Different physical locations and different molecular mechanisms of health and disease

By: James V. Kohl | Published on: September 29, 2014

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Reappraisal of known malaria resistance loci in a large multicenter study

Abstract excerpt: “The finding that G6PD deficiency has opposing effects on different fatal complications of P. falciparum infection indicates that the evolutionary origins of this common human genetic disorder are more complex than previously supposed.”
Reported as:

Long term genetic study finds geographical differences in human immune response to malaria

Excerpt: “…humans living in different physical locations have evolved different mechanisms for staving off the dreaded disease malaria.”
My comment: Placing the successful immune system response to malarial parasites in the context of mutations linked to hemoglobin variants such as the sickle cell hemoglobin S variant showed us all that evolutionary theorists have no understanding of biologically-based cause and effect,
Like all other 1180+ human hemoglobin variants, the S variant must arise in the context of nutrient-dependent RNA-directed DNA methylation and RNA-mediated events that lead from nutrient uptake to amino acid substitutions that stabilize DNA in the organized genomes of species from microbes to man via pheromone-controlled fixation of the substitutions. Even butterfly collectors should recognize the similarity between the molecular mechanisms of genome stability in moths and human populations. For example, moth larvae that ate lead- and manganese-contaminated leaves became pepper-colored because their nutrient-dependent pheromone-controlled physiology of reproduction stabilized their organized genome just as vitamin D stabilizes the genome in some human populations where malaria is endemic.

Reports that bird predation led from mutations and natural selection of fawn-colored to pepper-colored moths, and back (when industrial pollution was controlled) are another classic example of what pseudoscientists were taught to believe about nutrient-dependent pheromone-controlled ecological adaptations.

What we see here is another example of how researchers taught to believe in neo-Darwinian theory refuse to learn about biophysical constraints on thermodynamic cycles of protein biosynthesis and degradation. That leads them to attribute geographical differences in the immune system response to mutations — instead of to ecological variation and ecological adaptations. Serious scientists would ask, “What does Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency do to the stability of DNA in organized genomes. After learning about the epigenetic link from the biophysics and chemistry of glucose metabolism to cell type differentiation in all cells of all individuals of all species, the serious scientists would proceed to make progress in attempts at Combating Evolution to Fight Disease.
They would place pathology associated with cell type differentiation in blood cells into a model of biologically-based cause and effect. That model would eliminate the theory of mutation-initiated natural selection and evolution of moths via bird predation and the evolution of humans via snake predation as touted in a recent report on the snake-centric theory of human evolution. In fact, the model of nutrient-dependent pheromone-controlled ecological adaptations would eliminate all the pseudoscientific nonsense associated with evolutionary theories.