Information -sharing, adaptive epigenetics and human longevity

TL;DR

This paper explores how exposure to meaningful environmental information influences epigenetic mechanisms, potentially promoting healthy longevity by enhancing biological repair processes and reducing age-related diseases.

Contribution

It introduces a novel perspective on how adaptive responses to environmental information can impact epigenetics and longevity, emphasizing the importance of meaningful stimuli.

Findings

Environmental information acts as a hormetic stimulus enhancing biological repair.

Adaptive epigenetic responses may reduce age-related degeneration.

Information exposure influences resource allocation between somatic and germ-line cells.

Abstract

Emerging empirical and theoretical thinking about human aging places considerable value upon the role of the environment as a major factor which can promote prolonged healthy longevity. Our contemporary, information-rich environment is taken to mean not merely the actual physical surroundings of a person but it is also considered in a more abstract sense, to denote cultural, societal and technological influences. Our modern environment is far from being static or stable. In fact, it is continually changing in an exponential manner, necessitating constant adaptive responses on behalf of our developmental and evolutionary mechanisms. In this paper, I attempt to describe how a continual, balanced and meaningful exposure to a stimulating environment, including exposure to information-that-requires-action (but NOT trivial information), has direct or indirect repercussions on epigenetic mechanisms which may then act to prolong healthy longevity. Information gained from our environment acts as a hormetic stimulus which up-regulates biological responses and feedback loops, eventually leading to improved repair of age-related damage. The consequence of this biological information-processing mechanism may influence resource allocation and redress the imbalance between somatic cell versus germ-line cell repairs. This can eventually have evolutionary consequences resulting in the drastic reduction of age-related disease and degeneration.