You chose the wrong model of evolution

Choose your model …wisely
“Attempts to replicate recent molecular date estimates show that these estimates depend strongly on the choice of calibration points, on the dating method, and on the chosen model of evolution…” David Marjanović and Michel Laurin (2006)
David Marjanović (2013) “The base pair change you mention? That’s a mutation.”
David Marjanović makes it clear that his 2006 chosen model of evolution is mutation-initiated natural selection. His chosen model has never been experimentally validated.  Skull 5 validates the experimental evidence of my chosen model. My model has been experimentally validated with evidence found in species from microbes to man. In addition, nutrient-dependent pheromone-controlled adaptive evolution is consistent with the “multiregional theory” of humans as a single species suggested by the Skull 5 analyses. See for example:
1) Weidenreich pioneered the Polycentric (multiregional) or Weidenreich Theory, which proposed that that the human races have evolved independently in the Old World from Homo erectus to Homo sapiens sapiens, while at the same time there was gene flow between the various populations.
2) In 1962, Brace published a paper in American Anthropologist titled “Refocusing on the Neanderthal Problem” where he argued… that the archeological and fossil evidence did not necessarily support the idea that the Neanderthals were replaced by Cro-Magnon populations migrating into Europe, rather than being ancestral to early Homo sapiens.
3) According to Wolpoff, populations of Homo evolved together as a single species. Change in Pleistocene populations did not involve speciation (the splitting of one species into two): all this time, the geographically distinct populations maintained small amounts of gene flow. This idea directly challenges the Out of Africa model, which claims Homo sapiens evolved recently as a new species in Africa, and then dispersed throughout the Old World, replacing the existing human populations without mixing with them.
The fact that the historical record of thoughts about our single species evolution has not impressed upon David Marjanović that he chose the wrong model has left him in the untenable position of continuing to tout it after the right model has been detailed. I reiterate: he wrote “”The base pair change you mention? That’s a mutation.”
The evidence from Grossman et al., 2013 and Kamberov et al., 2013, which I cited in Nutrient-dependent/pheromone-controlled adaptive evolution: a model was added in the context of model organisms from species of nematodes, insects, and other mammals. However, these additions were merely extensions of what we reported in our 1996 Hormones and Behavior review in the context of molecular epigenetics
“Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes…. 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, Drosophila melanogaster and Caenorhabditis elegans…. That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.”
Although we did not state that epigenetically-effected alternative splicings were nutrient-dependent, we clearly indicated that sex differences were pheromone-controlled in species from microbes to man. “Parenthetically it is interesting to note even the yeast Saccharomyces cerevisiae has a gene-based equivalent of sexual orientation (i.e., a-factor and alpha-factor physiologies). These differences arise from different epigenetic modifications of an otherwise identical MAT locus
See also: Evolution by Splicing: “These are very important papers that provide for the first time a large-scale view of the evolution of alternative splicing in vertebrates,” said Brent Graveley, professor of genetics and developmental biology at the University of Connecticut, who was not involved in the research. “They demonstrate how dramatically rapidly alternative splicing evolves, and suggest that it might play a role in speciation.”
See also: The alpha-factor mating pheromone of Saccharomyces cerevisiae: a model for studying the interaction of peptide hormones and G protein-coupled receptors; and Signaling Crosstalk: Integrating Nutrient Availability and Sex
Elekonich and Robinson (2000) extended our 1996 model of hormone-organized and hormone-activated behavior to insects. Like the evidence from yeasts, the evidence from insects of nutrient-dependent pheromone-controlled reproduction is clear.
In Kohl (2013), I wrote: “Two additional recent reports link substitution of the amino acid alanine for the amino acid valine (Grossman et al., 2013) to nutrient-dependent pheromone-controlled adaptive evolution. The alanine substitution for valine does not appear to be under any selection pressure in mice. The cause-and-effect relationship was established in mice by comparing the effects of the alanine, which is under selection pressure in humans, via its substitution for valine in mice (Kamberov et al., 2013).
These two reports (Grossman et al., 2013; Kamberov et al., 2013) tell a new short story of adaptive evolution. The story begins with what was probably a nutrient-dependent variant allele that arose in central China approximately 30,000 years ago. The effect of the allele is adaptive and it is manifested in the context of an effect on sweat, skin, hair, and teeth. In other mammals, like the mouse, the effect on sweat, skin, hair, and teeth is due to an epigenetic effect of nutrients on hormones responsible for the tweaking of immense gene networks that metabolize nutrients to pheromones. The pheromones control the nutrient-dependent hormone-dependent organization and activation of reproductive sexual behavior in mammals such as mice and humans, but also in invertebrates as previously indicated. That means the adaptive evolution of the human population, which is detailed in these two reports, is also likely to be nutrient-dependent and pheromone-controlled, since there is no other model for that.”
David Marjanović made it clear that his chosen model of evolution is mutation-initiated natural selection. However, evolution is a biological process, and apparently, Marjanović  chose a mathematical model of a biological process. Perhaps people should choose their models after first determining whether they can be supported with biologically-based experimental evidence, since evolution is clearly biological but no experimental evidence suggests the biological basis of nutrient-dependent pheromone-controlled adaptive evolution can be mathematically modeled.
Is anyone willing to attempts replication of recent molecular date estimates that depend strongly on the choice of calibration points and on the dating method? It might be interesting to determine how accurately dated a model of nutrient-dependent pheromone-controlled adaptive evolution can be, compared to any other model that includes biological facts.

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