Published online by Cambridge University Press: 01 August 2014
The phenomenon of life, in its individual and collective expressions, develops through a sequence of times resulting from the interference of biological with physical time. While physical time is uniform, the biological one differs from one individual to the other, except for MZ twins.
The problem of biological time has been studied in physiology and informational genetics from the viewpoint of its succession of single times, although irrespective of the individual variability in their duration. This variability has already been shown by the authors to be hereditary, its inheritance being directly connected with the hereditary unit.
Biological time corresponds to the duration of degradation (“chronon”) of the energy of stability (“ergon”) possessed by the gene and, by extension, to the total chronon of the genotypes underlying a given structure or function. Ergon and chronon are correlated index values, thereby constituting a system (“E/C system”).
The individual variability of biological time depends on the A-T/G-G ratio in the DNA molecule, on the different amount of genie redundancy and on the different possibilities of repair of corresponding genes. The variability of these or possibly other causal factors determines the stability with respect to the environment in which the information operates, and especially to mutagenic agents.
The authors apply the E/C model to epidemiologic data concerning diabetes, lupus erythematosus, and peptic ulcer, and verify the consistency of the experimental data with the theoretical model.