Gompertz’ Hazard Law as a Network Principle of Aging
Jakob Korf 1, *, Arthur A. Sas2
Identifiers and Pagination:Year: 2019
First Page: 14
Last Page: 20
Publisher Id: TOBIOJ-7-14
Article History:Received Date: 03/12/2018
Revision Received Date: 25/03/2019
Acceptance Date: 22/04/2019
Electronic publication date: 31/05/2019
Collection year: 2019
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: (https://creativecommons.org/licenses/by/4.0/legalcode). This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Life-spanning population survivorship curves (the number of survivors versus age) are conventionally regarded as a demographic issue. Most often, the term hazard, the relative mortality per age-interval, is used as a typical survivorship parameter. Population survivorship curves are construed from cross-sectional data (single event per individual; here, mortality).
We tested (quantitatively) how Gompertz’ law describes the mortality pattern of a wide variety of organisms, some of them fed with lifespan affecting diets. Moreover, we tested (semi-quantitatively) whether Gompertz’ law describes the disintegration of a (biological) small-world network.
The Gompertz tests, explored in demographic data of humans (male/female) and 4 animal species (mice, honeybees, fruit flies, houseflies), were analyzed with conventional software. The Gompertz law was examined in a small-world network model.
Gompertz' law applies to all cohorts; thus, with or without exposure to experimental conditions. It describes in all cohorts old-age slowing of mortality. Gompertz’ law is compatible with a gradual and random increase of connections in the network model.
Old-age deceleration of mortality is a characteristic of many populations. Aging has to be understood as a lifetime increasing of excitatory or, alternatively, of decreasing inhibitory (biological) connections, thereby facilitating pathogenic mechanisms.