What Are Triglycerides?

Triglycerides are the most common type of fat in your body and in the foods you eat. When you consume more calories than your body needs immediately for energy—whether from fats, carbohydrates, or proteins—your body converts those excess calories into triglycerides and stores them in fat cells for later use. Between meals, hormones signal your fat cells to release triglycerides to provide energy.[1]

Triglycerides travel through your bloodstream packaged inside particles called lipoproteins. The main triglyceride-carrying particles are very low-density lipoproteins (VLDL), which are made by your liver, and chylomicrons, which are made by your intestines after you eat a fatty meal. These particles are collectively called "triglyceride-rich lipoproteins" or TRLs.[2][3]

Here's an important concept: while we measure triglycerides in a blood test, triglycerides themselves are not what directly damages your arteries. Instead, it's the cholesterol carried within these triglyceride-rich particles—called "remnant cholesterol"—that contributes to atherosclerosis.[4][5] Think of triglycerides as a useful marker that tells us about the number and activity of these potentially harmful particles circulating in your blood.

Why are Triglycerides Important in the Development of Heart Disease?

For many years, the relationship between triglycerides and heart disease was controversial. While observational studies consistently showed that people with higher triglycerides had more heart attacks and strokes, it was unclear whether triglycerides were a direct cause or simply a marker of other problems like obesity, diabetes, or low HDL cholesterol.[4][1]

We now have strong evidence from genetic studies that triglyceride-rich lipoproteins and their remnants are causally linked to cardiovascular disease—meaning they actually contribute to causing heart disease, not just predicting it.[4][6][7] This evidence comes from Mendelian randomization studies, which use genetic variants as natural experiments to test causality.

Here's how triglyceride-rich lipoproteins damage your arteries:[3][8][4]

1. Arterial penetration: Unlike the largest triglyceride-rich particles (chylomicrons), which are too big to enter the artery wall, smaller remnant particles can penetrate the inner lining of your arteries and become trapped there.

2. Cholesterol deposition: Once trapped, these remnant particles deposit their cholesterol cargo directly into the artery wall. Importantly, remnant particles can be taken up directly by macrophages (immune cells) without needing to be chemically modified first—unlike LDL particles, which require oxidation before macrophages will engulf them. This means remnants may actually be more efficiently converted into the "foam cells" that form the core of atherosclerotic plaques.[3][4]

3. Inflammation: Triglyceride-rich lipoproteins trigger inflammation in the artery wall. When these particles are broken down by an enzyme called lipoprotein lipase, they release free fatty acids and other molecules that activate inflammatory pathways, including the production of cytokines like tumor necrosis factor-α and interleukin-1β. This inflammatory component may explain why genetically elevated triglycerides are associated with increased levels of C-reactive protein (a marker of inflammation), while genetically elevated LDL cholesterol is not.[3][4]

4. Greater cholesterol content per particle: On a per-particle basis, triglyceride-rich remnants actually carry 20 to 40 times more cholesterol molecules than LDL particles. This means that even a relatively small number of remnant particles can deliver a substantial amount of cholesterol to your artery walls.[3]

The Remnant Cholesterol Concept

A key concept for understanding triglyceride-related cardiovascular risk is "remnant cholesterol." Remnant cholesterol refers to the cholesterol content of all triglyceride-rich lipoproteins—including VLDL, intermediate-density lipoproteins (IDL), and chylomicron remnants.[5][9][10]

Why does remnant cholesterol matter? A study from the Copenhagen population found that remnant cholesterol levels of 1 mmol/L (39 mg/dL) or higher—present in 22% of the population—were associated with more than double the risk of cardiovascular death compared to lower levels.[11] Remarkably, in the PREDIMED trial of older adults at high cardiovascular risk, remnant cholesterol was associated with cardiovascular events while LDL cholesterol was not.[5]

A large study from the Copenhagen population found that VLDL cholesterol accounts for approximately one-half of the myocardial infarction risk associated with all apoB-containing lipoproteins—meaning that triglyceride-rich particles contribute as much to heart attack risk as LDL particles do.[12]

How Are Triglycerides Measured?

Triglycerides are measured as part of a standard lipid panel blood test. The result is reported in milligrams per deciliter (mg/dL) in the United States or millimoles per liter (mmol/L) in many other countries.[16][2]

Fasting vs. non-fasting: Traditionally, triglyceride testing required an overnight fast (8-12 hours without eating) because triglyceride levels rise substantially after meals, particularly fatty meals. However, guidelines now recognize that non-fasting triglyceride levels are also clinically meaningful—and may actually be more relevant for cardiovascular risk assessment since we spend most of our lives in a non-fasting state.[2][17]

What do my Triglyceride Numbers Mean?

The American College of Cardiology and American Heart Association use the following categories for triglyceride levels:[17][16][2]

• Optimal: Less than 150 mg/dL (fasting) or less than 175 mg/dL (non-fasting)

• Borderline high: 150-199 mg/dL

• High (moderate hypertriglyceridemia): 200-499 mg/dL

• Very high (severe hypertriglyceridemia): 500 mg/dL or higher

• Extremely high: 1,000 mg/dL or higher—significantly increased risk of acute pancreatitis

The clinical significance of these levels differs:[17][16]

For moderate hypertriglyceridemia (150-499 mg/dL), the primary concern is increased cardiovascular risk. Elevated triglycerides in this range are considered a "risk-enhancing factor" that may influence decisions about preventive therapies like statins.[17]

For severe hypertriglyceridemia (≥500 mg/dL), there is an additional concern: acute pancreatitis. When triglyceride levels are very high, the excess triglycerides can be broken down in the pancreas, releasing toxic free fatty acids that cause inflammation and potentially life-threatening pancreatitis. The risk increases substantially when triglycerides exceed 1,000 mg/dL.[16][18]

What Causes High Triglycerides?

Hypertriglyceridemia usually results from a combination of genetic susceptibility and environmental or lifestyle factors. Understanding the causes is important because many are modifiable. Hypertriglyceridemia most often reflects a mix of genetic predisposition and modifiable lifestyle factors, particularly excess body fat, insulin resistance or diabetes, high intake of refined carbohydrates or alcohol, and low physical activity. Secondary medical conditions—such as hypothyroidism, kidney or liver disease, pregnancy, or autoimmune disorders—can also contribute and should be considered during evaluation. In addition, several commonly used medications, including beta-blockers, thiazide diuretics, estrogens, corticosteroids, antipsychotics, and certain immunosuppressants, are known to raise triglyceride levels.[19][18][17]

Why Is Triglyceride Testing Important?

Testing your triglycerides provides several important benefits for cardiovascular risk assessment and management:

1. Identifies cardiovascular risk. Elevated triglycerides are an independent risk factor for heart disease. The 2018 AHA/ACC cholesterol guidelines recognize persistently elevated triglycerides (≥175 mg/dL non-fasting) as a "risk-enhancing factor" that can help guide decisions about preventive therapy.[17]

2. Helps identify metabolic syndrome. Fasting triglycerides ≥150 mg/dL is one of the five criteria for metabolic syndrome, a condition that substantially increases cardiovascular and diabetes risk.[17]

3. Guides treatment decisions. For patients with established cardiovascular disease or diabetes who have elevated triglycerides despite statin therapy, specific triglyceride-lowering treatments like icosapent ethyl may provide additional cardiovascular protection.[17][21]

4. Identifies pancreatitis risk. Severely elevated triglycerides (≥500 mg/dL) require treatment to prevent acute pancreatitis, a potentially life-threatening condition.[16]

5. Reveals secondary causes. Very high triglycerides often signal an underlying condition (like uncontrolled diabetes or hypothyroidism) that needs to be addressed.[19][17]

6. Monitors treatment response. Triglycerides respond dramatically to lifestyle changes and medications, making them useful for tracking the effectiveness of interventions.[17]

How Can You Lower Your Triglycerides?

The good news is that triglycerides are highly responsive to lifestyle modifications—often more so than other lipid parameters. Comprehensive lifestyle changes can reduce triglycerides by 20% to 50%, and in some cases by as much as 70%.The encouraging news is that triglycerides are often very responsive to lifestyle change, with comprehensive interventions lowering levels by 20–50% and sometimes even more. Weight loss is the most powerful lever—losing just 5–10% of body weight can reduce triglycerides by about 20%, with larger losses leading to even greater improvements—while diet (reducing sugars and refined carbohydrates, limiting alcohol, choosing healthy fats, and increasing fiber) and regular aerobic exercise can each contribute meaningful additional reductions. When lifestyle measures aren’t enough, medications—most commonly statins in people with elevated cardiovascular risk—can provide further triglyceride lowering alongside their broader heart-protective benefits.[17][18][22][3][23]

References

1. Triglycerides and Cardiovascular Disease: A Scientific Statement From the American Heart Association. Miller M, Stone NJ, Ballantyne C, et al. Circulation. 2011;123(20):2292-333. doi:10.1161/CIR.0b013e3182160726.

2. Clinical Trial Design for Triglyceride-Rich Lipoprotein-Lowering Therapies: JACC Focus Seminar 3/3. Malick WA, Waksman O, Do R, et al. Journal of the American College of Cardiology. 2023;81(16):1646-1658. doi:10.1016/j.jacc.2023.02.034.

3. New Therapies for Lowering Triglyceride-Rich Lipoproteins: JACC Focus Seminar 3/4. Rosenson RS, Shaik A, Song W. Journal of the American College of Cardiology. 2021;78(18):1817-1830. doi:10.1016/j.jacc.2021.08.051.

4. Triglycerides and Cardiovascular Disease. Nordestgaard BG, Varbo A. Lancet (London, England). 2014;384(9943):626-635. doi:10.1016/S0140-6736(14)61177-6.

5. Remnant Cholesterol, Not LDL Cholesterol, Is Associated With Incident Cardiovascular Disease. Castañer O, Pintó X, Subirana I, et al. Journal of the American College of Cardiology. 2020;76(23):2712-2724. doi:10.1016/j.jacc.2020.10.008.

6. Mendelian Randomization of Blood Lipids for Coronary Heart Disease. Holmes MV, Asselbergs FW, Palmer TM, et al. European Heart Journal. 2015;36(9):539-50. doi:10.1093/eurheartj/eht571.

7. Genetics and Genomics for the Prevention and Treatment of Cardiovascular Disease: Update: A Scientific Statement From the American Heart Association. Ganesh SK, Arnett DK, Assimes TL, et al. Circulation. 2013;128(25):2813-51. doi:10.1161/01.cir.0000437913.98912.1d.

8. Triglyceride-Rich Lipoproteins, Remnants and Atherosclerotic Cardiovascular Disease: What We Know and What We Need to Know. Chapman MJ, Packard CJ, Björnson E, Ginsberg HN, Borén J. Atherosclerosis. 2025;410:120529. doi:10.1016/j.atherosclerosis.2025.120529.

9. Triglyceride-Rich Lipoproteins and Their Remnants: Metabolic Insights, Role in Atherosclerotic Cardiovascular Disease, and Emerging Therapeutic Strategies-a Consensus Statement From the European Atherosclerosis Society. Ginsberg HN, Packard CJ, Chapman MJ, et al. European Heart Journal. 2021;42(47):4791-4806. doi:10.1093/eurheartj/ehab551.

10. Cholesterol Remnants, Triglyceride-Rich Lipoproteins and Cardiovascular Risk. Baratta F, Cocomello N, Coronati M, et al. International Journal of Molecular Sciences. 2023;24(5):4268. doi:10.3390/ijms24054268.

11. Elevated Remnant Cholesterol, Plasma Triglycerides, and Cardiovascular and Non-Cardiovascular Mortality. Wadström BN, Pedersen KM, Wulff AB, Nordestgaard BG. European Heart Journal. 2023;44(16):1432-1445. doi:10.1093/eurheartj/ehac822.

12. VLDL Cholesterol Accounts for One-Half of the Risk of Myocardial Infarction Associated With apoB-Containing Lipoproteins. Balling M, Afzal S, Varbo A, et al. Journal of the American College of Cardiology. 2020;76(23):2725-2735. doi:10.1016/j.jacc.2020.09.610.

13. Association of Apolipoprotein B–Containing Lipoproteins and Risk of Myocardial Infarction in Individuals With and Without Atherosclerosis: Distinguishing Between Particle Concentration, Type, and Content. Marston NA, Giugliano RP, Melloni GEM, et al. JAMA Cardiology. 2022;7(3):250-256. doi:10.1001/jamacardio.2021.5083.

14. Association of Triglyceride-Lowering LPL Variants and LDL-C–Lowering LDLR Variants With Risk of Coronary Heart Disease. Ference BA, Kastelein JJP, Ray KK, et al. JAMA. 2019;321(4):364-373. doi:10.1001/jama.2018.20045.

15. Apolipoprotein B-Containing Lipoproteins in Atherogenesis. Borén J, Packard CJ, Binder CJ. Nature Reviews. Cardiology. 2025;22(6):399-413. doi:10.1038/s41569-024-01111-0.

16. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Grundy SM, Stone NJ, Bailey AL, et al. Journal of the American College of Cardiology. 2019;73(24):e285-e350. doi:10.1016/j.jacc.2018.11.003.

17. 2021 ACC Expert Consensus Decision Pathway on the Management of ASCVD Risk Reduction in Patients With Persistent Hypertriglyceridemia: A Report of the American College of Cardiology Solution Set Oversight Committee. Virani SS, Morris PB, Agarwala A, et al. Journal of the American College of Cardiology. 2021;78(9):960-993. doi:10.1016/j.jacc.2021.06.011.

18. Management of Hypertriglyceridemia: Common Questions and Answers. Oh RC, Trivette ET, Westerfield KL. American Family Physician. 2020;102(6):347-354.

19. Management of Hypertriglyceridemia. Simha V. BMJ (Clinical Research Ed.). 2020;371:m3109. doi:10.1136/bmj.m3109.

20. Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline. Berglund L, Brunzell JD, Goldberg AC, et al. The Journal of Clinical Endocrinology and Metabolism. 2012;97(9):2969-89. doi:10.1210/jc.2011-3213.

21. Cardiovascular Risk Reduction with Icosapent Ethyl for Hypertriglyceridemia. Bhatt DL, Steg PG, Miller M, et al. The New England Journal of Medicine. 2019;380(1):11-22. doi:10.1056/NEJMoa1812792.

22. Comprehensive Management of Cardiovascular Risk Factors for Adults With Type 2 Diabetes: A Scientific Statement From the American Heart Association. Joseph JJ, Deedwania P, Acharya T, et al. Circulation. 2022;145(9):e722-e759. doi:10.1161/CIR.0000000000001040.

23. Long-Chain Omega-3 Fatty Acids, Fibrates and Niacin as Therapeutic Options in the Treatment of Hypertriglyceridemia: A Review of the Literature. Ito MK. Atherosclerosis. 2015;242(2):647-56. doi:10.1016/j.atherosclerosis.2015.06.012.