Lift Decay and Interception Termination: The Physical Inevitability of Death and the Engineering Boundaries of Longevity

This paper deduces the physical inevitability of death from the second law of thermodynamics and electrochemical potential. Current aging research faces a fragmentation dilemma—the free radical, telomere, mitochondrial, and epigenetic theories are each valid in their own right, yet lack a unified underlying framework. This paper proposes the "Lift Decay Model," unifying these fragments as manifestations of the same physical process at different scales: aging is the inevitable process by which the "lifting force" that maintains the cross-scale electrochemical steady state of the organism relatively decays as the carbon-based carrier ages. The decline in mitochondrial respiratory chain proton pump efficiency, the deterioration of cell membrane potential maintenance capacity, and the degradation of autonomic nervous regulation of visceral rhythms—these three together constitute the decay of the lifting force. When the lifting force falls below the critical threshold required to maintain the steady state, the organism enters decompensation, ultimately progressing to multiple organ failure. Death is not a malfunction of life, but the inevitable thermodynamic relaxation that occurs when the lifting force falls below the critical threshold. Based on this, this paper proposes three intervention pathways: repairing the electrical properties of the carbon-based carrier, supplementing exogenous electrochemical potential, and decoupling externalized memory from the body. This paper provides testable predictions: if the above pathways are systematically developed and made universally accessible, the average human lifespan can be extended to the order of a century; in model organisms, combined interventions targeting membrane potential maintenance, mitochondrial efficiency, and autonomic nervous regulation should extend healthspan significantly more than any single intervention. This paper is a purely conceptual hypothesis containing no new experimental data, aiming to provide a common physical foundation for the fragments of aging research.