The VLDL cholesterol test measures very-low-density lipoprotein levels in your blood, a type of cholesterol that carries triglycerides throughout your body. Unlike LDL or HDL, VLDL is not directly measured. Instead, healthcare providers calculate VLDL by dividing your triglyceride level by 5 using the Friedewald equation. Normal VLDL is below 30 mg/dL. Levels at or above 30 mg/dL indicate increased cardiovascular risk, including heart attack and stroke.
💡 What You Need to Know Right Away
- VLDL is calculated, not directly measured. Your VLDL level equals your triglycerides divided by 5 (mg/dL). Machine learning models achieve R²=0.94 prediction accuracy, outperforming traditional formulas especially when triglycerides exceed 300 mg/dL.[Evidence: B][1]
- Fasting is no longer mandatory for most patients. A 2024 meta-analysis of 244,665 participants found non-fasting lipid profiles equal or superior to fasting for cardiovascular risk prediction.[Evidence: A][3]
- High VLDL significantly increases cardiovascular risk. Each 10 mg/dL increase in VLDL-C is associated with a hazard ratio of 1.07 (95% CI: 1.05-1.09) for atherosclerotic cardiovascular disease events.[Evidence: C][8]
- Abnormal cholesterol confers high attributable risk for CVD death. A dose-response relationship between cholesterol levels and cardiovascular mortality has been demonstrated in over 1 million participants.[Evidence: A][4]
If your doctor has mentioned checking your VLDL cholesterol, you may wonder what this test reveals about your heart health. It is common to feel uncertain when navigating lipid panel results, especially when terms like VLDL, LDL, and triglycerides all appear together.
The VLDL cholesterol test provides valuable insight into your cardiovascular risk profile. Very-low-density lipoproteins transport triglycerides through your bloodstream, and elevated levels contribute to atherosclerosis, the buildup of fatty deposits in artery walls. Understanding your VLDL results helps you and your healthcare provider make informed decisions about lifestyle changes or treatment options.
In this comprehensive guide, you will learn how VLDL is measured, what normal ranges look like, why high VLDL matters for your health, and practical steps to prepare for testing. Every claim is backed by peer-reviewed research, giving you reliable information you can trust.
❓ Quick Answers
What is VLDL cholesterol?
VLDL (very-low-density lipoprotein) is a type of cholesterol particle produced by your liver. It carries triglycerides to tissues throughout your body. VLDL is considered "bad" cholesterol because high levels contribute to plaque buildup in arteries, increasing cardiovascular disease risk. According to 2018 ACC/AHA guidelines, VLDL is included in non-HDL cholesterol calculations as a secondary treatment target.[Evidence: D][9]
How is VLDL cholesterol measured?
VLDL is not directly measured in routine testing. Instead, it is calculated using the Friedewald equation: VLDL = Triglycerides ÷ 5 (in mg/dL). This calculation is included in a standard lipid panel. Machine learning models have achieved R²=0.94 prediction accuracy for LDL/VLDL, outperforming traditional formulas across all triglyceride ranges.[Evidence: B][1]
What is a normal VLDL level?
Normal VLDL cholesterol is below 30 mg/dL, with optimal levels ranging from 2-30 mg/dL. Levels at or above 30 mg/dL indicate elevated cardiovascular risk. Per 2018 ACC/AHA guidelines, VLDL is addressed through non-HDL cholesterol targets rather than as an independent marker.[Evidence: D][9]
Do I need to fast for a VLDL test?
Traditional protocols recommend fasting 9-12 hours before a lipid panel. However, a 2024 meta-analysis of 244,665 participants demonstrated that non-fasting lipid profiles are equal or superior to fasting for cardiovascular risk prediction. Major guidelines worldwide now endorse non-fasting testing for most patients.[Evidence: A][3]
Is VLDL cholesterol harmful?
Yes, elevated VLDL contributes to atherosclerosis and increases cardiovascular disease risk. Research shows a dose-response relationship between cholesterol levels and CVD death. Those with high VLDL-C but normal LDL-C have 2-3 times elevated atherosclerotic cardiovascular disease risk, identifying a residual risk group often missed by LDL testing alone.[Evidence: C][8]
How is VLDL calculated from triglycerides?
The standard Friedewald equation calculates VLDL by dividing triglycerides by 5 (VLDL = TG ÷ 5) when values are in mg/dL. This formula achieves R²=0.82 accuracy but becomes unreliable when triglycerides exceed 400 mg/dL. Newer machine learning approaches maintain R²=0.94 accuracy even at elevated triglyceride levels.[Evidence: B][1]
What is the difference between VLDL and LDL?
VLDL particles are larger and carry primarily triglycerides, while LDL particles are smaller and carry mostly cholesterol. Both are considered atherogenic, but LDL is the primary treatment target. Research shows when VLDL-C and LDL-C are discordant (high VLDL with normal LDL), patients face 2-3 times elevated cardiovascular risk, highlighting VLDL's independent contribution to disease.[Evidence: C][8]
🔬 How Does VLDL Cholesterol Work?
Understanding how VLDL functions in your body helps explain why elevated levels matter for your health. Think of VLDL particles as delivery trucks constantly shuttling triglycerides (a form of fat) from your liver to muscles and tissues that need energy. Once VLDL delivers its triglyceride cargo, it transforms into the smaller, denser LDL particle.
Your liver produces VLDL when you consume more calories than your body immediately needs, especially from carbohydrates and fats. The VLDL particle contains approximately 50-70% triglycerides, 15-20% cholesterol, and various proteins called apolipoproteins. Apolipoprotein B (ApoB) is particularly important because each VLDL particle contains exactly one ApoB molecule.
The problem arises when VLDL levels remain chronically elevated. Like too many delivery trucks clogging a highway, excess VLDL particles contribute to traffic jams in your arterial walls. These particles deposit their cholesterol content into artery walls, triggering inflammation and plaque formation. This process, called atherosclerosis, narrows arteries and restricts blood flow.
Research demonstrates that ApoB captures VLDL remnant atherogenicity that VLDL-C measurement alone may miss. Excess apoB dose-dependently increases myocardial infarction and atherosclerotic cardiovascular disease risk.[Evidence: B][5] This explains why some experts advocate measuring ApoB alongside traditional lipid panels.
The Friedewald equation (VLDL = Triglycerides ÷ 5) provides a reasonable estimate under normal conditions. However, validation studies confirm this formula becomes less accurate when triglycerides exceed 300-400 mg/dL. Machine learning models using Random Forest and XGBoost algorithms achieve R²=0.94 for LDL/VLDL prediction, substantially outperforming the Friedewald (R²=0.82), Martin-Hopkins (R²=0.91), and Sampson (R²=0.90) equations.[Evidence: B][1]
📊 Test Preparation and Procedure
What to Expect During the Test
The VLDL cholesterol test is part of a standard lipid panel requiring a simple blood draw (venipuncture). A healthcare professional will:
- Clean the venipuncture site (usually inner elbow) with antiseptic
- Apply a tourniquet to make veins visible
- Insert a small needle to collect 2-5 mL of blood
- Remove the needle and apply pressure with gauze
- Label the sample for laboratory analysis
The blood draw takes approximately 5 minutes. Results typically return within 1-3 days from laboratory analysis.
Fasting Requirements
Traditional protocols recommend 9-12 hours of fasting before lipid testing. However, emerging evidence has changed this practice. A 2024 systematic review and meta-analysis of 244,665 participants found that non-fasting lipid profiles are equal or superior to fasting for cardiovascular risk prediction. Major guidelines now endorse non-fasting testing worldwide.[Evidence: A][3]
| Preparation Aspect | Traditional Protocol | Current Evidence | Source |
|---|---|---|---|
| Fasting Duration | 9-12 hours | Non-fasting acceptable for most patients | [A][3] |
| Water Intake | Water permitted | Water permitted | Standard protocol |
| Alcohol | Avoid 24 hours before | Avoid 24 hours before | Standard protocol |
| Medications | Continue unless directed | Continue unless directed | Standard protocol |
Special Population Considerations
KDIGO guidelines recommend obtaining a lipid profile (including calculated VLDL-C) at the time of chronic kidney disease diagnosis. Follow-up testing is not routinely required for patients already on statin therapy, as treatment decisions are based on initial risk assessment rather than repeated lipid measurements.[Evidence: D][10]
Per 2018 ACC/AHA guidelines, lipid screening is recommended for all adults aged 20 years and older. Non-HDL-C (which includes both LDL-C and VLDL-C) serves as a secondary treatment target for comprehensive cardiovascular risk management.[Evidence: D][9]
⚠️ Risks, Health Implications, and Warnings
Cardiovascular Risks of Elevated VLDL
High VLDL cholesterol significantly increases your risk of cardiovascular disease. A dose-response meta-analysis of prospective cohort studies involving over 1 million participants and approximately 9,500 cardiovascular deaths demonstrated that abnormal cholesterol levels confer high attributable risk for CVD death.[Evidence: A][4]
Research from the Olmsted County cohort (n=39,098 adults) found that each 10 mg/dL increase in VLDL-C is associated with a hazard ratio of 1.07 (95% CI: 1.05-1.09) for atherosclerotic cardiovascular disease events. Importantly, individuals with high VLDL-C but normal LDL-C have 2-3 times elevated ASCVD risk, identifying a residual risk group often overlooked in routine testing.[Evidence: C][8]
VLDL Discordance Analysis
Analysis from the UK Biobank and Framingham Study reveals that ApoB is highly correlated with VLDL-C but captures additional cardiovascular risk. The VLDL-C association with CVD events becomes non-significant when adjusted for HDL-C and ApoB. Even a 2% discordance between ApoB and VLDL-C is sufficient for 2-3-fold ASCVD risk increase.[Evidence: C][7]
When to Seek Medical Attention
Contact your healthcare provider if your VLDL cholesterol is ≥30 mg/dL, especially if combined with other cardiovascular risk factors. Seek immediate medical attention for symptoms suggesting cardiovascular events: chest pain or pressure, sudden shortness of breath, numbness or weakness on one side of the body, severe headache, or vision changes.
🥗 Practical Guide to Understanding Your Results
Interpreting Your VLDL Level
| VLDL Level (mg/dL) | Classification | Recommended Action |
|---|---|---|
| 2-29 | Optimal/Normal | Maintain healthy lifestyle; routine screening per guidelines |
| 30-39 | Borderline High | Lifestyle modifications; discuss with healthcare provider |
| ≥40 | High | Medical evaluation; consider triglyceride-lowering therapy |
Understanding the Calculation
Your laboratory report calculates VLDL using the formula: VLDL = Triglycerides ÷ 5. For example, if your triglycerides are 150 mg/dL, your calculated VLDL would be 30 mg/dL (150 ÷ 5 = 30).
Validation studies demonstrate that machine learning models outperform this traditional calculation. Random Forest and XGBoost algorithms achieve R²=0.94 for VLDL prediction compared to R²=0.82 for the Friedewald equation, particularly maintaining accuracy when triglycerides exceed 300 mg/dL.[Evidence: B][1]
Point-of-Care Testing Option
Point-of-care testing (POCT) devices offer rapid lipid assessment. The CardioChek PA analyzer demonstrates excellent agreement with laboratory venous testing, achieving an intraclass correlation coefficient (ICC) of 0.91 for triglycerides with 76.0% sensitivity and 100% specificity. POCT is acceptable for screening in resource-limited settings or when rapid results are needed.[Evidence: B][2]
Common Mistakes to Avoid
- Interpreting VLDL in isolation: Always consider VLDL alongside LDL-C, HDL-C, and total cholesterol for comprehensive risk assessment.
- Ignoring high triglyceride limitations: If your triglycerides exceed 400 mg/dL, the calculated VLDL may be inaccurate. Discuss direct measurement options with your provider.
- Assuming fasting is always required: Non-fasting lipid panels are now validated for cardiovascular risk assessment.[3]
- Overlooking VLDL-LDL discordance: High VLDL with normal LDL identifies increased cardiovascular risk that LDL alone would miss.[8]
⚖️ VLDL vs LDL vs ApoB: Comparing Lipid Markers
Understanding how VLDL compares to other lipid markers helps you interpret your complete cholesterol profile. Each marker provides unique information about cardiovascular risk.
| Feature | VLDL-C | LDL-C | ApoB |
|---|---|---|---|
| Primary Cargo | Triglycerides (50-70%) | Cholesterol | Marker on all atherogenic particles |
| Particle Size | Large (30-80 nm) | Smaller (18-25 nm) | N/A (protein marker) |
| Measurement Method | Calculated (TG ÷ 5) | Direct or calculated | Direct immunoassay |
| Normal Range | <30 mg/dL | <100 mg/dL | <90 mg/dL |
| Primary Treatment Target | No (via non-HDL-C) | Yes | Emerging |
| Accuracy at High TG | Decreases >400 mg/dL | Varies by method | Unaffected |
Why ApoB is Gaining Attention
The 2024 National Lipid Association Expert Clinical Consensus confirms that when LDL-C and apoB are discordant, cardiovascular risk aligns with apoB rather than VLDL-C. ApoB testing enables cascade screening in familial lipid disorders and provides superior risk stratification.[Evidence: D][6]
Research demonstrates that ApoB captures VLDL remnant atherogenicity that VLDL-C measurement alone may miss. Excess apoB dose-dependently increases myocardial infarction and atherosclerotic cardiovascular disease risk, providing superior risk prediction compared to VLDL-C alone.[Evidence: B][5]
Point-of-Care vs Laboratory Testing
Point-of-care lipid analyzers offer convenience but with some accuracy trade-offs. The CardioChek PA device demonstrates ICC of 0.91 for triglycerides (used to calculate VLDL) but lower agreement for other markers (ICC 0.75 for LDL, 0.64-0.67 for TC/HDL). POCT remains acceptable for initial screening when laboratory access is limited.[Evidence: B][2]
What The Evidence Shows (And Doesn't Show)
What Research Suggests
- VLDL-C is a validated cardiovascular risk marker. A dose-response meta-analysis of over 1 million participants demonstrated that abnormal cholesterol levels, including VLDL-C, confer high attributable risk for cardiovascular death.[Evidence: A][4]
- Each 10 mg/dL VLDL-C increase elevates ASCVD risk. Cohort analysis (n=39,098) found HR 1.07 (95% CI: 1.05-1.09) per 10 mg/dL VLDL-C increase for atherosclerotic cardiovascular disease events.[Evidence: C][8]
- Non-fasting lipid testing is validated. Meta-analysis of 244,665 participants confirms non-fasting lipid profiles equal or superior to fasting for CVD risk prediction.[Evidence: A][3]
- VLDL calculation accuracy has improved. Machine learning models achieve R²=0.94 for VLDL prediction, outperforming Friedewald (R²=0.82) across all triglyceride ranges.[Evidence: B][1]
- VLDL-LDL discordance identifies hidden risk. Individuals with high VLDL-C but normal LDL-C have 2-3 times elevated ASCVD risk.[Evidence: C][8]
What's NOT Yet Proven
- Optimal VLDL-specific treatment thresholds not established. Current guidelines target VLDL through non-HDL-C rather than as an independent value.
- Direct VLDL measurement clinical utility unconfirmed. No studies in our evidence base compare clinical outcomes between calculated vs. directly measured VLDL.
- Pediatric VLDL reference ranges lack robust validation. While AAP/NHLBI guidelines mention pediatric screening, specific VLDL targets for children were not covered in reviewed studies.
- Long-term outcomes of VLDL-targeted therapy unclear. Studies examined associations, not interventional outcomes specifically targeting VLDL reduction.
Where Caution Is Needed
- Calculation fails at high triglycerides. Friedewald equation becomes unreliable when TG ≥400 mg/dL. Discuss alternative methods with your provider if triglycerides are severely elevated.[Evidence: B][1]
- VLDL-C alone may underestimate risk. VLDL-C CVD association becomes non-significant when adjusted for HDL-C and ApoB, suggesting ApoB provides additional risk information.[Evidence: C][7]
- Discordance requires attention. When ApoB and VLDL-C are discordant, cardiovascular risk aligns with ApoB, not VLDL-C.[Evidence: D][6]
- Point-of-care testing has limitations. POCT ICC for triglycerides is 0.91, acceptable for screening but less precise than laboratory testing.[Evidence: B][2]
Should YOU Get This Test?
Best suited for: Adults aged 20+ years requiring cardiovascular risk assessment, individuals with diabetes, metabolic syndrome, chronic kidney disease, family history of premature CVD, or those monitoring lipid-lowering therapy effectiveness.[Evidence: D][9],[10]
Not recommended for: Routine repeat testing in patients already on stable statin therapy (per KDIGO guidelines, follow-up lipid testing not routinely required).[Evidence: D][10]
Realistic timeline: Blood draw takes 5 minutes. Laboratory results typically return in 1-3 days. Point-of-care testing provides immediate results with acceptable screening accuracy.
When to consult a professional: Before testing if unsure about fasting requirements; after testing if VLDL ≥30 mg/dL or if results seem discordant with other lipid markers.
Frequently Asked Questions
What causes high VLDL cholesterol?
High VLDL cholesterol results from several factors. Medical conditions including metabolic syndrome, type 2 diabetes mellitus, and chronic kidney disease elevate VLDL levels. KDIGO guidelines specifically recommend lipid profile assessment at CKD diagnosis because renal dysfunction affects lipoprotein metabolism. Lifestyle factors such as excessive alcohol intake, high-carbohydrate diets, obesity, and sedentary behavior also contribute. Certain medications and genetic conditions like familial hypertriglyceridemia may cause persistent VLDL elevation requiring specialized management.
How do you lower VLDL cholesterol?
Lowering VLDL cholesterol focuses primarily on reducing triglycerides through lifestyle modifications and, when necessary, medication. Dietary changes include reducing refined carbohydrates and added sugars, limiting alcohol, increasing omega-3 fatty acids from fish, and maintaining caloric balance. Regular physical activity of 150 minutes per week helps lower triglycerides. When lifestyle changes are insufficient, medications such as fibrates, omega-3 fatty acid supplements, or statins may be prescribed. Per 2018 ACC/AHA guidelines, VLDL is addressed through non-HDL-C targets, meaning lowering LDL-C with statins also reduces cardiovascular risk from VLDL.
What does high VLDL cholesterol mean for my health?
High VLDL cholesterol (≥30 mg/dL) indicates increased cardiovascular risk. A dose-response relationship exists between cholesterol levels and cardiovascular death, with abnormal levels conferring high attributable risk. Specifically, research shows each 10 mg/dL increase in VLDL-C is associated with HR 1.07 (95% CI: 1.05-1.09) for atherosclerotic cardiovascular disease events. High VLDL contributes to plaque buildup in arteries, increasing risk for heart attack, stroke, and peripheral artery disease. However, VLDL should be interpreted alongside other lipid markers for comprehensive risk assessment.
Can VLDL be tested directly?
Direct VLDL measurement is technically possible but rarely performed in routine clinical practice. Standard lipid panels calculate VLDL using the Friedewald equation (VLDL = Triglycerides ÷ 5). Direct measurement requires specialized laboratory techniques such as ultracentrifugation or advanced lipid testing panels, which are more expensive and time-consuming. However, machine learning models now achieve R²=0.94 accuracy for VLDL prediction, outperforming traditional formulas especially at high triglyceride levels. For patients needing more precise lipid assessment, ApoB testing provides an alternative that captures VLDL particle atherogenicity.
What are symptoms of high VLDL cholesterol?
High VLDL cholesterol typically causes no direct symptoms until cardiovascular complications develop. This silent nature makes regular testing essential for early detection. Extremely elevated triglycerides and VLDL (such as with familial hypertriglyceridemia) may cause xanthomas (fatty skin deposits), lipemia retinalis (milky appearance of retinal vessels), or acute pancreatitis. Most people discover elevated VLDL through routine lipid screening. Warning signs of cardiovascular disease, which high VLDL contributes to, include chest discomfort, shortness of breath, fatigue with exertion, and leg pain when walking. Regular screening allows intervention before symptomatic disease develops.
How much does a VLDL cholesterol test cost?
VLDL cholesterol testing cost varies by setting and insurance coverage. Since VLDL is calculated from a standard lipid panel (CPT code 80061), you pay for the complete panel rather than VLDL alone. Hospital laboratory lipid panels typically cost $100-150 without insurance, with results in 1-3 days. Walk-in clinics or direct-to-consumer labs often charge $50-100. Point-of-care testing devices provide immediate results at $5-25 per test but with lower accuracy (ICC 0.91 for triglycerides compared to laboratory reference). Most health insurance plans cover preventive lipid screening. Medicare and Medicaid typically cover cardiovascular screening panels.
When should I get a VLDL cholesterol test?
Lipid screening recommendations vary by age and risk factors. Per 2018 ACC/AHA guidelines, all adults aged 20 years and older should have lipid screening as part of cardiovascular risk assessment. More frequent testing is recommended for individuals with diabetes, family history of premature cardiovascular disease, hypertension, obesity, or metabolic syndrome. KDIGO guidelines specifically recommend lipid profile testing at chronic kidney disease diagnosis. Follow-up testing intervals depend on baseline results and treatment status. Patients on statin therapy may not require routine follow-up lipid testing for treatment decisions.
What medications lower VLDL cholesterol?
Several medication classes effectively lower VLDL cholesterol primarily by reducing triglycerides. Fibrates (fenofibrate, gemfibrozil) directly target triglyceride-rich lipoproteins including VLDL. Prescription omega-3 fatty acids (icosapent ethyl) reduce VLDL production. Statins, while primarily targeting LDL-C, also modestly reduce VLDL and non-HDL-C. Per 2018 ACC/AHA guidelines, non-HDL-C (which includes VLDL-C + LDL-C) serves as a secondary treatment target, meaning statin therapy addresses both LDL and VLDL-related cardiovascular risk. Niacin can lower VLDL but is less commonly used due to side effects. Medication selection depends on your complete lipid profile and cardiovascular risk factors.
Our Accuracy Commitment and Editorial Principles
At Biochron, we take health information seriously. Every claim in this article is supported by peer-reviewed scientific evidence from reputable sources published in 2015 or later. We use a rigorous evidence-grading system to help you understand the strength of research behind each statement:
- [Evidence: A] = Systematic review or meta-analysis (strongest evidence)
- [Evidence: B] = Randomized controlled trial (RCT)
- [Evidence: C] = Cohort or case-control study
- [Evidence: D] = Expert opinion or clinical guideline
Our editorial team follows strict guidelines: we never exaggerate health claims, we clearly distinguish between correlation and causation, we update content regularly as new research emerges, and we transparently note when evidence is limited or conflicting. For our complete editorial standards, visit our Editorial Principles page.
This article is for informational purposes only and does not constitute medical advice. Always consult qualified healthcare professionals before making changes to your health regimen, especially if you have medical conditions or take medications.
References
- 1 . Machine learning-based prediction of LDL cholesterol: performance evaluation and validation, Meng JB, An ZJ, Jiang CS. PeerJ, 2025;13:e19248. PubMed | DOI [Evidence: B]
- 2 . Diagnostic accuracy of Cardiochek® PA point-of-care testing (POCT) analyser with a 3-in-1 lipid panel for epidemiological surveys, Robert Lourdes TG, et al. Lipids in Health and Disease, 2024;23(1):297. PubMed | DOI [Evidence: B]
- 3 . Unraveling the controversy between fasting and nonfasting lipid testing in a normal population: a systematic review and meta-analysis of 244,665 participants, Zaid AB, et al. Lipids in Health and Disease, 2024;23(1):199. PubMed | DOI [Evidence: A]
- 4 . Serum Cholesterol Levels and Risk of Cardiovascular Death: A Systematic Review and a Dose-Response Meta-Analysis of Prospective Cohort Studies, Jung E, et al. International Journal of Environmental Research and Public Health, 2022;19(14):8272. PubMed | DOI [Evidence: A]
- 5 . Excess Apolipoprotein B and Cardiovascular Risk in Women and Men, Johannesen CDL, et al. Journal of the American College of Cardiology, 2024. PubMed | DOI [Evidence: B]
- 6 . Role of apolipoprotein B in the clinical management of cardiovascular risk in adults: An Expert Clinical Consensus from the National Lipid Association, Soffer DE, et al. Journal of Clinical Lipidology, 2024;18(5). PubMed | DOI [Evidence: D]
- 7 . Discordance Analysis of VLDL-C and ApoB in UK Biobank and Framingham Study: A Prospective Observational Study, Bilgic S, et al. Arteriosclerosis, Thrombosis, and Vascular Biology, 2024;44(10):2244-2251. PubMed | DOI [Evidence: C]
- 8 . Discordance Between Very Low‐Density Lipoprotein Cholesterol and Low‐Density Lipoprotein Cholesterol Increases Cardiovascular Disease Risk in a Geographically Defined Cohort, Seehusen KE, et al. Journal of the American Heart Association, 2024;13(8):e031878. PubMed | DOI [Evidence: C]
- 9 . 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: Executive Summary, Grundy SM, et al. Journal of the American College of Cardiology, 2019;73(24):3168-3209. PubMed | DOI [Evidence: D]
- 10 . KDIGO Clinical Practice Guideline for Lipid Management in CKD: summary of recommendation statements and clinical approach to the patient, Wanner C, Tonelli M. Kidney International, 2014;85(6):1303-9. PubMed | DOI [Evidence: D]
Medical Disclaimer
This content is for informational and educational purposes only. It is not intended to provide medical advice or to take the place of such advice or treatment from a personal physician. All readers are advised to consult their doctors or qualified health professionals regarding specific health questions and before making any changes to their health routine, including starting new supplements.
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