Excerpt: Despite the high heritability of depression and a clear genetic contribution to the disease, the identification of genetic risk factors for depression has been very difficult. The first published candidate to reach genome-wide significance in depression was SLC6A15, a neuronal amino acid transporter. With a reported 1,42 fold increased risk of suffering from depression associated with a single nucleotide polymorphism (SNP) in a regulatory region of SLC6A15, the polymorphism was also found to affect hippocampal morphology, integrity, and hippocampus-dependent memory.
My comment: We again see how the misplaced focus on genes has skewed the entirety of what might otherwise have been rapid progress towards linking RNA-mediated amino acid substitutions and RNA-mediated gene duplication from nutritional epigenetics to pharmacogenomics in the context of chromosomal rearrangements, cell type differentiation, pathology, and healthy longevity — without the pseudoscientific nonsense about mutations and neo-Darwinian theories.
For comparison, in my 2013 review, I reported that one SNP, which was linked to a single amino acid substitution, differentiated cell types in similar tissuesof mice and humans. Also, Dobzhansky (1973) linked a single amino acid substitution to cell type differentiation in chimps, humans, and gorillas. For contrast to everything known by serious scientists about ecology, olfaction, and RNA-mediated cell type differentiation, see:
Trichromatic vision allows humans and many other primates to perceive perhaps 10 million colours; its evolution probably keyed into the eating of fruit by our distant primate ancestors, allowing it to be distinguished against a forested backdrop of leaves.
Another recent study led by Kara Hoover of the University of Alaska Fairbanks compared the ability of humans from a range of populations across the globe to detect an odour called OR7D4.
This odd gene mutation allows us to detect a smell called androstenone that’s produced by pigs and wild boar, so may have played a role in diet among our ancestors.
For contrast, nutrient-dependent RNA-mediated events link microRNAs to DNA repair via the de novo creation of odor receptor genes, like OR7D4. However, when the genes are no longer required, they accumulate viral microRNAs that cause loss of function via the perturbed protein folding that is attributed to mutaitons. The mutations that limit our conscious perception of androstenone odor have been placed by neo-Darwinian theorists into the context of evolution of our ability to consciously detect an aversive odor. Simply put, they have turned the world of knowledge about olfaction upside down and reported top-down causation as if it was a bottom-up effect of a mutation.
For comparison, a consciously perceived aversive food odor would not typically be linked to evolution of our ability to detect it– even by a theorist. If conscious perception was required to respond to odors, consciousness could not have evolved. But that simply attests to the fact that consciousness didn’t evolve. So, what just happened to their ridiculous theory about the importance of evolution to human olfaction?
The unconscious affects of odors on behavior and the conscious perception of odors require fixation of nutrient-dependent RNA-mediated amino acid substitution in organized genomes. That suggests neo-Darwinian theorists understand nothing about the nutrient-dependent pheromone-controlled RNA-mediated metabolic networks and genetic networks of all genera that link the physiology of reproduction in all species .
The biophysically constrained nutrient-dependent chemistry of RNA-mediated protein folding links the fixation of amino acid substitutions to all cell type differentiation in all cells of all individuals of all genera via their physiology of reproduction and the conserved molecular mechanisms of molecular epigenetics detailed in this 1996 Hormones and Behavior review article.
Obviously, it is past time to move forward and examine Evolution beyond neo-Darwinism: a new conceptual framework.
But first, ask yourself this: “Why is Denis Noble still using the term “evolution” in an article about how ecological variation is linked to ecological adaptations in the context of an atoms to ecosystems model of biologically-based cause and effect?” Is it because, like others, he must use the term most associated with neo-Darwinism, even when use of the term has been consistently associated with ridiculous misrepresentations of how species ecologically adapt? See for example:
Description of the video:
Animation of the evolution in birds of the olfactory bulb, the part of the brain where smell information is processed, passing from a dinosaur (Bambiraptor) through early birds (Lithornis, Presbyornis) to a modern-day bird (pigeon).
Human pheromones, a controversial subject, seem to be a natural phenomenon, with a small number identified in clinical studies.
My comment: The sense of smell in birds was once a controversial subject, largely because it was ignored along with experimental evidence of biologically-based cause and effect that linked olfaction and pheromones to biodiversity in insects and in humans. The bird-watching Nobel Laureates of the past have been replaced by Nobel Laureates who understand the role of conserved molecular mechanisms.