Medicine 3.0 · Evidence-based
About this calculator
🫀
Why cumulative apoB exposure?
Atherosclerosis is driven not just by how high apoB is, but by how long it has been elevated. A person with apoB 100 mg/dL for 40 years has accumulated the same atherogenic burden as someone with apoB 200 mg/dL for 20 years — yet standard lipid panels capture only a snapshot. This calculator integrates apoB over time (mg/dL-years) to estimate total lifetime exposure, contextualizes it against validated population thresholds, and models how treatment timing changes the trajectory.
Step 1
Past Exposure
Reconstructs cumulative apoB from birth to today using measurements and validated population models. Outputs total mg/dL-years and CARDIA risk placement.
Step 2
Future Scenarios
Compares treat-now vs. delay 10/20/30 years vs. never treat. Quantifies exposure avoided and CHD risk reduction from apoB lowering (Thanassoulis 2014).
Step 3
Lifetime Graph
Overlays all scenarios from birth to age 90 with CARDIA cohort thresholds and Ference Mendelian randomization MI risk lines.
Scope: This tool estimates relative atherogenic burden — not absolute MACE probability. It does not incorporate blood pressure, smoking, diabetes, or inflammatory markers. Use alongside PCE / PREVENT / MESA for absolute risk. All assumptions are in the methodology notes below.
1Past Exposure — Birth to Present

Enter all available lipid measurements to reconstruct cumulative apoB burden. Surrogates (LDL-C, non-HDL-C) are converted automatically.

How to enter measurements
Enter all available apoB, LDL-C, or non-HDL-C values at any age, on or off therapy. On-therapy values are included in the AUC (they represent real exposure) but excluded from childhood quartile assignment (which requires natural, untreated apoB). Surrogates are converted to apoB using Sayed et al. JAMA Cardiol 2024 quantile regression (NHANES, n=12,688).[1][2]
Age (yrs) Value (mg/dL) Metric Therapy status Notes (optional)
About pediatric inputs
Direct apoB only (no surrogate conversion for pediatric window). Off therapy only. Age-specific norms from Perak et al. JAMA 2019 (NHANES, n=26,047).[3]
Age (yrs) ApoB (mg/dL)
Results — Birth to Age
Childhood Quartile — Birth to Age 18 [4]
Q1
Q2
Q3
Q4
<1,232
mg/dL-yrs
1,232–1,378
mg/dL-yrs
1,378–1,524
mg/dL-yrs
>1,524
mg/dL-yrs
Individual Trajectory — Birth to Present
Exposure breakdown by age window
Age WindowAvg ApoB (mg/dL)Duration (yrs) Exposure (mg/dL-yrs)Basis
📚 Methodology notes & evidence sources
  1. [1] On-therapy values: Measured apoB during lipid-lowering therapy represents actual atherogenic exposure and is included in the cumulative AUC. On-therapy values are excluded only from childhood quartile assignment, which requires natural (untreated) apoB. Statins lower LDL-C ~5 mg/dL more than apoB on average (Ridker et al. Eur Heart J 2016; Sniderman J Clin Lipidol 2008).
  2. [2] Surrogate conversions (LDL-C / non-HDL-C → apoB): Sayed et al. JAMA Cardiol 2024 (NHANES 2005–2016, n=12,688). At LDL-C=100 mg/dL, 95% population range of apoB is 66–99 mg/dL. Personal concordance offset applied when paired measurements exist.
  3. [3] Pediatric apoB norms: Nielsen et al. EHJ 2023 (cord blood, 2 months, 14–16 months); Srinivasan et al. Metabolism 1982 (Bogalusa, ages 6–18 scaled for modern assay); Perak et al. JAMA 2019 (NHANES, n=26,047). Population AUC birth–18: mean ~1,378 SD ~216 mg/dL-years.
  4. [4] Childhood quartile assignment: Earliest untreated adult apoB used for quartile inference via Wilkins et al. CARDIA 2022 (r=0.63, childhood apoB explains ~40% adult apoB variance). Quartile medians: Q1=1,103, Q2=1,309, Q3=1,447, Q4=1,652 mg/dL-years. ±1 quartile uncertainty at individual level.
  5. [5] Untreated apoB trajectory: +0.52 mg/dL/yr from Wilkins et al. J Lipid Res 2022 (CARDIA longitudinal). SD ~1.0 mg/dL/yr; observed range −6.26 to +9.21. Applied current age to 55, then plateau.
  6. [6] CARDIA risk thresholds (ages 18–40 only): Zheutlin et al. Eur Heart J 2025 (CARDIA, n=4,366, NMR-apoB). HR 1.30 per SD for incident ASCVD after 40. CARDIA Q1–Q4 event rates: 1.7, 1.8, 3.1, 5.0 per 1,000 person-years. Applies only to 18–40 window; not extrapolated.
  7. [7] Ference cumulative LDL-C thresholds: Mendelian randomization synthesis. ~5,000 mg/dL-years LDL-C ≈ 1% MI risk at age 40. Risk doubles each additional 1,250 mg/dL-years. Population-level MR constructs — not validated individual risk predictions. Shown as reference context only.
  8. [8] CHD risk reduction — Thanassoulis et al. JAHA 2014: 7 placebo-controlled statin RCTs. RRR 24.4% per 27 mg/dL apoB reduction (1 SD). Important: Thanassoulis measures the relationship between a change in concentration (baseline minus achieved level after ~1 year) and CHD event reduction — it does not model cumulative exposure over time. The apoB-years architecture derives from CARDIA (Zheutlin 2025) and Ference (MR). Thanassoulis is used solely to convert an apoB reduction goal to estimated RRR. Limitations: statin-only data; CHD events not full MACE; assumes sustained reduction; RRR is relative.
  9. [9] Ference→apoB concordance: Ference thresholds are in LDL-C-years. Converted using patient's personal apoB/LDL-C ratio when paired measurements exist (within 5 years, off therapy). Otherwise Sayed 2024 population median (~0.78 at LDL-C 125 mg/dL). Ratio varies 0.74–0.89 across LDL-C spectrum; ±20 mg/dL individual variation (Sayed IQR). This is an inferential extension not directly validated.