Eggs and cardiovascular disease.
Abstract
BACKGROUND: Consumption of dietary cholesterol from eggs has shown to increase the ratio of total to HDL cholesterol in humans, which has been suggested
to increase the risk of CHD (Weggemans RM. 2001). However, until now no systematic review has been published about the direct effects between egg consumption and CHD/CVD.
OBJECTIVES:
- To review all prospective studies which published information about eggs in relationship with total cardiovascular disease, heart disease, or stroke.
- To define the amount of consumption found to be related with possible effects on these diseases.
- To define possible effect modification by confounders.
DATA SOURCE: The Pubmed database was searched (No start date - May 25th, 2010) for relevant articles using
the keywords "dietary cholesterol, dietary fat, egg, or eggs" combined with "prospective, cohort, follow-up, or longitudinal". The exact search term is described
Here.
Prospective studies published in the English language were included. Reference lists were searched for additional articles.
RESULTS: 23 articles were found which provided information about 19 different cohorts. Of these, 0 articles were excluded.
- Disease risk.
-2 cohorts provided information about total CVD risk. Suggestive evidence was found for an increased CVD risk of egg consumption among subjects with pre-existing type 2 diabetes.
-10 cohorts provided information about CHD risk, including 5,678+ cases. No evidence was found for an association with any level of egg consumption. However, suggestive evidence was found for an increased CHD risk of high egg consumption among subjects with pre-existing type 2 diabetes.
-2 cohorts provided information about heart failure, including 2,224 cases. Suggestive evidence was found for an increased heart failure risk of high egg consumption.
-4 cohorts provided information about stroke risk, including 2,818 cases. No evidence was found for an association with any level of egg consumption. - Mortality risk.
-No data was found about the relation with total CVD mortality.
-8 cohorts provided information about CHD mortality, including 3,757+ cases. No evidence was found for an association with any level of egg consumption.
-4 cohorts provided information about stroke mortality, including 3,978 cases. Inconclusive evidence was found for an association.
CONCLUSION: No evidence was found for an overall association between any level of egg consumption and total CVD risk, CHD risk, stroke risk,
CHD mortality, and stroke mortality. However, suggestive evidence was found for an increased heart failure risk (+ 39%) of high egg consumption, and suggestive
evidence was found for an increased total CVD- (+ 68%) and CHD risk of high egg consumption (≥ 6-7 eggs/week) among subjects with type 2 diabetes.
Any increased risks were practically restricted to findings from Western cohorts, and any protective effects were practically restricted to findings from
Asian cohorts. No other effect modification was found by any variables, including baseline cholesterol levels and hypertension.
LIMITATIONS: No evidence was found for an overall association between any level of egg consumption and any CVD end point, except for a possible association
with the condition called heart failure. But since the amount of evidence is limited, and no results from cohorts of very large size were included, the possibility of
an effect on CVD among specific subgroups of the population can not be excluded. Though no evidence was found for an association with CVD, current evidence shows
high egg consumption might increase risk of all-cause mortality
(Hoenselaar R. 2010).
References:
Hoenselaar R. Eggs and mortality from all causes. Canceranddiet.nl June 28. 2010.
Full text
Weggemans RM. 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 May;73(5):885-91.
Full text
Eggs and total cardiovascular disease.
2 articles, providing information about 2 different cohorts were found. In both cases the association with disease risk was examined.
Results: Results about subjects without prevalent disease were restricted to one cohort of very small size (Houston DK). No association was found.
In both cohorts, results were shown about subjects with pre-existing type 2 diabetes (Houston DK; Tanasescu M). A significantly increased risk was found in both
cohorts, including 664 cases.
Effect modification: No data was found.

Conclusion: Significantly increased risk were found in both cohorts among subjects with type 2 diabetes. One cohort was of very small size. Suggestive evidence was found for an increased CVD risk of egg consumption among subjects with type 2 diabetes (+ 68%).
| Author | Cohort name | Cases | Relative Risk (RR) |
|---|---|---|---|
| 18) Houston DK (2010) | The Health ABC Study | 45 | HR = 5.02 (1.63-15.52; P = 0.005). |
| 8) Tanasescu M (2004) | The Nurses' Health Study | 619 | RR = 1.44 (1.05-1.98; P = < 0.001). |
| Total number of cases: 664 | Average RR = 1.68 |
Eggs and coronary heart disease risk (MI or total CHD).
9 articles, providing information about 10 different cohorts were found, including 5,678 + X CHD cases (the amount of cases was not defined in
3 articles).
Definition of CHD: Analysis of the relation between eggs and CHD included results about MI or total CHD (MI + fatal CHD). Results about heart failure or
angina pectoris as a single end point were not included. Effects on heart failure are discussed separately.
Results: A significantly increased risk was found in one study of very small size, examining Australian Aborigines (Burke V). No other associations were found,
except for a nonsignificant protective effect among women only in one cohort at the level of consumption of 1 egg/week (Hu FB).

Results among subjects with pre-existing type 2 diabetes: 5 articles, providing information about 6 different cohorts were found. No information was
available about the amounts of cases. Significantly increased risks (trend) were found in 2 cohorts (Hu FB), and a nonsignificantly increased risk was found in a third
cohort (Qureshi AI). No other associations were found.
Effect modification: No associations were found among subgroups stratified by hypercholesterolemia (Hu FB; Nakamura Y; Qureshi AI; Djoussé L),
systolic blood pressure (Qureshi AI), and smoking (Hu FB; Qureshi AI), or stratified by hypertension, BMI, alcohol use, age, vitamin supplement use, parental
history of MI, and intakes of saturated fat, polyunsaturated fat, and carbohydrates (Hu FB).

Conclusion: Almost no associations were found between high, or median vs low levels of egg consumption and CHD risk. No evidence was found for an overall association between any level of egg consumption and CHD risk (excluding incomplete data from cohorts 1-4: Average RR = 1.01). Among subjects with pre-existing type 2 diabetes, high consumption of eggs was associated with significantly increased risks in 2 cohorts of moderate-large size, and a nonsignificantly increased risk was found in a third cohort. Suggestive evidece was found for an increased CHD risk of high egg consumption (≥ 6-7 eggs/week) among subjects with pre-existing type 2 diabetes.
| Author | Cohort name | Cases | Relative Risk (RR) |
|---|---|---|---|
| 17) Djoussé L (2008) | The Physician's Health Study | 1,550 | HR = 0.90 (0.72-1.14; P = 0.88) |
| 14) Qureshi AI (2007) | The NHANES I | 1,584 | RR = 1.1 (0.9-1.3). |
| 13) Burke V (2007) | No cohort name | 130 | HR = 2.59 (1.11-6.04; P = 0.03). |
| 12) Nakamura Y (2006) | The JPHC Study | 462 | HR = 1.19 (0.86-1.64) for low vs high consumption. |
| 8) Hu FB (1999) | The Health Professional's Follow-up Study, and The Nurses' Health Study | 866 men, and 939 women | Men: RR = 1.08 (0.79-1.48; P = 0.75). Women: RR = 0.82 (0.60-1.13; P = 0.95). |
| 4) Tanaka H (1987) | The Shibata Study | Not defined | RR = 1.09 (No P-value). |
| 3) Fraser GE (1994) | The Adventist Health Study | Not defined | RH = 1.01 (No P-value). |
| 2) Dawber TR (1982) | The Framingham Study | 147 | No significant association. |
| 1) Medalie JH (1973) | No cohort name | Not defined | No significant association. |
| Total number of cases: 5,678 + X | Average RR = 1.01 |
| Author | Cohort name | Cases | Relative Risk (RR) |
|---|---|---|---|
| 17) Djoussé L (2008) | The Physician's Health Study | Not defined | RR = 1.06 (0.43-2.64; P = 0.93). |
| 16) Nettleton JA (2008) | The ARIC Study | Not defined | No association. |
| 14) Qureshi AI (2007) | The NHANES I | 132 | RR = 1.9 (1.0-3.5). |
| 12) Nakamura Y (2006) | The JPHC Study | Not defined | No association. |
| 8) Hu FB (1999) | The Health Professional's Follow-up Study, and The Nurses' Health Study | Not defined | Men: RR = 2.02 (1.05-3.87; P = 0.05). Women: RR = 1.49 (0.88-2.52; P = 0.008). |
| Total number of cases: ? |
Eggs and coronary heart disease mortality.
7 articles, providing information about 8 different cohorts were found, including 3,757 + X CHD cases (the amount of cases was not defined in
1 article providing data about 2 cohorts).
Results: Significantly increased risks were found in 2 cohorts (Snowdon DA; Mann JI) existing of primarily vegetarian subjects. In one cohort
this effect was restricted to women only (Snowdon DA). This analysis included 905 cases. A nonsignificant protective effect (trend) was found in a third cohort
among men only, and including 39 male cases (Nakamura Y). These associations were found of high vs low consumption (≥ 6-7 eggs/week), and no (non)significant
associations were found at median levels of consumption.
Effect modification: No data was found.

Conclusion: Few associations were found, and increased risks were restricted to primarily vegetarian cohorts. No evidence was found for an association between any level of egg consumption and CHD death (excluding incomplete data from Knekt P [5], and Hu FB [8]: Average RR = 1.08).
| Author | Cohort name | Cases | Relative Risk (RR) |
|---|---|---|---|
| 15) Iso H (2007) | The JACC Study | 624 men, and 407 women | Men: HR = 0.87 (0.72-1.05). Women: HR = 0.84 (0.66-1.06). |
| 11) Kelemen LE (2005) | The Iowa Women's Health Study | 739 | RR = 1.04 (0.75-1.45; P = 0.53). |
| 10) Nakamura Y (2004) | The NIPPON DATA80 | 39 men, and 41 women | Men: RR = 1 (P = 0.08). RR for Reference = 1.18 (0.26-5.42). Women: RR = 1.27 (0.16-9.80; P = 0.71). RR for Reference = 1.42 (0.56-3.62). |
| 8) Hu FB (1999) | The Health Professional's Follow-up Study, and The Nurses' Health Study | Not defined | No significant association. |
| 7) Mann JI (1997) | The Oxford Vegetarian Study | 64 | DRR = 268 (119-602; P = < 0.01). |
| 5) Knekt P (1994) | The Finnish Mobile Clinic Health Cohort | 244 | No association (P = 0.68). |
| 3) Snowdon DA (1984) | The Adventist Health Study | 758 men, and 841 women | Men: RR = 1.04 (No P-value). Women: RR = 1.31 (P = < 0.05). |
| Total number of cases: 3,757 | Average RR = 1.08 |
Eggs and heart failure.
2 articles, providing information about 2 different cohorts were found, including 2,224 cases.
Results: Significantly increased risks were found in both cohorts. In one cohort, the trend but not the effect was significant (Djoussé L).
Effect modification: No significant interactions were found with diabetes (Nettleton JA; Djoussé L), hypertension
(Nettleton JA; Djoussé L), baseline CVD/BMI/sex/race/dietary variables (Nettleton JA), or hypercholesterolemia/smoking (Djoussé L).
Conclusion: Significantly increased risks were found in 2 cohorts of small-moderate size. Suggestive evidence was found for an increased heart failure
risk of high egg consumption (+ 39%).
| Author | Cohort name | Cases | Relative Risk (RR) |
|---|---|---|---|
| 17) Djoussé L (2008) | The Physician's Health Study | 1,084 | RR = 1.56 (0.99-2.46; P = 0.006). |
| 16) Nettleton JA (2008) | The ARIC Study | 1,140 | RR = 1.23 (1.08-1.41; P = < 0.05). |
| Total number of cases: 2,224 | Average RR = 1.39 |
Eggs and stroke risk.
5 articles, providing information about 4 different cohorts were found, including 2,818 cases.
Results: No (non)significant association was found between eggs and total stroke risk in any cohort at any level of consumption. In addition, no
significant associations were found with ischemic or hemorrhagic stroke at any level of consumption.
Effect modification: No significant differences in effect were found in subgroups defined by serum cholesterol (Qureshi AI; Djoussé L),
systolic blood pressure (Qureshi AI), or cigarette smoking (Qureshi AI). And no significant associations were found among subjects with pre-existing
diabetes mellitus (Qureshi AI; Djoussé L).

Conclusion: No associations were found. No evidence was found for an association between any level of egg consumption and stroke risk (Average RR = 0.95).
| Author | Cohort name | Cases | Relative Risk (RR) |
|---|---|---|---|
| 17) Djoussé L (2008) | The Physician's Health Study | 1,342 | HR = 0.99 (0.80-1.23; P = 0.40). |
| 14) Qureshi AI (2007) | The NHANES I | 655 | RR = 0.9 (0.7-1.1). |
| 8) Hu FB (1999) | The Health Professional's Follow-up Study, and The Nurses' Health Study | 258 men, and 563 women | Men: RR = 1.00 (0.57-1.78; P = 0.95). Women: RR = 0.89 (0.60-1.31; P = 0.77). |
| Total number of cases: 2,818 | Average RR = 0.95 |
Eggs and stroke mortality.
4 articles, providing information about 4 different cohorts were found, including 3,978 cases.
Results: Significant protective effects of high vs low consumption were found in 2 cohorts. In one cohort the effect but not the trend was significant (Sauvaget C),
and in the other cohort the effect was restricted to women only (Iso H). The effects were found at the level of consumption of ≥ 5 eggs/week.
In another cohort a significantly increased risk was found at an intermediate level of consumption (0.5 egg/day) among women only (Nakamura Y).
Effect modification: No data was found.

Conclusion: Results were restricted to Asian populations. Though protective effects of high vs low consumption were found in 2 cohort of moderate-large size, the effect was once restricted to women only. Inconclusive evidence was found for an association between egg consumption and stroke death (excluding incomplete data from Ross RK [6]: Average RR = 0.84).
| Author | Cohort name | Cases | Relative Risk (RR) |
|---|---|---|---|
| 15) Iso H (2007) | The JACC Study | 1,225 men, and 1,030 women | Men: HR = 0.99 (0.86-1.14). Women: HR = 0.84 (0.72-0.97; P = < 0.05). |
| 10) Nakamura Y (2004) | The NIPPON DATA80 | 112 men, and 107 women | Men:RR = 0.25 (0.03-1.81; P = 0.11). Women: RR = 1.22 (0.29-5.17; P = 0.23). |
| 9) Sauvaget C (2003) | The Hiroshima/Nagasaki Life Span Study | 1,259 | HR = 0.70 (0.51-0.95; P = 0.185). |
| 6) Ross RK (1997) | No cohort name | 245 | No significant association. |
| Total number of cases: 3,978 | Average RR = 0.84 |