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Genetic Influences on Epigenetically Effected Disease

Posted on November 26, 2012 by James Kohl.

Science 23 November 2012: Vol. 338 no. 6110 pp. 1016-1017

Human Genetics

Genetic Influences on Disease Remain Hidden by Jocelyn Kaiser

Excerpt: “Some scientists, such as Harry Dietz of Johns Hopkins University in Baltimore, Maryland, suspect that much of the missing heritability lies in gene-gene interactions.”

My comment:

Adaptive evolution occurs via the epigenetic effects of nutrient chemicals on genetically predisposed food acquisition behaviors that alter intracellular signaling and intermolecular changes in DNA. The changes enable the metabolism of the nutrient chemicals to species-specific pheromones that control reproduction by altering nutrient chemical-dependent social behaviors.

This makes it clearer that gene-environment interactions result in sense-driven gene-gene interactions required to achieve cellular and organism-level homeostasis via the microRNA / messenger RNA balance. When perturbed (e.g., stressed) by the epigenetic effects of sensory input, it is that miRNA/mRNA balance that enables de novo gene expression.

If so, one reason we’re seeing less evidence for effects of specific de novo gene expression on disease is because there is first the bottom up epigenetic effect of nutrient chemicals followed by the top-down epigenetic effect of pheromones on adaptive evolution. Looking for a mutated gene that causes uncontrolled intracellular effects and pathology via intermolecular changes that occur via only either a 1)bottom-up,  or a 2)top-down approach,  seems less likely to reveal the underlying biochemical basis of disease than would examination of how and why nutrient chemical-dependent (e.g., bottom-up) pheromone-controlled (e.g., top-down) reproduction enables de novo gene expression-driven speciation.

After looking at the path from genes to behavior and back, the intracellular and intermolecular dynamics of typical speciation could then be compared to the null effects or deadly effects of mutations and show us why nutrient chemicals and pheromones are part of adaptive evolution and mutations are not. It is because mutations are not part of adaptive evolution that we can be sure olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans in the context of adaptive evolution.

Without that clear evolutionary trail of nutrient chemical-dependent pheromone-controlled reproduction, looking for mutations that cause one thing in vertebrates/mammals/primates or another in invertebrates seems a bit pointless. By the time you get to 4 or 5 million nutrient-chemical and pheromone-controlled DNA switches in the human genome, you will probably have missed something important to homeostasis even if you do find a mutated gene linked to endocrine disruption, toxins, deficient immune systems, or any mental or physical disease processes.



James Kohl
Retired medical laboratory scientist

James Kohl

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