EMF - Heavy Metals - Blood-Brain Barrier

Dr Kevin Baker wrote:

Can anyone help? I have had the thought (from wherever, certainly inspired by scanning this group) that as emfs disrupt the blood brain barrier and heavy metals may well act as an atomic antenna within any organism, plus many toxic effects are CNS related, that a vicious cycle could be set up here after a critical threshold is reached (that may of course vary for different individuals). I am wondering whether any of you have had thoughts along these lines and whether there is any published research available on this subject...? Apart from my own personal interest an influential sustainable development consultant acquaintance of mine who is relatively new to the emf toxicity debate has asked whether I could quote any relevant research. Many thanks for any responses


"Planet Earth is the lunatic asylum of the Universe. The problem is the inmates are in charge" Bertrand Russell



Posted by: Carlos Levachof

Sat Mar 8, 2008 10:10 am (PST) Dear Dr. Baker:

You could probably find more insights into this matter in classical quantum theory. This atomic "zitterbewegung" of heavy metals exposed to radiofrequency in the body, has recently been used by an engineer to develop a technique in the battle against cancer. There is, however, some limited literature on this respect. I would recommend the following publications:

1: J Alzheimers Dis. 2006 Nov;10(2-3):223-53.

Blood-brain barrier flux of aluminum, manganese, iron and other metals suspected to contribute to metal-induced neurodegeneration. Yokel RA. College of Pharmacy and Graduate Center for Toxicology, University of Kentucky Medical Center, Lexington, KY 40536-0082, USA. ryokel@email.uky.edu The etiology of many neurodegenerative diseases has been only partly attributed to acquired traits, suggesting environmental factors may also contribute. Metal dyshomeostasis causes or has been implicated in many neurodegenerative diseases. Metal flux across the blood-brain barrier (the primary route of brain metal uptake) and the choroid plexuses as well as sensory nerve metal uptake from the nasal cavity are reviewed. Transporters that have been described at the blood-brain barrier are listed to illustrate the extensive possibilities for moving substances into and out of the brain. The controversial role of aluminum in Alzheimer's disease, evidence suggesting brain aluminum uptake by transferrin-receptor mediated endocytosis and of aluminum citrate by system Xc;{-} and an organic anion transporter, and results suggesting transporter-mediated aluminum brain efflux are reviewed. The ability of manganese to produce a parkinsonism-like syndrome, evidence suggesting manganese uptake by transferrin- and non-transferrin-dependent mechanisms which may include store-operated calcium channels, and the lack of transporter-mediated manganese brain efflux, are discussed. The evidence for transferrin-dependent and independent mechanisms of brain iron uptake is presented. The copper transporters, ATP7A and ATP7B, and their roles in Menkes and Wilson's diseases, are summarized. Brain zinc uptake is facilitated by L- and D-histidine, but a transporter, if involved, has not been identified. Brain lead uptake may involve a non-energy-dependent process, store-operated calcium channels, and/or an ATP-dependent calcium pump. Methyl mercury can form a complex with L-cysteine that mimics methionine, enabling its transport by the L system. The putative roles of zinc transporters, ZnT and Zip, in regulating brain zinc are discussed. Although brain uptake mechanisms for some metals have been identified, metal efflux from the brain has received little attention, preventing integration of all processes that contribute to brain metal concentrations.

2: Neurosci Lett. 2006 Oct 9;406(3):189-93. Epub 2006 Aug 21.

Nanoparticle iron chelators: a new therapeutic approach in Alzheimer disease and other neurologic disorders associated with trace metal imbalance. Liu G, Men P, Harris PL, Rolston RK, Perry G, Smith MA. Department of Radiology, University of Utah, Salt Lake City, UT 84102, USA. gang.liu@m.cc.utah.edu Accumulating evidence suggests that oxidative stress may be a major etiologic factor in initiating and promoting neurodegeneration in Alzheimer disease. Contributing to this, there is a dyshomeostasis of metal ions in Alzheimer disease with abnormally high levels of redox-active metals, particularly iron, in affected areas of the brain. Although it is unclear whether metal excesses are the sole cause of oxidative stress and neurodegeneration or a by-product of neuronal loss, the finding that metal chelators can partially solubilize amyloid-beta deposits in Alzheimer disease suggests a promising therapeutic role for chelating agents. However, the blood-brain barrier and toxicity of known chelators limit their utility. In this study, we suggest that covalent conjugation of iron chelators with nanoparticles may help overcome the limitations in blood-brain barrier permeability of existing chelation therapy. Using in vitro studies, we have shown that a chelator-nanoparticle system and the chelator-nanoparticle system complexed with iron, when incubated with human plasma, preferentially adsorb apolipoprotein E and apolipoprotein A-I, that would facilitate transport into and out of the brain via mechanisms used for transporting low-density lipoprotein. Our studies suggest a unique approach, utilizing nanoparticles, to transport chelators and chelator-metal complexes in both directions across the blood-brain barrier, thus providing safer and more effective chelation treatment in Alzheimer disease and other neurodegenerative diseases.

Neurotoxicology. 2006 Sep;27(5):737-44. Epub 2006 Mar 20.

Molecular mechanism of distorted iron regulation in the blood-CSF barrier and regional blood-brain barrier following in vivo subchronic manganese exposure. Li GJ, Choi BS, Wang X, Liu J, Waalkes MP, Zheng W. School of Health Sciences, Purdue University, 550 Stadium Mall Drive, CIVL 1163D, West Lafayette, IN 47907, USA. Previous studies in this laboratory indicated that manganese (Mn) exposure in vitro increases the expression of transferrin receptor (TfR) by enhancing the binding of iron regulatory proteins (IRPs) to iron responsive element-containing RNA. The current study further tested the hypothesis that in vivo exposure to Mn increased TfR expression at both blood-brain barrier (BBB) and blood-cerebrospinal fluid (CSF) barrier (BCB), which contributes to altered iron (Fe) homeostasis in the CSF. Groups of rats (10-11 each) received oral gavages at doses of 5 mg Mn/kg or 15 mg Mn/kg as MnCl(2) once daily for 30 days. Blood, CSF, and choroid plexus were collected and brain capillary fractions were separated from the regional parenchyma. Metal analyses showed that oral Mn exposure decreased concentrations of Fe in serum (-66%) but increased Fe in the CSF (+167%). Gel shift assay showed that Mn caused a dose-dependent increase of binding of IRP1 to iron responsive element-containing RNA in BCB in the choroid plexus (+70%), in regional BBB of capillaries of striatum (+39%), hippocampus (+56%), frontal cortex (+49%), and in brain parenchyma of striatum (+67%), hippocampus (+39%) and cerebellum (+28%). Real-time RT-PCR demonstrated that Mn exposure significantly increased the expression of TfR mRNA in choroid plexus and striatum with concomitant reduction in the expression of ferritin (Ft) mRNA. Collectively, these data indicate that in vivo Mn exposure results in Fe redistribution in body fluids through regulating the expression of TfR and ferritin at BCB and selected regional BBB. The disrupted Fe transport by brain barriers may underlie the distorted Fe homeostasis in the CSF.

Dr. Baker:

Please check out the following links:






Best regards,



Blood brain barrier and mercury could certainly be involved in toxicity of microwaves.

Here's one of many possible places to start: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2235207

Also, the bioinitiative.org report.

At microwave frequencies you don't need much of an antenna anyway.


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