High Fat Meals Promote CVD

There is growing evidence that altered levels of blood fats after meals play a role in promoting atherosclerosis and cardiovascular disease (CVD). It is now known that increased release of inflammatory substances such as IL-6, IL-8, CRP, and TNF-alpha in the blood plays a role in promoting cardiovascular disease (CVD). Research has shown that a high-fat meal, but not a very high-carbohydrate meal, increases the release of these inflammatory substances in the blood.1 More recently, a single high-fat meal has been shown to increase these inflammatory substances in part via the enhanced uptake of bacterial toxins from the gut.2

High-fat meals tend to be calorie dense and associated with reduced satiety/calorie. A diet with less satiety over time promotes weight gain. Increased body fat stores, especially when accompanied by insulin resistance, are associated with increased free fatty acids (FFA) in the blood. Higher levels of FFA in the blood appear to promote inflammation and CVD. However, even a single high-fat meal was shown to markedly elevate FFA levels for several hours and this was accompanied by impaired blood flow. By contrast, this same study showed a high-carbohydrate meal and a mixed meal did not increase FFA levels nor did they impair endothelial function and reduce blood flow.3 Bottom Line: It is increasingly clear that each high-fat meal or snack consumed increases inflammation and impairs endothelial function for several hours due in part to increased FFA levels and perhaps an enhanced release of toxins from the gut. It seems likely that a diet high in fat may promote CVD even in people who maintain fairly healthy levels of LDL-C by taking statin drugs. Statin drugs likely do little to block the adverse effects of high-fat meals on inflammation and CVD. This may be why a very-low-fat, near vegetarian diet can reverse atherosclerosis, get rid of angina, and dramatically cut the risk of CVD, while statin drugs with more moderate changes in dietary fat intake only slow the progression of atherosclerosis. By James J. Kenney PhD, RD, FACN 1. J Am Coll Cardiol 2002;39:1145-50 2. Am J Clin Nutr 2007;86:1286-92 3. Am J Clin Nutr 2007;86:923-8