Evolutionary theories of epigenetic drift

By: James V. Kohl | Published on: September 15, 2017

Testing Two Evolutionary Theories of Human Aging with DNA Methylation Data
My summary: Outside the context of food energy-dependent biophysically constrained pheromone-controlled viral latency, mutation accumulation (MA) and disposable soma (DS) provide possible explanations for the existence of human aging. For example, age-differentially-methylated sites across the genome showed significant MA-consistent increases in heritability with age or significant DS-consistent decreases in heritability. Their results supposedly show that both MA and DS play a role in explaining aging and aging-related changes but their results do not link food energy-dependent RNA-directed DNA methylation to de novo gene creation or the virus-driven degradation of messenger RNA that serious scientists have linked from mutations to all pathology in all living genera.
See also: Caloric restriction delays age-related methylation drift

Epigenetic information encoded by DNA methylation is tightly regulated, but shows a striking drift associated with age that includes both gains and losses of DNA methylation at various sites.

Reported as: Researchers uncover mechanism behind calorie restriction and lengthened lifespan

Dr. Issa’s team made their discovery after first examining methylation patterns on DNA in blood collected from individuals of different ages for each of three species – mouse, monkey, and human.

Energy as information is epigenetically linked from the food that organisms eat to the physiology of pheromone-controlled reproduction in all living genera by RNA-directed DNA methylation and amino acid substitutions that differentiate all cell types in all individuals.
All serious scientists have linked RNA-mediated amino acid substitutions from the differentiation of cell types in yeasts to the differentiation of cell types in primates.
Nothing in Biology Makes Any Sense Except in the Light of Evolution 

…the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla.

See for example: Nutrient-dependent/pheromone-controlled adaptive evolution: a model

In the mouse model, the diet of the mice determines their nutrient-dependent pheromone production and social interactions with other mice. The mouse model also reveals something that was not revealed in the context of dogs and wolves (Axelsson et al., ; Lord, ). The aversive human body odor associated with fish odor syndrome can be epigenetically controlled by reducing dietary choline intake. It can also be controlled through antibiotic use (citations in Li et al., ). This may be important in the context of chemical ecology and epigenetic effects of genetically predisposed nutrient-dependent pheromone-controlled human interactions (Martin et al., ; Preti & Leyden, ).

See also the section on “An epigenetic continuum of nutrient-dependent / pheromone-controlled adaptive evolution”


Differences in the behavior of nematodes are determined by nutrient-dependent rewiring of their primitive nervous system…


The honeybee is currently an accepted model organism of nutrient-dependent pheromone-controlled adaptive evolution of the brain and behavior that is consistent with what is known about neurogenic niche construction in nematodes…


Species-specific health and reproductive fitness is associated with nutrient-dependent amino acid substitutions and with pheromone-controlled reproduction. Disease is associated with mutations exemplified in cancer where perturbations of the glucose-dependent thermodynamic/thermoregulatory equilibrium are equally clear (Locasale, ).


Two additional recent reports link substitution of the amino acid alanine for the amino acid valine (Grossman et al., ) to nutrient-dependent pheromone-controlled adaptive evolution. The alanine substitution for valine does not appear to be under any selection pressure in mice. The cause-and-effect relationship was established in mice by comparing the effects of the alanine, which is under selection pressure in humans, via its substitution for valine in mice (Kamberov et al., ).

See for comparison: Feynman on social science
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