![]() ![]() HDL is a collection of macromolecular particles that contain >80 different proteins ( 12, 13) and range in size from 14 nm ( 14). These discrepancies highlight a central question: Does HDL deficiency promote human atherosclerosis, or is it simply a marker for other risk factors, such as insulin resistance ( 2, 3)? To make this determination, it is critical to identify HDL metrics that truly reflect CVD risk. Furthermore, people with Tangier disease (who lack ATP-binding cassette transporter 1 (ABCA1), a key first step in cholesterol export from cells) have very low HDL-C levels and accumulate cholesterol-laden macrophages in many different tissues ( 10, 11). Also, humans with familial deficiency of apoA-I, the major HDL protein, suffer severe, early-onset CVD ( 9). For example, a polymorphism in apoA-I, the major HDL protein, associates with low HDL cholesterol (HDL-C) levels and premature coronary artery disease ( 8). It is important to note that many lines of evidence strongly suggest that HDL directly protects against vascular disease. These observations indicate that HDL-C levels do not always predict CVD risk and that elevating HDL-C is not necessarily therapeutic. Strikingly, a CETP inhibitor and niacin, two interventions that elevate HDL-C, failed to reduce CVD risk in statin-treated humans with established CVD ( 6, 7). For example, genetic variations that alter levels of HDL-C do not always predict CVD risk ( 5). However, recent work has cast doubt on the hypothesis that the concentration of HDL-C captures its proposed cardioprotective functions ( 2– 4). Indeed, there is a robust, inverse association of HDL-C with cardiovascular disease (CVD) risk in clinical, epidemiological and genetic studies ( 1). ![]() Plasma levels of high density lipoprotein cholesterol (HDL-C) are widely used clinically to assess HDL’s cardioprotective potential.
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