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Subject: Insignificance of inorganic mercury in the brain mercury poisoning ... Selenium, B12, C and lipoic
poison the brains by increasing meHg intake to brains and impairing liver meHg detox
Date: Mon, 6 Mar 2000 02:01:06 -0700 From: Ray S Reply-To: Mercury Poisoning from Dental Amalgam To: AMALGAM@LISTSERV.GMD.DE ++++++ 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 PĆecs, 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 ++++++++++++++ |