The most recent Australian Health Survey1, found one in three Australians aged 18 years and over have abnormal or high total cholesterol and/or LDL cholesterol levels. Since high plasma cholesterol levels, in particular high LDL cholesterol levels, are an important traditional risk factor for heart disease it is vital to understand the dietary and lifestyle factors which negatively impact these lipid levels.
Historically, research has focused on individual dietary components such as nutrients or single foods when it comes to assessing the factors that impact on blood cholesterol levels. More recently, however increasing attention has been given to dietary patterns and how the combination of foods, as well as the overall context of consumption influences lipid levels and overall heart disease risk2,3. To lower lipid levels and heart disease risk, the most recent advice from national and international heart associations emphasises an overall healthy eating pattern and a reduction in saturated and trans fat intake as the primary effective dietary changes2-5. Any specific limits or restrictions on dietary cholesterol intake are seldom included given a lack of evidence for a clear relationship between serum LDL cholesterol and dietary cholesterol intake2,6.
National and International recommendations
The most recent American Heart Association (AHA) guidelines for the prevention of cardiovascular disease7 emphasise the need for individuals to: “limit saturated fat, trans fat, sodium, red meat, sweets and sugar-sweetened beverages” with no specific guidelines given relating to egg or dietary cholesterol consumption7.
The Heart Foundation (Australia) states saturated fat intake is associated with coronary heart disease, and that dietary cholesterol increases total cholesterol and LDL-cholesterol but substantially less so than saturated and trans fats4. They recommend regular egg consumption within a cardio-protective, reduced saturated fat eating pattern5.
Dietary cholesterol, serum cholesterol and heart disease risk
It is known that individuals vary in their response to dietary cholesterol intake. Approximately 25% of the population have been defined as “hyper-responders”, a term used to describe those who experience an increase in serum LDL and HDL-cholesterol following intake of dietary cholesterol. Importantly, approximately 75% of the population experience moderate to no difference in serum cholesterol levels following intakes of dietary cholesterol, and are therefore described as “normal responders” or “hypo-responders” 8-11.
The potential mechanism by which the majority of the population regulates serum cholesterol levels is that when dietary cholesterol intake increases, there is a subsequent decrease in cholesterol absorption and/or endogenous cholesterol synthesis12.
Overall, evidence to date suggests the impact of dietary cholesterol intake on blood lipids is modest, particularly with respect to increasing LDL cholesterol levels13. Furthermore, even in hyper-responders when LDL-cholesterol is increased in response to dietary cholesterol intake, due to the simultaneous rise in serum HDL cholesterol levels, the overall LDL:HDL ratio is maintained. A 2015 systematic review and meta-analysis of evidence demonstrated dietary cholesterol intake increased the LDL:HDL ratio and failed to find an association between higher intakes of dietary cholesterol and CVD risk14.
Eggs, cholesterol and heart disease risk
Eggs are relatively low in saturated fat (3.4g per serve) and while they do contain cholesterol (398mg per serve), a number of studies have demonstrated they can be incorporated into a healthy dietary pattern without significant impact on cholesterol levels15-18. The most recent scientific evidence indicates no association between egg intake and increased risk of coronary heart disease in the general population14,19,20,21. This corroborates the 2013 Australian Dietary Guidelines review of scientific literature which concluded that the “consumption of eggs daily is not associated with increased risk of coronary heart disease”22.
Importantly, well-designed intervention studies do not indicate that higher egg intake has any adverse effects on CVD risk in individuals with or at risk of type 2 diabetes. A 2017 systematic review of six randomised controlled trials concluded that the consumption of 6 to 12 eggs per week, in the context of a diet that is consistent with guidelines on cardiovascular health promotion, has no adverse effect on major CVD risk factors in individuals at risk for developing diabetes or with type 2 diabetes20.
Furthermore, since the 2017 systematic review, the results of an Australian 12 month intervention study have been published which support the conclusion that eggs can be enjoyed by individuals with (or at risk of) type 2 diabetes. In the DIABEGG study, consuming ≥12 eggs per week produced no detrimental outcomes in CVD risk factors (including cholesterol, triglycerides, inflammatory markers, oxidative stress or measures of glycemia) for individuals with prediabetes or type 2 diabetes and overweight or obesity 21. These 12 month findings are an extension of the original 3-month DIABEGG study which showed that high egg (≥12 eggs per week) consumption vs low egg (<2 eggs per week) consumption, as part of a weight maintenance diet, had no detrimental effect on CVD risk factors23.
As well as data from cohort studies, a number of clinical trials have been conducted investigating the effect of short term egg consumption on various markers of heart disease and metabolic health. The majority of these trials have been conducted in at-risk populations such as individuals who are overweight or who have the metabolic syndrome, prediabetes or type 2 diabetes24-29.
In these studies, 2-3 eggs per day over 6-12 week study periods showed either no effect or in some cases improvements in blood lipids, particularly when they were consumed as part of a weight loss intervention or carbohydrate restricted diet25-27. Taken together, these results indicate that eating eggs fails to negatively affect some markers of cardiovascular disease risk and may have some favourable effects on other markers when consumed in appropriate dietary contexts.
Possible cardio-protective benefits of eggs
Meta-analyses14,30 to date show a small but significant increase in HDL cholesterol with increasing cholesterol intake from eggs. The Heart Foundation and the American Heart Association recognise low HDL as a risk factor for coronary heart disease31,32 with higher levels suggested to be cardio-protective33.
Eggs also provide nutrients that may be associated with protection from heart disease or its risk factors. For example, eggs provides folate and long chain omega-3 fatty acids34, as well as arginine, a precursor to nitric oxide, which in turn plays a central role in endothelial function35. They also contain the carotenoids lutein and zeaxanthin which have been associated with improved cardiometabolic health36,37 potentially by providing protection against lipid oxidation38 and inflammation39.
While definitive mechanisms by which eggs may provide some possible cardio-protection are limited, research increasingly suggests that the consumption of eggs does not increase the risk of CVD.
Scientific evidence shows little association between egg intake, serum cholesterol levels and coronary heart disease, particularly in the general population.
The Egg Nutrition Council therefore concludes the following:
- Eggs may be consumed daily as part of a healthy diet which is in line with the National Heart Foundation of Australia’s recommendations, as well as the NHMRC’s Australian Dietary Guidelines.
- Eggs should be considered in a similar way as other protein rich core foods and selected as part of a varied diet that is low in saturated fat and contains a variety of cardio-protective foods such as fish, wholegrains, fruit, vegetables, legumes and nuts.
- Reducing saturated fat intake is the primary dietary strategy recommended for reducing serum cholesterol levels.
- In individuals at high risk, such as people with diabetes, there is limited data based on a small number of studies to guide specific recommendations for egg consumption. However, prudent advice is that the inclusion of eggs in the context of a healthy eating pattern low in saturated fat and containing known cardio-protective foods is not associated with increased risk. Diabetes Australia recommends individuals with diabetes follow the Australian Dietary Guidelines which allows for the consumption of eggs daily. [Refer to the Egg Nutrition Council’s position statement on Eggs and Diabetes for more details in this area.]
This statement is for healthcare professionals only.
*One serve = 2x60g eggs (104g edible portion)
As diet-induced changes in total cholesterol and lipoproteins vary considerably between individuals, the Egg Nutrition Council recommends individual discussion of the recommendations regarding egg intake with their healthcare professional.
Heart Foundation: www.heartfoundation.org.au
Australian Dietary Guidelines: www.eatforhealth.gov.au/guidelines
- Australian Bureau of Statistics. Australian Health Survey: Biomedical Results for Chronic Diseases, 2011-12 (Australian Bureau of Statistics, Canberra, ACT, Australia, 2013).
- Eckel, R.H., et al. 2013 AHA/ACC guideline on lifestyle management to reduce cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 63, 2960-2984 (2014).
- Mozaffarian, D. Dietary and Policy Priorities for Cardiovascular Disease, Diabetes, and Obesity: A Comprehensive Review. Circulation [Epud ahead of print](2016).
- National Heart Foundation of Australia. Position statement. Dietary fats and dietary sterols for cardiovascular health, (2009).
- Australia, H.F.o. Eggs. (2016).
- Clayton, Z.S., Fusco, E. & Kern, M. Egg consumption and heart health: A review. Nutrition 37, 79-85 (2017).
- Wenger, N.K. Prevention of cardiovascular disease: highlights for the clinician of the 2013 American College of Cardiology/American Heart Association guidelines. Clin Cardiol 37, 239-251 (2014).
- Herron, K.L., et al. The ABCG5 polymorphism contributes to individual responses to dietary cholesterol and carotenoids in eggs. J Nutr 136, 1161-1165 (2006).
- Howell, W.H., McNamara, D.J., Tosca, M.A., Smith, B.T. & Gaines, J.A. Plasma lipid and lipoprotein responses to dietary fat and cholesterol: a meta-analysis. Am J Clin Nutr 65, 1747-1764 (1997).
- Katan, M.B. & Beynen, A.C. Characteristics of human hypo- and hyperresponders to dietary cholesterol. Am J Epidemiol 125, 387-399 (1987).
- Katan, M.B., Beynen, A.C., de Vries, J.H. & Nobels, A. Existence of consistent hypo- and hyperresponders to dietary cholesterol in man. Am J Epidemiol 123, 221-234 (1986).
- McNamara, D.J., et al. Heterogeneity of cholesterol homeostasis in man. Response to changes in dietary fat quality and cholesterol quantity. J Clin Invest 79, 1729-1739 (1987).
- Griffin, J.D. & Lichtenstein, A.H. Dietary Cholesterol and Plasma Lipoprotein Profiles: Randomized-Controlled Trials. Curr Nutr Rep 2, 274-282 (2013)
- Berger, S., Raman, G., Vishwanathan, R., Jacques, P.F. & Johnson, E.J. Dietary cholesterol and cardiovascular disease: a systematic review and meta-analysis. Am J Clin Nutr 102, 276-294 (2015).
- DiMarco, D.M., Norris, G.H., Millar, C.L., Blesso, C.N. & Fernandez, M.L. Intake of up to 3 Eggs per Day Is Associated with Changes in HDL Function and Increased Plasma Antioxidants in Healthy, Young Adults. J Nutr 147, 323-329 (2017).
- Katz, D.L., et al. Egg consumption and endothelial function: a randomized controlled crossover trial. Int J Cardiol 99, 65-70 (2005).
- Rueda, J.M. & Khosla, P. Impact of breakfasts (with or without eggs) on body weight regulation and blood lipids in university students over a 14-week semester. Nutrients 5, 5097-5113 (2013).
- Clayton, Z.S., et al. Influence of Resistance Training Combined with Daily Consumption of an Egg-based or Bagel-based Breakfast on Risk Factors for Chronic Diseases in Healthy Untrained Individuals. J Am Coll Nutr 34, 113-119 (2015).
- National Health and Medical Research Council. Australian Dietary Guidelines. (ed. National Health and Medical Research Council) (NHMRC, Canberra, ACT, Australia, 2013).
Richard, C., et al. Impact of Egg Consumption on Cardiovascular Risk Factors in Individuals with Type 2 Diabetes and at Risk for Developing Diabetes: A Systematic Review of Randomized Nutritional Intervention Studies. Can J Diabetes (2017).
- Fuller, N.R., et al. Effect of a high-egg diet on cardiometabolic risk factors in people with type 2 diabetes: the Diabetes and Egg (DIABEGG) Study—randomized weight-loss and follow-up phase. Am J Clin Nutr [Epud ahead of print], nqy048-nqy048 (2018).
- National Health and Medical Research Council. Australian Dietary Guidelines. (Commonwealth Department of Health and Ageing, Canberra, 2013).
Fuller, N.R., et al. The effect of a high-egg diet on cardiovascular risk factors in people with type 2 diabetes: the Diabetes and Egg (DIABEGG) study—a 3-mo randomized controlled trial. Am J Clin Nutr[Epub ahead of print](2015).
- Ratliff, J.C., Mutungi, G., Puglisi, M.J., Volek, J.S. & Fernandez, M.L. Eggs modulate the inflammatory response to carbohydrate restricted diets in overweight men. Nutr Metab (Lond)5, 6 (2008).
- Blesso, C.N., Andersen, C.J., Barona, J., Volek, J.S. & Fernandez, M.L. Whole egg consumption improves lipoprotein profiles and insulin sensitivity to a greater extent than yolk-free egg substitute in individuals with metabolic syndrome. Metabolism [Epub ahead of print](2012).
- Andersen, C.J., et al. Egg Consumption Modulates HDL Lipid Composition and Increases the Cholesterol-Accepting Capacity of Serum in Metabolic Syndrome. Lipids [Epub ahead of print](2013).
- Blesso, C.N., et al. Effects of carbohydrate restriction and dietary cholesterol provided by eggs on clinical risk factors in metabolic syndrome. J Clin Lipidol 7, 463-471 (2013).
- Katz, D.L., et al. Effects of egg ingestion on endothelial function in adults with coronary artery disease: a randomized, controlled, crossover trial. Am Heart J 169, 162-169 (2015).
- Fuller, N.R., et al. The effect of a high-egg diet on cardiovascular risk factors in people with type 2 diabetes: the Diabetes and Egg (DIABEGG) study—a 3-mo randomized controlled trial. Am J Clin Nutr [Epub ahead of print](2015).
- Weggemans, R.M., Zock, P.L. & Katan, M.B. Dietary cholesterol from eggs increases the ratio of total cholesterol to high-density lipoprotein cholesterol in humans: a meta-analysis. Am J Clin Nutr 73, 885-891 (2001).
- American Heart Association & National Heart Lung and Blood Institute. Recommendations regarding public screening for measuring blood cholesterol. (1995).
- National Heart Foundation of Australia & The Cardiac Society of Australia and New Zealand. Lipid Management Guidelines--2001. Med J Aust 175 Suppl, S57-85 (2001).
- Marcason, W. What Role Does HDL Cholesterol Have in CVD and What Is the Most Effective Way to Increase It? J Am Diet Assoc 111, 1266 (2011).
- National Health and Medical Research Council. Nutrient Reference Values for Australia and New Zealand including Recommended Dietary Intakes, (NHRMC, Canberra, 2006).
- Katz, D.L., et al. Egg consumption and endothelial function: a randomized controlled crossover trial. Int J Cardiol 99, 65-70 (2005).
- Leermakers, E.T., et al. The effects of lutein on cardiometabolic health across the life course: a systematic review and meta-analysis. Am J Clin Nutr 103, 481-494 (2016).
- Bonds, D.E., et al. Effect of long-chain omega-3 fatty acids and lutein + zeaxanthin supplements on cardiovascular outcomes: results of the Age-Related Eye Disease Study 2 (AREDS2) randomized clinical trial. JAMA Intern Med 174, 763-771 (2014).
- Ribaya-Mercado, J.D. & Blumberg, J.B. Lutein and zeaxanthin and their potential roles in disease prevention. J Am Coll Nutr 23, 567S-587S (2004).
- Hozawa, A., et al. Relationships of circulating carotenoid concentrations with several markers of inflammation, oxidative stress, and endothelial dysfunction: the Coronary Artery Risk Development in Young Adults (CARDIA)/Young Adult Longitudinal Trends in Antioxidants (YALTA) study. Clin Chem 53, 447-455 (2007).