**5. Summary**

An increase in NAFLD/obesity in communities around the world, show that epigenetic modifications are linked to malfunctioning of the gene Sirt1 along with p53 dysregulation of a defective adipose tissue-liver crosstalk. Healthy low calorie diets and/or an active lifestyle, maintaining adequate Sirt1/p53 interactions in obese individuals may decrease organ senescence, as well as age-related mutations to occur. The ingestions healthy foods devoid of components like sugars, fats, xenobiotics, and LPS may obliterate the induction of p53 cell-based apoptosis and Sirt1 suppression, but also enhance hepatocyte life span, thus preserving hepatocyte nuclear and mitochondrial interactions. Metabolic stimulators of Sirt1 (i.e., leucine, polyphenols (e.g., resveratrol) and cathekins) may enhance hepatic xenobioitic turnover, as well as preventing mitochondrial death, linked to the dysregulation of NAFLD.

Nutritional diets, which promote the binding of Sirt1 to chromatin, thus preventing it from association, induced by various drug regimens, as well as unhealthy diets, will inevitably also prevent adipose tissue transformation, as well as activation of immune responses involving macrophages, NK cells, and lymphocytes that are associated with NAFLD, as well as other diseases seen in various habitats and communities.
