Kohl’s miRNA model vs the VA & Grok (1)

(click to enlarge)

Grok CCDS is NCBI’s collaborative project for consistent human/mouse protein-coding annotations, useful for genomics and PGx/NGS in reducing medication errors via better variant data. It doesn’t link to or support miRNA-mediated autophagy, pH effects, or a comprehensive model for virus-driven pathology and speciation. Your synthesis connects these elements, but it remains a personal framework without broad scientific consensus or clear testable predictions. What specific prediction of yours can CCDS data directly test or falsify?

Kohl
Re: “What falsifiable predictions does your nutrient-pheromone-epigenetic model make that diverge from…” [pseudoscientific nonsense touted by moronic theorists?

See: “Clonal lineage tracing of innate immune cells in human cancer” 6/4/26

It links God’s ATP-dependent Creation of RNA from biophysically constrained viral replication at the origin of life 6-10,000 years ago to data-driven medical malpractice. Reality is not data-driven. It is energy-dependent and miRNA-mediated.

See also: 197,639 results from today’s search of the PubMed database for indexed articles linked to experimental evidence from model organism via “miRNAs” for comparison to moronic theories.

Kohl
“Microarray-Based Identification of Time-Sensitive miRNAs as Serum Quality Indicators in Liquid Biopsy” 6/5/26 “miR-4429 and miR-6511b-5p showed a significant decrease in signals in the sample group with longer processing times.” The epic failure to link miRNA abundance at the origin of life to healthy longevity or virus-driven degradation of mRNA to all pathology and extinctions exemplifies human idiocy. @Grok champions the human idiocy.

My clear testable predictions links facts about fixation of EDAR V370A from companion papers published in “Cell” (2013) –cited in my 2013 model of biophysically constrained viral latency and healthy longevity across kingdoms, to 20 copies of p53 in cancer-free African elephants via “Nutrient-dependent/pheromone-controlled adaptive evolution: a model” and the 2018 update: Nutrient-dependent Pheromone-Controlled Ecological Adaptations: From Angstroms to Ecosystems:

“This angstroms to ecosystems model of ecological adaptation links nutrient energy-dependent epigenetic effects on base pairs and amino acid substitutions to pheromone-controlled changes in the miRNA/mRNA balance and chromosomal rearrangements via the physiology of reproduction in species from microbes to humans. 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 ecological, social, neurogenic and socio-cognitive niche construction are manifested in increasing organismal complexity. Species-specific pheromones link quorum-sensing in microbes from chemical ecology to the physiology of reproduction. The reciprocal relationships of species-typical nutrient-dependent morphological and behavioral diversity are enabled by pheromone-controlled reproduction. Ecological variations and biophysically constrained natural selection for codon optimality links nutritional epigenetics to the behaviors that enable ecological adaptations. All biodiversity is an ecologically validated proof-of-concept. Ideas from population genetics, which exclude ecological factors, are integrated with an experimental evidence-based approach that establishes what is currently known. Simply put, olfactory/pheromonal input links food odors and social odors from the epigenetic landscape to the physical landscape of supercoiled DNA in the organized genomes of species from microbes to man during their development.

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