Behavioral Immune System model

By: James V. Kohl | Published on: November 21, 2015

Was the dawn of man among trees in the cradle of disease?

Reported on July 4, 2013

Excerpt (with my emphasis):

The impact of a forest home on the social structure of the first homo sapiens will be examined by the Division’s Dr Peter Walsh, who researches social networks in primate ecology. A major theme of the conference will be what’s known as Behavioural Immune System hypothesis – the idea that social behavior is an intrinsic part of the immune system, and infectious disease transmission can dictate social contact, especially in the heart of Africa.

The “Behavioural Immune System hypothesis” is not merely an idea. The facts about the “Behavioural Immune System” link microbes to humans in the context of an atoms to ecosystems model of biologically-based cause and effect.
The history of RNA-mediated gene duplication and RNA-mediated amino acid substitutions that differentiate all cell types in all individuals of all living genera can now be seen in the light of what has been known for several decades to serious scientists.
For accurate representations of the links from atoms to ecosystems, see: Biologists discover bacteria communicate like neurons in the brain
My comment: Another report linked communication in bacteria to brain health: Is nutrition the future of brain health? See the comments on these two reports for examples of what happens when I tried to tell neo-Darwinists that their ridiculous theories have been refuted by everything known to all serious scientists. Serious scientists have linked atoms to ecosystems across all species from microbes to humans via RNA-mediated amino acid substitutions in the context of the nutrient-dependent pheromone-controlled physiology of reproduction. There attention is now returning to the role that viruses play in pathology.

Discover Interview: The World’s Most Celebrated Virus Hunter, Ian Lipkin

Excerpt 1)

The Columbia University researcher describes his quest for HIV in San Francisco and SARS in China, the immune cascades that may cause autism, and the infectious roots of psychiatric disease.

My comment: I’m reading “Neurotribes,” which provides an interesting view of what the medical profession, and specifically the psychiatrists have done via their ignorance of cell type differentiation.
Excerpt 2)

We still need motive and opportunity. Motive is tropism [seeking nutrients or energy] and virulence [ability to multiply and cause disease].

My comment: The “motive” of viruses is to steal energy from cells to support their virulence, their ability to multiply and cause disease.  The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site. Amino acid substitutions in viruses are examples that show the success of energy theft. The energy theft links perturbed protein folding in different cell types in different tissues of different organs in different organs systems to pathology in the context of increasing organismal complexity that neo-Darwinian theorists claim is mutation-driven. See: Mutation-Driven Evolution.
Everything currently known to serious scientists about cell type differentiation in all living genera links ecological variation to ecological adaptation via nutrient-dependent RNA-directed DNA methylation and RNA-mediated gene duplication that links RNA-mediated amino acid substitutions to the supercoiled DNA that protects organized genomes from virus-driven entropy.  The link from nutrient-dependent immune system cascades shows up in a report of how a single amino acid substitution is linked to differences in behavior that vary with human life history transitions.
See: Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults. The function of the Val158Met amino acid substitution

“…is known to be affected by a functional single nucleotide polymorphism (SNP) in COMT (G-to-A base-pair substitution) leading to a methionine (Met) valine (Val) substitution at codons 108/158 (COMT Val158Met). Carriers of the Met allele have been found to display a fourfold decrease in enzymatic activity compared to Val allele carriers going along with an increase of prefrontal DA activity (Lachman et al. 1996; Lotta et al. 1995).

My comment: If you understand the fact that a single amino acid substitution is linked to differences in behavior via the dopaminergic reward system, help others to understand why the authors failed to mention that “…a methionine (Met) valine (Val) substitution…” is a nutrient-dependent RNA-mediated amino acid substitution. That incriminating fact may have been left out to avoid negative feedback from all researchers who have failed to link amino acids from nutrient-dependent metabolic networks and genetic networks to healthy longevity or to pathology.
For example, a researcher who reported links from beneficial mutations to evolution is not likely to appreciate the claim that all pseudoscientists must learn the difference between a mutation and an amino acid substitution before attempting to link biologically-based cause and effect from atoms to ecosystems. No one expects those who can only be referred to as biologically uninformed science idiots to admit that they are biologically uninformed.
For example,  the pathology of phenylketonuria is linked from metabolism of a single amino acid to brain damage that can be avoided by changes in nutrition during the first few years of life. That is why infants are tested for the presence of the mutation that links the transgenerational epigenetic inheritance of one allele from each parent to the pathology in their child. The combination of mutations is not beneficial. If not for the adjustment in the diet of the infant the link from the metabolic networks to genetic networks and pathology rapidly becomes increasingly clear.
If you were a psychiatrist who had ignored the link from phenylketonuria nutrient-dependent brain development and also ignored what is known about the methionine (Met) valine (Val) substitution in the context of life history transitions that link the honeybee model organism to humans, what would you tell someone who asked the following question:

Could the development of pathological behavior in adolescents be prevented by proper nutrition?

Do you know any medical profession who might be willing to admit that neo-Darwinian theory is largely responsible for their ignorance of how RNA-mediated amino acid substitutions are linked to brain development throughout life in all vertebrates and invertebrates?
See: Nutrient-dependent/pheromone-controlled adaptive evolution: a model

The honeybee already serves as a model organism for studying human immunity, disease resistance, allergic reaction, circadian rhythms, antibiotic resistance, the development of the brain and behavior, mental health, longevity, diseases of the X chromosome, learning and memory, as well as conditioned responses to sensory stimuli (Kohl, 2012).

Medical professionals need only admit to that fact for a new age of medicine to quickly replace practices that have ignored what is known to serious scientists about cell type differentiation in species from microbes to humans.

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