Dietary Cholesterol: Still a risk factor for CHD?

THE QUICK TAKE:  Contrary to long-standing perceptions, dietary cholesterol, whether from egg consumption, shellfish, or other foods of animal origin, does not have any adverse effect on serum lipids or risk of coronary vascular disease or stroke.  Recent studies have in fact shown positive effects on HDL cholesterol (which is why an elevated total cholesterol is now thought to be misleading), LDL/HDL ratio, and LDL and HDL particle size (which is associated with less atherogenic lipid particles), and lower risk of hemorrhagic stroke.  There no longer appears to be a need for an upper daily limit for dietary cholesterol consumption;  eggs are increasingly being viewed as health food.

THE ONE MINUTE VERSION: Although proponents of the Lipid Hypothesis have long promoted dietary cholesterol as a risk factor for elevated serum cholesterol and therefore also for increased coronary disease risk, recent researchers1 2 have called into question to rethink  this association.  Although the USA continues to put an upper daily limit of 300mg for dietary cholesterol, European countries, Australia, Canada, New Zealand, Korea and India have removed this restriction.  And, given the otherwise dense nutritional value of eggs, (widely thought of as the highest concentration of cholesterol in the Western diet), there seems to be pressure to reassess the decades-long vilification of dietary cholesterol.

Much recent research has supported this perspective.  A large prospective study reported that increased shellfish intake (another high source of dietary cholesterol) was associated with a significantly decreased risk of myocardial infarction in middle-aged men. The Tehran Lipid and Glucose Study found no relation of dietary cholesterol to serum LDL cholesterol, although it was positively correlated with HDL cholesterol levels.   Another study found that cholesterol-rich foods were associated with a decrease in plasma LDL cholesterol during a calorie restricted diet. And after following more than 20,000 men for 20 years, the Physician’s Health Study did not find any association with increasing egg consumption and myocardial infarction or stroke. And finally, a 2013 meta-analysis of prospective cohort studies reported  “no evidence of a curve linear association was seen between egg consumption and risk of coronary heart disease or stroke”, and in fact, “people with higher egg consumption had a 25% lower risk of developing hemorrhagic stroke.”

Some of the pre-eminent researchers in the diet-heart health hypothesis have subsequently refuted some of their previously held convictions.  Ancel Keys, the author of the Seven Countries Study, felt by many to be the father of the lipid hypothesis, “notes the often inaccurate publicity concerning the importance of dietary cholesterol”, as quoted in a letter to the editor of the New England Journal of Medicine:

Dietary cholesterol has an important effect on the cholesterol level in the blood of chickens and rabbits, but many controlled experiments have shown that dietary cholesterol has a limited effect in humans.  Adding cholesterol to a cholesterol-free diet raises the blood level in humans, but when added to an unrestricted diet it has a minimal effect.  …..(Instead), emphasis on the fatty acids in the diet is needed.” (Source: Ancel Keys:  “Letter: Normal Plasma Cholesterol in a Man Who Eats 25 Eggs aDay,”  New England Journal of Medicine, Aug 22, 1991; 325(8): 584.)

And this from George V. Mann, MD,  Associate Director of the Framingham Heart Study:

The diet‐heart idea [the notion that saturated fats and cholesterol cause heart disease] is the greatest scientific deception of our times. This idea has been repeatedly shown to be wrong, and yet, for complicated reasons of pride, profit and prejudice, the hypothesis continues to be exploited by scientists, fund‐raising enterprises,food companies and even governmental agencies. The public is being deceived by the greatest health scam of the century.

(Mann,George V., “Coronary heart disease – ‘Doing the wrong things.’”  Nutrition Today, Jul/Aug1985; 12‐14.)

And finally this quote from the longest standing director (1979-2005) of the Framingham Study, William Castelli, MD:

“….in Framingham, Mass, the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower the person’s serum cholesterol. The opposite of what one saw in the 26 metabolic ward studies, the opposite of what the equations provided by Hegsted et al and Keys et al.”

(Castelli, William, “Concerning the Possibility of a Nut. . .”  Archives of Internal Medicine, Jul 1992; 152(7):1371‐1372.)

So what can we say about and risk of dietary cholesterol with CVD?  In short, there appear to be no adverse effects of dietary cholesterol on lipid levels, but rather, there appear to be positive effects on HDL, LDL/HDL ratio, and LDL and HDL particle size. The introduction of this review summarizes it well:

“Dietary cholesterol has been shown to increase both LDL and HDL in those individuals who respond to a cholesterol challenge without altering the LDL cholesterol/HDL cholesterol ratio, a key marker of CVD risk. Further, dietary cholesterol has been shown to increase only HDL with no changes in LDL with average cholesterol consumption and during weight loss interventions. Ingestion of cholesterol has also been shown to increase the size of both LDL and HDL particles with the associated implications of a less atherogenic LDL particle as well as more functional HDL in reverse cholesterol transport. Other changes observed in lipoprotein metabolism are a greater number of large LDL and decreases in small LDL subfractions.”



Rethinking dietary cholesterol. Curr Opin Clin Nutr Metab Care. 2012 Mar;15(2):117-21. doi: 10.1097/MCO.0b013e32834d2259. Fernandez ML.

Exploring the factors that affect blood cholesterol and heart disease risk: is dietary cholesterol as bad for you as history leads us to believe? Kanter MM, Kris-Etherton PM, Fernandez ML, Vickers KC, Katz DL.  Adv Nutr. 2012 Sep 1;3(5):711-7. doi: 10.3945/an.111.001321.

Fish and Shellfish Consumption in Relation to Death from Myocardial Infarction among Men in Shanghai, ChinaJian-Min Yuan, Ronald K. Ross, Yu-Tang Gao and Mimi C. Yu. American Journal of Epidemiology Volume 154, Issue 9  Pp. 809-816.

Combined effects of saturated fat and cholesterol intakes on serum lipids: Tehran Lipid and Glucose Study.  Mirmiran P, Ramezankhani A, Azizi F. Nutrition. 2009 May;25(5):526-31. doi: 10.1016/j.nut.2008.11.018. Epub 2009 Jan 3.

Increased dietary cholesterol does not increase plasma low density lipoprotein when accompanied by an energy-restricted diet and weight loss. Harman NL, Leeds AR, Griffin BA.  Eur J Nutr. 2008 Sep;47(6):287-93. doi: 10.1007/s00394-008-0730-y. Epub 2008 Aug 26.

Egg consumption in relation to cardiovascular disease and mortality: the Physicians’ Health Study.  Luc Djoussé and J Michael GazianoAm J Clin Nutr April 2008vol. 87 no. 4 964-969.

Egg consumption and risk of coronary heart disease and stroke: dose-response meta-analysis of prospective cohort studies. Ying Rong, Li Chen, Tingting Zhu, Yadong Song, Miao Yu,  Zhilei Shan,  Amanda Sands, Frank B Hu, Liegang Liu. BMJ 2013; 346 doi: (Published 7 January 2013)

“Letter: Normal Plasma Cholesterol in a Man Who Eats 25 Eggs aDay,”  Ancel Keys. New England Journal of Medicine, Aug 22, 1991; 325(8): 584.
Dietary Cholesterol Affects Plasma Lipid Levels, the Intravascular Processing of Lipoproteins and Reverse Cholesterol Transport without Increasing the Risk for Heart Disease. Jacqueline Barona and Maria Luz Fernandez. Nutrients. 2012 August; 4(8): 1015–1025. Published online 2012 August 17. doi:  10.3390/nu4081015

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