Provider Tools

Advanced Lipid Panel Interpreter

2026 ACC/AHA Dyslipidemia Guideline implementation. Calculate, Personalize, Reclassify. PREVENT-ASCVD risk scoring with interactive intervention modeling.

Lipid Panel

~2.5 nmol/L per 1 mg/dL

The 2026 guideline recommends ApoB over LDL-P for clinical decision-making. LDL-P is shown for reference.

ASCVD Risk Assessment

PREVENT is for primary prevention only. If the patient has established ASCVD, check the box above instead.

Don't know your eGFR? It's calculated from creatinine on a metabolic panel.

Goal Setting and Gap Analysis

Enter lipid panel values and complete the risk assessment above for personalized targets.

Intervention Modeling

These interventions reduce cholesterol production in the liver. Select one.

50% LDL-C reduction
Atorvastatin 40-80 mg, rosuvastatin 20-40 mg
38% LDL-C reduction
Atorvastatin 10-20, rosuvastatin 5-10, simvastatin 20-40, pravastatin 40-80
25% LDL-C reduction
20% LDL-C reduction
Contains monacolin K, which is identical to lovastatin. Same mechanism, same interaction profile. Do not combine with a statin.

These interventions reduce cholesterol absorbed from the gut.

23% additional LDL-C reduction
9% LDL-C reduction
7% LDL-C reduction

These interventions increase the liver's clearance of LDL particles from the blood.

55% additional LDL-C reduction
50% additional LDL-C reduction
17% LDL-C reduction
Also suppresses PCSK9 expression and activates AMPK. Separate from PCSK9 inhibitor antibodies; stacking is reasonable.
20% LDL-C reduction
Upstream of HMG-CoA reductase. Can be combined with a statin; acts on a different enzyme in the same pathway.
20% LDL-C reduction
Evidence is limited; effect may be smaller than reported.
17% LDL-C reduction
Controlled metabolic ward studies show up to 35%. The 17% figure reflects real-world adherence.
-11 mg/dL LDL-C (absolute)
7% LDL-C reduction
-7 mg/dL LDL-C (absolute)
Exercise's cardiovascular benefit extends far beyond LDL-C reduction. Most benefit is through improved endothelial function, BP reduction, insulin sensitivity, and HDL functionality.
-1.28 mg/dL per kg
Each kg lost also reduces TG by ~4 mg/dL and increases HDL-C by ~0.5 mg/dL. Source: JCEM 2020 meta-analysis (73 RCTs, n=32,496).
Minimal LDL-C impact, but HDL-C increases ~5-10% and ASCVD risk drops substantially through non-lipid pathways. One of the highest-impact interventions for cardiovascular risk.
Lipoprotein Metabolism Pathway

Active interventions are highlighted where they act on the pathway.

How this works

This tool implements the 2026 ACC/AHA Dyslipidemia Guideline's CPR framework: Calculate risk with the PREVENT-ASCVD equations, Personalize with risk-enhancing factors, Reclassify with coronary artery calcium scoring.

PREVENT replaces the old Pooled Cohort Equations, which overestimated 10-year risk by 40-50% in modern populations. PREVENT is sex-specific, race-free, and incorporates kidney function and BMI. The PREVENT model uses a logistic regression framework with piecewise linear splines for systolic blood pressure (knot at 110 mmHg), eGFR (knot at 60 mL/min), and BMI (knot at 30 kg/m²), plus age-interaction terms for most predictors.

LDL-C is calculated three ways. Most US labs still report Friedewald (1972), which divides triglycerides by a fixed factor of 5. The Sampson-NIH equation (2020) uses a regression model that remains accurate at much higher triglyceride levels. When triglycerides are elevated, these equations diverge, and Friedewald systematically underestimates LDL-C, which means some patients appear to be at goal when they are not.

ApoB measures the number of atherogenic particles directly. Each LDL, VLDL, IDL, and Lp(a) particle carries exactly one ApoB molecule. When LDL-C looks normal but ApoB is elevated, the patient has more small, dense particles than the cholesterol content suggests. The 2026 guideline recommends ApoB measurement and provides numeric targets aligned with LDL-C categories.

The ancestral LDL-C baseline. Hunter-gatherer populations, healthy human neonates, free-living primates, and wild mammals maintain LDL-C levels of 50-70 mg/dL and do not develop atherosclerosis. The Tsimane of Bolivia, a forager-horticulturalist population, have a mean LDL of 91 mg/dL and the lowest reported prevalence of coronary atherosclerosis of any population studied. The modern Western average of 110-130 mg/dL is approximately double the ancestral baseline. Every intervention in this tool, whether cooking with whole foods, adding fiber, walking after dinner, or taking rosuvastatin, is moving the needle back toward where human biology expects it to be.

Interventions are organized by mechanism, not by "pharmaceutical vs natural." Red yeast rice and lovastatin are the same molecule acting on the same enzyme. Ezetimibe and plant sterols both reduce intestinal cholesterol absorption through overlapping mechanisms. The clinical question is not "drug or supplement" but "which combination closes the gap between where you are and where your body needs to be, given your risk and your values."

The stacking model uses multiplicative reduction because each successive intervention acts on a smaller remaining pool of LDL-C. A statin that reduces LDL-C by 50% plus ezetimibe that reduces the remainder by 23% yields a total reduction of about 62%, not 73%.

Low LDL-C achieved through treatment is safe for the brain. The brain synthesizes virtually all of its own cholesterol behind the blood-brain barrier; circulating LDL does not cross it in meaningful quantities. The largest meta-analysis to date (55 studies, 7+ million patients) found statin use associated with a 14% reduction in dementia risk. Participants in clinical trials with LDL-C below 25 mg/dL showed no cognitive decline.

References

  1. 2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia. Circulation. 2026.
  2. Khan SS, Matsushita K, Sang Y, et al. Development and Validation of the American Heart Association's PREVENT Equations. Circulation. 2024;149(6):430-449.
  3. Sampson M, Wolska A, Meeusen JW, Otvos J, Remaley AT. The Sampson-NIH Equation Is the Preferred Calculation Method for LDL-C. Clinical Chemistry. 2024;70(2):399-402.
  4. O'Keefe JH, Cordain L, Harris WH, Moe RM, Vogel R. Optimal Low-Density Lipoprotein Is 50 to 70 mg/dl. J Am Coll Cardiol. 2004;43(11):2142-2146.
  5. Kaplan H, Thompson RC, Trumble BC, et al. Coronary atherosclerosis in indigenous South American Tsimane. Lancet. 2017;389(10080):1730-1739.
  6. Westphal Filho FL, Lopes PRM, de Almeida AM, et al. Statin use and dementia risk: A systematic review and updated meta-analysis. Alzheimers Dement (N Y). 2025;11(1):e70039.
  7. Selma-Permana H, et al. Weight Loss and Serum Lipids in Overweight and Obese Adults: A Systematic Review and Meta-Analysis. J Clin Endocrinol Metab. 2020;105(12):3695-3703.
  8. Smart NA, et al. The Effect of Exercise Training on Blood Lipids: A Systematic Review and Meta-analysis. Sports Medicine. 2024.
  9. Chiavaroli L, et al. Portfolio Dietary Pattern and Cardiovascular Disease: Systematic Review and Meta-analysis. Prog Cardiovasc Dis. 2018;61(1):43-53.
This tool is for healthcare provider education and clinical decision support. It implements guideline-based risk assessment and intervention modeling using published clinical data. It does not replace individualized clinical assessment, shared decision-making, or serial lab monitoring. All therapy decisions should be made in the context of the whole patient.