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High-Density Lipoprotein Cholesterol (HDL-C) is often referred to as "good" cholesterol due to its well-established protective role against the development of cardiovascular disease. Its functions are largely antagonistic to those of LDL-C, and its concentration in the blood is a key indicator of cardiovascular health.
The primary beneficial function of HDL-C is its central role in a process called reverse cholesterol transport.24 HDL particles act as scavengers, actively removing excess cholesterol from peripheral cells, including the foam cells within atherosclerotic plaques, and transporting it back to the liver.5 Once in the liver, this cholesterol can be excreted from the body via bile. This process effectively counteracts the plaque-forming actions of LDL-C, and as a result, higher levels of HDL-C are consistently associated with a lower risk of heart attack and stroke.2
A unique feature of HDL-C is that its optimal levels differ between men and women, a distinction not typically seen with other lipid parameters. This is due to hormonal and genetic differences.11
The standard reference ranges for HDL-C in adults are as follows 5:
For Men:
Low (Increased Risk): Less than 40 mg/dL (<1.0 mmol/L)
Desirable: 40 mg/dL or higher
Best (Protective): 60 mg/dL or higher (≥1.6 mmol/L)
For Women:
Low (Increased Risk): Less than 50 mg/dL (<1.3 mmol/L)
Desirable: 50 mg/dL or higher
Best (Protective): 60 mg/dL or higher (≥1.6 mmol/L)
Various lifestyle factors can significantly influence HDL-C levels. Regular aerobic exercise is one of the most effective ways to raise HDL-C. Conversely, smoking is known to lower HDL-C levels. Other factors include genetic predisposition, body weight, and moderate alcohol consumption, which has been linked to higher HDL-C levels.2
While the inverse relationship between HDL-C levels and ASCVD risk is well-established, the clinical approach to modulating it is more complex than a simple "higher is always better" philosophy. This nuanced understanding stems from two key lines of evidence. First, numerous large-scale clinical trials of pharmacological agents designed specifically to raise HDL-C levels (such as niacin and CETP inhibitors) have failed to demonstrate a corresponding reduction in cardiovascular events.26 This suggests that the mere quantity of circulating HDL-C may be less important than the efficiency and quality of its function in reverse cholesterol transport. Second, observational studies have revealed a paradoxical association, where individuals with genetically determined, extremely high HDL-C levels (e.g., above 100 mg/dL) may actually have an increased risk of heart disease.26 This has led to the concept of "dysfunctional HDL," where the HDL particles, despite being numerous, are ineffective at their protective role. Taken together, these findings indicate that the relationship between HDL-C and cardiovascular risk is not strictly linear but may follow a J- or U-shaped curve, where both very low and potentially very high levels are associated with adverse outcomes. This shifts the clinical focus from simply increasing the HDL-C concentration to promoting overall HDL functionality, which is best achieved through lifestyle modifications like exercise and smoking cessation.
Triglycerides are the most abundant type of fat in the human body and a critical component of the lipid profile. While their primary role is in energy metabolism, elevated levels of triglycerides are increasingly recognized as an important independent risk factor for atherosclerotic cardiovascular disease.
Triglycerides are composed of a glycerol molecule attached to three fatty acid chains. They are derived from two main sources: dietary intake of fats and carbohydrates, and endogenous synthesis in the liver.2 When caloric intake exceeds the body's immediate energy needs, the excess calories, particularly from carbohydrates, are converted into triglycerides by the liver and stored in fat cells (adipocytes) for future use. Between meals, these stored triglycerides are released as fatty acids to provide energy for metabolic processes.19
Triglyceride levels are known to fluctuate significantly in response to food intake. For this reason, a standard lipid profile is typically performed after a 9- to 12-hour fast to obtain a baseline measurement.22
The standard classifications for fasting triglyceride levels in adults are 1:
Normal/Desirable: Less than 150 mg/dL (<1.7 mmol/L)
Borderline High: 150–199 mg/dL (1.7–2.2 mmol/L)
High: 200–499 mg/dL (2.3–5.6 mmol/L)
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