Every drug and hormone therapy in this category has a legitimate clinical use and a considerably less well-evidenced anti-aging use. The distance between those two is the recurring theme.
This is territory where talking to a doctor comes first, and the entries below are written to make that conversation better informed rather than to replace it.
TRT has a clear clinical indication and a much fuzzier anti-aging one, and the evidence differs sharply between them. This entry sets the two use cases side by side rather than treating them as the same prescription with the same expected result.
The original WHI results reshaped HRT prescribing almost overnight, and the later re-analysis reshaped it again. Inside: what changed, what the timing hypothesis proposes, and why this remains an individual decision rather than a general rule.
Semaglutide and its relatives act on appetite signalling, not on metabolism in the way most supplements claim to. What it sets out: the mechanism, the size of the gap between these drugs and their marketed "natural alternatives," and the downsides worth knowing first.
Read the full entry →In some observational data, diabetics taking metformin appeared to outlive non-diabetic controls, which is why the drug is now studied for aging itself. The detail: how strong that signal really is, and what the long-delayed TAME trial would settle.
No compound gets discussed more in longevity circles, and its mouse lifespan data genuinely is robust. The harder question is how much survives translation into humans, which is where this entry spends most of its attention.
Read the full entry →A single TSH reading is a snapshot of a system with several moving parts. It works through why Longevity Coach IQ holds thyroid static rather than projecting it forward, what an abnormal result should prompt you to do, and how it differs from markers you can train.
DHEA declines steadily with age, which is not the same as saying that topping it back up helps. This entry separates the well-documented decline from the genuinely mixed supplementation results, and notes the regulatory quirk behind its availability.
Growth hormone is prescribed for diagnosed deficiency and marketed for something else entirely. What follows: why the risk-benefit case looks unfavourable in healthy adults, and how different the picture becomes when a real deficiency has been diagnosed.
Less famous than metformin, and in mouse lifespan work arguably the more interesting of the two. Also here: the rodent data, the digestive tolerability trade-off that limits real-world use, and how it sits alongside rapamycin in the same conversation.
Two uses, two evidence bases. Testosterone replacement and menopause hormone therapy both treat diagnosed conditions with real evidence behind them, while being marketed considerably more broadly. Reading the trial evidence for the clinical use as though it supports the longevity use is the most common error in this category.
A decline is not automatically a deficiency. Several hormones here fall predictably with age. That pattern is well documented and does not by itself mean restoring the level helps. Growth hormone is the clearest case where the risk-benefit calculation in healthy adults does not favour use.
Repurposed drugs are a separate group. Some approved medications have genuinely interesting aging evidence, and the strongest of it is in mice rather than people. How much survives translation is the open question, and it is a different question from whether the drug works for its licensed purpose.
A single reading rarely settles anything. Hormone systems have several moving parts and daily rhythms, so one measurement is a snapshot rather than a diagnosis. That is also why some markers here are held static rather than projected forward, which is a deliberate limit rather than a gap.
The metabolic drugs overlap with everything else. Medications acting on appetite and glucose control land on the same outcomes as insulin resistance and HbA1c. They are a different route to the same markers, not a separate category of benefit.
Prescription is the dividing line. Everything here requires a clinician, which changes the calculation compared with the supplement aisle. It means real oversight and real side effects, and it means the evidence bar for approval was genuinely cleared for at least one use.
None has been shown to. Several approved medications have interesting evidence in animals, and the strongest lifespan data of any of them is in mice rather than people. Human trials measure surrogate markers or specific disease outcomes, not lifespan itself, so the honest answer stays negative.
Replacement treats a diagnosed deficiency against a clinical threshold. Optimisation is a marketing term for raising a level that is already within range. The evidence supports the first considerably more than the second, and conflating them is how the same trial data gets used to justify very different things.
Because everything in this category had to clear regulatory approval for at least one use. That means real trials, real oversight and real side effects. A supplement needs none of that before sale, which is why the same standard of proof cannot be applied to both.
Because large trials keep reframing it. Several recommendations in this category have reversed once and then partly reversed again after re-analysis. The pattern usually turns on who was studied and when treatment started, rather than on whether the drug works at all.
A clinical use treats a diagnosed condition against a threshold, with trial evidence behind it. A longevity use applies the same drug to healthy people hoping to slow aging. Almost every entry here has both, and the evidence for the first rarely transfers to the second.
Neither is approved for that use, and both are prescription medications with real side effects. Rapamycin has some of the most robust mouse lifespan data in aging research, and how much survives translation to humans is unresolved. This is a conversation for a doctor, not a page.
No, and conflating the two is the most common error in this category. Several hormones fall predictably with age, which is well documented. That pattern alone does not establish that restoring the level helps, and in some cases the risk-benefit calculation argues against it.
Because these systems have several moving parts and daily rhythms. One reading is a snapshot of a curve rather than a stable state. That is why some hormone markers are held static rather than projected forward, and why an abnormal result usually means retest before it means treat.
Every marker on this page, benchmarked against your own age and sex.
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