The Longevity Blueprint
Ongoing, six arms, one pick each
Everything on this page is free. The stack, why each pick beat its alternatives, every option, the bloodwork and the safety lines. The week-by-week schedule and the decision rules are the members half.
This is the goal with the widest gap between what is exciting and what is evidenced, and being straight about that is the whole value of the page. Five of the six arms below are mechanism-led: nutrient sensing, NAD+, senescence, autophagy, glycation. They are genuinely interesting biology and the human outcome data is thin to absent. The sixth arm is the one with actual mortality data — lipids, blood pressure, glucose — and it is the least discussed in this space because it is boring. A longevity protocol that runs the first five and ignores the sixth has the priorities exactly backwards. So this page puts the boring arm first.
Can you run all of them? Yes - and here is what it costs
This is a general protocol. You make the final call on how much of it to run — or have it built around your labs.
Which of these 6 is actually you?
This tells you where your biggest leverage is — where to start, not where to stop. Read the But line too: it is what each lane cannot do for you, which is the part a list of options never tells you.
Before any of it — the foundation
These four are not a disclaimer at the bottom of the page. They are the reason the rest of it works, and every one of them is free.
Growth hormone is released in pulses during deep sleep, insulin sensitivity is measurably worse after one bad night, and appetite regulation collapses without it. Every compound below works through a system that sleep already governs. This is not filler advice — it is the highest-leverage item on the page and it is free.
The single dietary variable with the most consistent evidence behind it for body composition, in both directions — building and preserving. Under-eating protein while running anything anabolic is paying for a signal with no substrate to act on.
Nothing here substitutes for mechanical tension. Compounds change how well you recover from and adapt to training; they do not replace the stimulus. A protocol run without training reliably produces the side effects and not the results.
Non-exercise activity is the largest and most variable component of daily energy expenditure, and it is the one that quietly falls when you start dieting. Tracking it stops the metabolic adaptation people blame on their thyroid.
The stack
Said once. Most of what follows is mechanism-led rather than outcome-proven — that is the state of longevity research, not a flaw in any particular compound. Unproven is not the same as ineffective, and the honest framing is that you are running an experiment on yourself that you should measure. What is different on this page from every other blueprint: arm six is not in that category. Statins, blood-pressure control and glucose management have hard mortality endpoints from very large trials. When something here has that kind of evidence, it is said plainly.
Each pick names what it was chosen over and why. That is the difference between a blueprint and a list — if you disagree with a choice, the alternative is right there and swapping it does not break the rest.
Peptides 3
Short amino-acid chains that signal rather than force. Almost all are injected or intranasal, they need reconstituting, and they are the reason most people are on this site.
*'For nutrient sensing I prefer MOTS-c here.'* Mitochondrially encoded, activates AMPK, and it does not carry rapamycin's immunosuppression or its glucose cost - which matters on a page someone runs for years rather than weeks.
Metformin activates AMPK and has the largest human dataset of anything here — though the TAME trial that would settle it has not reported, and it blunts training adaptations. Acarbose blunts the glucose curve and has mouse lifespan data. Canagliflozin has mouse data in males specifically. AICAR and MOTS-c activate AMPK directly. Rapamycin is the base because the animal evidence is the strongest and most replicated in the field. It is also the one where the dosing schedule is the difference between the intended effect and immunosuppression — which is why it is in the paid half of this page.
Stack this arm deeper5 optional add-ons
Each of these sits in this same pathway, so it starts the week this pathway starts. Swapping one in for the pick above does not change the schedule.
The previous pick for this arm, kept as an option. mTOR inhibition is the most reproducible life-extension intervention in animal models there is — it works across yeast, worms, flies and mice, which is unusual. **The schedule is the entire mechanism
The trade-off Cam moved it out of the lead spot on sign-off.
Blunts the post-meal glucose spike by slowing carbohydrate breakdown. Mouse lifespan data, and it acts on the glucose curve rather than on insulin signalling — a different lever from metformin.
The trade-off The GI cost is real and dose-dependent, because the undigested carbohydrate ferments. It also does nothing on a low-carbohydrate diet, which is worth knowing before buying it.
The other half of the nutrient-sensing argument, and the subject of the TAME trial — the first trial designed to treat ageing itself as an endpoint.
The trade-off Blunts the adaptations to exercise, and exercise has better longevity evidence than metformin does. That tension is unresolved and worth taking seriously.
A polyamine that induces autophagy independently of mTOR — so it reaches the same endpoint as rapamycin without immunosuppression, and it has human epidemiology behind it.
The trade-off Far weaker than rapamycin. The dietary intake data is observational and confounded by the foods it comes in.
The simplest Khavinson dipeptide, and the one with the most of that group's own lifespan data behind it in animals - which is the endpoint this entire blueprint is about.
The trade-off One group's animal work is the weakest possible basis for a human longevity claim, and this page has an arm with actual mortality data in it. Run it knowing which is which.
NAD+ & sirtuin signallingNad+4 options
4 options — 0 to swap in, 4 to stack ontap to collapse
Cellular senescence & senolyticsFoxo4-DRI2 options
2 options — 0 to swap in, 2 to stack ontap to collapse
Small molecules 1
Orally active compounds, most of them with a prescription history and a real clinical evidence base. Less exciting than the peptides and frequently better evidenced.
The unglamorous evidence — what actually has mortality dataRosuvastatin4 options
4 options — 0 to swap in, 4 to stack ontap to collapse
Health supplements & substrate
The floor underneath the compounds. Cheap, well tolerated, and the part that decides whether anything above it has a fair chance — a secretagogue on a magnesium deficiency is a rounding error.
Autophagy & mitochondrial quality controlUrolithin A4 options
4 options — 0 to swap in, 4 to stack ontap to collapse
Glycation, oxidation & protein damageBenfotiamine2 options
2 options — 0 to swap in, 2 to stack ontap to collapse
The 24-week schedule
What goes in, what comes out, and when. The exact doses for each phase are inside the Academy — the structure below is free because it is the part you need to decide whether this fits your life.
| 1–8 | 9–16 | 17–24 | Ongoing | Annual review | |
|---|---|---|---|---|---|
| Rosuvastatin | |||||
| Urolithin A | |||||
| Benfotiamine | |||||
| Nad+ | |||||
| Rapamycin | |||||
| Fisetin |
Each bar is a week block that compound is running. The shape is free — it is what tells you whether this fits your life. The doses for each phase are the members half.
Fix what has mortality data before adding what has mechanism.
Arm one only if your panel supports it. A statin with a normal ApoB is treating a number that was fine. Get the before-panel first — this is the one goal where starting without baseline data makes the whole protocol uninterpretable.
The most replicated mechanism in the field, on top of a foundation that is already working.
Rapamycin weekly, never daily. The schedule is the mechanism — pulsed dosing inhibits mTORC1 while sparing mTORC2, and continuous dosing does not. This is the single most important detail on the page.
Short high-dose pulses, not a daily addition.
2–3 days on, then weeks off. A senolytic taken daily is not a senolytic protocol — you are trying to trigger apoptosis in a cell population, not maintain a level.
Re-run the panel and drop anything that has not moved a number or a symptom.
This is the discipline the whole goal lacks. Most longevity stacks only grow. If twelve months of a compound has produced no change in any marker you can measure and nothing you can feel, that is a result — and the correct response is to stop paying for it.
The stack should get shorter over time, not longer.
This is the category most prone to accumulation — items get added on mechanism and never removed on evidence. Once a year, stop everything without hard outcome data and see what you miss. The ApoB and blood pressure arm is the part to never stop.
The doses for each phase are inside
Every compound above, dosed week by week, plus the reconstitution numbers and Coach Cam's notes on running it. $10/mo.
Unlock the schedule →Bloodwork
This is the goal where bloodwork is not optional — it is the only way to know whether any of it is working. Nothing here produces a feeling you can trust. ApoB and Lp(a) are the two that change what you do. ApoB counts the atherogenic particles and is a better predictor than LDL-C, which only estimates the cholesterol inside them. Lp(a) is largely genetic, is not lowered by statins, and is worth measuring exactly once in your life — if it is high, that reframes how aggressively everything else is worth treating. hs-CRP, HbA1c and fasting insulin are the three that move with the mechanism arms and tell you whether they are doing anything.
Before you start
Everything, drawn before you start. This is the one that decides which pathway is actually yours - and the only one you cannot go back and collect later.
Around week 8
The short list, drawn while you are running it. Not a progress report - it is the draw that catches the things that go wrong quietly.
After
Drawn at the end, against your own baseline. This is what turns the protocol into information rather than a feeling.
All three are drawn at Quest, 2,000+ US locations, no doctor visit, HSA/FSA eligible. Prefer to pick and choose? Every marker above links to its own page, and the panel builder assembles any combination.
Adjusting it
A protocol you cannot adjust is a protocol you abandon. Four situations come up on nearly every run of this — nausea that will not settle, a three-week stall, hair shedding, glucose moving the wrong way. Each one has a specific answer, and the wrong answer to a stall is the reason most people end up on six compounds that each do nothing.
The four decision rules are inside
What to change, what to leave alone, and how to tell a real stall from a water shift. $10/mo.
Unlock the decision rules →The lines I'd stop at
- Any unexplained lump, persistent night sweats, or unintended weight loss. Several arms here act on cell growth and clearance pathways, and nothing on this page is worth running while an unexplained finding is unexplained.
- Signs of infection while on rapamycin — fever, spreading redness, anything not resolving. It is an immunosuppressant, and that is not a theoretical property.
- Muscle pain with dark urine on a statin. That is the rhabdomyolysis presentation, it is rare, and it is a same-day problem rather than a wait-and-see one.
- Any new mouth ulcers, poor wound healing or repeated infection on rapamycin. That is the immunosuppressive effect and it is the reason the dosing is intermittent.
- Muscle pain with dark urine on a statin. Rare, and the reason the muscle question is taken seriously.
- New shortness of breath or a persistent dry cough on rapamycin — pneumonitis is uncommon but it is the serious one.
It is built for the common case, not for you specifically. Compound selection and dosing genuinely do change person to person — training age, bloodwork, what you have run before, what you react to. Adjust it against your own numbers using the panels above, or if you want it built around your labs rather than the average, that is what 1-on-1 coaching is for.