Diet-driven RNA interference and mental health (4)

By: James V. Kohl | Published on: February 13, 2018

See: Diet-driven RNA interference and mental health (3)

Social transmission and buffering of synaptic changes after stress

Transmission from the stressed subject to the naive partner required the activation of PVN CRH neurons in both subject and partner to drive and detect the release of a putative alarm pheromone from the stressed mouse.

Reported as: Researchers discover brain cells change following close contact with a stressed individual

“There has been other literature that shows stress can be transferred — and our study is actually showing the brain is changed by that transferred stress,” says Toni-Lee Sterley, an Eyes High postdoctoral fellow in Bains’s lab and the study’s lead author. “The neurons that control the brain’s response to stress showed changes in unstressed partners that were identical to those we measured in the stressed mice.”

The researchers discovered that the activation of the neurons causes the release of a chemical signal, an “alarm pheromone,” from the mouse that alerts the partner. The partner who detects the signal can, in turn, alert additional members of the group.

This links Bruce McEwen’s works on stress to my works. It completes details of how the mouse-to-human model links nutrient stress-linked and social stress-linked mutations from the virus-driven theft of quantized energy to all pathology. It predicts that fact that human pheromone-enhanced products will continue to be used to prevent or effectively treat Alzheimer’s disease and other neurodegenerative diseases, and to prevent suicide.
See: Formulation and evaluation of anti-suicidal nasal spray of Thyrotropin releasing hormone
See also: Pheromones and the luteinizing hormone for inducing proliferation of neural stem cells and neurogenesis
The unnecessary suffering and premature deaths of ~ 22 veterans per day and many others who commit suicide or who suffer through largely ineffective treatments for cancer can be place into the context of two reviews:
See: Nutrient-dependent/pheromone-controlled adaptive evolution: a model (2013)
and Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems
In my 2014 invited review of nutritional epigenetics, I linked one food energy-dependent base pair to fixation of one amino acid substitution and the stability of organized genomes in a modern human population. The stability was clearly linked from the creation of microRNAs via ingestion of sago palm-like leaves to an increase in endogenous vitamin C.
See also: Vitamins and Hormones Volume 106 Thyroid Hormone February 2018 (paywalled)
Vitamin C links a single base pair change to one amino acid substitution (V370A) in a modern human population. That fact can now be linked from my 2013 refutation of neo-Darwinian pseudoscientific nonsense to all biodiversity on Earth via the creation of sunlight and the Dependence of RNA synthesis in isolated thymus nuclei on glycolysis, oxidative carbohydrate catabolism and a type of “oxidative phosphorylation” (1964)

The synthesis of RNA in isolated thymus nuclei is ATP dependent.

The model organism that best represent the facts about epigenetic regulation of biophysically constrained ATP-dependent RNA-mediated viral latency is featured here: Meet the creature that can regenerate its brain and resist cancer.

A good model with a good model organism predicts. The mouse to human model predicts that one base pair and one fixed RNA-mediated amino acid substitution link the pheromone-controlled physiology of reproduction to all vertebrate biodiversity via food odors.  Predictably, in the axolotyl (aka the “walking fish”), an iodine isotope and cryo-EM technology will soon be used to establish the facts about how the creation of sunlight must be linked from the creation of ATP and the creation of RNA to DNA repair and all biodiversity via the physiology of reproduction and healthy longevity in all living genera.

See also: Researchers ID New Mechanism for Keeping DNA Protein in Line

The actions of a protein used for DNA replication and repair are guided by electrostatic forces known as phosphate steering, a finding that not only reveals key details about a vital process in healthy cells, but provides new directions for cancer treatment research.
Electrostatic forces are not known as phosphate steering.
See: What is an Electrostatic Force?

Electrostatic force between electrons and protons is one of the strongest forces in the universe, even more powerful than gravity. A hydrogen atom, which contains only one electron and one proton, has the fundamental force of gravity keeping it together. However, each subatomic particle can develop electrostatic force as well, which becomes even stronger.

Pseudoscientists are prepared to attack serious scientists at every level of examination that includes aspects of how subatomic particles contribute to oxidative phosphorylation. Who doesn’t know about the role that subatomic particles play in biophysically constraining viral latency?
See: Subatomic: An Atom Building Game (2017)

Subatomic is a deck building game where players are competing to build a number of available Elements, which score them points. Each player starts with the same small deck of cards that consist of Proton, Neutron, and Electron Cards. They use these cards to build upon their current Atom (by playing these cards face-up as Subatomic Particles) in an attempt to construct one of the available Element Cards. Or players may use their hand of cards to purchase more powerful cards for later use (by playing them in combinations of face-down as energy and face-up as Subatomic Particles!) Subatomic introduces a unique variation on deck building with a highly accurate chemistry theme…

The fact that Discover’s “My Science Shop” does not yet include information on the game “Subatomic” can be explained because the game is not yet available. The fact that Discover’s “My Science Shop” does not mention the availabilty of “Cytosis” suggests they are not willing to admit that their past representations of neo-Darwinian pseudoscientific nonsense were removed from consideration in 1944 when Schrödinger published “What is Life?”
See: Schrödinger at 75 – The Future of Biology – September 2018
The most accurate of all chemistry themes has continued to link Schrödinger’s claims from  quantum physics and quantum chemistry to quantum biology via the conserved molecular mechanisms of biophysically constrained protein folding chemistry. The conserved molecular mechanisms link energy-dependent epigenetics to healthy longevity. The conserved molecular mechanisms also link the virus-driven theft of quantized energy to all pathology.
See also: A quantum theory for the irreplaceable role of docosahexaenoic acid in neural cell signalling throughout evolution (2013)
Classical biophysics does not have a ready explanation for the role of docosahexanoic acid (DHA), which appears to be irreplaceable in the context of a light-activated endogenous substrate that functions as an electron tunnelling device. DHA provides precise quantized signals that are essential to visual accuity in the context of synaptic signaling. The link from quantum physics to classical physics helps to explain why the energy-dependent creation of photoreceptors has been linked to their counter intuitive orientation — away from the incoming light.
But, I digress. I am often forced to digress by theorists who invent new terms, such as phosphate steering, to obfuscate what is know about epigenetically-effected top-down causation, which starts with effects of sunlight linked to oxidative phosphorylation. Top-down causation does not start with phosphate steering. It starts with the creation of receptors. If any aspect of biophysically constrained life on Earth started with phosphate steering, there would be more than one citation to the claim. There is only one. See. “Phosphate steering.”
For comparison to what is known about the link from microRNAs to the brain and behavior, see:
microRNA brain and microRNA behavior
See also: Reduced expression of brain-enriched microRNAs in glioblastomas permits targeted regulation of a cell death gene (2011)
and Targeted expression of suicide gene by tissue-specific promoter and microRNA regulation for cancer gene therapy (2013)

See: Epigenetics study helps focus search for autism risk factors

Within the Shank3 promoter 6 region they identified a single nucleotide polymorphism (or SNP, a common type of genetic variation) known as rs6010065. Analyzing genomic data from a clinical study of 554 children with autism and 214 healthy controls, they found that rs6010065 is indeed associated with autism spectrum disorder.

I reiterate. The profiles are energy-dependent and the pheromone-controlled physiology of reproduction helps to ensure that viral latency is biophysically constrained by the dynamic processes. That fact can be compared to ridiculous claims about mutations and the “evolving profiles.”

See for example, this link from the food energy-dependent pheromone-controlled fixation of the BDNF val66met polymorphism amino acid substitution to behavior in human infants.

The BDNF val66met polymorphism and individual differences in temperament in 4-month-old infants: A pilot study

See for comparison: Stress dynamically regulates behavior and glutamatergic gene expression in hippocampus by opening a window of epigenetic plasticity

Reported as: Newly discovered windows of brain plasticity may help with treatment of stress-related disorders 

…they looked at mice genetically engineered to carry a genetic variant associated with development of depression and other stress-related disorders in humans [ the variant is (BDNF Val66Met)] and present in 33 percent of the population.

If you don’t know where to look, you might find where the information on the BDNF Val66Met is buried. But, if you look at the life’s works of Bruce S. McEwen, you will discover what is known to all serious scientists about stress linked RNA-mediated cell type differentiation.

Redefining neuroendocrinology: Epigenetics of brain-body communication over the life course (2017)

Heterozygous BDNF Val66Met mice are genetically susceptible to stress. The effects of stress on messenger RNA levels in wild-type mice was recapitulated but only via activation of immediate early genes when the heterozygous BDNF Val66Met mice were actually stressed. In the absence of stress, stress activated expression of immediate early genes is not worth studying. Similarly, it is not worth studying how nutrient stress is linked to social stress via c-fos activation in gonadotropin releasing hormone (GnRH) neuroscretory neurons.

However, if baseline studies had not already linked expression of the Fos protein to epigenetic effects of pheromones on luteinizing hormone in mice, the epigenetic effects of food odors and pheromones on humans might never have been linked to interethnic genetic differences in human morphology and behavior.

See: Influence of male rats on the luteinizing hormone-releasing hormone neuronal system in female rats: role of the vomeronasal organ (1993)

[Pheromonal regulation of genetic processes: research on the house mouse (Mus musculus L.)] (1994)

Human pheromones: integrating neuroendocrinology and ethology (2001)

Pheromones and the luteinizing hormone for inducing proliferation of neural stem cells and neurogenesis (2011)

The link from diet-driven RNA interference to mental health can now be considered in the context of gene gains and losses.

For example, see: APOBEC1

  1. Catalytic component of the apolipoprotein B mRNA editing enzyme complex which is responsible for the postranscriptional editing of a CAA codon for Gln to a UAA codon for stop in the APOB mRNA.
  2. Also involved in CGA (Arg) to UGA (Stop) editing in the NF1 mRNA.
  3. May also play a role in the epigenetic regulation of gene expression by participating in DNA demethylation.

Loss of APOBEC1 RNA-editing function in microglia exacerbates age-related CNS pathophysiology

These data provide powerful evidence supporting the critical role of APOBEC1-mediated RNA editing in maintaining the balance between the homeostatic and activated immune functions of MG.

See also: Psychological Stress and Mitochondria: A Conceptual Framework (Part 1) and Psychological Stress and Mitochondria: A Systematic Review (Part 2)

Reported as: Cellular ‘powerhouses’ may explain health effects of stress

The findings are especially exciting for the field of psychosomatic medicine, with its traditional focus on re-integrating the mind (“psyche”) and body (“soma”). Emerging evidence on the role of mitochondria in translating the effects of stress on health “extend the reach of mind-body research into the cellular-molecular domain that is the core foundation of current biomedical training and practice,” Drs. Picard and McEwen write. They emphasize the need for further studies to test various elements of their model, especially in humans. “Future research should consider the dynamic bi-directional interactions between mitochondria and other important physiological systems,” the authors conclude.

See also: Mitochondrial alterations and neuropsychiatric disorders

Mitochondria are membrane-enclosed organelle found in most eukaryotic cells, where they generate the majority of the cell’s supply of adenosine triphosphate (ATP), used as a source of chemical energy. In addition, they are involved in a range of other processes, such as signalling, cellular differentiation, cell death, as well as the control of the cell cycle and cell growth. Mitochondria have been implicated in several neuropsychiatric disorders, in particular, depression, anxiety, schizophrenia, autism, and Alzheimer’s dementia. Furthermore, the presence of mutations at the level of mitochondrial or nuclear DNA (mtDNA and nDNA, respectively) has been linked to personality disorders, behavioral disturbances, thought alterations, impulsivity, learning impairment, cognitive failures until dementia. The aim of this paper is to review the literature on the relationship between psychiatric symptoms or syndromes and mtDNA mutations or mitochondrial alterations, while highlighting novel therapeutic targets for a broad range of disorders.


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