Intermittent fasting influences immunity and metabolism.
AI Summary
This review examines how intermittent fasting (IF) affects immune and metabolic processes, with particular relevance to the Blueprint Nutrition Protocol's structured eating approach. The researchers found that IF creates distinct cellular responses compared to traditional caloric restriction, influencing metabolic flexibility and inflammation patterns. The study suggests IF can improve glucose metabolism and reduce metabolic inflammation even without weight loss, indicating benefits beyond simple calorie reduction. The research highlights that fasting periods force the body to use different energy substrates, promoting metabolic adaptability. Key organs including liver, fat tissue, skeletal muscle, and immune cells coordinate during fasting to relay metabolic signals. The findings suggest IF's effects are time-dependent and compartmentalized, meaning benefits occur in specific tissues at particular times. The gut microbiota also plays a role in mediating IF's immune and metabolic changes. While this review provides valuable insights into IF mechanisms, it focuses on obesity and type 2 diabetes contexts, which may limit broader applicability to healthy individuals following structured nutrition protocols.
Key Findings
- Intermittent fasting can lower metabolic inflammation and improve glucose metabolism without reducing obesity
- IF forces periods of metabolic flexibility and increases use of different energy substrates
- Liver, adipose tissue, skeletal muscle, and immune cells communicate to relay metabolic and immune signals during fasting
- IF produces time-dependent, compartmentalized changes in immunity that differ from classic caloric restriction
- Gut microbiota triggers changes in immunity and metabolism during fasting periods
Abstract
Intermittent fasting (IF) modifies cell- and tissue-specific immunometabolic responses that dictate metabolic flexibility and inflammation during obesity and type 2 diabetes (T2D). Fasting forces periods of metabolic flexibility and necessitates increased use of different substrates. IF can lower metabolic inflammation and improve glucose metabolism without lowering obesity and can influence time-dependent, compartmentalized changes in immunity. Liver, adipose tissue, skeletal muscle, and immune cells communicate to relay metabolic and immune signals during fasting. Here we review the connections between metabolic and immune cells to explain the divergent effects of IF compared with classic caloric restriction (CR) strategies. We also explore how the immunometabolism of metabolic diseases dictates certain IF outcomes, where the gut microbiota triggers changes in immunity and metabolism during fasting.
Authors
Daniel M Marko, Meghan O Conn, Jonathan D Schertzer