Saturated Fat Meal Damages Arteries

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More than 25 years ago, Dr. Zilversmit proposed that atherosclerosis may be caused in large part by changes in blood lipids that last for several hours after each fat- and cholesterol-rich meal. He suggested that simply relying on fasting blood lipid levels may not be the best way to predict the impact of diet on atherosclerosis.1 Growing evidence suggests Dr. Zilversmit’s hypothesis may be correct.

A recent study examined the impact of a single saturated-fat-rich meal, or one high in polyunsaturated fat, on the anti-inflammatory potential of HDL (good cholesterol) particles and the function of blood vessels. The researchers conclude that, “Consumption of saturated fat reduces the anti-inflammatory potential of HDL and impairs arterial endothelial function.”2

Another study that examined the impact of a single high-fat meal on patients with coronary heart disease (CAD) also showed impaired blood flow occurs for several hours after a single high-fat meal. They conclude “the postprandial state after a high-fat meal is critical in atherogenesis, as it induces endothelial dysfunction through an oxidative stress mechanism.”3

So while diets high in fat, and particularly saturated fat, may raise HDL, they appear to impair the functioning of the HDL particles. In addition, the increased oxidative stress and impaired blood flow that occur after a single high-fat meal, but not after a very-low-fat meal, may be atherogenic.4

Bottom Line: Perhaps it is time for the American Heart Association and the National Cholesterol Education Program to rescind their questionable warnings about a very-low-fat diet for treating and preventing coronary artery disease? In light of growing evidence that a very-low-fat-near-vegetarian diet, composed largely of minimally processed foods, may in fact be the safest and most effective dietary strategy for preventing and even reversing atherosclerosis,

By James J. Kenney, PhD, RD, FACN

1 Circulation 1979;60:473-85

2 J Am Coll Cardiol 2006;48:715-20

3 Clin Cardiol 2002;25:219-24

4 Nutr Rev 1998;56:182-5

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