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I have had all amalgams removed except one root canal. The info about

lipolic acid, and B-12, and sulphur makes me scared. I thought I was doing

something good for my body. joyce Also has anyone tried cholestrymine with

success? jamkaye@...

Ýlt: [adult-metal-chelation] Warning-who is right Andy Cutler or

others?

What about that?

Thanks.

Nil

++++++ Mercury Poisoning from Dental Amalgam ++++++

>TITLE: Speciation of mercury in the primate blood and brain

following long-

>term exposure to methyl mercury.

>AUTHORS: Vahter M; Mottet NK; Friberg L; Lind B; Shen DD;

Burbacher T

>AUTHOR AFFILIATION: Institute of Environmental Medicine,

Karolinska

>Institutet, Stockholm, Sweden.

>SOURCE: Toxicol Appl Pharmacol 1994 Feb;124(2):221-9

>ABSTRACT: Total (T-Hg) and inorganic (I-Hg) mercury in blood and

brain of

>female Macaca fascicularis monkeys, exposed to daily peroral doses

of methyl

>mercury (MeHg; 50 micrograms Hg/kg body wt) for 6, 12, or 18 months,

or to

>continuous iv infusion of HgCl2 (200 micrograms Hg/kg body wt) for 3

months,

>were determined. In normal weight monkeys (2.4-4.1 kg body wt)

exposed to

>MeHg, steady state of T-Hg in blood (1.1 micrograms Hg/g) was

reached in

>about 4 months. The elimination T1/2 in blood was 26 days. I-Hg

constituted

>7% of T-Hg in blood. The average concentration of MeHg in occipital

pole and

>thalamus was about 3 micrograms Hg/g at 6 months and 4.5 micrograms

Hg/g at

>12-18 months.

>Accumulation in brain seemed to be biphasic. Following

>termination of 12 months exposure, elimination T1/2 for MeHg in

brain was 35

>days. I-Hg constituted about 9% of T-Hg in brain at 6-12 months, 18%

at 18

>months, and 74% at 6 months after termination of exposure. The I-Hg

>concentrations were somewhat higher in thalamus than in occipital

pole. The

>elimination T1/2 for I-Hg was extremely long, on the order of years.

Most

>likely, the I-Hg was formed by demethylation of MeHg in the brain.

In monkeys

>exposed to HgCl2, blood levels of 0.6 micrograms I-Hg/g gave rise to

brain

>I-Hg levels of about 0.1 micrograms/g only. In three heavy weight

monkeys

>(5.0-6.1 kg body wt) exposed to MeHg, blood Hg increased to about 2

>micrograms Hg/g, indicating a limited distribution of MeHg to fat.

The Hg

>concentrations in brain (7-22 micrograms Hg/g) were considerably

higher than

>those in normal weight monkeys, due to the high blood Hg levels in

>combination with a high brain-to-blood distribution ratio.

>They have a figure that shows this all very nicely. Once they stop

putting

>methylmercury into the monkeys, methylmercury levels in the monkey

brains

>fall precipitiously. Inorganic mercury levels don't budge.

----------------

The same study shows very nicely that that there is no brain-

poisoning from inorganic mercury, as 4 times higher inorganic mercury

exposure ( HgCl2 ) resulted in ONLY 1/30th to 1/45th of the levels

the organic mercury did, ie, inorganic mercury accumulates 120 - 190

times less to brains per same dose as methyl-mercury does.

This means that practically ALL brain mercury poisoning is from

methyl-mercury entering the brains, converting there to inorganic,

and locking into the brains.

Therefore, taking agents that impair methyl-mercury detox causing

higher blood methyl-mercury levels will cause higher brain methyl-

mercury intake, which will result in higher brain mercury levels

for example Lipoic acid impairs methyl- mercury detox from liver,

which will naturally lead to higher blood methyl-mercury levels, and

therefore higher brain mercury intake from the methyl-mercury, as

inorganic mercury is not taken to brains practically at all ...

A reference that suggests LA may be bad idea for brains, as it

impairs liver methyl-mercury detox, and as Methyl-mercury is

responsible for up over 99 % of all mercury intake to brains, LA can

really cause increase intake to the brains ...

" Effect of lipoic acid on biliary excretion of glutathione and

metals. Gregus Z; Stein AF; Varga F; Klaassen CD Department of

Pharmacology, University Medical School of PÆecs, Hungary. Toxicol

Appl Pharmacol, 1992 May, 114:1, 88-96 Several metals are excreted in

bile as glutathione complexes, and their biliary excretion is

facilitated by increased hepatobiliary transport of glutathione. The

present study analyzed the effect of lipoic acid (LA; thioctic acid;

37.5-300 mumol/kg, iv),an endogenous disulfide which can be reduced

in vivo to a dithiol, on the hepatobiliary disposition of glutathione-

related thiols and the biliary excretion of metals (10 mumol/kg, iv)

in rats. Administration of LA enhanced the biliary excretion of

reduced glutathione in a dose-dependent fashion.

Despite increasing glutathione output, LA (150 mumol/kg, iv) did not

increase, but rather decreased, the biliary excretion of

methylmercury, cadmium, zinc, and coppe - !! - , which are

transported into bile in a glutathione-dependent manner, as indicated

by a marked reduction in their biliary excretion after diethyl

maleate-induced glutathione depletion.

It also showed that those who are heavy-weight and with excess body

fat, are going to absorb lot more mercury to their brains than those

who are thinner, and not overly fatty, who do not have as much

distribution of the methyl-mercury to their fats, and those that

circulate their brains.

So, a great way to get brains mercury poisoned is to eat plenty fatty

foods, taking excess doses of methylating nutrients such as TMG, B12,

C, Selenium, and at the same time, taking nutrients that impair

reduction of blood/liver methyl-mercury such as lipoic acid, and

keeping oneself overweight.

Selenium is also a great way to pump mercury to the brains, in

addition to B12+C combo, and blocking liver methyl-mercury detox with

lipoate, or taking SAMe that also methylates mercury and can together

therefore help methylate kidney, GI and oral deposits of inorganic to

methyl-mercury, and then cause the raising of blood and brain methyl-

mercury levels, and as the methyl-mercury is the main intake mode,

this is non-desireable.

This reference summarizes some of the nutrients causing

biomethylation :

Recent studies on biomethylation and demethylation of toxic elements.

Ridley WP; Dizikes L; Cheh A; Wood JM Environ Health Perspect, 1977

Aug, 19:, 43-6 Methylcobalamin (methyl-B12) has been implicated in

the biomethylation of the heavy metals (mercury, tin, platinum, gold,

and thallium) as well as the metalloids (arsenic, selenium, tellurium

and sulfur).

In addition, methylcobalamin has been shown to react with lead, but

the lead-alkyl product is unstable in water.

Details of the kinetics and mechanisms for biomethylation of arsenic

are presented, with special emphasis on synergistic reactions between

metal and metalloids in different oxidation states. This study

explains why synergistic, or antagonistic, processes can occur when

one toxic element reacts in the presence of another. The relative

importance of biomethylation reactions involving methylcobalamin will

be compared to those reactions where S-adenosylmethionine is is

involved.

>This also again raises the point that mercury does not methlyate

inside of

>you. In fact, it would be great if it did because if you could get

the

>mercury in your brain to methlyate it would come out.

>Andy Cutler

This also again raises the point that mostly all mercury to the

brains and nerves is from methyl-mercury, that is formed in vivo,

from B12+ C and selenium and methylating microbial contribution, and

that taking excess selenium, B12 + C vitamins, and having flora that

methylates mercury ( candida ) will all increase blood methyl-

mercury, and that is the major form of mercury taken into the brains

( absorbing up to 190 times better to brains than inorganic ) and

that the heavy-weighter one is, and the more one has fatty tissues,

the more will one get mercury taken into the brains.

The references that demonstrate how mercury methylates in you = in

vivo by C+B12 vitamin combo can be found from the list archives,

posted there NUMEROUS times, as well as the fact that seleium

increase organic mercury intake to brians has been also posted there,

and the above references posted by Andy as well as the Lipoate

reference suggest that one wants to keep BLOOD and LIVER methyl-

mercury levels to minimum to minimize brain methyl-mercury intake,

which is the absolutely major intake mode of mercury to the brains,

and once there, part demethylates back to inorganic and locks into

the brains, and won't come out easily anymore with anything else but

DMSA, and even with that, slowly, but at least it helps to reverse

what excess intake of LA, Vit C+B12+selenium and eating plenty fats

can cause.

So, if one wants to avoid pumping mercury to brains, one wants to :

1. Avoid eating oneself heavy-weight, putting up plenty fat, and

increasing brain methyl-mercury uptale

2. Avoid excess nutrients Lipoic acid, Selenium, S-

adesnosylmethionine, Methylcobalamin and C vitamin

That is while one still has plenty extra-brain inorganic mercury in

the tissues that can be converted to methyl-mercury and taken to

brains.

Numerous people have experienced getting foggy in the brains, and

developing the methyl-mercury twitches after eating fatty foods,

after takign lipoate, SAMe, C+Methylcobalamin, or Selenium in excess

( and also felt the arrythmias the methyl-mercury in the heart may

cause in addition to the foggyness and muscle twitches ... )

Regards, Ray Saarela

+++++++++++++ http://www.listserv.gmd.de/archives/amalgam.html

++++++++++++++

Top document

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where do I get tested for mercury and mycoplasmas?jamkaye@...

Ýlt: [adult-metal-chelation] Warning-who is right Andy Cutler or

others?

What about that?

Thanks.

Nil

++++++ Mercury Poisoning from Dental Amalgam ++++++

>TITLE: Speciation of mercury in the primate blood and brain

following long-

>term exposure to methyl mercury.

>AUTHORS: Vahter M; Mottet NK; Friberg L; Lind B; Shen DD;

Burbacher T

>AUTHOR AFFILIATION: Institute of Environmental Medicine,

Karolinska

>Institutet, Stockholm, Sweden.

>SOURCE: Toxicol Appl Pharmacol 1994 Feb;124(2):221-9

>ABSTRACT: Total (T-Hg) and inorganic (I-Hg) mercury in blood and

brain of

>female Macaca fascicularis monkeys, exposed to daily peroral doses

of methyl

>mercury (MeHg; 50 micrograms Hg/kg body wt) for 6, 12, or 18 months,

or to

>continuous iv infusion of HgCl2 (200 micrograms Hg/kg body wt) for 3

months,

>were determined. In normal weight monkeys (2.4-4.1 kg body wt)

exposed to

>MeHg, steady state of T-Hg in blood (1.1 micrograms Hg/g) was

reached in

>about 4 months. The elimination T1/2 in blood was 26 days. I-Hg

constituted

>7% of T-Hg in blood. The average concentration of MeHg in occipital

pole and

>thalamus was about 3 micrograms Hg/g at 6 months and 4.5 micrograms

Hg/g at

>12-18 months.

>Accumulation in brain seemed to be biphasic. Following

>termination of 12 months exposure, elimination T1/2 for MeHg in

brain was 35

>days. I-Hg constituted about 9% of T-Hg in brain at 6-12 months, 18%

at 18

>months, and 74% at 6 months after termination of exposure. The I-Hg

>concentrations were somewhat higher in thalamus than in occipital

pole. The

>elimination T1/2 for I-Hg was extremely long, on the order of years.

Most

>likely, the I-Hg was formed by demethylation of MeHg in the brain.

In monkeys

>exposed to HgCl2, blood levels of 0.6 micrograms I-Hg/g gave rise to

brain

>I-Hg levels of about 0.1 micrograms/g only. In three heavy weight

monkeys

>(5.0-6.1 kg body wt) exposed to MeHg, blood Hg increased to about 2

>micrograms Hg/g, indicating a limited distribution of MeHg to fat.

The Hg

>concentrations in brain (7-22 micrograms Hg/g) were considerably

higher than

>those in normal weight monkeys, due to the high blood Hg levels in

>combination with a high brain-to-blood distribution ratio.

>They have a figure that shows this all very nicely. Once they stop

putting

>methylmercury into the monkeys, methylmercury levels in the monkey

brains

>fall precipitiously. Inorganic mercury levels don't budge.

----------------

The same study shows very nicely that that there is no brain-

poisoning from inorganic mercury, as 4 times higher inorganic mercury

exposure ( HgCl2 ) resulted in ONLY 1/30th to 1/45th of the levels

the organic mercury did, ie, inorganic mercury accumulates 120 - 190

times less to brains per same dose as methyl-mercury does.

This means that practically ALL brain mercury poisoning is from

methyl-mercury entering the brains, converting there to inorganic,

and locking into the brains.

Therefore, taking agents that impair methyl-mercury detox causing

higher blood methyl-mercury levels will cause higher brain methyl-

mercury intake, which will result in higher brain mercury levels

for example Lipoic acid impairs methyl- mercury detox from liver,

which will naturally lead to higher blood methyl-mercury levels, and

therefore higher brain mercury intake from the methyl-mercury, as

inorganic mercury is not taken to brains practically at all ...

A reference that suggests LA may be bad idea for brains, as it

impairs liver methyl-mercury detox, and as Methyl-mercury is

responsible for up over 99 % of all mercury intake to brains, LA can

really cause increase intake to the brains ...

" Effect of lipoic acid on biliary excretion of glutathione and

metals. Gregus Z; Stein AF; Varga F; Klaassen CD Department of

Pharmacology, University Medical School of PÆecs, Hungary. Toxicol

Appl Pharmacol, 1992 May, 114:1, 88-96 Several metals are excreted in

bile as glutathione complexes, and their biliary excretion is

facilitated by increased hepatobiliary transport of glutathione. The

present study analyzed the effect of lipoic acid (LA; thioctic acid;

37.5-300 mumol/kg, iv),an endogenous disulfide which can be reduced

in vivo to a dithiol, on the hepatobiliary disposition of glutathione-

related thiols and the biliary excretion of metals (10 mumol/kg, iv)

in rats. Administration of LA enhanced the biliary excretion of

reduced glutathione in a dose-dependent fashion.

Despite increasing glutathione output, LA (150 mumol/kg, iv) did not

increase, but rather decreased, the biliary excretion of

methylmercury, cadmium, zinc, and coppe - !! - , which are

transported into bile in a glutathione-dependent manner, as indicated

by a marked reduction in their biliary excretion after diethyl

maleate-induced glutathione depletion.

It also showed that those who are heavy-weight and with excess body

fat, are going to absorb lot more mercury to their brains than those

who are thinner, and not overly fatty, who do not have as much

distribution of the methyl-mercury to their fats, and those that

circulate their brains.

So, a great way to get brains mercury poisoned is to eat plenty fatty

foods, taking excess doses of methylating nutrients such as TMG, B12,

C, Selenium, and at the same time, taking nutrients that impair

reduction of blood/liver methyl-mercury such as lipoic acid, and

keeping oneself overweight.

Selenium is also a great way to pump mercury to the brains, in

addition to B12+C combo, and blocking liver methyl-mercury detox with

lipoate, or taking SAMe that also methylates mercury and can together

therefore help methylate kidney, GI and oral deposits of inorganic to

methyl-mercury, and then cause the raising of blood and brain methyl-

mercury levels, and as the methyl-mercury is the main intake mode,

this is non-desireable.

This reference summarizes some of the nutrients causing

biomethylation :

Recent studies on biomethylation and demethylation of toxic elements.

Ridley WP; Dizikes L; Cheh A; Wood JM Environ Health Perspect, 1977

Aug, 19:, 43-6 Methylcobalamin (methyl-B12) has been implicated in

the biomethylation of the heavy metals (mercury, tin, platinum, gold,

and thallium) as well as the metalloids (arsenic, selenium, tellurium

and sulfur).

In addition, methylcobalamin has been shown to react with lead, but

the lead-alkyl product is unstable in water.

Details of the kinetics and mechanisms for biomethylation of arsenic

are presented, with special emphasis on synergistic reactions between

metal and metalloids in different oxidation states. This study

explains why synergistic, or antagonistic, processes can occur when

one toxic element reacts in the presence of another. The relative

importance of biomethylation reactions involving methylcobalamin will

be compared to those reactions where S-adenosylmethionine is is

involved.

>This also again raises the point that mercury does not methlyate

inside of

>you. In fact, it would be great if it did because if you could get

the

>mercury in your brain to methlyate it would come out.

>Andy Cutler

This also again raises the point that mostly all mercury to the

brains and nerves is from methyl-mercury, that is formed in vivo,

from B12+ C and selenium and methylating microbial contribution, and

that taking excess selenium, B12 + C vitamins, and having flora that

methylates mercury ( candida ) will all increase blood methyl-

mercury, and that is the major form of mercury taken into the brains

( absorbing up to 190 times better to brains than inorganic ) and

that the heavy-weighter one is, and the more one has fatty tissues,

the more will one get mercury taken into the brains.

The references that demonstrate how mercury methylates in you = in

vivo by C+B12 vitamin combo can be found from the list archives,

posted there NUMEROUS times, as well as the fact that seleium

increase organic mercury intake to brians has been also posted there,

and the above references posted by Andy as well as the Lipoate

reference suggest that one wants to keep BLOOD and LIVER methyl-

mercury levels to minimum to minimize brain methyl-mercury intake,

which is the absolutely major intake mode of mercury to the brains,

and once there, part demethylates back to inorganic and locks into

the brains, and won't come out easily anymore with anything else but

DMSA, and even with that, slowly, but at least it helps to reverse

what excess intake of LA, Vit C+B12+selenium and eating plenty fats

can cause.

So, if one wants to avoid pumping mercury to brains, one wants to :

1. Avoid eating oneself heavy-weight, putting up plenty fat, and

increasing brain methyl-mercury uptale

2. Avoid excess nutrients Lipoic acid, Selenium, S-

adesnosylmethionine, Methylcobalamin and C vitamin

That is while one still has plenty extra-brain inorganic mercury in

the tissues that can be converted to methyl-mercury and taken to

brains.

Numerous people have experienced getting foggy in the brains, and

developing the methyl-mercury twitches after eating fatty foods,

after takign lipoate, SAMe, C+Methylcobalamin, or Selenium in excess

( and also felt the arrythmias the methyl-mercury in the heart may

cause in addition to the foggyness and muscle twitches ... )

Regards, Ray Saarela

+++++++++++++ http://www.listserv.gmd.de/archives/amalgam.html

++++++++++++++

Top document

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Guest guest

I am very thin. I cannot gain weight. When I attempted to do Hulda clarks

wormwood complex for detoxing parasites I had to go off because it gave me

an upper respiratory bacterial infection.I think I must be very toxic. How

do I detox and clean out my cells? My hair is very thin because my cells are

not getting nutrients. Is this a slow death or fast one? joyce

jamkaye@...

Ýlt: [adult-metal-chelation] Warning-who is right Andy Cutler or

others?

What about that?

Thanks.

Nil

++++++ Mercury Poisoning from Dental Amalgam ++++++

>TITLE: Speciation of mercury in the primate blood and brain

following long-

>term exposure to methyl mercury.

>AUTHORS: Vahter M; Mottet NK; Friberg L; Lind B; Shen DD;

Burbacher T

>AUTHOR AFFILIATION: Institute of Environmental Medicine,

Karolinska

>Institutet, Stockholm, Sweden.

>SOURCE: Toxicol Appl Pharmacol 1994 Feb;124(2):221-9

>ABSTRACT: Total (T-Hg) and inorganic (I-Hg) mercury in blood and

brain of

>female Macaca fascicularis monkeys, exposed to daily peroral doses

of methyl

>mercury (MeHg; 50 micrograms Hg/kg body wt) for 6, 12, or 18 months,

or to

>continuous iv infusion of HgCl2 (200 micrograms Hg/kg body wt) for 3

months,

>were determined. In normal weight monkeys (2.4-4.1 kg body wt)

exposed to

>MeHg, steady state of T-Hg in blood (1.1 micrograms Hg/g) was

reached in

>about 4 months. The elimination T1/2 in blood was 26 days. I-Hg

constituted

>7% of T-Hg in blood. The average concentration of MeHg in occipital

pole and

>thalamus was about 3 micrograms Hg/g at 6 months and 4.5 micrograms

Hg/g at

>12-18 months.

>Accumulation in brain seemed to be biphasic. Following

>termination of 12 months exposure, elimination T1/2 for MeHg in

brain was 35

>days. I-Hg constituted about 9% of T-Hg in brain at 6-12 months, 18%

at 18

>months, and 74% at 6 months after termination of exposure. The I-Hg

>concentrations were somewhat higher in thalamus than in occipital

pole. The

>elimination T1/2 for I-Hg was extremely long, on the order of years.

Most

>likely, the I-Hg was formed by demethylation of MeHg in the brain.

In monkeys

>exposed to HgCl2, blood levels of 0.6 micrograms I-Hg/g gave rise to

brain

>I-Hg levels of about 0.1 micrograms/g only. In three heavy weight

monkeys

>(5.0-6.1 kg body wt) exposed to MeHg, blood Hg increased to about 2

>micrograms Hg/g, indicating a limited distribution of MeHg to fat.

The Hg

>concentrations in brain (7-22 micrograms Hg/g) were considerably

higher than

>those in normal weight monkeys, due to the high blood Hg levels in

>combination with a high brain-to-blood distribution ratio.

>They have a figure that shows this all very nicely. Once they stop

putting

>methylmercury into the monkeys, methylmercury levels in the monkey

brains

>fall precipitiously. Inorganic mercury levels don't budge.

----------------

The same study shows very nicely that that there is no brain-

poisoning from inorganic mercury, as 4 times higher inorganic mercury

exposure ( HgCl2 ) resulted in ONLY 1/30th to 1/45th of the levels

the organic mercury did, ie, inorganic mercury accumulates 120 - 190

times less to brains per same dose as methyl-mercury does.

This means that practically ALL brain mercury poisoning is from

methyl-mercury entering the brains, converting there to inorganic,

and locking into the brains.

Therefore, taking agents that impair methyl-mercury detox causing

higher blood methyl-mercury levels will cause higher brain methyl-

mercury intake, which will result in higher brain mercury levels

for example Lipoic acid impairs methyl- mercury detox from liver,

which will naturally lead to higher blood methyl-mercury levels, and

therefore higher brain mercury intake from the methyl-mercury, as

inorganic mercury is not taken to brains practically at all ...

A reference that suggests LA may be bad idea for brains, as it

impairs liver methyl-mercury detox, and as Methyl-mercury is

responsible for up over 99 % of all mercury intake to brains, LA can

really cause increase intake to the brains ...

" Effect of lipoic acid on biliary excretion of glutathione and

metals. Gregus Z; Stein AF; Varga F; Klaassen CD Department of

Pharmacology, University Medical School of PÆecs, Hungary. Toxicol

Appl Pharmacol, 1992 May, 114:1, 88-96 Several metals are excreted in

bile as glutathione complexes, and their biliary excretion is

facilitated by increased hepatobiliary transport of glutathione. The

present study analyzed the effect of lipoic acid (LA; thioctic acid;

37.5-300 mumol/kg, iv),an endogenous disulfide which can be reduced

in vivo to a dithiol, on the hepatobiliary disposition of glutathione-

related thiols and the biliary excretion of metals (10 mumol/kg, iv)

in rats. Administration of LA enhanced the biliary excretion of

reduced glutathione in a dose-dependent fashion.

Despite increasing glutathione output, LA (150 mumol/kg, iv) did not

increase, but rather decreased, the biliary excretion of

methylmercury, cadmium, zinc, and coppe - !! - , which are

transported into bile in a glutathione-dependent manner, as indicated

by a marked reduction in their biliary excretion after diethyl

maleate-induced glutathione depletion.

It also showed that those who are heavy-weight and with excess body

fat, are going to absorb lot more mercury to their brains than those

who are thinner, and not overly fatty, who do not have as much

distribution of the methyl-mercury to their fats, and those that

circulate their brains.

So, a great way to get brains mercury poisoned is to eat plenty fatty

foods, taking excess doses of methylating nutrients such as TMG, B12,

C, Selenium, and at the same time, taking nutrients that impair

reduction of blood/liver methyl-mercury such as lipoic acid, and

keeping oneself overweight.

Selenium is also a great way to pump mercury to the brains, in

addition to B12+C combo, and blocking liver methyl-mercury detox with

lipoate, or taking SAMe that also methylates mercury and can together

therefore help methylate kidney, GI and oral deposits of inorganic to

methyl-mercury, and then cause the raising of blood and brain methyl-

mercury levels, and as the methyl-mercury is the main intake mode,

this is non-desireable.

This reference summarizes some of the nutrients causing

biomethylation :

Recent studies on biomethylation and demethylation of toxic elements.

Ridley WP; Dizikes L; Cheh A; Wood JM Environ Health Perspect, 1977

Aug, 19:, 43-6 Methylcobalamin (methyl-B12) has been implicated in

the biomethylation of the heavy metals (mercury, tin, platinum, gold,

and thallium) as well as the metalloids (arsenic, selenium, tellurium

and sulfur).

In addition, methylcobalamin has been shown to react with lead, but

the lead-alkyl product is unstable in water.

Details of the kinetics and mechanisms for biomethylation of arsenic

are presented, with special emphasis on synergistic reactions between

metal and metalloids in different oxidation states. This study

explains why synergistic, or antagonistic, processes can occur when

one toxic element reacts in the presence of another. The relative

importance of biomethylation reactions involving methylcobalamin will

be compared to those reactions where S-adenosylmethionine is is

involved.

>This also again raises the point that mercury does not methlyate

inside of

>you. In fact, it would be great if it did because if you could get

the

>mercury in your brain to methlyate it would come out.

>Andy Cutler

This also again raises the point that mostly all mercury to the

brains and nerves is from methyl-mercury, that is formed in vivo,

from B12+ C and selenium and methylating microbial contribution, and

that taking excess selenium, B12 + C vitamins, and having flora that

methylates mercury ( candida ) will all increase blood methyl-

mercury, and that is the major form of mercury taken into the brains

( absorbing up to 190 times better to brains than inorganic ) and

that the heavy-weighter one is, and the more one has fatty tissues,

the more will one get mercury taken into the brains.

The references that demonstrate how mercury methylates in you = in

vivo by C+B12 vitamin combo can be found from the list archives,

posted there NUMEROUS times, as well as the fact that seleium

increase organic mercury intake to brians has been also posted there,

and the above references posted by Andy as well as the Lipoate

reference suggest that one wants to keep BLOOD and LIVER methyl-

mercury levels to minimum to minimize brain methyl-mercury intake,

which is the absolutely major intake mode of mercury to the brains,

and once there, part demethylates back to inorganic and locks into

the brains, and won't come out easily anymore with anything else but

DMSA, and even with that, slowly, but at least it helps to reverse

what excess intake of LA, Vit C+B12+selenium and eating plenty fats

can cause.

So, if one wants to avoid pumping mercury to brains, one wants to :

1. Avoid eating oneself heavy-weight, putting up plenty fat, and

increasing brain methyl-mercury uptale

2. Avoid excess nutrients Lipoic acid, Selenium, S-

adesnosylmethionine, Methylcobalamin and C vitamin

That is while one still has plenty extra-brain inorganic mercury in

the tissues that can be converted to methyl-mercury and taken to

brains.

Numerous people have experienced getting foggy in the brains, and

developing the methyl-mercury twitches after eating fatty foods,

after takign lipoate, SAMe, C+Methylcobalamin, or Selenium in excess

( and also felt the arrythmias the methyl-mercury in the heart may

cause in addition to the foggyness and muscle twitches ... )

Regards, Ray Saarela

+++++++++++++ http://www.listserv.gmd.de/archives/amalgam.html

++++++++++++++

Top document

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