Genetic mutations in healthy blood
April 26, 2014 | James Kohl
Here’s the problem when others take a mutation-driven evolution approach to across-species differences in morphological and behavioral phenotypes. Eventually, they find out that nutrient-dependent DNA methylation and amino acid substitutions, which stabilize the genome, enable the ecological adaptations that are responsible for individual diversity and species diversity.
For example of a correct approach, with her co-authors, Anna Di Cosmo cites “From a marine neuropeptide to antimicrobial pseudopeptides containing aza-beta(3)-amino acids: structure and activity.” Also, in a search of Anna’s text, there is no mention of “mutation.” Thus, the problem for others becomes their mention of “mutation” instead of accurately portraying the role of nutrient uptake in ecological adaptations of different cell types.
Anyone who touts theory will run up against the concept of genetic mutations in healthy blood, which means they will soon see their funding reduced or eliminated as more researchers detail aspects of biologically based cause and effect in the context of DNA methylation, amino acid substitutions and ecological adaptations.