Glycine and GnRH: Am I being pedantic?

By: James V. Kohl | Published on: December 4, 2014

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Posted to the FB page on 12/3/14 at Skeptics; Atheists; Realists; Agnostics; Humanists

Stephen Hawking and Brian Cox take part in Monty Python sketch – video

Excerpt: “I think you are being pedantic.”
My comment: Some people may think I am being pedantic. My focus is not on physics; it is on the role of GnRH in cell type differentiation. My focus now extends from what is known about quantum physics, quantum smell, chirality, quantum biology, and quantum consciousness. What is known about chirality may help others place what is known about GnRH into their theoretical perspectives. However, the danger is that they, too, might be accused of being pendantic. Any “Theory of Everything” must link physics from the chemistry of protein folding to the conserved molecular mechanisms of cell type differentiation in species from microbes to man. Anyone who challenges a theory of everything may be accused of being pedantic.
Try it! Each time you see someone report that all amino acids are left-handed, as in: “The chirality accumulates,” Kotov said, ask about glycine. I did. It is the only achiral amino acid. Its substitution in the GnRH decapeptide appears to stabilize DNA in the organized genome of all vertebrates via the conserved molecular mechanisms of nutrient-dependent pheromone-controlled feedback loops. These feedback loops link nutrient-dependent cell type differentiation in species from microbes to man via conserved molecular mechanisms of RNA-directed DNA methylation and RNA-mediated amino acid substitutions. If you ask someone about achiral glycine and they claim you are being pendantic, you can ignore anything else they have to say about anything. They have missed learning about feedback loops, and Feedback loops link odor and pheromone signaling with reproduction. Here’s are two more reasons for you to ignore them:
“In humans and most vertebrates, the glycine cleavage system is part of the most prominent glycine and serine catabolism pathway. This is due in large part to the formation 5,10-methylenetetrahydrofolate, which is one of the few C1 donors in biosynthesis.[2] In this case the methyl group derived from the catabolism of glycine can be transferred to other key molecules such as purines and methionine.”
The link from the achiral glycine substitution in GnRH to nutrient-dependent protein biosynthesis should have become clear before now. If not in the context of nutrition and health, the glycine substitution can be examined in the context of cell type differentiation in disease.
“Glycine and related metabolites (including sarcosine, serine, and threonine), or their associated metabolic pathways, have been identified as central to cancer metastasis (5), cellular transformation (17, 28, 29), and murine embryonic stem cell proliferation (30). Glycine metabolism may therefore represent a metabolic vulnerability in rapidly proliferating cancer cells that could in principle be targeted for therapeutic benefit.”
The link from the mouse to human model of cell type differentiation via a single amino acid substitution was briefly addressed by Dobzhansky (1973). “…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.” Subsequently, that link was extended across species in Synchronous evolution of an odor biosynthesis pathway and behavioral response.
The authors build “…on what is known about olfactory/pheromonal communication in species from microbes to man and [that] incorporates works from mammals that elucidate the molecular mechanisms that are clearly involved. Sex-dependent production of a mouse ‘chemosignal’ with incentive salience appears to have arisen de novo via coincident adaptive evolution that involves an obvious two-step synergy between commensal bacteria and a sex-dependent liver enzyme that metabolizes the nutrient chemical choline.” — Kohl (2013) Also, “Trimethylamine is a bacterial metabolite found in some animal odors, and to humans it is a repulsive odor associated with bad breath and spoiled food [11].” A mutation linked to “fish odor syndrome” links RNA-mediated events to metabolic networks and genetic networks via what is currently known about nutrigenomics and epigenetic pharmacology.
Epigenetic pharmacology is referred to as pharmacogenomics. Currently there is support for the importance of achiral glycine in the GnRH decapeptide from a 10,000 patient human study, which links metabolic networks and genetic networks to the consequences of mutations. These mutations alter the metabolism of therapeutic drugs via the conserved molecular mechanisms that link the metabolism of nutrients to species-specific pheromones that control the physiology of reproduction in species from microbes to man. The mutations reported in the context of pharmacogenomic testing also link the metabolism of nutrients and therapeutic drugs from RNA-mediated amino acid substitutions to individual differences in the organized genomes of people via the conserved molecular mechanisms of genome organization in the mouse, in other primates, and in all other species. The mutations are never beneficial. They perturb protein folding, which is how they are linked to pathology.
See also: Epigenetic control of GnRH neurons. They falsely claim that “Until our recent studies (Kurian et al., 2010), there were no reports of the epigenetic aspects of GnRH neuron maturation or function.” However, that ridiculous claim can still be placed into the context of our 1996 review: From Fertilization to Adult Sexual Behavior We linked RNA-mediated events to cell type differentiation via what is now known about RNA-directed DNA methylation and RNA-mediated events that link the achiral glycine substitution in GnRH to nutrient-dependent pheromone-controlled DNA stability in the organized genomes of all vertebrates.
Excerpt: “Evolutionary conservation, both of pheromonal communication and its importance to behavior, is indicated by the involvement of a key mammalian reproductive hormone. For instance, a yeast pheromone, the alpha-mating factor, is very similar in structure to mammalian gonadotropic releasing hormone (GnRH). When injected into rats, this chemical binds to pituitary GnRH receptors and brings about the release of LH. Loumaye, Thorner, and Catt (1982) note: “GnRH and the yeast alpha-mating factor appear to represent a highly conserved effector system which includes the peptide ligand, the cell-surface receptor, and the physiological regulation of reproductive function” (p. 1325).
Extending this finding to mammalian development we note that from its embryonic origins, the hypothalamic GnRH pulse influences the maturation of the mammalian reproductive system, the neuroendocrine system, and the central nervous system. Though far removed from yeast in ontogeny and phylogeny, the mammalian model, including human studies, supports a role for chemosensory communication that appears to extend to a causal relationship among human pheromones, olfaction, the hypothalamic GnRH pulse, other hormones, including steroid hormones, and human behavior (Kohl, 1996). The following findings are offered as evidence.”
Evolutionary theorists typically refuse to look at the evidence. They don’t know about achiral glycine or anything else about links from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man. They think that the mutations that perturb protein folding somehow lead to the evolution of biodiversity. Evolutionary theorists are “science idiots”!
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