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Evidence-based supplements similar to Telmisartan, ranked by shared goals and clinical evidence. Compare any of them head-to-head below.
A 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.
A fully human monoclonal-antibody PCSK9 inhibitor (Praluent), injected under the skin every 2 weeks, that lowers LDL cholesterol by ~50–60%. In the ODYSSEY OUTCOMES trial of ~18,900 post-heart-attack patients it reduced major cardiovascular events and showed a possible all-cause mortality signal. Generally well tolerated; injection-site reactions and high cost/access are the main trade-offs. Prescription drug, not a supplement.
An SGLT2-inhibitor diabetes drug (Invokana) that lowers glucose by excreting it in urine. It extended lifespan in male mice in the NIA aging program, and the SGLT2 class has strong proven cardiovascular, kidney, and heart-failure benefits in humans. Longevity benefit itself is unproven; carries genital-infection and (rarely) ketoacidosis risks. Prescription drug, not a supplement.
An SGLT2-inhibitor diabetes drug (Jardiance) with the strongest human outcome evidence of its class — it cuts cardiovascular death, heart-failure hospitalization, and kidney-disease progression even in non-diabetics. The most widely used SGLT2 for off-label 'longevity,' though longevity itself is unproven (the lifespan data are for sibling canagliflozin in mice). A prescription drug, not a supplement.
A prescription PCSK9-inhibitor monoclonal antibody (Repatha) given by subcutaneous injection. By binding circulating PCSK9 it spares LDL receptors and lowers LDL cholesterol by roughly 60%. The landmark FOURIER trial in ~27,500 statin-treated patients showed it cut cardiovascular events, and it produces dramatic LDL lowering in familial hypercholesterolemia. Very safe apart from injection-site reactions; cost and injection burden are the main trade-offs. A prescription drug, not a supplement.
A prescription oral statin (Crestor) that inhibits HMG-CoA reductase, the rate-limiting enzyme of cholesterol synthesis — one of the most potent statins, lowering LDL-C ~45–55%. In JUPITER (~17,800 people with elevated hsCRP), rosuvastatin cut major cardiovascular events and all-cause mortality; IVUS trials (ASTEROID, SATURN) show coronary plaque regression. Risks: myalgia, rare rhabdomyolysis, a small new-onset-diabetes signal, and transient liver-enzyme rise. Prescription drug, not a supplement.
An SGLT2-inhibitor diabetes drug (Farxiga/Forxiga) with broad, robust human outcome evidence — it cuts heart-failure hospitalization and cardiovascular death across the ejection-fraction spectrum and slows kidney-disease progression, including in non-diabetics. The sibling of empagliflozin, used off-label for 'longevity,' though longevity itself is unproven (the lifespan data are for sibling canagliflozin in mice). A prescription drug, not a supplement.
A prescription oral cholesterol-absorption inhibitor (Zetia) that blocks the intestinal NPC1L1 sterol transporter, lowering LDL-C ~15–20% on its own and more when added to a statin. In IMPROVE-IT (~18,000 post-ACS patients) ezetimibe added to simvastatin cut cardiovascular events — the first proof a non-statin LDL-lowering drug improves outcomes. Very well tolerated; rare myalgia and small liver-enzyme rise. Prescription drug, not a supplement.
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.