> > That's an interesting article. Does it seem to you that this study

> > does provide pretty strong evidence that the BBB indeed can repair

> > itself? I can't tell very well just from the abstract how

> > convincing it is.

>

> The peer reviewers let them say in the title that the barrier was restored, so

I'm convinced. I also found some papers about an MS drug currently in clinical

trials (fingolimod) that confirm that the BBB can be repaired. In rats

" Late-stage rescue therapy with FTY720, even up to 1 month after EAE onset,

reversed BBB leakiness and reduced demyelination, along with normalization of

neurologic function. " (PMID: 18540945). In humans, " After 24 months, 79 to 91%

of patients were free from Gd(+) lesions and up to 77% of patients remained

relapse free. " (PMID: 19122034) I think that Gd(+) lesions are those that are

currently inflamed by autoimmune T-cells getting into the brain through a

compromised BBB.

>

> > Obviously certain other chemicals (such as formaldehyde) can cross

> > the BBB themselves, but I've yet to hear about any others that can

> > cause perforations that will allow other chemicals to get in as

> > well. Are you aware of any that can do that?

>

> All I have in my notes is PMID: 12270692 where a cocktail of Gulf War

chemicals (pyridostigmine bromide, DEET, and permethrin) in the presence of

stress did it.

>

> > For me, it usually takes a day or two of reasonably large mold

> > exposures before the switch flips. In 's case, when I was

> > visiting, it was about six hours after his first exposure of the

> > day.

> >

> > The MCS turns off fairly quickly too....maybe 1-3 days after

> > avoidance is resumed.

>

> That does complicate things. Your first recovery from MCS took 8 months, so

perhaps the BBB matrix was chewed up then, and perhaps the brief mold exposures

are just interfering with cell adhesion. I wonder if a good analogy would be:

first the window is slid open, and then it gets smashed to bits.

>

> This abstract has just such a two-step process, and gives us one more chemical

that brings down the BBB: phorbol esters, a component of tung oil (which by the

way is associated with CFS). In the short term, cell-cell contacts get

disrupted. Long-term, MMP-9 gets upregulated and (I presume) munches away at the

matrix.

>

> Brain Res. 2005 Nov 30;1063(2):168-79.

> Phorbol ester induced short- and long-term permeabilization of the blood-CSF

barrier in vitro.

> Angelow S, Zeni P, Höhn B, Galla HJ.

> Institut für Biochemie, Westfälische Wilhelms-Universität,

Wilhelm-Klemm-Strasse 2, D-48149 Münster, Germany.

>

> Interconnected by tight junctions, the epithelial cells of the choroid plexus

form a barrier separating the cerebrospinal fluid (CSF) from blood. Using an in

vitro model based on porcine choroid plexus epithelial cells (PCPEC), we

investigated the influence of PKC activating phorbol 12-myristate 13-acetate

(PMA) on barrier properties and analyzed mechanisms involved in the regulation

of barrier tightness. Applied in concentrations of 5-25 nM, PMA induced a fast

and lasting decrease of the transepithelial electrical resistance (TER), which

could be blocked by rottlerin, indicating the involvement of PKCdelta in signal

transduction. The immediate impairment of barrier integrity was accompanied by

dephosphorylation of occludin and formation of actin bundles. Moreover, in the

presence of at least 25 nM PMA, changes of cell shape as well as discontinuities

of tight junction strands were observed, suggesting the disruption of cell-cell

contacts. Exposure to PMA for 1-2 days additionally induced down-regulation of

claudin-2 and up-regulation of barrier modulating matrix metalloproteinase

(MMP)-9, respectively. The results show that different interconnected mechanisms

directly and indirectly targeting at the tight junctions are released by PMA

contributing to the short-term and long-term decrease of TER and opening of the

blood-CSF barrier in vitro.

>

> PMID: 16271356

>

> Here's a paper called " Vascular matrix adhesion and the blood–brain barrier "

for more background.

>

> http://www.biochemsoctrans.org/bst/034/1261/bst0341261.htm

>

> I wonder if getting 25-OH vitamin D to 40-50 ng/ml (that's my target) would be

protective, since it induces adhesion proteins in colon and breast cancer

(PMIDs: 11470825 and 17288543) and lowers MMP-9 (PMID: 19615945 etc.).

>

> > (Note that a similar thing happens with alcohol. I went for years

> > and years not being able to drink anything. Now I have no problems

> > with any sort of alcohol, unless I've gotten some mold exposures

> > recently. Are Moldies sensitive to alcohol because of the MCS or

> > for other reasons, do you think?)

>

> Goldstein theorized that alcohol depletes an already low level of dopamine

and/or norepinephrine in neurosomatics. (His word for Dr. Pall's 10th Paradigm

diseases.) In parts of the brain involved in attention, whenever NMDA receptors

fire, DA and NE have to be released to get a decent signal to noise ratio. If

the NMDA receptors are overactive a la Dr. Pall's NO/ONOO- cycle, DA and NE get

depleted and the brain's circuits get totally messed up.

>

>

http://books.google.com/books?id=7ccB3CCAtYkC & printsec=frontcover & dq=tuning+the+\

brain#v=onepage & q=alcohol & f=false

>

> One final thought: would you characterize your first mold sabbatical

experience as moving from a masking state to the alarm state, in Dr. Rea's MCS

terminology?

>

>

http://books.google.com/books?id=bWIQWjR_MZEC & pg=PA24 & lpg=PA24 & dq=rea+masking+al\

arm & source=bl & ots=MTw0xCY8Z_ & sig=8SR8iULdRjXX5iJIDM4okkBdYAs & hl=en & ei=SWUkS5S_Go\

uMswO-xp3hDg & sa=X & oi=book_result & ct=result & resnum=1 & ved=0CAgQ6AEwAA#v=onepage & q=\

& f=false

>

[Guest guest]

heres a tip, maybe you overlooked with your math, you applied both of what I

mentioned below to lung effects and neither to the effects of what can happen on

from breathing paticles up the nose, enless you breath with your mouth open all

the time, and maybe you do, you might want to reconsider your thoughts, and you

have not considered the word " chronic " or applied in your theory of thinking.

if your here with the purpose of trying to convience people that the damage to

the brain is nothing, your in the wrong place.

>

> The lungs have at least four orders of magnitude more surface area available

for mass transfer than the nose, and they're probably more permeable. So with a

defective BBB, you get massively higher doses to the brain from the lungs than

from the nose. It seems perfectly reasonable to me that someone could shrug off

the trickle of chemicals getting in through the nose, but be devastated by the

flood of chemicals getting in through the lungs. Here are my calculations:

>

> is this based on dose or level or organ damage ?

> or are you talking about someone who received little or no organ damage?

>

> you just made my point, maybe it seems reasonable for you to think that way

because you have not live with or researched how the chronic assult of toxins

can damage the olfactory system and beyond.

>

> are you saying that after the damage is done that it still takes large doses

to cause the same reacuuring effects ?

>

> sorry, your message is just to generalized, again , assumpsion that everyone

recieves the same level of damage to all the same organs might leave your theory

lacking and I'm not up thinking or typeing much rught now as my sinuses are

bothering me.

>

[Guest guest]

krillin5@.The peer reviewers let them say in the title that the barrier was

restored, so I'm convinced.

>60 % of abstracts are wrong, you might fight want to do some major research on

how the mucus system,and olfactory system . but, like I said before, if if you

haven't lived it you just probably wont get it.

[Guest guest]

>krillin5@... wrote: I'm only hypersensitive to the volatile non-persistent mold

chemicals (1,4-dialdehydes are possible suspects) that activate the TRPA1

receptor and are only released when it's humid.

elium.

I dont think this quilifies you to make any theories about the nose to brain

effects,damage or anything else.

you can site abstracts all you want. you obviously dont have a clue about what

can happen with long term exposure, or anything beyond your version of MCS.

[Guest guest]

heres something else you might want to mix in with your theory,

the small airways, and what happens with reactive airway disorders,

you know, what most people suffer with MCS, reactive airways that tend to close

up, possably greatly cutting down on what actually makes it to the lungs.

>

> krillin5@... peer reviewers let them say in the title that the barrier was

restored, so I'm convinced.

>

> >60 % of abstracts are wrong, you might fight want to do some major research

on how the mucus system,and olfactory system . but, like I said before, if if

you haven't lived it you just probably wont get it.

>

[Guest guest]

>> The lungs have at least four orders of magnitude more surface area

>> available for mass transfer than the nose, and they're probably

>> more permeable. So with a defective BBB, you get massively higher

>> doses to the brain from the lungs than from the nose. It seems

>> perfectly reasonable to me that someone could shrug off the

>> trickle of chemicals getting in through the nose, but be

>> devastated by the flood of chemicals getting in through the lungs.

> sorry, your message is just to generalized, again , assumpsion that

> everyone recieves the same level of damage to all the same organs

> might leave your theory lacking and I'm not up thinking or typeing

> much rught now as my sinuses are bothering me.

Your irrational hatred of the set-up-a-tent-in-the-godforsaken-desert crowd has

blinded you to the fact that I'm merely proposing a mechanism to explain Slaya's

intriguing MCS observations. Carefully re-read my words above and note how I

wrote " someone could shrug off " and not " everyone does shrug off " .

Do you have a better mechanism, or is she just lying through her teeth?

[Guest guest]

>

> first you site a 2000 article that you might want to reed a little

> closer, claiming BBB heals itself, next you conclude that you think

> the effects to the brain from the nose route are minor, I'm telling

> you your wrong. you can post your theories all you want, I'm not

> reading them, I tell you some facts that you could go spend some

> time researching but I not helping anyone write their book.

What is your critique of the three references I provided to support the idea

that the BBB can be repaired under the right conditions? You can't just expect

us to take your word for it that they're all wrong.

I concluded that the nose route was minor compared to the lung route. I did not

say that the nose route was incapable of causing harm in anyone and I resent the

implication.

[Guest guest]

krillin5@...> wrote:Your irrational hatred of the

set-up-a-tent-in-the-godforsaken-desert crowd has blinded you to the fact that

I'm merely proposing a mechanism to explain Slaya's intriguing MCS observations.

Carefully re-read my words above and note how I wrote " someone could shrug off "

and not " everyone does shrug off " .

>

> Do you have a better mechanism, or is she just lying through her teeth?

>

I could care less who you live with or who your friends are.

I had already commented about the BBB,

what I said is that your theory of lung vs. up the nose, and your math is wrong.

to did not take everything into consideratation.

I also said that I'm not helping anyone write their book.

meaning, that if you want to come in here throwing a theory around

do your homework first.

now it may have made you angry that I believe your math and theory are greatly

lacking, but like I said, I dont think you can conclude anything by just what

you posted.

so, if it makes to fell better to bring my fellings about someone else up , than

fine, go right ahead cause at this point it's probably becomeing a reality

anyway.