Intermittent fasting and neurocognitive disorders: What the evidence shows

Intermittent fasting (IF) has emerged as a potential lifestyle intervention for mitigating cognitive decline and enhancing brain health in individuals with mild to major neurocognitive disorders. Unlike preventive strategies, this review evaluates IF as a therapeutic approach, focusing on its effects on neuroplasticity, inflammation, and cognitive function.

A narrative review was conducted using a comprehensive PubMed search with the terms "intermittent fasting AND neurocognition" and "intermittent fasting AND neuroplasticity". Studies published in English within the last ten years involving human and animal models were included. Exclusion criteria focused on studies primarily examining mood disorders or unrelated metabolic outcomes.

Preclinical evidence demonstrates that IF enhances hippocampal neurogenesis and synaptic plasticity through pathways involving BDNF and CREB. IF also reduces neuroinflammation, as shown in animal models of Alzheimer's disease, vascular cognitive impairment, and high-fat diet-induced cognitive impairment. Human studies, though limited, suggest that regular IF may improve cognitive function and reduce markers of oxidative stress and inflammation in individuals with mild cognitive impairment.

Current findings highlight the therapeutic potential of IF for individuals with existing cognitive impairment. While preclinical studies provide robust evidence of neuroprotective mechanisms, human studies remain sparse and require standardization. Further clinical research is necessary to confirm long-term safety and efficacy and to refine IF protocols for broader clinical application.