Autophagy is a fundamental cellular cleaning process that, when disrupted, contributes to serious diseases. Drugs such as rapamycin and metformin activate it in laboratory studies, but are not suitable for self-medication. For people without disease, no proven safe method currently exists for deliberately increasing autophagy.
Autophagy is the built-in clean-up and recycling system of every cell in your body. The word literally means 'eating oneself': the cell packages damaged proteins, worn-out components (organelles) and other cellular waste into small vesicles called autophagosomes, and then breaks them down. The released building blocks are reused. This process is active in all cells and is evolutionarily highly conserved, meaning that yeast cells and human cells both do it in virtually the same way (PMID 35892559, 38601984).
When a cell is under stress, for example during nutrient deprivation or a lack of growth factors, autophagy shifts into a higher gear. The cell then recycles more intensively to supply itself with energy and raw materials (PMID 35892559). This is a survival mechanism: brief stress can therefore increase clean-up activity. Neurons, the nerve cells in your brain, are particularly dependent on this: they no longer divide after birth, so they cannot 'share away' damaged components through cell division. Without adequate autophagy, waste accumulates in those cells (PMID 35892559, 37334842).
When autophagy does not function properly, that accumulation of cellular waste is associated with serious diseases: Alzheimer's, Parkinson's, liver diseases, cardiovascular diseases and cancer (PMID 35892559, 37334842). Excessive oxidative stress, caused by reactive oxygen species (ROS), can damage the membrane of lysosomes. Lysosomes are the 'stomach acids' of the cell that digest autophagic waste. When they are damaged, the entire clean-up system becomes blocked (PMID 38762757). The protein p62 also plays a key role: it clusters around marked waste and recruits the autophagy machinery. This mechanism has been mapped in greater detail recently, but has not yet been translated into concrete treatments for humans (PMID 40011090).
Then there is the question of whether you can 'switch on' autophagy yourself. At present, drugs exist that activate autophagy in laboratory studies. Rapamycin (an mTOR inhibitor) promoted autophagy and inhibited cellular ageing in cell culture and mouse models (PMID 39110121). Metformin, a diabetes drug, did something similar in a cell model of diabetic cataracts (PMID 39334185). But both are real medicines with serious side effects: rapamycin suppresses the immune system, and metformin is licensed for the treatment of type 2 diabetes. Neither is suitable for self-medication with the aim of stimulating autophagy.
What remains for the ordinary person, then, is the knowledge that stress from nutrient deprivation increases autophagy. Caloric restriction and fasting are therefore often mentioned in the same breath as autophagy, but the studies provided support that mechanism at the cellular level, not as a proven strategy for concrete health gains in humans. There is no evidence in the available sources that specific supplements, diets or lifestyle interventions safely and effectively increase autophagy in healthy people in a way that demonstrably prevents disease or slows ageing.
The claims are based on cell studies, mouse models and mechanistic research. No large randomised trials in humans on increasing autophagy through lifestyle or supplements were included. The pathological side (what goes wrong when autophagy is disrupted) is more strongly supported than the intervention side.