Nutritional epigenetics, exercise, and immune system integrity

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Anti-inflammatory mechanism of dieting and fasting revealed

Summary: Researchers have found that a compound produced by the body when dieting or fasting can block a part of the immune system involved in several inflammatory disorders such as type 2 diabetes, atherosclerosis, and Alzheimer’s disease.

My comment: For the obvious link from nutrition and exercise to reproduction and RNA-mediated transgenerational epigenetic effects on the morphological and behavioral phenotypes of all species that must “move” to find food or to find mates see: Chapter 5: “Epigenetic Modulation of Gene Expression by Exercise in “Nutrition, Exercise and Epigenetics: Ageing Interventions” Use the search inside feature to see what will be published in April, 2015

Excerpt: Among the highlights are chapter-length discussion of such topics as: how anti-inflammatory action of calorie restriction underlies the retardation of ageing and age-related diseases (Chapter 3); epigenetic modification of gene expression by exercise (Chapter 5); the role of functional foods and their bioactive components…

See also: Acute Exercise Remodels Promoter Methylation in Human Skeletal Muscle

Excerpt: “…the unifying trigger that orchestrates the genomic response to exercise is incompletely defined.”

Conclusion: Our finding that the patterns of DNA methylation change in differentiated nondividing somatic cells provides further evidence that the epigenetic marks across the genome are subject to more dynamic variations than previously appreciated.

My comment: In my model, RNA-directed DNA methylation and RNA-mediated amino acid substitutions link the anti-entropic effects of nutrient-dependent survival of individuals to the survival of species. Species adapt to ecological variation in the availability of food. Entropic plasticity is linked from the availability of food to the nutrient-dependent physiology of reproduction via the metabolism of nutrients to species-specific pheromones.

The link from viral microRNAs to entropy and from nutrient-dependent microRNAs to their anti-entropic effects on cell type differentiation in the context of the required entropic elasticity has been fully detailed. All examples from all model organisms attest to the fact that species arise in the context of nutrient-dependent pheromone-controlled reproduction. Other attempts to explain extant biodiversity fail to include what is currently known about physics, chemistry, and conserved molecular mechanisms that link epigenetic effects of the sun’s biological energy to cell type differentiation in plants and to the animals that eat the plants or that eat other animals to ensure their nutrient-dependent pheromone-controlled survival.

See also: An integrative analysis reveals coordinated reprogramming of the epigenome and the transcriptome in human skeletal muscle after training

Abstract excerpt: “A transcriptional network analysis revealed modules harboring distinct ontologies and, interestingly, the overall direction of the changes of methylation within each module was inversely correlated to expression changes. In conclusion, we show that highly consistent and associated modifications in methylation and expression, concordant with observed health-enhancing phenotypic adaptations, are induced by a physiological stimulus.”

My comment: RNA-directed DNA methylation is consistently linked to health-enhancing phenotypic adaptations via RNA-mediated amino acid substitutions. The epigenetically effected microRNA/messenger RNA balance is the determinant of alternative splicings that link the RNA-mediated substitutions to the stability of DNA. When viral microRNAs accumulate due to nutrient stress and/or social stress, they may lead to mutations that perturb protein folding and lead to the instability of DNA if the DNA is not repaired. This links the accumulation of viral microRNAs across the life history of humans to age-linked physiopathology.

For example, see: A molecular chaperone breaks the catalytic cycle that generates toxic Aβ oligomers  reported as: Molecular inhibitor breaks cycle that leads to Alzheimer’s

Excerpt: Alzheimer’s disease is one of a number of conditions caused by naturally occurring protein molecules folding into the wrong shape and then sticking together – or nucleating – with other proteins to create thin filamentous structures called amyloid fibrils. Proteins perform important functions in the body by folding into a particular shape, but sometimes they can misfold, potentially kick-starting this deadly process.

My comment: Thermodynamic cycles of protein biosynthesis and degradation are nutrient-dependent. Nutrient-stress and social stress are linked to perturbed protein folding via RNA-mediated events. The molecular inhibitor that breaks the cycle that leads to Alzheimer’s probably inhibits misfolding via the prevention of “heat shock.” That’s what some molecular chaperones do.

See: Emergency Alert in the Cell

Excerpt: “During the heat shock response, different stress proteins are synthesized. Their task is to prevent permanent damage to the organism.”

My comment: All of the above attests to what is currently known about how cell type differentiation occurs during life history transitions, and what leads to perturbed protein folding and physiopathology. Everything currently known about Epigenetic Modulation of Gene Expression by Exercise in “Nutrition, Exercise and Epigenetics: Ageing Interventions can be placed into the context of evolutionary theory by simply ignoring it.

If you ignore what’s currently known about physics, chemistry, and the conserved molecular mechanisms of nutrient-dependent RNA-directed DNA methylation and RNA-mediated amino acid substitutions that differentiate all cell types in all individuals of all species during their life history transitions, you will not be on the side of those who are Combating Evolution to Fight Disease.

Excerpt: “Another mechanism involves chaperones such as heat shock protein 90 (Hsp90), proteins that massage subideal (mutant) proteins into functional conformations but abandon their regular client proteins during heat and other stresses that destabilize proteins. This causes a stress-inducible release of phenotypic diversity, which may drive evolution (with phenotypes ultimately stabilized by subsequent genetic changes). Both of these molecular mechanisms of protein-based inheritance are major departures from the modern synthesis views of solely mutation-directed variation, solely genetic inheritance, and independence of the generation of variation from environmental conditions.”

My comment: If you are not on the same side as those who are Combating Evolution to Fight Disease, you may wish to join those who believe in the pseudoscientific nonsense about Mutation-Driven Evolution.

Alternatively, you can wait until the combat ends and join the winners simply by claiming that you knew all along that ecological adaptation was nutrient-dependent and pheromone-controlled and that the theorists were simply biologically uninformed science idiots who caused the suffering and death of millions.

See also: Evolution evolves: physiology returns to centre stage (with my emphasis)

Conclusions: “The wide-ranging set of articles published in this issue reveal a major challenge both for the physiological sciences and for evolutionary biology. As the integration between the two proceeds, neither can remain unchanged. Evolutionary theory requires extension or even replacement, while physiological science needs to address the exciting possibilities opened up for the future. We hope that our article, and those published here, will enable both disciplines to respond effectively to that challenge.”

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