Particle-level cardiovascular risk insight
Enter your lipid values first, then tap
Analyze My Particles
Imagine your blood vessels as a smooth highway. ApoB-containing particles are cars driving through. Inflammation creates potholes in the vessel walls. The more cars on the road, the more likely some will crash into those potholes — getting stuck and forming plaques.
Risk isn't about how heavy each car is — it's about how many cars are on the road. That's why ApoB (particle count) matters more than LDL-C (cholesterol weight).
Drag the slider to see how more particles increase collision risk with the artery wall.
Two people can have the exact same LDL-C (total cholesterol mass) but very different risk profiles. What matters is the number of particles carrying that cholesterol.
Each ApoB particle — regardless of size — can penetrate the artery wall and start plaque formation. More particles = more lottery tickets for a bad outcome. This is why ApoB (particle count) predicts risk better than LDL-C (particle weight).
Think of cholesterol and triglycerides as cargo. Lipoproteins are the ships carrying that cargo through your blood. Each ship has exactly one ApoB label — so counting ApoB = counting ships.
When triglycerides rise, each ship carries more triglyceride cargo — meaning less room for cholesterol per ship. Your body compensates by launching more ships to transport the same cholesterol. More ships = higher ApoB = higher risk — even if total LDL-C stays the same!
1. ApoB counts every atherogenic particle. It's the single best predictor of cardiovascular risk.
2. LDL-C measures cholesterol mass — useful but can be misleading when discordant with ApoB.
3. Lp(a) is genetically determined. If high, it demands even more aggressive ApoB reduction.
4. Peter Attia's target: ApoB under 60 mg/dL — the 5th population percentile. "As low as possible, as early as possible."