Elsevier

Atherosclerosis

Volume 224, Issue 2, October 2012, Pages 469-473
Atherosclerosis

Egg yolk consumption and carotid plaque

https://doi.org/10.1016/j.atherosclerosis.2012.07.032Get rights and content

Abstract

Background

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).

Methods

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).

Results

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.

Introduction

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) [1]. 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 [2], [3]. 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 [4], [5], [6], [7], [8] or impacts negatively on postprandial events, including vascular reactivity [9], [10]. Most importantly the association of egg consumption with CHD events in cohort studies has been inconsistent [11], [12], [13], [14]. We recently reviewed the evidence that consumption of cholesterol and egg yolk should not be considered benign in patients at risk of vascular disease [15]. 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 [15], [16].

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).

Section snippets

Methods

Patients in the database had been referred to vascular prevention clinics since we routinely began measuring carotid total plaque area (TPA) in 1995 [17], [18]. Plaque area was measured as previously described [19]: 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

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.

Fig. 1A shows that carotid atherosclerotic plaque burden increases linearly after age 40, among

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

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.

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

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