Of mice and men; accounting for the latest (2018) observation that the same cancers are found in man and animals (mice and rats) each cancer type being associated with very specific frequencies and modulation schemes of mobile phone telephony, by Dr Chris Barnes, Bangor Scientific and Educational Consultants e-mail Chris@bsec-wales.co.uk    April 2018

 

Main site  http://drchrisbarnes.co.uk

Important Caveat:  The IPR harmonics calculated in this paper are for a GMF of some 48 micro-Tesla the approximate GMF in the UK and Japan.  I intend to address the effects of GMF on a number of World Cancer distributions in some future publications.  I also intend to fully account for the effects of Tumour Treating Fields in some future papers.      

Abstract

The paper seeks to account for the latest (2018) US Department of Health  NTP observation (rodent study) that the same cancers are found in man and animals (mice and rats) each cancer type being associated with very specific frequencies and modulation schemes of mobile phone telephony.  The author’s previous hypothesis of Ion Parametric Resonance in quantum coherence with cellular soliton modes is further developed by considering specific ion channels relevant to specific cancers.    According to the NTP study  the rodent cancers associated with GSM are Glioma, Prostate and Pancreatic.  The present author has also shown some association in the North Wales and in the human epidemiological model with GSM and glioma and others have shown association of GSM with prostate cancer in humans.   According to the author’s  hypothesis the ion channels disturbed by GSM frequencies are the voltage gated chloride channel and the voltage gated sodium channel.      The data  of Bennett et al (2004) suggest that increased voltage-gated sodium channel expression alone is necessary and sufficient to increase the invasive potential of a set of human prostate cancer cell lines that serve as a model for prostate cancer metastasis. On the other hand,   the mechanism of 1900 CDMA is common to both liver and lung cancer and is a unique facet of  both frequency components which can coincide with TRPM 7,  proton and sodium and potassium IPR..    Far field effects on humans are also considered in a very small pilot study of 31 cancer cases. The hypothesis that RFR stimulation of cation IPR/soliton modes is either cancer causing or cancer promoting is supported.  Different cation modes are associated with different cancers.  The hypothesis that RFR stimulation of certain voltage gated chloride channels and their associated soliton modes may be anticancer, especially for lung cancer, and especially when applied for short transient periods is also supported.         The IPR ion/ soliton model of interaction too justifies further investigation.  RF and DC field can predict the IPR frequency but there is no reason to suppose that the soliton mode in itself does not set the  genetic expression of  or  shape  and size of the channel.    The work on ion channels is essentially a beginning, perhaps an oversimplification.  This is hardly surprising given that many ion channels encoding genes have ‘superfamilies’(ref).    No fewer than 10 genes encode for   sodium, 16 for potassium and a staggering 100 for potassium.  This probably explains the observation of common and personal tumour treating frequencies as mentioned by  Zimmermann et al (20120>  https://www.nature.com/articles/bjc2011523There is scope for considerable further work which could potentially be of immense benefit to human kind.  

 

1.         I propose getting cancer registries to release as much data as possible to be used with a GIS study to fully validate both the quantum and IPR/soliton hypotheses.    

2.         I propose that extensive laboratory studies are needed to look into RF and modulation duty cycle effects on the various phases of healthy and cancer cell cycles.

Only with such data can we fully understand this enthralling subject and develop a truly electromagnetic and drug free cancer medicine regime. 

 

Introduction

It has long been known that interactions of EMF and EMR with Biosystems appear to be quantised in some way with regard to both frequency and field strength.  This observation alone is sufficient to account for the fact that some 40% of known studies prove a negative association of any interaction or bioeffect per se.     Negative studies have been used by some to support the notion that EMF and EMR fields pose no threat to human health and to suggest that somehow the results of positive studies or associations are fundamentally flawed.   

 

Until very recently indeed there existed no adequate theory to fully explain the observable effects, in particular the so-called frequency windowing effect.  The present author has provided such theory (ref).   

 

 

Moreover, prior to the advent of mobile telephony most studies of the epidemiological effects of EMF/ EMR on the general public were limited to those living within the near field of power  lines, the near field of Medium Wave Broadcast Transmitters and the far field of TV and FM  radio transmitters.

 

Out of a significant number of studies the conclusions were that there was a slightly increased risk of certain types of leukaemia (refs).    One study suggested a slightly increased risk of melanoma skin cancer and this has recently been elucidated in much greater detail by others(refs).

 

One group of individuals exposed to EMF/EMR at probable higher field strengths and for more sustained times are professional and amateur radio operators. Milham (1988) studied death records for a significant number of US Radio Amateurs.  Three cancers had excess odds ratios which I have calculated from Milham’s data, these are namely;  Lymphoma (NHL)  ad Myeloma both odds ratio =2.8,     Myeloid Leukaemia, odds ratio  1.41 and  Prostate Cancer odds ratio 1.15.   

 

Another similar    study suggested a slight increase in the risk of ALS (MND). 

 

Radio Amateurs are exposed to high levels of 50/60 Hz fields from the power transformers associated with their equipment as well as to specific short wave frequencies in the 1.8 -30 MHz range and some also use VHF and UHF  frequencies. 

 

Interestingly the odds ratio I have calculated for Leukaemia is virtually the same as that given by Coleman (1988) for electricity workers.   Thus it could be argued that the 50/60 Hz fields the radio hams are exposed to are a most significant factor.        

 

 Taking the very largest example of EMR in our present radio frequency environment, namely mobile telephony and based solely on incidences of Glioma brain cancer, has led to various classifications over the years culminating in the 2011 W.H.O type 2b carcinogen classification.     Group 2b: an agent is ‘possibly carcinogenic to humans’. There is limited evidence in humans that it causes cancer and the evidence from animal studies is ‘less than sufficient’. This is the new classification for mobile phones. Cancer Research UK consider Group 2B to mean that, ‘there is some evidence for a risk but it’s not that convincing’.

 

Lloyd-Morgan (2015) reviews the epidemiology of glioma in adults with respect to mobile phone use and comes to the conclusion that previous assumptions of lack of association were, in fact, seriously flawed and require revision.

 

 

The above results are suggest yet with no real certainty, that different frequencies of EMF/EMR might either cause or promote different cancers.   

 

 

Mobile phone systems have developed rapidly since their general inception in the 1990’s.    There is now a myriad of operational frequencies and modulation techniques.    Intuitively and in the light of frequency windowing effects alone one would expect different types of mobile phone system to cause different, if any, biological effect. 

 

 

 

 

Part I : Near field effects

 

Ten years of planning went into the ‘NPT’ study, a 25 million-dollar US Government rodent study that proves RF radiation levels common to cell phone use can pose a risk of certain cancers and if so which.  Essentially   the rodents lived in the near field of a transmitting antenna but only being exposed the RF levels common to that of a mobile handset. 

 

The NTP study tested Global System for Mobile Communications (GSM) modulated exposures (AT&T and T-Mobile use GSM frequencies), concluding GSM bioeffects on male rats were seen in the prostate gland and in pancreatic islets, and granular cell tumours of the brain.

 

Such effects were NOT observed in Code Division Multiple Access (CDMA)–modulated -exposed rats (Sprint, Verizon, and US Cellular use CDMA frequencies).

 

Conversely, liver effects were noted only in CDMA-exposed male rats.

 

Findings At 900 MHz: AT&T and T-Mobile use GSM frequencies

Some evidence linking RFR with malignant schwannoma in the hearts of male rats, no evidence for same in female rats. Equivocal evidence linking exposure to malignant brain glioma in females. Other tumors of various types in both sexes “may have been related to cell phone RFR exposure,”. Less serious “nonneoplastic lesions” were more frequent in exposed males and females.

Findings At 1900 MHz: Sprint, Verizon, and US Cellular use CDMA frequencies

Equivocal evidence of carcinogenicity in lung, liver and other organ tissues in both male and female mice.

Otis Brawley, the chief medical officer of the American Cancer Society said, “The NTP report linking radiofrequency radiation to two types of cancer marks a paradigm shift in our understanding of radiation and cancer risk,”

 

 

Thus the  NTP study establishes a relationship between different exposure responses to GSM technology used by AT&T and T-Mobile or CDMA technology used by Sprint, Verizon, and US Cellular.  The NTP study supports evidence that the frequency of radiation exposure is as important as the intensity of RF exposure in differentiating potential health risk from one frequency of RF exposure over another.

Trying to find a control group of people not exposed to cell phone radiation sounds impossible in today’s age.  However, to validate the results of the NTP rodent radiation study in human terms, we need a group of people exposed to only CDMA radiation and  cut off  completely from the outside world’s GSM frequencies.

 

Lucky for us such a place exists and provides a natural human control group supporting the rodent study claims that GSM and CDMA wireless technology target different cells and organs.  More data proving that we are susceptible to different frequencies used by different phone network carrier technologies ought also to raise  a red flag for the rollout of new 5G technology known as millimeter wave technology.

 

Most of the world uses GSM to some extent, except for the island nation of Japan wherein GSM technology was never deployed.   Vast distances over water isolate everyone in Japan from anything but CDMA frequencies. GSM phones are simply of no use there.

 

The NTP study showed male rats exposed to GSM frequencies had higher rates of abnormal prostate cells, and if this is also true for humans then the population of  Japan without any exposure to GSM frequencies should have prostate cancers at a much lower rate than other developed countries that use GSM technology.

 

Japan has the lowest instance rate of prostate cancers in the world – nearly 300% lower than the USA.  Prostate gland effects were not observed in CDMA-exposed rats, and the entire population of Japan has always used CDMA technology.

 

Likewise, the NTP study found that CDMA frequencies caused liver damage whereas GSM did not. By extrapolation from rodent to human model we would expect an uptick in liver cancer in Japan compared to the rest of the world where CDMA is less common, and what is found is that Japan has the highest rate of liver cancer in any industrialized country.

 

Thus, now not only do we have frequency specific bio-effect i.e. frequency windowing but we also have for the first-time substantial evidence of frequency/organ specific carcinogenesis or at the very least frequency/organ specific cancer promotion seemingly equally pertinent to the rodent and human model.      

 

The remainder of this present publication will explain the above observations and consider other what other frequency/organ specific examples of carcinogenesis  can be found from within the author’s own work and within the scientific literature.  A universal hypothesis in terms of perturbation of relevant voltage gated ion channels will be tested   and strong support found.      

Explaining the NTP observations and human mirror.

 

Geesink and Meijer have recently suggested that cancer is promoted by electromagnetic decoherence (ref).   This is truly an elegant and exquisite piece of work but as usual with physical models there are sometimes as many questions as answers.   For example, when one feeds into their model the known Schumann resonance frequencies, some 50% fall on the life stabilising bands and some 50% on the destabilising bands.  It is hard to see why life should have developed in this way unless this directly drove the morphogenic fields of evolution itself through DNA mutation.    The model can suggest which frequencies ought to promote cancer and which frequencies ought to suppress it but cannot account for the fact that different frequencies seem to promote different cancers. 

 

 

The present author has previously provided a new hypothesis developed by extending the earlier work of Geesink (ref) and linking its frequency condensates scale to both Schuman resonances and Ion Parametric resonance.     

 

The hypothesis was carefully formulated to  bring together Bose Einstein ( Frolich ) condensate ‘Geesink’ modes  and Ion Parametric Resonance.  The conclusion is that these key frequencies work in concert with Schumann resonance to normalise biological systems at an ideal DC  magnetic field strength.    The hypothesis enjoys strong support in a number of directions. For example, the prediction that cancer incidences would vary according to the earth’s background DC field is fulfilled.       A number of healing frequencies are fully explained in terms of the particular ion channel being disturbed especially pertinent to cancer wherein cancer cells some ion channels are overexpressed.      Perturbation of very specific ion channels also explains dangerous effects of RF on biology.   

 

 

 

My previous assessment was that activation of voltage gated chloride channels is  biologically  dangerous and   explains   for the first time the few sparse observations of RF at   harmonics of 455-457 Hz  being classed by others as genotoxic.  I will discuss this at length further with regard to cell cycle dependent applications, see discussion and further work.   Further it provides another mechanism by which RF (EMR) can generate ROS.  I  also proposed that if voltage gated  magnesium channel   TRPM7  was also modulated by excessive frequency sources at harmonics of 320-374 Hz   both additional oxidative and nitrosative stresses occur and either initiation  of cancer  could follow or highly likely promotion  of existing cancer will follow.     This could account for why certain cancer latency or reoccurrence periods appear to be reducing.   Certainly ionising radiation has this effect for breast cancer, see Nguyen et al (2011).      Another great success of the theory was to explain why the team of Zimmerman and Pasche were able to use physiological heartbeat changes to define their so called ‘TTF’ tumour treating frequencies.     The same sorts of ion channels expressed in heart muscle and nerve fibres are also expressed in many cancer cells but not so much normal non-excitable tissue.  The theory also explained, for the first time  Hallberg’s  observations of FM radio antenna polarisation and melanoma.  Finally, regarding power windowing, the limit of human sensitivity is of the order of 1 picotesla, i.e. pretty much  the   same magnitude as Schumann resonance.   

 

 

Thus  in seeking to explain  the NTP observations and human mirror, I further extend and employ the above hypothesis.   GSM 900/1800 has been shown by the above study to be associated with Glioma and Prostate cancer.  

 

Whereas 1900 MHz CDMA has been shown to be associated with both Liver and Lung cancers in both the rodent and human models. 

 

All that is necessary is firstly, to reduce each carrier frequency and any modulation frequencies onto the acoustic scale by successive division by powers of 2.    Secondly to identify the ion channels perturbed for each of the calculated frequencies.   Finally, to check if there is equivalence between the involvement or expression of these ion channels in the specific cancers involved.  

 

First consider a 900 or 1800 MHz GSM signal.  The carrier frequency reduces 429.15 Hz on the Geesink acoustic scale.  There are major   modulation components at 217 Hz and 8.3 Hz. It is known that harmonics of IPR frequencies also stimulate IPR. When these are multiplied up appropriately they fall at 434Hz and 265.6 Hz on the same scale.

 

According to the NTP study  the rodent cancers associated with GSM are Glioma, Prostate and Pancreatic.  The present author has also shown some association in the North Wales and in the human epidemiological model with GSM and glioma and others have shown association of GSM with prostate cancer in humans.  

 

According to the author’s  hypothesis the ion channels disturbed by GSM frequencies are the voltage gated chloride channel and the voltage gated sodium channel.     

 

Thus a further and fitting test of the extended hypothesis is to enquire if and how these channels are relevant to the three associated cancers.    

 

Olsen et al (2003) state that voltage-gated chloride channels have recently been implicated as being important for cell proliferation and invasive cell migration of primary brain tumors cells. In their study they provide several lines of evidence that glioma Cl– currents are primarily mediated by ClC-2 and ClC-3, two genes that belong to the ClC superfamily.

 

Glioblastoma is the most common and aggressive primary malignant brain tumor. Voltage-gated chloride channels have been identified as crucial regulators of glioma cell migration and invasion by mediating cell shape and volume change.  Chloride channel blockers have been shown to be effective against glioma.   

 

It is proposed thus that the mechanism of GSM RF must be counter to blocking i.e. enhaning the chloride channel.

 

ClC-3 is also expressed in Human Prostate Cancer Epithelial Cells see Lemonnier et al (2004). 

 

FXYD3 is overexpressed in pancreatic ductal adenocarcinoma and influences pancreatic cancer cell growth.   FXYD3, a transmembrane protein that acts as a chloride channel or chloride channel regulator.   I postulate thus that the mechanism of GSM RFR in pancreatic cancer is to act synergistically with FXYD3 to further enhance chloride transport. 

 

Thus we have a common thread in all three cancers which is enhanced chloride channel and transport.   I have previously discussed the chloride channel as a dangerous route through which RF EMR can generate ROS.  

 

I next turn to the voltage gated sodium channel.  

 

Schrey (2002) has shown voltage-sensitive sodium channels appear to be an electrophysiological hallmark of gliomas.   Further, their  study gives clear evidence for a differential expression of sodium channel subtypes in gliomas and indicates a predominant expression of channels related to malignancy grades.  Sodium channel subtypes are: Nav1.1, Nav1.2, Nav1.3, Nav1.4, Nav1.6, and Nax (Nav2.1)  Nav1.6 however seemed to be almost absent in gliomas. 

 

Voltage‐gated Na+ channel (VGSC) activity has also been implicated in prostate cancer (PC) metastasis. Although VGSCs can occur as multiple‐subunit assemblies, the α‐subunits (VGSCαs) alone can encode functional channels.   Diss et al (2001) conclude that several VGSCα genes and their splice variants are expressed similarly in both rat and human PC cell lines. (2) Expression levels are much higher in the strongly metastatic (MAT‐LyLu/PC‐3) cells. (3) Levels of SCN9A mRNA specifically are predominant in MAT‐LyLu and PC‐3 cells; thus, SCN9A is highly likely to be the main source of the functional VGSC detected, see Prostate 48:165–178, 2001. © 2001 Wiley‐Liss, Inc.

Diss (2005) show Na v 1.7, to  be  associated with strong metastatic potential in prostate cancer.

 

 

Anderson et al 2003 have showed voltage-gated sodium channel blockers to be cytostatic inhibitors of the androgen-independent prostate cancer cell line PC-3.

 

Mycielska (2003) also showed a contribution of functional voltage‐gated Na+ channel expression to cell behaviours involved in the metastatic cascade in rat prostate cancer.

 

Thus the conclusion is here that GSM RFR enhances the channel or transport therein, I a similar manner to the chloride channel above.    

 

No significant references can be found as to the expression of voltage gated sodium channels in pancreatic cancer of humans or rodents.  Thus the conclusion most supported is that only the chloride channel is disturbed by GSM RFR in the case of pancreatic cancer whereas both the chloride and the sodium channel are disturbed in gliomas and prostate cancer. 

 

Glioma was the most abundant cancer observed in the rodent study.   

 

 

I next turn to the effects of Verizon 1900 CDMA.  The basic carrier frequency of 1900 MHz reduces to 452 Hz on the Geesink Scale and the modulation effectively has a spread comb   like quasi random spectrum from 2-16 Hz.   Thus the ion channels expected to be perturbed are the hydrogen ( proton) channel ( 452Hz )  and the sodium channel (256Hz ) and the potassium channel (    320 Hz) and the TRPM 7 channel (320-374 Hz).

The cancers observed are Liver and Lung in the rodent model and in Japan where 1900 CDMA has been exclusively used Liver cancer rates are very high and Lung cancer rates are comparable with other parts of the world.  

 

I next seek to confirm the involvement of the hydrogen and sodium channel  and TRPM 7 in these two cancers.  

 

Over activity of the proton channel HV1 increases proliferation in all types of cancer cells, see Hong et al (2014).   Fang et al ( 2013) have showed that inhibiting the TRPM 7 channel stops proliferation in rat liver cancer.  

Since 1900 CDMA produces TRPM 7 IPR and soliton mode interaction it is not surprising it is involved in proliferation of rat liver cancer.         Gao et al (2011) describes TRPM7 as a potential target for lung cancer treatment.   

Spugninni et al (2015) conclude:

• pH derangement is a common feature of cancers.

 

·         Major determinants of aberrant pH gradient in cancer are proton exchangers and transporters.

 

·         These include V-ATPase, Na+/H+ exchanger, MC transporters, CA.

·         Through proton transporters and exchangers tumors isolate themselves from the body.

·           Pharmacological inhibition of these molecules may represent the future of cancer therapy.

 

Proton channels may be considered as a class of Acid Sensing Channel or ASICS.  An acidic microenvironment promotes carcinoma cell proliferation and migration. Acid-sensing ion channels (ASICs) are H+, Ca2+, and Na+-gated cation channels that are activated by changes in the extracellular pH, and ASIC1α may be associated with tumor proliferation and migration.

 

Jin et al (2015)  investigated the role of ASIC1α in hepatocellular carcinoma (HCC) migration and invasion. The expression of ASIC1α was examined in 15 paired HCC and adjacent non-tumor tissues by immunohistochemistry.   A moderately acidic extracellular environment promoted ASIC1α expression, and silencing of ASIC1α expression inhibited the migration and invasion of HCC cells. Suppression of ASIC1α expression by RNAi attenuated the malignant phenotype of HCC cells, suggesting a novel approach for anticancer gene therapy.

 

Since ASICS can also be activated by Sodium it is not surprising that 1900 CDMA causes such a rise in HCC.     

 

Furthermore according to Yang et al (2011)  Na+/H+ exchanger 1 gene (NHE1) expression was increased in HCC tissues and cells in which its expression was associated with the increased tumour size, venous invasion and advanced tumour stages.

 

Finally, I turn to Potassium channels.   Blockage of voltage-gated K+ channels inhibits adhesion and proliferation of hepatocarcinomatous cells, see Zhou et al 2003.  Thus I would propose that RFR stimulation of IPR does the opposite and encourages proliferation. 

 

Since 1900 CDMA has the potential to cause IPR of proton, sodium and potassium  it is not surprising that associations are found. 

 

 

The experiments of Roger et al (2007) suggest that the functional expression of voltage-gated sodium channels might be an integral component of the metastatic process in non-small-cell lung cancer cells probably through its involvement in the regulation of intracellular sodium homeostasis. These channels could serve both as novel markers of the metastatic phenotype and as potential new therapeutic targets.

 

Similar to the work of Yang above, Li et al (2009) has also showed that inhibition of proliferation and apoptosis in drug-resistant human small cell lung cancer cells may be induced by a Na+/H+ exchanger-1 (NHE-1) antisense gene.

 

Finally, I consider the potassium channel and lung cancer.  Anti-proliferative effect of Kv1.3 blockers in A549 human lung adenocarcinoma in vitro and in vivo  have been studied by  Jang et al (2010).   In their  study, they investigated the effects of suppression of Kv1.3 expression on cell proliferation and cell cycle progression in human lung adenocarcinoma, A549 cells. Treatment with margatoxin (MgTX), a selective blocker of Kv1.3 or short hairpin RNA (shRNA) against Kv1.3, significantly blocked A549 cells' proliferation. In addition, selective inhibition of Kv1.3 significantly increased expression level of p21Waf1/Cip1 and significantly decreased the expression level of Cdk4 and cyclin D3.  They  also applied the MgTX into a xenograft model using nude mice, and MgTX caused a reduction of tumor volume when it was injected into the tumor tissues. Their  results suggest that Kv1.3 may serve as a novel therapeutic target for lung adenocarcinoma therapy.

 

I thus propose that the mechanism of 1900 CDMA is common to both liver and lung cancer and is a unique facet of  both frequency components which can coincide with TRPM 7,  proton and sodium and potassium IPR.   

 

Explaining some of the previous near field observations.

 

1.      Leukaemia in power workers

 

50/60 Hz are sufficiently  close to stimulate  sodium and magnesium IPR normally under the control of the 1st Schumann mode.

 

IPR is expected with 50Hz at the Sodium Channel and with 60 Hz at the Proton channel Hv1.

 

Enhancement of Voltage-gated Na+ Channel Current is Associated with Multidrug Resistance in Human Leukemia Cells,  Yamashita et al (1987).   

 

Endogenously expressed Mg2+‐dependent cation channels in K562 cells and the MIC channels in other hematopoietic cells might be formed by different channel proteins, see Semenova et al (2005).

 

The voltage-gated proton channel, H V 1, has been implicated in numerous biological functions diseases such as ischemic stroke, breast cancer, and chronic lymphocytic leukemia, see Dudev et al 2015.

 

Petheo et al (2010)  detected a significant amount of Hv1 in human eosinophil and neutrophil granulocytes and in PLB-985 leukaemia cells.   Using RNA interference, they obtained strong correlation between Hv1 expression and IHv density in PLB-985 cells. It was also demonstrated that a massive reduction in Hv1 expression can limit the Nox2 mediated superoxide production of PLB-985 granulocytes.

 

2.      Leukaemia in Radio Amateurs 

 

The study of Milham was of US Radio Amateurs thus the 60 Hz  IPR as above will be relevant.   Hence proton IPR will be highly relevant.  Different chloride channels are also expressed in leukemic and normal cells see Jiang (2002).   Coincidentally most of the frequencies that radio amateurs use would coincide with chloride frequencies or about 433 Hz on the Geesink scale.  It is doubtful if actual transmission periods will be relevant.  Most radio hams spend more time listening than transmitting but they do spend a lot of time sitting near power supplies which will be emitting 60 Hz fields.   I postulate that continuous radio frequency emissions from mobile phone base stations, pagers, TETRA and Commercial  Radio and TV  transmitters could be potentially far more hazardous than the short bursts of emission from a Ham Radio Station which do not last for significant durations of the cell cycle.   

 

 

Summary of Results

 

The results are most elegantly summarised in Table form.

 

Table 1

 

Further Discussion

 

Reference has been made above to the work of Geesink and Meijer ( refs).  In their latest (2018) work they make reference to over 200 individual studies of EMF and RFR on living systems and evaluate the results    according to factors such as carrier frequency, modulation frequency and bandwidth.   Carrier frequencies which are narrow and pure i.e. little or no phase noise and fall on the stabilising frequencies of the condensate produce either no or advantageous biological effect.  Those which fall on the dephasing or decohering (anti-condensate) frequencies seem to be associated with cancer initiation or proliferation.   Even those which fall on the stabilising frequencies have destabilisation effects if they have either modulation frequencies which fall in any of the destabilising zones and/or modulation bandwidth which exceeds ….% of the carrier frequency.     

 

1.      Effects of GSM man and rodents

It is logical therefore to attempt to retrospectively apply the Geesink model to the present results as a reinforcing test.    Referring then to Table 1 in the case of Glioma induced by GSM only the modulating frequencies lie in the ‘red’ destabilising zone and these are they which stimulate Sodium IPR.     I would expect to find evidence of sodium channel blockers inhibiting  glioma if the contrary is true and Sodium IPR by RFR is a promoter.

 

Smitherman and Sontheimer (2001) shoed the inhibition of Glial Na+ and K+ Currents by Tamoxifen (tmx) . Incubation with tmx significantly was seen to reduce cell proliferation as examined by 3[H]-thymidine uptake.

 

Kappor et al (2009) showed that knockdown of ASIC1 and Epithelial Sodium Channel Subunits Inhibits Glioblastoma Whole Cell Current and Cell Migration.  

 

The above evidence fits exactly with my expectations.  

 

Further I would expect the sodium channel  to be equally relevant to prostate cancer.     

 

 

Hoosein (2002) considered voltage-gated sodium ion channels in prostate cancer (Pca) both in terms of  expression and activity.  Their  results indicated increased expression of VGSCs in Pca and VGSC involvement in Pca growth.

 

Anderson et al (2003) examined voltage-gated sodium channel blockers as cytostatic inhibitors of the androgen-independent prostate cancer cell line PC-3.  Hydroxyamides and  a hydantoin were found to be effective. 

 

Hoosein (2001) showed that Phenytoin and carbamazepine, which inactivate voltage-gated sodium channels, inhibited the secretion of PSA by LNCaP and IL-6 by DU-145 and PC-3 cell lines.

 

The data  of Bennett et al (2004) suggest that increased voltage-gated sodium channel expression alone is necessary and sufficient to increase the invasive potential of a set of human prostate cancer cell lines that serve as a model for prostate cancer metastasis.

 

One again the above results exactly vindicate my hypothesis. 

 

2.       Effects of Verizon CDMA man and rodents: lung and liver cancers

 

The modulation frequencies suggest that both sodium and potassium could be relevant in the promotion of both lung and liver cancer by         CDMA.     Intuitively there has to potassium involvement else I would have expected GSM to produce these same cancers. 

 

 

To reiterate, the anti-proliferative effect of Kv1.3 blockers in A549 human lung adenocarcinoma in vitro and in vivo  have been studied by  Jang et al (2010).   In their  study, they investigated the effects of suppression of Kv1.3 expression on cell proliferation and cell cycle progression in human lung adenocarcinoma, A549 cells. Treatment with margatoxin (MgTX), a selective blocker of Kv1.3 or short hairpin RNA (shRNA) against Kv1.3, significantly blocked A549 cells' proliferation. In addition, selective inhibition of Kv1.3 significantly increased expression level of p21Waf1/Cip1 and significantly decreased the expression level of Cdk4 and cyclin D3.  They  also applied the MgTX into a xenograft model using nude mice, and MgTX caused a reduction of tumor volume when it was injected into the tumor tissues. Their  results suggest that Kv1.3 may serve as a novel therapeutic target for lung adenocarcinoma therapy.

 

 

 

Blockage of voltage-gated K+ channels inhibits adhesion and proliferation of hepatocarcinomatous cells, see Zhou et al 2003. 

 

 

Koch and Leffert (1979) showed that increased sodium ion influx is necessary to initiate rat hepatocyte proliferation. 

 

Only CDMA provides a mechanism for stimulating both the sodium and potassium channels by IPR by means of its modulation.  

 

Presently insufficient evidence exists in the literature to comment with great certainly on  potassium on Lung Cancer but there is evidence for TRPM7 on both lung and liver cancer.

Thus  increased activity in TRPM7 alone is probably sufficient to account    for  the association of  Verizon CDMA with lung and liver cancer. 

 

3.      Leukaemia 60 Hz 

 

Only proton channel Hv1 ( approx. 480Hz) is stimulated.  Asuage et al (2017) showed that Diphenhydramine inhibits voltage-gated proton channels (Hv1) and induces acidification in leukemic Jurkat T cells.  Not only does this represent a potential new pharmacological application and treatment for Leukaemia  but it 100% supports my hypothesis.  

 

 

Part II Far field effects.

 

So far, I have dealt with laboratory studies, mobile phone handsets and the radio ham station.  All three exposed either rodents or humans to near field conditions.

 

All three sets of results elegantly support the present hypothesis that different RF frequencies initiate or promote different cancers because of their coupling to cellular soliton modes coincident with cancer specific ion channels or groups of such channels.

 

Part II of this work explores if this possibility also applies to far field signals impinging with biology.     

 

Although there exist several public domain epidemiological studies of the effects of Powerful MW Broadcasting stations, FM Broadcasting stations, TV Broadcasting Stations and Mobile Phone Base stations the conclusions reached are very mixed.  Some suggest an  increased risk of haemopoietic cancers such as Leukaemia, NHL and Myelomas whilst others suggest increased risk of Brain cancers and Breast and Prostate cancers.           Some of the references are as follows:  Incidence of Cancer in the Vicinity of Korean AM Radio TransmitterMina Ha , Hyung-Jun Lim , Soo-Hun Cho , Hyung-Do Choi & Kwang-Yun Cho

Pages 756-762 | Published online: 07 Aug 2010,     Cancer Incidence near Radio and Television Transmitters in Great Britain I. Sutton Coldfield Transmitter

Helen Dolk Gavin Shaddick Peter Walls Chris Grundy Bharat Thakrar Immo Kleinschmidt Paul Elliott

American Journal of Epidemiology, Volume 145, Issue 1, 1 January 1997, Pages 1–9, https://doi.org/10.1093/oxfordjournals.aje.a009025,  Electromagnetic radiation: Environmental pollution and health

Anders Ahlbom Maria Feychting

British Medical Bulletin, Volume 68, Issue 1, 1 December 2003, Pages 157–165, https://doi.org/10.1093/bmb/ldg030

Published: 01 December 2003, 

 

Elmwood (1999)  makes the following conclusion:   ‘Several positive associations suggesting an increased risk of some types of cancer in those who may have had greater exposure to RF emissions have been reported. However, the results are inconsistent: there is no type of cancer that has been consistently associated with RF exposures.’

 

According to my present hypothesis this is exactly the conclusion to be expected because most commercial transmitting sites are multi-frequency installations and we have seen above how, at least in the near field,  different frequencies seem to promote different cancers via the appropriate soliton/ion channel link. 

 

Thus if I am to elucidate further in this far field  analysis, I have no choice but to both employ some of my own locally acquired experimental data  and to rely on anecdotal and press reports of cancer cases and deaths at various locations and employ ‘site finder’ to see which frequencies are active at nearby transmitters.     

 

The late Dr Neil Cherry (2002) was one of the first to realise that both the spatial and temporal evolution of a signal emitted from either a TV or mobile phone tower would be critical in determining related epidemiology      https://pdfs.semanticscholar.org/2848/19bae4232af253ec4073030e635172bedf32.pdf.

 

Following Cherry  and the arguments of Professor Cyril Smith, a world renounced expert in magnetics, water memory and more recently homeopathy,  I re-analysed some of the Dolk I and II data and found that the spatial distribution of biological effects was not simply due to antenna lobe effects but rather had a quantum mechanical origin.      

This additional piece of evidence facilitates my evaluation.    The  observation I previously made was  that biological effects  in the far field of any transmitting antenna  follows a quantum mechanical frequency/distance rule based   on the electromagnetic Aharonov–Bohm effect.  The same applies whether the effect in question relates to bio-damage to trees ( ref) or to bio-damage to humans.    

 

Recently it has been shown by van Vlaenderen (2001) that for electromagnetism the generalised Maxwell equations also contain scalar field terms which predict the existence of so called LES (longitudinal electro-scalar) waves in the vacuum which have an associated power flow term.    The experimental and theoretical  work of Ziamidorogoa (2016) during solar eclipses  confirms van Vlaenderen. http://realstrannik.com/media/kunena/attachments/208/JMP_ElectroScalar_EnergyoftheSun(2).pdf  Arbab (2014) also discusses ‘The modified electromagnetism and the emergent longitudinal wave.’   

 

 

 Evans (2004) has stressed the possible importance of the Electromagnetic Aharonov-Bohm effect in radar and signalling technologies and is convinced that the effect is responsible for certain effects of radio frequency radiation on animal and human physiology.  I will endeavour to confirm this below.

 

Tomilin (2013) discusses The Potential-Vortex Theory of Electromagnetic Waves and explains the properties of the elctroscalar wave and the magnetic vector potential.   Concluding that there are ‘new opportunities for  communications technologies’.

 

Additionally, if Batteaus’ (1968) hypothesis on nerve function proves correct, then the  A –potential with its ability to perturb electron wave function at a distance may be able to directly influence nerve and brain tissue.  

 

For instance, and as first suggested by Smith http://cwl2004.powerwatch.org.uk/programme/posters/day4-smith.pdf

  the electromagnetic radiation (E- and B-fields) from a transmitter will experience refractive index and propagate at  the velocity of light in air i.e. less than that in the vacuum, but the magnetic vector potential-A (A-field), following the Aharonov-Bohm effect, does not interact with matter (instead it alters the phase of the electron wave-function) and so propagates at the vacuum velocity of light. At 5 km distance from a 100 MHz VHF FM transmitter, there will thus be a transit time difference of 5 ns between the A and B fields, based on standard values for the dielectric constant and refractive index of air.  At 100MHz, this distance or time delay represents a 180º or pi/2 phase difference. I have expanded on this elsewhere and have shown that the condition is also value for npi/2 when n is odd (ref). 

 

Smith has suggested that frequency could  be imprinted into water alone, see https://hpathy.com/scientific-research/homeopathy-how-it-works-and-how-it-is-done-5/2/

or that  present such as living tissues.

 

Returning to the analysis of  Dolk, the frequency band 70MHz-130MHz would cover the standard deviations in Smith’s data as plotted. In the UK VHF FM broadcasts can be made anywhere within the band 88-108 MHz.  

 

The full mathematics  of the AB effect has been recently and elegantly  been developed by Bright et al (2015).

https://link.springer.com/article/10.1140/epjc/s10052-015-3670-8#

 

As an alternative to water molecules as a receiver,  DNA and whole cellular toroidal and caduceus structures may act as  receiving antennas of  electro-scalar waves.    Ion channels  too can display toroidal geometry.  Analytical solutions of Poisson's equations satisfying the Dirichlet boundary conditions for a toroidal dielectric boundary are presented. The electric potential computed anywhere in the toroidal conduit by the analytical method agrees with the value derived from an iterative numerical method.  Kuyucak (1998) show that three different channel geometries, namely, bicone, catenary, and toroid, give similar potential profiles as an ion traverses along their central axis. They then examine the effects of dipoles in the toroidal channel wall on the potential profile of ions passing through the channel. The presence of dipoles eliminates the barrier for one polarity of ion, while raising the barrier for ions of the opposite polarity. They also examine how a uniform electric field from an external source is affected by the protein boundary and a mobile charge. The channel distorts the field, reducing it in the vestibules, and enhancing it in the constricted segment. The presence of an ion in one vestibule effectively excludes ions of the same polarity from that vestibule but has little effect in the other vestibule. Finally, they discuss how the solutions we provide here may be utilized to simulate a system containing a channel and many interacting ions.    Toroidal cell membranes are occasionally observed, e.g., in specialized structures of plant cells like the prolamellar body,  see ‘From sphere to torus: a topological view of the metazoan body plan’ ( Jockusch and Dress 2003). 

 

Scalar field radio emission as distinct from transverse wave was first predicted by Nikola Tesla.  Some recent experiment shows positive results that are in qualitative agreement with the presented predictions of scalar field effects, but further quantitative tests are required in order to verify or falsify the presented theory. The importance of Nikola Tesla's pioneering research, with respect to the predicted effects, cannot be overstated, see van Vlaenderen (2003).  Experimental   Scalar radio signals have been sent which penetrate a Faraday screen using caduceus coils and toroid   https://www.google.com/patents/US5845220, see also Froning   http://www.sciencedirect.com/science/article/pii/S1875389211005773, works by considering theory of Marengo (2002).

 

Not only do biological systems and their structures from DNA to whole cells and sub-cellular structures have suitable scalar wave antennas, they also have Bose -Einstein condensates, see Frolich (ref) and more latterly Geesink and Meijner (refs).    An ideal scalar (information) receiver is an AC Josephson junction.  It has recently been shown that a Bose Einstein condensate behaves as such.    The possibility of AC Josephson Junctions in biology was first discussed almost four decades ago by  Achimowicz (1982).  Only now is the realisation.

 

Using the notion of scalar wave information, I have shown it is possible to separate out the biological effects of radio waves in the far field even those originating from multi-frequency transmitting sites.    One simply seeks the distance or time delay which represents a 180º or pi/2 phase  difference at each given frequency and then explores the distribution of cancers in radial locations defined by the given distance and frequency.  The same can also be done for odd integer (n) multiples of this distance.  Biological effects can sometimes be seen   out to n=5 or even n=7.      Antenna main beam and secondary side lobe interactions (SSL) can produce e-field fluctuations at distances similar to but not equal to those predicted by the quantum model advanced here. For instance re-evaluation of the famous Sutro transmitter study results gives better fits to the recorded cancer epidemiology according to the quantum model than it does to SSL.

 

 

Indeed, the very fact that this technique works at all and works well is a testimony as to the correctness   of Frolich’s original assertions of coherence in biology as recently and elegantly expanded upon by Geesink  and Meijer.  

 

Experimental

A number of experimental sites were chosen on the basis of known association with various cancers.  Some of these were associated with the demise of personal friends and even family members and others were more anecdotally related or as a result of investigative work following press reports.     Site -finder was used initially to find the locations of nearby transmitters and since its closure more recently  mast  data dot com https://mastdata.com/.  Where it was physically possible to visit premises the expected RF spectra were confirmed using a hand-held spectrum analyser see www.rf-explorer.com  and RF field strengths were measured using Cornet Microsystems ED88T 100MHz-8GHz tri-field meter.   In all cases  distances between the site   and nearby transmitter masts were calculated using an on-line postcode distance calculator.  

 

Only frequencies which fulfilled the necessary phase distance condition were tabulated. 

 

 I have previously discussed what I have termed ‘RF’ cancers on the basis of their association with the inception of TV Broadcasting http://www.drchrisbarnes.co.uk/Meta.htmla and   with RF fields at certain locations.   http://www.drchrisbarnes.co.uk/CancerHouses.htm. 

 

A number of individual cases are discussed in terms of my quantum mechanical location model are to be found at  http://drchrisbarnes.co.uk/More%20egg%20than%20chicken.html.

 

On the basis of the proposed quantum mechanical far field interaction it  is possible to identify which cancers are associated with various  transmission frequencies by  only considering cases which satisfy the necessary  phase distance equation for each given  frequency as explained   above. 

 

The results of the pilot study are shown in Table 2 below.

 

 

 

Table 2.

Analysis of results and Discussion

 

Far field conditions are confirmed.   The nearest point of approach to a transmitting antenna in the results is condition ‘D’ at 2100 MHz which represents a distance of 238 m.

The largest distance of possible interaction identified is 3D FM which is circa 15 Km.

 

To be considered far field a signal  needs to be interacting at least two wavelengths from an antenna.  This is 28 cm at 2100 MHz and  6m at FM.    

 

Hence, we can see the interaction is well in the far field.

 

In Part 1 of the study the link established by others for GSM with regard to glioma and prostate cancer was confirmed and also strongly supported the present hypothesis of soliton/ion channel interaction.   Amongst the so called ‘RF cancers I have previously discussed, I established my own link between breast and prostate cancer.   If the same modes of interaction are relevant in the far field    I would expect integer and odd integer quantum phase relationships as explained above for GSM and any frequencies which reduce to the same on the Geesink scale.

 

There are 31 cases of human cancer and 3 cases of animal cancer and 1 young age stoke in this pilot sample. 

 

There are 6 cases of breast cancer and at first sight the most common frequencies appear to be DVB 530 MHz.  However, it should be borne in mind that two of these cases also fulfils the correct phase relationship for GSM 900 and the other four for GSM 1800.  In this respect it should be noted that all have common modulation frequencies and that bot reduce to the same places on the Geesink scale.   In reality then it would appear to be  GSM that is the true common denominator for breast cancer.  

 

There are 5 cases of haemopoietic cancers some with apparent involvement of GSM some with DVB but no consistent theme. 

 

There are 4 cases of colon cancer GSM being the common denominator three of which also associated with    DVB 570 MHz .  I have previously shown colon cancer to be correlated   as an ‘RF’ cancer. 

 

There are 3 cases of brain cancer and all are related to 2100 MHz UMTS. The structure of a WCDMA signal is very complex and can be 1.5 or 5 MHz channel widths with modulation components including 800 and 1500Hz.  The fundamental frequency reduces to 250 Hz on the Geesink scale.          The modulation frequencies reduce to 375 and 400 Hz on the Geesink scale.  250 Hz has the potential to interfere with voltage gated sodium channels.   Geesink has recently commented on a bandwidth effect in bio-destabilisation.  The W-CDMA channel has far more bandwidth than GSM so possibly more potency to promote glioma?    375 Hz relates to either magnesium or calcium channels and 400 Hz to hydrated proton channels.  

 

 

 

There is one case of lung cancer with a possible association with GSM or Tetra.

 

There are 3 cases of Melanoma skin cancer but only one associated with FM as has been suggested a possibility by Halberg and Johansson. 

 

There is 1 case of Prostate cancer seemingly associated with GSM. This is as would be expected from the near-field study.  

 

There are 4 cases of Larynx cancer either potentially associated with GSM or DVB 530 or both. 

 

There are 3 cases of animal cancer, 1 dog lymphoma, 1 cat colon and 1 dog spleen all potentially associated with GSM. 

 

There is 1 Pancreatic cancer, potentially associated with GSM 900MHz. 

 

  There is one case of young age stroke at a the location exposed to the most frequencies which fulfil the quantum phase relationship, incidentally this was also the location of a terminal case of triple negative breast cancer.  

 

No further frequency division analysis needs to be done for the GSM cases since the carrier and modulation frequencies are the same as those for the near field study. However, in order to complete the analysis it is still necessary to check the effects of any other frequencies which satisfy the quantum interaction phase relationship and check which ion channels are involved. 

 

 

In the UK as a whole one might expect roughly equal probabilities of breast and prostate cancer, but this is not borne out here. However, the sample size is very small.     

 

Voltage-gated Na+ channels (VGSC) have been implicated in the metastatic potential of human breast, prostate, and lung cancer cells. Specifically, the SCN5A gene encoding the VGSC isotype Nav1.5 has been defined as a key driver of human cancer cell invasion. Voltage-gated Na+ channel SCN5A is a key regulator of a gene transcriptional network that controls colon cancer invasion, see House et al 2010. 

 

Re- consider a 900 or 1800 MHz GSM signal.  The carrier frequency reduces 429.15 Hz on the Geesink acoustic scale.  There are major   modulation components at 217 Hz and 8.3 Hz. It is known that harmonics of IPR frequencies also stimulate IPR. When these are multiplied up appropriately they fall at 434Hz and 265.6 Hz on the same scale.  These modulation frequencies are capable of soliton/ion channel interaction, in particular for voltage gated sodium channels. 

 

There is thus support for the notion that human breast, prostate, colon and lung cancer could all be initiated or promoted by RFR in the far field at either 900 or 1800 MHz with GSM modulation.   Somewhat surprisingly and contrary to the near field study no evidence of GSM association with glioma at a distance was found.    On the other hand 2100 MHz W-CDMA is associated with glioma.  Calculation shows its fundamental frequency to disturb sodium channels.   The apparent preference may simply be a facet of small sample size. However, WCDMA is a very wide bandwidth transmission and Geesink has remarked about the destabilising effects of such bandwidth.   

 

Unexpected possible associations of GSM  with larynx and pancreatic cancer are suggested. DVB 530 MHz also reduces to 252 Hz on the Geesink scale.  These can only be regarded as possibilities because the sample size is so small.  Nevertheless it is instructive to check for ion channel involvement.    An extensive literature search shows no reference to the expression of such channels in these two cancers.   I am forced therefore to assume that larynx and pancreatic cancers are not in any way associated with RFR.   Larynx cancers have known and strong associations with other factors such as smoking and HPV.   Tobacco and Obesity  and heavy alcohol use are strong risk factors for Pancreatic cancer.   Pancreatic cancer has also been associated with exposure to various pesticides. 

 

 

There is insufficient data to comment on the cases of individual Haemopoietic cancer observed which simply leaves the melanomas.  However taken as a group the result for Haemopoietic cancers is interesting.  A 530 MHz DVB carrier can have a modulation bandwidth of 8 MHz.  at the low end of the scale this corresponds with the voltage gated proton channel Hv1 and is thus consistent with the Radio Ham near field study.  

 

 

   There are  no significant literature references to voltage gate Sodium ion channels being relevant to Melanoma.  According to Hallberg and Johansson FM radio emissions are a causative factor in melanoma.  However the centre of the FM broadcast band reduces to 335.4 Hz on the Geesing scale which they would view as    a ‘life stabilising frequency’.     A note of caution is required, however, since there are multiple stations broadcasting at similar power levels within the bandwidth giving the effect of a potentially 20 MHz wide information carrier.  Following  Geesink and Meijner    such a scenario would behave as highly destabilising.   Examination of the ion channels which could be perturbed are the potassium channel    and the magnesium/calcium channel.   Some cases of Melanoma have been seen associated with DVB 670 MHz and with TETRA 390 MHz.  These reduce to 313 HZ( Potassium) and 374 Hz (Magnesium) on the Gessink scale both in life destabilising bands.   There are 2 skin cancers associated with 2100 WCDMA.  The modulation frequencies provide  300 and 400  Hz when reduced to the Geesink scale.  300 Hz can stimulate the potassium channel.

 

I must enquire, therefore,  if voltage gated potassium and magnesium channels are involved in Melanoma and especially if  pharmaceutical blocking of such channels  inhibits the disease.  Such a finding would strongly reinforce the present hypothesis. 

 

Silencing the KCNK9 potassium channel (TASK-3) gene disturbs mitochondrial function, causes mitochondrial depolarization, and induces apoptosis of human melanoma cells, see Nagy et al (2014).    There is some limited reference to the involvement of the TRPM gene family of magnesium channels

 

 TRPM7 can be a protector and detoxifier in both melanocytes and melanoma cells. TRPM8 can mediate agonist‐induced melanoma cell death. Therefore, we propose that TRPM1, TRPM2, TRPM7 and TRPM8 play crucial roles in melanocyte physiology and melanoma oncology and are excellent diagnostic markers and therapeutic targets, see Guo et al 2012. 

 

It would seem thus that RFR stimulation of either    voltage gated potassium and magnesium channels is suggested and supports the hypothesis as drafted.

 

The results for the fields study have been summarised in  table 3  below. 

 

 

 

Table 3.

 

Discussion of Results

The results of the far field study support the observation made by others that different RF frequencies and/or modulation schemes are capable of initiating or promoting different cancers.

 

The results of both studies support the hypothesis of the author the RFR increases activity in the over-expressed ion channels of cancers by means of soliton mode /IPR coupling.  Some cancers have more than one over-expressed ion channel whereas ion channels are normally reserved for excitable tissue.     Even in the cases of cancers with multiple overexpressed channels there is sufficient evidence in the scientific literature to suggest that if a very specific type    is pharmaceutically blocked proliferation can be slowed or halted. RFR on a specific frequency seems to single out and enhance this specific or ‘key player’ channel.   

The common denominator with the laboratory rodent study ( ref) and 21st century RFR exposure is the it is all but continuous i.e. applied over the entire cell cycle.    Even with the rodent study it was applied for 19 hours per day over the animal’s entire life times.

 

The near field study of Milham on Radio Amateurs may shed further light on the matter.  Radio Amateurs use many different frequencies which ought to be capable of exciting many different IPR’s and soliton modes and hence an excess of more than one type of cancer ought to be expected. In fact this is NOT found to be the case and  the data shows that hemopoietic  cancers are the only ones found in this group to excess.    I have proposed here that the 60 Hz fields form amateur power supplies etc. may be sufficient to cause the observed excess.   The Milham study also shows that the group of radio amateurs as a whole had considerably and statistically significantly less lung cancer than the public as a whole.  It ascribed the reason as ‘higher’ socioeconomic class.    My understanding of radio amateurs is that the great majority are ordinary people,     I wonder therefore, if short intermittent exposure to certain RF frequencies is actually beneficial.  

 

Analysis of the common frequencies used by radio hams suggests that with the exception of the 15 metre band   most fall on the Geesink 433 Hz condensate and would stimulate the chloride IPR.   15 metre band reduces to 324 Hz on the Geesink condensate which would stimulate potassium IPR and TRPM7.     

 

Intermittent exposure to low level modulated RF has also recently been used as an experimental treatment method for advanced hepatic carcinoma, see……

 

A carrier frequency of 27.12 MHz was employed modulated by a number of amplitude modulated frequencies, the so called TTF’s ( tumour treating frequencies) applied in sequence. 

 

This carrier frequency reduces to 413 Hz on the Geesink scale close to the chloride channel.

The 2,221.323 Hz  TTF reduces to 277.63 Hz, very close to the 278.9 Hz condensate/Ca2+   and Cl- (aq) IPR coherence.

10,454.4 Hz TTF Reduces to 326.7 condensate/ potassium channel and/or  TRPM7. 

6530.24 TTF

 

 Reduces to 408.14 Hz close to but not on either harmonic of hydronium ion or anhydrous chloride. 

 

All of the channels that seem to promote cancer as identified in this present study are cation channels,  NaV1. Etc,  Hv1, Potassium and TRPM. 

 

I enquire therefore if RFR stimulation of anion channels specifically inhibits cancer?   I hypothesise that this is why Radio Hams may have less lung cancer than the population at large?   The common channel between Ham Radio exposure and some of the TTF’s above is the   chloride channel.   The paradox is I have previously shown the dangers and genotoxic aspects of the chloride channel. (REF).

 

I hypothesise that the effects of RFR     on the chloride channel are duty cycle specific.  In the world at large RF emissions are continuous.  However, in the amateur radio shack   RF emissions are highly intermittent.

The cell cycle times for malignant cells are very short and mitosis continues unchecked. Normal cells have long cell cycles.  I suspect the short bursts of RF from Ham radio signals and TTF frequencies interfere effectively with the cell’s cycle. 

  

 

I enquire if there is evidence in the literature that an upregulated chloride channel can be used for cancer treatment.    The work of Okada et al (2006) confirms my argument exactly.  

 

According to Okada et al, apoptosis is an essential process in organ development, tissue homeostasis, somatic cell turnover, and the pathogenesis of degenerative diseases. Apoptotic cell death occurs in response to a variety of stimuli in physiological and pathological circumstances. Efflux of K+ and Cl− leads to apoptotic volume decrease (AVD) of the cell. Both mitochondrion-mediated intrinsic, and death receptor-mediated extrinsic, apoptotic stimuli have been reported to rapidly activate Cl− conductances in a large variety of cell types.

 

In epithelial cells and cardiomyocytes, the AVD-inducing anion channel was recently determined to be the volume-sensitive outwardly rectifying (VSOR) Cl− channel which is usually activated by swelling under non-apoptotic conditions. Blocking the VSOR Cl− channel prevented cell death in not only epithelial and cardiac cells, but also other cell types, by inhibiting the induction of AVD and subsequent apoptotic events. Ischemia-reperfusion-induced apoptotic death in cardiomyocytes and brain neurons was also prevented by Cl− channel blockers. Furthermore, cancer cell apoptosis induced by the anti-cancer drug cisplatin was recently found to be associated with augmented activity of the VSOR Cl− channel and to be inhibited by a Cl− channel blocker. The apoptosis-inducing VSOR Cl− channel is distinct from ClC-3 and its molecular identity remains to be determined. 

 

Min et al (2011) have obtained results which suggest that impaired activity of VSOR Cl− channels contributes to the cisplatin resistance in A549/CDDP cells.

 

Bustin et al have showed that certain classes of chloride channel gene are  down regulated in some cancers. Their results suggest that CLCA1 could specify a new tumour suppressor and that, as in breast cancer, CLCA2 may function as a tumour suppressor in colorectal cancer, see     Stephen A. Bustin, Shu-Rui Li, and Sina Dorudi.DNA and Cell Biology. Jun 2001.ahead of printhttp://doi.org/10.1089/10445490152122442

 

The behaviour of some chloride channels is a double-edged sword. See   Suh et al, 2005.They find   that chloride intracellular channel (CLIC)4 is a p53- and tumor necrosis factor α (TNFα)-regulated chloride channel protein that is localized to the mitochondria and cytoplasm of mouse and human keratinocytes. CLIC4 protein increases in differentiating keratinocytes and in keratinocytes exposed to DNA-damaging agents and metabolic inhibitors. Increasing CLIC4 levels by transduction of recombinant CLIC4 causes apoptosis. CLIC4 translocates to the nucleus under a variety of conditions of cell stress, and nuclear CLIC4 is associated with cell cycle arrest and accelerated apoptosis.  Yet reduction of CLIC4 and several other CLIC family members by expressing a doxycycline-regulated CLIC4 antisense also causes apoptosis in squamous cancer cell lines.

Again I suspect both loss of p53 and cell cycle times are involved in the latter case.   

 

Conclusions and further work.

 

A new hypothesis to explain the observation of different cancers being associated with different frequencies and modulations in a recent very large rodent near field RFR/cancer study  ( ref)  has been developed and fully supported,.    There is considerable support also when the model is extended to the far field and linked with the authors quantum mechanical frequency distance interaction model to be expected when dealing with soliton modes. 

 

The hypothesis that RFR stimulation of cation IPR/soliton modes is either cancer causing or cancer promoting is supported.  Different cation modes are associated with different cancers. 

 

The hypothesis that RFR stimulation of certain voltage gated chloride channels and their associated soliton modes may be anticancer, especially for lung cancer, and especially when applied for transient periods is also supported.        

 

The IPR ion/ soliton model of interaction too justifies further investigation.  RF and DC field can predict the IPR frequency but there is no reason to suppose that the soliton mode in itself does not set the  genetic expression of  or  shape  and size of the channel.   

 

The work on ion channels is essentially a beginning, perhaps an oversimplification.  This is hardly surprising given that many ion channels encoding genes have ‘superfamilies’(ref).    No fewer than 10 genes encode for   sodium, 16 for potassium and a staggering 100 for potassium.  This probably explains the observation of common and personal tumour treating frequencies as mentioned by  Zimmermann et al (20120>  https://www.nature.com/articles/bjc2011523

 

 

There is scope for considerable further work which could potentially be of immense benefit to human kind.  

 

1.      I propose getting cancer registries to release as much data as possible to be used with a GIS study to fully validate both the quantum and IPR/soliton hypotheses.     

2.      I propose that extensive laboratory studies are needed to look into RF and modulation duty cycle effects on the various phases of healthy and cancer cell cycles.

Only with such data can we fully understand this enthralling subject and develop a truly electromagnetic and drug free cancer medicine regime.