The Miracles of Smell and Taste: Evolutionists Cannot Account for the Origin of the Sense of Smell
Excerpt:
Professor of Biology John T. Caprio of Louisiana State University states that initially, the sense of smell developed in order to identify amino acid-like chemical substances soluble in water. The ability to determine molecules floating in the air is an adaptation of that original mechanism.96 (p. 106)
How The Nose Knows: Research On Smell Boosted
Excerpt:
In an interesting side note, Caprio observed that a pheromone which excites sex in an elephant is the same one that excites sex in a moth.
Origins of magic: review of genetic and epigenetic effects
What is already known on this topic
Magical abilities may be heritable
Complete family lineages to study this topic have only recently become available
What this study adds
Some components of magical ability clearly have a genetic basis
This is not a simple single gene effect and may be related to “magical enhancer” elements
My comment: Is life about miracles or about magic?
See also: What is Life? (1944)
Excerpt:
Indeed, in the case of higher animals we know the kind of orderliness they feed upon well enough, viz. the extremely well-ordered state of matter in more or less complicated organic compounds, which serve them as foodstuffs. After utilizing it they return it in a very much degraded form -not entirely degraded, however, for plants can still make use of it. (These, of course, have their most power supply of ‘negative entropy’ the sunlight)
See also: What is Life?: The Intellectual Pertinence of Erwin Schrödinger with a forward by Roger Penrose
Excerpt:
How often do we still hear that quantum effects can have little relevance in the study of biology, or even that we eat food in order to gain energy?
My comment: Is life supported by “magical enhancer” elements, or by photosynthesis and nutrition in accord with Schrodinger, Penrose, and Darwin’s nutrient-dependent “conditions of life?” Darwin’s “conditions of life” also are controlled by the energy-dependent physiology of reproduction.
Will debate over the facts that link angstroms to ecosystems via energy-dependent changes in hydrogen-atom transfer in DNA base pairs in solution lead to resolve of any issues invented by pseudoscientists. See, for example: Watch the Great Debate on Connectomics (April 7, 2016 – video)
Excerpt:
On one side was Moritz Helmstaedter of the Max Planck Institute, arguing that understanding neuronal circuit structure is key to modeling the mind. On the other side was Anthony Movshon of NYU, arguing that functional models that carefully analyze behavior are the key.
See also: Toward Predicting Personalized Neural Responses (April 7, 2016)
Individual brains differ in shape, architecture, and connectomes, impacting how different parts of the brain communicate. A long-standing question in neurobiology is to what extent brain architecture and/or neural connections underlie behavioral differences observed among people.
What aspect of the biophysically constrained chemistry of RNA-mediated protein folding, which links the innate immune system to supercoiled DNA in all living genera, do pseudoscientists think is questionable?
At a time when all models are supported by experimental evidence of biologically-based cause and effect that links angstroms to ecosystems, who wonders if energy-dependent hydrogen-atom transfer in DNA base pairs in solution links the anti-entropic energy of the sun from the morphological and behavioral phenotypes of microbes to humans?
See also: What is life when it is not protected from virus driven entropy? (6 minute video)
See also: The science behind bodily secretions (April 5, 2016)
Excerpt: “…all four parts must be activated (turned on) for calcium to increase in a cell and start processes like fluid secretion.”
My comment: The four parts are nutrient-dependent and controlled by the physiology of reproduction, which links RNA-mediated events to transgenerational epigenetic inheritance of cell type differentiation via the biophysically constrained four parts in species from microbes to humans.
All four parts of the biophysically constrained receptor-mediated events involve the sensing and secreting of molecules that allow different cell types and organisms to achieve the versatile social behaviors, which are controlled by the metabolism of nutrients to species-specific pheromones in species from microbes to humans.
See also my comment on:Secreting and Sensing the Same Molecule Allows Cells to Achieve Versatile Social Behaviors
Re: “Evolution appears to favor efficient circuits and signaling elements that can accomplish many different tasks…”
That was inferred in our 1996 Hormones and Behavior review: From Fertilization to Adult Sexual Behavior. We started with the conserved molecular epigenetics of yeasts and extended nutrient-dependent genetic diversity from the metabolism of nutrients to the pheromone-controlled physiology of reproduction in species from microbes to man.
Four years later our yeast-to-mammalian model was extended by others to hormone-organized and hormone-activated invertebrate behavior, and 5 years after that to the life history transitions of the honeybee model organism.
Since then, “Signaling Crosstalk: Integrating Nutrient Availability and Sex” has linked yeasts to “Feedback loops link odor and pheromone signaling with reproduction” in other species and to “Nutrient-dependent/pheromone-controlled adaptive evolution: a model”
Placing all these published works into the context of evolution as Youk and Lim have done seems somewhat problematic for some evolutionary theorists. The conserved molecular mechanisms appear to represent adaptations to ecological variation via nutrient-dependent secretion of pheromones and the sensing of pheromones.
That links the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man.
The fact that ecological adaptations occur via a nutrient-dependent signaling pathway, which regulates a pheromone-controlled signalling pathway shows how unicellular and multicellular organisms produce a coordinated response to multiple stimuli with no consideration for mutations or for natural selection of anything except food.
That does not present a problem in the context of biologically-based food odor- and social odor-driven cause and effect, but it makes mutation-driven evolution appear to be not only biologically implausible but also to not be an ecologically valid approach to species diversity.
See also: Modern men lack Y chromosome genes from Neanderthals, researchers say
Excerpt:
…a woman’s immune system might attack a male fetus carrying Neanderthal H-Y genes. If women consistently miscarried male babies carrying Neanderthal Y chromosomes, that would explain its absence in modern humans. So far this is just a hypothesis, but the immune systems of modern women are known to sometimes react to male offspring when there’s genetic incompatibility.
My comment: The innate immune system links ecological variation to ecological adaptation in species from microbes to humans via RNA-mediated events that link amino acid substitutions to supercoiled DNA, which protects all organized genomes from virus-driven energy theft and entropy. Energy theft links mutations to all pathology.
See: Species of Drosophila (1972)
Excerpt 1)
A biological species concept is therefore necessary. Its beginning goes back to John Ray, who stated in 1686 that “one species never springs from the seed of another” [quoted in (1)].
Excerpt 2)
They [species] are separated by any one, or by a combination of several, reproductive isolating mechanisms, (1, 4-7). Hybrid inviability and sterility are among such mechanisms, but there are others (for example, ethological and ecological isolations) which may be just as effective in nature.
My comment: Nutrient-dependent pheromone-controlled cell type differentiation links supercoiled DNA and chromosomal rearrangements to protection against virus driven entropy in all vertebrates. That is why modern men lack Y chromosome genes from Neanderthals. The experience-dependent de novo creation of olfactory receptor genes links chemotaxis and phototaxis to other sensory input and to behavior via supercoiled DNA, which protects organized genomes from virus-driven entropy.
See also: Natural Selection on the Olfactory Receptor Gene Family in Humans and Chimpanzees (2003) — co-authored by Carlos D. Bustamante
Conclusion:
…humans may identify the selected changes and shed light on what olfactory stimuli have exercised selective pressures on the human OR gene repertoire.
My comment: Food odors and pheromones exercise selective pressure that enable the olfactory receptor gene repertoire, which links supercoiled DNA to protection against virus-driven entropy in the organized genomes of all living genera. As it always has been, supercoiled DNA is the link from metabolic networks to genetic networks that typically prevents hybridization. By preventing hybridization, food odors and pheromones establish the niche construction that is exemplified in every species.
See also: The Divergence of Neandertal and Modern Human Y Chromosomes (2016) — co-authored by Carlos D. Bustamante
My comment: Scientific progress has led all serious scientists to explanations that link angstroms to ecosystems in all living genera. Serious scientists have linked what is known about molecular diagnostics across all species. When will neo-Darwinian theorists admit that they have known how odors and pheromones link biophysically constrained RNA-mediated cell type differentiation to supercoiled DNA in all living genera?
Obviously, not all theorists are committed to telling “Just So” stories about mutations and human evolution. For example, see: Clustered mutations in hominid genome evolution are consistent with APOBEC3G enzymatic activity, which was reported as: Human evolution fast-tracked by mutations from anti-viral enzyme
Excerpt (with my emphasis):
…when examining the locations of the clustered mutations, the researchers found they were enriched in transcriptionally active and regulatory regions of the human genome. Over a third of mutations overlapping coding regions led to amino acid changes, and in several cases an entire mutation cluster overlapped, resulting in up to five amino acid substitutions in a single exon.
“Our results are at odds with assumptions of mutational models that are at the basis of most genetic analyses, including in medical genetics, evolutionary genetics, and population genetics,” co-corresponding author Keinan said.
My comment: Those assumptions were based on de Vries 1904 definition of mutation. [W]hat Haldane, Fisher, Sewell Wright, Hardy, Weinberg et al. did was invent…. Evolution was defined as “changes in gene frequencies in natural populations.” The accumulation of genetic mutations was touted to be enough to change one species to another…. Assumptions, made but not verified, were taught as fact.
The facts have since been repeatedly stated and often succinctly stated, as in: Feedback loops link odor and pheromone signaling with reproduction; and in Combating Evolution to Fight Disease and in MicroRNA-Based Single-Gene Circuits Buffer Protein Synthesis Rates against Perturbations.
In my invited review of nutritional epigenetics I placed the facts into the context of nutrient-dependent pheromone-controlled biophysically constrained cell type differentiation and changes in the microRNA/messenger RNA balance, which are linked from RNA-mediated amino acid substitutions to cell type differentiation in all living genera.
See: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems (April 11, 2014)
Abstract excerpt:
This atoms to ecosystems model of ecological adaptations links nutrient-dependent epigenetic effects on base pairs and amino acid substitutions to pheromone-controlled changes in the microRNA / messenger RNA balance and chromosomal rearrangements. The nutrient-dependent pheromone-controlled changes are required for the thermodynamic regulation of intracellular signaling, which enables biophysically constrained nutrient-dependent protein folding; experience-dependent receptor-mediated behaviors, and organism-level thermoregulation in ever-changing ecological niches and social niches. Nutrient-dependent pheromone-controlled ecological, social, neurogenic and socio-cognitive niche construction are manifested in increasing organismal complexity in species from microbes to man.
My comment: My invited review was promptly returned without review.
For comparison, see this award-winning invited review: The Mind’s Eyes: Human pheromones, neuroscience, and male sexual preferences
In his review of my award-winning review, David A. Puts wrote:
James Kohl authors the Handbook’s final chapter, “The mind’s eyes: Human pheromones, neuroscience, and male sexual preferences.” Kohl posits innate sex differences in preferences for sexually dimorphic pheromones. These sex pheromones act as unconditioned stimuli that become associated with visual and tactile stimuli through classical conditioning. Consequently, men with innate preferences for women’s odors come to prefer the appearance and feel of women, for example. Homosexuality results from incomplete sexual differentiation of the olfactory system.
Kohl marshals supporting evidence, though it is often subject to alternative interpretation. For example, Kohl suggests that exposure to sex pheromones is “the most likely explanation for the recent finding that saliva [testosterone] levels in men increase with exposure to a young woman, but do not increase with exposure to a young man” (p. 327). Is it not likely that the young woman’s appearance raised men’s testosterone levels?
Multiple studies by independent researchers leave little doubt that odor affects human mate choice, but Kohl probably grossly overstates its importance. Why postulate that humans evolved only obligate olfactory/pheromonal preferences? Isn’t there likely to be useful information about mates that is better obtained through vision and touch than through smell? If so, selection would probably favor more reliable developmental patterns for visual and tactile preferences than classical conditioning to olfactory ones. Moreover, there is a trend among anthropoid primates, including humans, for reduced olfaction and increased reliance on vision for locating food and mates. This is witnessed in our tiny olfactory bulbs, which are relatively many times smaller than in rats; and our apparent lack of a functional vomeronasal organ, which is used by many mammals to detect pheromones.
Ironically, a seemingly fatal blow follows from a condition that Kohl presents in support of his hypothesis. Prior to treatment, people with Kallmann Syndrome (KS) lack both a sense of smell and much of a libido. Superficially, these facts appear to support Kohl’s hypothesis that olfaction is primary in sexual interest. However, the relation between olfaction and libido here is not causal. In most fetuses, some cells in the olfactory placode develop into olfactory cells while others migrate to the hypothalamus to become cells that trigger sex hormone secretion by the gonads. A mutation in one of three known genes can disrupt the development of these cells, so that a person not only lacks a sense of smell but also has gonads that do not produce sex hormones. It is the low sex hormone levels, rather than a lack of olfaction, that leads to reduced libido in adults with KS: Testosterone treatment at least partially restores libido in men with KS, but there is no known treatment for their anosmia.
My comment: David A. Puts is one of the most personable and intelligent antagonists I have ever met, but he failed to realize that I was not detailing a hypothesis. The model I detailed has been supported by all experimental evidence of biologically-based cause and effect since the time I first presented it in 1992, and subsequently co-authored The Scent of Eros: Mysteries of Odor in Human Sexuality (1995/2002).
See also: On April 9, 2016 at 1145 AM, on the sexnet listserver, David A. Puts, PhD (Associate Professor, Department of Anthropology, Center for Brain, Behavior, and Cognition, Center for Human Evolution and Diversity, Penn State University, University Park, PA 16802, wrote:
“Modern humans may also have abducted Neandertal females, so that the flow of Neandertal genes into modern human populations was primarily through females. Hypergynous marriage along the lines that Ray describes is also a possibility, but my gut is that relations between “us” and “them” weren’t so civil.
A less sexy possibility that the authors mention is simply that the Neandertal Y was lost due to drift. (The effective population size of Y chromosomes is half that of autosomes, and drift is stronger in smaller populations.)
Gene flow primarily through females and loss of Neandertal Y’s through drift are not mutually exclusive, but drift seems more consistent with also losing Neandertal mtDNA.
And of course there could be selection against the Neandertal Y in human-Neandertal hybrids, as the authors suggest.”
My comment: None of his claims are supported by experimental evidence of biophysically constrained biodiversity in any species.
For comparison, see: Formation of novel PRDM9 allele by indel events as possible trigger for tarsier-anthropoid split
Abstract excerpt:
The first mutation event interrupts the reading frame and function while the second compensates both. The fixation of this peculiar allele variant in tarsiers led to hypothesize that de- and reactivation of the zinc finger domain drove the speciation in early haplorhine primates.
My comment: Only if you believe that mutations are fixed in organized genomes can you link virus-driven energy theft from pathology to neo-Darwinian pseudoscientific nonsense in which alleles are somehow formed outside the context of the nutrient-dependent physiology of reproduction. Only if you believe that mutations are fixed in organized genomes can you link weekend evolution of the bacterial flagellum from mutations the evolution of primates. But as all serious scientists know, those who link mutations to the evolution of microbes into primates never learned the difference between mutations and nutrient-dependent RNA-mediated amino acid substitutions that link de novo gene creation to biodiversity in the context of the innate immune system and supercoiled DNA.
