Why we measure it

Atherosclerosis begins when an atherogenic lipoprotein particle enters the subendothelial space of an arterial wall. The probability of that event is determined by particle number, not by how much cholesterol each particle carries. LDL cholesterol measures the cargo; ApoB measures the number of delivery vehicles. Large-scale analyses — including a meta-analysis of over 300,000 patients — have found ApoB to be a superior predictor of cardiovascular events compared to LDL-C, non-HDL-C, and the total-to-HDL cholesterol ratio. The discordance between LDL-C and ApoB is particularly important in people with metabolic syndrome, insulin resistance, or elevated triglycerides, where small dense LDL particles carry less cholesterol per particle — meaning LDL-C can appear normal while ApoB, and therefore particle number, is substantially elevated. The 2019 ESC/EAS Guidelines for Dyslipidaemias and the European Atherosclerosis Society now formally recommend ApoB as the preferred metric for assessing atherogenic burden and treatment targets. ApoA-I, measured alongside ApoB, is the principal structural protein of HDL particles. The ApoB/ApoA-I ratio captures the balance between atherogenic and atheroprotective particles — a more complete cardiovascular risk signal than either alone.

Why every 3 months

Lipid particle concentrations respond to diet, exercise, body weight, medications, and metabolic state on a timescale of weeks to months — comparable to LDL cholesterol. Quarterly measurement provides the resolution to see the directional effect of lifestyle changes and to distinguish a true sustained shift from normal biological variation. For people actively working on cardiovascular risk reduction, annual measurement means waiting 12 months to learn whether an intervention is working. Quarterly measurement allows meaningful course correction within a year rather than waiting for the next annual cycle.

What movement means

The 2019 ESC/EAS Guidelines for the Management of Dyslipidaemias set ApoB targets that vary by individual risk profile — below 100 mg/dL for moderate-risk individuals, below 80 mg/dL for high-risk, and below 65 mg/dL for very high-risk individuals with established cardiovascular disease. These are clinical targets set by external guideline bodies, not by Nexuses. What the data provides is the trend across draws: the direction and rate of change in response to whatever is happening in your life — diet, exercise, medication, metabolic state.

In the protocol