Hyper-Excitability Followed by Functional Quiescence in Neuronal Cells Caused by Insufficient Cellular Energy (ICE): Treatable by Enhancing the Alternative Cellular Energy (ACE) Pathway

Abstract

Living organisms derive energy for cellular activities through three primary mechanisms. The first is photosynthesis, which is restricted to plants and certain bacteria. It uses energy in sunlight to combine carbon dioxide with water to form carbohydrates plus oxygen. The second is chemical energy, which is ob-tainable by all organisms from the cellular metabolism of carbohydrates and other organic molecules. The third mechanism of obtaining cellular energy is the alternative cellular energy (ACE) pathway. The ACE pathway is expressed as an added dynamic (kinetic) quality of the body’s fluids. It results from the absorption of an environmental force termed KELEA (kinetic energy limiting electrostatic attraction). The fundamental role of KELEA is presumably to pre-vent the fusion and annihilation of electrostatically attracted opposing electrical charges. KELEA can loosen the hydrogen bonding between fluid molecules. KELEA benefits living organisms in part by enabling more efficient biochemical reactions. Cells require a minimal amount of energy to remain viable. Additional energy is required to undertake specialized cellular functions. Illnesses result if cells have insufficient cellular energy (ICE) for their specialized functions. Since KELEA is attracted to separated electrical charges, it is presumably attracted to the electrical charges comprising the membrane potential of cells. It is proposed that the depolarization of neuronal cells leads to the partial release of KELEA for use by the depolarized cell and as a contribution to the overall activation of the body’s fluids. Many brain illnesses currently attributed to cellular neurodegeneration are explainable as neuronal cells’ adaptations to ICE. The adaptations likely comprise initial hyper-excitability to obtain additional KELEA, followed by functional quiescence prior to actual neuronal cell death. Clinical recovery during both the hyper-excitable and hypoactive phases is potentially achievable by enhancing the ACE pathway. Furthermore, among the restored specialized functions of quiescent neuronal cells may be the capacity to again attract KELEA, leading to sustainable recovery. The opportunity exists for extended clinical trials involving the ACE pathway in neurological and psychiatric illnesses.