Abstract
A compelling regimen that has recently gained popularity is intermittent fasting (IF), which aims to improve metabolic function and promote weight loss. Recent research suggests that IF has complex effects, influencing metabolic regulators like insulin sensitivity and lipolytic pathways as well as causing epigenetic changes, which are thought to be responsible for a significant portion of its therapeutic efficacy. Epigenetic remodeling controls inflammatory responses, fat deposition, and energy homeostasis by modifying chromatin structure and transcription dynamics in a way that is reversible and inheritable while leaving the nucleotide sequence unchanged. Metabolic abnormalities are characterized by an increase in visceral adipose tissue, which is a risk factor for obesity and type 2 diabetes. This review focuses on the inhibitory effect of IF on this expansion and how it leads to epigenetic changes. This sudy examines IF and its influence on certain epigenetic changes regulating ‘master’ genes and ‘core’ metabolic pathways parameters involved in fat storage, mitochondrial bioenergetics, and inflammation related to oxidative stress. In light of recent studies on targeted epigenomic remodeling and visceral fat loss, this text examines how time-restricted fasting may provide clinically relevant cardiometabolic benefits and explores personalized approaches to energy restriction based on epigenetic predictive factors. Such prediction may represent a selective point of relevance to offer therapeutic intervention in a day-to-day manner. This article ends with a set of prioritized suggestions for longitudinal studies that delineate the overlapping time frame of epigenetic fasting and its influence on the genome in the context of obesity and its associated cardiovascular components.