Unscrambling the research: eggs, serum cholesterol and coronary heart disease.

Abstract

The role of dietary cholesterol in raising plasma cholesterol levels has been debated over the past 25 years. Consequently, eggs, as a food high in dietary cholesterol, have been targeted as a food to limit when advising patients on a diet to lower serum cholesterol levels. The aim of the present review was to evaluate the literature to address the effects of dietary cholesterol from eggs on serum cholesterol levels and risk of coronary heart disease. An increase in dietary cholesterol from eggs by 100 mg daily, equivalent to half a medium egg or three to four eggs a week, results in an increase of approximately 0.05 mmol/L in LDL cholesterol. Adding 100 mg of cholesterol per day (equivalent to three to four eggs a week) to a high saturated fat diet caused an increase in LDL cholesterol of 0.061 [+ or -] 0.006 mmol/L, whereas adding the same quantity of cholesterol to a low saturated fat diet caused an increase in LDL cholesterol of only 0.036 [+ or -] 0.004 mmol/L (P= 0.03). Despite the small increase in LDL-cholesterol levels with increasing egg intake, most epidemiological studies have shown little or no association between egg intake and risk of coronary heart disease. However, the impact of dietary cholesterol for people with type 2 diabetes has been poorly studied. In conclusion, in a healthy Western population, there is insufficient evidence to excessively restrict egg intake as part of a healthy diet. Eggs should be considered in a similar way as other protein-rich 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, fruits, vegetables, legumes and nuts.

Key words: cholesterol, coronary heart disease, dietary cholesterol, egg, LDL cholesterol.

INTRODUCTION

Coronary heart disease (CHD) is a major cause of morbidity and mortality in Australia. (1) Dietary intervention and lifestyle changes are an important component of the management of CHD and its risk factors, and play a major role in reducing the risk of developing CHD. As elevated serum LDL cholesterol is one of the most important treatable risk factors, the public has been advised to reduce dietary cholesterol intake as a strategy for reducing serum cholesterol levels. Consequently, eggs, as a food high in dietary cholesterol, have been targeted as one to limit when advising patients to lower serum cholesterol levels. (2,3)

This dietary advice was based on early animal studies and studies using simple regression models that demonstrated a linear relationship between dietary cholesterol and serum cholesterol. (4) However, early work by Keys found that within the context of a typical Western diet, significant reductions in dietary cholesterol can be expected to have only minimal effects on reducing serum cholesterol, and that changes in the fatty acid composition of the diet are significantly more important. (5) More recent reviews have confirmed Keys' early work and concluded that saturated fat in the diet has a greater effect on serum cholesterol than dietary cholesterol. (6,7) Despite this, recommendations around optimal dietary cholesterol intakes for the general population and those at high risk of CHD have remained controversial.

In addition, recent market research indicates both consumers and health professionals have misconceptions about the role of eggs in a healthy diet. (8,9) One of the key barriers to including eggs in the diet is the perceived contribution that eggs have to elevating serum cholesterol levels. Sixty-three per cent of general practitioners believe the consumption of eggs leads to a moderate or significant increase in serum cholesterol levels and more than half of the general practitioners surveyed indicated that the potential increase in serum cholesterol outweighs the dietary benefits obtained from egg consumption. (9) However, eggs are a highly nutritious food providing 18 vitamins and minerals, and contain 618 kJ per serve. The macronutrient content of eggs include minimal carbohydrates (0.3 g), 10.5 g total fat, with 3.2 g saturated fat, 4.5 g monounsaturated and 1.0 g polyunsaturated fat and 13.3 g of protein per serve. They have the highest nutritional quality protein of any food (10) and are a useful source of the antioxidants lutein and zeaxanthin. (11) Eggs can therefore be a nutritious inclusion in the diet for people of all ages and at different life stages, but may play a particularly useful role in the diets of those at risk of low nutrient intakes such as the elderly, pregnant women and children.

The aim of the present review was to clarify the role of eggs in a healthy Western diet by examining the literature to assess the effects of dietary cholesterol from eggs on serum cholesterol levels and the risk of CHD. Medline and CINAHL electronic databases were used to search for publications. In addition, the references listed within retrieved publications were also manually searched for relevant articles. Because of the scope of the project, identified meta-analyses and key randomised controlled trials were included for review.

EGGS AND CHOLESTEROL

The lack of a consistent association between egg intake and risk of CHD may be explained by the small increase in serum cholesterol levels following egg consumption that has been observed in experimental studies. Three meta-analyses have been conducted investigating the effects of eggs or dietary cholesterol on serum cholesterol levels. These studies varied in inclusion criteria. The Weggemans et al.'s meta-analysis published in 2001 reviewed all experimental studies on eggs, total cholesterol and lipoproteins conducted between 1989 and 1999 that met strict inclusion criteria. (12) The Howell et al.'s meta-analysis retrieved studies published between 1960 and 1994. (13) The inclusion criteria were clearly specified and included comparative dietary cholesterol interventions in adults. The Hopkins's meta-analysis published in 1992 reviewed studies from 1960 to 1990 that were controlled dietary interventions investigating cholesterol-feeding in humans. (14) The inclusion criteria were not described clearly, but all studies included baseline dietary cholesterol concentrations. Since 2001 two additional studies have been published investigating the impact of eggs on serum cholesterol or CHD. One study showed that the consumption of two eggs daily for six weeks had no effect on serum total cholesterol or on endothelial function in healthy adults. (15) The second study reported that adding four eggs a day to a low-fat diet for four weeks increased HDL cholesterol levels in all subjects, and increased inflammatory markers and non-HDL cholesterol levels in lean insulin-sensitive subjects but not in lean or obese insulin-resistant subjects. (16) To our knowledge, there have been no further experimental studies investigating the impact of eggs on serum cholesterol, other than these two studies, since publication of the Weggemans et al.'s meta-analysis in 2001.

In this meta-analysis, 17 human experimental studies met the inclusion criteria including 556 subjects. Using a linear regression analysis the study showed that, on average, increasing dietary cholesterol from eggs by 100mg daily, equivalent to half a medium egg* or three to four eggs a week, results in the serum lipid changes shown in Table 1. (12) The results indicated that egg consumption has little effect on serum cholesterol levels and may therefore be expected to have little effect on CHD risk. The authors concluded that the small change in serum lipid levels with increasing egg intake does contribute to a rise in CHD risk. However, this assertion is not supported by the majority of epidemiological studies in this area. (17-22)

The results of the Weggemans et al.'s study are consistent with the meta-analysis by Howell et al., on the serum lipid and lipoprotein responses to dietary fat and cholesterol, showing that a 100 mg decrease in dietary cholesterol results in a 0.057 mmol/L decrease in serum cholesterol translating to an approximate 1% decrease in the average population cholesterol concentration. (13)

The Hopkins's meta-analysis of the effects of dietary cholesterol on serum cholesterol found higher baseline intakes of dietary cholesterol, that is, levels around the average Australian intake of 300-400 mg daily, attenuated the increase in serum cholesterol seen with increasing intakes. (14) Subsequent studies have shown that this occurs only at baseline cholesterol intakes greater than 1000-1200 mg/day. (23,24) Only three of the 17 studies included in the Weggemans et al.'s meta-analysis involved subjects with a cholesterol intake greater than 1000 mg daily, therefore linear regression models were used in the analysis showing the following serum LDL changes with increasing dietary cholesterol intake up to 1000 mg/day (Figure 1). (12)

The changes in serum cholesterol levels outlined in Table 1 and Figure 1 represent maximal estimates because the increase in serum LDL cholesterol in response to increased egg consumption is attenuated when the background diet is low in saturated fat. (25-27) This finding was confirmed when studies were divided into two groups: those with a background diet relatively high in saturated fat, and those with a background diet relatively low in saturated fat.12 As demonstrated in Figure 2, adding 100 mg of cholesterol to a high saturated fat diet caused an increase in LDL cholesterol of 0.061 [+ or -] 0.006 mmol/L, whereas adding the same quantity of cholesterol to a low saturated fat diet caused an increase in LDL cholesterol of only 0.036 [+ or -] 0.004 mmol/L (P = 0.03). The effect on LDL cholesterol from an increase in dietary cholesterol from eggs is therefore 1.7 times greater when the background diet is high in saturated fat compared with a low saturated fat background diet. Dietary saturated fat has a significant impact on serum cholesterol levels with research showing that for every 1% increase in total daily kilojoules from saturated fatty acids, serum LDL cholesterol rises by about 2%. (28)

[FIGURE 1 OMITTED]

[FIGURE 2 OMITTED]

The Weggemans et al.'s study also showed a small increase in HDL cholesterol with increasing cholesterol intake from eggs. (12) Body weight may also affect the response to dietary cholesterol. The Chicago Western Electric Study, a prospective cohort study of 1903 middle-aged men, showed a change in intake of dietary cholesterol was positively associated with a change in serum cholesterol for men in the lowest tertile of body mass index (<24.2 kg/[m.sup.2]) who would be at lower risk of CHD but not for men in the highest tertile (>26.6 kg/[m.sup.2]). (29) This has since been supported by studies conducted in obese insulin-resistant postmenopausal women consuming up to four eggs per day showing no change in LDL cholesterol levels. (30)

Overall, the increase in total and LDL cholesterol levels seen with increased dietary cholesterol intake from eggs is small and is even less when the background diet is low in saturated fat. The effect may be attenuated even further in overweight, insulin-resistant people; however, further research is required in this area.

APOLIPOPROTEINS

Apolipoproteins are the protein component of lipoproteins and are responsible for receptor-mediated uptake. A number of studies have assessed the effect of changes in dietary cholesterol intake from eggs on apolipoprotein levels with varying results. Some have shown no change in apolipoprotein B (the main protein of LDL and VLDL levels and the protein that is associated with CHD development) with increased dietary cholesterol from eggs (31-34) whereas others have shown an increase. (35-39) Most studies have found no change in apolipoprotein A-1 (the main protein of HDL) levels with increased intakes of dietary cholesterol from eggs (31-33,35,36,38,39)

HYPER-RESPONDERS

It has been estimated that 15-25% of the population are hyper-responders to dietary cholesterol. (24) It used to be thought that people with hyperlipidaemia were more likely to be hyper-responders and that restriction of dietary cholesterol intake was therefore prudent in this group. However, recent research shows that despite hyper-responders experiencing an almost threefold greater response to dietary cholesterol compared with the remainder of the population, the LDL : HDL ratio is not significantly changed. (40-42) Randomised controlled trials are yet to show how these findings translate to changes in cardiovascular disease risk.

Herron et al. showed that female hyper-responders to dietary cholesterol experienced an increase in LDL and HDL cholesterol levels with the addition of 640 mg/day of dietary cholesterol from eggs (equivalent to 3.5 eggs a day). (42) However, there was no change in the LDL : HDL ratio. (42) Similar results were shown in men, where although there was an increase in the LDL : HDL ratio with the addition of 640 mg dietary cholesterol from eggs, the ratio correlated with a low risk of CHD according to the clinical guidelines of the National Cholesterol Education Program Adult Treatment Panel. (28) Another study found hyper-responders had a consistently lower LDL : HDL ratio compared with hypo-responders before, during and after an experimental period that involved the consumption of three eggs a day for 28 days in addition to their habitual diet. (40) The studies by Herron et al. also showed that an increase in dietary cholesterol from eggs enhances reverse cholesterol transport pathways in hyper-responders that mobilise the excess cholesterol to the liver, the major site of cholesterol elimination from the body. (41,42)

HIGH-RISK GROUPS

People with hypercholesterolaemia have been shown to demonstrate the same degree of response to increased dietary cholesterol from eggs as the remainder of the population; (12,25,43) however, studies in this area are limited. A study by Edington et al. included 33 patients with hyperlipidaemia (a combination of subjects with hypercholesterolaemia, combined hyperlipidaemia and hypertriglyceridaemia). The addition of either two or seven eggs a week to a reduced-fat, high-fibre diet resulted in no change to total cholesterol, LDL, HDL or triglycerides after eight weeks. (25) In this study, combined hyperlipidaemic subjects (those with high triglyceride and total cholesterol levels) experienced the same lack of response to egg feeding as other subjects; however, the numbers were small (three of 33 subjects).

In contrast, another study showed that patients with combined hyperlipidaemia exhibited greater increases in serum cholesterol levels with increased egg intake compared with hypercholesterolaemic patients. (43) In this study, combined hyperlipidaemic subjects following the American Heart Association Step 1 diet for six weeks showed an increase in LDL cholesterol levels of 0.31 mmol/L with the addition of two eggs a day (P < 0.001) and an increase in HDL cholesterol levels of 0.08 mmol/L (P = 0.02). In comparison, and in support of Edington et al.'s findings, there was a non-significant increase in LDL cholesterol levels in hypercholesterolaemic subjects (0.07 mmol/L P = 0.49) and a significant increase in HDL cholesterol levels (0.10 mmol/L P = 0.003).

People with type 2 diabetes are another high-risk group for cardiovascular disease; however, no experimental studies on the effect of egg feeding on serum cholesterol and lipoprotein levels have been conducted in this group. One study in people with insulin resistance showed the increase in LDL cholesterol that occurred with ingesting four eggs a day over four weeks was less in people with insulin resistance compared with insulin-sensitive subjects. (30)

EGGS AND CARDIOVASCULAR DISEASE

Nine epidemiological, including two case-control studies, have assessed egg intake and subsequent development of CHD. The Nurses Health Study (80 082 women) and the Health Professionals Follow Up Study (37 851 men) showed no association between levels of egg consumption of up to one a day and risk of CHD or stroke in both men and women (P for trend = 0.36 and 0.73, respectively). (17) However, in a subgroup analysis of both cohorts, higher egg consumption was associated with increased risk of CHD in people with diabetes; however, statistical interpretation of this result shows that the increase in risk was not due to the presence of diabetes. (17) In a Finnish cohort of 5133 men and women, there was no difference in egg consumption between individuals who developed fatal CHD and those who did not (P = 0.68 men; P = 0.94 women). (18) The Framingham Study also found no association between egg intake and subsequent development of CHD in a subsample of 912 subjects. (19) The Oxford Vegetarian Study (11 140 vegetarians and meat-eating subjects) showed a positive association between egg intakes of six or more a week and mortality from ischaemic heart disease (P < 0.01). (44) In contrast, the Adventist Health Study (34 192 vegetarian and non-vegetarian Seventh Day Adventists) found individuals consuming more than two eggs per week were at the same risk of developing CHD compared with those consuming less than one egg a week. (20) A case-control study of Italian women (287 cases, 649 controls) found no association between egg consumption and non-fatal myocardial infarction. (22)

A Japanese case-control study (660 cases, 1277 controls) that examined the relationship of selected foods to non-fatal acute myocardial infarction found no association between egg intakes up to four or more a week and incidence of acute myocardial infarction. (21) Another Japanese study showed no effect of egg consumption on risk of fatal CHD events, stroke and cancer in men consuming up to two or more eggs a day; however, there was an increased risk in women eating one egg a day or more (P = 0.02). (45)

Most of the above studies adjusted the data for non-dietary coronary risk factors, including hyperlipidaemia. No data are available on the effect of eggs on recurrent coronary events in those with existing CHD.

Using the results of the Weggemans et al.'s meta-analysis, McNamara predicts that the increase in risk of myocardial infarction associated with a 100 mg increase in dietary cholesterol from eggs, equivalent to half a medium egg daily or three to four eggs a week, ranges from 0.5% to 1.5%. (2) However, these figures may represent maximal estimates as the level of saturated fat in the background diet may attenuate the rise in serum cholesterol levels from eggs even further, therefore virtually eliminating the risk of myocardial infarction altogether. (2) The effect of adding eggs to a diet already low in saturated fat may therefore be clinically insignificant.

In addition, although an elevated serum cholesterol level is a major risk factor for CHD, the theoretical degree of increase that occurs with moderate egg consumption is considered minimal compared with other risk factors. Figure 3 shows there is a 72% increase in risk associated with increased body mass index, (46) a 42% decrease in risk associated with replacement of 5% of energy from saturated fat with unsaturated fat (47) and a 51% decrease in risk associated with 90 minutes of vigorous walking one day a week. (48)

The contribution of various food groups to saturated fat and cholesterol intakes in the Australian diet is shown in Figure 4. As indicated, egg products and dishes contribute only a small proportion of daily cholesterol and saturated fat intake in the context of the total diet. (49)

The American Heart Association when revising their dietary guidelines for the general population in 2000 concluded that 'dietary cholesterol can increase LDL cholesterol levels, although to a lesser extent than saturated fat' and 'cholesterol-rich foods that are relatively low in saturated fatty acid content (notably egg yolks) have smaller effects on LDL cholesterol levels' when compared with saturated fat. They suggest that daily targets for dietary cholesterol intake 'can readily be achieved even with periodic consumption of eggs'. (6) In addition, the National Heart Foundation of Australia has set no specific target for either dietary cholesterol or egg consumption; (50) however, the 2001 guidelines state, 'limit cholesterol-rich foods such as egg yolk and offal' as part of the dietary management of abnormal lipids and prevention of CHD. (50) A position statement, published as an interim update report by the National Heart Foundation of Australia, makes no reference to recommendations for dietary cholesterol intake for CHD risk factor management. (51) The National Heart Foundation of Australia also recently recognised eggs as a nutritious food, with regular eggs becoming eligible for the healthy eating Tick of approval.

CONCLUSIONS

Egg consumption results in only a small increase in serum cholesterol levels in most people. It is therefore not surprising that there is no convincing evidence in the literature of increased cardiovascular disease risk with increased consumption of eggs. Reducing saturated fat intake is the primary dietary strategy recommended for reducing serum cholesterol levels and the present review further supports this strategy. In a healthy Western population, there is insufficient evidence to excessively restrict egg intake as part of a healthy diet. Eggs are a nutrient-dense food and provide an economical source of protein. They should be considered in a similar way as other protein-rich 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, fruits, vegetables, legumes and nuts. Substituting eggs for other animal protein foods in the diet may result in even smaller changes to LDL cholesterol than predictive equations, as the net dietary cholesterol increase is smaller. Further research is required to fully assess the effects of egg consumption in those with CHD, hyperlipidaemias (especially combined hyperlipidaemias), type 2 diabetes and hyper-absorbers of dietary cholesterol. However, prudent advice is that the inclusion of eggs in the context of a diet low in saturated fat and containing known cardio-protective foods is not associated with increased risk.

ACKNOWLEDGEMENT

This review is authored by the Egg Nutrition Advisory Group, an expert group convened by the Australian Egg Corporation Limited.

REFERENCES

1 AIHW Australia's Health 2004: Ninth Biennial Health Report. Canberra: Australian Institute of Health and Welfare, 2004. Report No.: 1 74024 382 X.

2 McNamara DJ. Eggs and heart disease risk: perpetuating the misperception. Am J Clin Nutr 2002; 75: 333-5.

3 Krauss RM, Deckelbaum RJ, Ernst N et al. Dietary guidelines for healthy American adults. A statement for health professionals from the Nutrition Committee, American Heart Association. Circulation 1996; 94: 1795-800.

4 Hegsted DM, McGandy RB, Myers ML, Stare FJ. Quantitative effects of dietary fat on serum cholesterol in man. Am J Clin Nutr 1965; 17: 281-95.

5 Keys A. Serum cholesterol response to dietary cholesterol. Am J Clin Nutr 1984; 40: 351-9.

6 Krauss RM, Eckel RH, Howard B et al. AHA Dietary Guidelines: revision 2000: a statement for healthcare professionals from the Nutrition Committee of the American Heart Association. Circulation 2000; 102: 2284-99.

7 National Heart Foundation of Australia. A review of the relationship between dietary fat and cardiovascular disease. Aust J Nutr Diet 1999; 56 (4 Suppl.): S5-22.

8 Newspoll Market Research. Eggs Study. Sydney: Saatchi and Saatchi Healthcare, 2004.

9 Decisions Research. GPReach: Understanding Egg Consumption and Its Effect on Cholesterol. Reed Weir: Saatchi and Saatchi Healthcare, 2004.

10 Mann J, Truswell AS. Essentials of Human Nutrition, 2nd edn. New York: Oxford University Press, 2002.

11 Handelman GJ, Nightingale ZD, Lichtenstein AH, Schaefer EJ, Blumberg JB. Lutein and zeaxanthin concentrations in plasma after dietary supplementation with egg yolk. Am J Clin Nutr 1999; 70: 247-51.

12 Weggemans RM, Zock PL, Katan MB. Dietary cholesterol from eggs increases the ratio of total cholesterol to high-density lipoprotein cholesterol in humans: a meta-analysis. Am J Clin Nutr 2001; 73: 885-91.

13 Howell WH, McNamara DJ, Tosca MA, Smith BT, Gaines JA. Plasma lipid and lipoprotein responses to dietary fat and cholesterol: a meta-analysis. Am J Clin Nutr 1997; 65: 1747-64.

14 Hopkins PN. Effects of dietary cholesterol on serum cholesterol: a meta-analysis and review. Am J Clin Nutr 1992; 55: 1060-70.

15 Katz DL, Evans MA, Nawaz H et al. Egg consumption and endothelial function: a randomized controlled crossover trial. Int J Cardiol 2005; 99: 65-70.

16 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.

17 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.

18 Knekt P, Reunanen A, Jarvinen R, Seppanen R, Heliovaara M, Aromaa A. Antioxidant vitamin intake and coronary mortality in a longitudinal population study. Am J Epidemiol 1994; 139: 1180-89.

19 Dawber TR, Nickerson RJ, Brand FN, Pool J. Eggs, serum cholesterol, and coronary heart disease. Am J Clin Nutr 1982; 36: 617-25.

20 Fraser GE. Associations between diet and cancer, ischemic heart disease, and all-cause mortality on non-hispanic white California Seventh-day Adventists. Am J Clin Nutr 1999; 70 (Suppl.): 532S-38S.

21 Sasazuki S. Case-control study of nonfatal myocardial infarction in relation to selected foods in Japanese men and women. Jpn Circ J 2001; 65: 200-206.

22 Gramenzi A, Gentile A, Fasoli M, Negri E, Parazzini F, La Vecchia C. Association between certain foods and risk of acute myocardial infarction in women. BMJ 1990; 300 (6727): 771-3.

23 Hegsted DM, Ausman LM, Johnson JA, Dallal GE. Dietary fat and serum lipids: an evaluation of the experimental data. Am J Clin Nutr 1993; 57: 875-83.

24 McNamara DJ. The impact of egg limitations on coronary heart disease risk: do the numbers add up? J Am Coll Nutr 2000; 19 (5 Suppl): 540S-48S.

25 Edington J, Geekie M, Carter R et al. Effect of dietary cholesterol on plasma cholesterol concentration in subjects following reduced fat, high fibre diet. BMJ (Clin Res Ed) 1987; 294 (6568): 333-6.

26 Edington JD, Geekie M, Carter R, Benfield L, Ball M, Mann J. Serum lipid response to dietary cholesterol in subjects fed a low-fat, high-fiber diet. Am J Clin Nutr 1989; 50: 58-62.

27 Chenoweth W, Ullmann M, Simpson R, Leveille G. Influence of dietary cholesterol and fat on serum lipids in men. J Nutr 1981; 111: 2069-80.

28 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.

29 Goff DC Jr, Shekelle RB, Moye LA, Katan MB, Gotto AM Jr, Stamler J. Does body fatness modify the effect of dietary cholesterol on serum cholesterol? Results from the Chicago Western Electric Study. Am J Epidemiol 1993; 137: 171-7.

30 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.

31 Blanco-Molina A, Castro G, Martin-Escalante D et al. Effects of different dietary cholesterol concentrations on lipoprotein plasma concentrations and on cholesterol efflux from Fu5AH cells. Am J Clin Nutr 1998; 68: 1028-33.

32 Schonfeld G, Patsch W, Rudel LL, Nelson C, Epstein M, Olson RE. Effects of dietary cholesterol and fatty acids on plasma lipoproteins. J Clin Invest 1982; 69: 1072-80.

33 Applebaum-Bowden D, Haffner SM, Hartsook E, Luk KH, Albers JJ, Hazzard WR. Down-regulation of the low-density lipoprotein receptor by dietary cholesterol. Am J Clin Nutr 1984; 39: 360-67.

34 Kestin M, Clifton PM, Rouse IL, Nestel PJ. Effect of dietary cholesterol in normolipidemic subjects is not modified by nature and amount of dietary fat. Am J Clin Nutr 1989; 50: 528-32.

35 Sacks FM, Salazar J, Miller L et al. Ingestion of egg raises plasma low density lipoproteins in free-living subjects. Lancet 1984; 1 (8378): 647-9.

36 Ginsberg HN, Karmally W, Siddiqui M et al. Increases in dietary cholesterol are associated with modest increases in both LDL and HDL cholesterol in healthy young women. Arterioscler Thromb Vase Biol 1995; 15: 169-78.

37 Sutherland WH, Ball MJ, Walker H. The effect of increased egg consumption on plasma cholesteryl ester transfer activity in healthy subjects. Eur J Clin Nutr 1997; 51: 172-6.

38 Brown SA, Morrisett J, Patsch JR, Reeves R, Gotto AM Jr, Patsch W. Influence of short term dietary cholesterol and fat on human plasma Lp[a] and LDL levels. J Lipid Res 1991; 32: 1281-9.

39 Johnson C, Greenland P. Effects of exercise, dietary cholesterol, and dietary fat on blood lipids. Arch Intern Med 1990; 150: 137-41.

40 Oh SY, Miller LT. Effect of dietary egg on variability of plasma cholesterol levels and lipoprotein cholesterol. Am J Clin Nutr 1985; 42: 421-31.

41 Herron KL, Vega-Lopez S, Conde K, Ramjiganesh T, Shachter NS, Fernandez ML. Men classified as hypo- or hyperresponders to dietary cholesterol feeding exhibit differences in lipoprotein metabolism. J Nutr 2003; 133: 1036-42.

42 Herron KL, Vega-Lopez S, Conde K et al. Pre-menopausal women, classified as hypo- or hyperresponders, do not alter their LDL/HDL ratio following a high dietary cholesterol challenge. J Am Coll Nutr 2002; 21: 250-58.

43 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.

44 Appleby PN, Thorogood M, Mann JI, Key TJ. The Oxford Vegetarian Study: an overview. Am J Clin Nutr 1999; 70 (3 Suppl.): 525S-31S.

45 Nakamura Y, Okamura T, Tamaki S et al. Egg consumption, serum cholesterol, and cause-specific and all-cause mortality: the National Integrated Project for Prospective Observation of Non-communicable Disease and Its Trends in the Aged, 1980 (NIPPON DATA80). Am J Clin Nutr 2004; 80: 58-63.

46 Rimm EB, Stampfer MJ, Giovannucci E et al. Body size and fat distribution as predictors of coronary heart disease among middle-aged and older US men. Am J Epidemiol 1995; 141: 1117-27.

47 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.

48 Lee IM, Rexrode KM, Cook NR, Manson JE, Buring JE. Physical activity and coronary heart disease in women: is 'no pain, no gain' passe? JAMA 2001; 285: 1447-54.

49 National Nutrition Survey Nutrient Intakes and Physical Measurements 1995. Canberra: Australian Bureau of Statistics (ABS) and Commonwealth Department of Health and Aged Care, 1998. Report No.: Cat. No. 4805.0.

50 National Heart Foundation of Australia, The Cardiac Society of Australia and New Zealand. Lipid Management Guidelines--2001. Med J Aust 2001; 175 (Suppl.): S57-85.

51 Tonkin A, Barter P, Best J et al. National Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand: position statement on lipid management--2005. Heart Lung Circ 2005; 14: 275-91.

Sharon NATOLI, (1) Tania MARKOVIC, (2) David LIM, (3) Manny NOAKES (4) and Karam KOSTNER (5)

(1) Food and Nutrition Australia, (2) Royal Prince Alfred Hospital, (3) Church Street medical Practice, Sydney, New South Wales, (4) CSIRO Health Sciences and Nutrition, Adelaide, South Australia, and (5) University of Queensland, Brisbane, Queensland, Australia

S. Natoli, BNutDiet, APD, Director

T. Markovic, MB BS, PhD, FRACP Endocrinologist

D. Lim, MB BS, FRACGP, General Practitioner

M. Noakes, PhD, DipNutDiet, Research Dietitian 

K. Kostner, PhD, MD, Cardiologist

Correspondence: S. Natoli, GPO Box 222, Sydney, NSW 2001, Australia. Email: [e-mail]

*One medium egg = 52 g edible portion.

Table 1 Predicted changes in serum total cholesterol concentration,
induced by a 100 mg/day increase in dietary cholesterol from eggs
alone (12)

Serum cholesterol concentration  Predicted change (95% CI)

Total cholesterol (mmol/L)       0.056 [+ or -] 0.005 (0.046-0.065)
HDL cholesterol (mmol/L)         0.008 [+ or -] 0.001 (0.005-0.010)
LDL cholesterol (mmol/L)         0.050 [+ or -] 0.004 (0.042-0.058)

                          Change in risk of CHD (%)

Egg Consumption*            1.5%
Increase in BMI            72%
Altering Fat Intake^      -42%
90 min Physical Activity  -51%

Figure 3 The change in risk of developing coronary heart disease (CHD)
By increasing egg consumption compared with an increase in body mass
Index (BMI), altering fat intake and increasing physical* activity. *Egg
consumption = three to four eggs per week. ^Replacing 5% of daily energy
from saturated fat with unsaturated fat.

Note: Table made from bar graph.

                                       Percentage contribution to diet
                                      Saturated fat  Dietary cholesterol

Meat, poultry and game products and   21%            37%
  dishes
Milk products and dishes              27%            16%
Cereal-based products and dishes      20%            15%
Egg products and dishes                2%            17%
Fish and seafood products and dishes   2%             7%

Figure 4 The 1995 Australian National Nutrition Survey results comparing
The contribution of food groups to total dietary intake of saturated fat
And dietary cholesterol. (49)

Note: Table made from bar graph.