The end of human evolution: Ecological adaptations
April 18, 2014 | James Kohl
Excerpt: DNA methylation is a key hallmark of gene activity in mammals…
My comment: That is an understatement! DNA methylation is the end of human evolution. Methylation is THE hallmark of nutrient-dependent hormone-organized and hormone-activated changes in the organized genome of mammals. The changes epigenetically link olfactory/pheromonal input to the physical landscape of DNA via methylation. The changes in the organized genomes are manifested in morphological and behavioral phenotypes in vertebrates and invertebrates. For examples, see: Nutrient-dependent/pheromone-controlled adaptive evolution: a model.
In that literature review, I uncovered the epigenetic basis for phenotypic differences among invertebrates and vertebrates, which include species of mammals, and I explained the development of differences between present-day and archaic humans. For example, the nutrient-dependent pheromone-controlled epigenetic basis of differences in morphological and behavioral phenotypes in mice and humans clearly involves base pair changes. One base pair change leads from methylation to an amino acid substitution and changes in the teeth, hair, sweat glands, and mammary tissue of the mouse. Those changes are paralleled by changes in a modern human population that ecologically adapted during approximately the past ~30,000 years in what is now central China. The physiology of reproduction is nutrient-dependent and pheromone-controlled in all species, which links species-specific pheromone-production in mice to pheromone-controlled reproduction in humans via the same model.
In the context of my model of nutrient-dependent pheromone-controlled ecological adaptations in mice and humans, claims about the recent evolution of our lineage can be replaced with experimental evidence of biologically-based cause and effect. Cause and effect is biophysically constrained, which means any ideas that remove ecological variation must also insert constraint-breaking mutations. However, the constraint-breaking mutations do not lead to ecological adaptations.
As these authors show, mutations lead to disease. The fact that the disease-linked genes are involved in neurological and psychiatric disorders links nutrient-dependent pheromone-controlled ecological, social, neurogenic, and socio-cognitive niche construction from ecological variation to detrimental changes in the modern human brain. The detrimental changes are associated with nutrient stress and social stress in other animals.
Nutrient-stress and social stress are the primary and secondary contributors to the end of human evolution in my model, because they limit ecological adaptation.
Nutrient stress and social stress have always limited ecological adaptations in the cell types of individuals of all species. Thus, nutrient-stress and social stress now limit use of the term evolution and replace it via a model of Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems.