Four very important studies below that prove that microwave sickness/EHS is a physiological/medical condition, identifying predisposing factors and biomarkers including cell membrane changes from microwave radiation exposure that lead to harmful effects impacting every system in the body as well as changes in the expression of 178 genes affecting critical biological processes including the cell cycle, DNA replication and repair, cell death, cell signaling, nervous system development and function, immune system response, lipid metabolism, and carcinogenesis and affecting pathways of “Calcium Signaling,” “Synaptic Long Term Potentiation,” “Production of Nitric Oxide and Reactive Oxygen Species in Macrophages,“Serine Biosynthesis,” and “Signaling in Neurons.”
1) Deluca et al, 2014. https://www.hindawi. com/journals/mi/2014/924184/
Statistically significant genetic and metabolic differences were seen in EHS compared to non-EHS, also reduced levels of glutathione and impaired detoxification ability in EHS. Risk of EHS development was increased 9.7 times in individuals who are missing two genes GSTM1 and GSTT1, which are glutathione S-transferase (GST) enzymes that detoxify by conjugation with glutathione
proved that EHS is a medical condition by showing
- a certain genotype (cytochrome P450 isoenzyme CYP2C19 (*1/*1)) was present in 89.7% of EHS (see Table 1 in study)
- a risk of EHS development was increased 9.7 times in individuals who are homozygously missing two genes GSTM1 and GSTT1, which are glutathione S-transferase (GST) enzymes that detoxify by conjugation with glutathione (see Table 1 in study)
- a statistically significant lowered level of antioxidant/detoxification enzymatic activity of GST (glutathione S-transferase) in EHS compared to non-EHS (~1.9 in EHS vs. ~2.5 in non-EHS, p=0.000001, see Figure 5a)
- a statistically significant increased level of antioxidant/detoxification enzymatic activity of GPX (glutathione peroxidase) in EHS compared to non-EHS (~24.9 in EHS vs. ~22.8 in non-EHS, p=0.012151, see Figure 5b)
- a statistically significant lowered level of GSH (reduced glutathione) in EHS compared to non-EHS (~315 EHS vs. ~350 non-EHS, p=0.000031, see figure 6a)
- a statistically significant lowered level of omega-6 phospholipid content in the red blood cell membranes of EHS compared to non-EHS (~11.3% EHS vs.~11.9% non-EHS, p=0.000181, see Figure 8a)
- there was statistically significant higher levels of oxidized /total CoQ10 in EHS compared to non-EHS (~0.345 EHS vs. ~0.327 non-EHS, p=0.000181, see figure 6d). The higher levels of oxidized CoQ10 could explain the dermatitis/eczema seen in 41% of EHS sufferers.
- EHS group showed a trend to the increase in erythrocyte CuZnSOD activity Fig. 5c and to the depletion of the main lipophilic antioxidants in plasma-reduced coenzyme Q10 and alpha-tocopherol (vitamin E) (Figures 5 and 6).
identifed biomarkers in many of those with EHS and/or MCS that are out of normal range:
High-sensitivity C reactive protein (hs-CRP)
Low Vitamin D2-D3 (this study showed that low vitamin D is not a cause of EHS but an effect from electromagnetic radiation exposure)
High Histamine
High IgE
High Protein S100B
High Nitrotyrosine (NTT)
High Heat shock protein 70 (HSP70)
High Heat shock protein 27 (HSP27)
High Anti-O-myelin autoantibodies
Low Hydroxy-melatonin sulfate (6-OHMS)
Low 6-OHMS/creatinine
Abnormal blood flow in brain in temporal lobes
3) 2016 Belyaev et al, EUROPAEM Guidelines for Prevention, Diagnosing and Treating EHS https://www.degruyter.com/ downloadpdf/j/reveh.2016.31. issue-3/reveh-2016-0011/reveh- 2016-0011.pdf
It covers all aspects of EHS, including skin effects (elevated mast cells in the upper dermis of the skin and histamine release from the mast cells), neurological symptoms, effects on endocrine system, liver and organ systems, and increased vulnerability of children.
Mechanisms also discussed: Increased peroxynitrite, malfunctioning cell membranes, mitochondrial dysfunction, decreased glutathione, cellular stress proteins.
It also gives treatment recommendations: These include a balanced homeostasis in order to increase the “resistance” to EMF. There is increasing evidence that a main effect of EMF on humans is the reduction of their oxidative and nitrosative regulation capacity. This hypothesis also explains observations of changing EMF sensitivity and the large number of symptoms reported in the context of EMF exposure. Based on currently available knowledge it appears useful to recommend a treatment approach, as those gaining ground for multisystem illnesses, that aims at minimizing adverse peroxynitrite effects. Measures that enhance the immune system and reduce stress in combination with detoxification will promote EHS recovery."
Supplements needed to combat the oxidative stress, like antioxidants, detoxifying agents, supportive nutrients, NAC, ALA, vitamin E, C, methylfolate, methylcobalamin, etc.
Also genetic mutations MTHFR and COM-T increases need for nutrients like methylated B vitamins to combat EHS symptoms.
4) Fragopoulou et al 2018 found a marker and mechanism for EHS/wireless health effects , i.e. the cell membrane becomes more permeable from RF exposure by changes in the phospholipid composition. https:// onlinelibrary.wiley.com/doi/ epdf/10.1002/brb3.1001
In this study, mice were exposed to 2hr of 1800 MHz radiation from an actual cell phone in talk mode at a distance of 3 cm
(exposure is well within government exposure limits; SAR calculated exposure to be 0.02-0.366 W/kg to the head in the experiment, and phones sold in the US cannot exceed a SAR of 1.6 W/kg http://content.time.com/time/ magazine/article/0,9171, 2029493,00.html ; 6 hours after exposure, the mice were sacrificed.
Results of the study, statistically significant:
- the levels of four fatty acids [16:0, 16:1 (6c + 7c), 18:1 9c, eicosapentaenoic acid omega-3 (EPA, 20:5 ω3)] and the two fatty acid sums of saturated and monounsaturated fatty acids (SFA and MUFA) were significantly altered (p < 0.05) in the exposed group, resulting in changes to the cell membrane, reducing SFA and EPA, while increasing MUFA residues. (These changes to the cell membrane make it more fluid and more permeable)
- expression of 178 genes changed significantly (p < 0.05), revealing an impact on genes involved in critical biological processes, such as cell cycle, DNA replication and repair, cell death, cell signaling, nervous system development and function, immune system response, lipid metabolism, and carcinogenesis.
- Pathway analysis identified 16 canonical pathways, which were significantly enriched (p ≤ 0.05) with the 178 DEGs , including“Calcium Signaling,” “Synaptic Long Term Potentiation,” “Production of Nitric Oxide and Reactive Oxygen Species in Macrophages,“Serine Biosynthesis,” and “Signaling in Neurons.”
- 10 functional networks that were significantly affected by mobile phone radiation, in order of ranking:
- 1) Cancer, Cell Death and Survival, Organismal Injury and Abnormalities
- 2) Cellular Assembly and Organization, Cellular Functionand Maintenance, Molecular Transport
- 3) Dermatological Diseases and Conditions, Gastrointestinal Disease, Immunological Disease
- 4) Nucleic Acid Metabolism, Small Molecule Biochemistry, Cellular Function and Maintenance
- 5) Cancer, Protein Degradation, Protein Synthesis
- 6) Cell Cycle, Cancer, Cellular Development
- 7) Lipid Metabolism, Small Molecule Biochemistry, Molecular Transport
- 8) Cell Cycle, Cellular Development, Embryonic Development
- 9) Lipid Metabolism, Molecular Transport, Small Molecule Biochemistry
- 10) Cellular Compromise, Hematological System Development and Function, Auditory Disease
- "This study provides preliminary evidence that mobile phone radiation induces hippocampal lipidome and transcriptome changes that may explain the brain proteome changes and memory deficits"
For more info. on Cell membrane composition https://en. wikipedia.org/wiki/Cell_ membrane
5) Panagopoulos 2019, a very significant paper explaining the mechanisms involved in DNA damage from cell phone radiation, and that the extreme variability in the intensity and waveform of wireless communication signals are responsible for the biological effects [because voltage-gated ion channels in all cell membranes switch between open and closed states whenever a change exceeding ∼30% in the
membrane voltage takes place, and all physiological cellular effects are initiated by changes in ionic concentrations mediated by ion channel gating]. A highlighted copy is attached.
The exposure levels of radiation from the cell phone were from typical exposure conditions and well under goverment exposure limits, including that of the US. The radiation exposure was from actual cell phones in talk mode placed next to the vials containing the egg cells. The RF radiation intensity was ∼0.378±0.059 mW/cm2, and the U.S. exposure limit is 1mW/cm2 for 30 minutes.
The DNA damage from 6 different types of EMF sources on the eggs of the fruit fly Drosophila melanogaster were compared, and found that the EMF from cell phones are the most damaging, even more so than magnetic fields from power lines, and that they were significantly more bioactive than the other EMFs even at much shorter exposure durations.
Furthermore, the damage from cell phone radiation was found to be even more damaging than that caused by cytotoxic chemical agents.
While cytotoxic chemical agents caused damage only at certain stages of the egg's development, cell phone radiation was found to cause damage at ALL stages of egg development and heritable DNA mutations which could be passed on to the next generation.
Results were statistically significant:
There was 35.77% more DNA damage from GSM 1800 cell phone exposure at 36 minutes compared to non-exposed eggs (p<0.0005),
and 50.16% more DNA damage from GSM 900 cell phone exposure at 36 minutes compared to non-exposed eggs (p<0.0002).
In contrast, DNA damage from magnetic fields comparable to power lines for 120 hours was only up to 7.5% (p<0.001)
These results apply to humans as well, because insects and humans have the same type of cell membranes, utilize calcium (Ca+2), potassium (K+), sodium (Na+) etc, to initiate and accompany all cellular events, and have the same intracellular organelles.
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