Triglycerides are concentrated form of fat found in the diet, in adipose tissue, and circulating in the blood. They are composed of a glycerol backbone attached in different combinations to three fatty acid types that include monounsaturated, polyunsaturated, and saturated. Triglycerides increase after a meal but should return to normal fairly quickly.
Persistently elevated triglycerides are a sign of metabolic dysfunction and are associated with obesity, CVD, metabolic syndrome, mitochondrial dysfunction, and pancreatitis. Low triglycerides in the blood can be associated with poor absorption, inadequate intake, and hyperthyroidism.
Standard Range: 0.00 - 150.00 mg/dL (0.00 - 1.69 mmol/L)
The ODX Range: 70 - 80 mg/dL (0.79 - 0.90 mmol/L)
Low triglycerides are associated with malabsorption, malnutrition, and hyperthyroidism. Drugs that may decrease triglycerides include asparaginase, fibrates, clofibrate, colestipol, and statins, as well as ascorbic acid (Pagana 2021).
High triglycerides are associated with insulin resistance (Hong 2019), elevated glucose, poorly controlled diabetes, glycogen storage disease, hypothyroidism, cirrhosis, pregnancy, nephrotic syndrome, peripheral vascular disease, hypertension, hyperlipidemias, atherosclerotic coronary disease, myocardial infarction, and excess intake of carbohydrate, fat, and alcohol. Drugs that may increase triglycerides include estrogen, oral contraceptives, and cholestyramine (Pagana 2021), anti-depressants, thiazides, non-cardiac beta-blockers, bile acid sequestrants, and tamoxifen (Parhofer 2019).
Elevated levels may also be seen with excess fat or sugar intake, pancreatitis, obesity, metabolic syndrome, lupus, sepsis, pregnancy (Parhofer 2019), elevated cortisol (Le-Ha 2016), pesticide exposure (Aminov 2013), and the APOA5 gene (Arsenault 2011).
Triglycerides (TGs) are a form of fat found in food and stored in adipose tissue. They may also be referred to as triacylglycerols. Triglycerides are found circulating in the blood, carried primarily by VLDLs but also by LDLs. They can be produced by the liver de novo from glycerol and fatty acids (Pagana 2021). The glycerol backbone may be attached to various types of fatty acids, such as monounsaturated, polyunsaturated, and/or saturated fatty acids (Gropper 2021). Triglycerides can also be synthesized from glucose, a major source of 3-glycerol phosphate (Reshef 2003).
Measuring triglycerides in the blood is typically done in the fasting state as levels can vary widely after a meal though they usually remain below 400 mg/dL (4.52 mmol/L) even after a high-fat meal. Hypertriglyceridemia increases risk of atherosclerosis, an effect mediated by the apoB-containing lipoproteins that carry TGs. Elevated triglycerides that are commonly seen with obesity, metabolic syndrome, and diabetes may be reduced by moderation of alcohol intake, decreased intake of rapidly metabolized carbohydrates (e.g., sugary beverages), blood glucose control, weight loss, increased physical activity, intake of 2-4 grams of omega-3 fatty acids, and use of medium-chain triglycerides in severe hypertriglyceridemia (Parhofer (2019).
Elevated triglycerides, especially in the fasting state, reflect metabolic dysfunction and are associated with increased cardiometabolic risk. Review of data from the Atherosclerosis Risk in Communities (ARIC) and Framingham Offspring Study revealed an association between fasting serum triglycerides and “hard” CVD endpoints, i.e., myocardial infarction, stroke, and death. The association was clear even below the cut-off of 150 mg/dL (1.69 mmol/L) for “normal” fasting TGs. A tighter optimal range is consistent with the American Heart Association’s recommendation for TGs of less than 100 mg/dL (1.13 mmol/L). Those in the lowest quartile of TGs (less than 83 mg/dL [0.93 mmol/L] had the lowest probability of a CVD event. Incidence increased as average TGs increased. Individuals at the highest TG quartile (153 mg/dL [1.73 mmol/L] or above) had highest CVD risk as well as higher fasting glucose, LDL-C, and non-HDL-C, and were more likely to be male, diabetic, and on cholesterol-lowering medication (Aberra 2020).
High triglycerides are associated with pancreatitis and can induce the condition if levels exceed 1000 mg/dL (11.3 mmol/L). Additional causes of high triglycerides include obesity, metabolic syndrome, diabetes, lupus, excess calorie intake from fat or rapidly metabolized carbohydrates, sepsis, pregnancy, anti-depressants, thiazides, non-cardiac beta-blockers, bile acid sequestrants, tamoxifen (Parhofer 2019), and elevated cortisol (Le-Ha 2016). High triglycerides may also have a genetic component related to the APOA5 gene (Arsenault 2011). Persistent organic pollutants, including PCBs, DDT, and fat-soluble pesticides, may also be associated with elevated triglycerides (Aminov 2013).
Hypertriglyceridemia may lead to mitochondrial dysfunction and increased insulin resistance. In one cross-sectional study of 935 hypertensive patients, higher triglycerides, as well higher LDL-C/HDL-C ratio, were significantly associated with newly diagnosed diabetes (Hong 2019).
One prospective randomized double-blind study of 15,355 subjects demonstrated an association between elevated triglycerides and 22-year all-cause mortality. Risk increased by 68% for those with TGs above 500 mg/dL (5.65 mmol/L) versus those with TGs below 100 mg/dL (1.13 mmol/L). The study found that even triglycerides in the range of 100-149 mg/dL (1.13-1.68 mmol/L) were associated with increased mortality risk (Klempfner 2016).
Although established ranges currently refer to fasting triglycerides, researchers suggest that evaluation of post-prandial triglycerides may also have clinical value (Arsenault 2011). Triglycerides are expected to rise 20-30% following a meal and sustain elevations for approximately 2 hours. Various non-fasting cut-offs have been proposed including the American Heart Association’s recommended 200 mg/dL (2.26 mmol/L). A lower non-fasting threshold of 175 mg/dL (1.98 mmol/L) to reduce risk of CVD incidents was suggested by a prospective study of 6,391 subjects in the Women’s Health Study (White 2015).
However, even lower non-fasting triglyceride levels may be desirable. Data review from the Copenhagen City Heart Study found that individuals with the lowest non-fasting triglycerides, i.e., below 89 mg/dL (1 mmol/L), had the lowest all-cause mortality, possibly due to genetic factors as well as reductions in remnant cholesterol (Thomsen 2014).
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