Electrosmog and autoimmune disease

Abstract

Studies in mice have shown that environmental electromagnetic waves tend to suppress the murine immune system with a potency similar to NSAIDs, yet the nature of any Electrosmog effects upon humans remains controversial. Previously, we reported how the human Vitamin-D receptor (VDR) and its ligand, 1,25-dihydroxyvitamin-D (1,25-D), are associated with many chronic inflammatory and autoimmune diseases. We have shown how olmesartan, a drug marketed for mild hypertension, acts as a high-affinity partial agonist for the VDR, and that it seems to reverse disease activity resulting from VDR dysfunction. We here report that structural instability of the activated VDR becomes apparent when observing hydrogen bond behavior with molecular dynamics, revealing that the VDR pathway exhibits a susceptibility to Electrosmog. Further, we note that characteristic modes of instability lie in the microwave frequency range, which is currently populated by cellphone and WiFi communication signals, and that the susceptibility is ligand dependent. A case series of 64 patient-reported outcomes subsequent to use of a silver-threaded cap designed to protect the brain and brain stem from microwave Electrosmog resulted in 90 % reporting “definite” or “strong” changes in their disease symptoms. This is much higher than the 3–5 % rate reported for electromagnetic hypersensitivity in a healthy population and suggests that effective control of environmental Electrosmog immunomodulation may soon become necessary for successful therapy of autoimmune disease.

Electronic supplementary material
The online version of this article (doi:10.1007/s12026-016-8825-7) contains supplementary material, which is available to authorized users.

Full text

ENVIRONMENT AND AUTOIMMUNITY
Electrosmog and autoimmune disease
Trevor G. Marshall
1
•Trudy J. Rumann Heil
2
Published online: 13 July 2016
ÓThe Author(s) 2016. This article is published with open access at Springerlink.com
Abstract Studies in mice have shown that environmental electromagnetic waves tend to suppress the murine immune
system with a potency similar to NSAIDs, yet the nature of any Electrosmog effects upon humans remains controversial.
Previously, we reported how the human Vitamin-D receptor (VDR) and its ligand, 1,25-dihydroxyvitamin-D (1,25-D), are
associated with many chronic inflammatory and autoimmune diseases. We have shown how olmesartan, a drug marketed
for mild hypertension, acts as a high-affinity partial agonist for the VDR, and that it seems to reverse disease activity
resulting from VDR dysfunction. We here report that structural instability of the activated VDR becomes apparent when
observing hydrogen bond behavior with molecular dynamics, revealing that the VDR pathway exhibits a susceptibility to
Electrosmog. Further, we note that characteristic modes of instability lie in the microwave frequency range, which is
currently populated by cellphone and WiFi communication signals, and that the susceptibility is ligand dependent. A case
series of 64 patient-reported outcomes subsequent to use of a silver-threaded cap designed to protect the brain and brain
stem from microwave Electrosmog resulted in 90 % reporting ‘‘definite’’ or ‘‘strong’’ changes in their disease symptoms.
This is much higher than the 3–5 % rate reported for electromagnetic hypersensitivity in a healthy population and suggests
that effective control of environmental Electrosmog immunomodulation may soon become necessary for successful
therapy of autoimmune disease.
Keywords Electrosmog VDR Autoimmune disease PPPM WiFi Electromagnetic hypersensitivity
Introduction
‘‘Electrosmog’’ describes the electromagnetic waves sur-
rounding us in our environment. According to NASA [1]:
‘‘As you sit watching TV, not only are there visible
light waves from the TV striking your eyes, but also
radio waves, transmitting from a nearby station, and
microwaves carrying cellphone calls and text mes-
sages, and waves from your neighbor’s WiFi, and
GPS units in the cars driving by. There is a chaos of
waves from all across the spectrum passing through
your room right now.’’
Every year, the quantity and nature of radio and
microwaves contained in this Electrosmog increases.
However, research into whether they might interact with
human biology, and exactly how they might interact, is a
field clouded by the jargon and complexity of each
technology and hampered by inadequate experimental
guidelines.
The only known natural source of microwave electro-
magnetic radiation is the negligibly weak cosmic radiation
from space, although significant sources of natural
Electronic supplementary material The online version of this
article (doi:10.1007/s12026-016-8825-7) contains supplementary
material, which is available to authorized users.
&Trevor G. Marshall
trevor.m@AutoimmunityResearch.org
1
Autoimmunity Research Foundation, Thousand Oaks, CA,
USA
2
NP-Private Practice Associates, Scottsdale, AZ, USA
Trevor G. Marshall
123
Immunol Res (2017) 65:129–135
DOI 10.1007/s12026-016-8825-7
Content courtesy of Springer Nature, terms of use apply. Rights reserved.

radiation have existed at lower radio frequencies due to
atmospheric phenomena such as the aurora borealis and
thunderstorms. Until the 1950s, Electrosmog frequencies
remained out of the microwave region, but by the 1960s
television channels began microwave transmissions. Cel-
lular phone technologies emerged during the 1980s; WiFi
during the 1990s. Both extensively use microwave fre-
quency bands. The recent release of WiGig and anti-col-
lision vehicle radars in the 60 GHz region embody a
1000-fold increase in frequency, and photon energy, over
the exposures mankind experienced up until the 1950s.
It is generally accepted that exposure to low-energy
radio waves does not produce any sign of harm. However,
low-level exposures to ionizing radiation, for example the
exposures caused by nuclear energy accidents, do indeed
affect human biology. It may take years of accumulated
exposure before the subsequent symptoms become
apparent.
Both ionizing X-rays and non-ionizing microwaves are
forms of electromagnetic radiation. The energy in X-rays,
however, is much higher, usually above a thousand elec-
tron volts (1 keV), while the energy in each microwave
photon is usually just a few micro-electron volts (leV) [1].
A primary effect of low-dose ionizing radiation (from
radon and X-rays) is suppression of our body’s immune
defenses [2,3], something which often does not become
apparent until the body catastrophically fails to overcome
an acute challenge. The emerging use of radon exposure to
mitigate rheumatoid arthritis symptoms in humans [4]isan
interesting exploitation of radiation’s immunosuppressive
properties.
With low-level non-ionizing electromagnetic radiation,
Lushnikov [5] found a suppressed immune response in
mice. Subsequently, Gapeev (aka Gapeyev) [6,7] showed
that the effect on mice of low-intensity non-ionizing
electromagnetic waves was roughly equivalent to effect of
the NSAID diclofenac. Most recently, some suppression of
inflammation was reported in lizards which had been
exposed to pulsed DECT radiation simulating the cordless
phones used in many homes [8].
Proteins are continually in motion, responsive
to electromagnetic waves
We have previously reported [9–13] that the drug olme-
sartan could be retargeted to produce immunostimulation
in patients with autoimmune disease. During that research,
we used the emerging field of molecular dynamics (MD) to
analyze the actions of both the drug olmesartan and the
native ligand, 1,25-dihydroxyvitamin-D (1,25-D) on the
VDR [14]. Molecular dynamics is computationally inten-
sive, as interactions between each atom in the VDR pro-
tein, its activating ligand, and the surrounding water are
calculated incrementally as a function of time. We found
that hydrogen bond exchange within the VDR exhibited
structural resonances at frequencies typically found in
modern Electrosmog.
Turton et al. [15]inNature Communications 2013 used
MD to study the interaction between lysozyme and its
ligand triacetylchitotriose at much higher frequencies than
Electrosmog. They were then able to confirm that the
lysozyme complex was indeed underdamped by using
femtosecond optical Kerr Effect spectroscopy. They con-
cluded that the lysozyme complex was marginally unstable,
and non-ionizing terahertz electromagnetic radiation is
likely to alter ‘‘proper biological function.’’
1
We used MD software to create a movie which allowed
us to easily visualize the relative motion of each atom in
the VDR as a function of time. The MD output comprises a
very large number of incremental combinations of protein
and ligand, which can be displayed as frames of a movie
film. This allows the relative motions of each atom in the
interaction to be studied.
Two frames from a movie of a VDR molecule being
activated by olmesartan are shown in Fig. 1(the movie is
available as ‘‘olmesartan.MP4’’ in the ‘‘Supplementary
Information’’ file). These frames, separated by a time
interval of 900 femtoseconds, show the VDR helical
‘‘backbone’’ and the position of several key atoms. The
circular area labeled as ‘‘B’’ highlights the carboxyl group
of glutamine at position GLU420 in PDB:1DB1, a crystal
structure model of the VDR [14].
How Electrosmog interacts with human metabolism
There is no need to go into detail to understand the action
of Electrosmog on human proteins. All one needs to notice
is that, in Fig. 1, the two oxygen atoms of the carboxyl
group at ‘‘B’’ have spun by 90°in the time between the two
frames. Although all the atoms of the VDR are constantly
in motion, these two oxygens are key because they are
involved in forming hydrogen bonds with the DRIP205
coactivator. When the VDR is not activated, this carboxyl
group binds with the lysine to its left (LYS264) and cannot
position the coactivator where it needs to be for proper
gene transcription. Activation forces these residues apart so
they can bind with the coactivator. The shape of the
1
Our emulation protocol was essentially similar to that of Turton
et al. except that we used Gromacs 3.3 running on a multiprocessor
Linux operating system. Because the VDR is a much larger molecule
than lysozyme, we had to emulate 239 amino acids containing a total
of 2415 atoms. They were bathed in thousands of molecules of water.
For each of our dozens of experiments, we computed 500,000
emulation steps to get 750 picoseconds of real time data. Each run
often took several days of CPU time. We used the NDLP bounding
box of Wassenaar [16,17] to keep the number of water molecule
calculations to a minimum.
130 Environment and Autoimmunity (2017) 65:129–135
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whole VDR molecule changes as it is activated by the
drug.
Whenever an electromagnetic field is present, a Lorentz
Force [18] will act upon any charged atom in motion, such
as these moving oxygen atoms, a force which could either
boost or hinder the proper activation of the VDR molecule.
Whether activation is assisted or blocked depends on the
frequency content of the molecular interactions, and that of
the impinging electromagnetic waves.
So why do not human beings suffer immediate symp-
toms when exposed to Electrosmog? Recall the time
interval between the two frames in Fig. 1—900 fem-
toseconds—corresponding to a wave frequency near
1 terahertz (THz). Very few waves oscillating at that fre-
quency are able to reach the molecules of a human body,
and none of them are currently present in Electrosmog.
Consequently, Electrosmog does not yet directly affect
motions of the individual atoms.
However, at least in the case of the VDR activation, the
bulk of the molecule changes shape with characteristic
frequencies already found in today’s Electrosmog. Groups
of hundreds of atoms which form the helical ‘‘backbone’’
of the VDR do shift together at the lower frequencies
present in Electrosmog.
The number of hydrogen bonds formed between olme-
sartan and the VDR over time shows many periods of
marginally stable activation, as can be seen in Fig. 2.
Despite an initial 170 ps sinusoidal instability, the number
of hydrogen bonds builds to a stable range within 300 ps of
the olmesartan getting to the binding pocket. However,
even this ‘‘stable’’ region beyond 300 ps shows consider-
able fluctuation, with a noticeable tendency to oscillations
having the same characteristic 170 ps period. An FFT of
the data
2
confirmed a primary response peak at a frequency
just below 6 GHz (which corresponds to the 170 ps inter-
val). WiFi routers operate in this frequency range, and
these routers already comprise a significant proportion of
indoor Electrosmog.
The VDR is even more susceptible when bound
with its natural ligand
The primary natural ligand for the VDR is 1,25 dihy-
droxyvitamin-D, a ligand with fewer oxygen atoms than
olmesartan. The hydrogen bond count for this 1,25-D and
Fig. 2 A plot (from the Gromacs g_hbond software) of the instan-
taneous number of hydrogen bonds formed between olmesartan and
the VDR sampled every 37.5 femtoseconds during the first 750 ps of
VDR activation
Fig. 1 Frames 131 and 155 from a movie showing activation of the
VDR by olmesartan, obtained using Gromacs for molecular dynamics
emulation. Most of the 239 amino acid residues making up the
PDB:1DB1 VDR are shown in helical representation, with the atoms
of GLU420 and LYS264 highlighted in ‘‘ball and stick’’ notation. The
ligand olmesartan can be seen within circle ‘‘A’’ and GLU420 within
‘‘B’’
2
The mathematics package ‘GNU Octave’’ was used to compute the
FFTs in this study. It is an open source mathematics package similar
to Wolfram’s MATLAB.
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VDR combination is therefore lower. Consequently, the
VDR ‘‘backbone’’ is less rigid than when olmesartan is
used as the ligand. Figure 3shows 2250 ps of activity,
three times as long a time frame as is shown in Fig. 2.
The modes of functional resonance in the natural ligand/
VDR combination are slower, and the FFT (Fig. 4) con-
firms multiple hydrogen bond exchange rate peaks in the 3,
5 and 6 GHz, frequency bands, close to those typically
found in Electrosmog from WiFi and 4G-LTE cellular
communication devices.
Electromagnetic waves in Electrosmog exert
sufficient force to affect biological function
The force exerted on a moving charge by an electromag-
netic wave is dependent on the charge’s velocity, the
wave’s frequency and the wave’s amplitude [18]. With
environmental Electrosmog, the amplitude is an uncon-
trolled variable, and amplitudes can easily exceed
-16 dBm
3
(1 V/m at 1 GHz) when close to cell phones,
cell towers and WiFi access points.
There are many studies which document biological
effects at these higher levels, and the 2012 ‘‘BioInitiative’’
consensus [19] collated and summarized many of them.
However, very few studies tried to define the lowest level at
which electromagnetic waves might start to affect biology.
Bise [20] reported in 1978 that human EEG was changed by
wave amplitudes as low as -100 dBm, with -60 dBm
giving multiple subjects immediate frontal headache. Sadly,
such levels are impossible to replicate in 2016 without the
use of a Faraday cage, as the Electrosmog background levels
in our cities rarely fall below -50 dBm (100,000 times
stronger than the -100 dBm signals used by Bise).
While investigating the report of Gapeev [21] that the
near-field zone of an antenna seemed more biologically active
than the far-field zone, we received reports that 27.12 MHz
signals from our near-field (capacitive wave) antenna, similar
in design to Figure 9 of Sacco and Tomilin [22], could be
sensed by patients, but not by healthy individuals. This
occurred at levels around -90 dBm, levels below wideband
thermal noise. Even though Bise reported human responses at
similarly low levels, our observation needs independent
replication before we would claim it as definitive.
However, the BioInitiative report noted ‘‘At least five
new cell tower studies are reporting bioeffects in the range
of 0.003–0.05 lW/cm
2
researchers report headaches, con-
centration difficulties and behavioral problems in children
and adolescents; and sleep disturbances, headaches and
concentration problems in adults.’’ This level corresponds
to -36 dBm, an exposure frequently being reported by
slow responders in our olmesartan immunostimulation
follow-up cohort. After consultation, and some initial data
gathering with electromagnetic level meters, we decided to
suggest that these slow responders might be wise to take
steps to protect themselves from Electrosmog.
The sleeping caps case series
Patients began to initiate protection by purchasing com-
mercially available shielded clothing and tenting from
retailers. This clothing typically has silver-coated polyester
threads interwoven with the supporting fabric so that the
Fig. 3 A plot (from the Gromacs g_hbond software) of the instan-
taneous number of hydrogen bonds formed between 1,25-D and the
VDR sampled every 37.5 femtoseconds during the first 2250 ps of
VDR activation
Fig. 4 A fast Fourier transform of the hydrogen bond data from
Fig. 2
3
Just as there are many units of measurement for ionizing radiation,
so there are many ways of measuring non-ionizing electromagnetic
radiation. For ionizing, one can choose dose units of Rad, Grey,
Roentgen, Rem, Sieverts and the common dps (disintegrations per
second, often metered as counts per minute). For non-ionizing, one
can use Volts/metre as a measure of field strength, Watts/metre
2
,or
Decibels relative to 1 mW (dBm). The authors usually use dBm, as,
being logarithmic, the dBm measure can easily denote wide variations
in field strengths (it is easier to visualize -7 0dBm than ‘‘0.002 V/
m’’). Once the wave’s frequency is known, it is simple to convert
between each non-ionizing unit of measurement.
132 Environment and Autoimmunity (2017) 65:129–135
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garment is capable of partially blocking microwave Elec-
trosmog (see Fig. 5).
We quickly realized that frequent anecdotal reports of
symptomatic improvement, especially when the brain and
brain stem were ‘‘shielded’’ during sleep, warranted stan-
dardization with a garment whose electromagnetic shield-
ing performance could be more easily analyzed and
optimized. ‘‘Sleeping caps’’ (Fig. 6) were sewn and, upon
informed request, distributed free of charge to members of
our follow-up olmesartan cohort. A total of 64 patients took
part in this case series, with a variety of immune diagnoses
including arthritis, lupus, multiple sclerosis, sjogrens and
celiac. As these patients were all ill, many undergoing
olmesartan treatment with therapeutic intent, we decided
that ethical considerations precluded the distribution of
‘‘placebo caps’’ without the silver threads.
We decided to make the reporting task minimally
onerous by asking patients to initially wear the cap once
for 4 h during sleeping and once for 4 h during normal
activity (many are house-bound). We sought patient-re-
ported outcomes (PRO) of whether the garment had ‘‘No
Effect,’’ a ‘‘Weak Effect,’’ a ‘‘Definite Effect’’ or a
‘‘Strong Effect,’’ regardless of whether the effect was
good or bad (Fig. 7).
A full 90 % of the 64 patients reported a ‘‘Definite’’ or
‘‘Strong’’ change in their symptoms. This compares with
the 3 % incidence for electromagnetic hypersensitivity
typically expected in the population as a whole [23].
While a placebo or nocebo effect might be expected to
bias our PRO data, follow-up reports have indicated a
durable response over many months. Additionally, Dieu-
donne [24] has questioned the likelihood of nocebo cau-
sation in EHS.
Immunopathology from Electrosmog
When the Electrosmog in a patient’s environment is
reduced, the immune system tends to become more active.
This may result in immunopathology. Indeed, some
patients have reported a surge in disease symptoms,
occasionally an intolerable surge, after WiFi routers and
cell phones have been switched off in their homes. Others
have reported that travel to a very quiet area, such as a
remote canyon, caused a surge in their immune symptoms.
While further research is needed to clarify these reac-
tions, autoimmune patients seem predisposed to Electros-
mog hypersensitivity at levels currently existing in typical
home and work environments, and this factor may be
affecting their therapeutic response.
Fig. 5 A X20 micrograph of a microwave-blocking fabric woven
with a mesh of silver-coated polyester strands among the supporting
bamboo fibers
Fig. 7 Abar chart of the 64 PRO patient responses reporting
whether there was no change in symptoms from wearing the cap for
4 h during sleep and work, or a weak, definite, or strong change
Fig. 6 A photograph of a sleeping cap sewn from the microwave-
shielding fabric
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Discussion
The experiments described in this paper confirm that bio-
logical molecules are constantly moving and interact with
timescales measured in picoseconds. As a result, forces will
be exerted on the charged atoms within these molecules by
incident electromagnetic fields, including Electrosmog.
There is no reason to suspect that a pulsed electro-
magnetic wave of 1 ls duration (1000 times slower than a
typical molecular response) might cause any less damage
to biology than a continuous wave of the same magnitude.
It is therefore important to have very-fast-acting peak-
reading signal level meters when measuring the biological
interaction potential of electromagnetic waves.
Much of the research literature in this field is criticized
as not being sufficiently authoritative because experiments
have not been conducted under the current pragma of
placebo control and simplistic (p=0.05) analysis of
results. Research in this area will only move forward when
critics start to examine qualitative study outcomes—for
example, observations which might indicate that a Faraday
cage should have been an element of a study’s experi-
mental methodology, or that a 2–3 days acclimatization or
immune—washout might have changed the study results.
Furthermore, it seems likely that signals a million times
lower than those currently being used in research may be
sufficient to elicit a tangible change in human biology. In
order to better understand the amplitude at which bioeffects
become apparent, it is important that experimental guide-
lines be delineated which ensure that Electrosmog does not
confound a study’s results.
Finally, we need to plan how to handle subjects whose
symptoms become untenable (due to immunopathology)
during acclimatization to an Electrosmog-quiet environ-
ment, or during immune washout. We cannot ignore the
increasing body of evidence showing electromagnetic
effects on the immune system. The ‘‘controversial’’ nature of
electromagnetic hypersensitivity will not diminish until we
grasp the complexity of the task we face in defining exactly
how electromagnetic waves interact with human biology.
Acknowledgments The authors wish to thank Joyful Smith, Amy
Proal and Paul Albert for their assistance, Tsjerk A. Wassenaar for
helping with Gromacs internals, the Drug Design Laboratory at the
University of Milan for its Vega-ZZ software, and Greg P. Blaney
MD (recently deceased) for having worked tirelessly on our project.
Funding This study was supported by the Autoimmunity Research
Foundation, an IRS 501(c)3 charitable nonprofit organization.
Compliance with ethical standards
Conflict of interest The authors have no conflicts of interest to
declare.
Ethical approval The authors state that they have obtained appro-
priate institutional review board approval or have followed the prin-
ciples outlined in the Declaration of Helsinki for all human or animal
experimental investigations. In addition, for investigations involving
human subjects, informed consent has been obtained from the par-
ticipants involved.
Informed consent Informed consent has been obtained from the
participants involved.
Open Access This article is distributed under the terms of the
Creative Commons Attribution 4.0 International License (http://
creativecommons.org/licenses/by/4.0/), which permits unrestricted
use, distribution, and reproduction in any medium, provided you give
appropriate credit to the original author(s) and the source, provide a
link to the Creative Commons license, and indicate if changes were
made.
References
1. Science@NASA. N.A.S.A.: an introduction to the electromag-
netic spectrum. 2010 [cited 2016 May 13]. https://www.youtube.
com/watch?v=cfXzwh3KadE.
2. Large M, Hehlgans S, Reichert S, Gaipl US, Fournier C, Rodel C,
et al. Study of the anti-inflammatory effects of low-dose radia-
tion: the contribution of biphasic regulation of the antioxidative
system in endothelial cells. Strahlenther Onkol. 2015;191:742–9.
3. Thangaraj G, Manakov V, Cucu A, Fournier C, Layer PG.
Inflammatory effects of TNFaare counteracted by X-ray irradi-
ation and AChE inhibition in mouse micromass cultures. Chem
Biol Interact. 2016. doi:10.1016/j.cbi.2016.03.027.
4. Shreder K, Cucu A, Deloch L, Frey B, Gaipl US, Durante M,
et al. A7. 20 Low-dose ionising radiation inhibits adipokine
induced inflammation in rheumatoid arthritis. Ann Rheum Dis.
2016;75:A64.
5. Lushnikov KV, Gapeev AB, Sadovnikov VB, Cheremis NK.
Effect of extremely high frequency electromagnetic radiation of
low intensity on parameters of humoral immunity in healthy
mice. Biofizika. 2001;46:753–60.
6. Gapeev AB, Lushnikov KV, Chemeris NK, Shumilina IV.
Pharmacological analysis of anti-inflammatory effects of low-
intensity extremely high-frequency electromagnetic radiation.
Biofizika. 2006;51:1055–68.
7. Gapeyev AB, Mikhailik EN, Chemeris NK. Anti-inflammatory
effects of low-intensity extremely high-frequency electromag-
netic radiation: frequency and power dependence. Bioelectro-
magnetics. 2008;29:197–206.
8. Mina D, Sagonas K, Fragopoulou AF, Pafilis P, Skouroliakou A,
Margaritis LH, et al. Immune responses of a wall lizard to whole-
body exposure to radiofrequency electromagnetic radiation. Int J
Radiat Biol. 2016;92:162–8.
9. Proal AD, Albert PJ, Marshall TG, Blaney GP, Lindseth IA.
Immunostimulation in the treatment for chronic fatigue syndrome/
myalgic encephalomyelitis. Immunol Res. 2013;56:398–412.
10. Proal AD, Albert PJ, Marshall TG. The human microbiome and
autoimmunity. Curr Opin Rheumatol. 2013;25:234–40.
11. Proal AD, Albert PJ, Blaney GP, Lindseth IA, Benediktsson C,
Marshall TG. Immunostimulation in the era of the metagenome.
Cell Mol Immunol. 2011;8:213–25.
12. Blaney GP, Albert PJ, Proal AD. Vitamin D metabolites as
clinical markers in autoimmune and chronic disease. Ann N Y
Acad Sci. 2009;1173:384–90.
13. Proal AD, Albert PJ, Marshall TG. Inflammatory disease and the
human microbiome. Discov Med. 2014;17:257–65.
134 Environment and Autoimmunity (2017) 65:129–135
123
Content courtesy of Springer Nature, terms of use apply. Rights reserved.

14. Marshall TG. Molecular static and dynamic analyses reveal flaw
in murine model used by US FDA to detect drug carcinogenicity.
Nat Prec. 2007. http://precedings.nature.com/documents/52/
version/1.
15. Turton DA, Senn HM, Harwood T, Lapthorn AJ, Ellis EM,
Wynne K. Terahertz underdamped vibrational motion governs
protein-ligand binding in solution. Nat Commun. 2014;5:3999.
16. Wassenaar TA, de Vries S, Bonvin AM, Bekker H. SQUEEZE-E:
the optimal solution for molecular simulations with periodic
boundary conditions. J Chem Theory Comput. 2012;8:3618–27.
17. Wassenaar TA, Mark AE. The effect of box shape on the
dynamic properties of proteins simulated under periodic bound-
ary conditions. J Comput Chem. 2006;27:316–25.
18. Purcell EM. Electricity and magnetism. Cambridge: Cambridge
University Press; 2013.
19. BioInitiative Working Group, Cindy Sage, David O. Carpenter.
BioInitiative report: a rationale for biologically-based public
exposure standards for electromagnetic radiation. 2012 [cited
2016 May 12]. http://www.bioinitiative.org.
20. Bise W. Low power radio-frequency and microwave effects on
human electroencephalogram and behavior. Physiol Chem Phys.
1978;10:387–98.
21. Gapeev AB, Safronova VG, Chemeris NK, Fesenko EE. Modi-
fication of the activity of murine peritoneal neutrophils upon
exposure to millimeter waves at close and far distances from the
emitter. Biofizika. 1996;41:205–19.
22. Sacco B, Tomilin AK. The study of electromagnetic processes in
the experiments of Tesla; 2012. Available from: http://vixra.org/
abs/1210.0158.
23. Levallois P, Neutra R, Lee G, Hristova L. Study of self-reported
hypersensitivity to electromagnetic fields in California. Environ
Health Perspect. 2002;110(Suppl):619–23.
24. Dieudonne M. Does electromagnetic hypersensitivity originate
from nocebo responses? Indications from a qualitative study.
Bioelectromagnetics. 2016;37:14–24.
Environment and Autoimmunity (2017) 65:129–135 135
123
Content courtesy of Springer Nature, terms of use apply. Rights reserved.

1.
2.
3.
4.
5.
6.
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