LDL Cholesterol as a Predictor of Mortality, and Beyond
To Fast or Not to Fast, That Is the Question?
The necessity of a fasting lipid panel for assessment of atherosclerotic cardiovascular disease (ASCVD) risk has been assumed now for decades. The rationale for this position has been the estimation of levels of low-density lipoprotein cholesterol (LDL-C), a major risk factor for ASCVD, by correcting for nonfasting changes in plasma triglycerides using the so-called Friedewald equation developed during the 1960s at the then National Heart Institute.1 Because LDL-C determination by ultracentrifugation is time consuming and expensive and direct LDL-C measurements have proven no more accurate than the Friedewald equation, the calculation of LDL-C has remained more than adequate, and was recently endorsed by the 2013 American College of Cardiology (ACC)/American Heart Association (AHA) Risk Assessment Work Group2 and used in the 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Disease Risk in Adults.3 The equation estimates LDL-C after measuring total cholesterol, high-density cholesterol (HDL-C) and triglycerides (TG), and then subtracting from the total cholesterol concentration the HDL-C plus very-low-density lipoprotein cholesterol (VLDL-C), which is estimated by TG/5. This formula is not used when plasma TG >400 mg/dL because in this metabolic setting VLDL particles contain relatively less cholesterol and VLDL-C contribution is therefore overestimated and the calculated LDL-C is falsely low.
Article see p 546
The scientific rationale for addressing the importance of fasting versus nonfasting is that food consumption results in variable increases in plasma TG. Here the effect is not only that of dietary fat but also carbohydrate. Carbohydrate intake increases VLDL TG secretion within 30 to 90 minutes after ingestion, whereas fat intake in normotriglyceridemic people increases plasma TG via …