Why Testing Your ‘Good and Bad’ Cholesterol Doesn’t Tell the Whole Story: Understanding ApoB and Lp(a)
Introduction - The Limits of Standard Cholesterol Testing
For decades, cholesterol was simplified into “good” (HDL) and “bad” (LDL). That model, while helpful, overlooks a crucial reality: heart-disease risk is determined not only by how much cholesterol you have, but by how many particles are carrying it [1–3].
Two people can share the same LDL value yet have very different risks. The difference lies in Apolipoprotein B (ApoB) - a test now considered by many experts to be the most accurate predictor of atherosclerotic cardiovascular disease (ASCVD).
At LifespanMD™, we use advanced lipid testing to measure true cardiovascular risk - including ApoB, Lp(a), and hs-CRP - as part of every Comprehensive Wellness Assessment.
What Is ApoB and Why It Matters - Each Particle = Potential Plaque
Every atherogenic lipoprotein (LDL, IDL, VLDL, Lp(a)) carries exactly one ApoB protein on its surface [4]. Each of those particles can infiltrate arterial walls, trigger inflammation, and form plaque. Therefore, ApoB concentration reflects the number of “particles of risk,” not just the cholesterol inside them.
Traditional LDL-C can appear normal even when ApoB is elevated - especially in insulin resistance or metabolic syndrome. Measuring ApoB gives a clear, particle-based assessment of vascular stress [5].
Lp(a): The Genetic Risk Few People Test For
Lipoprotein(a) - Lp(a) - is an LDL-like particle with an added sticky apolipoprotein(a) chain. Lp(a) raises inflammation, promotes clotting, and accelerates plaque buildup [6]. About 20 % of Canadians have high Lp(a); it’s purely genetic and often missed by standard panels. Although lifestyle has little effect, knowing your Lp(a) level allows your physician to intensify prevention and, soon, prescribe new targeted drugs now in Phase III trials [7].
Dr. Sam Hetz on Early Detection
“Two people can have identical LDL numbers but entirely different risks,” explains Dr. Sam Hetz, Co-Founder of LifespanMD™. “ApoB and Lp(a) testing moves us to a more accurate risk stratification.” Detecting elevated ApoB and Lp(a) in your 30s or 40s lets you intervene decades before symptoms appear.
Lifestyle Interventions That Lower ApoB Naturally
Nutrition: Limit refined carbs and trans fats; favour extra-virgin olive oil, oily fish, nuts, legumes, and soluble fibre [8].
Exercise: 150 min/week of Zone 2 training and one Zone 5 session improve lipid particle size and insulin sensitivity [9].
Sleep: 7–8 hours nightly lowers cortisol and triglycerides [10].
Stress control: Mindfulness, breathwork, and consistent recovery blunt sympathetic drive and endothelial injury.
Even modest weight loss can drop ApoB by 10–15 %.
When to Consider Therapy
If ApoB remains elevated despite lifestyle optimization - or if Lp(a) is high - medical therapy may be warranted.
Statins: Lower ApoB by 30–50 % and reduce events ~25 % [11].
Ezetimibe: Adds 15–20 % additional ApoB reduction.
PCSK9 inhibitors: Lower ApoB and Lp(a) by ≈ 60 %; proven outcome benefit [12].
Emerging agents: Inclisiran (siRNA) and pelacarsen (antisense to Lp(a)) show > 80 % reductions in trials [13].
How LifespanMD Integrates These Tests Into Prevention
Your Comprehensive Wellness Assessment includes:
ApoB and Lp(a) bloodwork
Inflammation markers (hs-CRP) and other metabolic health biomarkers.
VO₂ max testing for cardiorespiratory fitness
Visbody S30 composition.
This integrative approach connects metabolic, cardiovascular, and hormonal data into one personalized prevention plan, with 6-month follow-ups to ensure measurable progress. Heart disease is still Canada’s #1 killer - but it’s largely preventable. By adding to classic “good vs bad” cholesterol models with advance testing such as ApoB and Lp(a) testing, you can quantify your risk and act early.
References
Sniderman AD et al. Apolipoprotein B and atherosclerotic cardiovascular disease: pathophysiology and clinical significance. Nat Rev Cardiol. 2019;16(4):222-233.
Ference BA et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease: 1 consistent evidence from genetics and clinical trials. Eur Heart J. 2017;38(32):2459-2472.
Grundy SM et al. 2018 AHA/ACC Cholesterol Guideline. Circulation. 2019;139:e1082-e1143.
Nordestgaard BG, Varbo A. Triglycerides and ApoB-containing lipoproteins as causes of ASCVD. Lancet. 2014;384:626-635.
Wilkins JT et al. Discordance between LDL-C and ApoB levels and cardiovascular risk. JAMA Cardiol. 2016;1(6):619-626.
Tsimikas S. Lp(a): novel target and marker for residual cardiovascular risk. Curr Atheroscler Rep. 2023;25:33-45.
Nissen SE et al. Pelacarsen for Lp(a) reduction. N Engl J Med. 2022;387:1833-1844.
Hu FB et al. Mediterranean diet and risk of cardiovascular disease. N Engl J Med. 2018;378: e34.
Ross R et al. Cardiorespiratory fitness and risk of coronary heart disease. Circulation. 2016;134(24):e653-e699.
Irwin MR et al. Sleep and inflammation: partners in illness. J Clin Invest. 2016;126(10):3762-3773.
Cholesterol Treatment Trialists’ (CTT) Collaboration. Lancet. 2010;376:1670-1681.
Sabatine MS et al. Evolocumab and clinical outcomes in patients with cardiovascular disease. N Engl J Med. 2017;376:1713-1722.
Ray KK et al. Inclisiran for LDL cholesterol lowering. N Engl J Med. 2020;382:1507-1519.
