Olfaction, ecology, and intelligence

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“I should think we might fairly gauge the future of biological science, centuries ahead by estimating the time it will take to reach a complete comprehensive understanding of odor. It may not seem a profound enough problem to dominate all the life sciences, but it contains, piece by piece, all the mysteries” (p. 732). — Lewis Thomas (1980)

See also: The Scent of Eros: Mysteries of Odor in Human Sexuality (1995/2002)

Olfaction and odor receptors an epigenetic link between what you can read about here or at RNA-mediated.com and at Searching for the Mind.com

See for example: Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors.

Excerpt: “Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans (Keller et al., 2007; Kohl, 2007; Villarreal, 2009; Vosshall, Wong, & Axel, 2000).”

Jon Lieff incorporates what is known about that evolutionary trail in his brief review of how ecological variation is linked to intelligence in the context of ecological adaptations.

“The act of smelling is remarkably like the act of thinking itself” (p. 732). — Lewis Thomas (1980)

See also:

Dr. Lieff’s 10 Most Intelligent Animals for Discover Channel

    Bee

Excerpt: “Bees have approximately one million neurons in 0.5 mm; humans have 100 billion neurons. And yet bees can learn, and understand abstract concepts, and make complex decisions.”

My comment: “The honeybee already serves as a model organism for studying human immunity, disease resistance, allergic reaction, circadian rhythms, antibiotic resistance, the development of the brain and behavior, mental health, longevity, diseases of the X chromosome, learning and memory, as well as conditioned responses to sensory stimuli (Kohl, 2012).” Excerpted from Nutrient-dependent/pheromone-controlled adaptive evolution: a model.

    Octopus

See also: Role of olfaction in Octopus vulgaris reproduction

Excerpt: “…olfactory organ could exert regulatory action on the OL via epigenetic effects of nutrients and pheromones on gene expression (Kohl, 2013; Elekonich and Robinson, 2000).

Kohl (2013) is: “Nutrient-dependent/pheromone-controlled adaptive evolution: a model.

Elekonich and Robinson (2000) is: “Organizational and activational effects of hormones on insect behavior.”

Excerpt: “The development of species-typical and sex-specific adult behaviors in vertebrate animals is influenced by gonadal steroid hormones, non-gonadal hormones, and non-hormonal factors working on the underlying neural circuitry (reviewed in Diamond et al., 1996; Kawata,1995; Schlinger, 1998).”

Diamond et al. (1996) is: “From Fertilization to Adult Sexual Behavior

Excerpt: “Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism…” (1996) See also: Alternative RNA Splicing in Evolution by Jon Lieff

Excerpt: “Alternative RNA splicing in evolution is one of the critical factors in the development of the complexity of human beings” (2012)

My comment: Ecological variation is linked directly to ecological adaptation by the sun’s anti-entropic biological energy and also by alternative splicing techniques of pre-mRNA (now called microRNAs). Ecological adaptations are consistently portrayed in the context of the evolution of biodiversity. No matter how many times ecological variation and ecological adaptations are linked from entropic elasticity via what is currently known about the biophysically constrained chemistry of protein folding and conserved molecular mechanisms of RNA-mediated cell type differentiation in species from microbes to man, we will see horrid misrepresentations like this:

“…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world. In this view of evolution there is no need of considering teleological elements” (p. 199).

The pseudoscientific nonsense about mutations and evolution has been taught to several generations of student who never asked themselves or their teachers if it made sense.

This makes sense: 1) Ecological variation is the raw material by which natural selection can drive evolutionary divergence [1–4].
This makes sense: 2) The differences in amino acid composition among different tissues can lead to large differences in trophic discrimination [38].

The RNA-mediated amino acid substitutions that differentiation the cell types of all cells in all tissues of all organs and all organ systems of mammals exemplify nutrient-dependent ecological adaptations. Serious scientists have become consistently more aware of that fact, at the same time pseudoscientists misrepresent the facts, like this:

“…the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla” (p. 127).

Jon Lieff is one of very few ecologically adapted humans whose search for the intelligent minds of others who are ecologically adapted may bring us closer to learning the difference between how ecological variation leads to ecological adaptations and how mutations lead to physiopathology. Mutations do not lead to the evolution of new species because the nutrient-dependent chemistry of protein folding is biophysically constrained by the physiology of reproduction, which enables fixation of the RNA-mediated amino acid substitutions that differentiate all cell types in all individuals of all species during their life history transitions.

Mitochondrial and plastid genome architecture: Reoccurring themes, but significant differences at the extremes

Excerpt: “Organelle genomes are truly a playground for genomic diversity, but we have yet to see if there is a unifying explanation for the bizarre array of changes to structure, function, and content that they have sustained.”

My comment: The most obvious unifying explanation links nutrient-dependent RNA-mediated DNA repair to the physiology of reproduction and fixation of the amino acid substitutions in ecologically adapted populations via the physiology of their reproduction. If not, “The honeybee…[would not be] a model organism for studying human immunity, disease resistance, allergic reaction, circadian rhythms, antibiotic resistance, the development of the brain and behavior, mental health, longevity, diseases of the X chromosome, learning and memory, as well as conditioned responses to sensory stimuli (Kohl, 2012).” Excerpted from Nutrient-dependent/pheromone-controlled adaptive evolution: a model.

See also: Spatial and temporal variation of body size among early Homo

Conclusion: “A better understanding of body size–even on strictly relative grounds–is crucial to obtain a more complete and coherent picture of the origin, adaptive strategies,and evolution of the genus Homo. We consider our contribution as a small part of this process.”

Reported as: Earliest humans had diverse range of body types, just as we do today

Excerpt: “Basically every textbook on human evolution gives the perspective that one lineage of humans evolved larger bodies before spreading beyond Africa. But the evidence for this story about our origins and the dispersal out of Africa just no longer really fits,” said Stock. “The first clues came from the site of Dmanisi in Georgia where fossils of really small-bodied people date to 1.77 million years ago. This has been known for several years, but we now know that consistently larger body size evolved in Eastern Africa after 1.7 million years ago, in the Koobi Fora region of Kenya.”

My comment: 1) “…no longer really fits…” 2) “has been known for several years” and 3) “…we now know…” are phrases that attest to what is not known about RNA-mediated cell type differentiation in species from microbes to man.

For example, see: Clinically Actionable Genotypes Among 10,000 Patients With Preemptive Pharmacogenomic Testing. What is known about nutrient-dependent pheromone-controlled RNA-mediated amino acid substitutions enables the extension of what is known about the clinically actionable genotypes to behavioral phenotypes that develop during life history transitions. See: Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults

Excerpt (with my emphasis): “Its function is known to be affected by a functional single nucleotide polymorphism (SNP) in COMT (G-to-A base-pair substitution) leading to a methionine (Met) valine (Val) substitution [an amino acid substitution] at codons 108/158 (COMT Val158Met). Carriers of the Met allele have been found to display a fourfold decrease in enzymatic activity compared to Val allele carriers going along with an increase of prefrontal DA activity (Lachman et al. 1996; Lotta et al. 1995).

If you did not know the “Met” allele included an amino acid substitution, you would probably never link it from nutrient-dependent metabolic networks and genetic networks to differences in behavior. See, for instance:Rs4680

In genetics, rs4680 (Val158Met) is a genetic variant. It is a single nucleotide polymorphism (SNP) in the COMT gene that codes catechol-O-Methyltransferase. The single nucleotide substitution between G–> A results in an amino acid change from valine to methionine at codon 158.

The A or Met allele is associated with lower enzymatic activity (due to thermoinstability), and with exploratory behaviour.

If you knew nothing about nutrient-dependent organism-level thermoregulation, you would not link the amino acid substitution to the stability of the organized human genome. If you knew nothing about how the sun’s anti-entropic energy linked light-induced amino acid substitutions in plants and animals to nutrient-dependent amino acid substitutions that differentiate the cell types of individuals of all genera, you would not link the nutrient-dependent physiology of reproduction to differences in their morphological phenotypes of plants and/or differences in the morphological and behavioral phenotypes of animals. You would be more likely to believe that the differences somehow “evolved.” You would probably fit into a category reserved for evolutionary theorists and theoretical physicists who are biologically uninformed supporters of the evolution industry and “big bang” cosmology industry.

You could never become a serious scientist who knows that links from what is known about nutritional epigenetics and pharmacogenomics predict the response to different therapeutic drugs used to treat undesirable behaviors that are linked to a single amino acid substitution in the organized genomes of humans. The responses to therapeutic drugs link enzymes to metabolic networks and genetic networks based on what is currently known about the biophysically constrained nutrient-dependent chemistry of RNA-mediated protein folding and what is known about the role of a single amino acid substitution in behavior. The different responses can be compared to what is known about evolution of differences in morphological and behavioral phenotypes. For example:

1) “…the re-evolved flagella enabled the bacteria to access food supplies at the farthest reaches of the Petri dish…

My comment: It “re-evolved” over-the-weekend.

2) “…a family of microbes has persisted essentially unchanged for the past 2.3 billion years—half the age of Earth.

3)  “[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.

My comment: Theorists need to invent another theory of evolution to replace neo-Darwinism. They will almost undoubtedly include other assumptions about how long it takes for something to evolve into something else. There is no doubt in the intelligent minds of serious scientists that theorists should have learned — long ago — the difference between a ridiculous theory and a fact.

See also: Force for ancient and recent life: viral and stem-loop RNA consortia promote life

Excerpt: “…ribosomes are composed of a complex set of covalently linked stem-loop RNAs that interact in complex ways to provide it with its core function, the catalytic synthesis of peptide bonds.72 Given that their individual stem loops appear to have various and distinct evolutionary histories, the ribosome seems to represent a consortium of stem loops that was built up over time.73 Thus, when it became a resident of DNA, the stem-loop RNA consortium created a stable habitat. But the massive creative power of a cooperative RNA consortium (QS-C) remains crucial for life. QS-C was made known to us only recently by virus evolution (e.g., HIV-1). Its role in the origin of life, the emergence of complexity and the creation of group identity should now receive our combined attention.”

See also: Nutrient-dependent/pheromone-controlled adaptive evolution: a model.

Excerpt: “…the model represented here is consistent with what is known about the epigenetic effects of ecologically important nutrients and pheromones on the adaptively evolved behavior of species from microbes to man. Minimally, this model can be compared to any other factual representations of epigenesis and epistasis for determination of the best scientific ‘fit’.”

My comment: Luis P. Villarreal’s “…massive creative power of a cooperative RNA consortium…” “virus evolution” and the “complexity and the creation of group identity” should have receive the combined attention of all serious scientists from the time it was linked to pheromonal communication in a new human sub-species by Greg Bear in his science fiction novels: “Darwin’s Radio” (1999) and “Darwin’s Children” (2003).

See: Greg Bear, “When Genes Go Walkabout”(video)

Excerpt: HERV seemed to be something weird, something wonderful and counter-intuitive–and they were somehow connected with HIV, a species-crossing retrovirus that had become one of the major health scourges on the planet. I couldn’t understand the lack of papers and other source material on HERV. Why weren’t they being investigated by every living biologist?

My comment: The answer to his question: “Why weren’t they being investigated by every living biologist?”

Most biologists were taught to believe in the theory of evolution.

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