Low-density lipoprotein, or "bad"cholesterol
21 of 22 providers
Lipid Panel / Cardiovascular Health
Optimal:<100 mg/dL, Near optimal:100-129 mg/dL, Borderline high:130-159 mg/dL, High:≥160 mg/dL
LDL Cholesterol (Low-Density Lipoprotein Cholesterol) is often called "bad cholesterol"because elevated levels drive atherosclerosis—the buildup of cholesterol plaques in arteries causing heart attacks and strokes. LDL particles transport cholesterol from the liver to peripheral tissues. When LDL levels are excessive, cholesterol infiltrates artery walls, triggering inflammation and plaque formation.
LDL cholesterol is either directly measured or calculated using the Friedewald equation:LDL=Total Cholesterol - HDL - (Triglycerides/5). This calculation is inaccurate when triglycerides >400 mg/dL, requiring direct LDL measurement. Modern guidelines emphasize that LDL reduction is the primary target of lipid-lowering therapy—each 40 mg/dL reduction in LDL decreases cardiovascular events by ~20%.
While LDL-C (cholesterol content) is widely used, it has limitations. Two people with identical LDL-C can have different numbers of LDL particles. Someone with many small dense LDL particles (Pattern B) has higher cardiovascular risk than someone with fewer large buoyant particles (Pattern A) despite the same LDL-C. This is why advanced testing (ApoB, LDL particle number) provides superior risk assessment, especially when triglycerides are elevated.
| Range Type | Level | Significance |
|---|---|---|
| Optimal (Longevity) | <70 mg/dL | Associated with lowest cardiovascular risk. Population studies show LDL <70 mg/dL dramatically reduces atherosclerosis progression. Infants have LDL 30-70 mg/dL—likely our evolutionary baseline. Modern guidelines recommend <70 mg/dL for secondary prevention, <55 mg/dL for very high risk. |
| Near Optimal | 70-100 mg/dL | Acceptable for primary prevention in low-risk individuals. However, even this range causes gradual plaque accumulation over decades. Consider targeting <70 mg/dL if family history, diabetes, or other risk factors present. |
| Borderline to Moderately High | 100-189 mg/dL | 100-129 (Borderline):Lifestyle modification essential. Consider statin if diabetes or 10-year risk >7.5%. 130-159 (Moderately High):Statin therapy indicated if diabetes, known heart disease, or multiple risk factors. 160-189 (High):Statin strongly recommended. If no contraindication, start moderate to high-intensity statin. |
| Very High (Likely Familial Hypercholesterolemia) | ≥190 mg/dL | Very high cardiovascular risk. Strongly suggests familial hypercholesterolemia (FH), especially if <40 years old or family history of early heart disease. Requires high-intensity statin (atorvastatin 40-80 mg or rosuvastatin 20-40 mg). If LDL not <100 mg/dL on maximum statin, add ezetimibe 10 mg. If still not at goal, add PCSK9 inhibitor. Untreated FH causes heart attacks by age 50. |
Reduce saturated fat:Limit to <7% of calories. Each 1% reduction lowers LDL 2-3 mg/dL. Major sources:red meat, butter, cheese, palm/coconut oil
Eliminate trans fats:Avoid partially hydrogenated oils. Trans fats raise LDL and lower HDL
Plant-based diet:Vegan/vegetarian diets reduce LDL 15-25 mg/dL. Emphasize legumes, whole grains, vegetables, fruits
Soluble fiber:10-25g daily. Oats, barley, psyllium, beans, apples. Each 5-10g reduces LDL 5% (7-10 mg/dL)
Plant sterols/stanols:2g daily from fortified foods or supplements. Block cholesterol absorption, reduce LDL 6-15%
Portfolio diet:Combines plant sterols, viscous fiber, soy protein, almonds. Can lower LDL 25-30% without medication
Moderate-intensity statins:Atorvastatin 10-20 mg or rosuvastatin 5-10 mg. Lower LDL 30-40%
High-intensity statins:Atorvastatin 40-80 mg or rosuvastatin 20-40 mg. Lower LDL 50-60%
Primary prevention indications:LDL ≥190 mg/dL (any age), diabetes age 40-75, 10-year ASCVD risk ≥7.5%
Secondary prevention:All patients with heart disease, stroke, PAD require high-intensity statin regardless of LDL level
Monitoring:Check LDL 4-12 weeks after starting. Goal LDL <100 primary prevention, <70 high risk, <55 very high risk
Side effects:Myalgias occur in 5-10%. Try different statin, alternate-day dosing, or CoQ10 100-200 mg daily
Ezetimibe:10 mg daily. Blocks intestinal cholesterol absorption. Lowers LDL additional 15-25%. Add to statin if not at goal. IMPROVE-IT trial showed cardiovascular benefit
PCSK9 inhibitors:Evolocumab or alirocumab subcutaneous injection every 2-4 weeks. Lower LDL 50-60%. For FH, statin-intolerant, or LDL not at goal on max therapy. Expensive but highly effective
Bempedoic acid:180 mg daily. Inhibits cholesterol synthesis upstream of statins. Lowers LDL 15-25%. For statin-intolerant patients
Inclisiran:siRNA injection every 6 months. Lowers LDL 50% by silencing PCSK9 gene. Convenient dosing
Bile acid sequestrants:Cholestyramine, colesevelam. Lower LDL 15-30% but significant GI side effects limit use
Weight loss:Each 10 lbs lost reduces LDL 5-8 mg/dL. Target BMI <25 or waist <40"(men), <35"(women)
Aerobic exercise:150-300 min/week moderate intensity. Lowers LDL modestly (5-10 mg/dL) but improves particle size and reduces small dense LDL
Smoking cessation:Smoking oxidizes LDL, making it more atherogenic. Quitting improves LDL quality even if level unchanged
Limit alcohol:Heavy drinking raises LDL. Limit to ≤1-2 drinks daily
Stress management:Chronic stress increases LDL via cortisol. Meditation, adequate sleep (7-9 hours) help
Intermittent fasting:Time-restricted eating or alternate-day fasting may reduce LDL 5-10%
ApoB measurement:More accurate than LDL-C for risk assessment. Each LDL particle has one ApoB. Target <90 mg/dL primary prevention, <80 secondary, <65 very high risk
LDL particle number (LDL-P):If triglycerides elevated, LDL-P may be high despite "normal"LDL-C (discordance). Target LDL-P <1000 nmol/L
Non-HDL cholesterol:Total - HDL=non-HDL. Captures LDL + VLDL + remnants. Target <100 mg/dL (30 mg/dL higher than LDL target)
CAC score:Coronary artery calcium quantifies atherosclerosis. CAC >100 indicates LDL target should be <70 mg/dL regardless of calculated risk
Aggressive targets:Recent trials (FOURIER, ODYSSEY) show benefit down to LDL 20-30 mg/dL. "Lower is better"with no lower threshold
Mendelian randomization studies prove LDL is causal in atherosclerosis, not just associated. Genetic variants causing lifelong LDL reduction (PCSK9, NPC1L1, HMGCR loss-of-function) reduce cardiovascular events proportional to LDL lowering. Each 40 mg/dL lower lifelong LDL reduces cardiovascular risk by 50-60%—double the benefit of LDL lowering later in life, proving cumulative LDL exposure drives disease.
Source:Ference BA, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. Eur Heart J. 2017;38(32):2459-2472.
CTT Collaboration meta-analysis of 170,000 patients shows each 40 mg/dL (1 mmol/L) reduction in LDL reduces major cardiovascular events by 22%, regardless of baseline LDL. Benefit continues down to LDL 30-40 mg/dL with no safety concerns. This established "lower is better"principle—no threshold below which LDL lowering becomes ineffective.
Source:CTT Collaboration. Efficacy and safety of LDL-lowering therapy among men and women:meta-analysis. Lancet. 2015;385(9976):1397-1405.
FOURIER and ODYSSEY OUTCOMES trials demonstrated PCSK9 inhibitors reduce LDL to median 30 mg/dL and reduce cardiovascular events by 15% beyond statin therapy. Patients achieving LDL <20 mg/dL had greatest benefit with no safety concerns. This definitively proved very low LDL (<50 mg/dL) is safe and beneficial.
Source:Sabatine MS, et al. Evolocumab and clinical outcomes in patients with cardiovascular disease. N Engl J Med. 2017;376(18):1713-1722.
FH affects 1 in 250 people (1 in 300,000 for homozygous FH). Untreated heterozygous FH causes heart attacks 20 years earlier than general population. LDL is markedly elevated from birth (>190 mg/dL). Early statin treatment (starting in childhood for FH) prevents cardiovascular events. Cascade screening identifies affected relatives.
Source:Sturm AC, et al. Clinical genetic testing for familial hypercholesterolemia. J Am Coll Cardiol. 2018;72(6):662-680.
When triglycerides are elevated (>150 mg/dL), LDL-C underestimates cardiovascular risk. These patients often have high LDL particle number despite "normal"LDL-C. ApoB (which counts particles, not cholesterol content) more accurately predicts risk. LDL-C <100 mg/dL with ApoB >90 mg/dL indicates high particle number and elevated risk requiring treatment.
Source:Sniderman AD, et al. Apolipoprotein B particles and cardiovascular disease:a narrative review. JAMA Cardiol. 2019;4(12):1287-1295.
| Provider | Includes | Annual Cost | Biomarkers |
|---|---|---|---|
 Superpower | ✓ | $199 | 100+ (150 with ratios) |
 WHOOP Advanced Labs | ✓ | $349 | 65 |
 Labcorp OnDemand | ✓ | $398 | 30+ |
| ✓ | $486 | 40+ | |
| ✓ | $468 | 83 | |
| ✓ | $349 | 100+ | |
 InsideTracker | ✓ | $680 | 54 |
 Function Health | ✓ | $365 | 100+ |
| ✓ | $250 | 65 | |
| ✓ | $495 | 70+ | |
| ✓ | $895 | 100+ | |
| ✓ | $1950 | 150+ | |
| — | $399 | 100+ | |
| — | $Varies | 75+ | |
| ✓ | $190 | 100+ | |
| ✓ | $99 | 50 | |
| ✓ | $125 | 60 | |
| ✓ | $199 | 50 | |
| ✓ | $499 | 120+ | |
| ✓ | $4188 | 80+ | |
| ✓ | $375 | 85 | |
| ✓ | $700 | 129 |
21 providers include this biomarker in their panels
This information is for educational purposes only and is not medical advice. Always consult with a qualified healthcare provider about your specific health needs.
