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Quick Reference
  • Desirable: <200 mg/dL
  • Borderline High: 200-239 mg/dL
  • High: ≥240 mg/dL
  • Primary Use: Cardiovascular risk assessment and screening
  • Sample Type: Serum or plasma (fasting preferred but not required for screening)
  • Key Point: Total cholesterol alone is insufficient - must evaluate HDL, LDL, and non-HDL for complete risk assessment

Test Description

What is Cholesterol?

Cholesterol is a waxy, fat-like substance that is essential for life. It serves multiple critical functions in the body:

  • Cell membrane structure: Cholesterol is a vital component of all cell membranes, providing structural integrity and fluidity
  • Hormone synthesis: Serves as precursor for steroid hormones (cortisol, aldosterone, testosterone, estrogen, progesterone)
  • Bile acid production: Liver converts cholesterol into bile acids needed for fat digestion and absorption
  • Vitamin D synthesis: Cholesterol in skin is converted to vitamin D3 by sunlight exposure
  • Nerve function: Myelin sheaths surrounding nerves contain high cholesterol concentrations

Types of Cholesterol

Total cholesterol represents the sum of all cholesterol-containing lipoproteins circulating in blood:

  • LDL cholesterol (Low-Density Lipoprotein): "Bad cholesterol" - deposits cholesterol in arterial walls, promoting atherosclerosis
  • HDL cholesterol (High-Density Lipoprotein): "Good cholesterol" - removes cholesterol from arterial walls and transports it to liver for excretion
  • VLDL cholesterol (Very Low-Density Lipoprotein): Carries triglycerides and some cholesterol; estimated as triglycerides ÷ 5
  • IDL and Lp(a): Intermediate-density lipoprotein and lipoprotein(a) - minor contributors to total cholesterol
Total Cholesterol = LDL + HDL + (Triglycerides ÷ 5)
This equation estimates total cholesterol from its components. The "triglycerides ÷ 5" term approximates VLDL cholesterol (valid when triglycerides <400 mg/dL).

Cholesterol Sources

The body obtains cholesterol from two sources:

  • Endogenous synthesis (70-80%): Liver and other cells synthesize most cholesterol via HMG-CoA reductase pathway (target of statin drugs)
  • Dietary intake (20-30%): Cholesterol from animal products (meat, eggs, dairy) is absorbed in small intestine

How Total Cholesterol is Measured

Total cholesterol is measured directly from blood sample using enzymatic methods. While traditionally measured fasting, recent guidelines recognize that non-fasting total cholesterol is acceptable for screening purposes, as it varies minimally with food intake (unlike triglycerides).

Normal Ranges

The NCEP ATP III (National Cholesterol Education Program Adult Treatment Panel III) established cholesterol classification based on cardiovascular risk rather than strict "normal" values.

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Category Total Cholesterol Cardiovascular Risk
Desirable <200 mg/dL Lower risk
Borderline High 200-239 mg/dL Moderate risk - further evaluation needed
High ≥240 mg/dL High risk - treatment usually indicated
Important Considerations:
  • Total cholesterol is insufficient alone: A person with total cholesterol 250 mg/dL and HDL 90 mg/dL may have lower cardiovascular risk than someone with total cholesterol 180 mg/dL and HDL 25 mg/dL
  • Complete lipid panel required: Must evaluate LDL, HDL, non-HDL cholesterol, and triglycerides for accurate risk assessment
  • Risk calculators: ACC/AHA Pooled Cohort Equations incorporate multiple factors beyond cholesterol (age, blood pressure, diabetes, smoking)
  • Children and adolescents: Different cutoffs apply - desirable <170 mg/dL, borderline 170-199 mg/dL, high ≥200 mg/dL
Clinical Significance

Elevated Total Cholesterol (Hypercholesterolemia)

Elevated total cholesterol increases cardiovascular disease risk through atherosclerosis formation. Causes include:

Primary (Genetic) Hyperlipidemia

  • Familial hypercholesterolemia (FH): LDL receptor defects causing severe elevation (often >300 mg/dL); heterozygotes 1:250, homozygotes 1:160,000-300,000; presents with tendon xanthomas, corneal arcus, premature CAD
  • Familial combined hyperlipidemia: Most common genetic dyslipidemia (1:100); elevated total cholesterol, LDL, and triglycerides; strong family history of premature CAD
  • Polygenic hypercholesterolemia: Multiple genetic variants causing modest elevations (200-300 mg/dL)
  • Familial defective apoB-100: Defective apolipoprotein B prevents LDL uptake; similar phenotype to FH

Secondary Causes of Elevated Cholesterol

  • Hypothyroidism: Decreased LDL receptor expression and clearance; check TSH in all patients with hyperlipidemia
  • Nephrotic syndrome: Protein loss triggers hepatic lipoprotein overproduction; cholesterol often >300 mg/dL with marked proteinuria
  • Cholestasis/liver disease: Impaired bile acid synthesis and cholesterol excretion
  • Diabetes mellitus: Insulin resistance alters lipid metabolism; typically elevates triglycerides more than cholesterol
  • Obesity: Increased VLDL production and decreased HDL
  • Pregnancy: Physiologic increase (20-40%) due to hormonal changes; returns to baseline postpartum

Medications That Increase Cholesterol

  • Thiazide diuretics: Modest increase in total cholesterol and LDL
  • Beta-blockers (non-selective): May increase triglycerides and decrease HDL
  • Corticosteroids: Increase LDL and total cholesterol
  • Cyclosporine/tacrolimus: Immunosuppressants cause hyperlipidemia
  • Protease inhibitors: Antiretrovirals commonly cause dyslipidemia
  • Anabolic steroids: Decrease HDL, increase LDL
  • Progestins (some oral contraceptives): Variable effects on lipids

Dietary and Lifestyle Factors

  • Saturated fat intake: Raises LDL cholesterol (main dietary culprit)
  • Trans fats: Raise LDL and lower HDL (worst dietary fat)
  • Dietary cholesterol: Modest effect in most people (body compensates by reducing synthesis)
  • Sedentary lifestyle: Contributes to elevated triglycerides and low HDL
  • Excessive alcohol: Raises triglycerides; moderate intake may raise HDL

Low Total Cholesterol (Hypocholesterolemia)

Very low cholesterol (<120 mg/dL) is less common and usually not clinically significant, but may indicate:

  • Malnutrition/malabsorption: Inadequate dietary intake or intestinal absorption
  • Severe liver disease: Decreased hepatic cholesterol synthesis in cirrhosis or hepatic failure
  • Hyperthyroidism: Increased cholesterol catabolism and LDL receptor upregulation
  • Chronic infection/inflammation: Sepsis, chronic inflammatory diseases
  • Malignancy: Advanced cancer may cause hypocholesterolemia
  • Abetalipoproteinemia: Rare genetic disorder preventing lipoprotein assembly; severe fat malabsorption, neurologic disease
  • Hypobetalipoproteinemia: Genetic defect in apoB-100 causing low LDL
  • Statin overtreatment: Excessive cholesterol lowering (though no clear harm from very low LDL if achieved with statins)
Low Cholesterol and Mortality: Some observational studies suggested U-shaped mortality curve with increased risk at very low cholesterol, but this likely reflects underlying disease (cancer, liver disease) rather than cholesterol itself. Randomized trials of statins show no increased mortality with low LDL.
Interpretation Guidelines

Complete Lipid Panel Interpretation

Total cholesterol must be interpreted in context of complete lipid profile:

Non-HDL Cholesterol Calculation:
Non-HDL Cholesterol = Total Cholesterol - HDL Cholesterol

Non-HDL represents all atherogenic lipoproteins (LDL + VLDL + IDL + Lp(a)) and is a secondary treatment target. Goal is typically <130 mg/dL or 30 mg/dL above LDL goal.

ACC/AHA Cholesterol Management Guidelines

Current guidelines focus on overall cardiovascular risk assessment rather than treating cholesterol targets alone:

Swipe to see more
Risk Category Definition Treatment Approach
Clinical ASCVD Prior MI, stroke, TIA, PAD, ACS High-intensity statin (goal LDL ≥50% reduction); consider adding ezetimibe or PCSK9 inhibitor if LDL ≥70 mg/dL
LDL ≥190 mg/dL Severe hypercholesterolemia (likely genetic) High-intensity statin; often requires combination therapy
Diabetes (40-75 years) Type 1 or 2 diabetes, no ASCVD Moderate to high-intensity statin based on 10-year ASCVD risk
Primary Prevention LDL 70-189 mg/dL, no diabetes or ASCVD Calculate 10-year ASCVD risk; consider statin if risk ≥7.5-10%

Screening Recommendations

  • Adults 20-75 years: Lipid panel every 4-6 years (more frequently if abnormal or high risk)
  • Children and adolescents: Universal screening at ages 9-11 and 17-21; earlier if family history of premature CAD or familial hyperlipidemia
  • Men ≥35 years, Women ≥45 years: Consider more frequent screening
  • High-risk patients: Annual screening if diabetes, known ASCVD, strong family history
Interfering Factors

Factors That Increase Total Cholesterol

  • Medications: Thiazide diuretics, beta-blockers, corticosteroids, anabolic steroids, cyclosporine, protease inhibitors, some progestins
  • Dietary factors: High saturated fat, trans fats, excessive dietary cholesterol (modest effect)
  • Physiologic states: Pregnancy (20-40% increase), standing position during blood draw (5-15% higher than sitting)
  • Medical conditions: Hypothyroidism, nephrotic syndrome, diabetes, obesity, cholestatic liver disease
  • Seasonal variation: Cholesterol may be 3-5% higher in winter months

Factors That Decrease Total Cholesterol

  • Medications: Statins, ezetimibe, PCSK9 inhibitors, fibrates, niacin, bile acid sequestrants
  • Dietary factors: High fiber intake, plant sterols/stanols, soy protein, omega-3 fatty acids
  • Lifestyle: Regular aerobic exercise, weight loss, smoking cessation
  • Medical conditions: Hyperthyroidism, malabsorption, severe liver disease, chronic infections, malignancy
  • Acute illness: Cholesterol drops 10-40% during acute MI, infection, surgery, trauma (wait 6-8 weeks after acute event for accurate measurement)

Pre-analytical Considerations

  • Fasting status: Total cholesterol varies <2% with food intake (fasting not required for screening); triglycerides much more affected
  • Posture: Total cholesterol 5-15% higher when standing vs. lying down due to hemoconcentration
  • Tourniquet time: Prolonged tourniquet application causes hemoconcentration and falsely elevated values
  • Biological variation: Individual cholesterol varies ±8% on different days; average of 2-3 measurements recommended before treatment decisions
Clinical Pearls
Clinical Pearl
"Total cholesterol tells you the total story, not the whole story": Total cholesterol alone cannot differentiate between favorable and unfavorable lipid profiles. A high total cholesterol with high HDL may be lower risk than borderline total cholesterol with low HDL. Always review complete lipid panel.
Clinical Pearl
Fasting vs. non-fasting: Recent guidelines accept non-fasting lipid panels for initial screening since total cholesterol and HDL change minimally with meals. However, if triglycerides >400 mg/dL on non-fasting sample, repeat fasting for accurate LDL calculation.
Clinical Pearl
Check thyroid function: Hypothyroidism is a common, correctable cause of elevated cholesterol. Always check TSH in patients with new hyperlipidemia, especially if accompanied by fatigue, weight gain, or other hypothyroid symptoms.
Don't check lipids during acute illness: Total cholesterol and LDL drop 10-40% during acute MI, infection, surgery, or trauma. Wait 6-8 weeks after acute event for accurate baseline measurement. Exception: very high cholesterol during acute illness still indicates underlying hyperlipidemia.
Biological variation requires averaging: Total cholesterol naturally varies ±8% day-to-day in same individual. Obtain 2-3 measurements separated by 1-2 weeks and average them before making treatment decisions (unless cholesterol is very high or patient has clinical ASCVD).
Clinical Pearl
Familial hypercholesterolemia screening: Consider FH if: total cholesterol >300 mg/dL, LDL >190 mg/dL, family history of premature CAD, tendon xanthomas, or corneal arcus before age 45. FH patients need aggressive treatment and family cascade screening.
Clinical Pearl
Pregnancy effects: Total cholesterol rises 20-40% during pregnancy due to hormonal changes and is not an indication for treatment. Lipid testing should be deferred until 3-6 months postpartum. Statins are contraindicated in pregnancy.
Non-HDL cholesterol as secondary target: Non-HDL cholesterol (Total Chol - HDL) represents all atherogenic particles and is a secondary treatment target. Goal is typically 30 mg/dL above LDL goal. Advantage: doesn't require fasting and valid even when triglycerides are high.
References
  1. Kratz, A., Ferraro, M., Sluss, P. M., & Lewandrowski, K. B. (2004). Laboratory reference values. New England Journal of Medicine, 351, 1548-1564.
  2. Lee, M. (Ed.). (2009). Basic skills in interpreting laboratory data. Ashp.
  3. Farinde, A. (2021). Lab values, normal adult: Laboratory reference ranges in healthy adults. Medscape. https://emedicine.medscape.com/article/2172316-overview?form=fpf
  4. Nickson, C. (n.d.). Critical Care Compendium. Life in the Fast Lane • LITFL. https://litfl.com/ccc-critical-care-compendium/
  5. Farkas, Josh MD. (2015). Table of Contents - EMCrit Project. EMCrit Project. https://emcrit.org/ibcc/toc/
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