Autophagy & mitochondrial quality control
One of 6 mechanistic pathways to ⏳ Longevity & healthspan · 9 options
Damaged proteins and mitochondria accumulate because clearance slows with age. Autophagy is the recycling programme; mitophagy is the mitochondria-specific arm. This is arguably the most tractable longevity mechanism because fasting alone moves it.
Autophagy is suppressed by nutrient abundance, so insulin and HbA1c are the levers you can actually see. Roughly 40% of people cannot produce Urolithin A from food at all, which is the argument for supplementing the metabolite.
HbA1c (Hemoglobin A1c)Fasting InsulinCoenzyme Q10Comprehensive Metabolic Panel (CMP)⏳ Longevity Baseline covers these in one panel →
What engages this pathway
Ordered by how directly each one acts on the mechanism above — never by how much trial evidence exists. Each links to its full breakdown with dosing, half-life and vendor.
🧬 Spermidine
Induces autophagy and extends lifespan in yeast, flies, worms and mice. The human evidence is epidemiological — higher dietary intake, lower mortality — which is suggestive rather than causal.
🧬 Urolithin A
The one mitophagy inducer with randomised human trials. A gut-bacterial metabolite of ellagitannins that most people cannot produce — roughly 40% of the population lacks the microbiome to make it, which is exactly why supplementing the metabolite makes sense.
💉 SS-31
Repairs cristae architecture by binding cardiolipin. In clinical development, with human exercise-capacity data in mitochondrial disease.
🧬 Pomegranate Extract
The ellagitannin source Urolithin A is made from — useful only if you have the microbiome to convert it.
🧬 PQQ
Mitochondrial biogenesis via PGC-1α — adding new mitochondria as the complement to clearing damaged ones.
🧬 CoQ10
Electron transport substrate; declines with age and with statin use.
🧬 Ubiquinol
The reduced form, better absorbed in older adults whose conversion capacity has fallen.
💉 Methylene Blue
Alternative electron carrier that bypasses damaged complexes.
🧬 GliSODin (SOD)
Oral superoxide dismutase protected by a gliadin coating so it survives digestion — supplying the enzyme rather than a scavenger.
The other 5 routes to longevity & healthspan
Pick the pathway that matches where you are actually stuck. An appetite drug does nothing for someone who already undereats.
Want the protocols behind these?
Dosing schedules, stacking, cycle timing and Coach Cam's notes live inside the Academy — plus the full interactive Vault.
Join the Academy — $10/mo →← Open this pathway in the interactive Vault
Frequently asked questions
Damaged proteins and mitochondria accumulate because clearance slows with age. Autophagy is the recycling programme; mitophagy is the mitochondria-specific arm. This is arguably the most tractable longevity mechanism because fasting alone moves it.
9 options are mapped to this pathway in the Vault, including Spermidine, Urolithin A, SS-31, Pomegranate Extract. They are grouped by the mechanism they act through rather than ranked by how much trial evidence exists — 5 carry clinical validation and 3 are mechanistic predictions.
Autophagy is suppressed by nutrient abundance, so insulin and HbA1c are the levers you can actually see. Roughly 40% of people cannot produce Urolithin A from food at all, which is the argument for supplementing the metabolite. The markers worth checking are HbA1c (Hemoglobin A1c), Fasting Insulin, Coenzyme Q10, Comprehensive Metabolic Panel (CMP).
Unproven is not the same as ineffective. Of the 9 options on this pathway, 5 have clinical validation and 3 are graded theoretical — meaning the mechanism is sound but the specific human trial has not been run, which is true of a great deal of what works in this space. Nothing on this page is ordered by evidence tier, because sorting by trial count would bury the compounds you came looking for.