Modern life risks due to neuropsychiatric effects of light choices

The major non-thermal effect of nnEMF is a net increase of deuterium in the TCA cycle with a change in the pool of hydrogen in the NADPH pool and a loss of melatonin which causes more deuterium in the cells. This single change destroys cell membranes where DHA is located. DHA controls the lipid cytosocial regions on lipid rafts in cell membranes to perform the movement of electrons on a liquid crystalline semiconductive circuit. The most important one connects the retina to the SCN to control all growth metabolism in animals because it controls the circadian mechanism which determines how the clock genes work everywhere in your body. When you live in a nnEMF world, say like musicians, you become depressed and quickly collect deuterium in your matrix and you might kill yourself or become addicted to opiates. We've recently seen it in Prince, the King of Pop, Houston, Winehouse, Cobain, Cornwell, and Bennington. "Non-thermal microwave/lower frequency electromagnetic fields (EMFs) act via voltage-gated calcium channel (VGCC) activation.


Did you know sunlight is a natural calcium channel blocker? Calcium channel blockers block EMF effects and several types of additional evidence confirm this mechanism. Low-intensity microwave EMFs have been proposed to produce neuropsychiatric effects, sometimes called microwave syndrome, and the focus of this review is whether these are indeed well documented and consistent with the known mechanism(s) of action of such EMFs. VGCCs occur in very high densities throughout the nervous system and have near-universal roles in the release of neurotransmitters and neuroendocrine hormones.

Soviet and Western literature shows that much of the impact of non-thermal microwave exposures in experimental animals occurs in the brain and peripheral nervous system, such that nervous system histology and function show diverse and substantial changes. These may be generated through roles of VGCC activation, producing excessive neurotransmitter/neuroendocrine release and oxidative/nitrosative stress and other responses. Excessive VGCC activity has been shown from genetic polymorphism studies to have roles in producing neuropsychiatric changes in humans. Two U.S. government reports from the 1970s to 1980s provide evidence for many neuropsychiatric effects of non-thermal microwave EMFs, based on occupational exposure studies.

18 more recent epidemiological studies, provide substantial evidence that microwave EMFs from cell/mobile phone base stations, excessive cell/mobile phone usage, and from wireless smart meters can each produce similar patterns of neuropsychiatric effects, with several of these studies showing clear dose–response relationships. Lesser evidence from 6 additional studies suggests that short wave, radio station, occupational, and digital TV antenna exposures may produce similar neuropsychiatric effects. Among the more commonly reported changes are sleep disturbance/insomnia, headache, depression/depressive symptoms, fatigue/tiredness, dysesthesia, concentration/attention dysfunction, memory changes, dizziness, irritability, loss of appetite/body weight, restlessness/anxiety, nausea, skin burning/tingling/dermographism, and EEG changes. In summary, then, the mechanism of action of microwave EMFs, the role of the VGCCs in the brain, the impact of non-thermal EMFs on the brain, extensive epidemiological studies performed over the past 50 years, and five criteria testing for causality, all collectively show that various non-thermal microwave EMF exposures produce diverse neuropsychiatric effects."
https://www.sciencedirect.com/science/article/pii/S0891061815000599

 

@Dr Jack Kruse has said over and over -> "Neuroprotective DHEA marine derived peptides are a rich solar source for nourishing our cells with the full spectrum synthesis of our sun."

For the reader's reference: .

https://www.mdpi.com/1660-3397/13/7/4006/pdf
The neuroprotective peptide (HTP-1) Gly-Thr-Glu-Asp-Glu-Leu-Asp-Lys from the seahorse Hippocampus trimaculatus exerted a protective action on PC12 cells and prevented them from the deleterious action of amyloid β42 which is associated with the pathogenesis of Alzheimer’s disease, as evidenced by the enhancement of cell viability and expression of the pro-survival gene (Bcl-2).

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