Thursday, June 27, 2019

Chapter 3. Strong Evidence for Cumulative and Irreversible EMF Effects



Chapter 3. Strong Evidence for Cumulative and Irreversible EMF Effects 

Two questions that must be raised about the effects of these low-intensity EMFs producing biological effects is are they cumulative and are they reversible? I am aware of several different types of evidence for cumulative effects and also for irreversible effects.



Three of the human occupational exposure studies from the 1970’s reviewed in the Raines, National Aeronautics and Space Administration (NASA) study [26], showed that effects increased substantially with increasing time of exposure to a particular type and intensity of EMF. While these three studies each show cumulative effects but they provide no data on possible irreversibility of these neurological/neuropsychiatric effects. However the largest review of such occupational exposures (Hecht [28]) does provide substantial evidence on the cumulative nature and irreversibility of these neurological/neuropsychiatric effects.

Hecht [28] reviewed 60 different studies of occupational exposures that were done between 1960 and 1990 in the Soviet Union and East Germany. These were occupational exposure studies of over 3500 people, who were exposed to microwave frequency EMFs at intensities of less than 1/1000th of our safety guidelines. These studies [28] found that these EMFs produced neuropsychiatric effects similar to those found in my much more recent study [3], listed in Chapter 1 as well as on cardiac effects. Neither the neuropsychiatric findings nor the cardiac findings were unique however. Similar neuropsychiatric effects have been found to be caused by low intensity EMF exposures [27,29-34]. Cardiac effects have also been found in humans [26,29,30,32,34,35] similar to those found by Hecht [28].

Hecht [28] reports that exposures at those very low intensities for up to 3 years produced increased sympathetic nervous system activity, apparently in response to the EMF stress, following the classic stress sequence described by Hans Selye in 1953. No other effects were apparent during this circa 3 year period.

However longer exposure produced observable neurological/neuropsychiatric and cardiac effects as well as other effects which were initially modest. Exposures of 3 to 5 years typically produced effects that could be largely reversed after 2 to 3 years in a no-EMF exposure environment. Hecht states that “if detected early, effective therapy is possible.” However longer than 4 to 5 years exposures produced more severe effects which did not reverse when the persons were subsequently put into a no-EMF exposure environment. These and other effects continued to worsen with 10 years of exposure or longer. This cumulative nature of such EMF exposures was noted in two earlier reviews cited by Hecht et al [36,37]. These studies, then, provide very large amounts of evidence both for the cumulative nature of these neuropsychiatric effects, as well as the apparent irreversibility of these effects as they become more severe. Hecht also notes that “decline in health status increasingly amplifies EMF effects.” This a pattern of increasing apparent sensitivity produced by previous exposure is similar to that described in the Western literature on electromagnetic hypersensitivity (EHS), something that Hecht recognizes [28]. EHS something that is discussed very briefly below in this section.
There are strong similarities between the Hecht [28] findings on microwave frequency EMFs in humans and the impacts of such EMFs on cellular and organ histology in rodents, as were reviewed in Tolgskaya and Gordon [38] and discussed in Pall [3]. In rodents, initially non- thermal exposures over periods of 1 to 2 months produced modest changes in structure of the brain and of the neurons. When such exposures ceased, most of the structural changes
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disappeared – that is the changes were largely reversed when the animals were placed back into a no-EMF environment. However more months of exposure produced much more severe impacts on brain and neuronal structure and these were irreversible [38, 3]. More recent, Western country and other country studies cited in [3], provide much further support for brain impacts similar to those found in Soviet and also other country brain studies reviewed by Tolgskaya and Gordon[38]. Tolgskaya and Gordon [38,3] also reported findings that in histological studies, the nervous system was the most sensitive organ in the body, followed closely by effects on the heart and the testis, although many other organs were also impacted. Thus, the Tolgskaya and Gordon review [38,3] provides very important support for the findings of neurological/neuropsychiatric effects, the cardiac effects, discussed immediately above and below, and the reproductive effects discussed in Chapter 1. By comparing the animal studies with the human studies, one can see the striking similarities, with the major difference being that the effects in rodents are much more rapid than the effects on humans. Given the much higher metabolic rates in rodents and much lower life spans in rodents, the timing difference is not surprising. With regard to the issues of cumulative nature and irreversibility, both rodent and human studies provide strong support for both neurological and neuropsychiatric effects showing both cumulative nature and irreversibility and show a similar pattern of cumulative effects with the cardiac effects.

What are the cardiac effects discussed briefly above, that are produced by non-thermal microwave frequency EMF exposures? The effects include tachycardia (rapid heartbeat) where some people with apparent EHS, on blinded exposure to cordless phone radiation have instantaneous tachycardia, an effect that is also essentially instantaneously reversible on cessation of exposure [28,35,36]. So tachycardia can be an almost instantaneous response to EMFs and it is sometimes also found with arrhythmia. Prolonged exposures produce both arrhythmias and bradycardia (slow heart beat) [26-30,32]. Similar EMF cardiac effects were seen in animal studies, with the earliest of these going back to the late 1960s.

Some of the early studies on long-term EMF cardiac effects are listed in Table 2, below. They show that such chronic exposures produce bradycardia and sometimes arrhythmia. The early Soviet studies (labeled USSR) reported similar findings to those found in the western studies (Table 2).

Table 2. Chronic Exposure, Non-Thermal EMF Cardiac Effects from NASA Review [26]
Study
Effects Reported
Schwan 1977
Cardiology changes
Dwyer 1978
Bradycardia, hypotension
Sadicikova (USSR)
Bradycardia, hypo & hypertension, cardiac pain, systolic murmur
Kalyada (USSR)
“cardiovascular changes”
Sadichikova (USSR)
Changes in cardiovascular system
Pressman 1970
QRS interval in ECG increased (bradycardia), also arrhythmia
Domanski (USSR)
Bradycardia, hypotension, ECG changes (shows both bradycardia and arrhythmia)
Lerner (1980)
Bradycardia
Stuchley (1978)
Bradycardia (measured in 2 ways), hyper & hypotension, cardiac pain, systolic murmur.


Arrhythmias, especially when they are accompanied by bradycardia, are often associated with sudden cardiac death. We are having an epidemic of young, apparently healthy athletes dying in
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the middle of an athletic competition of apparent sudden cardiac death, which may, therefore be possibly caused by EMF exposures [39]. Some of these individuals have been saved from death [39] and subsequently found to be suffering from bradycardia and arrhythmias. Another type of cardiac effect is that when apparent EHS people are exposed to Wi-Fi, cell phone, cell phone tower or smart meter radiation, they are reported to suffer from heart palpitations. Each of these four types of cardiac effects, tachycardia, arrhythmias, bradycardia and heart palpitations involve aberrations in the electrical control of the heartbeat. How can these be produced?

The heartbeat is controlled by pacemaker cells in what is called the sino-atrial node of the heart. Those pacemaker cells have been shown to have very high densities of the T-type VGCCs which may make these cells particularly susceptible to direct effects of the EMFs (recall that EMFs act via VGCC activation). The T-type and the L-type VGCCs have essential roles in controlling the heartbeat. It follows that EMF exposures, acting directly on the pacemaker cells of the heart, can produce tachycardia responses. Furthermore, gene mutations in a VGCC gene that produce increased VGCC activity can produce both tachycardia and arrhythmia in young babies carrying those mutations; these young children die of sudden cardiac death at a very young age. How then do we get bradycardia? Bradycardia is produced when EMFs chronically impact the sino-atrial node, such that the dysfunction involved in heart failure, which is very complex, produces dysfunction of the pacemaker cells of the heart, producing bradycardia [40].

It follows from this that EMF-produced bradycardia and chronic arrhythmias are likely to be caused by heart-failure-like changes that particularly impact the sino-atrial node of the heart, including the tissue remodeling found in heart failure. This model has been confirmed by the findings of Liu et al [41], who found that pulsed microwave frequency EMF produced tissue remodeling that specifically impacted the sino-atrial node of the heart with remodeling changes similar to those found in heart failure [40]. Heart failure develops in a cumulative fashion and, based on current medicine at least, is an irreversible process involving tissue remodeling and a large number of other biochemical and physiological changes [41]. It seems likely, therefore, that the EMF effects on the heart are both cumulative and irreversible.

You will recall, from the discussion at the beginning of Chapter 1, that there are 18 reviews documenting that EMF produces lowered fertility. These act via diverse mechanisms. These include tissue remodeling changes in the testis, lowered sperm count and sperm quality, lowered female fertility including ovary remodeling and oocyte apoptosis, lowered estrogen, progesterone and testosterone levels (that is sex hormone levels), increased spontaneous abortion incidence, and lowered libido. We already have sperm count drops to below 50% of normal in every technologically advanced country on earth [1]. We also have fertility drops to well below replacement levels in every technologically advanced country on earth, with one exception. Clinical observations argue that while there are sometimes technical fixes that allow some reproduction, infertility appears to be inherently irreversible. The Magras and Xenos [2] in mice, also discussed in Chapter 1 shows that radiofrequency radiation exposures well below our safety guidelines, produce immediate drops in mouse reproduction in the first litter. Further exposures to the same EMF levels produced a crash in reproduction essentially to zero, a crash that appeared to be essentially irreversible.

We don’t know that humans will behave very similarly to mice. We do know that the EMFs produce the diverse effects on human reproduction listed in the previous paragraph. My prediction is that even if exposures level off where they are now, we will start seeing crashes in reproduction within about 5 years. If we go ahead with 5G, that crash may be almost instantaneous.
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Mutation accumulation produced by cellular DNA damage is likely to be both cumulative and irreversible, as well, because later mutations are highly unlikely to reverse previously occurring mutations. It has been estimated that all we need to have is an increase in germ line mutation of 2 1⁄2 to 3-fold, to become over time, extinct from the very high levels of mutations in each newborn. From the high levels of DNA damage produced in human sperm from common EMF exposures, we may be already well above that level.

It follows from this that we already face four existential threats produced by microwave frequency EMF exposures to the survival of every technologically advanced society on earth:
1.    Cumulative and irreversible neurological/neuropsychiatric effects.
2.    Cumulative and irreversible reproductive effects.
3.    Cumulative and irreversible cardiac effects, leading to sudden cardiac death.
4.    DNA effects in germ line, including sperm cells, leading to major impacts on our gene
pool and high mutation frequencies.
Any one of these can destroy us on its own and with the ever increasing exposures and especially the vast increases in exposure that the 5G rollout will inevitably produce, that destruction is likely to be imminent. These don’t even take into consideration the cancer effects, the hormonal effects or other effects produced by increased oxidative stress or increased apoptotic cell death. There is extraordinary evidence for each of these effects of EMF exposure, which have been repeatedly documented in the reviews listed in Chapter 1.

The following information is derived from an abstract that I used for a talk at the Neuroscience 2016 meeting in Los Angeles, a meeting that was focused on Alzheimer’s disease and similar dementias. The discussion here raises the question of whether Alzheimer’s and other dementias may be still another set of irreversible diseases where cumulative effects of microwave frequency EMFs may have important causal roles. Dementias and other types of neurological deaths have had unexplained rapid recent increases [42-44]. The parallel between these increases and the increases in cell phone and other EMF exposures suggested that such exposures may cause dementia increases [45]. Reports show people circa age 30 developing Alzheimer’s or other very early onset dementias and even younger people are reported to develop digital dementias, dementias caused by heavy use of digital devices [46-48]. One of the questions being raised here, is whether digital dementias are caused, at least in part, by the EMF exposures produced by these digital devices and the Wi-Fi fields involved in their usage, rather than solely by such things as screen time, as is often assumed. As you have seen in chapter 2, microwave and lower frequency EMFs act via activation of the VGCCs, leading to increases in intracellular calcium ([Ca2+]i) and downstream effects including increased Ca2+ signaling, NO, superoxide, peroxynitrite, free radicals, oxidative stress, NF-kappaB and mitochondrial dysfunction.

Each of these downstream effects have been shown to have important roles in causing Alzheimer’s disease and other neurodegenerative diseases [49-51]. These all suggest plausible mechanisms for action for EMFs causing Alzheimer’s disease. Furthermore the amyloid-beta protein (Aβ) which has an specific role in causing Alzheimer’s disease, is produced in increasing amounts by elevated [Ca2+]i, and small Aβ aggregates form Ca2+ channels in the plasma membrane and aggregates also raise [Ca2+]i via increased VGCC and RYRr activity, suggesting a vicious cycle between Aβ and [Ca2+]i in Alzheimer’s disease. This argues that increased intracellular calcium levels, produced by the EMFs increases Aβ and increased Aβ increases intracellular calcium, in what may be the central mechanism in causing Alzheimer’s disease.
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Four rodent studies support an EMF role in Alzheimer’s disease. A series of short pulses of EMFs in young rats, produced the following in the equivalent of middle aged rats: elevated brain Aβ and oxidative stress; lowered cognition and memory [52,53]. 900 MHz exposures produces oxidative stress, increased Aβ and lowered miR-107, all found in Alzheimer’s disease brains [52- 55]. There are many animal studies showing roles for [Ca2+]i through both VGCCs and RYRs in causing Alzheimer’s disease in rodent models; these include studies with calcium channel blockers and studies of transgenic mice with varying VGCC and RYR expression. Very low EMF exposures can produce, however, protective responses [56,57]; this is not surprising because EMF therapy is thought to act via NO signaling and protein kinase G (see Fig.1, Chapter 2) and this pathway is reported to protect from Alzheimer’s disease. Epidemiological studies have shown that exposure of humans of 50/60 Hz EMFs, which also act via VGCC activation, can cause elevated Alzheimer’s disease incidence [58,59]. Interestingly, a 1997 article in Microwave News, discussing two such epidemiological findings on EMFs and Alzheimer’s disease in humans, found that occupational exposures to EMFs produced as much as a four-fold increase in Alzheimer’s disease [59A]. That same article [59A] suggested a similar mechanism to the mechanism suggested here, namely that increased [Ca2+]i following EMF exposure produces increases in Aβ. In conclusion, a wide range of studies support the view that low intensity microwave frequency exposures acting via VGCC activation and [Ca2+]i, can produce increases in Aβ and other causal factors of Alzheimer’s disease in humans and in animals and EMFs have been shown to produce Alzheimer’s effects in rats.

These various findings on EMFs and Alzheimer’s disease, the increasingly early onset of dementias and the occurrence of digital dementias, all suggest we may have another very high level threat caused by EMF exposures, possibly involving cumulative EMF effects and leading to severe, irreversible brain damage.

Chapter 4 EMFs Including Wi-Fi May Be Particularly Damaging to Young People

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