Cell phones and the brain

Townsend Letter for Doctors and Patients,  July, 2002  by John D. MacArthur

• E-mail
• Print
• Link

Not only did they find it possible to differentiate between thermal and nonthermal stress, but the stress proteins induced by low frequency served as "biomarkers" to monitor the early stages of the cellular stress reaction to EMFs -- prior to activation by increased temperature. They believe this will make it possible to establish a lower, more accurate safety threshold for cell phones and towers.

Electromagnetic Fields and Enzymes

Another pathway by which living organisms are influenced by radiofrequency radiation in a nonthermal way may be through an alteration in the activity of important enzymes. A well-studied example is ornithine decarboxylase (ODC), an enzyme involved in the regulation of cell growth. High ODC activity is characteristic of the unregulated growth of tumor cells, and ODC activity has been shown to be sensitive to both extremely low frequency magnetic fields and to radiofrequency fields. (25, 26)

Scientists are learning more and more about intracellular communication pathways. Signals originating at the cell membrane initiate a production sequence of enzyme "cascades" within the cell. These signaling pathways are proving to be sensitive to weak EMFS. (27, 28)

In his summary of "Cell and Molecular Biology Associated with Radiation Fields of Mobile Telephones," longtime EMF researcher Dr. W. Ross Adey writes: "Microwave bioeffects at the cellular level support concepts of athermal responses not mediated by tissue heating. A spectrum of these biological responses show dependence on ELF amplitude- or pulse-modulation of the imposed fields. Cell membranes have been identified as the site of transduction of many of these responses, with initiation of enzyme cascades that chemically couple cell surface radiofrequency signals to intracellular systems, including some that reach cell nuclei and regulate processes of cell growth and division." (29)

Programmed-Cell-Death

Dr. Adey also points to evidence that suggests these same enzyme cascades have probable continuing roles in programmed-cell-death (apoptosis), in the promotional phase of tumor formation, and in the pathophysiology of certain neurodegenerative diseases such as Parkinson's and Alzheimer's.

In the process of programmed-cell-death, caspase enzymes are unleashed to destroy cells that are abnormal or are no longer needed. In Lou Gehrig's disease (ALS), scientists believe the process of caspase-mediated apoptosis is misdirected and begins to destroy neurons. (30)

Researchers at Howard Hughes Medical Institute and at Harvard Medical School have identified an enzyme that may be involved in the pathogenesis of Alzheimer's disease. Calpain, a calcium-dependent cysteine protease, appears to be a common mechanistic link between the death of primary cortical neurons and known causes of neurotoxic damage, including oxidative stress, excitotoxic chemicals, and oxygen starvation. (31)

Enzymes and Free Radicals

Reduced activity of a key mitochondrial enzyme complex has been observed in the brains of patients with Alzheimer's disease. Neuroscientists at Cornell University think a reduction in alpha-ketoglutarate dehydrogenase complex (KGDHC) may be responsible for the decreases in brain metabolism characteristic of many neurodegenerative disorders. Their research suggests "KGDHC participates in a deleterious cascade of events related to oxidative stress that are critical in selective neuronal loss in neurodegenerative diseases." (32,33)