Abstract
There is consensus among biogerontologists that aging occurs either as the result of a purposeful genome-based, evolved program or due to spontaneous, randomly occurring, maladaptive events. Neither concept has yet identified a specific mechanism to explain aging’s emergence and acceleration during mid-life and beyond. Presented herein is a novel, unifying mechanism with empirical evidence that describes how aging becomes continuous with development. It assumes that aging emerges from deterioration of a regulatory process that directs morphogenesis and morphostasis. The regulatory system consists of a genome-wide “backbone” within which its specific genes are differentially expressed by the local epigenetic landscapes of cells and tissues within which they reside, thereby explaining its holistic nature. Morphostasis evolved in humans to ensure the nurturing of dependent offspring during the first decade of young adulthood when peak parental vitality prevails in the absence of aging. The strict redundancy of each morphostasis regulatory cycle requires sensitive dependence upon initial conditions to avoid initiating deterministic chaos behavior. However, when natural selection declines as midlife approaches, persistent, progressive, and specific DNA damage and misrepair changes the initial conditions of the regulatory process, thereby compromising morphostasis regulatory redundancy, instigating chaos, initiating senescence, and accelerating aging thereafter.
Highlights
Aging is generally thought to occur by programmed or non-programmed processes [1,2]
Assuming that somatic maintenance is active during the period of exponentially increasing death rates, and since human and captive animal mortality curves approximate the physiological aging curve, the authors felt that opposition to aging via the somatic maintenance program (SMP) could be graphically represented as an inverse plot of the Gompertz function [91] which begins in humans at approximately age 30 [92]
Relevant to the mechanism of aging that occurs within the proposed process of morphostasis is the fact that the soma is under threat of constant assault by double-stranded breaks (DSBs) damage to DNA
Summary
Aging is generally thought to occur by programmed (adaptive) or non-programmed (non-adaptive/stochastic) processes [1,2]. Adaptive theories presume that aging evolved to benefit species, not individuals [3,4]. They provide reasons why, but not the mechanism by which, aging benefits evolution; its progression has often been said to appear programmatic. Non-adaptive theories view aging as resulting from molecular damages that accumulates because chemical and physical constraints prevent their elimination by evolutionary processes. Events that promote senescence occur “within the scope of the developmental program”, causing the progression of aging to appear programmatic. (a) A holistic regulatory program guides morphogenesis and morphostasis in the absence of aging;. (d) Progressively chaotic regulatory behavior erodes morphostasis redundancy initiating senescence and accelerating the rate of aging
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