Thrombosis, Lp(a) & residual risk
One of 5 mechanistic pathways to 🫀 Heart, cholesterol & blood pressure · 13 options
Plaque doesn't kill you — the clot on a ruptured plaque does. And Lp(a) is genetically determined, unaffected by diet and lifestyle, raised in about one in five people, and almost never tested. If you measure one unusual thing in your life, measure this once.
Measure Lp(a) once in your life. It is genetic, unmoved by diet or exercise, raised in about one in five people, and almost never ordered — and it changes how aggressively everything else on this page should be treated.
Lipoprotein(a) — Lp(a)Fibrinogen ActivityD-DimerLp-PLA2 ActivityMyeloperoxidase (MPO)Factor V Leiden Mutation, DNAFactor II Activity (Prothrombin)Homocysteine🩸 Clotting & Advanced Cardiac Risk covers these in one panel →
What engages this pathway
Ordered by how directly each one acts on the mechanism above — never by how much trial evidence exists. Each links to its full breakdown with dosing, half-life and vendor.
💉 Icosapent Ethyl
Purified EPA. REDUCE-IT showed a 25% relative risk reduction in cardiovascular events beyond statin therapy — larger than triglyceride lowering alone explains, implying plaque stabilisation.
🧬 Super EPA (Fish Oil)
High-EPA concentrate — the fraction that carried the benefit in trials.
🧬 Omega-3 (Fish Oil)
Mixed EPA/DHA. Trial results are more mixed than EPA-only, which is itself informative about which component matters.
🧬 Nattokinase
A fibrinolytic enzyme from fermented soy with trials showing reduced fibrinogen and, in one, reduced carotid plaque. Real anticoagulant interaction risk.
🧬 Lumbrokinase
A more potent fibrinolytic enzyme complex. Same interaction caution.
🧬 Serrapeptase
Proteolytic with fibrinolytic claims; weaker evidence than nattokinase.
🧬 Aged Garlic Extract
Reduced coronary calcium progression in randomised trials using CT scoring — one of very few supplements with a structural imaging endpoint.
🧬 Niacin (Flush)
Lowers Lp(a) by 20–30% — the only widely available agent that does — and failed to improve outcomes in two large trials. The disconnect is worth understanding.
🧬 Vitamin K2 Complex
Activates matrix Gla protein, which inhibits arterial calcification. The Rotterdam study linked higher K2 intake to substantially lower cardiac mortality.
🧬 NAC
Small studies show it lowers Lp(a) and homocysteine; the mechanism involves disrupting the disulfide bond that assembles the Lp(a) particle.
🧬 Methylfolate (5-MTHF)
Lowers homocysteine reliably. Lowering homocysteine has not reduced events in trials, which is another instructive marker-versus-outcome gap.
🧬 SPMs (Pro-Resolving Mediators)
Plaque instability is an inflammatory process; resolution signalling is the mechanistically correct target.
🧬 Curcumin
Reduces hs-CRP in meta-analysis. Residual inflammatory risk is real — CANTOS proved reducing inflammation alone reduces events.
The other 4 routes to heart, cholesterol & blood pressure
Pick the pathway that matches where you are actually stuck. An appetite drug does nothing for someone who already undereats.
Want the protocols behind these?
Dosing schedules, stacking, cycle timing and Coach Cam's notes live inside the Academy — plus the full interactive Vault.
Join the Academy — $10/mo →← Open this pathway in the interactive Vault
Frequently asked questions
Plaque doesn't kill you — the clot on a ruptured plaque does. And Lp(a) is genetically determined, unaffected by diet and lifestyle, raised in about one in five people, and almost never tested. If you measure one unusual thing in your life, measure this once.
13 options are mapped to this pathway in the Vault, including Icosapent Ethyl, Super EPA (Fish Oil), Omega-3 (Fish Oil), Nattokinase. They are grouped by the mechanism they act through rather than ranked by how much trial evidence exists — 10 carry clinical validation and 3 are mechanistic predictions.
Measure Lp(a) once in your life. It is genetic, unmoved by diet or exercise, raised in about one in five people, and almost never ordered — and it changes how aggressively everything else on this page should be treated. The markers worth checking are Lipoprotein(a) — Lp(a), Fibrinogen Activity, D-Dimer, Lp-PLA2 Activity.
Unproven is not the same as ineffective. Of the 13 options on this pathway, 10 have clinical validation and 3 are graded theoretical — meaning the mechanism is sound but the specific human trial has not been run, which is true of a great deal of what works in this space. Nothing on this page is ordered by evidence tier, because sorting by trial count would bury the compounds you came looking for.