Mosaic Epigenetic Dysregulation of Ectodermal Cells in Autism Spectrum Disorder clearly links the de novo creation of olfactory receptor gene OR2L13, from decreased nutrient-dependent DNA methylation to sensory processing in ASD’s.
A series of published works I posted yesterday in Ecological variation leads to ecological adaptations links failed adaptations manifested in autism spectrum disorders (ASDs) via the sensing of chemicals that are typically called “odors.” Although the complexity of nutrient-dependent signaling and de novo creation of an olfactory receptor (OR) gene via conserved molecular mechanisms of cell type differentiation in species from microbes to man that lead to my atoms to ecosystems model is overwhelming, scientific progress is not made by ignoring the complexity.
That’s why I was surprised to read this sentence from Maximum information entropy: a foundation for ecological theory (in press). “Given that there are so many mechanisms, processes, and trait-specific interactions at work in an ecosystem, they can effectively be ignored.”
Biophysical constraints on experience-dependent protein folding allow the natural genetic engineering of the cell to create the receptors that allows the nutrient(s) to enter the cell and to alter the microRNA/messenger RNA balance, which leads to the cell’s nutrient-dependent ability to create more ORs via gene duplication. However, gene duplication seems unlikely to occur in the context of entropy. I suspect that’s why a new definition of entropy is used in the context of maximum information entropy. What else can be done by theorists when what’s known about atoms and ecosystems refutes their theories with experimental evidence that appears to violate the Second Law of Thermodynamics, which implies that order does not arise from disorder. The molecular mechanisms of gene duplication show that order does result from disordered nutrient-dependent intercellular signaling in all cells of all individuals in all species. Since gene duplication defies entropy, it must now be defined in the terms of population genetics or neo-Darwinism will be exposed to be pseudoscientific nonsense.
Creation of ORs and other proteins via seemingly futile cycles of protein biosynthesis and degradation then stabilizes cell type differentiation that occurs with nutrient uptake and “pheromone”-controlled reproduction at the unicellular level (e.g., in bacteria and yeasts) and multicellular levels of organism-level sensing and signaling via the complexities of biophysically constrained thermodynamics and thermoregulation.
Transgenerational epigenetic inheritance of the molecular mechanisms required for organism-level thermoregulation enable ecological variation to be manifested in ecological adaptations. These ecological adaptations are found in the morphological and behavioral phenotypes of species from microbes to man.
ASDs represent failed ecological adaptations that are readily linked to nutrient stress and social stress, which link the epigenetic landscape to the physical landscape of DNA in organized genomes whether or not Darwin’s ‘conditions of life’ are all-together favorable.
His ‘conditions of life’ may require atomic level changes that link micronutrients and macronutrients from one-carbon metabolism, base pair changes, DNA methylation, and amino acid substitutions to the Creation of novel cell types via the differentiation of cell types during their nutrient-dependent maturation.
Use of the big “C” in the context of the Creation of novel cell types led to Dobzhansky’s claims. In 1973, he stated that he was a Creationist and an Evolutionist
Anyone who is not an evolutionary theorist now recognizes the likelihood that Dobzhansky and others like him have always been Creationists and Ecological Adaptationists who realize that mutations perturb protein folding, which means they are not naturally selected to become fixed in the organized genome of any species. Therefore, entropy must be redefined in another attempt to fit what population geneticists have ignored into their theories.
They have ignored the fact that only nutrient-dependent fixation of amino acid substitutions and the pheromone-controlled physiology of reproduction can result in increasing organismal complexity that is manifested in biodiversity via the conserved molecular mechanisms that link microbes to man. That fact led Queitsch & Rosenberg to conclude an article about Combating Evolution to Fight Disease with this statement, which echoes the sentiments I have repeatedly expressed: “The evolutionary biologist Theodosius Dobzhansky famously noted that “nothing in biology makes sense except in the light of evolution,” but perhaps, too, “nothing in evolution makes sense except in the light of biology.” Although the latter might be an exaggeration, an important gap is being filled by molecular understanding of the genesis of variation that confers the ability to evolve.”
Variation in the availability of nutrients confers the ability to ecological adapt. Nothing that makes sense in the light of biology confers the ability to evolve. The theory of evolution was invented to explain what could not be explained by biology after the Scopes trial in 1925. Examples of ecological adaptations in species from microbes to man now explain how ecological variation leads to biodiversity via the nutrient-dependent pheromone-controlled physiology of reproduction. But: “Given that there are so many mechanisms, processes, and trait-specific interactions at work in an ecosystem…,” they must be ignored by theorists, lest their theories be removed from any further consideration whatsoever in the context of biological facts about the origins of ASDs and other developmental disorders that theorists want others to attribute to mutations and natural selection.
