Is the brain influenced by a phone call?
Study: Is the brain influenced by a phone call? An EEG study of resting wakefulness
Abstract: Resting electroencephalogram of 20 healthy subjects in order to investigate the effect of electromagnetic field (EMF) exposure on EEG waking activity and its temporal development was recorded. The subjects were randomly assigned to two groups and exposed, in double-blind conditions, to a typical mobile phone signal (902.40 MHz, modulated at 217 Hz, with an average power of 0.25 W) before or during the EEG recording session. The results show that, under real exposure as compared to baseline and sham conditions, EEG spectral power was influenced in some bins of the alpha band. This effect was greater when the EMF was on during the EEG recording session than before it. The present data lend further support to the idea that pulsed high-frequency electromagnetic fields can affect normal brain functioning, also if no conclusions can be drawn about the possible health effects.
Bibliographic Information: Curcio G, Ferrara M, Moroni F, D'Inzeo G, Bertini M, De Gennaro L, Neurosci Res. 2005 Aug 12; [Epub ahead of print]
http://www.ncbi.nlm.nih.gov/
From FGF-Infoline, 25.08.2005
Is the brain influenced by a phone call? An EEG study of resting wakefulness.
Curcio G, Ferrara M, Moroni F, D'Inzeo G, Bertini M, De Gennaro L.
Department of Psychology, "La Sapienza" University of Rome, Via dei Marsi 78, I-00185 Rome, Italy.
We recorded the resting electroencephalogram of 20 healthy subjects in order to investigate the effect of electromagnetic field (EMF) exposure on EEG waking activity and its temporal development. The subjects were randomly assigned to two groups and exposed, in double-blind conditions, to a typical mobile phone signal (902.40MHz, modulated at 217Hz, with an average power of 0.25W) before or during the EEG recording session. The results show that, under real exposure as compared to baseline and sham conditions, EEG spectral power was influenced in some bins of the alpha band. This effect was greater when the EMF was on during the EEG recording session than before it. The present data lend further support to the idea that pulsed high-frequency electromagnetic fields can affect normal brain functioning, also if no conclusions can be drawn about the possible health effects.
PMID: 16102863 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16102863&query_hl=1
--------
Moreover we also have the studies demonstrating that blood flow in the brain, to the optic nerve etc. are also affected, and that this is possibly related to vasodilation response to levels of nitric oxide (NO) caused by EMF impact on NO synthase, since exhaled NO can also be measured under EMF exposure.
NO is also a neurotransmitter, produced as required, not stored, and could well be responsible for some aspects of cognitive disruption. It also regulates REM sleep.
So there are some very interesting chain reactions that could explain why these observed effects happen. Of course there is more, and the ideas of Konstantin Meyl relating to electric field vortices concentrating energy in a small space may add to the argument regarding momentum in the EM photon (previous Omega post) going beyond the predicted energy of a photon.
But at least we certainly cannot say that we have no plausible reasons why the observed effects take place.
EMFs and enzyme behaviours should be a big research issue.
Andy
--------
Dear Andy and All:
I have found in my archive some more details about NO that may clear the whole picture: Nitric oxide, a friend or foe ?
The nitric oxide (NO) is a neurotransmitter and vascular smooth muscle relaxant, synthesized by deamination of arginine (an amino acid) by the enzyme NO synthetase (=NOS). Nitroglycerol (taken by angina pectoris patients) is metabolized also to NO, then relaxed smooth muscles. NO is well bound to RBC haemoglobin (Hb), when blood circulated in the lungs: The thiol groups in the two cysteines in the Hb molecule, bind the NO, and prevent the haems from inactivating it. Whereupon, the NO is released in oxygen-poor blood vessels along with oxygen, stabilizes blood pressure. NO raised concentration of cyclic guanosine monophosphate (cGMP), that in turn, is active in membrane ion channels, and in numerous biochemical pathways. NO is a homeostasis signaling molecule, but also a potent free radical effector, acting in pathogenesis (Liaudet et al 2000). This paradoxical fate generated confusion, but well defining NO biological actions dissociated beneficial from toxic consequences: Normally at low concentration, NO acted as a 2nd messenger and a cytoprotective (antioxidant) factor, via direct interactions with transition metals and other free radicals. But when due to conditions high NO concentrations produced, and modified the formation of superoxide radical, the NO turned into indirect effects to form N2O3, ONOO-(peroxynitrite), NO2*, and NO3-. They in turn mediated oxidative and nitrosative cytotoxic stresses, attributed to NO, in inflammation, circulatory shock, and ischemia-reperfusion injury. Radicals excess in neurons derail neural and muscular activities. Dawson and Dawson (1996) showed that excess of NO, formed in the brain and at other neurons, reacted with superoxide anion, to make ONOO- that together with oxygen free radicals inflicted severe neural damage. Boczkowski (2001) showed that exogenous and endogenous peroxynitrite altered the structure and function of mitochondrial proteins, resulted in dysfunction and cellular or organ injury. NO produced in atherosclerotic-damaged vascular endothelial cells, promoted vasodilitation and oxidized low density lipoprotein (LDL), that enhanced atherosclerosis Thus inhaling vehicular emitted NOx, adds to such detrimental activity. In the nervous system, overactive phagocytic cells produced NO that entered neurons, and generated superoxide radical, that disrupted cellular structures. NO inhibited synthesis of mitochondrial complex 1 enzyme, that resulted in energy deficit, and more free radicals produced, thus wasting the cellular antioxidant pools to defuse them. This in turn, led to develop neurological ailments. Buzard and Kasprzak (2000) reported that oxidative stress was resulted from imbalance in cellular oxidation/reduction, by metals redox reactions with endogenous oxidants, and from effects on cellular antioxidant systems. The stress impaired (redox-sensitive) signaling molecules: NO, S-nitrosothiols, AP-1, NF-kappaB (in cell nucleus), IkappaB (its inhibitor), p53, and p21ras, resulting in variety of toxic effects such as carcinogenesis. Supportive experimental data for these toxicity and carcinogenicity for two toxic metals indicated that: Fe, Cu, and metal carcinogens: Ni, Cr, and Cd were bound selectively to particular cell constituents and affected Ca signaling. Oxidative stress caused, suggested the pathogenicity of toxic Pb, Hg and As. Yoshikawa et al (2000) showed that NO generated in mice by injected enterobacterial endotoxin (lipopolysaccharide, LPS), was enhanced by exposure to ELF-EMF (0.1 mT, 60 Hz). Considering that enterobacterial mass was a major human colon contents, the LPS in contact with colon wall cells probably enhanced generation of NO, that was enhanced further by EMF exposure.
Best,
Zamir
--------
Thanks Zamir!
At risk of being tedious, I have over 60 pages of citations and abstracts all pertaining to NO, (all three kinds of ) NOS, superoxide and superoxide dismutase (SOD) and peroxynitrite, and the knock on effects as relating to exhibited symptoms of microwave sickness, including all the longer latency diseases. The key fits the lock disturbingly well. What I want to know is what it is about enzymes (such as nitric oxide synthase) that makes them particularly susceptible to modulated microwaves, what frequencies matter most, and whether it is the enzyme precursors (eg arginine), metals in their structure (eg Mg, Zn, Cu), or the genes that express them. Knowing this and being able to demonstrate it reliably would be a seriously powerful argument.
I don't believe this is the only problem, but it is presenting an amazing array of consistent pointers. I have yet to investigate any attributed microwave syndrome disorder that is not in some way directly mediated by the NO cascade.
Andy
From Mast Sanity
Abstract: Resting electroencephalogram of 20 healthy subjects in order to investigate the effect of electromagnetic field (EMF) exposure on EEG waking activity and its temporal development was recorded. The subjects were randomly assigned to two groups and exposed, in double-blind conditions, to a typical mobile phone signal (902.40 MHz, modulated at 217 Hz, with an average power of 0.25 W) before or during the EEG recording session. The results show that, under real exposure as compared to baseline and sham conditions, EEG spectral power was influenced in some bins of the alpha band. This effect was greater when the EMF was on during the EEG recording session than before it. The present data lend further support to the idea that pulsed high-frequency electromagnetic fields can affect normal brain functioning, also if no conclusions can be drawn about the possible health effects.
Bibliographic Information: Curcio G, Ferrara M, Moroni F, D'Inzeo G, Bertini M, De Gennaro L, Neurosci Res. 2005 Aug 12; [Epub ahead of print]
http://www.ncbi.nlm.nih.gov/
From FGF-Infoline, 25.08.2005
Is the brain influenced by a phone call? An EEG study of resting wakefulness.
Curcio G, Ferrara M, Moroni F, D'Inzeo G, Bertini M, De Gennaro L.
Department of Psychology, "La Sapienza" University of Rome, Via dei Marsi 78, I-00185 Rome, Italy.
We recorded the resting electroencephalogram of 20 healthy subjects in order to investigate the effect of electromagnetic field (EMF) exposure on EEG waking activity and its temporal development. The subjects were randomly assigned to two groups and exposed, in double-blind conditions, to a typical mobile phone signal (902.40MHz, modulated at 217Hz, with an average power of 0.25W) before or during the EEG recording session. The results show that, under real exposure as compared to baseline and sham conditions, EEG spectral power was influenced in some bins of the alpha band. This effect was greater when the EMF was on during the EEG recording session than before it. The present data lend further support to the idea that pulsed high-frequency electromagnetic fields can affect normal brain functioning, also if no conclusions can be drawn about the possible health effects.
PMID: 16102863 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16102863&query_hl=1
--------
Moreover we also have the studies demonstrating that blood flow in the brain, to the optic nerve etc. are also affected, and that this is possibly related to vasodilation response to levels of nitric oxide (NO) caused by EMF impact on NO synthase, since exhaled NO can also be measured under EMF exposure.
NO is also a neurotransmitter, produced as required, not stored, and could well be responsible for some aspects of cognitive disruption. It also regulates REM sleep.
So there are some very interesting chain reactions that could explain why these observed effects happen. Of course there is more, and the ideas of Konstantin Meyl relating to electric field vortices concentrating energy in a small space may add to the argument regarding momentum in the EM photon (previous Omega post) going beyond the predicted energy of a photon.
But at least we certainly cannot say that we have no plausible reasons why the observed effects take place.
EMFs and enzyme behaviours should be a big research issue.
Andy
--------
Dear Andy and All:
I have found in my archive some more details about NO that may clear the whole picture: Nitric oxide, a friend or foe ?
The nitric oxide (NO) is a neurotransmitter and vascular smooth muscle relaxant, synthesized by deamination of arginine (an amino acid) by the enzyme NO synthetase (=NOS). Nitroglycerol (taken by angina pectoris patients) is metabolized also to NO, then relaxed smooth muscles. NO is well bound to RBC haemoglobin (Hb), when blood circulated in the lungs: The thiol groups in the two cysteines in the Hb molecule, bind the NO, and prevent the haems from inactivating it. Whereupon, the NO is released in oxygen-poor blood vessels along with oxygen, stabilizes blood pressure. NO raised concentration of cyclic guanosine monophosphate (cGMP), that in turn, is active in membrane ion channels, and in numerous biochemical pathways. NO is a homeostasis signaling molecule, but also a potent free radical effector, acting in pathogenesis (Liaudet et al 2000). This paradoxical fate generated confusion, but well defining NO biological actions dissociated beneficial from toxic consequences: Normally at low concentration, NO acted as a 2nd messenger and a cytoprotective (antioxidant) factor, via direct interactions with transition metals and other free radicals. But when due to conditions high NO concentrations produced, and modified the formation of superoxide radical, the NO turned into indirect effects to form N2O3, ONOO-(peroxynitrite), NO2*, and NO3-. They in turn mediated oxidative and nitrosative cytotoxic stresses, attributed to NO, in inflammation, circulatory shock, and ischemia-reperfusion injury. Radicals excess in neurons derail neural and muscular activities. Dawson and Dawson (1996) showed that excess of NO, formed in the brain and at other neurons, reacted with superoxide anion, to make ONOO- that together with oxygen free radicals inflicted severe neural damage. Boczkowski (2001) showed that exogenous and endogenous peroxynitrite altered the structure and function of mitochondrial proteins, resulted in dysfunction and cellular or organ injury. NO produced in atherosclerotic-damaged vascular endothelial cells, promoted vasodilitation and oxidized low density lipoprotein (LDL), that enhanced atherosclerosis Thus inhaling vehicular emitted NOx, adds to such detrimental activity. In the nervous system, overactive phagocytic cells produced NO that entered neurons, and generated superoxide radical, that disrupted cellular structures. NO inhibited synthesis of mitochondrial complex 1 enzyme, that resulted in energy deficit, and more free radicals produced, thus wasting the cellular antioxidant pools to defuse them. This in turn, led to develop neurological ailments. Buzard and Kasprzak (2000) reported that oxidative stress was resulted from imbalance in cellular oxidation/reduction, by metals redox reactions with endogenous oxidants, and from effects on cellular antioxidant systems. The stress impaired (redox-sensitive) signaling molecules: NO, S-nitrosothiols, AP-1, NF-kappaB (in cell nucleus), IkappaB (its inhibitor), p53, and p21ras, resulting in variety of toxic effects such as carcinogenesis. Supportive experimental data for these toxicity and carcinogenicity for two toxic metals indicated that: Fe, Cu, and metal carcinogens: Ni, Cr, and Cd were bound selectively to particular cell constituents and affected Ca signaling. Oxidative stress caused, suggested the pathogenicity of toxic Pb, Hg and As. Yoshikawa et al (2000) showed that NO generated in mice by injected enterobacterial endotoxin (lipopolysaccharide, LPS), was enhanced by exposure to ELF-EMF (0.1 mT, 60 Hz). Considering that enterobacterial mass was a major human colon contents, the LPS in contact with colon wall cells probably enhanced generation of NO, that was enhanced further by EMF exposure.
Best,
Zamir
--------
Thanks Zamir!
At risk of being tedious, I have over 60 pages of citations and abstracts all pertaining to NO, (all three kinds of ) NOS, superoxide and superoxide dismutase (SOD) and peroxynitrite, and the knock on effects as relating to exhibited symptoms of microwave sickness, including all the longer latency diseases. The key fits the lock disturbingly well. What I want to know is what it is about enzymes (such as nitric oxide synthase) that makes them particularly susceptible to modulated microwaves, what frequencies matter most, and whether it is the enzyme precursors (eg arginine), metals in their structure (eg Mg, Zn, Cu), or the genes that express them. Knowing this and being able to demonstrate it reliably would be a seriously powerful argument.
I don't believe this is the only problem, but it is presenting an amazing array of consistent pointers. I have yet to investigate any attributed microwave syndrome disorder that is not in some way directly mediated by the NO cascade.
Andy
From Mast Sanity
Starmail - 27. Aug, 22:13
