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Intermolecular thermodynamics and thermoregulation of adaptive evolution

Posted on February 24, 2013 by James Kohl.

Pigeon Study Contradicts Darwinian Natural Selection

Excerpt: “…the role of incremental adaptive selection (i.e., Darwinism) in rationalizing morphological evolution becomes highly questionable.”

H. Allen Orr’s review of Mind and Cosmos: Why the Materialist Neo-Darwinian Conception of Nature Is Almost Certainly False by Thomas Nagel.

Excerpt: “…natural selection responds only to the present environment and evolution cannot, therefore, be aiming for any goal. This view, Nagel tells us, is “almost certainly false.”

“Awaiting a New Darwin”
My comment: There’s no need to wait. The epigenetic effects of nutrient chemicals and pheromones are on immense gene networks. For example, the epigenetic effect of one nutrient causes the formation of a receptor that lets it enter the cell. When it enters the cell it alters the thermodynamics of intracellular signaling and intermolecular interactions between the mitochondrial tRNA and its nuclear-encoded tRNA synthetase. That allows the epigenetic landscape to become the physical landscape of the cell’s DNA. What happens next is that histone-driven chromatin remodeling and de novo protein biosynthesis occur. Nutrient-dependent de novo protein biosynthesis is required for stochastic gene expression and pheromone-controlled adaptive evolution.

Recent reports link the thermodynamics of antibiotic resistance in bacteria to sexually dimorphic traits that can be selected in a human population. The traits are associated with organism-level thermoregulation in the bacteria and in humans. That means I can again link nutrient-dependent pheromone-controlled adaptive evolution across species from microbes to man, sans mutations theory. This time, there is proof of the link from physics to biology (e.g., in the “RNA world” mentioned in Orr’s review).

Arguments can now proceed in the context of whether or not the 2nd law of thermodynamics has been invalidated by a single base pair change that results in substitution of one amino acid for another. This occurs within the closed system of the cell. It results in organism-level changes in thermoregulation.

Since I’m not a physicist, I cannot predict the outcome of those arguments, except from what I know about biology. Physicists may simply state that the cell is not a closed system because nutrients enter. They may say that’s why the reduction in entropy via de novo protein biosynthesis does not invalidate the 2nd law. Biologists may redefine mutations to make it appear as if they can cause adaptive evolution. I don’t think they can get away with that, since a recent report on G-protein coupled receptors distinguishes between natural variants and disease-causing mutations. Evolutionary theorists may continue to say anything they like.

Nevertheless, whatever the argument is from physics or from biology, it is not likely to result in support for a mutation-driven model of adaptive evolution because there is no model for that. There never has been. I doubt that there will be. Even the population geneticists have realized that what’s known about molecular epigenetics has forced them to think in terms of what’s being selected. And, as we’ve seen in the pigeon study results, it’s not the visual appeal of the head crest or other associated physical features — except in theory. The truth hasn’t changed, however.  Natural selection occurs for nutrients and social selection is enabled by the metabolism of nutrients to species-specific pheromones. Sexual selection is a subset of social selection in many organisms.

Jay R. Feierman: “Random gene mutation is the variance generator upon which natural selection operates.”

My question: How does natural selection “select” for a random gene mutation?

The obvious answer: It doesn’t. It can’t. Natural selection “selects” at the molecular level for thermodynamic interactions that result in adaptive evolution via thermoregulation.

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James Kohl
Retired medical laboratory scientist

James Kohl




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