Posted on 12/11/2013 at 08:39:57 AM by Student BloggerBy Larry Istrail, ACCN13 Blogger
Dr. Ronald Krauss, a world-renowned physician and researcher, spoke at ACCN 2013 about the evidence implicating saturated fats and dietary cholesterol in the etiology of cardiovascular disease. It was discovered in his lab that the “LDL” we all hear about in the media is actually a conglomerate of many different LDL particles—large buoyant ones and small dense others—that are largely determined by the foods we eat.
Dr. Krauss's talk began by covering the counterintuitive finding that dietary cholesterol has a very small and variable effect on blood cholesterol, citing one study that found no correlation between egg consumption of up to 10 eggs per week and cardiovascular risk. This is likely due to the fact that your liver has the ability to detect dietary cholesterol and adjust its cholesterol production accordingly. A review of the historical literature regarding dietary cholesterol can be viewed here. This has very important implications for dietary policy, since this fact first appeared in the literature as far back as 1955 yet we are still told to limit our cholesterol intake to less than 300mg per day.
Dr. Krauss went on to discuss the role of saturated fats in the development of heart disease. The logic explaining its role is a linear one: eating saturated fat results in a rise in LDL and total cholesterol (surprisingly HDL as well), and high cholesterol is associated with heart disease. But this logic does not differentiate between pharmacologic and dietary increases in LDL. There is documented benefit to cholesterol lowering with statin therapy in subjects with known heart disease, but the evidence that lowering LDL by decreasing saturated fat results in less heart disease has yet to be convincingly demonstrated.
This logic also does not address the sub fractionation of LDL particles. As I described in a previous post documenting Krauss's work, “when Dr. Krauss and other researchers began testing the effects of diet on these LDL particles, he consistently found that the dietary carbohydrates seemed to be changing the density of the LDL particles. As the carbohydrate content of the diet increased, along with a concomitant decrease in dietary fat, the LDL particles migrated from their buoyant form to the small, dense, atherogenic form.”
This would suggest that the carbohydrates – not saturated fats – in the diet may be the bigger contributor to the development of heart disease. “Carbohydrates,” Dr. Krauss described in Friday's lecture, “have a major influence on the smaller LDL particles. They can increase small LDL without increasing total LDL. The main effect of saturated fats is on larger LDL particles, which is less strongly associated with CVD risk than small LDL.” A summary of the randomized clinical trials and prospective studies related to saturated fat and heart disease can be found at the link. Krauss concluded his controversial talk by stating that “LDL is important but making recommendations for saturated fat is really not good science.”