Nutritional epigenetics vs perturbed metabolism in defective cells
April 12, 2014 | James Kohl
Excerpt: “[The dietary intervention] is a general shift in what we’re feeding the cells to get them to do something different with their whole nutrient metabolism,” Friis noted. “There are signaling pathways that allow a cell to sense its environment and co-ordinate events to allow the cell to adapt to what’s going on. In this case, [cells are responding to] which nutrients are available.”
My comment: Dietary intervention (e.g., nutritional epigenetics) exemplifies what naturally occurs in the context of biophysically constrained ecological variations and natural selection for nutrient-dependent pheromone-controlled ecological adaptations. See : Signaling Crosstalk: Integrating Nutrient Availability and Sex. In yeasts, the “…Snf1-dependent pathway that senses limiting amounts of glucose acts on the mating pathway to reduce mating efficiency during times of nutrient stress. The mechanism by which one signaling pathway regulates a second provides insight into how cells integrate multiple stimuli to produce a coordinated response.”
Simply put, the coordinated response to nutrient stress (e.g., food availability) and social stress (e.g., the number of conspecifics requiring food) is controlled by the metabolism of nutrients (e.g., glucose) to species-specific pheromones that control the physiology of reproduction. See also: “The diverse social behaviors that are enabled by the functional flexibility of the secrete-and-sense circuits (Fig. 5C) may explain the frequent occurrence of this class of circuits in nature.”
Details of the systems biology that link nutrient stress and social stress from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man have consistently been provided in the extant literature. However, the details have been placed into the context of evolutionary theory. Unfortunately, the misrepresentations of theory have been accepted despite the lack of experimental evidence that might otherwise have supported the claims made by evolutionary theorists. Thus, their unsupported claims have become popular — if only due to their simplicity.
We now know there are at least two ways that heritable variation can be generated by proteins, not DNA. Nutrient-dependent base pair flipping may result in spontaneous self-aggregating alternative splicings of pre-mRNA and alternative conformations of proteins that change a cell’s phenotype “… in an environmentally responsive manner with no change to DNA. The change is transmissible vertically, parent to offspring cell, as well as horizontally, to other cells in which the proteins come in contact. Another mechanism involves chaperones such as heat shock protein 90 (Hsp90), proteins that massage subideal (mutant) proteins into functional conformations but abandon their regular client proteins during heat and other stresses that destabilize proteins. This causes a stress-inducible release of phenotypic diversity, which may drive evolution (with phenotypes ultimately stabilized by subsequent genetic changes). Both of these molecular mechanisms of protein-based inheritance are major departures from the modern synthesis views of solely mutation-directed variation, solely genetic inheritance, and independence of the generation of variation from environmental conditions (Rosenberg & Queitsch, 2014, p. 1088).”
For contrast, the two ways that heritable variation can be generated by proteins involve the conserved molecular mechanisms of nutritional epigenetics, which means there is only one way to link biologically-based cause and effect to species diversity. For example, nutrient stress and social stress alter the seemingly futile thermodynamic cycles of protein biosynthesis and degradation. Epigenetic effects of olfactory/pheromonal input on heritable variation generated by proteins links biophysically-constrained conserved molecular mechanisms that enable ecological variations to result in ecological adaptations manifested in the stability of protein folding that is required for organism-level thermoregulation and species diversity. The ecological adaptations in protein-folding are manifested in species-specific morphological and behavioral phenotypes.
The idea that mutations could somehow result in morphological phenotypes, which were also somehow correlated with species-specific behavioral phenotypes, should be replaced with the facts of how food odors and pheromones epigenetically cause the species diversity that is manifested in ecological adaptations. Only the popularity of bastardized evolutionary theory can prevent accurate representations of cause and effect. However, now that the “…major departures from the modern synthesis views…” have been addressed by Rosenberg & Queitsch, 2014, others may be inclined to stop touting the pseudoscientific nonsense of evolutionary theory and begin to examine biological facts that have been established by experimental evidence in species from microbes to man.
Clearly, nutritional epigenetics and ecological adaptations make sense in the context of what is currently known about physics, chemistry, and molecular biology, which shows that nothing nothing about evolution makes sense. That explains why experimental evidence continues to support the detailed concept of “Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems” that dismisses current misrepresentations of evolutionary theory. Darwin’s theory can now be examined in the context of ‘conditions of life,’ which are nutrient-dependent and pheromone-controlled.
Note: All but one of the reviewers who were invited to review my invited submission refused to review “Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems.” The article on dietary intervention and two articles on on 1) and 2) link nutrient stress and social stress to ecological adaptations via conserved molecular mechanisms of protein folding. The only comment on my review was that it was not focused and self-aggrandizing.