The Cardiovascular Blueprint
Five arms — and most people only need two of them
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.
Cardiovascular risk is not one number and it is certainly not cholesterol alone. Five separable things drive it, and the interventions do not substitute for each other. How many atherogenic particles are circulating — that is ApoB, and it is the arm with the strongest causal evidence in all of medicine. Whether the vessel wall itself is working — endothelial function, which is where blood pressure actually lives. Whether your blood clots too readily, and what your Lp(a) is — the residual risk that stays after the LDL is fixed. Whether the muscle has the energy to pump. Whether blood gets back from your legs. One panel and one blood-pressure cuff sorts you into the two that matter for you. That is the entire job of this page.
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 5 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
The ApoB arm is the single best-evidenced intervention on this website and it is not close. Randomised trials, mendelian randomisation and dose-response all agree, across hundreds of thousands of people. Nothing else in the Vault has that. That is worth stating plainly because it cuts against the temptation of this space: the most interesting compound on this page is not the most useful one. The supplement lanes here are real and several have genuine randomised data, but where a prescription option has outcome trials and a botanical has surrogate markers, the page says so rather than flattening the difference.
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.
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.
Purified EPA with no DHA, and the distinction is the whole point: mixed EPA/DHA preparations raise LDL, and the outcome trial that showed a genuine event reduction on top of a statin used the DHA-free formulation. It lowers triglycerides, stabilises plaque and has an antithrombotic effect.
Fish oil is a fraction of the price and it lowers triglycerides too. It also raises LDL, because the DHA does — which on this page is working against the arm above it. That is the entire argument, and it is why the trials that used mixed EPA/DHA at these doses did not show what the EPA-only trial did. If triglycerides are only mildly raised and ApoB is already at target, ordinary omega-3 is a perfectly reasonable, much cheaper answer.
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.
A fibrinolytic enzyme from fermented soy — it degrades fibrin directly. The only lane here acting on clot breakdown rather than clot prevention.
The trade-off Genuine bleeding risk stacked with aspirin, anticoagulants or surgery. Stop two weeks before any procedure.
The only widely available thing that lowers Lp(a) — by roughly 20–30%. That matters because Lp(a) is genetic, common, and almost nothing touches it.
The trade-off The outcome trials were negative on top of a statin, and it raises glucose and uric acid. Flushing is universal. Never use the slow-release form — that is the hepatotoxic one.
Aged extract specifically — it has randomised data on coronary calcium progression, which is a structural endpoint rather than a lipid one, and almost nothing over the counter has that.
The trade-off Aged extract is not fresh garlic and not garlic oil; the data does not transfer. Mild antiplatelet effect that stacks.
Activates matrix Gla protein, which is the body's own inhibitor of arterial calcification — it directs calcium into bone and away from the vessel wall.
The trade-off Directly antagonises warfarin. The trial data on reversing existing calcification is weaker than the mechanistic case suggests.
A more potent fibrinolytic than nattokinase per milligram, with a longer half-life.
The trade-off Same bleeding considerations, magnified. Very little Western trial data and it is expensive.
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.
ApoB & LDL particle reductionPlant Sterols & Stanols5 options
5 options — 1 to swap in, 4 to stack ontap to collapse
Endothelial function & nitric oxideBeetroot (Nitrates)6 options
6 options — 0 to swap in, 6 to stack ontap to collapse
Cardiac energetics & heart failure supportUbiquinol5 options
5 options — 0 to swap in, 5 to stack ontap to collapse
Venous & microcirculationDiosmin4 options
4 options — 0 to swap in, 4 to stack ontap to collapse
The 16-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.
| 0 | 1–6 | 7–8 | 9–16 | Ongoing | |
|---|---|---|---|---|---|
| Rosuvastatin | |||||
| Beetroot (Nitrates) | |||||
| Icosapent Ethyl |
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.
ApoB, a full lipid panel, Lp(a), hs-CRP, CMP, HbA1c.
Lp(a) is genetic and does not meaningfully change, so it is a one-time test that reframes everything else. A high result moves the ApoB target down and makes the residual-risk arm relevant regardless of your other numbers. Most people have never had it drawn.
Start the arm your numbers assigned.
Home readings beat clinic readings for deciding anything. Seated, five minutes rest, arm at heart level, twice a day for a week. One clinic number is not a diagnosis and it is not a reason to start a drug.
Lipids and a CMP. Six weeks is when a statin effect is fully expressed.
Statin effect plateaus by about six weeks — there is no reason to wait three months to find out whether it worked. If ApoB has not moved enough, that is the point to add ezetimibe rather than double the statin: doubling buys about 6% more, adding ezetimibe buys about 20%.
Residual risk, energetics or venous — whichever applies.
Triglycerides above 150 with ApoB already at target is the specific signature that says the residual-risk arm is next, rather than more of the first one.
Cumulative exposure is the thing that causes the event.
Atherosclerosis is driven by particle-years, not by your current number. A statin taken for two years and stopped returns you to the original trajectory. This is the one arm on the entire site where stopping because you feel fine is the mistake.
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
ApoB is the number, not LDL-C. LDL-C estimates how much cholesterol is being carried; ApoB counts the particles carrying it, and one ApoB molecule sits on every atherogenic particle. When the two disagree — which happens constantly in insulin resistance and high triglycerides — ApoB is right and LDL-C is reassuring you wrongly. Lp(a) is the once-in-a-lifetime draw. It is genetic, roughly one in five people has a raised level, and it is invisible on a standard panel. hs-CRP is the inflammation half of risk and it is independent of lipids — raised ApoB with raised hs-CRP is a materially different situation from raised ApoB alone. Lp-PLA2 and MPO extend that picture toward plaque activity specifically.
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
- Chest pain, pressure or jaw and arm pain on exertion. That is not something to titrate around — it is an emergency assessment.
- Sudden severe leg swelling with pain and warmth, particularly one side. That is the deep vein thrombosis presentation, and the venous arm does not treat it.
- Any unusual bleeding or bruising on nattokinase, lumbrokinase or high-dose omega-3, especially alongside aspirin or an anticoagulant.
- Dark urine with severe generalised muscle pain on a statin — rhabdomyolysis is rare, and it is the reason the muscle question is always taken seriously.
- New or worsening breathlessness lying flat, or waking short of breath. That is a heart failure presentation and the energetics arm is an adjunct to treatment, not a substitute for diagnosis.
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.