Re: 's Lipoic Acid Article and his questions about Dr. Kane's research

[Guest guest]

I'm finally back after several busy weeks in OB department- it's the month

for inductions (tax deductions) and end of the year female surgeries (before

starting a new calendar year and new deductibles)!

I have now read about a hundred or more actual full text articles on mercury

toxicity and hundreds of abstracts. I have read several now on Lipoic Acid

including one (not the one recently posted by ) claiming it was a metal

chelator. On CAREFUL review, however, they discussed it as " chelating Fe2+ " ,

and " protection of Cu2+ peroxidation, and Cd2+peroxidation was prevented " .

(No mention of MERCURY chelation at all.)

Ok, so now looking at both these articles, ('s and the one I just

mentioned), one might assume that the problem is lipid peroxidation- BUT the

exact mechanism for merury neurotoxicity is not known.

Here is an abstract from another article:

Abstract Mercury in both organic and inorganic forms is neurotoxic.

Methylmercury (MeHg) is a commonly encountered form of mercury in the enviro

nment. Early electrophysiological experiments revealed that MeHg potently

affects the release of neurotransmitter from presynaptic nerve terminals.

Recently, the hypothesis that these alterations may be mediated by changes in

the intracellular concentration of Ca2+ has been supported. MeHg alters Ca2+

by at least 2 mechanisms. First, it disrupts regulation of Ca2+ from an

intracellular Ca2+ pool and second, it increases the permeability of the

plasma membrane to Ca2+. MeHg also blocks plasma membrane voltage-dependent

Ca2+ and Na+ channels in addition to activating a nonspecific transmembrane

cation conductance. Chronic MeHg exposure results in ultrastructural changes

and accumulation of MeHg within mitochondria. In vitro, MeHg inhibits several

mitochondrial enzymes and depolarizes the mitochondria membrane subsequently

reducing ATP production and Ca2+ buffering capacity. Inhibition of protein

synthesis is observed after in vivo or in vitro exposures of MeHg and may be

an early effect of MeHg. Thus, the early cellular effects of exposure to MeHg

are diverse and cell damage likely occurs by more than one mechanism, the

effects of which may be additive or synergistic.

Atchison, W.D., Hare, M.F.: Mechanisms of methylmercury-induced

neurotoxicity.

FASEB Journal 8:622-629; 1994

Here is some information from the article: " MeHg accumulates in the brain and

becomes associated with motochondria, endoplasmic reticulum, golgi complex,

nuclear envelopes an lisosomes. In nerve fibers, MeHg is localized primarily

in myelin sheaths and mitochondria. " ... " Studies of MeHg neurotoxicity have

traditionally involved behavioral or pathological observations in animals

treated for days or weeks with MeHg, or observations of acute or semiacute

effects of MeHg primarily using in vitro systems. There have been few

mechanistic studies using animals treated chronically with MeHg. "

" Toxicity with MeHg probably does not result from action on a single target.

Instead, because of it's highly reactive nature, a complex series of many unr

elated effects may occur more or less simultaneously, initiating a sequence

of additional events that may ultimately lead to cell death. "

I read an article somewhere a while back, that stated that Methyl Mercury and

Ethyl Mercury were virtually the same in their role toxicity in the human

body. Thimerisol is Ethyl Mercury. Also virtually all mercury is methylated

in the body and therefor the problem we are dealing with is methylmercury. It

may eventually become unmethylated, but it takes years for this reaction to

occur. I will see if I can relocate the article on Methyl/Ethyl Mercury.

's article did a 35 day study that they called " long term exposure " and

they gave the ALA simultaneously as prophylactic, in the " short term

exposure " portion of that study they gave mercury for 10 days followed by 10

days of ALA. I fail to see quite how any of this is equivalent to our kids

who are mercury poisoned from shots they received MONTHS to YEARS before we

ever heard of this connection.

More to follow on Lipoic Acid.

Now to the other part of my post.

said: <<I have gone back through all of the bodybio posts, and I

simply do

not understand what the problem is. Either something is a fact or

it is not. I have NEVER accepted Dr. Cutler's " opinions " on the use

of lipoic acid. Now that I have found studies proving Dr. Cutler to

be correct I am now using lipoic acid in a VERY aggressive way. Dr.

Cutler was right but he had no proof or studies in english to back

him up. He does now, and one of his most serious detractors found

the study, and posted it. Me. If bodybio has a way of doing

something, great post the thoughts and ideas back them up with

references and studies, and that is it.>>

If you want to read any of Dr.Kane's well documented research papers, you can

call BodyBio to order them. One of the paper's I have is called " The

Neurochemistry and Neurophysics of Autistic Spectrum Disorders " and has a 40

page biblography! I'm sure you could go to any medical library and get the

articles. (I have looked at a few of them, but I've been too busy reading

about mercury to follow up on more of them at the moment.) Also, Dr. Kane

wrote a medical detoxification protocol for children with autism with Dr.

Dietrich Klinghardt which was presented at the BRAIN 2000 course in Seattle

Washington December 2-4. Their protocol is an active working model in clinics

in the US, Canada and Europe.

Ruth(RN) mom to ,16,

Autism/LKS

[Guest guest]

Hi Ruth. You read the Biewenga review article on lipoic acid because

it is in english. It IS very good, but is not complete.

The better article on LA's use in mercury is in Russian, by Leskova in

Gigiena Truda ... You can find an abstract on medline.

It also helps to know enough chemistry to understand what makes

something a chelating agent. Dihydrolipoate has the same arrangement

of sulfur atoms that makes DMPS and DMSA good chelators.

Your ultimate proof, of course, is the big stack of 'clinical reports'

of improvement presented by people on this list - if you believed all

the peer reviewed journal papers you read you'd think thimerosal and

mercury has nothing to do with autism.

Andy Cutler

> I'm finally back after several busy weeks in OB department- it's the

month

> for inductions (tax deductions) and end of the year female surgeries

(before

> starting a new calendar year and new deductibles)!

>

> I have now read about a hundred or more actual full text articles on

mercury

> toxicity and hundreds of abstracts. I have read several now on

Lipoic Acid

> including one (not the one recently posted by ) claiming it

was a metal

> chelator. On CAREFUL review, however, they discussed it as

" chelating Fe2+ " ,

> and " protection of Cu2+ peroxidation, and Cd2+peroxidation was

prevented " .

> (No mention of MERCURY chelation at all.)

>

> Ok, so now looking at both these articles, ('s and the one I

just

> mentioned), one might assume that the problem is lipid peroxidation-

BUT the

> exact mechanism for merury neurotoxicity is not known.

>

> Here is an abstract from another article:

>

> Abstract Mercury in both organic and inorganic forms is neurotoxic.

> Methylmercury (MeHg) is a commonly encountered form of mercury in

the enviro

> nment. Early electrophysiological experiments revealed that MeHg

potently

> affects the release of neurotransmitter from presynaptic nerve

terminals.

> Recently, the hypothesis that these alterations may be mediated by

changes in

> the intracellular concentration of Ca2+ has been supported. MeHg

alters Ca2+

> by at least 2 mechanisms. First, it disrupts regulation of Ca2+ from

an

> intracellular Ca2+ pool and second, it increases the permeability of

the

> plasma membrane to Ca2+. MeHg also blocks plasma membrane

voltage-dependent

> Ca2+ and Na+ channels in addition to activating a nonspecific

transmembrane

> cation conductance. Chronic MeHg exposure results in ultrastructural

changes

> and accumulation of MeHg within mitochondria. In vitro, MeHg

inhibits several

> mitochondrial enzymes and depolarizes the mitochondria membrane

subsequently

> reducing ATP production and Ca2+ buffering capacity. Inhibition of

protein

> synthesis is observed after in vivo or in vitro exposures of MeHg

and may be

> an early effect of MeHg. Thus, the early cellular effects of

exposure to MeHg

> are diverse and cell damage likely occurs by more than one

mechanism, the

> effects of which may be additive or synergistic.

>

> Atchison, W.D., Hare, M.F.: Mechanisms of methylmercury-induced

> neurotoxicity.

> FASEB Journal 8:622-629; 1994

>

> Here is some information from the article: " MeHg accumulates in the

brain and

> becomes associated with motochondria, endoplasmic reticulum, golgi

complex,

> nuclear envelopes an lisosomes. In nerve fibers, MeHg is localized

primarily

> in myelin sheaths and mitochondria. " ... " Studies of MeHg

neurotoxicity have

> traditionally involved behavioral or pathological observations in

animals

> treated for days or weeks with MeHg, or observations of acute or

semiacute

> effects of MeHg primarily using in vitro systems. There have been

few

> mechanistic studies using animals treated chronically with MeHg. "

>

> " Toxicity with MeHg probably does not result from action on a single

target.

> Instead, because of it's highly reactive nature, a complex series of

many unr

> elated effects may occur more or less simultaneously, initiating a

sequence

> of additional events that may ultimately lead to cell death. "

>

> I read an article somewhere a while back, that stated that Methyl

Mercury and

> Ethyl Mercury were virtually the same in their role toxicity in the

human

> body. Thimerisol is Ethyl Mercury. Also virtually all mercury is

methylated

> in the body and therefor the problem we are dealing with is

methylmercury. It

> may eventually become unmethylated, but it takes years for this

reaction to

> occur. I will see if I can relocate the article on Methyl/Ethyl

Mercury.

> 's article did a 35 day study that they called " long term

exposure " and

> they gave the ALA simultaneously as prophylactic, in the " short term

> exposure " portion of that study they gave mercury for 10 days

followed by 10

> days of ALA. I fail to see quite how any of this is equivalent to

our kids

> who are mercury poisoned from shots they received MONTHS to YEARS

before we

> ever heard of this connection.

>

> More to follow on Lipoic Acid.

>

> Now to the other part of my post.

>

> said: <<I have gone back through all of the bodybio posts,

and I

> simply do

> not understand what the problem is. Either something is a fact or

> it is not. I have NEVER accepted Dr. Cutler's " opinions " on the

use

> of lipoic acid. Now that I have found studies proving Dr. Cutler to

> be correct I am now using lipoic acid in a VERY aggressive way.

Dr.

> Cutler was right but he had no proof or studies in english to back

> him up. He does now, and one of his most serious detractors found

> the study, and posted it. Me. If bodybio has a way of doing

> something, great post the thoughts and ideas back them up with

> references and studies, and that is it.>>

>

> If you want to read any of Dr.Kane's well documented research

papers, you can

> call BodyBio to order them. One of the paper's I have is called " The

> Neurochemistry and Neurophysics of Autistic Spectrum Disorders " and

has a 40

> page biblography! I'm sure you could go to any medical library and

get the

> articles. (I have looked at a few of them, but I've been too busy

reading

> about mercury to follow up on more of them at the moment.) Also, Dr.

Kane

> wrote a medical detoxification protocol for children with autism

with Dr.

> Dietrich Klinghardt which was presented at the BRAIN 2000 course in

Seattle

> Washington December 2-4. Their protocol is an active working model

in clinics

> in the US, Canada and Europe.

>

> Ruth(RN) mom to

,16,

> Autism/LKS

[Guest guest]

Andy,

You'll have to forgive me, but I searched both PubMed (8 articles from

Gigiena Truda-none by Leskova and none about mercury OR Lipoic Acid) and

MedLine Pro (has hundreds of search engines) found several things like " Names

in italics are not to be trusted " which took me to a site listing a multitude

of journals- looked under G, no " Gigiena Truda "

I also tried WebMedLine-- usually I can type in the authors name and Journal

name of almost anything that would be on medline and come up with an

abstract- this came up with zero citations.

Could you please post where the abstract is available on line at? Even

better, could you send me the article in ENGLISH to read. If it isn't

translated (and from Sweden pointed out before that virtually

everything of importance is translated into English these days) perhaps you

would be so kind as to translate it for me. As ANY good researcher knows,

abstracts are only guides to finding information- but the article in it's

entirety must be read to find out the actual information presented therein-

research and the authors findings and intent. So, I am assuming that you have

the actual article and can read and translate Russian. I will send you my fax

# privately if that is easier for you, but you have my e-mail address, so you

could also send it as an attachment.

I am really curious what the article says that is beyond the " Biwenda "

article, since that article also only pointed to the antioxidant properties

of LA and protection against neuro damage by that pathway.

None of the articles I have read say ANYTHING about LA pulling mercury out

any tissues and eliminating it, increasing mercury levels in urine or stool,

or any other method of causing the body to release mercury. That is the

definitive test of a chelator is it not? If LA actually did that, one would

think there would be an article somewhere that says so.

And since many articles (I only posted one this morning that gave concise

info about this issue for the sake of not taking up the whole list and all MY

time, since I am the mother of an autistic child as well as a nurse, and I do

have other things to do) I have read on mercury call attention to the fact

that there are probably MANY pathways, not just the oxidative one or even the

ones addressed in the Atchison article, by which mercury causes damage, I

would like see these issues addressed as well if LA does such a good job

" chelating " .

As to your comment that this list is a good resource of how well LA is

working, MALARKEY! There have been multiple posts about problems children

have had when adding in LA, many others have just not come to the group with

their problems because of the attitude found in just such statements as

yours, and many other parents have left the list because their child did not

do well. Even a " poll " on this list would not be accurate because it only

counts those who actually voted- those interested in the subject, those on

the list at the present time, etc. We already found out about flawed polls on

several other lists. I am in contact with several physicians and other health

care professionals involved with ACAM, and the reports are coming in that

many of these doctors are seeing children or being consulted about children

who have done very poorly, and indeed regressed, on the LA protocol.

I will post more later on articles, etc., on LA, but I felt I needed to

address your statements as soon as possible. Now I'm off to get out of

mischief and help my husband with a repair job on the bathroom floor.

Ruth(RN), mom to ,16,

Autism/LKS

Andy wrote :

<<Message: 23

Date: Mon, 01 Jan 2001 19:45:32 -0000

From: " Cutler " <AndyCutler@...>

Subject: Re: 's Lipoic Acid Article and his questions about Dr. Kane's

research

Hi Ruth. You read the Biewenga review article on lipoic acid because

it is in english. It IS very good, but is not complete.

The better article on LA's use in mercury is in Russian, by Leskova in

Gigiena Truda ... You can find an abstract on medline.

It also helps to know enough chemistry to understand what makes

something a chelating agent. Dihydrolipoate has the same arrangement

of sulfur atoms that makes DMPS and DMSA good chelators.

Your ultimate proof, of course, is the big stack of 'clinical reports'

of improvement presented by people on this list - if you believed all

the peer reviewed journal papers you read you'd think thimerosal and

mercury has nothing to do with autism.

Andy Cutler>>

[Guest guest]

With all this talk of DMSA and Alpha Lipoic Acid for chelation, has

anyone considered that these chelators may not make it through the

impaired sulfoxidation/sulfation detox pathways in the liver? Are Ray

Saalera and I the only ones that have noticed that DMSA is like

giving sulfites to those who are allergic to it? Does DMSA really

oxidize in the capsule to a sulfite before it is ever ingested?

If mercury indeed replaces molybdenum in the sulfite oxidase enzyme,

thus deactivating it of sorts, then what are we doing with DMSA and

ALA, further depleting what few sulfates we have to latch on to toxic

metals? Impaired sulfoxidation leads to impaired sulfation-and we

all know by now that loose sulfites, sulfhydrils, sulfides (such as

insulin) can wreak havoc on the immune system (see autoimmune, on

bowel integrity (undersulfated GAGS) and lipoproteins in the brain

(see neurodegenerative diseases). So, it is the lesser of two evils.

If you take ALA or DMSA, you deplete your sulfates, increasing the

toxic metal load. If you don't, your metals stay put or increase

with consumption. Either way, you lose. First 1/8 capsule of DMSA

causes rash, asthma. Second dose causes pneumonia, every time-are we

chelating the weakest link first, namely zinc? Are we chelating

anything else at those low levels? How do we build up sulfoxidation

to be able to tolerate all this extra sulfuration? B-12? Folic acid?

Molybdenum (is it even going to be able to compete with mercury, the

strongest link and do any good?)- is the impaired sulfoxidation

genetic or metal-induced by defective metallothionein function

secondary to pyroluria, as HRI-Pfeiffer is postulating?