This meta-analysis identified no significant association between egg consumption and risk of coronary heart disease or stroke. Higher intake of eggs (up to one egg per day) was not associated with risk of coronary heart disease or stroke. Similar results were obtained in subgroup analyses. However, among diabetic participants, higher egg consumption was associated with a significantly elevated risk of coronary heart disease. On the other hand, higher egg intake was associated with a lower risk of hemorrhagic stroke. These subgroup results should be interpreted with caution, because only a few studies focused on diabetic participants and particular stroke subtypes.
Results in relation to other studies
To date, the majority of prospective studies have found no significant association between egg consumption and risk of coronary heart disease or stroke. However, Burke and colleagues43 analyzed data from 514 Western Australian aborigines with almost 14 years of follow-up and found that risk of coronary heart disease increased in participants consuming eggs more than twice per week. But this study was small and analyzed multiple dietary and lifestyle exposures.
Some studies have found an inverse association between egg consumption and stroke risk. For example, an analysis of the Third National Health and Nutrition Examination Survey 1988-1994 (NHANES III) dataset found a significant inverse association between higher egg consumption and stroke mortality among men.34 A cohort study from Japan found that increased consumption of animal products (including eggs) was associated with reduced risk of total and hemorrhagic stroke death.39
We considered several potential reasons for the lack of an overall association between egg consumption and coronary heart disease or stroke. Although dietary cholesterol influences plasma concentrations of serum cholesterol, the effects are relatively small.10 In addition, epidemiologic studies have found weak or little association between dietary cholesterol intake and cardiovascular disease risk.10 Apart from dietary cholesterol, saturated fat and dietary patterns might also influence blood cholesterol levels,444546 suggesting that compliance with general dietary recommendations instead of simply reducing egg consumption could have a greater effect on the risk of cardiovascular disease. Additionally, individual differences in response to dietary cholesterol vary greatly, which could affect the association between egg consumption and risk of coronary heart disease and stroke. Moreover, several studies have shown that egg consumption favors the formation of larger LDL and HDL particles, which might enhance protection against atherosclerosis.4748
Other than cholesterol, eggs are a good source of other nutrients such as high quality protein and vitamin D. In the Diet, Obesity, and Gene (Diogenes) Project, increased protein consumption together with a modest reduction in glycemic index was beneficial for weight control.49 Substituting protein for carbohydrate also partly resulted in lower blood pressure, improved lipids levels, and concomitantly reduced cardiovascular risk.50 Higher vitamin D intake might have beneficial effects on the reduction of visceral adipose tissue51 and other cardiovascular risk factors52.
Another possibility is that lifestyle factors associated with egg consumption might have obscured a positive association between egg consumption and risk of coronary heart disease and stroke. However, regular egg consumption tends to be associated with unhealthy lifestyle factors such as smoking and physical inactivity.343653 Higher consumption of eggs is also likely to be associated with increased consumption of red and processed meats.36 These confounding factors tend to exaggerate rather than mask the association between egg consumption and cardiovascular disease risk. One study found that participants with high levels of cholesterol in the blood were more likely to reduce their egg consumption than others.40 However, our subgroup analysis showed that the association between egg consumption and coronary heart disease was similar in the models, with or without adjustment for cholesterol levels.
Recently, a cross sectional study assessed the total plaque area in patients attending Canadian vascular prevention clinics to determine whether the atherosclerosis burden was related to dietary egg intake.54 The study found a strong positive association between the number of egg yolks and the degree of atherosclerosis measured by plaque areas. However, the study did not assess or adjust for other dietary or lifestyle factors and did not examine hard cardiovascular disease endpoints. The cross sectional nature of the study also limited causal interpretation of the data. Therefore, the results from this cross sectional analysis should be interpreted with caution.55 The findings from our meta-analyses of prospective cohort studies do not support a positive association between egg consumption and cardiovascular disease outcomes in the general population.
Subgroup analyses have suggested a positive association between egg consumption and coronary heart disease risk in diabetic patients. Among diabetic populations, decreased plasma levels of apolipoprotein E, together with increased levels of apolipoprotein C-III could lead to abnormal cholesterol transport, which might increase the risk of coronary heart disease.5657 The adverse effect of egg consumption on lipoprotein profile and glycemic control could contribute to the elevated risk of coronary heart disease in diabetic populations.
In addition, insulin sensitivity could influence HDL metabolism and cholesterol transport.5859 Riemens and colleagues60 found that people with lower insulin sensitivity had increased levels of plasma cholesterol, very low density lipoprotein cholesterol, and LDL cholesterol, compared with those with higher insulin sensitivity. Activities of plasma lecithin, cholesterol acyl transferase, phospholipid transfer protein, and hepatic lipase were negatively correlated with insulin sensitivity, which could have enhanced reverse cholesterol transport.60 These findings suggest a biological mechanism for possible adverse effects of insulin resistance on risk of coronary heart disease in diabetic populations through cholesterol metabolism. Nonetheless, this subgroup finding of a positive association between egg consumption and coronary heart disease risk was based on a small number of studies and thus needs to be replicated in further studies.
Several prospective cohort studies showed that hemorrhagic stroke had an inverse association with serum levels of cholesterol.61626364 In particular, the result of a meta-analysis including 13 cohorts from China and Japan showed that decreased cholesterol concentrations conferred an increased risk of hemorrhagic stroke.65 It has been suggested that low cholesterol levels promote necrosis of medial muscle cells and reduce platelet aggregability, which could lead to plasmatic arterionecrosis and the incidence of hemorrhagic stroke.6667 It is unclear whether the inverse association between egg consumption and hemorrhagic stroke is mediated through low levels of serum cholesterol or other mechanisms. Since this subgroup finding was based on a small number of studies, the results should be interpreted with caution.
Strengths and limitations
Our study has several strengths. Our meta-analysis included prospective cohort studies with large sample size and long duration of follow-up, which significantly increased the statistical power to detect potential associations. We investigated a dose-response relation between egg consumption and risk of coronary heart disease and stroke, allowing us to examine the shape of this possible association. Linear and non-linear relations were also tested to quantify the associations. In addition, we used models adjusting for most established risk factors and did stratified analyses to explore whether some factors could explain the results.
Several limitations of our study should also be acknowledged. Firstly, errors in measurement of egg intake and other dietary habits could have attenuated individual study results and led to the null association between egg consumption and risk of coronary heart disease and stroke. All the studies in our analysis assessed egg consumption using food frequency questionnaires, several of which have been validated with reasonable reproducibility and validity of self reported egg intake. However, misreporting of intake was still inevitable.686970
The cooking methods of eggs and the amount of salt added to eggs were not available in most of the included studies. The nutrient contents of eggs could alter depending on different cooking methods or feeding methods of chicken. In addition, we could not uniformly quantify the size of eggs in each study. Moreover, participants with higher egg intake consumed more dietary cholesterol and protein but fewer carbohydrates and were more likely to have lower levels of education than those with lower egg intake.3436 Several studies adjusted for those confounding factors. To reduce this bias, we conducted a stratified analysis and found the results to be robust in different strata of covariates.
Secondly, during the long follow-up, participants may have changed their diets. However, in our meta-analysis, nearly half the included studies updated the diet information from food frequency questionnaires. Stratified analysis indicated that the associations between egg consumption and risk of coronary heart disease and stroke were similar, regardless of whether repeated egg consumption measurements were considered.
Thirdly, some studies considered the intake of foods in which egg was the main ingredient. However, the results suggested that the amount of eggs estimated in other foods was relatively small and was unlikely to affect the aforementioned associations. Finally, the statistical power was limited in subgroup analyses of diabetic patients or subtypes of stroke.
In summary, results from our meta-analysis do not support that higher egg consumption is associated with elevated risk of coronary heart disease and stroke. Subgroup analyses suggest a positive association between higher egg intake and risk of coronary heart disease in diabetic patients, and an inverse association between higher egg consumption and incidence of hemorrhagic stroke. Studies with larger sample sizes and longer follow-up times are warranted to confirm these subgroup results.
What is already known on this topic
Cardiovascular disease affects millions of people in both developed and developing countries
As a major source of dietary cholesterol, eggs have been investigated by several epidemiologic studies in relation to risk of coronary heart disease and stroke
However, whether egg consumption increases the future risk of coronary heart disease and stroke remains unclear
What this study adds
Consumption of up to one egg per day was not associated with increased risk of coronary heart disease or stroke
Subgroup analysis suggested that consumption of up to one egg per day was associated with a significantly elevated risk of coronary heart disease in diabetic populations, and a reduced risk of hemorrhagic stroke
1. Beck L. The Globe and Mail. April 16. 2008. Heart health concerns? You can still get cracking.
2. Beck L. The Globe and Mail. March 4. 2009. Cracking nutrition myths.
3. Taylor V. Regular eggs ‘no harm to health’ British Heart Foundation, BBC news. November 2. 2009. [Accessed on April 12, 2010]. < http://news.bbc.co.uk/2/hi/health/7882850.stm>.
4. McDonald BE. The Canadian experience: Why Canada decided against an upper limit for cholesterol. J Am Coll Nutr. 2004;23(6 Suppl):616S–20S.[PubMed]
5. Eggs: They can be part of a healthy diet! Heart and Stroke Foundation. February 10. 2010. Insider.
6. Harman NL, Leeds AR, Griffin BA. Increased dietary cholesterol does not increase plasma low density lipoprotein when accompanied by an energy-restricted diet and weight loss. Eur J Nutr. 2008;47:287–93.[PubMed]
7. Majumder K, Wu J. Angiotensin I converting enzyme inhibitory peptides from simulated in vitro gastrointestinal digestion of cooked eggs. J Agric Food Chem. 2009;57:471–7.[PubMed]
8. Willett WC, Stampfer MJ. Rebuild the food pyramid. Sci Am. 2003;1:64–71.[PubMed]
9. Adult Treatment Panel III. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation. 2002;106:3143–421.[PubMed]
10. Krauss RM, Eckel RH, Howard B, et al. Revision 2000: A statement for healthcare professionals from the Nutrition Committee of the American Heart Association. J Nutr. 2001;131:132–46.[PubMed]
11. Healthy People 2000: National Health Promotion and Disease Prevention Objectives. United States Department of Health and Human Services; 1991.
12. Ernst ND, Sempos CT, Briefel RR, Clark MB. Consistency between US dietary fat intake and serum total cholesterol concentrations: The National Health and Nutrition Examination Surveys. Am J Clin Nutr. 1997;66(4 Suppl):965S–72S.[PubMed]
13. Hardee’s Monster Thickburger. [Accessed on August 22, 2009]. < http://www.hardees.com/menu/lunch-and-dinner/23-lb-monster-thickburger/Hardee's> .
14. Ginsberg HN, Barr SL, Gilbert A, et al. Reduction of plasma cholesterol levels in normal men on an American Heart Association Step 1 diet or a Step 1 diet with added monounsaturated fat. N Engl J Med. 1990;322:574–9.[PubMed]
15. Hu FB, Stampfer MJ, Manson JE, et al. Dietary fat intake and the risk of coronary heart disease in women. N Engl J Med. 1997;337:1491–9.[PubMed]
16. Steinberg D, Glass CK, Witztum JL. Evidence mandating earlier and more aggressive treatment of hypercholesterolemia. Circulation. 2008;118:672–7.[PubMed]
17. Sacks FM, Salazar J, Miller L, et al. Ingestion of egg raises plasma low density lipoproteins in free-living subjects. Lancet. 1984;1:647–9.[PubMed]
18. Ginsberg HN, Karmally W, Siddiqui M, et al. A dose-response study of the effects of dietary cholesterol on fasting and postprandial lipid and lipoprotein metabolism in healthy young men. Arterioscler Thromb. 1994;14:576–86.[PMC free article][PubMed]
19. The Lipid Research Clinics Coronary Primary Prevention Trial results. II. The relationship of reduction in incidence of coronary heart disease to cholesterol lowering. JAMA. 1984;251:365–74.[PubMed]
20. Spence JD. Fasting lipids: The carrot in the snowman. Can J Cardiol. 2003;19:890–2.[PubMed]
21. Levy Y, Maor I, Presser D, Aviram M. Consumption of eggs with meals increases the susceptibility of human plasma and low-density lipoprotein to lipid peroxidation. Ann Nutr Metab. 1996;40:243–51.[PubMed]
22. Schwab US, Ausman LM, Vogel S, et al. Dietary cholesterol increases the susceptibility of low density lipoprotein to oxidative modification. Atherosclerosis. 2000;149:83–90.[PubMed]
23. Dubois C, Armand M, Mekki N, et al. Effects of increasing amounts of dietary cholesterol on postprandial lipemia and lipoproteins in human subjects. J Lipid Res. 1994;35:1993–2007.[PubMed]
24. Fielding CJ, Havel RJ, Todd KM, et al. Effects of dietary cholesterol and fat saturation on plasma lipoproteins in an ethnically diverse population of healthy young men. J Clin Invest. 1995;95:611–8.[PMC free article][PubMed]
25. Hegsted DM, Nicolosi RJ. Individual variation in serum cholesterol levels. Proc Natl Acad Sci U S A. 1987;84:6259–61.[PMC free article][PubMed]
26. Steiner G. Triglyceride-rich lipoproteins and atherosclerosis, from fast to feast. Annals Med. 1993;25:431–5.[PubMed]
27. Gronholdt ML, Nordestgaard BG, Nielsen TG, Sillesen H. Echolucent carotid artery plaques are associated with elevated levels of fasting and postprandial triglyceride-rich lipoproteins. Stroke. 1996;27:2166–72.[PubMed]
28. Terasaka N, Yu S, Yvan-Charvet L, et al. ABCG1 and HDL protect against endothelial dysfunction in mice fed a high-cholesterol diet. J Clin Invest. 2008;118:3701–13.[PMC free article][PubMed]
29. Vogel RA, Corretti MC, Plotnick GD. Effect of a single high-fat meal on endothelial function in healthy subjects. Am J Cardiol. 1997;79:350–4.[PubMed]
30. Plotnick GD, Corretti MC, Vogel RA. Effect of antioxidant vitamins on the transient impairment of endothelium-dependent brachial artery vasoactivity following a single high-fat meal. JAMA. 1997;278:1682–6.[PubMed]
31. Connor WE, Hodges RE, Bleiler RE. The serum lipids in men receiving high cholesterol and cholesterol-free diets. J Clin Invest. 1961;40:894–901.[PMC free article][PubMed]
32. Mattson FH, Erickson BA, Kligman AM. Effect of dietary cholesterol on serum cholesterol in man. Am J Clin Nutr. 1972;25:589–94.[PubMed]
33. Sacks FM, Salazar J, Miller L, et al. Ingestion of egg raises plasma low density lipoproteins in free-living subjects. Lancet. 1984;1:647–9.[PubMed]
34. Lehtimaki T, Moilanen T, Solakivi T, Laippala P, Ehnholm C. Cholesterol-rich diet induced changes in plasma lipids in relation to apolipoprotein E phenotype in healthy students. Ann Med. 1992;24:61–6.[PubMed]
35. Knopp RH, Retzlaff B, Fish B, et al. Effects of insulin resistance and obesity on lipoproteins and sensitivity to egg feeding. Arterioscler Thromb Vasc Biol. 2003;23:1437–43.[PubMed]
36. Knopp RH, Retzlaff BM, Walden CE, et al. A double-blind, randomized, controlled trial of the effects of two eggs per day in moderately hypercholesterolemic and combined hyperlipidemic subjects taught the NCEP step I diet. J Am Coll Nutr. 1997;16:551–61.[PubMed]
37. Tannock LR, O’Brien KD, Knopp RH, et al. Cholesterol feeding increases C-reactive protein and serum amyloid A levels in lean insulin-sensitive subjects. Circulation. 2005;111:3058–62.[PubMed]
38. Subramanian S, Han CY, Chiba T, et al. Dietary cholesterol worsens adipose tissue macrophage accumulation and atherosclerosis in obese LDL receptor-deficient mice. Arterioscler Thromb Vasc Biol. 2008;28:685–91.[PMC free article][PubMed]
39. Subramanian S, Chait A. The effect of dietary cholesterol on macrophage accumulation in adipose tissue: Implications for systemic inflammation and atherosclerosis. Curr Opin Lipidol. 2009;20:39–44.[PubMed]
40. Rull A, Rodriguez F, Aragones G, et al. Hepatic monocyte chemoattractant protein-1 is upregulated by dietary cholesterol and contributes to liver steatosis. Cytokine. 2009;48:273–9.[PubMed]
41. Vogel RA, Corretti MC, Plotnick GD. The postprandial effect of components of the Mediterranean diet on endothelial function. J Am Coll Cardiol. 2000;36:1455–60.[PubMed]
42. Fuentes F, Lopez-Miranda J, Sanchez E, et al. Mediterranean and low-fat diets improve endothelial function in hypercholesterolemic men. Ann Intern Med. 2001;134:1115–9.[PubMed]
43. Mancini M, Parfitt VJ, Rubba P. Antioxidants in the Mediterranean diet. Can J Cardiol. 1995;11(Suppl G):105G–9G.[PubMed]
44. Keys A. Serum cholesterol response to dietary cholesterol. Am J Clin Nutr. 1984;40:351–9.[PubMed]
45. Hegsted DM. Serum-cholesterol response to dietary cholesterol: A re-evaluation. Am J Clin Nutr. 1986;44:299–305.[PubMed]
46. Andrus SB, Mann GV. Xanthomatosis and atherosclerosis produced by diet in an adult rhesus monkey. J Lab Clin Med. 1956;48:533–50.[PubMed]
47. Gresham GA, Leat WM, Howard AN, Jennings IW. Pathological changes in pigs reared on semi-synthetic diets containing no fat, beef tallow and maize oil. Br J Exp Pathol. 1964;45:128–34.[PMC free article][PubMed]
48. Kritchevsky D. Dietary protein, cholesterol and atherosclerosis: A review of the early history. J Nutr. 1995;125(3 Suppl):589S–93S.[PubMed]
49. Finking G, Hanke H. Nikolaj Nikolajewitsch Anitschkow (1885–1964) established the cholesterol-fed rabbit as a model for atherosclerosis research. Atherosclerosis. 1997;135:1–7.[PubMed]
50. Friedman M, Byers S, St George S. Cortisone and experimental atherosclerosis; effects upon administration. Arch Pathol. 1964;77:142–58.[PubMed]
51. Staprans I, Pan XM, Rapp JH, Feingold KR. Oxidized cholesterol in the diet is a source of oxidized lipoproteins in human serum. J Lipid Res. 2003;44:705–15.[PubMed]
52. Salonen JT, Nyyssonen K, Salonen R, et al. Lipoprotein oxidation and progression of carotid atherosclerosis. Circulation. 1997;95:840–5.[PubMed]
53. Kushi LH, Lew RA, Stare FJ, et al. Diet and 20-year mortality from coronary heart disease. The Ireland-Boston Diet-Heart Study. N Engl J Med. 1985;312:811–8.[PubMed]
54. Shekelle RB, Shryock AM, Paul O, et al. Diet, serum cholesterol, and death from coronary heart disease. The Western Electric study. N Engl J Med. 1981;304:65–70.[PubMed]
55. Markus RA, Mack WJ, Azen SP, Hodis HN. Influence of lifestyle modification on atherosclerotic progression determined by ultrasonographic change in the common carotid intima-media thickness. Am J Clin Nutr. 1997;65:1000–4.[PubMed]
56. Hu FB, Stampfer MJ, Rimm EB, et al. A prospective study of egg consumption and risk of cardiovascular disease in men and women. JAMA. 1999;281:1387–94.[PubMed]
57. Qureshi AI, Suri FK, Ahmed S, Nasar A, Divani AA, Kirmani JF. Regular egg consumption does not increase the risk of stroke and cardiovascular diseases. Med Sci Monit. 2007;13:CR1–8.[PubMed]
58. Djousse L, Gaziano JM. Egg consumption in relation to cardiovascular disease and mortality: The Physicians’ Health Study. Am J Clin Nutr. 2008;87:964–9.[PMC free article][PubMed]
59. Liese AD, Weis KE, Schulz M, Tooze JA. Food intake patterns associated with incident type 2 diabetes: The Insulin Resistance Atherosclerosis Study. Diabetes Care. 2009;32:263–8.[PMC free article][PubMed]
60. Djousse L, Gaziano JM, Buring JE, Lee IM. Egg consumption and risk of type 2 diabetes in men and women. Diabetes Care. 2009;32:295–300.[PMC free article][PubMed]
61. Fraser GE. A comparison of first event coronary heart disease rates in two contrasting California populations. J Nutr Health Aging. 2005;9:53–8.[PubMed]