Re: 2 grand mals in two days

[Guest guest]

Jeannie on the list had a cool list one time about the properties of essiac,

oh jeannie ?

sleep@...

Kathy

Re: [ ] 2 grand mals in two days

>

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

>

>Crystal

>

>

[Guest guest]

Hi-I am new to the list,but I wanted to comment on essiac tea. To my

knowledge,I was the first parent to try it with one of our kids,and in

's case,the improvement in health and behavior was dramatic. He went

from sixty pounds to eight seven in a year,pretty good for a severely under

weight twelve year old. He went from aspergers to " a regular kid " ,although

an infection with toxoplasmosis has caused a regression since. I tried to

investigate this in a scientific way,giving surveys to parents to find out

what was going on. Most of the changes parents see initially are in vision

and behavior. essiac was initially used as a " cancer cure "

and continues to have a good reputation with diabetes and autoimmune

disorders. I have found benefit to many mothers of autistic kids with

CFIDS. the most interesting provable change in was that his blood

lead level,which had been 6 since the age of three,was 2 last october.

Nothing else could have done that. has been off of essiac for

several months,while the " powers that be " were trying to pinpoint the cause

of his current problems. He is saying that his stomach hurts again,which he

hasn't said in the year and a half since he started essiac tea. I plan to

restart the tea this week.

Re: [ ] 2 grand mals in two days

>

>

>>

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

>>

>>Crystal

>>

>>

[Guest guest]

,

He is 20. He has autism/mild CP (or should we just lump it all together and

say mercury poisoning!) He is extremely bright. His whole body is affected

by a movement disorder--in other words, difficulty stopping, starting,

continuing movement, also transitioning. The same is true for his speech.

He communicates primarily using facilitated communication. The touch

support helps him initiate and stop movement. He graduated from high school

with honors this spring!

He has trouble with social stuff, quite a lot of sensory overload, (has had

years of SI therapy, used to have petit mal seizures and was on Depakote for

a while, (maybe still has them occasionally, I'm not sure). Shows no

evidence of mindblindness--is extremely socially aware, but just can't act

on what he knows sometimes. He is gentle in spirit, and very caring about

people.

We are chelating--now added the ALA this fourth round. He showed little on

the one-month test, just some arsenic, nickel, and a few other trace

things--not very high levels. I've been giving him supplements per Dr.

Amy's protocol, so and TMG, so maybe we lowered his aluminum (with magnesium

maalate?) and antimony with the TMG. Who knows? All we tested the first

round was mercury, and we haven't gotten any of that yet. I'm guessing his

is in the brain.

Craig seemed perfectly okay until about 4 months--2 months after his first

DPTand whatever else they gave him. Then we had the motor changes, (head

lag, etc.) and eye focusing problems. Then delayed motor development, and on

and on. Every symptom he's had can be traced to mercury!

How's that for starters?

Barb

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

>> >

>> >

[Guest guest]

So what is in the stuff? And what do the herbs do? Anyone with knowledge

of American Indian lore?

Barb

Re: [ ] 2 grand mals in two days

>>

>>

>>>

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

>>>

>>>Crystal

>>>

>>>

[Guest guest]

Barb

Are you living my life, my kids sound like yours

Kathy

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

>>> >

>>> >

[Guest guest]

In a message dated 9/2/00 7:09:24 PM Central Daylight Time,

kblanco@... writes:

<< Can mercury poisining " congest " the liver, make the detox pathways not

work? What natural supplementation would help " decongest " the liver. >>

yes yes yes! Go to the archives and look up the homeopathic drainers for

liver I posted awhile back and someone else posted a website or phone number

where you can order them from. Or, if the person who posted that contact

could repost, that would be helpful. My computer died after I saved it so I

don't have the contact any more or I'd repost it myself. The contact number

I have can only be ordered by doctors or medical professionals. It's Health

America in Houston, Texas 888-593-1581. We see an increase in seizures,

sluggishness and overall not feeling well every 4-5 months of detoxing and

these clear things right up and help him release more of the bad stuff.

<< What exactly in mercury poisining is the process of doing something to the

pancreas? >>

I can't answer this one knowledgably but wanted to say that I tend to have

more pancreatic problems when detoxing. I get these little alternating pains

in my liver and pancreas areas when I get a bit overloaded. I just started

the homeopathic drainers myself and am hoping that will take care of it.

Gaylen

[Guest guest]

I am trying to clarify a few things. There seems to be alot of anomosity on

this board about chelation therapy. I plan on doing it with my son under the

the supervision of his Dr. , Dr. Amy Holmes. Is the group opposed to any

chelation or just that attempted without a Dr.'s supervision. I know that

there has been great success with this, But just like chemotherapy, for

example, with therapy comes some side effects. I personally feel that it is

worth short term discomfort for long term better health. So many diseases

can occur later in life as a direct cause of mercury poisoning. I live in

Louisiana, and today on the front page of our newspaper was a story on how

the sstate gov. is funding research into this because of high mercury levels

in fish in our surrounding waters. They said it causes brain damage but the

effects can be reversed. I guess I'd just like to know if the majority of

you are attempting this on your own or are you under a Dr. close supervision?

[Guest guest]

Tell us more about this, please. What is in them?

Re: [ ] 2 grand mals in two days

>

>In a message dated 9/2/00 7:09:24 PM Central Daylight Time,

>kblanco@... writes:

>

><< Can mercury poisining " congest " the liver, make the detox pathways not

>work? What natural supplementation would help " decongest " the liver. >>

>

>yes yes yes! Go to the archives and look up the homeopathic drainers for

>liver I posted awhile back and someone else posted a website or phone

number

>where you can order them from. Or, if the person who posted that contact

>could repost, that would be helpful. My computer died after I saved it so

I

>don't have the contact any more or I'd repost it myself. The contact

number

>I have can only be ordered by doctors or medical professionals. It's

Health

>America in Houston, Texas 888-593-1581. We see an increase in seizures,

>sluggishness and overall not feeling well every 4-5 months of detoxing and

>these clear things right up and help him release more of the bad stuff.

>

><< What exactly in mercury poisining is the process of doing something to

the

>pancreas? >>

>

>I can't answer this one knowledgably but wanted to say that I tend to have

>more pancreatic problems when detoxing. I get these little alternating

pains

>in my liver and pancreas areas when I get a bit overloaded. I just started

>the homeopathic drainers myself and am hoping that will take care of it.

>Gaylen

>

>

[Guest guest]

I can't speak for everyone, but I think most people are working with a

doctor or at least following a protocol. It's safer that way.

Barb

Re: [ ] 2 grand mals in two days

>

>I am trying to clarify a few things. There seems to be alot of anomosity

on

>this board about chelation therapy. I plan on doing it with my son under

the

>the supervision of his Dr. , Dr. Amy Holmes. Is the group opposed to any

>chelation or just that attempted without a Dr.'s supervision. I know that

>there has been great success with this, But just like chemotherapy, for

>example, with therapy comes some side effects. I personally feel that it

is

>worth short term discomfort for long term better health. So many diseases

>can occur later in life as a direct cause of mercury poisoning. I live in

>Louisiana, and today on the front page of our newspaper was a story on how

>the sstate gov. is funding research into this because of high mercury

levels

>in fish in our surrounding waters. They said it causes brain damage but

the

>effects can be reversed. I guess I'd just like to know if the majority of

>you are attempting this on your own or are you under a Dr. close

supervision?

>

>

[Guest guest]

I took ALA off of becuase I think it is inaffective for removing

mercury out of him, instead, it stirs it up and redeposits. Of late, it has

been a tongue movement/pain/seizure that is definately related. I do have

him on milk thistle, but then Great plains told me that this may be

something to take off, becuase 's meds go through the liver and could

make them either more potent or less potent because he is detoxing them

better. I am going to go to a homeopath and do what they call homeopathic

drainage. It basically means detoxing the body safely instead of with DMSA

and ALA. They call it sequential therapy, and the doctor who invented it is

calling me over the weekend. (www.hvslabs.com). IT was recommened by Judith

Bluestone of the Handle Institute. I sort of trust her instincts with

as she has followed him for many years and knows of his specific weaknesses.

I don't like experimenting on my kids, not one least bit. I would also

confer that this increasing pain is a consequence of not getting the mercury

out fast enough. Along those lines, for a child with c4 b anulle, which

means he already doesn't encode proteins to eliminate virals TOXINS and

fungals, what am I suppose to do without all of the equations? What is that

protein? BAsically, what I have found is that if I can build T cell

immunity, then this helps encode the protein. That can be handily taken

care of by Ambrotose, but along those lines, of late have been giving

and MICROHYDIN (look on search) and other operating system types of

adjuncts (this was given him after the seizures). I have seen wonderful

things with it so far! Along those lines too, have read that MONOLAURIN

does enhance t cell immunity, so I am upping the dosage on that. If my kids

dont encode proteins to get rid of mercury, I have to teach the immune

system all over again what to do. If there is something that builds the

immune system enough without putting into overdrive, I am all for it. Look

to see if there is some baddies in his school classroom as far as PST is

concerened, damn that bugger, it hits my kids at times too and I question,

where in the heck did this come from? Our kids are truly mutlifacited, it

is not just the mercury, it is also other poisins invading them that their

little bodies just can eradicate, darn it. The seizures MAY have been

becuase is going off of dilantin (as I insisted) so this may explain

that, but not the tongue thing?

Kathy

Re: 2 grand mals in two days

>Dear Kathy,

> I am very sorry to hear that is still experiencing serious

seizures.

> Although I don't have any answers to your many questions, I was very

curious

>about the answers that you might have received since. (I assume is

>already on Milk Thistle for liver detox as that is what Williss had

>recommended to me.)

> Just as a side note, had been having increased pain since about

the

>1st of September and it kept getting worse. His multi-vitamin has 50mg of

>Alpha Lipoic Acid in it (daily total) and I am certain that this was the

>cause of the increasing pain. Williss assured me that it's half-life was

>very short--and it was--he feels much better today now that he's been

>ALA-free for 3 days. It just reminded me to remind you to look to see if

> is getting any natural (but effective!) chelators hidden in his

>supplements. It probably has nothing to do with the seizures, but may be

>worth a mental note.

> I so wish all could be well for him....

>

>Love, Audrey