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Prescription medication — not a dietary supplement
Captoprilis a prescription (or investigational) drug, not a supplement. It is included here for reference because people research and discuss it (often used off-label) — not as a recommendation. Take it only under a qualified clinician's supervision and only as prescribed; do not source it from grey-market vendors, where identity, purity, and dosing are unverified. The evidence below reflects its clinical trials.
What the evidence says
Most Captopril studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from mixed-quality randomised trials published 2003–2025.
Based on 5 studies · 1 RCT
Confidence
LowBy outcome
Captopril has an evidence score of 3.5/10 — emerging evidence based on 5 indexed studies. An ACE-inhibitor blood-pressure/heart drug studied as a geroprotector by targeting the renin-angiotensin system. ACE inhibition extends lifespan in C. elegans (and captopril specifically modulates a worm aging pathway), and the class has decades of human cardiovascular/kidney-protective evidence — but human longevity itself is unproven. A prescription drug used off-label, not a supplement. Representative study: PMID 14610160.
The commonly studied dose of Captopril is Off-label longevity use mirrors low antihypertensive dosing (captopril is short-acting; longer-acting ACE inhibitors like lisinopril/ramipril are often used) under a clinician. Not an approved longevity regimen; blood pressure and potassium should be monitored.. Individual needs vary — start at the lower end of the range and adjust based on how you respond.
Nicotinamide Riboside
Mostly mechanism / observationalA vitamin B3 precursor that reliably raises cellular NAD+ levels and is well tolerated — but human trials have so far shown mostly null or mixed results on the functional outcomes (muscle, metabolism, blood pressure, cognition) that elevation is meant to drive.
MitoQ
Mostly mechanism / observationalLast reviewed June 2026 · evidence from 5 studies · how we score
This information is for educational purposes only. It is not a substitute for professional medical advice. Always consult a qualified healthcare provider before starting, stopping, or changing any supplement or medication.
Captopril (ACE inhibitor)
An ACE-inhibitor blood-pressure/heart drug studied as a geroprotector by targeting the renin-angiotensin system. ACE inhibition extends lifespan in C. elegans (and captopril specifically modulates a worm aging pathway), and the class has decades of human cardiovascular/kidney-protective evidence — but human longevity itself is unproven. A prescription drug used off-label, not a supplement.
ACE/renin-angiotensin inhibition is a conserved aging pathway — captopril and ACE inhibitors extend lifespan in C. elegans and reduce cardiovascular/cardiac aging in rodents — and the class has strong human cardiovascular/renal outcome data, but no human trial shows captopril extends lifespan, so the geroprotector use is mechanistically grounded yet unproven.
Captopril is the prototype angiotensin-converting-enzyme (ACE) inhibitor — a cornerstone drug for hypertension, heart failure, post-myocardial-infarction care, and diabetic kidney protection.
Its geroscience interest centers on the renin-angiotensin system (RAS), an ancient signaling axis that, beyond blood pressure, influences inflammation, mitochondrial function, oxidative stress, and the senescence program.
Inhibiting ACE/RAS has emerged as a candidate longevity intervention with cross-species support: ACE inhibition extends lifespan in the worm C. elegans, captopril specifically inhibits the worm ACE homolog ACN-1 to influence dauer formation and aging, and reviews now frame RAS modulation as a conserved aging pathway across C. elegans, Drosophila, and rodents (where ACE inhibitors reduce cardiac and vascular aging).
On the human side, the evidence base is unusually deep — but it is cardiovascular and renal, not longevity: large randomized trials show ACE inhibitors reduce mortality and morbidity in heart failure and after myocardial infarction (e.g. the captopril arm of VALIANT) and slow kidney-disease progression.
The honest distinction is that no human trial shows captopril extends lifespan or healthspan in healthy people; the longevity case rests on conserved model-organism biology plus the drug's real (but disease-specific) human outcome benefits.
It is generally well tolerated; the characteristic effects are a dry cough (bradykinin-mediated), possible high potassium, first-dose hypotension, and a contraindication in pregnancy. Captopril is a prescription drug used off-label for its proposed geroprotective/RAS effects; it is not a dietary supplement.
The score reflects a conserved, mechanistically attractive aging pathway plus strong human cardiovascular evidence, against unproven human longevity.
Captopril blocks angiotensin-converting enzyme, lowering angiotensin II and modulating the renin-angiotensin system — a conserved axis influencing aging, inflammation, and mitochondrial function.
ACE inhibition raises bradykinin and nitric-oxide signaling (vasodilation and the characteristic cough), with vascular-protective effects.
In C. elegans, captopril inhibits the ACE homolog ACN-1 to affect dauer/aging; RAS modulation extends lifespan across invertebrate models.
How Captopril works — from molecular targets to health outcomes. Click an edge to see supporting research.This visualization is in beta — pathways are being refined and expanded.
Tap node to isolate • Pinch to zoom • Tap edge for research
Off-label longevity use mirrors low antihypertensive dosing (captopril is short-acting; longer-acting ACE inhibitors like lisinopril/ramipril are often used) under a clinician. Not an approved longevity regimen; blood pressure and potassium should be monitored.
Can be taken without food
| Form | Type |
|---|---|
| 💊Oral tablet (or a longer-acting ACE inhibitor) | Recommended |
| 💊Lisinopril / ramipril (longer-acting ACE inhibitors) | Alternative |
Captopril is the prototype; longer-acting ACE inhibitors are more convenient and share the class effects.
Minimum: 12 weeks
Optimal: 52 weeks
Cycling: Not required
Note: Captopril on an empty stomach, 2–3×/day; monitor blood pressure and potassium. Longer-acting ACE inhibitors allow once-daily dosing.
Dose-response data unavailable. The current published research for Captopril does not provide sufficient dose-specific outcome data to generate reliable dose-response curves.
Refer to the Dosage & Timing section above for recommended dose ranges based on available evidence.
ACE inhibition extends lifespan in C. elegans and reduces cardiac/vascular aging in rodents — not shown in humans.
Reduces mortality and morbidity in heart failure and after myocardial infarction (human RCTs).
Slows progression of chronic and diabetic kidney disease.
Dry cough (bradykinin), high potassium, and first-dose hypotension; contraindicated in pregnancy.
Contraindicated — ACE inhibitors cause fetal harm.
Monitor kidney function and potassium closely.
Caution — first-dose hypotension; start low.
Additive hyperkalemia risk — can be dangerous.
Reduce ACE-inhibitor effect and can worsen renal function (the 'triple whammy' with diuretics).
ACE inhibitors raise lithium levels and toxicity risk.
Tip: Bradykinin-mediated; switch to an ARB if intolerable.
Tip: Monitor potassium; avoid potassium supplements/salt substitutes.
Tip: Stop immediately and seek care; a class effect, more common in some groups.
Timing is flexible for Captopril — consistent daily use matters more than the time of day. Captopril is taken on an empty stomach (food reduces absorption); it is short-acting (2–3×/day).
Captopril should be used with caution — talk to a healthcare provider before taking it. The most commonly reported side effects are dry cough, hyperkalemia, angioedema. Use caution if any of these apply to you: Pregnancy (fetal harm); History of ACE-inhibitor angioedema; Bilateral renal artery stenosis.
A mitochondria-targeted antioxidant — CoQ10 conjugated to a triphenylphosphonium (TPP+) cation so it accumulates several-hundred-fold inside mitochondria. Sold OTC as a supplement. Its best human signal is improved endothelial/vascular function in older adults (one small RCT); several trials are null (Parkinson's, exercise adaptation), and almost all outcomes are surrogate/biomarker, not hard clinical endpoints.