A common misconception is that because statin drugs lower fasting cholesterol levels by approximately one-half and a low-fat diet only lowers cholesterol levels by approximately 10% (14
), there is no point in worrying about diet – simply take a statin, and it will be okay to eat anything! Nothing could be further from the truth. Although statins lower coronary artery disease risk by 25% to 40% and possibly more, it has been estimated that diet may account for 85% of coronary risk (15
), and in the best of circumstances, statins still leave a residual coronary risk in the order of 70% in major clinical trials (16
In human subjects, a high intake of dietary cholesterol increased fasting low-density lipoprotein (LDL) levels by approximately 10% (17
) in a dose-dependent manner (18
). A 10% increase in fasting cholesterol levels may not seem like much, but in the first study to show that diet and cholestyramine reduced coronary risk, a 12% reduction of fasting LDL levels reduced coronary risk by 19% (19
). Even the relatively permissive Step 1 American Heart Association diet (300 mg/day of cholesterol and 30% of calories from fat) reduced fasting LDL levels by approximately 10%, compared with a typical western diet (14
Furthermore, diet is not all about fasting lipids; it is mainly about the three-quarters of the day that we are in the nonfasting state (20
). Fasting lipids can be thought of as a baseline; they show what the endothelium was exposed to for the last few hours of the night. Then we get up and eat breakfast. For the next several hours, the endothelium is exposed to sugars, fats, cholesterol and free radicals from that meal, on top of the baseline. Then we have lunch followed by supper and by the time we retire to bed, we have been in a nonfasting state for approximately 18 h of the day. This is determined without even considering snacks between meals.
A focus on fasting LDL and dietary cholesterol levels per se has obscured three important issues. The first is that dietary cholesterol increased susceptibility of LDL to oxidation by 37% (21
) in one study and by 39% in another (22
). The latter study was performed with cooked egg yolks fed for periods of 32 days. The second issue is that the consumption of more than 140 mg dietary cholesterol in a single meal markedly increases postprandial lipemia (23
). Third, dietary cholesterol potentiates the adverse effects of dietary saturated fat (the bacon and egg effect), as discussed below.
In a study of normolipidemic young men (52 Caucasian and 32 non-Caucasian), Fielding et al (24
) compared the effects of diets high or low in saturated and polyunsaturated fat (polyunsaturated/saturated fat ratio 0.8 versus 0.3). The study also compared diets high versus low in cholesterol (200 mg versus 600 mg). At the lower cholesterol intake, the high saturated fat diet had only a modest effect on LDL cholesterol level in Caucasians (increase of 6 mg/dL [0.16 mmol/L])
and no effect in non-Caucasians. However, the diet with 600 mg cholesterol and high in saturated fat led to a substantial mean increase in LDL cholesterol level, which was significantly greater in Caucasian than in non-Caucasian subjects (increase of 31 mg/dL [0.82 mmol/L] versus 16 mg/dL [0.41 mmol/L], P<0.005). In contrast, 600 mg of cholesterol with increased polyunsaturated fat gave a mean LDL level increase of 16 mg/dL (0.42 mmol/L) – lower than that found when the same high cholesterol intake was coupled with increased saturated fat. Variation in cholesterol level rather than the proportions of saturated and polyunsaturated fat had the most influence on LDL cholesterol levels. Among non-Caucasians in this study, it was the only significant factor.