Context Reduction in egg consumption has been widely
recommended to lower blood cholesterol levels and prevent coronary
heart disease (CHD). Epidemiologic studies on egg consumption and risk
of CHD are sparse.
Objective To examine the association between egg consumption and
risk of CHD and stroke in men and women.
Design and Setting Two prospective cohort studies, the Health
Professionals Follow-up Study (1986-1994) and the Nurses' Health Study
(1980-1994).
Participants A total of 37,851 men aged 40 to 75 years at
study outset and 80,082 women aged 34 to 59 years at study
outset, free of cardiovascular disease, diabetes, hypercholesterolemia,
or cancer.
Main Outcome Measures Incident nonfatal myocardial
infarction, fatal CHD, and stroke corresponding to daily egg
consumption as determined by a food-frequency questionnaire.
Results We documented 866 incident cases of CHD and 258
incident cases of stroke in men during 8 years of follow-up and 939
incident cases of CHD and 563 incident cases of stroke in women during
14 years of follow-up. After adjustment for age, smoking, and other
potential CHD risk factors, we found no evidence of an overall
significant association between egg consumption and risk of CHD or
stroke in either men or women. The relative risks (RRs) of CHD across
categories of intake were less than 1 per week (1.0), 1 per week
(1.06), 2 to 4 per week (1.12), 5 to 6 per week (0.90), and ≥1 per day
(1.08) (P for trend=.75) for men; and less
than 1 per week (1.0), 1 per week (0.82), 2 to 4 per week (0.99), 5 to
6 per week (0.95), and ≥1 per day (0.82) (P for
trend=.95) for women. In subgroup analyses, higher egg
consumption appeared to be associated with increased risk of CHD only
among diabetic subjects (RR of CHD comparing more than 1 egg per day
with less than 1 egg per week among diabetic men, 2.02 [95%
confidence interval, 1.05-3.87; P for
trend=.04], and among diabetic women, 1.49
[0.88-2.52; P for trend=.008]).
Conclusions These findings suggest that consumption of up to 1 egg
per day is unlikely to have substantial overall impact on the risk of
CHD or stroke among healthy men and women. The apparent increased risk
of CHD associated with higher egg consumption among diabetic
participants warrants further research.
Elevated
low-density lipoprotein (LDL) cholesterol is a major risk factor for
coronary heart disease (CHD).1 Dietary cholesterol raises
LDL cholesterol levels and causes atherosclerosis in numerous
animal models.2 In controlled metabolic studies
conducted in humans, dietary cholesterol raises levels of total and LDL
cholesterol in blood,3,4 but the effects are relatively
small compared with saturated and transfatty
acids.5,6 Studies have found that individuals vary widely
in their responses to dietary cholesterol based on monitoring their
plasma levels.7,8 Prospective cohort studies on the
relationship of dietary cholesterol with risk of CHD have been
inconsistent, with a significant association found in
some,9,10 but not in most studies.11-17
To avoid elevations in blood cholesterol and reduce CHD risk, the
public has been advised to consume no more than 300 mg/d of cholesterol
and limit consumption of eggs, which contain about 213 mg of
cholesterol per egg.1,18 However, eggs contain many other
nutrients
besides cholesterol, including unsaturated fats,
essential amino acids, folate, and other B vitamins. In addition,
consumption of eggs instead of carbohydrate-rich foods may raise
high-density lipoprotein (HDL) cholesterol levels19,20 and
decrease blood glycemic and insulinemic responses.21 For
these reasons, it is useful to study directly the relationship of egg
consumption with risk of CHD, but few epidemiologic studies have
addressed this association.22-24 In this article, we
examine prospectively the association between egg consumption and risk
of CHD and stroke in 2 large cohorts of men and women.
The Health Professionals Follow-up Study
The Health Professionals Follow-up Study (HPFS) began in 1986 when
51,529 men who were US health professionals (dentists,
optometrists, pharmacists, podiatrists, and veterinarians), aged 40 to
75 years, answered a detailed questionnaire that included a
comprehensive diet survey and items on lifestyle practice and medical
history. Follow-up questionnaires were sent in 1988, 1990, 1992, and
1994 to update information on potential risk factors and to identify
newly diagnosed cases of cardiovascular and other diseases. We excluded
from the analysis men who did not satisfy the a priori criteria of
reported daily energy intake between 3360 and 17,640 kJ or who
left blank more than 70 items of the 131 total food items in the diet
questionnaire (n=1152). We also excluded men with
prior diagnoses of cardiovascular disease (n=5182) or
cancer (n=1644) at baseline. In the primary analyses,
we also excluded men who reported diabetes mellitus
(n=1187) or hypercholesterolemia
(n=4458) at baseline because these diagnoses could have
led to changes in diet. Incidence of CHD and stroke during the
subsequent 8 years was monitored for 37,851 men during
follow-up. The follow-up rate for nonfatal events was 97% of the total
potential person-years of follow-up.
The Nurses' Health Study (NHS) cohort was established in
1976 when 121,700 women who were registered nurses residing in
11 large states, aged 30 to 55 years, provided detailed information
about their medical history and lifestyle
characteristics.25 Every 2 years, follow-up questionnaires
have been sent to update information on potential risk factors and to
identify newly diagnosed cases of CHD, stroke, and other diseases. In
1980, a 61-item food frequency questionnaire was included to assess
intake of specific fats and other nutrients. In 1984, the food
frequency questionnaire was expanded to include 116 items. Similar
questionnaires were used to update diet in 1986 and 1990. The
reproducibility and validity of the food frequency questionnaires have
been described in detail elsewhere.26,27
After up to 4 mailings, 98,462 women returned the 1980 diet
questionnaire. We excluded those who left 10 or more items blank, those
with implausibly high or low scores for total food intake or energy
intake (ie, <2100 kJ/d or >14,700 kJ/d)
(n=5994), and those with previously diagnosed cancer
(n=3526), cardiovascular disease
(n=1812), high blood cholesterol
(n=1821), or diabetes (n=4122) at
baseline. Incidence of CHD and stroke during the subsequent 14 years
was monitored for 80,082 women during follow-up. The follow-up
rate for nonfatal events was 98% of the total potential person-years
of follow-up.
Assessment of Egg Consumption
Validated dietary questionnaires were sent to the HPFS participants in
1986 and 1990 and the NHS participants in 1980, 1984, 1986, and 1990.
In all the questionnaires, we asked the participants how often, on
average, during the previous year they had consumed eggs (unit of
consumption was 1 egg). Nine responses were possible, ranging from
never to 6 or more times per day. We divided the participants into 5
categories (<1 per week, 1 per week, 2-4 per week, 5-6 per week, ≥1
per day) based on the frequency distribution of egg consumption. In a
validation study in a subsample of the participants, the correlation
coefficent between intakes of eggs assessed by the diet questionnaire
and by multiple week diet records was 0.8 for both men28
and women.29 We also computed intake of eggs included in
other foods such as cakes, cookies, pancakes, muffins, sweet rolls, and
donuts. The amount of eggs estimated from other foods was relatively
small in both cohorts (men, 0.4 egg per week; women, 0.3 egg per week),
so we used the reported egg consumption as our primary exposure
variable. In a secondary analysis, we examined the effect of computed
total egg consumption.
The end points were incident CHD (including nonfatal myocardial
infarction [MI] and fatal CHD) and stroke occurring between return of
the baseline questionnaires and January 31, 1994 (men), or June 1, 1994
(women). We inquired about occurrence of cardiovascular end points on
each biennial questionnaire. Participants reporting an incident MI or
stroke were asked for permission to review medical records. Nonfatal MI
was confirmed by symptoms plus either typical electrocardiographic
changes or increased activities in cardiac enzymes (World Health
Organization criteria).30 Infarctions that required
hospital admission and for which confirmatory information was obtained
by interview or letter, but for which no medical records were
available, were designated as probable. We included all confirmed and
probable cases in the analyses because results were the same after
excluding probable cases. Strokes were confirmed if characterized by a
typical neurological defect of sudden or rapid onset, lasting at least
24 hours, and attributable to a cerebrovascular event. Strokes caused
by infection or neoplasia were excluded. Strokes were subclassified
according to the criteria of the National Survey of Stroke as due to
ischemia (embolism or thrombosis), subarachnoid hemorrhage,
intracerebral
hemorrhage, or unknown cause.31 If no
records could be obtained, strokes were considered probable if they
required hospitalization and were corroborated by additional
information provided by letter or interview.
Deaths were reported by next of kin, coworkers, postal authorities, or
the National Death Index. Using all sources combined, we estimate that
follow-up for the deaths was more than 98% complete.32
Fatal CHD was defined as fatal MI if this was confirmed by hospital
records or autopsy, or if CHD was listed as the cause of death on
the death certificate and this was the underlying and most plausible
cause, and evidence of previous CHD was available. The statement of the
cause of death on the death certificate was never relied on by itself
as providing sufficient confirmation of death due to CHD. Sudden death
within an hour of the onset of symptoms in subjects with no other
plausible cause of death (other than coronary disease) was also
included. Fatal stroke was also confirmed by medical records or autopsy
reports, or considered probable if these were not obtainable but stroke
was listed as the underlying cause on the death certificate.
Participants contributed follow-up time from the return of the
1986 (men) or the 1980 (women) questionnaire up to the occurrence of a
confirmed end point, death, or the end of follow-up (January 31, 1994,
for men and June 1, 1994, for women). The relative risks (RRs) were
calculated by dividing the incidence of CHD or stroke among men and
women in various categories of egg consumption by the incidence among
those in the lowest category of intake (<1 egg per week), adjusting
for age (5-year categories). To adjust for other risk factors, we used
pooled logistic regression,33 which is asymptotically
equivalent to Cox regression for time-dependent covariates.
Multivariate models included as covariates were (1) total energy intake
(quintiles); (2) smoking (never, past, current 1-14, 15-24, and ≥25
cigarettes/d); (3) alcohol consumption (0-4, 5-9, 10-14, 15-29, and
≥30 g/d); (4) history of hypertension; (5) parental history of MI; (6)
body mass index (calculated as weight in kilograms divided by the
square of height in meters) (quintiles); and (7) current multivitamin
use, and (8) vitamin E supplement use. In HPFS, we also adjusted for
physical activity in metabolic equivalents per week
(quintiles).34 In NHS, we adjusted for regular vigorous
exercise (once or more per week) and menopausal status and
postmenopausal hormone use. Tests of linear trend across increasing
categories of egg consumption were conducted by treating the median
values of consumption in categories (servings per day) as a continuous
variable.
To reduce intra-individual variation and best represent long-term diet,
we used repeated measures of diet in our primary
analyses.35 In particular, CHD or stroke incidence was
related to the cumulative average of egg consumption from all available
questionnaires prior to the beginning of each 2-year follow-up
interval. For example, in HPFS, CHD or stroke incidence during the
1986-1990 period was related to egg consumption assessed in 1986, while
the incidence during 1990-1994 period was related to the average intake
assessed in 1986 and 1990. For those who failed to complete the 1990
diet questionnaire (24%), we used the 1986 values to replace the
missing values and a missing data indicator was included in the model
to correct for potential bias. Average egg consumption at baseline was
the same between the respondents and nonrespondents. In alternative
analyses, we analyzed the incidence of CHD in relationship to egg
consumption at baseline only. We also related the incidence to the most
recent diet by using the baseline diet to predict incidence during
1986-1990, and the 1990 diet to predict incidence during 1990-1994.
Because the diagnosis of hypercholesterolemia, diabetes, or
hypertension may lead to changes in egg consumption and therefore
confound the associations between egg consumption and risk of
cardiovascular disease, we did not update diets for those who developed
these conditions.35
In men, the average egg consumption declined from 2.3 eggs per week in
1986 to 1.6 eggs per week in 1990. In women, the average egg
consumption declined from 2.8 eggs per week in 1980 to 1.4 eggs per
week in 1990. At baseline, egg consumption was positively associated
with smoking in men but inversely associated with smoking in women (Table 1). Those with higher egg
intake consumed more dietary cholesterol and protein but less
carbohydrates. Egg consumption was positively associated with bacon
intake among both men (r=0.35) and women
(r=0.21). Men with higher egg consumption were
more likely to consume whole milk, red meat, and bread, and less likely
to consume skim milk, chicken, vegetables, and fruits. These
relationships were less clear in women.
We documented 866 incident cases of CHD in men during 8 years of
follow-up (1986-1994) and 939 cases of CHD in women during 14 years of
follow-up (1980-1994). The age-adjusted RR of CHD comparing more than 1
egg per day with less than 1 egg per week was 1.15 (95% confidence
interval [CI], 0.85-1.55; P for trend=.37)
for men and 0.85 (95% CI, 0.62-1.16; P for
trend=.50) for women (Table
2). After adjustment for smoking and other
covariates, the corresponding RRs were 1.08 (95% CI, 0.79-1.48;
P for trend=.75) for men and 0.82 (95% CI,
0.60-1.13; P for trend=.95) for women.
Additional adjustment for dietary fiber intake had little impact on the
RRs for women but it further attenuated the association for men (RR for
>1 egg per day, 1.01; 95% CI, 0.74-1.38). Because of the relatively
strong correlation between consumption of eggs and bacon, we further
adjusted for bacon intake. The adjusted RRs across categories of egg
consumption are less than 1 per week (1.0), 1 per week (1.00), 2 to 4
per week (1.04), 5 to 6 per week (0.78), and 1 or
more per day (0.93) (P for
trend=.36) for men; and less than 1 per week (1.0), 1
per week (0.81), 2 to 4 per week (0.96), 5 to 6 per week (0.91), and 1
or more per day (0.78) (P for trend=.73) for
women. Additional adjustment for other foods including whole milk,
fish, beef as main dish, chicken, or cereal had little impact on the
results.
In further analyses egg consumption had no significant relationship
with either fatal CHD or nonfatal MI (data not shown). After excluding
cases with events occurring during the first 2 years of follow-up to
reduce the effect of change in diet due to preclinical conditions, the
results remained unchanged. In analyses excluding participants who
reported changes in egg consumption in the previous decade from
baseline, we observed a significant inverse association for men but a
nonsignificant positive association for women. The results from
analyses including eggs estimated from other foods were similar to
those from the main analyses. We also observed no
significant increase in risk when either only baseline
or only recent egg consumption was analyzed. Only 4.8% women reported
almost never consuming eggs and 1.6% women reported consuming 2 eggs
or more per day. When these 2 extreme groups were compared (using never
consumers as the reference group), the multivariate RR was 0.76 (95%
CI, 0.43-1.35). The corresponding RR was 1.10 (95% CI, 0.67-1.79) for
men.
In all above analyses, participants with diabetes or
hypercholesterolemia at baseline were excluded. When these subjects
were included in the analyses, the results did not appreciably change.
The multivariate RRs as in Table 2 across categories of egg intake were
less than 1 per week (1.0), 1 per week (1.05), 2 to 4 per week (1.04),
5 to 6 per week (0.96), and 1 or more per day (1.10) (95% CI,
0.83-1.45; P for trend=.78) for men; and less
than 1 per week (1.0), 1 per week (0.87), 2 to 4 per week (0.98), 5 to
6 per week (1.03), and 1 or more per day (0.95) (95% CI, 0.74-1.22;
P for trend=.54) for women.
Associations According
to Risk Factor Status
To examine the possibility that a positive association with egg intake
is limited to certain subgroups, we conducted additional multivariate
analyses stratified by risk factor status including
hypercholesterolemia, diabetes, hypertension, smoking, alcohol use,
body mass index, age, vitamin supplement use, parental history of MI,
and intakes of saturated fat, polyunsaturated fat, and carbohydrates.
We found no evidence of a positive association with higher consumption
of eggs in any subgroup except a suggestion that the risk might be
elevated among individuals with diabetes. Among diabetic men, the
multivariate RRs of CHD across categories of intake were less than 1
per week (1.0), 1 per week (1.0), 2 to 4 per week (1.16), 5 to 6 per
week (1.16), and 1 or more eggs per day (2.02); (95% CI, 1.05-3.87;
P=.04 for trend and
P=.18 for interaction between egg consumption
and diabetes status). The corresponding RRs for diabetic women were
1.0, 0.91, 1.05, 1.87, and 1.49 (95% CI, 0.88-2.52;
P=.008 for trend and
P=.07 for interaction). To investigate the
possibility that an effect of egg consumption may be more apparent
among those with a low-background cholesterol diet,36 we
conducted analyses stratified by dietary cholesterol from foods other
than eggs. The RRs for more than 1 eggs per day were 1.05 (95% CI,
0.61-1.79) for the men and 0.97 (95% CI, 0.13-7.10) for the women
whose non-egg cholesterol intake was low (mean intakes were 88.4
mg/4200 kJ for men and 118.8 mg/4200 kJ for women), compared with 0.97
(95% CI, 0.64-1.46) for the men and 0.79 (95% CI, 0.57-1.11) for the
women whose non-egg cholesterol intake was relatively high (mean
intakes were 135.9 mg/4200 kJ for men and 175.9 mg/4200 kJ for women).
The Association With Stroke
We documented 258 incident cases of stroke in men during 8 years of
follow-up and 563 cases of stroke in women during 14 years of
follow-up. In multivariate analyses (Table
3), egg consumption was not significantly
associated with risk of total stroke; the RRs for 1 egg or more per day
were 1.07 (95% CI, 0.66-1.75; P for
trend=.50) for men and 0.89 (95% CI, 0.60-1.31;
P for trend=.77) for women. Adjustment for
intake of bacon, vegetables, and fruit further attenuated the
association for men (RR for ≥1 egg per day, 1.00; 95% CI, 0.57-1.78;
P for trend = 0.95). In both cohorts, no significant
association was observed between egg consumption and risk of ischemic
or hemorrhagic stroke.
In these 2 large prospective cohort studies of men and women, we found
no overall significant association between egg consumption (up to 1 egg
per day) and risk of CHD or stroke. We specifically found no evidence
for a significant increase in risk with either recent or relatively
long-term (over the past decade) egg consumption. Despite somewhat
different patterns of egg consumption in men and women, the results
from the 2 cohorts were remarkably consistent.
In subgroup analyses, egg consumption appeared to be associated with
increased risk of CHD among individuals with diabetes. This result
should be interpreted cautiously due to numerous subgroup analyses, but
the consistency of the association in the 2 cohorts argues against a
chance finding. The increased risk may be related to abnormal
cholesterol transport due to decreased levels of apolipoprotein
E37 and increased levels of apolipoprotein
C-III38 among patients with diabetes.
We considered the possibility that inaccurate self-reports of egg
consumption or confounding by intake of other foods could explain the
observed null results. Egg consumption was reported on food frequency
questionnaires with relatively high accuracy (correlations were 0.8
between the self-report and multiple week dietary records in our
validation studies28,29). Also, egg consumption was
assessed several times in both cohorts so that our analyses using
updated dietary information could dampen measurement error and take
into account changes in eating behavior.
Several metabolic studies have suggested a hypocholesterolemic
effect of decholesterolized eggs (ie, Eggbeaters) on blood cholesterol
levels compared with whole eggs.39,40 We were not able to
examine the effect of such products on the risk of CHD because they
were not included in the dietary questionnaires on the printed form.
However, our questionnaires permit respondents to report other foods
that are frequently consumed. In NHS, only 48 women recorded consuming
Eggbeaters in the 1984 dietary questionnaire and 105 recorded this in
the 1990 questionnaire.
Egg consumption was positively associated with smoking, lower physical
activity, and a generally unhealthy eating pattern (ie, more whole
milk, red meat, and bacon and less skim milk, vegetables, and fruits)
in men. Confounding due to these factors would artifactually produce an
elevated risk for egg consumption. As expected, an apparent positive
association with higher egg consumption in the age-adjusted analysis in
men was attenuated after adjustment for smoking and other covariates.
After further adjusting for bacon intake, which was positively
associated with risk of CHD in our cohorts, the RRs became weakly
inverse. This speaks to the importance of considering overall eating
patterns when examining the effects of egg consumption.
It is possible that participants with high serum cholesterol
levels were more likely to reduce their egg intake than others, which
might obscure a positive association between egg consumption and risk
of CHD. However, in our primary analyses, we excluded subjects with
diagnosed hypercholesterolemia at baseline. Also, in our analyses by
using updated dietary information, we stopped updating egg consumption
at the beginning of the time interval during which individuals reported
hypercholesterolemia to avoid confounding due to change in diet during
follow-up.41 Finally, we did not measure blood cholesterol
levels in our cohorts. However, blood cholesterol should not be
controlled in the analyses as it is an intermediate variable when
assessing the relationship between dietary cholesterol and CHD.
In controlled metabolic studies, ingestion of cholesterol by eating egg
yolks or whole eggs raises serum total and LDL
cholesterol levels.5-7,42 In most egg feeding studies,
intakes of other nutrients such as fatty acids, carbohydrates, and
protein were balanced between egg and no egg groups so that only
dietary cholesterol varied. In our cohorts, participants who consumed
more eggs had lower intakes of carbohydrates, suggesting that, in
reality, people often substitute eggs for carbohydrate-rich foods such
as breakfast cereals. The effects of egg cholesterol on blood
cholesterol can be predicted from well-established equations derived
from metabolic studies. A 50-g egg contains about 213 mg of
cholesterol, 6 g of protein, and 5 g of fat.43 Of the fat,
nearly half is monounsaturated fat and 16% is polyunsaturated fat. The
equation derived by Keys and Parlin4 predicts that adding 1
egg to an average diet (assume 200 mg background cholesterol and 7560
kJ/d) will result in about a 4% increase in total serum cholesterol
for a normocholesterolemic person (assume total blood cholesterol of
5.17 mmol/L [200 mg/dL]). If we assume that raising cholesterol
levels is the only effect of egg consumption, this would translate into
about an 8% increase in CHD risk,44 an effect generally
too small to be detectable in this and most epidemiologic studies or
clinical trials. In NHS, dietary cholesterol (but not eggs) was
nonsignificantly associated with CHD,17 raising the
possibility that eggs contain other nutrients that may be beneficial in
preventing CHD.
The equation developed by Mensink and Katan45 predicts that
substituting fatty acids from 1 egg for carbohydrates would raise HDL
cholesterol by about 2% (assume HDL level of 1.03 mmol/L [40 mg/dL])
and decrease triglycerides also by about 2% (assume triglyceride level
of 2.82 mmol/L [250 mg/dL]). The effects of egg consumption on
raising HDL levels have been observed in some metabolic
studies,19,20 but not in others.36,40 Also, in
egg feeding studies, triglyceride levels were significantly reduced in
some,19,20 but not other studies.36,46 In
particular, Schnohr et al19 observed a reduction of
triglycerides by 0.09 mmol/L (7.97 mg/dL) by adding 2 eggs to the usual
diet. Packard et al20 observed a reduction of triglycerides
by 0.19 mmol/L (16.8 mg/dL) by adding 6 eggs to the diet. In addition,
egg intake decreased blood glycemic and insulinemic
responses,47 especially when egg yolk was ingested
(compared with whole egg or egg white).21 This might result
from further delayed gastric emptying after yolk ingestion. Moreover,
adding eggs to pasta produced lower insulin and C-peptide
responses.48 Holt et al49 tested 38 common
foods and found that eggs were among the foods that have the lowest
glycemic and insulin indexes.
Based on the 116 food items in the 1984 food frequency
questionnaire in NHS, we estimated that egg consumption contributed to
32% of total dietary cholesterol. Eggs also made contributions to
dietary intakes of many other nutrients, including vitamin D (5%),
retinol (4%), folate (4%), α-tocopherol (3%), monounsaturated fat
(3%), vitamin B12 (3%), vitamin B2 (3%),
protein (3%), saturated fat (2.5%), linoleic acid (2%), calcium
(1.3%), vitamin B1 (1.2%), and vitamin B2
(1.2%). It is conceivable that the small adverse effect of cholesterol
in an egg on plasma LDL levels is counterbalanced by potential
beneficial effects on HDL and triglycerides, and of other nutrients
including antioxidants, folate, other B vitamins, and unsaturated fats.
Since there is no single biochemical measurement that can represent the
effects of various nutrients, it is important to examine the direct
relationship between egg consumption and risk of CHD. Only 2 previous
prospective cohort studies reported on the association between egg
consumption and risk of CHD. In the Framingham Study, egg consumption
was not significantly associated with either serum cholesterol or risk
of CHD (RR was not provided).22 In the California
Adventists Study, the RR for higher intake (≥3 per week) vs lowest
intake (<1 per week) was 1.01.23 In a case-control study
conducted in Italy,24 the RR comparing women in the upper
third of egg intake with those in the lower third was 0.8.
One potential alternative explanation for the null finding is that
background dietary cholesterol may be so high in the usual Western diet
that adding somewhat more has little further effect on blood
cholesterol. In a randomized trial, Sacks et al36 found
that adding 1 egg per day to the usual diet of 17 lactovegetarians
whose habitual cholesterol intake was very low (97 mg/d) significantly
increased LDL cholesterol level by 12%. In our analyses, differences
in non-egg cholesterol intake did not appear to be an explanation for
the null association between egg consumption and risk of CHD. However,
we cannot exclude the possibility that egg consumption may increase the
risk among participants with very low background cholesterol intake.
Also, we have limited power to examine the effect of high egg
consumption (eg, ≥2 eggs per day). Nevertheless, the average egg
consumption was 0.64 eggs per day in 1995 in the United
States,50 which is well within the range of consumption in
our analyses.
We found no significant association between egg consumption and
risk of total stroke or its subtype. Epidemiologic
studies51 have revealed no clear patterns between blood
cholesterol and stroke although secondary prevention
trials52,53 showed significant reductions in stroke
incidence among patients with MIs and who were treated with
cholesterol-lowering drugs (statins). A recent report from the
Framingham Heart Study54 indicated that intakes of total
fat, saturated fat, and monounsaturated fat were associated with
reduced risk of ischemic stroke, but the study did not examine the
effects of dietary cholesterol or egg consumption.
In conclusion, our data suggest that consumption of up to 1
egg per day is unlikely to have substantial overall impact on the risk
of cardiovascular disease among healthy men and women. The apparent
increased risk of CHD associated with higher egg consumption among
diabetics warrants further research.
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