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Quick Reference
  • Normal: <150 mg/dL
  • Borderline High: 150-199 mg/dL
  • High: 200-499 mg/dL
  • Very High: ≥500 mg/dL
  • Critical (Pancreatitis Risk): ≥1000 mg/dL
  • Primary Use: Cardiovascular risk assessment; pancreatitis risk when very elevated
  • Sample Type: Serum or plasma - FASTING REQUIRED (8-12 hours)
  • Key Point: Triglycerides ≥1000 mg/dL significantly increase acute pancreatitis risk; fasting status critical for accurate measurement

Test Description

What are Triglycerides?

Triglycerides are the most common type of fat in the body and in the diet. Chemically, a triglyceride molecule consists of a glycerol backbone attached to three fatty acid chains. Triglycerides serve as the body's primary form of energy storage and fuel.

Structure and Function

  • Glycerol backbone: Three-carbon alcohol molecule
  • Three fatty acids: Can be saturated or unsaturated, varying in chain length
  • Energy storage: Stored in adipose tissue; provides 9 calories per gram (more than twice that of carbohydrates or protein)
  • Energy source: Released from adipose tissue during fasting or exercise; metabolized for fuel
  • Insulation and protection: Adipose tissue provides thermal insulation and cushioning for organs

Sources of Triglycerides

Blood triglycerides come from two main sources:

Dietary (Exogenous) Triglycerides:

  • Dietary fats: Directly absorbed from food (butter, oils, meat, dairy)
  • Packaged in chylomicrons: Intestine packages dietary triglycerides into large chylomicron particles
  • Cleared by lipoprotein lipase: Enzyme on blood vessel walls breaks down chylomicron triglycerides
  • Timing: Appear in blood 2-4 hours after meal; cleared within 8-12 hours in healthy individuals

Hepatic (Endogenous) Triglycerides:

  • Synthesized in liver: Liver converts excess carbohydrates, protein, and alcohol into triglycerides
  • Packaged in VLDL: Very low-density lipoprotein particles carry triglycerides from liver to tissues
  • Insulin's role: Insulin promotes triglyceride synthesis; insulin resistance increases VLDL production
  • VLDL metabolism: VLDL triglycerides are cleaved by lipoprotein lipase; VLDL remnants become IDL, then LDL

Why Fasting is Required

Triglycerides rise dramatically after meals (postprandial lipemia) due to chylomicron appearance. A non-fasting triglyceride measurement includes both baseline VLDL triglycerides plus dietary chylomicron triglycerides, making interpretation difficult.

Fasting Requirements:
  • 8-12 hour fast required: Water, black coffee, and medications OK; no food or caloric beverages
  • Avoid alcohol 24 hours before: Alcohol significantly raises triglycerides; abstain for at least 24 hours
  • No exercise immediately before: Strenuous exercise can transiently alter triglycerides
  • Consistent fasting state: If repeating triglycerides, use similar fasting duration for comparison

Clinical Significance of Triglycerides

  • Cardiovascular risk marker: Elevated triglycerides, especially with low HDL, increase ASCVD risk
  • Pancreatitis risk: Triglycerides ≥1000 mg/dL significantly increase acute pancreatitis risk
  • Metabolic syndrome indicator: Elevated triglycerides (≥150 mg/dL) are one of five metabolic syndrome criteria
  • Diabetes and insulin resistance: High triglycerides often signal insulin resistance or poorly controlled diabetes
  • LDL calculation: Friedewald equation requires triglycerides <400 mg/dL for accurate calculated LDL
Normal Ranges

Triglyceride levels are classified based on cardiovascular risk and pancreatitis risk. All values assume proper 8-12 hour fasting.

Swipe to see more
Category Triglyceride Level Clinical Significance
Normal <150 mg/dL Optimal for cardiovascular health
Borderline High 150-199 mg/dL Increased cardiovascular risk; lifestyle modifications recommended
High 200-499 mg/dL Significantly increased cardiovascular risk; treatment usually indicated
Very High 500-999 mg/dL Very high cardiovascular risk; emerging pancreatitis risk; urgent treatment needed
Severe/Critical ≥1000 mg/dL HIGH RISK OF PANCREATITIS - medical emergency; immediate triglyceride lowering required
Pancreatitis Risk Threshold: Triglycerides ≥1000 mg/dL carry significant risk of acute pancreatitis (estimated 5-10% annual risk). Risk increases further above 1500-2000 mg/dL. Patients with severe hypertriglyceridemia require urgent treatment to prevent this life-threatening complication. Even one episode of pancreatitis can cause permanent pancreatic damage.

Updated Guidelines

Recent guidelines increasingly recognize triglycerides as an independent cardiovascular risk factor:

  • AHA Scientific Statement (2011): Triglycerides <100 mg/dL may be optimal for cardiovascular health
  • 2018 ACC/AHA Guidelines: Consider fibrates or omega-3 fatty acids for persistent triglycerides 200-499 mg/dL after statin therapy
  • Severe hypertriglyceridemia (>500 mg/dL): Prioritize triglyceride lowering to prevent pancreatitis before addressing LDL
Clinical Significance

Elevated Triglycerides (Hypertriglyceridemia)

High triglycerides result from overproduction, decreased clearance, or both. Causes are often multifactorial.

Primary (Genetic) Hypertriglyceridemia

  • Familial hypertriglyceridemia: Autosomal dominant; triglycerides 200-500 mg/dL; often presents in adulthood; increased cardiovascular risk
  • Familial combined hyperlipidemia: Most common genetic dyslipidemia (1:100); elevated triglycerides AND LDL; strong family history of premature CAD
  • Familial chylomicronemia syndrome: Rare autosomal recessive; lipoprotein lipase or apoC-II deficiency; triglycerides often >1000-5000 mg/dL; recurrent pancreatitis, eruptive xanthomas, lipemia retinalis; onset in childhood
  • Familial dysbetalipoproteinemia (Type III): ApoE2/E2 genotype; accumulation of VLDL and chylomicron remnants; triglycerides 400-800 mg/dL; palmar xanthomas, premature atherosclerosis

Secondary Causes (Most Common)

  • Obesity: Especially visceral obesity; increased hepatic triglyceride synthesis
  • Metabolic syndrome: Insulin resistance drives VLDL overproduction; classic triad: high triglycerides, low HDL, small dense LDL
  • Type 2 diabetes: Poor glycemic control increases hepatic triglyceride synthesis; insulin deficiency impairs lipoprotein lipase activity
  • Excessive alcohol consumption: Alcohol stimulates hepatic triglyceride synthesis and impairs clearance; even moderate intake can raise triglycerides
  • High carbohydrate diet: Especially refined sugars and starches; excess carbohydrates converted to triglycerides in liver
  • Sedentary lifestyle: Physical inactivity reduces lipoprotein lipase activity and triglyceride clearance

Medical Conditions

  • Hypothyroidism: Reduced lipoprotein lipase activity; check TSH in all patients with hypertriglyceridemia
  • Chronic kidney disease: Impaired triglyceride clearance; worsens with declining GFR
  • Nephrotic syndrome: Urinary protein loss triggers hepatic lipoprotein overproduction; often severe hypertriglyceridemia
  • Pregnancy: Physiologic increase in third trimester (usually <300 mg/dL); can unmask familial hypertriglyceridemia and cause gestational pancreatitis
  • Liver disease: Cirrhosis impairs triglyceride metabolism
  • Autoimmune disorders: Lupus, monoclonal gammopathies can cause secondary hypertriglyceridemia

Medications That Increase Triglycerides

  • Alcohol: Dose-dependent increase; even moderate consumption
  • Estrogens (oral): Estrogen therapy, oral contraceptives; transdermal estrogen has less effect
  • Glucocorticoids: Prednisone and other steroids increase hepatic triglyceride production
  • Beta-blockers (non-selective): Propranolol, atenolol; cardioselective less effect
  • Thiazide diuretics: Dose-dependent; high doses more problematic
  • Protease inhibitors: HIV medications commonly cause dyslipidemia
  • Antipsychotics (atypical): Olanzapine, clozapine, quetiapine; significant metabolic effects
  • Isotretinoin (Accutane): Can markedly elevate triglycerides; monitor during treatment
  • Tamoxifen: Estrogen receptor modulator; increases triglycerides
  • Bile acid sequestrants: Paradoxically raise triglycerides while lowering LDL
  • Immunosuppressants: Cyclosporine, tacrolimus, sirolimus

Complications of Severe Hypertriglyceridemia

Acute Pancreatitis (Triglycerides ≥1000 mg/dL):
  • Mechanism: Excess triglycerides hydrolyzed by pancreatic lipase, releasing toxic free fatty acids that cause local pancreatic inflammation and necrosis
  • Risk: ~5-10% annual risk when TG >1000 mg/dL; higher above 1500-2000 mg/dL
  • Presentation: Severe epigastric pain radiating to back, nausea, vomiting; lipemic serum may appear milky white
  • Severity: Hypertriglyceridemia-induced pancreatitis can be severe with high morbidity/mortality
  • Recurrence: High recurrence risk if triglycerides not controlled

Other Complications:

  • Eruptive xanthomas: Yellowish papules on buttocks, elbows, knees when triglycerides >2000 mg/dL; resolve with triglyceride lowering
  • Lipemia retinalis: Creamy appearance of retinal vessels when triglycerides >2000-3000 mg/dL; visible on fundoscopy
  • Hepatosplenomegaly: Fatty infiltration of liver and spleen in severe cases
  • Pseudohyponatremia: Falsely low sodium due to lipemic interference with lab measurement (true sodium normal)
  • Laboratory interference: Severe lipemia interferes with many lab tests; sample appears milky

Low Triglycerides

Low triglycerides (<50 mg/dL) are uncommon and rarely clinically significant:

  • Malnutrition/malabsorption: Inadequate dietary fat intake or absorption
  • Hyperthyroidism: Increased triglyceride catabolism
  • Very low-fat diet: Extreme dietary restriction
  • Abetalipoproteinemia: Rare genetic disorder; cannot produce apoB-containing lipoproteins; fat malabsorption, neurologic disease
  • Certain medications: Fibrates, omega-3 fatty acids, niacin can lower triglycerides below normal range
Interpretation Guidelines

Treatment Approach Based on Triglyceride Level

Swipe to see more
Triglyceride Level Priority Treatment Approach
<150 mg/dL No specific TG therapy Focus on LDL lowering if indicated; maintain healthy lifestyle
150-199 mg/dL Lifestyle modifications Weight loss, exercise, limit refined carbs and alcohol, improve diabetes control
200-499 mg/dL Lifestyle + consider medication Aggressive lifestyle changes; if persistent after 3-6 months on statin, add fibrate or omega-3 fatty acids
500-999 mg/dL Prevent pancreatitis Immediate lifestyle changes + medication (fibrate, omega-3, niacin); goal TG <500 mg/dL
≥1000 mg/dL URGENT - prevent pancreatitis Very low-fat diet (<20g fat/day), eliminate alcohol, optimize diabetes control, high-dose omega-3 + fibrate; may require plasmapheresis if acute pancreatitis; goal TG <500 mg/dL urgently

Lifestyle Modifications (First-Line for TG 150-499 mg/dL)

  • Weight loss: 5-10% weight loss reduces triglycerides 20-30%; most effective intervention
  • Reduce refined carbohydrates and sugars: Limit sweets, sugary beverages, white bread, white rice; choose whole grains
  • Limit fructose: High-fructose corn syrup in sodas and processed foods strongly raises triglycerides
  • Reduce/eliminate alcohol: Even moderate alcohol consumption elevates triglycerides; complete abstinence if TG >500 mg/dL
  • Increase omega-3 fatty acids: Fatty fish (salmon, mackerel, sardines) 2-3 times/week; flaxseed, walnuts
  • Regular aerobic exercise: 150 min/week moderate or 75 min/week vigorous; reduces triglycerides 20-30%
  • Replace saturated fats with unsaturated fats: Use olive oil, nuts, avocado instead of butter and animal fats
  • Control diabetes: Improve glycemic control; each 1% reduction in HbA1c lowers triglycerides

Pharmacologic Therapy

Fibrates (First-line for TG >200 mg/dL):

  • Mechanism: Activate PPAR-alpha, increasing lipoprotein lipase and decreasing VLDL production
  • Effect: Reduce triglycerides 30-50%; increase HDL 10-25%; modest LDL increase possible
  • Agents: Fenofibrate (preferred; fewer drug interactions), gemfibrozil
  • Caution: Monitor for myopathy, especially with statins; fenofibrate safer than gemfibrozil with statins

Omega-3 Fatty Acids (Prescription or OTC):

  • Prescription (Vascepa, Lovaza): High-dose EPA or EPA+DHA; reduce triglycerides 20-50% at 2-4 g/day
  • Mechanism: Reduce hepatic VLDL synthesis; increase triglyceride clearance
  • Vascepa (icosapent ethyl): Pure EPA; shown to reduce cardiovascular events in REDUCE-IT trial
  • OTC fish oil: Variable quality; need 3-4 g/day omega-3 for therapeutic effect

Niacin (Nicotinic Acid):

  • Effect: Reduces triglycerides 20-40%; raises HDL 15-35%
  • Limitations: Flushing, glucose intolerance, GI symptoms; limited cardiovascular benefit in statin era
  • Use: Reserved for severe hypertriglyceridemia unresponsive to other therapies

Statins:

  • Effect: Modest triglyceride reduction (10-30%); primarily lower LDL
  • Use: First-line for cardiovascular risk reduction; may modestly help triglycerides

Emergency Management (TG ≥1000 mg/dL)

Immediate Actions:
  1. Very low-fat diet: <20 grams fat per day; prevents chylomicron formation
  2. Eliminate alcohol completely: Critical for triglyceride reduction
  3. Start fibrate + high-dose omega-3: Immediate pharmacologic therapy
  4. Optimize diabetes control: Insulin if needed to control hyperglycemia
  5. Stop offending medications: Estrogens, isotretinoin, etc.
  6. Plasmapheresis: Consider if acute pancreatitis or TG remains >2000 mg/dL despite medical therapy
  7. Monitor closely: Recheck triglycerides in 2-7 days; goal <500 mg/dL urgently
Interfering Factors

Factors That Increase Triglycerides

  • Dietary: High carbohydrate diet (especially refined sugars), high fructose corn syrup, excess calories, saturated fats
  • Alcohol: Even moderate consumption; dose-dependent effect; abstain 24 hours before testing
  • Non-fasting state: Triglycerides rise 50-100+ mg/dL after meals; MUST fast 8-12 hours
  • Medications: Estrogens, corticosteroids, beta-blockers, thiazides, protease inhibitors, atypical antipsychotics, isotretinoin, tamoxifen, bile acid sequestrants
  • Medical conditions: Obesity, diabetes, metabolic syndrome, hypothyroidism, CKD, nephrotic syndrome, pregnancy
  • Lifestyle: Sedentary behavior, obesity, smoking

Factors That Decrease Triglycerides

  • Medications: Fibrates (30-50% reduction), omega-3 fatty acids (20-50%), niacin (20-40%), statins (10-30%)
  • Lifestyle: Weight loss, regular exercise, low-carb diet, alcohol abstinence
  • Fasting: Prolonged fasting (>12 hours) lowers triglycerides below true baseline
  • Medical conditions: Hyperthyroidism, malabsorption, severe malnutrition

Pre-analytical Errors

  • Non-fasting sample: MOST COMMON ERROR; triglycerides can be 50-200+ mg/dL higher postprandially; always verify fasting status
  • Recent alcohol: Alcohol within 24 hours falsely elevates triglycerides
  • Glycerol-containing IV solutions: Propofol, parenteral nutrition cause falsely elevated triglycerides
  • Improper storage: Triglycerides stable at room temp 24 hours, refrigerated 7 days
  • Recent illness or stress: Triglycerides may be altered; wait 6-8 weeks after acute event
Clinical Pearls
"Triglycerides ≥1000 mg/dL = pancreatitis risk": This is a medical emergency requiring immediate treatment to prevent life-threatening acute pancreatitis. Very low-fat diet (<20g/day), eliminate alcohol, start fibrate + omega-3, optimize glucose control. Goal is to get triglycerides <500 mg/dL urgently. Consider plasmapheresis if acute pancreatitis or TG >2000 mg/dL.
Clinical Pearl
Fasting status is CRITICAL: Always verify patient fasted 8-12 hours before accepting triglyceride result. Non-fasting triglycerides can be 50-200+ mg/dL higher than true fasting value. If unsure about fasting status, repeat fasting sample. Document fasting duration in chart.
Clinical Pearl
Alcohol and carbs raise triglycerides more than dietary fat: Counterintuitively, excess carbohydrates (especially refined sugars and fructose) and alcohol have greater impact on triglycerides than dietary fat. Liver converts excess carbs and alcohol into triglycerides. Low-carb diets often more effective than low-fat diets for hypertriglyceridemia.
Clinical Pearl
TG ≥400 mg/dL invalidates Friedewald equation: When triglycerides ≥400 mg/dL, calculated LDL (Friedewald equation) becomes inaccurate. Must use direct LDL measurement or non-HDL cholesterol (Total Chol - HDL) as treatment target. Non-HDL goal is typically 30 mg/dL above LDL goal.
Low HDL + high triglycerides = metabolic syndrome: This pattern is hallmark of metabolic syndrome and insulin resistance. Often accompanies central obesity, pre-diabetes/diabetes, and hypertension. Indicates high cardiovascular risk and need for aggressive lifestyle intervention (weight loss, exercise).
Clinical Pearl
Check TSH in all patients with hypertriglyceridemia: Hypothyroidism commonly causes elevated triglycerides. Treating hypothyroidism may normalize triglycerides without need for lipid-lowering drugs. Always check TSH as part of secondary cause workup.
Clinical Pearl
Milky/lipemic serum when TG >500-1000 mg/dL: Severe hypertriglyceridemia causes blood to appear creamy or milky white (lipemia). This is visible in phlebotomy tube before centrifugation. Lipemia interferes with many lab tests. If you see milky blood, immediately think severe hypertriglyceridemia and pancreatitis risk.
Estrogen (oral) can markedly raise triglycerides: Oral estrogen (HRT, OCPs) increases hepatic VLDL production. Can unmask familial hypertriglyceridemia. In women with baseline TG >300 mg/dL, oral estrogen can push TG >1000 mg/dL, causing pancreatitis. Use transdermal estrogen instead (less hepatic first-pass effect) or avoid estrogen if TG elevated.
Clinical Pearl
Weight loss is most effective lifestyle intervention: 5-10% weight loss reduces triglycerides 20-30%. More effective than any single dietary change. Combine with exercise (another 20-30% reduction) for dramatic improvement. Most patients with TG 200-400 mg/dL can normalize with 10% weight loss + exercise.
Vascepa (icosapent ethyl) reduces cardiovascular events: REDUCE-IT trial showed high-dose EPA (4g/day) reduced cardiovascular events by 25% in patients with elevated triglycerides (135-499 mg/dL) on statin therapy. First triglyceride-lowering therapy proven to reduce hard outcomes. Covered by many insurance plans for this indication.
Clinical Pearl
Fenofibrate safer than gemfibrozil with statins: If combining fibrate with statin (for mixed dyslipidemia), use fenofibrate. Gemfibrozil inhibits statin metabolism, dramatically increasing myopathy risk. Fenofibrate has less interaction. Monitor CK and symptoms closely with any statin-fibrate combination.
Clinical Pearl
Pregnancy can unmask familial hypertriglyceridemia: Physiologic triglyceride increase in third trimester (usually <300 mg/dL) can push women with underlying genetic hypertriglyceridemia above 1000 mg/dL. Gestational pancreatitis is life-threatening for mother and fetus. Monitor triglycerides in pregnant women with history of hypertriglyceridemia.
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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