A theory for the temperature dependence of lifespan

Abstract

Human aging occurs at rates that vary widely between organisms and cell types. We hypothesize that in both cases, variation is due to differences in heat production, heat management and molecular susceptibility to heat-induced change.;A negative correlation has been observed between metabolic rates and lifespan. Free radicals are frequently assumed to be the agent of change, but we suggest that concurrently produced, minute quantities of thermal energy may also play a role.;We assume that the amount of heat produced by an individual will depend on the metabolic rate of each cell type and the proportion of body mass made up by each cell type. Similarly, an individual's ability to dissipate heat will depend on the thermal properties of each cell type, and the proportion of body mass made up by each cell type. These factors introduce substantial variation and can account for differential rates of aging between but not within tissue types ("mosaicism"), as well as between individuals of a species.;Existing theories of aging suggest that damage occurs to the conformations or sequences of molecules, which only shifts focus onto the implied failure of repair mechanisms. Contrarily, we suggest that heat-induced changes affect only the behavioral characteristics of molecules such as binding affinities, kinetics, motilities and functionalities. In this way, altered proteins would be able to persist undetected by heat shock proteins and other canalizing mechanisms, which recognize only physical aberrancies.;We hypothesize that the behaviors of a protein are dependent on minute energetic fields within and between its atoms. Minute quanta of heat alter behaviors by eliciting shifts in these energetic fields, which in turn, alter molecular interaction schemes. The appearance of novel protein interaction schemes can be thought of as a decrease in the integrity of existing genetic and epigenetic networks and an increase in variability.;Restructured topologies and increased variability lead to diverging emergent network properties, which correlate with the decreased functionality associated with "aging". Finally, we assume that a variability threshold exists such that once it is surpassed, an organism can no longer perform the functions required to sustain life and will die.