Actual or potential effects of ELF and RF/MW radiation on enhancing violence and homicide, and accelerating aging of human, animal or plant cells
Abstract
The brain is a very sensitive Bioelectromagnetic organ sat through classical resonance
processes can be halted and damage of external electromagnetic fields and radiation. This
review will explore the possibility that this could result in violence enhanced rates of
homicide. The evidence that electromagnetic fields and radiation electromagnetic are
genotoxic means that exposure to any electromagnetic fields and radiation will enhance cell
death (Apoptosis). The natural ageing process involves oxygenated free radicals from the
breathing process causing enhanced rates DNA damage, cancer and cell death. Exposure
to electromagnetic fields and radiation also reduces melatonin which limits a body’s ability
to scavenge the free radicals and therefore contributes to enhanced Apoptosis and cancer
rates. Melatonin is also necessary for a healthy immune system. Reduced melatonin is also
associated depression and suicide and therefore is likely to be associated with violence of
homicide. Since electromagnetic radiation damages the DNA and reduces melatonin it is
scientifically logical that it also enhances many of the natural paging process in people,
animals and plants. These conclusions are strongly supported by robust evidence that
natural weather related effects are caused by natural electromagnetic fields and radiation
with extremely small intensities. Therefore it is logical and proven that humanly generated
fields and radiation at intensities from a thousand to many billion times higher, also
significantly enhance a wide range of adverse health effects, including cancer, heart
disease, sleep disturbance, depression, suicide, anger, rage, violence, homicide,
neurological disease and mortality.... [Show full abstract]
Keywords
violence; homicide; human health effects; electromagnetic fields; Electromagnetic Radiation (EMR); ageing; MelatoninDate
2002-08-30Type
Journal ArticleCollections
Copyright © The Author.