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.

Highlights

  • It is widely assumed that work performed by living organisms is fueled entirely, either directly or indirectly, from the energy in sunlight via photosynthesis [1]

  • Since kinetic energy limiting electrostatic attraction (KELEA) is attracted to separated electrical charges, it is presumably attracted to the electrical charges comprising the membrane potential of cells

  • The alternative cellular energy (ACE) pathway is defined as a dynamic quality of the body fluids resulting from the attraction of an external force termed KELEA

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Summary

Introduction

It is widely assumed that work performed by living organisms is fueled entirely, either directly or indirectly, from the energy in sunlight via photosynthesis [1]. The proton motive force enables the ATP synthase enzymes to add a third phosphate from the phosphoryl (PO3) molecule to adenosine diphosphate (ADP) [4]. The reconversion of photosynthetically-derived ATP back to ADP provides the rubisco enzymes in plants with chemical energy to link carbon dioxide with water to form glucose and to release oxygen [7]. The oxidation of glucose in plants, as well as animals, occurs in the cells’ mitochondria [9] and yields ATP from ADP for numerous cellular activities [10] These activities include the synthesis of other types of organic molecules, including the many structural and functional components of organisms. Energy consumption in an average sized human is equivalent to approximately two thousand kilocalories (2000 kcal), expressed as 2000 Calories [12]

Additional Cellular Energy beyond the Metabolism of Food
Possible Involvement of KELEA in Conversion of Electrical to Chemical Energy
Hyper- and Hypo-Excitability of Neuronal Cells as Responses to ICE
ACE Pigments and KELEA Activation of Water
Brain and Muscle Activities in Support of the ACE Pathway
Conclusion
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