Excerpt: “How can it be that so many influential, powerful, wealthy, in-the-public people can be so confidently wrong about evolutionary biology? How did that happen? Why does it happen? Why does it persist? It really is a bit of a puzzle if you think about how they’d be embarrassed not to know that the world is round.”
My comment: Why aren’t evolutionary theorists embarrassed by the biological facts that have come from the past few decade’s-worth of works by serious scientists? It’s difficult for me to see someone reference David Haig’s work and then take it out of the context of nutrient-dependent pheromone-controlled epigenetic imprinting and mosaic copy number variation in human neurons.
Therefore, while it’s great to see someone admit that they’ve been wrong about how theorists first conceptualized the brain, it’s past time to look at the experimental evidence that links the epigenetic landscape to the physical landscape of DNA in the organized genome of every organism on the planet. The experimental evidence attests to ecological variation and the biologically-based cause of adaptations, which explains why the theorists are wrong, and why “…so many influential, powerful, wealthy, in-the-public people can be so confidently…” RIGHT — and continue to ignore the ridiculous theorists until they provide experimental evidence of cause and effect in the model organisms that have been the basis of scientific progress.
See for example: Mosaic Copy Number Variation in Human Neurons with my comments, which were published on the Science Magazine site:
My comment: 1) Re: Aplysia. Why not nematodes?
“High-throughput imaging of neuronal activity in Caenorhabditis elegans”https://www.pnas.org/content/110/45/E4266.full
The article helps to elucidate the conserved molecular epigenetics of cause and effect in a model organism of ecological, social, and neurogenic niche construction sans mutations theory.
Altered transcription can be associated with minimal variability in epigenetic landscapes that results in neurons with different genomes and distinct molecular phenotypes.
Effects of olfactory/pheromonal input appear to directly link the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man. In nematodes, conserved molecular mechanisms now link pulsing food odors and observed responses to the pulsatile secretion of gonadotropin releasing hormone (GnRH) in vertebrates. GnRH pulses links the epigenetic effects of food odors and pheromones to human behavior via systems biology and the ability of pulses to integrate information and rapidly transmit it throughout neuronal networks.
We can better understand the development of subtle differences in human behavior that are genetically predisposed and epigenetically effected. This will help us distinguish between genetic predisposition (nature) and effects of the sensory environment (nurture)during behavioral development.
The advantage is that we can also avoid attributing differences to mutations-initiated natural selection or to mutation-driven evolution by using what is known about biologically based cause and effect.
My comment: 2) The neuronal copy number variation (CNV) can be traced to its origins in yeasts, when epigenetically-effected CNVs enable self vs non-self recognition at the advent of immune system function and sexual reproduction, albeit sans neurons.
Olfactory/pheromonal input is subsequently associated with alternative splicings that link the epigenetic ‘landscape” to the physical landscape of DNA in the organized genome of species from microbes to man via CNVs and other variants. During adaptive evolution the CNVs in neurons are directly linked from olfactory/pheromonal input via ecological, social, neurogenic, and socio-cognitive niche construction. For example, neuronal niche construction in nematodes proceeds across species via conserved molecular mechanisms required for the thermodynamics of seemingly futile nutrient-dependent cycles of protein synthesis and degradation to species-specific pheromones. Pheromones control the physiology of reproduction and help to control nutrient-dependent organism-level thermoregulation.
In a mammal, see for example: “Odorant receptor gene choice and axonal wiring in mice with deletion mutations in the odorant receptor gene SR1.” However, see also my ISHE Summer Institute poster session uploaded to figshare: Nutrient-dependent / Pheromone-controlled adaptive evolution: (a mammalian model of thermodynamics and organism-level thermoregulation). I included details that eliminate mutations from further consideration in adaptive evolution. To do that I used examples from nematodes, insects, other mammals, and a human population that arose in what is now central China during the past ~30,000 years.
Non-random experience-dependent adaptive evolution appears to occur due to a thermodynamically controlled single base pair change and nutrient-dependent amino acid substitution best exemplified in the mouse model via what is neuroscientifically known about nutrient-dependent pheromone-controlled reproduction, which establishes the role of neuronal CNVs.