Military combat training to fight disease
Q: What is the extent of your formal scientific education? I see that you attended the University of Nevada at some point.
A: I had already been trained in the military to combat evolutionary theory (see also Combating Evolution to Fight Disease). After time spent in the hospital medical records department, I became the liaison between people who were being processed for medical discharge and the Medical Evaluation Board, I organized case histories that included all testing and learned about diagnostic medicine.
The testing established clear links between injuries and diseases or disorders due to mutations. Those links can be compared in the context of what is known about epigenetically-effected feedback loops to healthy cell type differentiation, which is perturbed by injuries or physiopathology.
I extended my enlistment to learn more about pathology. I finished formal training in the lab in 1974. See Dobzansky’s (1973) claim in “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.”
There are now known to be more than 1180 hemoglobin variants that differentiate different human populations. Evolutionary theorists still place the variants into the context of mutations in their ridiculous theories about biologically-based cause and effect. The dean of the biology department at the University of Nevada (Las Vegas) became very angry with me when I refused to declare a major and also refused to cut and paste chromosomes to exemplify “matching” in the context of mutations and evolution. I refused to “cut and paste” anything, although the “lab exercise” was 25% of the final grade. I finished the genetics course with a D. Then, in my conversation with the dean about declaring a major, I learned that the cut and paste nonsense was a “lab exercise” he designed — after telling him I thought it was like something I remembered from kindergarten.
Much of what I continue to see reported appears to be based on “lab exercises” from 35 years ago. See:Genetic Mutation
Excerpt: “For example, sickle-cell anemia is a disease caused by the smallest of genetic changes. Here, the alteration of a single nucleotide in the gene for the beta chain of the hemoglobin protein (the oxygen-carrying protein that makes blood red) is all it takes to turn a normal hemoglobin gene into a sickle-cell hemoglobin gene. This single nucleotide change alters only one amino acid in the protein chain, but the results are devastating.”
Researchers seem to have failed to grasp the basic principles of biology and levels of biologically-based cause and effect that link nutrient uptake and the pheromone-controlled physiology of reproduction to morphological and behavioral phenotypes in species from microbes to man, which are linked to physiopathology via the conserved molecular mechanisms of RNA-mediated cell type differentiation. I began to detail the aspects of these conserved molecular mechanisms in a series of published works starting with book publication in 1995. Other serious scientists now understand how:
Excerpt: “When I give talks about network medicine,” he said, “I’ve gotten three kinds of responses. At one end of the spectrum are generally young people … who say this is a great idea, I hadn’t thought about this before.
My comment: When I have presented or published reviews that incorporate every aspect of my model, I am often told that beneficial mutations cause cell type differentiation in species from microbes to man, via their evolution. I could not tolerate that pseudoscientific nonsense, and am even less tolerant now. But it’s still being taught today. For example, see: Mutation-Driven Evolution: “…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world. In this view of evolution there is no need of considering teleological elements.” (p. 199)
I hope others will attempt to understand my model in the context of what is currently known about nutrigenomics and pharmacogenomics, which links metabolic networks to genetic networks in species from microbes to man. It takes less that ten minutes to link current information to my model and to presentations for a general audience like this one from the 2010 Annual Gathering of Mensa in Dearborn, Michigan.