Noise-driven onset time of biodemographic aging

The lifespan of each individual, even in an isogenic cohort and a uniform environment, is quite different. The genetic factors influencing the lifespan in humans as well as animal models are few. The balance is attributed to “chance” variations. In this study, we focus on a third factor, noise or chance variations, as well as on genetic and environmental factors and examine how biodemographic aging is related to stochastic fluctuations, or noise. To elucidate the third factor in relation to aging and lifespan, we employed the nematode Caenorhabditis elegans, which can provide an ideal system for analyzing the mathematical and biophysical models. An amplification of ATP noise was clearly evident from around the onset of biodemographic aging (t0) as if the t0 was synchronized with or derived from the amplification of noise. Furthermore, the expression noise of the unc-54 gene, which encodes the myosin heavy chain, increased from around the t0. In contrast, the noise of genes related to the mitochondrial respiratory chain was almost constant with aging. There is a high energy barrier between life and death. Here we propose that the transition from living to dying may be facilitated by noise amplification. The finite value (or non-zero) of t0 is essential to the lifespan equation derived from the diffusion model. •We focus on a third factor, noise, as well as on genetic and environmental factors.•Biodemographic aging is related to stochastic fluctuations, or noise.•An amplification of ATP noise was clearly evident from around the onset of biodemographic aging.•The expression noise of the unc-54 gene increased from around the onset of biodemographic aging.•The transition from living to dying may be facilitated by noise amplification.