In one sentence
Every particle that can lodge in an artery wall (LDL, the triglyceride-rich VLDL and IDL, and lipoprotein(a)) carries exactly one molecule of apolipoprotein B, so measuring ApoB counts those particles instead of weighing the cholesterol inside them.
Why it matters
Two particles can carry the same cholesterol and be very different in number: many small, cholesterol-poor particles or a few large, cholesterol-rich ones. The particle count is what the cohorts followed. Among 389,529 UK Biobank adults not taking lipid-lowering medicines, followed for a median of 11.1 years, ApoB, non-HDL cholesterol and triglycerides were each associated with incident myocardial infarction on their own, but when assessed together only ApoB remained (adjusted hazard ratio 1.27 per standard deviation), and for a given ApoB the mix of particle types no longer added anything (Marston 2022). A meta-analysis of twelve studies with 233,455 participants and 22,950 events put ApoB ahead of non-HDL cholesterol, and non-HDL ahead of LDL cholesterol, as a marker of ischemic cardiovascular events (Sniderman 2011). The European consensus that LDL causes atherosclerotic cardiovascular disease made the same point: the benefit of lowering LDL cholesterol holds where the fall in cholesterol is matched by a fall in particle number (Ference 2017).
What moves it
The same things that move LDL cholesterol, and one more: insulin resistance and high triglycerides fill the blood with small, dense particles that carry little cholesterol each, so ApoB rises while LDL cholesterol may not. Weight, saturated fat, an underactive thyroid and the familial hypercholesterolemia genes raise it; the changes that lower LDL cholesterol lower it too, over weeks.
How to measure it well
No fasting is needed; ApoB is unaffected by a meal (Nordestgaard 2016). Ask for the result in g/L, the New Zealand unit; VT converts mg/dL by dividing by 100. It is usually a self-pay addition to the same draw in New Zealand. Re-test ten to twelve weeks after a diet or treatment change; a re-test before week eight is early.
How Vitality Tracker uses it
Stored as reported, with the laboratory's range and flag, never overridden. Typical New Zealand laboratory reference < 1.2 g/L; VT's working optimal (v0.1) < 0.8 g/L, shown beneath in smaller type with the word working until the clinical advisor has reviewed it. When a lipid profile from the same draw exists, VT computes the ApoB-to-LDL discordance (its own entry) and shows it in the lipids panel and the pre-visit report; a result outside the laboratory's own range prompts the consultation suggestion in the How it works page's words.
How far to trust the number
Laboratory: an immunoassay standardized against an international reference material, with small analytical error; it varies less from day to day within a person than LDL cholesterol does, because it does not depend on the triglyceride result the way a calculated LDL does.
The ranges
The laboratory’s range and flag are shown with your result and never overridden; the working optimal stays beneath, in smaller type, until the clinical advisor has reviewed it.
Sources
- Marston NA, et al. Association of apolipoprotein B-containing lipoproteins and risk of myocardial infarction in individuals with and without atherosclerosis: distinguishing between particle concentration, type, and content. JAMA Cardiol 2022;7:250–6. doi:10.1001/jamacardio.2021.5083
- Sniderman AD, et al. A meta-analysis of low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, and apolipoprotein B as markers of cardiovascular risk. Circ Cardiovasc Qual Outcomes 2011;4:337–45. doi:10.1161/CIRCOUTCOMES.110.959247
- Ference BA, et al. Eur Heart J 2017. doi:10.1093/eurheartj/ehx144
- Nordestgaard BG, et al. Eur Heart J 2016. doi:10.1093/eurheartj/ehw152
- Vitality Tracker, Recommended baseline lab panel v0.1; optimal set v0.1 (working).