Purpose of ReviewThis research aims to elucidate the molecular mechanisms by which intermittent fasting (IF) induces autophagy and to evaluate its therapeutic potential across a range of pathologies. By synthesizing findings from preclinical and clinical studies, the review seeks to clarify the roles of key signaling pathways-such as the AMPK-mTOR axis, sirtuins, and beta-hydroxybutyrate-mediated signaling-in orchestrating autophagic processes, thereby enhancing cellular resilience and metabolic homeostasis.Recent FindingsRecent evidence demonstrates that IF robustly activates autophagy in metabolically active tissues through conserved molecular pathways. Experimental studies reveal that fasting increases AMPK phosphorylation and inhibits mTOR activity, leading to enhanced expression of autophagy markers like LC3-II, Beclin-1, and ATG proteins. Additionally, IF has been shown to improve insulin sensitivity, reduce hepatic lipid accumulation, and mitigate neurodegenerative processes by promoting the clearance of toxic protein aggregates. Emerging clinical data further support these findings, indicating that tailored fasting protocols can modulate autophagy to yield benefits in metabolic, oncological, and neurodegenerative disorders.SummaryThe scoped literature underscores IF as a promising non-pharmacological strategy to induce autophagy and improve overall health. While robust preclinical and clinical evidence supports its beneficial effects, challenges remain in standardizing fasting protocols and identifying optimal biomarkers for monitoring autophagic activity. Future research should focus on long-term, well-controlled trials and combined therapeutic approaches to refine IF strategies, ultimately translating these insights into personalized dietary interventions for disease prevention and health optimization.