No yolk: eating the whole egg as dangerous as smoking?
By Melissa Healy, Los Angeles Times
For the Booster Shots Blog
August 14, 2012, 10:34 a.m.
Just as you were ready to tuck into a nice three-egg omelet again, comforted by the reassuring news that eggs are not so bad for you, here comes a study warning that for those over 40, the number of egg yolks consumed per week accelerates the thickening of arteries almost as severely as does cigarette smoking.
Server, can you make that an egg-white omelet instead, please?
The study, published Tuesday in the journal Atherosclerosis, measured the carotid wall thickness — a key indicator of heart disease risk — of 1,231 patients referred to a vascular prevention clinic, and asked each to detail a wide range of their health habits, from smoking and exercise to their consumption of egg yolks. Just as smoking is often tallied as “pack-years” (the number of cigarette packs smoked per day for how many years), egg-yolk consumption was tallied as “egg yolk years” (the number of egg yolks consumed per week times the number of years they were eaten).
The study subjects were typically referred to the clinic after having suffered a clot-induced stroke or a transient ischemic attack — a “mini-stroke” in which symptoms may disappear quickly but which often presage a more serious stroke to come.
Smoking tobacco and eating egg yolks increased carotid wall thickness in similar fashion — which is to say, the rate of increase accelerated with each stair-step up in cigarette smoking or yolk consumption. By contrast, for those who did not smoke, or who rarely consumed egg yolks, carotid wall thickness increased after 40, but at a slow-steady rate.
For those whose consumption of whole eggs was in the highest 20%, the narrowing of the carotid artery was on average about two-thirds that of the study’s heaviest smokers.
“We believe our study makes it imperative to reassess the role of egg yolks, and dietary cholesterol in general, as a risk factor for coronary heart disease,” the study authors write.
In recent years, nutritionists have begun to agree with egg purveyors that chicken eggs — cheap and packed with protein — have gotten a bad rap as a dangerous source of cholesterol. Some studies have suggested that eggs may increase HDL, or “good cholesterol” that protects against heart disease, even as it contributes to the artery-clogging LDL cholesterol, making egg consumption something of a wash. And regular egg-eaters may form larger lipoprotein particles that help clear the blood of fat particles and are not as likely to settle in artery walls.
Still, the National Heart Blood and Lung Institute recommends that to limit their risk of developing heart disease, Americans limit their cholesterol intake to no more than 300 mg per day (an egg yolk has just over 200 mg), and eat no more than four whole eggs weekly, including those in baked goods or processed foods. Those who already have heart disease, diabetes or high LDL-cholesterol, or who have had a stroke, should limit their cholesterol to less than 200 mg per day.
OK found the article. Full text is this:
Increasingly the potential harm from high cholesterol intake, and specifically from egg yolks, is considered insignificant. We therefore assessed total plaque area (TPA) in patients attending Canadian vascular prevention clinics to determine if the atherosclerosis burden, as a marker of arterial damage, was related to egg intake. To provide perspective on the magnitude of the effect, we also analysed the effect of smoking (pack-years).
Consecutive patients attending vascular prevention clinics at University Hospital had baseline measurement of TPA by duplex ultrasound, and filled out questionnaires regarding their lifestyle and medications, including pack-years of smoking, and the number of egg yolks consumed per week times the number of years consumed (egg-yolk years).
Data were available in 1262 patients; mean (SD) age was 61.5 (14.8) years; 47% were women. Carotid plaque area increased linearly with age after age 40, but increased exponentially with pack-years of smoking and with egg-yolk years. Plaque area in patients consuming <2 eggs per week (n = 388) was 125 ± 129 mm2, versus 132 ± 142 mm2 in those consuming 3 or more eggs per week (n = 603); (p < 0.0001 after adjustment for age). In multiple regression, egg-yolk years remained significant after adjusting for coronary risk factors. Interpretation Our findings suggest that regular consumption of egg yolk should be avoided by persons at risk of cardiovascular disease. This hypothesis should be tested in a prospective study with more detailed information about diet, and other possible confounders such as exercise and waist circumference. Highlights ► Carotid total plaque area (TPA) increases linearly with age. ► TPA increases exponentially with smoking pack-years. ► TPA increases exponentially with egg-yolk years. ► The effect size of egg yolks appears to be approximately 2/3 that of smoking. ► Probably egg yolks should be avoided by persons at risk of vascular disease.
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The underpinning of what used to be the step 2 diet and later became the diet recommended for CHD risk reduction by NCEP ATP III was a diet low in saturated fat (<7%) and dietary cholesterol (<200 mg) . This diet if strictly applied tended to drive the consumer towards a more plant based diet with other potential advantages in terms of CHD risk reduction. In addition to saturated fat in meat (especially red meat) and full fat dairy products, eggs were also restricted due to their significant cholesterol content. Currently, however, serious doubts have been expressed over the relevance of these dietary components to cardiovascular disease , . In the case of cholesterol much of the debate has been focused on the lack of clear consensus on whether egg consumption consistently raises serum cholesterol , , , ,  or impacts negatively on postprandial events, including vascular reactivity , . Most importantly the association of egg consumption with CHD events in cohort studies has been inconsistent , , , . We recently reviewed the evidence that consumption of cholesterol and egg yolk should not be considered benign in patients at risk of vascular disease . Much of the controversy in this area is about effects of egg yolk consumption on fasting lipids; however the main impact of diet is on the post-prandial state, not on the fasting state , . To address the key issue of whether egg yolk intake relates to vascular damage we report the association of egg consumption with carotid plaque area assessed by ultrasound as an indication of atheromatous change in patients attending vascular clinics at an University Hospital. To provide perspective on the magnitude of the effect, we also analysed the effect of smoking (pack-years). Back to Article Outline 2. Methods Patients in the database had been referred to vascular prevention clinics since we routinely began measuring carotid total plaque area (TPA) in 1995 , . Plaque area was measured as previously described : each plaque identified in the common, external and internal carotid artery on both sides was measured in a longitudinal view, in the plane in which it was biggest. The perimeter of each plaque was traced using a cursor on the screen to measure the area of the plaque, and the sum of all plaque areas was TPA. In earlier years, data on smoking and egg consumption were recorded by patients into a lifestyle questionnaire at the time of referral. Since 2000, when our referrals were scheduled on an urgent basis soon after transient ischeamic attacks or strokes, a more limited set of lifestyle questions were asked at the time the history was obtained. These data were entered, along with the history, medications, physical examination and recommendations into fields in the database, from which clinic notes were generated. The responses for smoking and egg yolk consumption were used to compute pack-years of smoking (number of packs per day of cigarettes times the number of years of smoking) and egg-yolk years (number of egg yolks per week times number of years consumed). This was not done for alcohol consumption, licorice intake or exercise, because the textual responses were mainly not quantifiable (e.g. “quit drinking six years ago”, “plays golf twice a week”). All patients with complete data for each analysis were included. Egg yolks per week were computed by one observer from text entries in the lifestyle field of the database; for example one whole egg per month was entered as 0.25 eggs per week, consumption of 2 whole eggs per day was entered as 14 eggs per week. Egg whites or egg substitutes were counted as 0 yolks. For example, a person who consumed 3 eggs per week for 50 years would have a score of 150 egg-yolk years. Data were analysed anonymously from electronic medical records; patients provided signed consent to participate in the database, approved by the University of Western Ontario ethics board (review number 12107E). Data range checks were performed and data entry errors such as decimal errors were identified by scatter plots of age against each continuous variable; outliers were identified using the data label mode in SPSS, and such errors were corrected by re-entering the correct value. Analyses were performed using IBM SPSS 20. Mean and standard deviation were computed for normally distributed baseline variables, median and interquartile range for non-normally distributed variables, and percent for categorical variables. As total plaque area is highly skewed, it was normalized for multiple regression analysis by a cube root transformation (exponent 1/3), as previously described , . Back to Article Outline 3. Results There were 2831 patients with data on egg yolk consumption. Of these, consent to use the data, and data on pack-years of smoking and carotid total plaque area were available in 1231 patients. The mean age was 62 years; 47% were women. Baseline characteristics of the patients are shown in Table 1. Table 2 shows the baseline characteristics of the patients grouped by quintiles of egg-yolk years. Table 1. Baseline characteristics of the subjects. Mean Std. deviation Age at first visit 61.50 14.82 Systolic pressure (mmHg) 141.75 23.01 Diastolic pressure (mmHg) 83.37 23.96 Total cholesterol (mmol/L) 4.91 1.21 Triglycerides (mmol/L) 1.90 1.28 HDL cholesterol (mmol/L) 1.33 0.44 Body mass index 27.38 6.44 Median Interquartile range Plaque area (mm2) 85.0 179.0 Smoking (pack-years) 5.0 25.0 Egg-yolk years 132 133 Percent Female 47.1% Diabetic 13.3% Table 2. Baseline characteristics of the participants by quintile of egg-yolk years. Egg-yolk years Quintile of egg-yolk years p <50 50–110 110–150 150–200 ≥200 Normally distributed variables: mean ± SD Age at first visit 55.70 ± 17.03 57.97 ± 16.32 56.82 ± 12.35 64.55 ± 12.00 69.77 ± 11.38 0.0001 Eggs per week 0.41 ± 0.44 1.37 ± 0.54 2.30 ± 0.53 2.76 ± 0.59 4.68 ± 3.03 0.0001 Systolic pressure (mmHg) 141 ± 24 139 ± 24 142 ± 22 144 ± 22 145 ± 23 0.001 Diastolic pressure (mmHg) 83 ± 12 82 ± 12 85 ± 13 82 ± 13 80 ± 13 0.001 Total cholesterol (mmol/L) 4.93 ± 1.16 4.94 ± 1.17 5.0 ± 1.14 4.90 ± 1.16 4.81 ± 1.19 0.47 Triglycerides (mmol/L) 1.88 ± 1.41 1.84 ± 1.08 1.96 ± 1.31 1.94 ± 1.40 1.85 ± 1.17 0.77 HDL cholesterol (mmol/L) 1.34 ± 0.48 1.33 ± 0.42 1.33 ± 0.42 1.29 ± 0.42 1.35 ± 0.45 0.58 LDL cholesterol (mmol/L) 2.76 ± 1.04 2.75 ± 1.02 2.81 ± 1.09 2.73 ± 1.19 2.67 ± 1.06 0.62 Body mass index 27.62 ± 5.62 27.42 ± 5.53 28.71 ± 9.91 27.00 ± 4.81 26.31 ± 4.48 0.001 Plaque area (mm2) 101.45 ± 125.64 110.35 ± 129.02 113.58 ± 138.82 135.76 ± 137.67 175.77 ± 147.61 0.0001 Age-dependent variables: age-adjusted marginal mean ± SE Smoking (pack-years) 14.14 ± 1.37 14.37 ± 1.40 16.57 ± 1.25 13.88 ± 1.30 17.00 ± 1.20 0.24 Categorical variables: percent Female 48.6% 51.7% 44.8% 45.0% 46.7% 0.56 Diabetic 11.8% 14.5% 11.8% 13.4% 14.6% 0.80 Fig. 1A shows that carotid atherosclerotic plaque burden increases linearly after age 40, among Canadian patients referred to cardiovascular prevention clinics. Online Supplemental Fig. 2 shows the distribution of weekly egg yolk consumption, and of pack-years of smoking and egg-yolk years. As 39.9% of patients never smoked, smoking groups were divided for analysis not into quintiles, but into roughly equal groups among those who ever smoked, using groupings that made sense clinically: 0 pack-years (39.9%), >0 < 10 pack-years 17.8%, 10–20 pack-years 13.1%, 20–40 pack-years 17.6%, >40 pack-years 11.6%. Fig. 1B and C shows that compared to age, both tobacco smoking and egg yolk consumption accelerate atherosclerosis, in a similar fashion: the increase in plaque area is linear with age, but it is exponential with smoking history and egg consumption. Curve fitting with the cases that had non-zero values for egg yolks and smoking showed that an exponential fit was better than a linear fit. The total plaque area among people who consumed 2 or fewer eggs per week (n = 388) was 125 ± 129.62 mm2, whereas it was 132.26 ± 142.48 mm2 in those consuming 3 or more eggs per week (n = 603). Because plaque area increases steeply with age, as shown in Fig. 1, it was important to adjust for age; this difference was statistically significant after adjustment for age in a General Linear Model (p < 0.0001). In linear multiple regression analysis (Table 3), egg-yolk years remained a significant predictor of baseline TPA after adjustment for sex, serum total cholesterol, systolic blood pressure, diabetes, body mass index and pack-years of smoking. As reflected in the Beta (proportion of explained variance), egg-yolk years was more predictive than fasting cholesterol or BMI. Triglycerides, HDL cholesterol and LDL cholesterol were not significant predictors of baseline TPA in stepwise linear regression (Online Supplemental Table 4). View Large Image Download to PowerPoint Fig. 1 Carotid total plaque area: effect of age, smoking (pack-years) and egg yolks (egg-yolk years) panel A shows how plaque area increases by age groups in all patients, including smokers and eaters of eggs; panel B shows plaque area by pack-years of smoking (number of packs of cigarettes per day times number of years smoked); panel C shows plaque area by quintiles of egg-yolk years (number of eggs per week times number of years consumed). Plaque area increases linearly with age, but exponentially with smoking and egg yolk consumption. Table 3. Multiple regression analysis. Egg-yolk years remained a significant predictor of carotid plaque area after adjustment for sex, total cholesterol, pack-years of smoking, systolic blood pressure, diabetes and body mass index. (Age is incorporated into pack-years and egg-yolk years). Coefficientsa Model Unstandardized coefficients Standardized coefficients t Sig. B Std. error Beta 1 (Constant) 2.073 0.460 4.502 0.000 Female sex −0.803 0.113 −0.184 −7.110 0.000 Total cholesterol −0.171 0.046 −0.095 −3.712 0.000 Systolic blood pressure 0.023 0.002 0.247 9.767 0.000 Smoking (pack-years) 0.031 0.003 0.280 10.930 0.000 Diabetes 0.914 0.161 0.144 5.669 0.000 Body mass index −0.033 0.009 −0.097 −3.828 0.000 Egg-yolk years 0.002 0.000 0.124 4.897 0.000 R2 = 0.277. aDependent variable: baseline plaque area (normalized by a cube root transformation). There was no significant correlation between egg yolk consumption and smoking history: R = 0.046; p = 0.10; the partial correlation, adjusted for age, was also not significant: R = 0.01; p = 0.70. Back to Article Outline 4. Interpretation Our data suggest a strong association between egg consumption and carotid plaque burden. The exponential nature of the increase in TPA by quintiles of egg consumption follows a similar pattern to that of cigarette smoking. The effect of the upper quintile of egg consumption was equivalent in terms of atheroma development to 2/3 of the effect of the upper quintile of smoking. In view of the almost unanimous agreement on the damage caused by smoking, we believe our study makes it imperative to reassess the role of egg yolks, and dietary cholesterol in general, as a risk factor for CHD. At present many jurisdictions include no consideration of cholesterol in their guidelines including the European Union, Canada, India, Korea, New Zealand . Part of the reason is the inconsistency in the data relating change in cholesterol intake to change in blood levels. Early on, analysis of the data at the time, independently by Keys and Hegsted, lead to the development of predictive equations in which dietary cholesterol was recognized to determine a proportion, albeit limited, of the change in serum cholesterol , . These equations formed the basis for subsequent dietary advice. Since then the data have been mixed with some studies supporting an increase in serum cholesterol with cholesterol feeding , ,  while others have not , . Notably egg consumption has resulted in divergent effects on serum cholesterol. In some studies raising serum cholesterol , ,  and in other studies being without effect , , , , . In addition, similarly to saturated fat, dietary cholesterol has also been shown to raise HDL-C , , . Part of the explanation for the differences in lipid responses may relate to genetic differences, such as in the apo-E4 polymorphism with carriers of apoE4 showing higher fasting LDL-C levels  and differences in the ABCG 5/8 sterol transporter where ABCG 5 polymorphism increasers sterol absorption , , . This situation is further complicated by the fact that cholesterol feeding may reduce the efficiency of cholesterol absorption  and depress hepatic cholesterol biosynthesis  so confounding a clear dose response. However none of these considerations negate the possible existence of significant vulnerable populations. Indeed a meta-analysis involving 395 experiments among 129 groups of individuals demonstrated that avoiding 200 mg/d dietary cholesterol, the amount similar to that found in a large egg, reduced LDL-C by 0.10 mmol/L . The outcome of increased vascular damage as demonstrated in the present study, or hard outcomes, including CHD events or deaths, assessed in relation to eggs, remains the critical issue. Here again the literature which is derived from cohort studies is divided. Analysis of the Health Professionals and Nurses Health studies by Hu and colleagues noted no overall effect of egg consumption on CHD events and mortality after 8 years of follow up, among participants who remained non-diabetic . However, among participants who became diabetic during follow-up, daily egg consumption doubled CHD mortality . The same pattern was seen in another large population-based study: among participants who became diabetic during follow-up, intake of eggs was associated with a doubling of cardiovascular risk . Extending these findings further, a later assessment of the Physicians Health Study demonstrated a relation of egg consumption to total mortality and confirmed an even stronger relation to mortality in those with diabetes , and a Greek study in diabetics showed that daily egg consumption increased coronary risk more than 5-fold . In view of the predicted increase in the incidence of diabetes both in western cultures and in the developing world the deleterious effect of egg consumption in diabetes is of particular concern. Furthermore there is also emerging evidence that egg consumption itself may be related to increased diabetes incidence . Therefore egg yolk consumption remains a public health concern. The study weakness includes its observational nature, the lack of data on exercise, waist circumference and dietary intake of saturated fat and sources of cholesterol other than eggs, and the dependence on self-reporting of egg consumption and smoking history, common to many dietary studies. Study strengths include the large number of patients on whom data were available, the significant egg consumption despite recommendations to high risk individuals to limit egg consumption and most importantly the use of carotid plaque burden as the study end point rather than risk factors such as fasting cholesterol levels. Carotid plaque area strongly predicts cardiovascular risk. We reported in 2002  that after adjustment for age, sex, systolic blood pressure, diabetes, serum total cholesterol, plasma total homocysteine and treatment of blood pressure and cholesterol, patients in the top quartile of plaque area had 3.4 times higher 5-year risk of stroke, death or myocardial infarction compared to patients in the lowest quartile. These findings were corroborated in the Tromsø study , a population-based study in Norway. A meta-analysis by Inaba et al. in this journal  confirmed that plaque area is a stronger predictor of cardiovascular events than carotid intima-media thickness. We conclude that the prevailing tendency to ignore dietary cholesterol as a risk factor for coronary heart disease requires reassessment, including the consumption of cholesterol from eggs. Although low fat egg dishes may be less harmful than meals high in both saturated fat and cholesterol (even if the latter have somewhat lower cholesterol content), meals high in cholesterol should not be consumed regularly by those at risk for cardiovascular diseases, as dietary cholesterol itself is harmful, and potentiates the effect of saturated fats . Increasingly studies are showing that vegetable oils and plant protein sources low in cholesterol and saturated fats confer benefits in terms of heart disease risk and diabetes incidence ,  with improvements in the blood lipid profile . This approach to diet has been captured in the idealized description of the Mediterranean diet now considered by many as the ideal diet for CHD risk reduction. Ansel Keys, who first drew attention to the Mediterranean diet, commented that “the heart of this diet is mainly vegetarian, and differs from the American and Northern European diets in that it is much lower in meat and dairy products and uses fruit for dessert” . Our study supports a return to earlier concepts of the therapeutic diet, including a continued prohibition on high dietary cholesterol intakes. Back to Article Outline 5. Conclusion Our findings suggest that regular consumption of egg yolk should be avoided by persons at risk of cardiovascular disease. This hypothesis should be tested in a prospective study with more detailed information about diet, and other possible confounders such as exercise and waist circumference. Back to Article Outline Acknowledgements Carotid plaque area measurements were performed by Maria DiCicco RVT and Janine DesRoches RVT. Data on egg consumption were converted from text fields in the database to egg-yolk years by Timothy Spence during a summer job at the Stroke Prevention & Atherosclerosis Research Centre. The maintenance of the database was made possible by funding from the Heart & Stroke Foundation of Ontario, including grant numbers T2956, T5017, NA4990, T5704, NA6018, and NA5912. It was also supported by donations to the Stroke Prevention & Atherosclerosis Research Centre. Back to Article Outline Appendix A. Supplementary material download text Back to Article Outline References D'Agostino RB, Vasan RS, Pencina MJ, et al. Executive summary of the 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) general cardiovascular risk profile for use in primary care: the Framingham heart study. 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