The long-range consequences of food energy-dependent social factors predictably link everything known about social odors called pheromones from the quantized energy in food to metabolism and biophysically constrained viral latency.  Sympatric speciation exemplifies what is known about how quantized energy links the pheromone-controlled physiology of reproduction to biophysically constrained viral latency in species from microbes to humans. In this review of biophysically constrained viral latency and biodiversity, I linked energy-dependent changes from angstroms to ecosystems in the mouse-to-human model of microRNA-mediated amino acid substitutions.

Nutrient-dependent Pheromone-Controlled Ecological Adaptations: From Angstroms to Ecosystems (2018)

For a historical perspective on pheromone-controlled pathology, which must be linked to ecological adaptations, see: The role of social factors in the regulation of stability of the cell genetic machinery in animals (2010)

The authors conclude that the evolutionary conservation of chemocommunicational mechanisms links the importance of studying olfaction to “…unpredictable long-range consequences.”

See also: Effect of two pyrazine-containing chemosignals on cells of bone marrow and testes in male house mice (Mus musculus L.) (2012)

The evolutionarily conservative 2,5-dimethylpyrazine chemosignal, a pheromone released by female mice, has been shown to increase frequency of mitotic disturbances in bone marrow cells assessed by using metaphase and ana-telophase analyses. The substitution of methyl radical in the molecule of pheromone by carboxyl reveals specificity of the effect of the latter derivative: the frequency of disturbances revealed by the ana-telophase analysis alone increases, whereas no induction of disturbance is detected by the metaphase analysis. An increase of the anomalies induced by both compounds has been shown in a sperm head test. Possible mechanisms underlying specific action of the tested substances on stability of the genetic apparatus of bone marrow dividing cells in the house mouse are discussed.

Daev, E. V. et al., (2012) cited my award-winning review and concurrently published book chapter Kohl, J.V., (2007) The Mind’s Eyes: Human pheromones, neuroscience, and male sexual preferences, J. Psychol. Human Sexual., vol. 18, pp. 313–369. Author’s copy here:

See also: Chemosignals from isolated females have antimutagenic effect in dividing the cells of bone marrow from male mice of the CBA strain (2014)

Humans also have various pheromone-induced physiological effects, especially those associated with reproduction [46, 47]. This suggests that the human olfactory system is still an effective pathway for influencing environmental factors on the human nervous system.

Daev, E. V. et al., (2014) cited [46] our award-winning review:  Kohl, J.V. et al., 2001 Human pheromones: integrating neuroendocrinology and ethology, Neuroendocrinol. Lett., 2001, vol. 22, pp. 309–321.

Daev may sometimes have failed to cite any of my additional published works if he is an evolutionary theorist. In 2012, I published Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors.

In 2013, I published a refutation of neo-Darwinian evolutionary theory. Nutrient-dependent/pheromone-controlled adaptive evolution: a model

In mammals, food odors and pheromones cause changes in hormones such as LH, which has developmental affects on pheromone-controlled sexual behavior in nutrient-dependent reproductively fit individuals across species of vertebrates.

For an attempt to discuss new research and the ridiculous claim that: New research reveals our brains are fixated on our social lives, see the Neuroscience FB group

In the past, after Pat Sweeney has thoroughly embarrassed himself, he has removed the OP from the group. I do not think there is any point to continuing my attempts to discuss his OP until he admits to being the first author of this publication, or when he denies it.

Protein misfolding in neurodegenerative diseases: implications and strategies (2017)

There is active research ongoing to uncover the mechanisms by which disease-associated proteins misfold, aggregate, and cause cellular toxicity. Continued progress in our ability to interrogate amyloid-forming proteins and their interactions with other cellular proteins provide confidence that novel therapies will be identified for multiple disease states. Therapeutic options now being explored include targeting misfolded protein-chaperone interactions at various points in the proteostatic pathway, promoting protein clearance, and large-scale rebalancing of proteostatic network. However, the identification and in vivo validation of new therapeutic compounds is impeded by the shortage of known disease drivers and the lack of reliable biomarkers for monitoring therapeutic responses in relevant animal models.

Quantized energy-dependent changes in the microRNA/messenger RNA balance have been clearly linked to healthy longevity or from the virus-driven degradation of messenger RNA to all pathology in species from microbes to humans.

See for comparison these recently published works from Eugene Daev or in the context of his collaborations with others

Genome-wide 5-hydroxymethylcytosine patterns in human spermatogenesis are associated with semen quality (2017)

We performed immunofluorescent analysis of DNA hydroxymethylation and methylation in human testicular spermatogenic cells from azoospermic patients and ejaculated spermatozoa from sperm donors and patients from infertile couples. In contrast to methylation which was present throughout spermatogenesis, hydroxymethylation was either high or almost undetectable in both spermatogenic cells and ejaculated spermatozoa. On testicular cytogenetic preparations, 5-hydroxymethylcytosine was undetectable in mitotic and meiotic chromosomes, and was present exclusively in interphase spermatogonia Ad and in a minor spermatid population. The proportions of hydroxymethylated and non-hydroxymethylated diploid and haploid nuclei were similar among samples, suggesting that the observed alterations of 5-hydroxymethylcytosine patterns in differentiating spermatogenic cells are programmed. In ejaculates, a few spermatozoa had high 5-hydroxymethylcytosine level, while in the other ones hydroxymethylation was almost undetectable. The percentage of highly hydroxymethylated (5-hydroxymethylcytosine-positive) spermatozoa varied strongly among individuals. In patients from infertile couples, it was higher than in sperm donors (P<0.0001) and varied in a wider range: 0.12-21.24% versus 0.02-0.46%. The percentage of highly hydroxymethylated spermatozoa correlated strongly negatively with the indicators of good semen quality – normal morphology (r=-0.567, P<0.0001) and normal head morphology (r=-0.609, P<0.0001) – and strongly positively with the indicator of poor semen quality: sperm DNA fragmentation (r=0.46, P=0.001). Thus, the immunocytochemically detected increase of 5hmC in individual spermatozoa is associated with infertility in a couple and with deterioration of sperm parameters. We hypothesize that this increase is not programmed, but represents an induced abnormality and, therefore, it can be potentially used as a novel indicator of semen quality.

Genome and stress-reaction in animals and humans (2018 in Russian)

Current data on the effects of stress at the level of the cell genomes of the central nervous system and peripheral organs in animals are discussed. Regulatory and structural genomic changes in the cells of the central nervous system under stress are considered as a mechanism for regulating the functions of the brain and peripheral organs that form the organism manifestations of stress. Based on the Yu.Ya. Kerkis and M.E. Lobashev point of view, we consider stress as a special physiological state of the nervous system, affecting the work and integrity of the genome in target cells in animals, and thus playing a major role in microevolutionary transformations.

The authors cite four works published by my mentor,  Bruce S. McEwen.

See:

McEwen BS, Bowles NP, Gray JD, et al. Mechanisms of stress in the brain. Nat Neurosci. 2015;18(10):1353-1363. doi: 10.1038/nn.4086.
McEwen BS, Nasca C, Gray JD. Stress Effects on Neuronal Structure: Hippocampus, Amygdala, and Prefrontal Cortex. Neuropsychopharmacology. 2016;41(1):3-23. doi: 10.1038/npp.2015.171.
Hunter RG, Gagnidze K, McEwen BS, Pfaff DW. Stress and the dynamic genome: Steroids, epigenetics, and the transposome. Proc Natl Acad Sci USA. 2015;112(22):6828-6833. doi: 10.1073/pnas.1411260111.
McEwen BS, Gianaros PJ. Stress- and allostasis-induced brain plasticity. Annu Rev Med. 2011;62:431-45. doi: 10.1146/annurev-med-052209-100430.

In the early 1990s, BS McEwen told me to start with gene activation in GnRH neurosecretory neurons or my model could not be validated. It has since been validated at every level of examination.

For comparison, see John Greally’s lament: My review, pictured. The journal, today: “Dear Professor John Greally, Thank you once again for reviewing the above-referenced paper. With your help the following final decision has now been reached: Accept” This. Is. Why. I. Think. I’m. Wasting. My. Time. Doing. Reviews.

See also: The flimsy evidence that environmentally-induced “epigenetic” changes in DNA are transmitted between generations of humans (2018)

Claims about “flimsy evidence” can be placed into the context of the evidence that links quantum physics to classical physics and biophysically constrained energy-dependent biodiversity via the physiology of reproduction in all living genera.

See: Photosynthetic Energy Transfer at the Quantum/Classical Border

For comparison, Jerry Coyne cited this blog post by Kevin Mitchell: Grandma’s trauma – a critical appraisal of the evidence for transgenerational epigenetic inheritance in humans

See also by Kevin Mitchell: What are the Laws of Biology?

He cites: What is Life?: With Mind and Matter and Autobiographical Sketches (Canto Classics) Reprint Edition but fails to link this claim about sunlight to biophysically constrained viral latency and all biodiversity via the physiology of pheromone-controlled reproduction.

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.)

The supply of “negative entropy” clearly links Photosynthetic Energy Transfer at the Quantum/Classical Border from viral latency to all biodiversity in the context of game play for ages 10+. See: Cytosis.

Watch for the release of Subatomic and news about conference presentations at Schrödinger at 75 – The Future of Biology – September 2018

Kevin Mitchell, Jerry Coyne and others like them are about to come face-to-face with Kohl’s Laws of Biology from Nutrient-dependent Pheromone-Controlled Ecological Adaptations: From Angstroms to Ecosystems (2018).

Kohl’s Laws of Biology

Life is nutrient-dependent. That is a Biological Law. The ecological origin of all biological laws is apparent 1) in the context of systems biology [87]; 2) in the context of the metabolism of nutrients by microbes [153]; and 3) in the context of how the metabolism of nutrients results in species-specific pheromones that control the physiology of reproduction [154]. Taken together, the systems biology of nutrient metabolism to species-specific pheromones, which control the physiology of reproduction, can be expressed in a summary of Kohl’s Laws of Biology: 1) Life is nutrient-dependent. See for review [27,155]. The physiology of reproduction is pheromone-controlled. See for review [26]. In the context of nutrient-dependent epigenetically-effected human reproduction, it is clearer that the epigenetic effects of human pheromones integrate neuroendocrinology and behavior [100], which includes the neuroendocrinology of mammalian behavior associated with the development of sexual preferences [156].

Kohl’s Laws help to explain what was missing from Darwin’s ‘conditions of life.’ Darwin knew nothing about genetics, which means he knew nothing about the epigenetic effects of food odors or pheromones.

See also: Biological and Social Aspects of Human Sexual Orientation: Chemocommunicative Hypothesis (2016/2018)

Failure to understand the role of biological and social factors in the formation of some socially important traits in humans could result in unjustified tension in interpersonal relationships. It is caused by a distorted perception of frequently unreliable information, its ambiguity due to the uncertainty of the terminology used and, as a consequence, the impossibility of its correct analysis. Using the term sexual orientation demonstrated the way how genetic understanding of the trait’s formation and data on the control mechanisms of sex formation may clarify and complement our knowledge on the subject. The hypothesis of the chemocommunicative model in the formation of sexual orientation in humans is discussed.

There is no hypothesis of the chemocommunicative model in the formation of sexual orientation in humans. There is only my model and Eugene Daev knows it. In 2012, see above, he cited:  The Mind’s Eyes: Human pheromones, neuroscience, and male sexual preferences (2007) without the subtitle: Human pheromones, neuroscience, and male sexual preferences. 

In 2018, he cited it again: 29. Kohl, J.V., The mind’s eyes: Human pheromones, neuroscience, and male sexual preferences, J. Psychol. Human Sex., 2006, vol. 18, no. 4, pp. 313–369. doi 10.1300/J056v18n04_03

The link from stress to all pathology has been thoroughly detailed. It would be odd if stress did not effect the hormones that affect human behavior and sexual orientation.

See: From Fertilization to Adult Sexual Behavior

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 (Runge and Zakian, 1996; Wu and Haber, 1995).

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