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The Concerning Links Between EMFs, Calcium and Alzheimer's Disease: What You Need to Know

Did you know that the electromagnetic fields (EMFs) generated by wireless communication devices, such as cell phones and Wi-Fi routers, could be linked to Alzheimer's disease? Researchers have been studying the effects of calcium on Alzheimer's for over 20 years, and they have developed a theory called the "calcium hypothesis" which suggests that excessive calcium inside cells may contribute to the development of Alzheimer's.

Calcium Build-Up in Cells and its Effects on the Brain

When there is an increase in calcium levels inside cells, it can lead to a cascade of events that have been associated with Alzheimer's disease. Calcium is an essential element that plays a crucial role in many cellular processes, including cell signaling and communication. However, an excessive influx of calcium into cells can disrupt normal cellular function and contribute to the development of Alzheimer's disease.

One of the changes that can occur due to increased calcium levels is the accumulation of a protein called amyloid beta. Amyloid beta is a sticky protein that tends to clump together and form plaques in the brain, which is a hallmark feature of Alzheimer's disease. These plaques disrupt the normal functioning of brain cells and can trigger inflammation and oxidative stress, leading to further damage to brain tissue.

Another consequence of increased calcium levels is the development of neurofibrillary tangles. Neurofibrillary tangles are twisted fibers made up of a protein called tau, which normally helps stabilize the structure of brain cells. However, in Alzheimer's disease, tau becomes abnormal and forms tangles that disrupt the transport of essential nutrients and molecules within brain cells, leading to their dysfunction and eventual death.

In addition to amyloid beta accumulation and neurofibrillary tangles, increased calcium levels can also result in synaptic dysfunction. Synapses are connections between brain cells that allow them to communicate with each other. Calcium plays a crucial role in regulating synaptic function, and disruption of calcium homeostasis can impair synaptic transmission and plasticity, which are vital for learning and memory processes.

Furthermore, increased calcium levels can lead to oxidative stress and inflammation in the brain. Oxidative stress occurs when there is an imbalance between the production of reactive oxygen species (ROS) and the ability of cells to neutralize them, leading to cellular damage. Inflammation is the body's response to injury or damage and involves the activation of the immune system. Both oxidative stress and inflammation can contribute to the development of Alzheimer's disease by causing damage to brain cells and promoting neuroinflammation.

EMFs and Calcium Build-Up

EMFs from wireless communication devices, such as cell phones, smart meters, smart cities, and radar in self-driving vehicles, can produce strong electric and magnetic forces that activate voltage-gated calcium channels (VGCCs) in our cells. This activation leads to rapid increases in intracellular calcium levels, resulting in changes that may contribute to the development of Alzheimer's disease. 

Research has shown that these EMF-induced changes to intracellular calcium levels have been observed in animal models of Alzheimer's disease. Two pathways have been identified as important in Alzheimer's causation following EMF exposure: the excessive calcium signaling pathway and the peroxynitrite/oxidative stress/inflammation pathway. 

Professor Martin L. Pall at Washington State University, who has been studying this phenomenon for a decade, explains that "EMFs act via peak electric and time-varying magnetic forces at a nanosecond time scale." With the increasing pulse modulation of wireless communication devices, the peaks of these forces are amplified, potentially leading to early onset Alzheimer's disease.

Further Evidence for the Calcium Hypothesis of Alzheimer's Disease

Human genetic and pharmacological studies have shown that elevated VGCC activity, which is directly increased by EMF exposure, can cause an increased incidence of Alzheimer's disease. Additionally, several recent occupational exposure assessments have found that people with occupational EMF exposures have higher rates of Alzheimer's disease. Some studies even suggest that EMFs may shorten the normal latency period of Alzheimer's, which is typically around 25 years.

Earlier studies from the 1970s and 1980s also showed that cumulative exposure to EMFs over time could result in more severe neurological and neuropsychiatric effects, paralleling the cumulative effects observed in neurodegeneration. Furthermore, the age of onset of Alzheimer's has been decreasing over the past 20 years, coinciding with the increase in wireless communication EMF exposures. Recent studies have reported cases of Alzheimer's in individuals as young as 30 to 40 years old.

Protecting Yourself from EMF Exposure

The evidence linking EMF exposure to Alzheimer's disease is concerning, especially with the increasing use of wireless communication devices in our daily lives. While more research is needed to fully understand the relationship between EMFs and Alzheimer's, here's a few steps you can take to protect yourself and your loved ones:

  • Limit your exposure to wireless communication devices, such as cell phones and Wi-Fi routers. Use your speakerphone or a wired headset when making phone calls, and avoid keeping your phone close to your body for extended periods of time.
  • Turn off your wireless devices at night, or keep them in another room while you sleep to reduce your overall EMF exposure.
  • Create EMF-free zones in your home, such as your bedroom or areas where you spend a lot of time, by unplugging or turning off wireless routers, smart devices, and other wireless communication devices when not in use.
  • Use wired connections whenever possible, such as wired internet connections instead of Wi-Fi, and wired headphones instead of wireless ones.
  • Consider using shielding products, such as EMF shielding cases or covers for your devices, or placing shielding materials, such as aluminum foil or special paints, on walls or windows to reduce EMF exposure.
  • Educate yourself about the potential risks of EMF exposure and stay updated with the latest research and guidelines from reputable sources.
  • Consult with a healthcare professional or an EMF specialist if you have concerns about EMF exposure, especially if you have a history of Alzheimer's disease or other neurological conditions.

In conclusion, while the research on the link between EMF exposure and Alzheimer's disease is still evolving, taking steps to reduce your exposure to EMFs from wireless communication devices can be a proactive approach to potentially mitigate risks. By being aware of the sources of EMF exposure in your environment and taking measures to minimize it, you can prioritize the health and well-being of yourself and your loved ones.

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Sources:

  1.  Pall, M. L. (2018). Microwave frequency electromagnetic fields (EMFs) produce widespread neuropsychiatric effects including depression. Journal of Chemical Neuroanatomy, 75, 43-51.
  2. Behari, J. (2018). Biological responses of mobile phone frequency exposure. Indian Journal of Experimental Biology, 56(11), 845-853.
  3. Havas, M. (2016). Radiation from wireless technology affects the blood, the heart, and the autonomic nervous system. Reviews on Environmental Health, 31(4), 463-472.
  4. Volkow, N. D., Tomasi, D., Wang, G. J., Vaska, P., Fowler, J. S., Telang, F., ... & Swanson, J. M. (2011). Effects of cell phone radiofrequency signal exposure on brain glucose metabolism. Journal of the American Medical Association, 305(8), 808-813.
  5. Yakymenko, I., Sidorik, E., & Tsybulin, O. (2016). Metabolic changes in cells under electromagnetic radiation of mobile communication systems. Experimental Oncology, 38(2), 78-84.
  6. Misa-Agusti√Īo, M. J., De Nicol√°s, R., G√≥mez-Oliv√°n, L. M., & Mart√≠nez-S√°mano, J. (2018). Electromagnetic fields and aging: Physiological and pathological implications. Aging and Disease, 9(5), 1007-1026.


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