Stimulation of the Brain With Radiofrequency Electromagnetic Field Pulses Affects Sleep-Dependent Performance Improvement

https://drive.google.com/open?id=1ZmjXSrwhrxLJUtNuQPCN8-DdEookfSMm

Comment; Alpha waves in the brain operate at 7.5-12.5 Hz arising from “pacemaker” thalamic cells.  This study used pulsed 900 MHz.  Deeper in the paper, the methods were reviewed to find: The 900 MHz RF signal was pulsed, with 7 consecutive 7.1 ms pulses forming one 500 ms burst. These 500 ms bursts were repeated every 4 s (Intermittent-1 phase, 0.25 Hz, corresponding approximately to occurrence of sleep spindles), and every 1.25 s (Intermittent-2 phase, 0.8 Hz, corresponding approximately to frequency of slow oscillations), respectively. Exposure of 5 min Intermittent-1 was followed by 1 min with no exposure (OFF phase), then 5 min Intermittent-2 was followed by a 7 min OFF phase. This 18 min sequence was repeated throughout the night.  The peak spatial specific absorption rate averaged over any 10 g tissue (psSAR10 g) during the 7.1 ms pulses was set to 10 W/kg. This resulted in a burst average of 1.0 W/kg. The whole night psSAR10 g averaged to 0.15 W/kg. A detailed description of the exposure setup and the dosimetric exposure assessment is given in the Supplementary material.  There was clearly interference in neural function with decreased learning activity at these frequencies, durations & doses that were in the range expected from cell phones, smart-meter transmitters

Caroline Lustenberger a,b, Manuel Murbach c,d, Roland Dürr e, Marc Ralph Schmid b,e, Niels Kuster c,d, Peter Achermann b,e,f, Reto Huber a,b,f,*

Background: Sleep-dependent performance improvements seem to be closely related to sleep spindles (12-15 Hz) and sleep slow-wave activity (SWA, 0.75-4.5 Hz). Pulse-modulated radiofrequency electromagnetic fields (RF EMF, carrier frequency 900 MHz) are capable to modulate these electroencephalographic (EEG) characteristics of sleep.

Objective: The aim of our study was to explore possible mechanisms how RF EMF affect cortical activity during sleep and to test whether such effects on cortical activity during sleep interact with sleep dependent performance changes.

Methods: Sixteen male subjects underwent 2 experimental nights, one of them with all-night 0.25

-0.8 Hz pulsed RF EMF exposure. All-night EEG was recorded. To investigate RF EMF induced changes in overnight performance improvement, subjects were trained for both nights on a motor task in the evening and the morning.

Results: We obtained good sleep quality in all subjects under both conditions (mean sleep

efficiency >90%). After pulsed RF EMF we found increased SWA during exposure to pulse-modulated RF-EMF compared to sham exposure (P <0.05) toward the end of the sleep period. Spindle activity was not affected. Moreover, subjects showed an increased RF EMF burst-related response in the SWA range, indicated by an increase in event-related EEG spectral power and phase changes in the SWA range. Notably, during exposure, sleep-dependent performance improvement in the motor sequence task was reduced compared to the sham condition (20.1%, P ¼0.03).

Conclusion: The changes in the time course of SWA during the exposure night may reflect an interaction of RF EMF with the renormalization of cortical excitability during sleep, with a negative impact on sleep-dependent performance improvement.