mTOR and Autophagy

The article favors cycling between challenge and recovery over remaining constantly in growth or deprivation states. Autophagy is presented as cellular recycling that breaks down damaged components and reuses materials. Rapamycin inhibits mTOR and is presented as promising for longevity, but human dosing remains uncertain. Fasting and exercise inhibit mTOR and increase autophagy. Autophagy removes damaged proteins, dysfunctional mitochondria, and free-radical-damaged molecules. The mTOR pathway is activated by glucose and amino acid availability after eating. mTOR regulates growth and protein synthesis and is necessary for building muscle and tissue. Active mTOR promotes glucose uptake, amino acid uptake, protein synthesis, and growth. Chronic mTOR activation can suppress autophagy and increase aging risk. Modern constant food availability is said to suppress fasting and scarcity signals that activate repair systems.