Two keys to success from Elon Musk (at the end of the video): Pay attention to negative feedback (especially when it comes from friends), and study physics to learn how to reason from first principles (instead of by analogy).
Q. Why are theorists attempting to remove physics and reason from biophysics and to remove natural selection from mutation-initiated natural selection (in the context of mutation-driven evolution)?
A. There is no such thing as mutation-initiated natural selection.
That’s what you learn when you study physics and you begin to reason using the first principles of conserved molecular mechanisms in species from microbes to man.
Excerpts: From Fertilization to Adult Sexual Behavior (Diamond, Binstock et al. 1996)
1) “…epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans…”
2) “Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species…”
3) “That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.”
Excerpt from Un-junking junk DNA with my emphasis
“Eukaryotic cells use alternative pre-mRNA splicing to generate protein diversity in development and in response to the environment. By selectively including or excluding regions of pre-mRNAs, cells make on average ten versions of each of the more than 20,000 genes in the genome. RNA-binding proteins are the class of proteins most closely linked to these decisions, but very little is known about how they actually perform their roles in cells.”
My comment: RNA-binding proteins generate protein diversity via alternative splicings that stabilize species-wide differences in protein folding. The claim that very little is known about how selective inclusion or exclusion of regions of pre-RNAs results in RNA-binding proteins ignores what we wrote in 1996 about biological basis of evolved sex differences and species differences, and it ignores what has been discovered since then.
Sex differences and species differences are due to differences in protein folding. Ignoring those facts allows theorists to continue touting random mutations theory, as if mutation-driven evolution caused sex differences or species-specific differences that are clearly due to epigenetically effected changes in protein folding. In mutations theory, the differences that are clearly due to differences in RNA-binding proteins “just happen” to be manifested as important differences that contribute to differences in DNA. In a word, mutations have automagical effects on something that affects evolution.
In reality, sex differences do not just automagically happen. They are genetically predisposed and epigenetically effected by sensory input. The inferred claim that sex differences “just happen” eliminates epigenetic effects and natural selection from any further consideration in the context of mutation-driven evolution.
This is my explanation of the new theory of evolution without natural selection: Mutations cause something associated with sex differences in protein biosynthesis. The mutations are not naturally selected. Thus, the sex differences in protein biosynthesis are differences that just happen to be somehow associated with inclusion or exclusion of regions of pre-RNAs, RNA-binding proteins and protein diversity in species from microbes to man.
If, until now, you thought that mutation-initiated natural selection lacked explanatory power, you may not like the new version of mutation-driven evolution sans natural selection. Theorists never before told us what was selected, except via predation, and now mutation-driven evolution occurs without selection for anything.
1) In our 1996 review, we did not consider the possibility that others would fail to recognize that that protein biosynthesis does not “just happen.” What is known about biophysics tells us that protein biosynthesis is nutrient-dependent and thermodynamically controlled. Perhaps that fact is assumed when reports mention how little is known about how RNA-binding proteins contribute to differences in DNA, which must result in organism-level thermoregulation. However, given the importance of differences in protein folding to sex differences and species differences, assumptions about thermodynamics and organism-level thermoregulation should be clearly stated. The sex differences and species differences in protein folding should not simply be ignored.
Ignoring sex differences and species differences in protein folding means we must also ignore ignoring the fact that thermodynamically-controlled organism-level thermoregulation must result in epistasis. If not, individuals do not survive. That means species do not reproduce. Unless mutations can somehow be linked to thermodynamically-controlled organism-level thermoregulation, mutation-driven natural selection can be elimionated from any further consideration whatsoever in the context of differences in protein biosynthesis, which are required for differences in species.
2) Similarly, we did not consider the possibility that others would not recognize the fact that that metabolism of nutrients to species-specific pheromones controls the physiology of reproduction.
We did not consider the possibility that others would not recognize cause and effect in the context of alternative splicings. Looking back 17 years later, we must have expected that others would realize that the thermodynamics of organism-level thermoregulation is nutrient-dependent and pheromone-controlled when we inferred that fact in our comprehensive review. It now appears that the conserved molecular epigenetics that enable unicellular reproduction and multicellular sexual reproduction in species from microbes to man was buried in the content of our integrative review. We failed to make the facts perfectly clear. Alternatively, others have simply ignored the role of molecular epigenetics in the gonadotropin-releasing hormone modulated control of fertilization and adult sexual behavior in mammals, which is what we detailed.
Perhaps we should have predicted something about people who accepted the theory that random mutations are the substrates on which directional natural selection acts. For example, we might have correctly predicted that they would cling tightly to that theory and attempt to limit discussion of the basic principles of biology and levels of biological organization that are required to link sensory cause to effects on genes. Clearly, there are those who continue to ignore the biological facts that directly link the epigenetic ‘landscape’ to the physical landscape of DNA in the organized genomes of species from microbes to man via food odors and pheromones. At the same time, they seem to deny the obvious fact that the sensory environment must be linked to the conserved molecular mechanisms of all species that have adaptively evolved.
By default, those people are now denying that RNA-binding proteins change the molecular bonds that alter protein folding in RNA, which leads to changes in DNA-coded protein folding. If these nutrient-dependent changes in protein folding were not epigenetically controlled by the metabolism of nutrients to pheromones via the same signaling pathway, there would be no finely-tuned physical constraints on cellular metabolism. Every cell could potentially exhibit the properties of cancerous cells that successfully compete for nutrients in their uncontrolled environment.
Mutated cells would cause mutation-driven evolution. Mutation-driven evolution is still widely touted by science journalists and many university professors. Nutrient-dependent pheromone-controlled adaptive evolution has received little to no consideration whatsoever, despite its obvious explanatory power and the fact that it is the only model that is based on experimental evidence. For comparison, mutation-driven evolution is based in experimentally unsubstantiated theories.
See, for example, anything published during the past 50 years that incorporates biological facts. But also see (Cook and Saccheri 2013) and (Van Le, Isbell et al. 2013) or anything else that attempts to link mutations to natural selection via predation of moths by birds or predation of humans by snakes or via any other hypothesis that has not been supported with experimental evidence of cause and effect (Longo, Montévil et al. 2012). If you cannot see why theorists continue attempts to remove physics from the biophysics of protein synthesis required to link sensory cause and effect to adaptive evolution, you may never need to question any theory about anything. You can simply continue to accept what you are told by people you think know about such things.
James V. Kohl detailedl how quantized energy-dependent microRNA biogenesis links the pheromone-controlled physiology of reproduction to biophysically constrained viral latency and healthy longevity. Links from what organisms eat to the enzyme-dependent metabolism of food also link metabolic networks to microRNA-mediated genetic networks in the context of RNA interference. Drug therapies alter RNA interference by altering cell type differentiation in all cells of all individuals of all species. For comparison, during the past 26 years, Kohl has detailed how the chemistry of protein folding is biophysically constrained at every level of biological organization by conserved molecular mechanisms.