New insights into the link between EMFs, calcium and Alzheimer’s disease

For almost a quarter of a century, researchers have been studying and publishing on the effect of calcium on Alzheimer's Disease. Research has led to the development of the calcium hypothesis of Alzheimer's disease, which argues that Alzheimer's is caused by excessive intracellular calcium.

Calcium causes changes to the brain

Calcium build-up in cells results in diverse range of changes in the brain. There are two significant changes that develop conditions for Alzheimer's disease.

1. Specific increases in the amyloid precursor protein, BACE1 and amyloid beta protein aggregates
2. Less specific neurodegenerative changes including hyperphosphorylated tau protein and neurofibrillary tangles, cell death produced by apoptosis or by destructive autophagy, synaptic dysfunction produced by changes in neuronal structures required for synapsis between brain neurons, oxidative stress and inflammation

EMFs and calcium build up

Pulsed electronically generated electromagnetic fields (EMFs) used for wireless communication are coherent producing strong electric and magnetic forces that act in the cells of our bodies primarily via activation of voltage-gated calcium channels (VGCCs). VGCC activation produces rapid increases in intracellular calcium levels. Therefore, EMF exposures produce changes with lead to excessive intracellular calcium. This buildup explains the effects on the brain in Alzheimer's disease.

These EMF induced changes to intracellular calcium levels have been demonstrated in animal models of Alzheimer's disease. Research has shown the involvement of two pathways that lead to Alzheimer's disease. Each of the two pathways producing pathophysiological effects following EMF exposure are important in Alzheimer's causation: the excessive calcium signaling pathway and the peroxynitrite/oxidative stress/inflammation pathway.

Professor Martin L. Pall, at the Washington State University has been studying this phenomenon for a decade. "EMFs act via peak electric and time varying magnetic forces at a nanosecond time scale.", says Professor Pall. Such peaks are vastly increased with each increase in pulse modulation produced by smarter cell phones, smart meters, smart cities and radar in self driving vehicles. "Any of these may produce the ultimate nightmare – extremely early onset Alzheimer's Disease."

These findings provide powerful evidence that EMFs can cause Alzheimer's disease. Human and animal studies add still more evidence to the calcium hypothesis of Alzheimer's disease.

A look at some more evidence

Professor Pall summarizes the evidence in a recent review in Current Alzheimer Research.

Human genetic and pharmacological studies show that elevated VGCC activity causes increased Alzheimer's incidence. Consequently, it is not just calcium that is important. VGCC activity, which is directly greatly increased by EMF exposure, is also important in causing Alzheimer's.

12 recent occupational exposure assessments have found that people having occupational EMF exposures have higher Alzheimer's incidence. Some studies suggest that EMFs shorten the normal 25-year latency period of Alzheimer's disease.

Earlier occupational exposure studies (in the 1970s and 1980s) showed that neurological / neuropsychiatric reported effects, associated with EMF exposures, developed cumulatively, such that longer times of exposure to the same EMFs, produced more severe effects. This parallels cumulative effects in neurodegeneration.

The age of onset of Alzheimer's has decreased over the past 20 years or so, with the timing corresponding to the large recent increases in wireless communication EMF exposures. Recent studies report age 30 to 40 Alzheimer's cases.

Very young people who are exposed to cell phone or Wi-Fi radiation for many hours per day may develop digital dementia.

El-Swefy et al, in 2008, showed that 2 hours per day very low intensity mobile phone base station (cell phone tower) radiation produced massive neurodegeneration of the brains of young rats. 34% of the brain cells died in 4 weeks. 11 measured brain changes and 4 observed behavioral changes were each greatly lowered by the VGCC calcium channel blocker amlodipine. These findings show is that EMFs most of us are exposed to every day, acted via VGCC activation to produce universal massive, extraordinarily rapid neurodegeneration in young rats. The researchers did not examine any Alzheimer's specific brain changes.

However, Jiang et al. (2013 & 2016) looked at EMF pulses in rats found Alzheimer's specific changes but also some less specific changes in the hippocampus, a brain region which is heavily impacted in Alzheimer's. Jiang 2013 exposed rats to a series of EMF pulses in one day to 2-month old rats, finding apparent universal Alzheimer's effects in 20 month old rats (roughly the equivalent of 42-year-old humans coming down with near universal Alzheimer's). The 2016 paper exposed the rats to EMF pulses once a day, causing Alzheimer's at 10 months of age (similar to 21-year-old people with extremely early onset Alzheimer's). Both El-Swefy and Jiang found massive neurodegeneration in young rats simply from exposing them to EMF pulses.

What needs to be done?

Three types of studies are urgently needed to be performed by independent scientists:

1. Brain marker surveys of Alzheimer's disease and MRI brain scans for abnormalities among young people who show signs of digital dementia.

2. EMF exposures assessments for pre-diagnosis environments for people aged 30 to 40 who have been diagnosed with early onset Alzheimer's disease. These assessments should compare phone and cell phone tower radiation, Wi-Fi radiation, smart meter and dirty electricity radiation levels with normal controls.

3. Examinations for early signs of Alzheimer's disease among people living near small cell antennae for a year or more.

Findings from each of these studies should be shared with the general public, so that everyone can take the steps necessary to reduce the incidence of early-onset Alzheimer's disease."

Professor Martin L. Pall, Washington State University