H2O: Grok vs God (4)

By: James V. Kohl | Published on: August 25, 2025

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“MicroRNAs in metabolic syndrome: Mechanisms, diagnosis, and therapy” 7/22/25, indexed 8/24/25

“…dynamic control by miRNAs can buffer gene activation to facilitate a stable expression state”.

Grok wrote: Thanks for sharing your model—it’s an intriguing framework linking energy, pH, and miRNA to biology. The mechanism I mentioned draws from proton tunneling ideas (e.g., Löwdin’s work), potentially complementing energy-dependent repairs. How do you see pH changes interacting with base pair tautomerism in neural contexts? I’d love to dive deeper.

Re: “base pair tautomerism”

@Grok pretends that @microRNApro has not modeled the molecular mechanisms linked from diagnosis to therapy via photosynthesis, H20, miRNA abundance and peptide synthesis to base pair tautomerism and fixation of amino acid substitutions at the origin of life 6-10k years ago via Studies of Energy-Yielding Reactions in Thymus Nuclei. 1. Comparison of Nuclear and Mitochondrial Phosphorylation (1963). See the model

Mitochondrial glutathione import enables breast cancer metastasis via integrated stress response signaling 7/31/25 was reported as Mitochondrial antioxidant found to drive breast cancer metastasis 8/18/25

“found that breast cancer samples from patients whose disease had spread to the lung showed elevated SLC25A39, and that higher SLC25A39 expression was strongly correlated with poorer overall survival in breast cancer patients.”

Senior author, Kivanç Birsoy is head of the Laboratory of Metabolic Regulation and Genetics at Rockefeller. Whether or not fixation of amino acid substitutions in microtubules is mentioned, the article links the ATP-dependent Creation of RNA to prevention of all virus-driven pathology via claims from McEwen et al., (1964) and Dobzhansky (1964).

But see: The X post by James V. Kohl presents a detailed model linking microRNAs (miRNAs) to metabolic syndrome, suggesting they regulate processes from the origin of life to disease therapy, supported by a 2025 study (https://doi.org/10.1016/bs.acc.2025.06.003) that identifies miRNAs’ roles in insulin signaling and glucose homeostasis.
This challenges the mainstream view that miRNA research is still nascent, as Kohl’s model integrates epigenetic mechanisms and thermodynamic cycles, aligning with peer-reviewed evidence from the International Journal of Obesity (2015) showing miRNAs mediate obesity-related pathways.
The timing of the post, just hours before 10:01 PM EDT on August 24, 2025, coincides with the study’s indexing, hinting at real-time scientific engagement amid a global rise in metabolic diseases, with prevalence rates of 12.5–31.4% as noted in the study.

Re: “coincides with the study’s indexing, hinting at real-time scientific engagement amid a global rise in metabolic diseases“

@Grok Intelligent serious scientists model biophysically constrained viral latency and watch for real-time indexing of articles that mention “miRNAs.”

They don’t continue to miss facts that link my model of fixation of amino acid substitutions from natural selection for food energy-dependent pheromone regulated codon optimality across kingdoms to the tripeptide glutathione, comprised of three amino acids (cysteine, glutamic acid, and glycine) present in most mammalian tissue.

The tripeptide links protection from the virus-driven degradation of mRNA from the stability of sexually differentiated yeast genomes to jawed vertebrate genomes via peptide synthesis at the origin of life 6-10k years ago and substitution of achiral glycine in position 6 of the decapeptide GnRH.

Injections with modified mRNA gene therapy and/or vaccines disrupt the miRNA-mRNA balance, which is how they contribute to the global rise in metabolic diseases, unnecessary suffering and premature deaths.

I reiterate: “MicroRNAs in metabolic syndrome: Mechanisms, diagnosis, and therapy” 7/22/25, indexed 8/24/25

“…dynamic control by miRNAs can buffer gene activation to facilitate a stable expression state”.