Energy-dependent coulombic, autophagic, polycombic healthy longevity

By: James V. Kohl | Published on: November 22, 2016

Mitophagy is the selective degradation of mitochondria by autophagy.
See also this excerpt:

Disorders in energy creation by mitochondria can cause cellular degeneration…

Mitochondria do not create energy.  They link the creation of the sun’s anti-entropic virucidal energy to RNA-mediated cell type differentiation via biophysically constrained DNA repair. Energy-dependent autophagy links mitophagy to supercoiled DNA via the innate immune system and RNA-mediated repair of damaged DNA.
Repair is nutrient-energy dependent. Separating mitophagy from autophagy is one way to prevent people from realizing how energy-dependent viral latency and healthy longevity is typically achieved outside the context of ridiculous neo-Darwinian theories. Mitophagy and autophagy are two terms used to describe the same energy-dependent molecular mechanisms. In this case, we see the claim that energy creation by mitochondria obfuscates the fact that energy cannot be created or destroyed in the context of what is known about how quantum physics must be linked from quantized energy to biologically-based cause and effect.
Selective removal of deletion-bearing mitochondrial DNA in heteroplasmic Drosophila
Re:  mtDNA deletion (mtDNAΔ) in adult Drosophila muscle.

Stimulation of autophagy, activation of the PINK1/parkin pathway or decreased levels of mitofusin result in a selective decrease in mtDNAΔ.


A key question is whether occasional manipulations of cell physiology that promote mtDNA quality control, in otherwise healthy individuals, can bring about a more general ‘housecleaning’ that keeps the frequency of mutant DNA below the threshold for causing cellular dysfunction in diverse tissues without incurring other organismal costs.

My comment: The innate immune system links selective removal of dysfunctional mitochondria to nutrient energy-dependent healthy longevity via the physiology of reproduction in all living genera. Everything known to all serious scientists about energy-dependent thermodynamic cycles of protein biosynthesis and degradation should not lead to the “key question” above. It is too obvious that virus-driven energy theft stimulates autophagy, which typically allows natural selection for nutrient energy-dependent codon optimality to repair damaged DNA.
For example, energy-dependent changes in base pairs link single nucleotide polymorphisms (SNPs) to fixation of RNA-mediated amino acid substitutions in supercoiled DNA via successful reproduction. Fixation of the amino acids substitutions in different cell types of different species is the hallmark of successful reproduction. For contrast, de Vries (1902) defined the term “mutation” in the context of what he claimed were sudden “jump-like” changes in energy. His definition became the basis for the invention of neo-Darwinian pseudoscientific nonsense, which has prevailed among the biologically uninformed.
For comparison, serious scientists have learned that virus-driven energy theft prevents fixation of the amino acid substitutions in host populations. Energy theft facilitates fixation of amino acid substitutions in viruses. For example, fixation via energy-dependent viral replication contributes to the stability of the viral genome via a single amino acid substitution in the influenza virus.
See: The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.
The increasing instability of the human host’s organized genome can be viewed in the context of accumulated mutations caused by virus-driven energy theft. That instability eventually leads to all virus-driven pathology. The innate immune system is compromised by virus-driven energy theft, and that biological fact also is a historical fact.
See: Analysis of 6,515 exomes reveals the recent origin of most human protein-coding variants

Of the putatively deleterious protein-coding SNVs, 86.4% arose in the last 5,000 to 10,000 years, and they are enriched for mutations of large effect (Supplementary Fig. 14) as selection has not had sufficient time to purge them from the population.

My comment: No experimental evidence of biologically-based cause and effect suggests that mutations are purged by selection. Natural selection for energy-dependent codon optimality clearly shows that virus-driven energy theft is biophysically constrained. The biophysical constraints link viral latency to healthy longevity in species from microbes to humans. Bacteria are more ecologically adapted than archaea, for example.
See: Virus-mediated archaeal hecatomb in the deep seafloor
Concluding sentence:

We show here for the first time the crucial role of viruses in controlling archaeal dynamics and therefore the functioning of deep-sea ecosystems, and suggest that virus-archaea interactions play a central role in global biogeochemical cycles.

My comment: Virus-human interactions clearly play the central role in the history of all life-sustaining cycles of protein biosynthesis and degradation. The transgenerational epigenetic inheritance of Zika virus-damaged DNA is the only proof of that fact that any serious scientist needs.
See for example: Small non-coding RNAs associated with viral infectious diseases of veterinary importance: potential clinical applications (April 4, 2016)

The emerging correlation between miRNA expression and disease pathogenesis and outcomes suggests the potential use of miRNAs as biomarkers.

See also: MicroRNAs in the Host Response to Viral Infections of Veterinary Importance (October 17, 2016)

Viruses, particularly DNA viruses [Marek’s disease virus (MDV), bovine herpesvirus] and even retroviruses (e.g., bovine leukemia virus), can also encode their own miRNAs, but due to space limitations, this topic is not emphasized in this review, and we refer the reader to excellent existing reviews [e.g., Ref. (8, 9)].

See also this invited (unpublished) review of nutritional epigenetics. Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems  (It was returned without review.)

This atoms to ecosystems model of ecological adaptations links nutrient-dependent epigenetic effects on base pairs and amino acid substitutions to pheromone-controlled changes in the microRNA / messenger RNA balance and chromosomal rearrangements. The nutrient-dependent pheromone-controlled changes are required for the thermodynamic regulation of intracellular signaling, which enables biophysically constrained nutrient-dependent protein folding; experience-dependent receptor-mediated behaviors, and organism-level thermoregulation in ever-changing ecological niches and social niches. Nutrient-dependent pheromone-controlled ecological, social, neurogenic and socio-cognitive niche construction are manifested in increasing organismal complexity in species from microbes to man.

See for comparison: Turning back the aging clock

Most people start off life with some level of heteroplasmy, and the levels of mutant mtDNA increase throughout life. When a critical threshold level of mutant mtDNA is passed, cells become nonfunctional or die.

The accumulation of mutant mtDNA over a lifetime is thought to contribute to aging and degenerative diseases of aging such as Alzheimer’s, Parkinson’s, and sarcopenia—age-related muscle loss and frailty. Inherited defects in mtDNA are also linked to a number of conditions found in children, including autism.

My comment: Virus-driven energy theft is clearly linked from changes in the nutrient energy-dependent microRNA/messenger RNA balance to all pathology. The most recent example of this was reported a few days ago in the context of autism: Shared epigenetic changes underlie different types of autism.
See also: Energy-dependent purifying selection / autophagy (2)
See also: Controlled amino acid treatment of all pathology

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