KELEA Excellerated Water and the Alternative Cellular Energy (ACE) Pathway

Abstract

It has generally been assumed that humans and animals can only obtain energy from food; with the mitochondria being the principal cellular component for food metabolism. Basic calculations of the daily work output of humans indicate an energy expenditure far in excess of the approximately two thousand Calories consumed each day in a typical diet. Humans must, therefore, have an alternative cellular energy (ACE) pathway that is empowered by an environmental force. Indeed, based on experimental observations, some of which are detailed herein, this force has been designated as KELEA; an abbreviation for Kinetic Energy Limiting Electrostatic Attraction. KELEA is seemingly reversibly bound to both positive and negative electrical charges. It likely provides the repulsive mechanism that prevents the ultimate fusion of electrostatic attracted opposing electrical charges. It is further proposed that KELEA is drawn to the isolated electrical charges on dipolar molecules, including water. Increasing the level of KELEA in water weakens the attachments between the electrostatically bonded water molecules. Consequently, the water molecules become kinetically more active; as can be shown in specific assays. The term “excellerated water” is being used rather than “activated water” to more specifically define water with a significantly heightened level of a non-thermal kinetic activity. The added kinetic energy present in KELEA excellerated water can be transferred from the water molecules to other types of molecules. The energy is also transferable between the molecules involved in linked chemical reactions. As such, it can be equated with chemical energy. It is likely that the fluctuating electrical activity of the normally functioning brain acts as the major receiver of KELEA from the environment. This is consistent with one of the consequences of brain damage being an overall insufficiency of energy for the ACE pathway. Individual neurons probably derive some of the energy for their own cellular needs from the repetitive depolarization of the cell. This may explain why hyperexcitability of neurons can occur in response to cell damage. Such an adaptive mechanism is unlikely to be sustainable, however, especially because of the continuing need to synthesize neurotransmitters and membrane ion channels.