Pheromones and neuroscience vs definitions and social science

Psychiatry in Crisis! Mental Health Director Rejects Psychiatric “Bible” and Replaces With… Nothing By John Horgan | May 4, 2013

Article excerpt: “Insel said that the NIMH will be replacing the DSM with the “Research Domain Criteria (RDoC),” which define mental disorders based not just on vague symptomology but on more specific genetic, neural and cognitive data. But then, immediately after making this dramatic announcement, Insel added that “we cannot design a system based on biomarkers or cognitive performance because we lack the data.”

Hunh? So the NIMH is replacing the DSM definitions of mental disorders, which virtually everyone agrees are profoundly flawed, with definitions that even he admits don’t exist yet!”

My comment: Note the subtle switch from “…design a system based on biomarkers…” to “…definitions that…don’t exist yet! Attention is directed away from what is known about the epigenetic effects of sensory input on the adaptively evolved gene-cell-tissue-organ-organ system pathway of mammals, and attention is refocused on definitions (i.e., meaningless classifications that someday might somehow lead to meaningful assessments). Clearly, many psychologists and psychiatrists will go kicking and screaming as they are dragged into the realm of what is currently neuroscientifically known.

What’s known includes information on biomarkers (e.g., indicators of the microRNA / messenger RNA balance required for epistasis). However, the information must be taken in the context of a model, sans definitions and dichotomies that obfuscate neuroscientifically established facts.

For example, “This model of systems biology represents the conservation of bottom-up organization and top-down activation via:
1) Nutrient stress-induced and social stress-induced intracellular changes in the microRNA  (miRNA)  /  messenger RNA  (mRNA) balance;
2) Intermolecular changes in DNA (genes) and alternative splicing;
3) Non-random experience-dependent stochastic variations in de novo gene expression and biosynthesis of odor receptors;
4) The required gene-cell-tissue-organ-organ system pathway that links sensory input directly to gene activation in neurosecretory cells and to miRNA-facilitated learning and memory in the amygdala of the adaptively evolved mammalian brain;
5) The required reciprocity that links gene expression to behavior that alters gene expression (i.e., reciprocity from genes to behavior and back) in model organisms like the honeybee.

The model is an adaptation of The Mind’s Eyes: Human pheromones, neuroscience, and male sexual preferences, which also indirectly addresses embodied cognition in the context of differences between classical conditioning of hormone-organized and hormone-activated behaviors, and contingencies of reinforcement via non-olfactory/pheromonal input. Contingencies of reinforcement do not epigenetically effect the adaptive evolution of the brain and behavior.  Olfactory/pheromonal input does epigenetically effect the adaptive evolution of the brain and behavior, which is why classical conditioning precedes operant conditioning of behavior in species from microbes to man (i.e., unless you’re a behaviorist like Glen Sizemore who cannot grasp the difference between classical (Pavlovian) conditioning, and operant conditioning.

Author: James Kohl

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