Epigenetically Mediated Health Effects of Intermittent Fasting

Globally, the prevalence of chronic diseases such as obesity, cardiovascular disorders, diabetes, and cancer is rising. These conditions are influenced by both genetic and environmental factors, with nutrition being one of the most critical environmental determinants. Intermittent fasting (IF) is a dietary pattern that has gained attention for its potential health benefits and impact on metabolic regulation. Recent studies in the field of nutrition-epigenetics suggest that IF may exert these effects through epigenetic modifications, including DNA methylation, histone modifications, and regulation by non-coding RNAs. IF encompasses various approaches such as alternate-day fasting, time-restricted feeding, and whole-day fasting. Evidence indicates that IF can enhance lipid and glucose metabolism, support healthy aging, reduce inflammation, and improve mitochondrial and immune function by modulating gene expression epigenetically. It may also promote autophagy, stem cell renewal, and anti-cancer responses, suggesting its potential role in preventing or mitigating metabolic and neurodegenerative diseases. Despite these benefits, adverse effects of IF have also been reported. Particularly concerning are findings related to maternal IF, which may impair fetal development and metabolic health in offspring via epigenetic inheritance. Additionally, in other life stages, IF may lead to micronutrient deficiencies, hypoglycemia, hormonal imbalances, fatigue, and increased metabolic disease risk, especially in vulnerable populations or when fasting is prolonged or poorly planned. This review aims to summarize the current evidence on how IF influences health and disease through epigenetic mechanisms. Personalized recommendations considering age, health status, and nutritional needs are essential. More comprehensive human studies are needed to clarify IF’s dual role and to optimize its application for health promotion.