Re: 2 grand mals in two days

September 3, 2000

Kathy,

I have liver congestion at times (been mercury detoxing for years) and take

Thorne's Lipotrepein which is a mix of a few vitamins & herbs. Milk thistle

is also supposed to help. Surprising they didn't " prescribe " anything to

help the liver let down more bile. Could the meds he's on be contributing?

Also, is he getting enough EFAs? I know when I'm bile deficient by lighter

colored stools. Do you have Andy's book? I can't remember if its mentioned

in there or not.

My prayers go out to you.

Janice in TX

September 3, 2000

Kathy,

I once had epilepsy too. Lots of grand mals. Seizures began around

puberty. If I forgot to take my dilantin, I was sure to have a grand

mal. Perhaps you are weaning too fast from the dilantin. I also had

lots of petit mals.

About 20 years ago, I was weaned VERY SLOWLY from dilantin. I've

never had a seizure again. I'm in my mid-40s now.

(Cary, NC)

persistentC@...

[ ] 2 grand mals in two days

> -------------------------- eGroups

Sponsor -------------------------~-~>

> GET A NEXTCARD VISA, in 30 seconds! Get rates

> of 2.9% Intro or 9.9% Ongoing APR* and no annual fee!

> Apply NOW!

> 1/7872/9/_/705339/_/967939738/

> --------------------------------------------------------------------

-_- >

>

> All

> Have just come back from ER with my son, had a grand mal last night,

and one

> today. Both bad. Was wondering, we did a WBC count as well as

metabolic

> panel. Of interest, all the time, my two with autism have elevated

Alkaline

> phosphatase Norms being around 120 are from 300 to 527. The Er doc

told me

> that this has everything to do with a congested liver function. Can

mercury

> poisining " congest " the liver, make the detox pathways not work?

What

> natural supplementation would help " decongest " the liver. He said

many

> times people with gallstones show this high of a number? We are

taking off/

> weaning Dilantin on to tegretol time released, could be why...but I

find

> this all very interesting, as secretin helped one daughter and not

my son

> with seizures which helps increase bile?

> Do any of your kids have bile insufficiency problems and SEIZURES?

Is this

> connected? What exactly in mercury poisining is the process of

doing

> something to the pancreas? What stealth or viral components of the

vaccines

> attack the pancreatic processes? Are liver detox pathways

hereditary?

> Kathy

>

> <!--See my SuperSig:

http://proxy.supersig.com/sig?45002326_45002140-->

> <HTML><HEAD><TITLE>See my SuperSig:

> http://proxy.supersig.com/sig?45002326_45002140</TITLE></HEAD><BODY

> BGCOLOR=#FFFFFF><IMG

SRC= " http://supersig.com/temp/confetti_n_360.gif "

> BORDER=0> <IMG SRC= " http://supersig.com/temp/confetti_w1_80.gif "

> BORDER=0><IMG SRC= " /temp/45002140_157045583618.gif " BORDER=0><A

>

HREF= " http://supersig.com/r.php3?url=http://home1.gte.net/jblanco2 & id=

450023

> 26_45002140 " ><IMG SRC= " /temp/45002140_157061315664.gif "

BORDER=0></A><IMG

> SRC= " /temp/45002140_10580_956175606.gif " BORDER=0><IMG

> SRC= " http://supersig.com/temp/confetti_e1_80.gif " BORDER=0> <IMG

> SRC= " http://supersig.com/temp/confetti_s_360.gif " BORDER=0> <A

>

HREF= " http://supersig.com/r.php3?url=http://supersig.com/?45002326_450

02140 &

> id=45002326_45002140 " ><IMG

> SRC= " http://supersig.com/images/sigmaker/button_getyours.gif "

ALT= " get your

> supersig! " HSPACE=227 VSPACE=2 BORDER=0

ALIGN=LEFT></A> </BODY></HTML>

>

September 3, 2000

Kathy

I thought the essiac tea was able to let down bile. I thought I read that

it was a suppliment that you used. good luck kelly

September 3, 2000

Excuse me for interrupting, but my daughter has had light colored stools off

and on for years. The gastroenterologist shows no interest or concern

whatsoever but I know it's got to mean SOMETHING's amiss! What is it and

what do you do about your light stools/bile issue?

thankyou!

Re: [ ] 2 grand mals in two days

>

> Kathy,

> I have liver congestion at times (been mercury detoxing for years) and

take

> Thorne's Lipotrepein which is a mix of a few vitamins & herbs. Milk

thistle

> is also supposed to help. Surprising they didn't " prescribe " anything to

> help the liver let down more bile. Could the meds he's on be

contributing?

> Also, is he getting enough EFAs? I know when I'm bile deficient by

lighter

> colored stools. Do you have Andy's book? I can't remember if its

mentioned

> in there or not.

>

> My prayers go out to you.

> Janice in TX

>

September 3, 2000

We are titrating it correctly, but for autism, who knows what correct is?

He had another seizure tonight, and we did a cat scan to make sure

everything is ok. Perfectly normal Cat scan, which is good, but I could

have told them that. Someone mentioned a neurospect or MRI that looks at

mitochondrial encephalopathy in the brain, could you let me know what that

is called again? (looking at blood flow etc)

Kathy

Re: [ ] 2 grand mals in two days

>

>Kathy,

>

>I once had epilepsy too. Lots of grand mals. Seizures began around

>puberty. If I forgot to take my dilantin, I was sure to have a grand

>mal. Perhaps you are weaning too fast from the dilantin. I also had

>lots of petit mals.

>

>About 20 years ago, I was weaned VERY SLOWLY from dilantin. I've

>never had a seizure again. I'm in my mid-40s now.

>

> (Cary, NC)

>persistentC@...

>

> [ ] 2 grand mals in two days

>

>> -------------------------- eGroups

>Sponsor -------------------------~-~>

>> GET A NEXTCARD VISA, in 30 seconds! Get rates

>> of 2.9% Intro or 9.9% Ongoing APR* and no annual fee!

>> Apply NOW!

>> 1/7872/9/_/705339/_/967939738/

>> --------------------------------------------------------------------

> -_- >

>>

>> All

>> Have just come back from ER with my son, had a grand mal last night,

>and one

>> today. Both bad. Was wondering, we did a WBC count as well as

>metabolic

>> panel. Of interest, all the time, my two with autism have elevated

>Alkaline

>> phosphatase Norms being around 120 are from 300 to 527. The Er doc

>told me

>> that this has everything to do with a congested liver function. Can

>mercury

>> poisining " congest " the liver, make the detox pathways not work?

>What

>> natural supplementation would help " decongest " the liver. He said

>many

>> times people with gallstones show this high of a number? We are

>taking off/

>> weaning Dilantin on to tegretol time released, could be why...but I

>find

>> this all very interesting, as secretin helped one daughter and not

>my son

>> with seizures which helps increase bile?

>> Do any of your kids have bile insufficiency problems and SEIZURES?

>Is this

>> connected? What exactly in mercury poisining is the process of

>doing

>> something to the pancreas? What stealth or viral components of the

>vaccines

>> attack the pancreatic processes? Are liver detox pathways

>hereditary?

>> Kathy

>>

>> <!--See my SuperSig:

>http://proxy.supersig.com/sig?45002326_45002140-->

>> <HTML><HEAD><TITLE>See my SuperSig:

>> http://proxy.supersig.com/sig?45002326_45002140</TITLE></HEAD><BODY

>> BGCOLOR=#FFFFFF><IMG

>SRC= " http://supersig.com/temp/confetti_n_360.gif "

>> BORDER=0> <IMG SRC= " http://supersig.com/temp/confetti_w1_80.gif "

>> BORDER=0><IMG SRC= " /temp/45002140_157045583618.gif " BORDER=0><A

>>

>HREF= " http://supersig.com/r.php3?url=http://home1.gte.net/jblanco2 & id=

>450023

>> 26_45002140 " ><IMG SRC= " /temp/45002140_157061315664.gif "

>BORDER=0></A><IMG

>> SRC= " /temp/45002140_10580_956175606.gif " BORDER=0><IMG

>> SRC= " http://supersig.com/temp/confetti_e1_80.gif " BORDER=0> <IMG

>> SRC= " http://supersig.com/temp/confetti_s_360.gif " BORDER=0> <A

>>

>HREF= " http://supersig.com/r.php3?url=http://supersig.com/?45002326_450

>02140 &

>> id=45002326_45002140 " ><IMG

>> SRC= " http://supersig.com/images/sigmaker/button_getyours.gif "

>ALT= " get your

>> supersig! " HSPACE=227 VSPACE=2 BORDER=0

>ALIGN=LEFT></A> </BODY></HTML>

>>

September 3, 2000

My friend bought Andy's book in which I will borrow in a few weeks . I

think Dilantin can do things to the liver, but my daughter who shows higher

numbers is not on any meds or has any seizures? I will look into the

product though? I have read about lipotropics, what would that do to

someone with seizures I wonder? (Fat metabolism?). He takes NEUROMINS

which is a balance of fatty acids.

Kathy

Re: [ ] 2 grand mals in two days

>

>Kathy,

>I have liver congestion at times (been mercury detoxing for years) and take

>Thorne's Lipotrepein which is a mix of a few vitamins & herbs. Milk

thistle

>is also supposed to help. Surprising they didn't " prescribe " anything to

>help the liver let down more bile. Could the meds he's on be contributing?

>Also, is he getting enough EFAs? I know when I'm bile deficient by lighter

>colored stools. Do you have Andy's book? I can't remember if its

mentioned

>in there or not.

>

>My prayers go out to you.

>Janice in TX

>

September 3, 2000

spect scan

September 3, 2000

There is a reason, I will send you a paper

Kathy

Re: [ ] 2 grand mals in two days

>

>Excuse me for interrupting, but my daughter has had light colored stools

off

>and on for years. The gastroenterologist shows no interest or concern

>whatsoever but I know it's got to mean SOMETHING's amiss! What is it and

>what do you do about your light stools/bile issue?

> thankyou!

>

> Re: [ ] 2 grand mals in two days

>

>>

>> Kathy,

>> I have liver congestion at times (been mercury detoxing for years) and

>take

>> Thorne's Lipotrepein which is a mix of a few vitamins & herbs. Milk

>thistle

>> is also supposed to help. Surprising they didn't " prescribe " anything to

>> help the liver let down more bile. Could the meds he's on be

>contributing?

>> Also, is he getting enough EFAs? I know when I'm bile deficient by

>lighter

>> colored stools. Do you have Andy's book? I can't remember if its

>mentioned

>> in there or not.

>>

>> My prayers go out to you.

>> Janice in TX

>>

September 3, 2000

We have used it, haven't seen wonderful benefits, but some. I am looking

into the Cabot diet.

Kathy

Re: [ ] 2 grand mals in two days

>

>Kathy

>

> I thought the essiac tea was able to let down bile. I thought I read that

>it was a suppliment that you used. good luck kelly

>

September 3, 2000

OOOH. That is what I am going to do next. Any centers that do that best?

Kathy

Re: [ ] 2 grand mals in two days

>

>spect scan

>

September 3, 2000

Kathy,

I know that you are very much into the alternative medicine but be

careful............ someof these thing casue fatal interaction with

anticonvulsants.

julie

September 4, 2000

In a message dated 09/03/2000 12:40:47 AM, kblanco@... writes:

<< He takes NEUROMINS

which is a balance of fatty acids. >>

Where do you get them?

September 4, 2000

O believe me, I am stepping lightly, more than you think

Kathy

Re: [ ] 2 grand mals in two days

>

>Kathy,

>I know that you are very much into the alternative medicine but be

>careful............ someof these thing casue fatal interaction with

>anticonvulsants.

>julie

>

>_

>

September 4, 2000

Mother nature.com carries them

Kathy

Re: [ ] 2 grand mals in two days

>

>In a message dated 09/03/2000 12:40:47 AM, kblanco@... writes:

>

><< He takes NEUROMINS

>which is a balance of fatty acids. >>

>

>Where do you get them?

>

September 4, 2000

All the seizure meds go through the liver except the new one Keppra which is

not yet approved for kids though many are already using it and some think it

is the best drug yet.

September 4, 2000

In a message dated 9/3/2000 1:41:14 AM Eastern Daylight Time,

kblanco@... writes:

<< He takes NEUROMINS

which is a balance of fatty acids. >>

Kathy where Can i get some info on Neuromins. ?? kelly

September 4, 2000

Kathy,

See any of Hulda 's books (recommend the most recent, regardless of title)

for great liver cleansing recipes that are pretty simple and literally allow you

to pass the gallstones out. Basic ingredients include fresh grapefruit juice,

olive oil and epsom salts.

aa

September 4, 2000

also how do you mix it?

Crystal

September 4, 2000

Can anyone remind me what the essiac tea was for??

Crystal

September 4, 2000

Mother nature.com carries it

Kathy

Re: [ ] 2 grand mals in two days

>

>In a message dated 9/3/2000 1:41:14 AM Eastern Daylight Time,

>kblanco@... writes:

>

><< He takes NEUROMINS

> which is a balance of fatty acids. >>

>Kathy where Can i get some info on Neuromins. ?? kelly

>

September 4, 2000

Kathy,

At 9/2/2000 -070005:18 PM, you asked:

Can mercury

>poisining " congest " the liver, make the detox pathways not work?

The liver is one of those filtering sorts of organs whose function makes it

a more likely target for mercury to collect. It is also a major (some

would say THE major) site of detoxication, so it is one place where an

impairment of the sulfate chemistry would be expected to produce

consequences. Mercury can block the transport of sulfate across membranes

(outside and maybe inside the cell), making it hard for the cell to utilize

sulfate.

Sulfate in the liver particularly is rate-limited (hampered by) the ability

of liver cells to convert sulfate into its activated form. That takes some

work. It has been noticed that a single dose of tylenol can use up the

liver's available activated sulfate in one to two minutes, and it takes a

long time to recover.

But bile is collected in the gall bladder, and the gall bladder's release

of bile is regulated by cholecystokinin, a peptide neurotransmitter which

needs to be sulfated to work right at its CCKA receptor. If the body is

unable to retain sulfate or absorb it from the diet (which would happen if

mercury were shutting down the transporters that accomplish that) then

CCKA's action would be inhibited.

> What

>natural supplementation would help " decongest " the liver.

Well, if the problem is the release of bile, I would put a wager on epsom

salts! (Magnesium is also needed to form activated sulfate.)

> He said many

>times people with gallstones show this high of a number?

I'd like to chase that! I've put some articles below showing that

gallstones may be seeded by the unsulfated GAG called hyaluronic acid or by

" neutral " sugars which wouldn't be the sulfated ones. Another article

looking for sulfated GAGs found that they were increased in the bile of

animals whose immune system was responding to the presence of bacteria in

the biliary tract, but it is difficult without the study in hand to find

out if they determined if the sulfated GAGs were normally sulfated or

not. When you run out of sulfate, which makes the sulfated GAGs you

normally produce become randomly undersulfated, then they lose their

biological effect, and depending upon feedback loops, that might encourage

the production of more of them, but again, if their production was

upregulated, you might keep producing GAGs that might not have the proper

" sulfate code " attached.

Running out of sulfate also apparently encourages the production of

hyaluronic acid, which is the unsulfated GAG that two studies below

suspected of being involved in beginning stone formation.

> We are taking off/

>weaning Dilantin on to tegretol time released, could be why...but I find

>this all very interesting, as secretin helped one daughter and not my son

>with seizures which helps increase bile?

Secretin and cholecystokinin are partners, and CCK's action here is sulfate

dependent. Girls do not have the same sulfation demands as boys,

especially in the brain. The way testosterone regulates sulfotransferases

is really amazing, and even differences in boy cells and girl cells

regarding sulfation has been replicated in vitro. I suspect this alone may

be the reason that boys with autism so much outnumber girls.

Do any of your kids have bile insufficiency problems and SEIZURES? Is this

>connected?

Seizures may involve problems in cell-to-cell communication, and much of

that is mediated by sulfated glycosaminoglycans (GAGS) and gap junctions

which they in some way regulate. For that reason, nerve-to-nerve

connections which have been studied ad nauseum may not be the critical site

of problems.

Scientists are only recently beginning to realize these other

" connections " need to be studied. The cellular machinery which makes GAGS

does not shut down when sulfate runs out inside the cell, but will churn

out molecules which will have lost their specificity and activity because

the " code " was in the sulfate.

That is like finding a page in a book where the ink never touched the page,

mixed in with pages of full text. You cannot read the " missing "

paragraphs, and neither can the cell decipher the meaning of a GAG that

never became appropriately sulfated. It is not surprising that this

jumbling of signalling would produce consequences in the nervous

system. Neuroscientists tend to know very little to nothing about sulfated

molecules, so it is not surprising that any connection with seizure has not

been investigated.

>What exactly in mercury poisining is the process of doing

>something to the pancreas?

Mercury poisoning apparently can block the transport of sulfate through the

cell, and may impair body supplies by its effects on cells in the kidney

and intestine, and in some cases may be responsible for the sort of

systemic lack of sulfate that has been well-documented in autism.

The pancreas, like the gall bladder, is also regulated by sulfated

cholecystokinin. Insufficient sulfate for cholecystokinin = no proper signal.

Just the report of children on chelation getting allergic shiners and

having a temporary worsening of behaviors and/or seizure makes me suspect

that the " loosened " mercury is collecting in the kidneys and temporarily

may be making sulfate retention a bit more difficult. This is something

that needs to be studied formally. I really wonder if " transdermal "

sulfate may be helpful in working around this temporary state of affairs.

1: Eur J Gastroenterol Hepatol 1995 Feb;7(2):135-40

Extracellular matrix proteins in human bile and gallstones.

Lohr M, Scherer R, Schneider HT, May A, Hahn EG, Zirngibl H, Kloppel G, Ell C

Department of Medicine, University of Rostock, Germany.

OBJECTIVE: To investigate the presence of extracellular matrix (ECM)

proteins in

human bile and gallstones and to determine whether they play a role in

gallstone

formation. METHODS: ECM components [procollagen-III-peptide (P-III-P), laminin,

and hyaluronic acid] in bile from patients with (n = 22) and without (n = 6)

gallstone disease were investigated by immunoassay. Bile, gallstones, and serum

were assayed for extracellular matrix components in an additional 19 patients

with gallstone disease and gallstones were analysed in a third set of 26

patients. The expression of hyaluronic acid synthetase in bile duct and gall

bladder epithelia was investigated by immunocytochemistry. RESULTS: Hyaluronic

acid levels were significantly elevated in hepatic and gall bladder bile, but

not in the serum of patients with compared with those without gallstone disease

(137 versus 81 micrograms/l, respectively; P < 0.05). No differences were found

between hepatic and gall bladder bile. Procollagen-III-peptide and laminin were

detected in the hepatic bile of patients in both groups. Laminin levels were

higher in gall bladder bile than in serum in all patients and measurable

amounts

of hyaluronic acid were found in gallstones. The amount of hyaluronic acid was

inversely correlated to the volume of the gallstone, i.e., the smallest

gallstones contained the highest levels of hyaluronic acid. No

procollagen-III-peptide or laminin was found in the gallstones.

Immunocytochemistry of the epithelial cells of bile duct and gall bladder

mucosa

stained strongly for hyaluronic acid synthetase. CONCLUSIONS: Hyaluronic

acid as

a progenitor of ECM can be detected in bile and is significantly elevated in

patients with gallstone disease. Small gallstones contain more hyaluronic acid

than large stones, suggesting that hyaluronic acid may play a role in gallstone

formation, particularly since it is produced by the epithelial lining of bile

ducts and is found in gall bladder mucosa.

PMID: 7712305, UI: 95227835

3: Nippon Shokakibyo Gakkai Zasshi 1990 Nov;87(11):2483-93

[study of glycosaminoglycan in human bile--especially in relationship to

gallstone formation].

[Article in Japanese]

Nakamura K

Second Department of Surgery, Nagasaki University School of Medicine.

Human bile glycosaminoglycan (GAG) was examined in eight normal controls and 87

patients with hepatobiliary diseases, in order to elucidate a role and

significance of GAG in gallstone formation. Each crude mucopolysaccharides

(c-MP) were examined by carbohydrate analysis, additional two dimensional

electrophoresis and DEAE Sephacel column chromatography. The yield of c-MP and

total hexosamine concentration, a marker for mucin, were significantly

higher in

gallstone patients than controls both in gallbladder and hepatic bile. They

were

marked high values especially in cholestatic bile. Electrophoresis of GAG from

normal and pathological bile identically showed single spot at unique position

which mobility were similar to standard hyaluronic acid, but lower at both run,

and they resisted enzymatic digestion. More detail analysis by chromatography

revealed three peaks and second peak eluted at 0.85 M NaCl was thought to

be the

most important fraction. This fraction was rich in neutral sugar and its amino

acid [sco--This is an error; it should have said hexosamine, as glucosamine

is NOT an

amino acid.] was composed almost entirely of glucosamine. [sco--This is

odd, because

these sugars usually come in pairs of two different sugar moeities. I can't

recall seeing this sort of GAG described before...]Present results

suggested that

these GAG were peculiar to human bile and played a significant role in

gallstone

formation by quantitative change.[sco--The enzymes that run the sulfation

of GAGs

know where to attach sulfate by recognizing patterns of the sugars and previous

changes made by other enzymes. What they describe here is very peculiar

indeed! I

wish it weren't in Japanese...]

PMID: 2277439, UI: 91116743

4: Hua Hsi I Ko Ta Hsueh Hsueh Pao 1989 Dec;20(4):417-20

[Mucus histochemical study of bilirubin cholangiolithiasis in rabbit model].

[Article in Chinese]

Li N, Xiao LJ, Chen SW, Li L, Xiao BL, Chen WB, Gao XK, Gu SJ

Sulfated mucopolysaccharides have an important role in pigment gallstone

formation. In this experiment, the animal model of bilirubin cholangiolithiasis

was made with Japanese hybrid big-ear white rabbits. The source, nature,

quantity and distribution of sulfated mucopolysaccharides in the cause of

bilirubin cholangiolithiasis were observed by means of mucous histochemical

study. There were three characteristic pathologic changes observed in this

experiment: 1. In normal condition, the sulfated mucopolysaccharides were

secreted by epithelium of biliary tracts and the quantity was minimum. When

bacterial infection was present in the biliary tracts, they were secreted

mainly

by the proliferative glands in submucosa of the bile duct; 2. In 26 rabbits

where the bilirubin cholangiolithiasis developed, there were many proliferative

glands in submucosa of the bile duct. Most of the glands produced sulfonated

acid mucin. In 5 rabbits where the gallstones did not develop in the stone

growing stage, the proliferative glands were not present in the bile duct. It

was suggested that there was a close relationship between the proliferative

glands and the formation of bilirubin cholangiolithiasis, and 3. The glands in

submucosa of the biliary tract provided the refuge where the bacteria could not

be cleaned out easily and so it was difficult to control the infection of the

biliary tract. [sco-Sulfate, not attached to GAGs, is needed to detoxify

bilirubin,

which is why kids with sulfation problems are prone to get allergic shiners.

Perhaps at an upstream place in this infection, sulfate had already failed to

do its job, making these stones with bilirubin in them more likely to form.]

PMID: 2534303, UI: 90201893

September 4, 2000

Kathy-havev you tried adding red clover blossoms to the tea? I know two

parents who did that,and it really helped their kids:) On the other

hand,red clover did really bad things to Mike LOL,but who knows?

Re: [ ] 2 grand mals in two days

>

>>

>>Kathy

>>

>> I thought the essiac tea was able to let down bile. I thought I read

that

>>it was a suppliment that you used. good luck kelly

>>

September 5, 2000

Barb,

I can't really say that I developed an opinion about how much oral mag

sulfate is equivalent to a bath or topical application to the skin. I do

know some children respond very quickly to the " baths " , but there are many

differences among children on the autism spectrum.

Can you tell me a little more about your son? What has made a difference,

and what sort of testing have you had done with what sort of

results? Maybe we can learn something.

At 9/4/2000 -070009:32 PM, you wrote:

>

>,

>What do you think of Andy's idea of taking a little epsom salts orally each

>day? Is that as effective as the transdermal? We tried the epsom salts

>baths with my son, but didn't see much difference. Also tried MSM, with the

>same kind of results. So I thought maybe Craig didn't have the sulfation

>problems others have?

>Barb

>

>P.S. Is it not a good idea to do this while chelating? Or doesn't matter?

>Someone said Jane El Dar said not to do the TMG while chelating.

>P.P.S. Your comments about cell-to-cell communication intrigue me because

>we've always felt Craig was like that--someone who had all the pieces but

>couldn't always put them together. He can do Algebra for hours, yet has

>greater difficulty with motor planning and movement, both in body and

>speech. We use a lot of humming and music to keep him going.

> Re: [ ] 2 grand mals in two days

>

> >

> >Kathy,

> >

> >At 9/2/2000 -070005:18 PM, you asked:

> >

> > Can mercury

> >>poisining " congest " the liver, make the detox pathways not work?

> >

> >The liver is one of those filtering sorts of organs whose function makes it

> >a more likely target for mercury to collect. It is also a major (some

> >would say THE major) site of detoxication, so it is one place where an

> >impairment of the sulfate chemistry would be expected to produce

> >consequences. Mercury can block the transport of sulfate across membranes

> >(outside and maybe inside the cell), making it hard for the cell to utilize

> >sulfate.

> >

> >Sulfate in the liver particularly is rate-limited (hampered by) the ability

> >of liver cells to convert sulfate into its activated form. That takes some

> >work. It has been noticed that a single dose of tylenol can use up the

> >liver's available activated sulfate in one to two minutes, and it takes a

> >long time to recover.

> >

> >But bile is collected in the gall bladder, and the gall bladder's release

> >of bile is regulated by cholecystokinin, a peptide neurotransmitter which

> >needs to be sulfated to work right at its CCKA receptor. If the body is

> >unable to retain sulfate or absorb it from the diet (which would happen if

> >mercury were shutting down the transporters that accomplish that) then

> >CCKA's action would be inhibited.

> >

> >> What

> >>natural supplementation would help " decongest " the liver.

> >

> >Well, if the problem is the release of bile, I would put a wager on epsom

> >salts! (Magnesium is also needed to form activated sulfate.)

> >

> >> He said many

> >>times people with gallstones show this high of a number?

> >

> >I'd like to chase that! I've put some articles below showing that

> >gallstones may be seeded by the unsulfated GAG called hyaluronic acid or by

> > " neutral " sugars which wouldn't be the sulfated ones. Another article

> >looking for sulfated GAGs found that they were increased in the bile of

> >animals whose immune system was responding to the presence of bacteria in

> >the biliary tract, but it is difficult without the study in hand to find

> >out if they determined if the sulfated GAGs were normally sulfated or

> >not. When you run out of sulfate, which makes the sulfated GAGs you

> >normally produce become randomly undersulfated, then they lose their

> >biological effect, and depending upon feedback loops, that might encourage

> >the production of more of them, but again, if their production was

> >upregulated, you might keep producing GAGs that might not have the proper

> > " sulfate code " attached.

> >

> >Running out of sulfate also apparently encourages the production of

> >hyaluronic acid, which is the unsulfated GAG that two studies below

> >suspected of being involved in beginning stone formation.

> >

> >> We are taking off/

> >>weaning Dilantin on to tegretol time released, could be why...but I find

> >>this all very interesting, as secretin helped one daughter and not my son

> >>with seizures which helps increase bile?

> >

> >Secretin and cholecystokinin are partners, and CCK's action here is sulfate

> >dependent. Girls do not have the same sulfation demands as boys,

> >especially in the brain. The way testosterone regulates sulfotransferases

> >is really amazing, and even differences in boy cells and girl cells

> >regarding sulfation has been replicated in vitro. I suspect this alone may

> >be the reason that boys with autism so much outnumber girls.

> >

> >Do any of your kids have bile insufficiency problems and SEIZURES? Is this

> >>connected?

> >

> >Seizures may involve problems in cell-to-cell communication, and much of

> >that is mediated by sulfated glycosaminoglycans (GAGS) and gap junctions

> >which they in some way regulate. For that reason, nerve-to-nerve

> >connections which have been studied ad nauseum may not be the critical site

> >of problems.

> >

> >Scientists are only recently beginning to realize these other

> > " connections " need to be studied. The cellular machinery which makes GAGS

> >does not shut down when sulfate runs out inside the cell, but will churn

> >out molecules which will have lost their specificity and activity because

> >the " code " was in the sulfate.

> >

> >That is like finding a page in a book where the ink never touched the page,

> >mixed in with pages of full text. You cannot read the " missing "

> >paragraphs, and neither can the cell decipher the meaning of a GAG that

> >never became appropriately sulfated. It is not surprising that this

> >jumbling of signalling would produce consequences in the nervous

> >system. Neuroscientists tend to know very little to nothing about sulfated

> >molecules, so it is not surprising that any connection with seizure has not

> >been investigated.

> >

> >>What exactly in mercury poisining is the process of doing

> >>something to the pancreas?

> >

> >Mercury poisoning apparently can block the transport of sulfate through the

> >cell, and may impair body supplies by its effects on cells in the kidney

> >and intestine, and in some cases may be responsible for the sort of

> >systemic lack of sulfate that has been well-documented in autism.

> >

> >The pancreas, like the gall bladder, is also regulated by sulfated

> >cholecystokinin. Insufficient sulfate for cholecystokinin = no proper

>signal.

> >

> >Just the report of children on chelation getting allergic shiners and

> >having a temporary worsening of behaviors and/or seizure makes me suspect

> >that the " loosened " mercury is collecting in the kidneys and temporarily

> >may be making sulfate retention a bit more difficult. This is something

> >that needs to be studied formally. I really wonder if " transdermal "

> >sulfate may be helpful in working around this temporary state of affairs.

> >

> >1: Eur J Gastroenterol Hepatol 1995 Feb;7(2):135-40

> >

> >Extracellular matrix proteins in human bile and gallstones.

> >

> >Lohr M, Scherer R, Schneider HT, May A, Hahn EG, Zirngibl H, Kloppel G, Ell

>C

> >

> >Department of Medicine, University of Rostock, Germany.

> >

> >OBJECTIVE: To investigate the presence of extracellular matrix (ECM)

> >proteins in

> >human bile and gallstones and to determine whether they play a role in

> >gallstone

> >formation. METHODS: ECM components [procollagen-III-peptide (P-III-P),

>laminin,

> >and hyaluronic acid] in bile from patients with (n = 22) and without (n =

>6)

> >gallstone disease were investigated by immunoassay. Bile, gallstones, and

>serum

> >were assayed for extracellular matrix components in an additional 19

>patients

> >with gallstone disease and gallstones were analysed in a third set of 26

> >patients. The expression of hyaluronic acid synthetase in bile duct and

>gall

> >bladder epithelia was investigated by immunocytochemistry. RESULTS:

>Hyaluronic

> >acid levels were significantly elevated in hepatic and gall bladder bile,

>but

> >not in the serum of patients with compared with those without gallstone

>disease

> >(137 versus 81 micrograms/l, respectively; P < 0.05). No differences were

>found

> >between hepatic and gall bladder bile. Procollagen-III-peptide and laminin

>were

> >detected in the hepatic bile of patients in both groups. Laminin levels

>were

> >higher in gall bladder bile than in serum in all patients and measurable

> >amounts

> >of hyaluronic acid were found in gallstones. The amount of hyaluronic acid

>was

> >inversely correlated to the volume of the gallstone, i.e., the smallest

> >gallstones contained the highest levels of hyaluronic acid. No

> >procollagen-III-peptide or laminin was found in the gallstones.

> >Immunocytochemistry of the epithelial cells of bile duct and gall bladder

> >mucosa

> >stained strongly for hyaluronic acid synthetase. CONCLUSIONS: Hyaluronic

> >acid as

> >a progenitor of ECM can be detected in bile and is significantly elevated

>in

> >patients with gallstone disease. Small gallstones contain more hyaluronic

>acid

> >than large stones, suggesting that hyaluronic acid may play a role in

>gallstone

> >formation, particularly since it is produced by the epithelial lining of

>bile

> >ducts and is found in gall bladder mucosa.

> >

> >PMID: 7712305, UI: 95227835

> >

> >3: Nippon Shokakibyo Gakkai Zasshi 1990 Nov;87(11):2483-93

> >

> >[study of glycosaminoglycan in human bile--especially in relationship to

> >gallstone formation].

> >

> >[Article in Japanese]

> >

> >Nakamura K

> >

> >Second Department of Surgery, Nagasaki University School of Medicine.

> >

> >Human bile glycosaminoglycan (GAG) was examined in eight normal controls

>and 87

> >patients with hepatobiliary diseases, in order to elucidate a role and

> >significance of GAG in gallstone formation. Each crude mucopolysaccharides

> >(c-MP) were examined by carbohydrate analysis, additional two dimensional

> >electrophoresis and DEAE Sephacel column chromatography. The yield of c-MP

>and

> >total hexosamine concentration, a marker for mucin, were significantly

> >higher in

> >gallstone patients than controls both in gallbladder and hepatic bile. They

> >were

> >marked high values especially in cholestatic bile. Electrophoresis of GAG

>from

> >normal and pathological bile identically showed single spot at unique

>position

> >which mobility were similar to standard hyaluronic acid, but lower at both

>run,

> >and they resisted enzymatic digestion. More detail analysis by

>chromatography

> >revealed three peaks and second peak eluted at 0.85 M NaCl was thought to

> >be the

> >most important fraction. This fraction was rich in neutral sugar and its

>amino

> >acid [sco--This is an error; it should have said hexosamine, as glucosamine

> >is NOT an

> >amino acid.] was composed almost entirely of glucosamine. [sco--This is

> >odd, because

> >these sugars usually come in pairs of two different sugar moeities. I

>can't

> >recall seeing this sort of GAG described before...]Present results

> >suggested that

> >these GAG were peculiar to human bile and played a significant role in

> >gallstone

> >formation by quantitative change.[sco--The enzymes that run the sulfation

> >of GAGs

> >know where to attach sulfate by recognizing patterns of the sugars and

>previous

> >changes made by other enzymes. What they describe here is very peculiar

> >indeed! I

> >wish it weren't in Japanese...]

> >

> >PMID: 2277439, UI: 91116743

> >

> >4: Hua Hsi I Ko Ta Hsueh Hsueh Pao 1989 Dec;20(4):417-20

> >

> >[Mucus histochemical study of bilirubin cholangiolithiasis in rabbit

>model].

> >

> >[Article in Chinese]

> >

> >Li N, Xiao LJ, Chen SW, Li L, Xiao BL, Chen WB, Gao XK, Gu SJ

> >

> >Sulfated mucopolysaccharides have an important role in pigment gallstone

> >formation. In this experiment, the animal model of bilirubin

>cholangiolithiasis

> >was made with Japanese hybrid big-ear white rabbits. The source, nature,

> >quantity and distribution of sulfated mucopolysaccharides in the cause of

> >bilirubin cholangiolithiasis were observed by means of mucous histochemical

> >study. There were three characteristic pathologic changes observed in this

> >experiment: 1. In normal condition, the sulfated mucopolysaccharides were

> >secreted by epithelium of biliary tracts and the quantity was minimum. When

> >bacterial infection was present in the biliary tracts, they were secreted

> >mainly

> >by the proliferative glands in submucosa of the bile duct; 2. In 26 rabbits

> >where the bilirubin cholangiolithiasis developed, there were many

>proliferative

> >glands in submucosa of the bile duct. Most of the glands produced

>sulfonated

> >acid mucin. In 5 rabbits where the gallstones did not develop in the stone

> >growing stage, the proliferative glands were not present in the bile duct.

>It

> >was suggested that there was a close relationship between the proliferative

> >glands and the formation of bilirubin cholangiolithiasis, and 3. The glands

>in

> >submucosa of the biliary tract provided the refuge where the bacteria could

>not

> >be cleaned out easily and so it was difficult to control the infection of

>the

> >biliary tract. [sco-Sulfate, not attached to GAGs, is needed to detoxify

> >bilirubin,

> >which is why kids with sulfation problems are prone to get allergic

>shiners.

> >Perhaps at an upstream place in this infection, sulfate had already failed

>to

> >do its job, making these stones with bilirubin in them more likely to

>form.]

> >

> >PMID: 2534303, UI: 90201893

> >

September 5, 2000

,

What do you think of Andy's idea of taking a little epsom salts orally each

day? Is that as effective as the transdermal? We tried the epsom salts

baths with my son, but didn't see much difference. Also tried MSM, with the

same kind of results. So I thought maybe Craig didn't have the sulfation

problems others have?

Barb

P.S. Is it not a good idea to do this while chelating? Or doesn't matter?

Someone said Jane El Dar said not to do the TMG while chelating.

P.P.S. Your comments about cell-to-cell communication intrigue me because

we've always felt Craig was like that--someone who had all the pieces but

couldn't always put them together. He can do Algebra for hours, yet has

greater difficulty with motor planning and movement, both in body and

speech. We use a lot of humming and music to keep him going.

Re: [ ] 2 grand mals in two days

>

>Kathy,

>

>At 9/2/2000 -070005:18 PM, you asked:

>

> Can mercury

>>poisining " congest " the liver, make the detox pathways not work?

>

>The liver is one of those filtering sorts of organs whose function makes it

>a more likely target for mercury to collect. It is also a major (some

>would say THE major) site of detoxication, so it is one place where an

>impairment of the sulfate chemistry would be expected to produce

>consequences. Mercury can block the transport of sulfate across membranes

>(outside and maybe inside the cell), making it hard for the cell to utilize

>sulfate.

>

>Sulfate in the liver particularly is rate-limited (hampered by) the ability

>of liver cells to convert sulfate into its activated form. That takes some

>work. It has been noticed that a single dose of tylenol can use up the

>liver's available activated sulfate in one to two minutes, and it takes a

>long time to recover.

>

>But bile is collected in the gall bladder, and the gall bladder's release

>of bile is regulated by cholecystokinin, a peptide neurotransmitter which

>needs to be sulfated to work right at its CCKA receptor. If the body is

>unable to retain sulfate or absorb it from the diet (which would happen if

>mercury were shutting down the transporters that accomplish that) then

>CCKA's action would be inhibited.

>

>> What

>>natural supplementation would help " decongest " the liver.

>

>Well, if the problem is the release of bile, I would put a wager on epsom

>salts! (Magnesium is also needed to form activated sulfate.)

>

>> He said many

>>times people with gallstones show this high of a number?

>

>I'd like to chase that! I've put some articles below showing that

>gallstones may be seeded by the unsulfated GAG called hyaluronic acid or by

> " neutral " sugars which wouldn't be the sulfated ones. Another article

>looking for sulfated GAGs found that they were increased in the bile of

>animals whose immune system was responding to the presence of bacteria in

>the biliary tract, but it is difficult without the study in hand to find

>out if they determined if the sulfated GAGs were normally sulfated or

>not. When you run out of sulfate, which makes the sulfated GAGs you

>normally produce become randomly undersulfated, then they lose their

>biological effect, and depending upon feedback loops, that might encourage

>the production of more of them, but again, if their production was

>upregulated, you might keep producing GAGs that might not have the proper

> " sulfate code " attached.

>

>Running out of sulfate also apparently encourages the production of

>hyaluronic acid, which is the unsulfated GAG that two studies below

>suspected of being involved in beginning stone formation.

>

>> We are taking off/

>>weaning Dilantin on to tegretol time released, could be why...but I find

>>this all very interesting, as secretin helped one daughter and not my son

>>with seizures which helps increase bile?

>

>Secretin and cholecystokinin are partners, and CCK's action here is sulfate

>dependent. Girls do not have the same sulfation demands as boys,

>especially in the brain. The way testosterone regulates sulfotransferases

>is really amazing, and even differences in boy cells and girl cells

>regarding sulfation has been replicated in vitro. I suspect this alone may

>be the reason that boys with autism so much outnumber girls.

>

>Do any of your kids have bile insufficiency problems and SEIZURES? Is this

>>connected?

>

>Seizures may involve problems in cell-to-cell communication, and much of

>that is mediated by sulfated glycosaminoglycans (GAGS) and gap junctions

>which they in some way regulate. For that reason, nerve-to-nerve

>connections which have been studied ad nauseum may not be the critical site

>of problems.

>

>Scientists are only recently beginning to realize these other

> " connections " need to be studied. The cellular machinery which makes GAGS

>does not shut down when sulfate runs out inside the cell, but will churn

>out molecules which will have lost their specificity and activity because

>the " code " was in the sulfate.

>

>That is like finding a page in a book where the ink never touched the page,

>mixed in with pages of full text. You cannot read the " missing "

>paragraphs, and neither can the cell decipher the meaning of a GAG that

>never became appropriately sulfated. It is not surprising that this

>jumbling of signalling would produce consequences in the nervous

>system. Neuroscientists tend to know very little to nothing about sulfated

>molecules, so it is not surprising that any connection with seizure has not

>been investigated.

>

>>What exactly in mercury poisining is the process of doing

>>something to the pancreas?

>

>Mercury poisoning apparently can block the transport of sulfate through the

>cell, and may impair body supplies by its effects on cells in the kidney

>and intestine, and in some cases may be responsible for the sort of

>systemic lack of sulfate that has been well-documented in autism.

>

>The pancreas, like the gall bladder, is also regulated by sulfated

>cholecystokinin. Insufficient sulfate for cholecystokinin = no proper

signal.

>

>Just the report of children on chelation getting allergic shiners and

>having a temporary worsening of behaviors and/or seizure makes me suspect

>that the " loosened " mercury is collecting in the kidneys and temporarily

>may be making sulfate retention a bit more difficult. This is something

>that needs to be studied formally. I really wonder if " transdermal "

>sulfate may be helpful in working around this temporary state of affairs.

>

>1: Eur J Gastroenterol Hepatol 1995 Feb;7(2):135-40

>

>Extracellular matrix proteins in human bile and gallstones.

>

>Lohr M, Scherer R, Schneider HT, May A, Hahn EG, Zirngibl H, Kloppel G, Ell

C

>

>Department of Medicine, University of Rostock, Germany.

>

>OBJECTIVE: To investigate the presence of extracellular matrix (ECM)

>proteins in

>human bile and gallstones and to determine whether they play a role in

>gallstone

>formation. METHODS: ECM components [procollagen-III-peptide (P-III-P),

laminin,

>and hyaluronic acid] in bile from patients with (n = 22) and without (n =

6)

>gallstone disease were investigated by immunoassay. Bile, gallstones, and

serum

>were assayed for extracellular matrix components in an additional 19

patients

>with gallstone disease and gallstones were analysed in a third set of 26

>patients. The expression of hyaluronic acid synthetase in bile duct and

gall

>bladder epithelia was investigated by immunocytochemistry. RESULTS:

Hyaluronic

>acid levels were significantly elevated in hepatic and gall bladder bile,

but

>not in the serum of patients with compared with those without gallstone

disease

>(137 versus 81 micrograms/l, respectively; P < 0.05). No differences were

found

>between hepatic and gall bladder bile. Procollagen-III-peptide and laminin

were

>detected in the hepatic bile of patients in both groups. Laminin levels

were

>higher in gall bladder bile than in serum in all patients and measurable

>amounts

>of hyaluronic acid were found in gallstones. The amount of hyaluronic acid

was

>inversely correlated to the volume of the gallstone, i.e., the smallest

>gallstones contained the highest levels of hyaluronic acid. No

>procollagen-III-peptide or laminin was found in the gallstones.

>Immunocytochemistry of the epithelial cells of bile duct and gall bladder

>mucosa

>stained strongly for hyaluronic acid synthetase. CONCLUSIONS: Hyaluronic

>acid as

>a progenitor of ECM can be detected in bile and is significantly elevated

in

>patients with gallstone disease. Small gallstones contain more hyaluronic

acid

>than large stones, suggesting that hyaluronic acid may play a role in

gallstone

>formation, particularly since it is produced by the epithelial lining of

bile

>ducts and is found in gall bladder mucosa.

>

>PMID: 7712305, UI: 95227835

>

>3: Nippon Shokakibyo Gakkai Zasshi 1990 Nov;87(11):2483-93

>

>[study of glycosaminoglycan in human bile--especially in relationship to

>gallstone formation].

>

>[Article in Japanese]

>

>Nakamura K

>

>Second Department of Surgery, Nagasaki University School of Medicine.

>

>Human bile glycosaminoglycan (GAG) was examined in eight normal controls

and 87

>patients with hepatobiliary diseases, in order to elucidate a role and

>significance of GAG in gallstone formation. Each crude mucopolysaccharides

>(c-MP) were examined by carbohydrate analysis, additional two dimensional

>electrophoresis and DEAE Sephacel column chromatography. The yield of c-MP

and

>total hexosamine concentration, a marker for mucin, were significantly

>higher in

>gallstone patients than controls both in gallbladder and hepatic bile. They

>were

>marked high values especially in cholestatic bile. Electrophoresis of GAG

from

>normal and pathological bile identically showed single spot at unique

position

>which mobility were similar to standard hyaluronic acid, but lower at both

run,

>and they resisted enzymatic digestion. More detail analysis by

chromatography

>revealed three peaks and second peak eluted at 0.85 M NaCl was thought to

>be the

>most important fraction. This fraction was rich in neutral sugar and its

amino

>acid [sco--This is an error; it should have said hexosamine, as glucosamine

>is NOT an

>amino acid.] was composed almost entirely of glucosamine. [sco--This is

>odd, because

>these sugars usually come in pairs of two different sugar moeities. I

can't

>recall seeing this sort of GAG described before...]Present results

>suggested that

>these GAG were peculiar to human bile and played a significant role in

>gallstone

>formation by quantitative change.[sco--The enzymes that run the sulfation

>of GAGs

>know where to attach sulfate by recognizing patterns of the sugars and

>indeed! I

>wish it weren't in Japanese...]

>

>PMID: 2277439, UI: 91116743

>

>4: Hua Hsi I Ko Ta Hsueh Hsueh Pao 1989 Dec;20(4):417-20

>

>[Mucus histochemical study of bilirubin cholangiolithiasis in rabbit

model].

>

>[Article in Chinese]

>

>Li N, Xiao LJ, Chen SW, Li L, Xiao BL, Chen WB, Gao XK, Gu SJ

>

>Sulfated mucopolysaccharides have an important role in pigment gallstone

>formation. In this experiment, the animal model of bilirubin

cholangiolithiasis

>was made with Japanese hybrid big-ear white rabbits. The source, nature,

>quantity and distribution of sulfated mucopolysaccharides in the cause of

>bilirubin cholangiolithiasis were observed by means of mucous histochemical

>study. There were three characteristic pathologic changes observed in this

>experiment: 1. In normal condition, the sulfated mucopolysaccharides were

>secreted by epithelium of biliary tracts and the quantity was minimum. When

>bacterial infection was present in the biliary tracts, they were secreted

>mainly

>by the proliferative glands in submucosa of the bile duct; 2. In 26 rabbits

>where the bilirubin cholangiolithiasis developed, there were many

proliferative

>glands in submucosa of the bile duct. Most of the glands produced

sulfonated

>acid mucin. In 5 rabbits where the gallstones did not develop in the stone

>growing stage, the proliferative glands were not present in the bile duct.

It

>was suggested that there was a close relationship between the proliferative

>glands and the formation of bilirubin cholangiolithiasis, and 3. The glands

in

>submucosa of the biliary tract provided the refuge where the bacteria could

not

>be cleaned out easily and so it was difficult to control the infection of

the

>biliary tract. [sco-Sulfate, not attached to GAGs, is needed to detoxify

>bilirubin,

>which is why kids with sulfation problems are prone to get allergic

shiners.

>Perhaps at an upstream place in this infection, sulfate had already failed

to

>do its job, making these stones with bilirubin in them more likely to

form.]

>

>PMID: 2534303, UI: 90201893

>

September 5, 2000

no, haven

't tried that one yet

Kathy

Re: [ ] 2 grand mals in two days

>>

>>>

>>>Kathy

>>>

>>> I thought the essiac tea was able to let down bile. I thought I read

>that

>>>it was a suppliment that you used. good luck kelly

>>>

Sign In

Re: 2 grand mals in two days

Recommended Posts

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Guest guest

Link to comment

Share on other sites

Join the conversation

Activity