Unopposed Oxidative Stress Leads to Pro-inflammatory Phenotype.. Metabolic Cellular Health Produces and Maintains Anti-inflammatory Phenotype..

Here is a discussion of beta hydroxybutyrate mechanisms of action in part listing some of the "starvation gene set" stimulated by nuclear beta hydroxybutyrate.  It further emphasizes the strategic goal of protecting against oxidative stress.  This, in effect, prevents cellular drift to pro-inflammatory senescent cells which prevents stem cell replacement.

The result?

Beta hydroxybutyrate is anti-aging anti-inflammatory and prevents phenotypic pro-inflammatory senescent cell drift and promotes stem cell replacement to maintain tissue integrity and function.

Metabolic cell health practices and supplements strategically and tactically achieves the young anti-inflammatory cell phenotype that simultaneously builds and maintains vigorous stem cell.

Maintaining a clean senescent reduced anti-inflammatory environment and resilient stem cells allows biological age to greatly lag chronological age.  It prevents inflamaging and other diseases derived from various oxidative stresses.

https://www.ncbi.nlm.nih.gov/pubmed/28371201

Ketone bodies mimic the life span extending properties of caloric restriction.

The extension of life span by caloric restriction has been studied across species from yeast and Caenorhabditis elegans to primates. No generally accepted theory has been proposed to explain these observations. Here, we propose that the life span extension produced by caloric restriction can be duplicated by the metabolic changes induced by ketosis. From nematodes to mice, extension of life span results from decreased signaling through the insulin/insulin-like growth factor receptor signaling (IIS) pathway. Decreased IIS diminishes phosphatidylinositol (3,4,5) triphosphate (PIP₃ ) production, leading to reduced PI3K and AKT kinase activity and decreased forkhead box O transcription factor (FOXO) phosphorylation, allowing FOXO proteins to remain in the nucleus. In the nucleus, FOXO proteins increase the transcription of genes encoding antioxidant enzymes, including superoxide dismutase 2, catalase, glutathione peroxidase, and hundreds of other genes. An effective method for combating free radical damage occurs through the metabolism of ketone bodies, ketosis being the characteristic physiological change brought about by caloric restriction from fruit flies to primates. A dietary ketone ester also decreases circulating glucose and insulin leading to decreased IIS. The ketone body, d-β-hydroxybutyrate (d-βHB), is a natural inhibitor of class I and IIa histone deacetylases that repress transcription of the FOXO3a gene. Therefore, ketosis results in transcription of the enzymes of the antioxidant pathways. In addition, the metabolism of ketone bodies results in a more negative redox potential of the NADP antioxidant system, which is a terminal destructor of oxygen free radicals. Addition of d-βHB to cultures of C. elegans extends life span. We hypothesize that increasing the levels of ketone bodies will also extend the life span of humans and that calorie restriction extends life span at least in part through increasing the levels of ketone bodies. An exogenous ketone ester provides a new tool for mimicking the effects of caloric restriction that can be used in future research. The ability to power mitochondria in aged individuals that have limited ability to oxidize glucose metabolites due to pyruvate dehydrogenase inhibition suggests new lines of research for preventative measures and treatments for aging and aging-related disorders. © 2017 The Authors IUBMB Life published by Wiley Periodicals, Inc. on behalf of International Union of Biochemistry and Molecular Biology, 69(5):305-314, 2017.

Joseph Thomas (Tony) Liverman, Jr.