Waking up dead-tired? Losing interest in sex? Could be the WiFi.

Here's what it's doing to our minds and bodies—and also to our unborn children.And if you think that's bad, 5G will be far worse (unless we stop it).



Oxidative stressProduced by elevated levels of peroxynitrite and the free radical breakdown products of peroxynitrite and its C02 adduct. Four studies of EMF exposure, cited in Pall (2013)showed that oxidative stress following exposure was associated with major elevation of 3-nitrotyrosine, a marker of peroxynitrite, thus confirming this interpretation. Two other studies each found 3-nitrotyrosine elevation, both following 35 GHz exposures (Sypniewska et al. (2010)Kalns et al., 2000).
Lowered male/female fertility, elevated spontaneous abortion, lowered libidoBoth the lowered male fertility and lowered female fertility are associated with and presumably caused by the oxidative stress in the male and female reproductive organs. Spontaneous abortion is often caused by chromosomal mutations, so the germ line mutations may have a causal role. Lowered libido may be caused by lowered estrogen, progesterone and testosterone levels. It seems likely that these explanations may be greatly oversimplified. One mechanism that may be important in lowered fertility is that VGCC activation and consequent high {Ca2+]i levels is known to have a key role in avoiding polyspermy. Consquently, if this if triggered before any fertilization of an egg has occurred, it may prevent any sperm from fertilizing and egg.
Neurological/ neuropsychiatric effectsOf all cells in the body, the neurons have the highest densities of VGCCs, due in part to the VGCC role and [Ca2+]i role in the release of every neurotransmitter in the nervous system. Calcium signaling regulates synaptic structure and function in 5 different ways, each likely to be involved here. Oxidative stress and apoptosis are both thought to have important roles. Lowered sleep and increased fatigue are likely to involve lowered nocturnal melatonin and increased nocturnal norepinephrine.
ApoptosisApoptosis can be produced by excessive Ca2+ levels in the mitochondria and by double strand breaks in cellular DNA; it seems likely that both are involved following EMF exposure. A third mechanism for triggering apopotosis, endoplasmic reticulum stress (see bottom row in this Table), may also be involved.
Cellular DNA damageCellular DNA damage is produced by the free radical breakdown products of peroxynitrite directly attacking the DNA [see Pall (2018) for discussion].
Changes in non-steroid hormone levelsThe release of non-steroid hormones is produced by VGCC activation and [Ca2+]i elevation. The immediate effects of EMF exposures is to increase hormone release and to raise, therefore, hormone levels. However many hormone systems become “exhausted” as a consequence of chronic EMF exposures. The mechanism of exhaustion is still uncertain, but it may involve oxidative stress and inflammation.
Lowered steroid hormoneSteroid hormones are synthesized through the action of cytochrome P450 enzymes; activity of these hormones is inhibited by binding of high levels of nitric oxide (NO) leading to lowered hormone synthesis.
Calcium overloadProduced by excessive activity of the VGCCs; secondary calcium overload is produced by oxidative stress activation of TRPV1, TRPM2 and possibly some other TRP receptors, opening the calcium channel of these receptors.
Heat shock protein inductionThere is a large literature showing that excessive [Ca2+]i induces very large increases in heat shock proteins. This is thought to be produced by complex calcium signaling changes involving the endoplasmic reticulum, mitochondria and the cytosol and also involving excessive [Ca2+]i producing increasing protein misfolding (Garbuz, 2017Park et al., 2014Krebs et al., 2011). It should be noted that some calcium is essential for proper protein folding in the endoplasmic reticulum such that only excessive calcium leads to misfolding and consequent endoplasmic reticulum stress.

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