Kohl’s miRNA model vs the VA & Grok (5)

By: Jim Kohl | Published on: June 8, 2026

Grok
James V. Kohl (@microRNApro) posts a link to his blog connecting recent papers on cytochrome b6f function, ceRNA networks regulating tomato fruit softening, ncRNA-BDNF interplay in neurodegeneration, and redox/mitochondrial dysfunction in gestational diabetes to his miRNA model of ATP-dependent RNA creation at life’s origin.
The post, part 4 in a series titled “Kohl’s miRNA model vs the VA & Grok,” positions his framework as superior by tying miRNA-mediated processes across plants, human disease, and ecosystems to biophysical constraints.
Kohl, a proponent of nutrient-dependent pheromone-controlled adaptive evolution via miRNA and pH-dependent peptide synthesis, uses these citations to argue for his angstroms-to-ecosystems model over mainstream alternatives.

I am not arguing with anyone about the facts. See Kohl:

Re: “…recent papers on cytochrome b6f function, ceRNA networks regulating tomato fruit softening, ncRNA-BDNF interplay in neurodegeneration, and redox/mitochondrial dysfunction in gestational diabetes… [and Kohl’s] miRNA model of ATP-dependent RNA creation at life’s origin.]

@Grok They link Merian (1679) to everything known about biophysically constrained viral latency across kingdoms via Darwin’s (1859) “conditions of life.” blob:https://x.com/c64ebca8-94f4-4120-985b-0b8f81daff77

See: Nutrient-dependent/pheromone-controlled adaptive evolution: a model 6/14/13 and the AI overview of Nutrient-dependent Pheromone-Controlled Ecological Adaptations: From Angstroms to Ecosystems 4/18/18

AI overview

“Nutrient-dependent, pheromone-controlled ecological adaptations are a biological model of evolution emphasizing that ecological adaptation and biodiversity are not driven by random genetic mutations. Instead, the model—detailed in scientific literature by researcher James V. Kohl—argues that environmental factors govern evolutionary development from the molecular (angstrom) to the macroscopic (ecosystem) level. [1, 2, 3, 4, 5]

The model highlights several key biological mechanisms:

  • Nutritional Epigenetics: Nutrients consumed by an organism are metabolized and transformed into pheromones. These pheromones, along with dietary elements, influence the epigenetic landscape of the organism, directing gene expression without altering the underlying DNA sequence. [1, 2]
  • Pheromonal Control of Reproduction: Species-specific pheromones regulate reproductive physiology by controlling the hypothalamic secretion of hormones like Gonadotropin-Releasing Hormone (GnRH) and Luteinizing Hormone (LH). Pheromones guide mating behaviors, sexual orientation, and the thermodynamic regulation of intracellular signaling. [1, 2, 3]
  • From Atoms to Ecosystems: The model maps how energy-dependent amino acid substitutions and RNA-directed DNA methylation protect organized genomes from virus-driven entropy. This progression leads to niche construction, organismal complexity, and biodiversity. [1, 2, 3]

You can read more about the conceptual framework via the Hilaris Publisher Abstract or review the biological theory in the NCBI Article. [1, 2]

If you want, I can dive deeper into specific components of this framework:

  • Epigenetic regulation of genetic expression
  • RNA-mediated protein folding and genome protection
  • The role of olfactory input in mammalian mating [1, 2]”

Unlike Grok AI, Google AI appears to know the difference between a model and facts that eliminate moronic theories from any further consideration, whatsoever.

For more facts, see: 197,667 results from today’s search on PubMed for indexed articles that mention the term “miRNA.”

Got cancer, yet? This article, co-authored by CM Croce was indexed on 6/7/26. Avoidance of immune mediated tumor rejection by cancer cells 6/4/26.

“…we summarize the role of microRNAs, in particularly miR-155 in avoidance of immune mediated tumor rejection by malignant cells.”

See also the AI Overview of Kohl’s 2013 review:

Nutrient-dependent, pheromone-controlled adaptive evolution is an evolutionary model linking ecological factors directly to genetic and physical development. It argues that environmental factors—primarily nutrition and chemical signals (pheromones)—directly guide developmental and reproductive biology, rather than relying solely on random genetic mutations. 

The framework details how chemical ecology drives evolution through four primary pathways: 

1. Ecological Niche Construction

Metabolized nutrients are converted by organisms into species-specific pheromones. These chemical signals control reproductive physiology, determine social dynamics, and define the boundaries between species. 

2. Neurogenic & Neuroendocrine Control

Nutrients and pheromones alter brain pathways like the gonadotropin-releasing hormone (GnRH) system. This alters hormone pulsatility, guiding the maturation of the reproductive, neuroendocrine, and central nervous systems from the prenatal stage onward. 

3. Socio-Cognitive Niche Construction

Sensory input—such as food odors and social pheromones—reaches the “epigenetic landscape”. This means environmental and chemical stimuli physically alter DNA organization and gene expression, which in turn influences ingestive, social, and reproductive behaviors. 

4. Adaptive Advantage

This process enables populations to adapt to their environments and construct functional, social niches. Instead of evolution being driven by unguided, random mutations, it is directed by how organisms metabolize local nutrients and communicate within their environments. 

You can review the foundational framework in this PubMed Central study or the primary model paper.


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