Anti-Aging Genes Improve Appetite Regulation and Reverse Cell Senescence and Apoptosis in Global Populations

Abstract

Appetite regulation by nutritional intervention is required early in life that involves the anti-aging gene Sirtuin 1 (Sirt 1) with Sirt 1 maintenance of other cellular anti-aging genes involved in cell circadian rhythm, senescence and apoptosis. Interests in anti-aging therapy with appetite regula-tion improve an individual's survival to metabolic disease induced by gene-environment interac-tions by maintenance of the anti-aging genes connected to the metabolism of bacterial lipopoly-saccharides, drugs and xenobiotics. Interventions to the aging process involve early calorie re-striction with appetite regulation connected to appropriate genetic mechanisms that involve mi-tochondrial biogenesis and DNA repair in neurons. In the aging process as the anti-aging genes are suppressed as a result of transcriptional dysregulation chronic disease accelerations and con-nected to insulin resistance, non-alcoholic fatty liver disease (NAFLD) and neurodegenerative diseases such as Parkinson's disease and Alzheimer's disease. Interests in the gene-environment interaction indicate that the anti-aging gene Sirt 1that regulates food intake has been repressed early in the aging process in various global populations. The connections between Sirt 1 and other anti-aging genes such as Klotho, p66Shc (longevity protein) and Forkhead box proteins (FOXO1/ FOXO3a) have been associated with programmed cell death and alterations in these anti-aging genesregulate glucose, lipid and amyloid beta metabolism that are important to various chronic diseases.