Aging and magnetism: Presenting a possible new holistic paradigm for ameliorating the aging process and the effects thereof, through externally applied physiologic PicoTesla magnetic fields

Abstract

A new holistic paradigm is proposed for slowing our genomic-based biological clocks (e.g. regulation of telomere length), and decreasing heat energy exigencies for maintenance of physiologic homeostasis. Aging is considered the result of a progressive slow burn in small volumes of tissues with increase in the quantum entropic states; producing desiccation, microscopic scarring, and disruption of cooperative coherent states. Based upon piezoelectricity, i.e. photon–phonon transductions, physiologic PicoTesla range magnetic fields may decrease the production of excessive heat energy through target specific, bio molecular resonant interactions, renormalization of intrinsic electromagnetic tissue profiles, and autonomic modulation.

Prospectively, we hypothesize that deleterious effects of physical trauma, immunogenic microbiological agents, stress, and anxiety may be ameliorated. A particle–wave equation is cited to ascertain magnetic field parameters for application to the whole organism thereby achieving desired homeostasis; secondary to restoration of structure and function on quantum levels. We hypothesize that it is at the atomic level that physical events shape the flow of signals and the transmission of energy in bio molecular systems. References are made to experimental data indicating the aspecific efficacy of non-ionizing physiologic magnetic field profiles for treatment of various pathologic states.

Introduction

Theories about the process of aging address two sets of factors – those intrinsic and those extrinsic to the organism. Intrinsic factors operate on the body from within, such as the impact of genetic programming. Extrinsic factors are influences on the body essentially from the environment, such as the impact of cumulative stresses. From an intrinsic perspective, human telomeres are approximately 15–20 kb in length at birth, and shorten gradually throughout life in dividing cells; suggesting that telomere length may serve as a biological (as opposed to a calendar) timing mechanism. Cell senescence is activated once a critical shortened telomere length is attained. There are many published correlative studies demonstrating a connection between telomere length and aging, and there is evidence supporting an inherited component to telomere length [1], [6], [10], [28], [31], [32], [33], [34].

The first component of our hypothesis resides in the possibility that extrinsically sourced physiologic PicoTesla electromagnetic fields (PTEMF’s) may be utilized to prevent telomere shortening. Theoretically, magnetic resonant energies may be target-specific, and through the mechanism of photon–phonon transduction, i.e. piezoelectricity, PTEMF’s may stabilize the structural integrity of telomeres to prevent shortening upon cell division. Studies supporting this possibility will be discussed.

Secondly, extrinsic challenges of life produce various stressors, stimulation of the hypothalamic–pituitary–adrenal axis (HPA axis), and production of the stress hormone cortisol, a glucocorticoid naturally secreted during a stress response. Cortisol’s primary function is the redistribution of energy through gluconeogenesis to regions that need it most, i.e. the brain and major muscles during a fight-or-flight situation.

Cortisol also acts to suppress the body’s immune system, while aiding in fat and protein metabolism. Thus, we hypothesize that the natural exigencies of life produce increased heat energy, enhancing desiccation of tissue microstructures, increasing microscopic scarring, quantum entropy or disorder, and aging. Therefore, the second component of our hypothesis concerns electromagnetic field modulation of vagal innervation and sympathetic innervation [1], [2], [3], [4], [5].

It is proposed that the challenges of life (physical, chemical, and emotional) all contribute to the actual longevity of an organism; seldom actualizing the maximum life span determined by the predisposing inherited characteristics of the genome. While the neuroendocrine system has been scrutinized as a major contributor to aging, we note that many lower organisms known to age over time have no well-developed neuroendocrine system. Neuronal loss in humans occurs in selective areas in the brain and age-related neuronal losses may be considered secondary to the production of biological senescence. Despite the fact that elderly individuals tend to develop hypertension possibly related to increased sympathetic system reactivity, impaired glucose tolerance, diminished thyroid function, and decline in gonadal function, these and other factors may be considered contributory to the aging process. It should be noted that most brain functions involved with intelligence are quite remarkably preserved throughout life [1], [2], [3], [4], [5], [6], [7], [8].