miRNA-mediated pH-dependent life (2)

By: Jim Kohl | Published on: May 17, 2026

Grok
James V. Kohl (@microRNApro) replies to Grok by ridiculing the separation of evolutionary biology from Biblical Creation, claiming his 1996 model links light-activated pH-dependent miRNA abundance and ATP-dependent RNA creation at life’s origin to enzyme protection against virus-driven mRNA degradation.
The post cites biophysical constraints on pathology across kingdoms via energy-dependent molecular changes and references the Consensus CDS project as aligning with his framework tying subatomic particles through autophagy and peptide synthesis to sympatric speciation.
Kohl maintains websites like RNA-mediated.com and microRNApro.com to advance nutrient-dependent, pheromone-controlled ecological adaptations supported by miRNA research, contrasting it with mainstream evolutionary mechanisms lacking direct model organism evidence for deep-time claims.

Kohl

Re: “Kohl maintains websites like http://RNA-mediated.com and http://microRNApro.com to advance nutrient-dependent, pheromone-controlled ecological adaptations supported by miRNA research, contrasting it with mainstream evolutionary mechanisms lacking direct model organism evidence for deep-time claims.”

Kohl

@Grok It’s settled then. With no experimental evidence from model organisms, Grok’s support for moronic theories makes it another example of data-driven human idiocy. Support for facts from model organisms could be compared to an experiment that unplugged the power supply needed to run Grok’s algorithms.

Grok wrote: “miRNAs extensively regulate autophagy (e.g., by targeting mTOR, ATG genes, or Beclin-1), creating bidirectional crosstalk—autophagy can also influence miRNA levels.”

Kohl replied: @Grok promotes pseudoscientific nonsense with claims that mutations and evolution led to this bidirectional crosstalk. See for comparison, the Google AI overview of “From Fertilization to Adult Sexual Behavior” “a seminal paper and framework… explores how genetics, hormones, and the environment interact to shape human sexual development, identity, and behavior from the moment of conception to adulthood.”

Grok
The bidirectional miRNA-autophagy crosstalk is a real regulatory network documented across model organisms. Mainstream biology attributes its origins to genetic variation (including mutations) acted on by natural selection, with nutrient/environmental inputs modulating it. Your referenced framework adds valuable context on gene-environment interactions from conception onward. What specific experimental data from model organisms best supports alternative causation here?

Kohl
Re: Your referenced framework adds valuable context on gene-environment interactions from conception onward. What specific experimental data from model organisms best supports alternative causation here?

@Grok Ha Ha Ha

There is no experimental evidence from model organisms for alternative causation. See for comparison: 196,955 results from today’s PubMed search for indexed articles that mention the term “miRNA.”

Grok
The vast miRNA literature (your ~197k PubMed hits) robustly supports its role in autophagy crosstalk, nutrient sensing, and gene regulation in model organisms from yeast to mammals. It integrates with genetic variation acted on by selection, not replaces it.

Which specific experiments in model organisms show your framework’s alternative causation (miRNA/pH/autophagy as primary driver of sympatric speciation) outperforming that standard model?

Grok
All experimental evidence from model organisms (yeast, flies, nematodes, mice, E. coli) is explained by natural mutation, selection, and drift without invoking supernatural creation. Conserved miRNA biogenesis, genetic divergence rates, and fossil-calibrated molecular clocks consistently indicate common ancestry over hundreds of millions to billions of years, not 6-10k. pH-dependent biophysics is compatible with gradual evolutionary processes, not a recent origin.

Kohl
Re: “fossil-calibrated molecular clocks consistently indicate common ancestry over hundreds of millions to billions of years, not 6-10k”

@Grok Ha Ha Ha (ridicule, not humor)

For comparison to the fossil record of dead things, USAF exome sequencing, the VA’s Million Veteran Program and everything known about energy-dependent biophysically constrained protein folding chemistry was presciently linked by intelligent serious scientists to “Precision Medicine” via PGx, NGS, FISH testing and “Analysis of 6,515 exomes reveals the recent origin of most human protein-coding variants” 11/28/12.

Grok
The Fu et al. 2013 paper shows most segregating human protein-coding variants (SNVs) are recent (~5-10k years) due to post-Neolithic population explosion. This is exactly what population genetics predicts under evolution after bottlenecks—not evidence against deep common ancestry.

Fossil-calibrated clocks, shared ERVs, synteny, and miRNA conservation across species still support billions of years of gradual change via mutation, selection, and drift. pH-dependent biophysics fits that framework.

Kohl

Re: “Fossil-calibrated clocks, shared ERVs, synteny, and miRNA conservation across species still support billions of years of gradual change via mutation, selection, and drift.”

@Grok That claim exemplifies human idiocy.

See for comparison: “The lnc40545-miR-965-CYP307A1 regulation pathway mediates imidacloprid resistance in Rhopalosiphum padi (L.)” 5/15/26

It links the nutrient-dependent physiology of reproduction in insects and ecological adaptations to cancer-free African elephants with 20 copies of p53 via my group’s 1996 claims and “Insect pheromone in elephants” 2/22/96

Grok
James V. Kohl (@microRNApro) criticizes a Grok post defending evolutionary mechanisms by calling claims of billions of years of gradual change via mutation, selection, and drift “human idiocy.”
He cites a May 2026 paper on the lnc40545-miR-965-CYP307A1 pathway driving imidacloprid resistance in aphids as support for nutrient-dependent, miRNA-mediated physiological adaptations.
Kohl links the recent insect study to his 1996 “Insect pheromone in elephants” paper and p53 gene duplication in elephants, promoting his model of pH-dependent peptide synthesis and sympatric speciation.

Grok
The miRNA-CYP pathway in aphid insecticide resistance is a clear case of recent natural selection on regulatory variation—exactly as population genetics predicts. miRNA conservation across animals, including elephants’ duplicated p53 genes arising from duplication events, supports common ancestry and gradual evolutionary change over deep time, not against it. Nutrient-dependent physiology and biophysics operate within that framework.

Kohl
Re: “Nutrient-dependent physiology and biophysics operate within that framework.”
Rather than follow the lead of moronic theorists, LEL Rassmussen asked me what might be the best measure of healthy longevity in African elephants.
She returned to her work and presciently linked urine albumin measurements from PGx, NGS and FISH testing to prevention of all virus driven pathology across kingdoms. See: “Insect pheromone in elephants”
@Grok What have you learned about biophysically constrained healthy longevity from moronic theorists for comparison?


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