Nutrition 37 (2017) 79–85

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Nutrition
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Review

Egg consumption and heart health: A review

Zachary S. Clayton M.S. a, *, Elizabeth Fusco M.S., R.D. b,
Mark Kern Ph.D., R.D., C.S.S.D. c
a
Department of Human Physiology, University of Oregon, Eugene, OR
b
United States Olympic Committee, Chula Vista, CA
c
Department of Exercise and Nutritional Science, San Diego State University, San Diego, CA

a r t i c l e i n f o a b s t r a c t

Article history: Cardiovascular disease is the leading cause of death in the United States. Until recently, reducing
Received 27 August 2016 dietary cholesterol has been a part of the American Heart Association (AHA) and American College
Accepted 17 December 2016 of Cardiology (ACC) guidelines on lifestyle management, despite inconclusive evidence to support
the recommendation. Considering eggs are a rich source of dietary cholesterol (typically containing
Keywords: 141–234 mg per egg), individuals with increased risk for CVD are advised not to consume eggs.
Eggs
Furthermore, based on the 2012 AHA/ACC guidelines, individuals with lower risk for CVD have
Dietary cholesterol
previously been advised to avoid consuming eggs due to the high content of dietary cholesterol.
Blood lipids
Cardiovascular disease Rather than strictly limiting cholesterol intake, the AHA and ACC guidelines now recommend di-
Dietary guidelines etary patterns that emphasize fruits, vegetables, whole grains, low-fat dairy products, poultry, fish,
and nuts as an approach to favorably alter blood lipid levels. Of note, the 2015–2020 Dietary
Guidelines for Americans have removed the recommendation of limiting cholesterol intake to no
more than 300 mg per day; however, the guidelines advise that individuals should eat as little
dietary cholesterol as possible while consuming a healthy eating pattern. The purpose of this re-
view is to summarize the documented health risks of egg consumption in individuals with low and
high risk for CVD and determine whether current recommendations are warranted based on the
available literature. We also aim to provide guidance for future studies that will help further
elucidate the health modulating effect of eggs.
Ó 2016 Elsevier Inc. All rights reserved.

Introduction been diagnosed with hypertension and hypercholesterolemia,

Cardiovascular disease (CVD) accounted for $444 billion in
healthcare expenditures in 2010 and remains the leading cause
of death in the United States [1,2]. Until recently, reducing
dietary cholesterol has been part of the American Heart Asso-
ciation (AHA) and American College of Cardiology (ACC)
guidelines on lifestyle management, despite inconclusive
evidence to support the recommendation. The current
AHA/ACC guidelines [3] now recommend dietary patterns that
emphasize fruits, vegetables, whole grains, low-fat dairy
products, poultry, fish, and nuts, rather than strictly limiting
cholesterol intake, as an approach to decrease serum
low-density lipoprotein-cholesterol (LDL-C) and hypertension.
Considering approximately one third of the US population has
* Corresponding author. Tel.: 541-346-9139.
E-mail address: zclayton@uoregon.edu (Z. S. Clayton).
the AHA/ACC recommend the Therapeutic Lifestyle Changes
(TLC) and the Dietary Approaches to Stop Hypertension (DASH)
diet to help attenuate development of CVD. The TLC and the
DASH diet recommended consuming less than 200 mg and
150 mg of cholesterol per day [4,5], respectively. Of note, the
2015–2020 Dietary Guidelines for Americans [6] have removed
the recommendation of limiting cholesterol intake to no more
than 300 mg/d; however, the guidelines state that “individuals
should eat as little dietary cholesterol as possible while
consuming a healthy eating pattern.”
Considering eggs are a rich source of dietary cholesterol
(typically containing 141–234 mg per egg, depending on size),
individuals with increased risk for CVD are often advised not to
consume eggs. Moreover, based on the 2012 AHA/ACC guide-
lines [3], individuals with lower risk for CVD have previously
been advised to avoid consuming eggs due to the high content
of dietary cholesterol. The purpose of this review is to

http://dx.doi.org/10.1016/j.nut.2016.12.014
0899-9007/Ó 2016 Elsevier Inc. All rights reserved.
80 Z. S. Clayton et al. / Nutrition 37 (2017) 79–85
Table 1
Current dietary cholesterol recommendations from various governing bodies
Organization/Diet Dietary cholesterol recommendation (mg/d)
Dietary Guidelines for Removed the previous (2010–2015 guidelines)
Americans (2015–2020) recommendation of limiting to <300 mg/d.
Now emphasizes that individuals should eat
as little dietary cholesterol as possible while
consuming a healthy eating pattern.
Therapeutic Lifestyle <200
Change (TLC) Diet
Dietary Approaches to Considering eggs are high in cholesterol,
Stop Hypertension limit egg yolk intake to no more than 4/wk.
(DASH) Diet
American Heart No specific recommendation. Emphasizes
Association/American eating an overall healthy dietary pattern
College of Cardiology consisting of fruits, vegetables, whole grains,
low-fat dairy products, skinless poultry and
fish, nuts, legumes, and
nontropical vegetable oils.
summarize the documented health risks of egg consumption in
individuals with low and high risk for CVD and determine
whether current recommendations (Table 1) are warranted
based on the available literature. Furthermore, considering
insulin resistance places an individual at increased risk for
development of CVD and stroke [7], we describe the effect of
eggs on glucose metabolism. Lastly, we aim to provide guidance
for future studies that will help further elucidate the health
modulating effect of eggs.
The relationship between serum cholesterol and CVD risk
Elevated serum LDL-C is a long-established risk factor for the
development of heart disease; however, the relationship between
serum concentrations of LDL-C and dietary cholesterol is not clear.
Researchers from the Framingham Heart Study were among the
first to demonstrate increased CVD risk with elevations in serum
cholesterol [8]. They suggested limitations on cholesterol intake,
yet no association between cholesterol intake and elevated serum
cholesterol had been reported. An early meta-analysis on the topic
indicated that for every 100 mg increase in dietary cholesterol,
serum total cholesterol (TC), LDL-C, and high-density lipoprotein
cholesterol (HDL-C) concentrations increased by 2.2 to 2.5, 1.9, and
0.4 mg/dL, respectively [9]. Subsequent feeding studies have not
always detected negative impacts of cholesterol consumption on
the serum lipid profile [10,11]. Variability in response to dietary
cholesterol among individuals is likely responsible for the
observed discrepancies. Researchers have used the term
“hyper-responders,” to describe individuals who experience an
increase in both circulating LDL-C and HDL-C following
consumption of dietary cholesterol. It is crucial to note that
approximately 75% of the population experience moderate to no
difference in plasma cholesterol following the consumption of
dietary cholesterol, and have been described as “normal
responders” or “hypo-responders” [12–14]. The potential
mechanism driving the “normal” or “hypo” response is a decrease
in cholesterol fractional absorption and/or endogenous choles-
terol synthesis, in response to increased cholesterol intake [15].
Reducing dietary cholesterol as a strategy to lower serum
cholesterol has been questioned by researchers for many years [16].
It has been suggested that dietary and lifestyle factors aside from
cholesterol consumption likely modulate blood lipid profiles to a
greater extent, and therefore may pose greater risks to cardiovas-
cular health [17]. Recently, the statistical significance of dietary
intake data was shown to be affected by differences in the
statistical methods used to analyze these data, which may impact
studies that associate disease risk factors with dietary intake. These
researchers suggested that the common assumption that nutrients
and food components are measured with a high degree of accuracy
is incorrect, and that care is warranted in 1) choosing a statistical
method that is unbiased, 2) objectively interpreting the results, and
3) adequately controlling for potentially confounding variables [18].
This is especially true for epidemiologic studies designed to assess
diet-disease relationships.
Eggs and CVD risk: Prior conceptions and current evidence
As previously mentioned, cholesterol intake reduction in
recent times has been a unifying characteristic of the DASH, TLC,
and AHA/ACC diets. Since a single egg yolk typically contains
between 141 mg and 234 mg of cholesterol, the TLC and DASH
diets recommend no more than two or four egg yolks per week,
respectively. In early research, elevations in serum TC concen-
trations were detected following whole egg consumption; how-
ever, the concentration of cholesterol among lipoproteins was not
determined [19]. Because HDL particles exhibit antiatherogenic
properties [20], drawing conclusions based solely on measure-
ments of TC can be misleading. Researchers for the Framingham
Heart Study reported that egg consumption was linked to higher
dietary cholesterol intake; however, no relationships to serum
cholesterol, all-cause mortality, coronary heart disease, myocar-
dial infarction, or angina were detected [8]. They concluded that
rather than simply limiting egg consumption, diet as a whole
must be considered as a means of decreasing CVD risk. Impor-
tantly, a clear connection between egg consumption and
increased CVD risk have not been established by meta-analyses of
dose response prospective cohort studies [10] and other
prospective studies [11,21]. In fact, some researchers have
actually detected that HDL-C increases with the consumption of
whole eggs during moderate carbohydrate restriction in over-
weight individuals, suggesting that eggs may even promote some
heart-healthy effects [22]. Because moderate carbohydrate
restriction alone can independently decrease TG [23], consider-
ation must be made when studying egg consumption during
normal carbohydrate intake.
Controlled dietary intervention trials demonstrating wide-
spread negative effects of egg consumption on CVD risk are not
available in individuals who are at either lower risk or higher risk
for heart disease. The lack of detection of negative effects can be
explained through two types of reasoning. One issue is that eggs
are a rich source of key nutrients that may protect against heart
disease. For example, lutein and zeaxanthin, which are within
the xanthophyll class of antioxidants, may protect against lipid
oxidation [24]. The other is that when increased dietary
cholesterol via egg intake has been demonstrated to elevate
circulating LDL-C in individuals classified as “hyper-responders,”
minimal changes in the overall ratio of LDL-C to HDL-C have been
detected due to proportional increases in HDL-C [12]. It is critical
to note that 75% of the population appears to experience little or
no alteration in plasma cholesterol concentration following
challenges of high cholesterol intake [12].
Egg consumption by individuals at lower risk for CVD
In the past, limiting egg consumption has frequently been
recommended as a means of decreasing CVD risk in the population
rather than only for individuals at higher risk. Multiple groups of
researchers have examined the potential lipid modulating effects
of eggs in low- and high-risk individuals alike. Here we describe
 Z. S. Clayton et al. / Nutrition 37 (2017) 79–85 81

the available research conducted with respect to the impacts of Table 2

egg intake (with and without simultaneous exercise intervention) Nutrient composition of one large, whole, raw, fresh egg (USDA Nutrient
Database)
on lipid profiles of individuals at low risk for CVD. Also included is
a discussion of studies that have not utilized weight loss Nutrient Concentration
interventions, since weight loss likely alters blood lipid Water 38.08 g
concentrations independent of cholesterol intake [25]. Energy 72 kcal
Protein 6.28 g
Differences in blood lipid concentrations have been reported
Total lipid (fat) 4.76 g
based on both ethnicity [26] and age [27]; therefore, determining Carbohydrate, by difference 0.36 g
blood lipid responses to egg intake across various populations is Fiber, total dietary 0.0 g
important. Eggs are a key constituent of the diet in Mexico, a Sugars, total 0.18 g
country often characterized by dyslipidemia and high risk of CVD Minerals
Calcium 28 mg
[28]. The addition of 2 eggs/d to usual intake of Mexican children Iron 0.88 mg
for 30 d failed to alter the LDL-C to HDL-C ratio, yet a change Magnesium 6 mg
toward a higher proportion of larger, less atherogenic LDL particle Phosphorus 99 mg
size was detected in comparison to when subjects consumed an Potassium 69 mg
Sodium 71 mg
egg substitute that was free of cholesterol [29]. Researchers of
Zinc 0.64 mg
another study conducted in subjects attending college similarly Copper 0.036 mg
concluded that ingestion of two eggs as part of breakfast five Manganese 0.014 mg
times per week for 14 wk failed to impact blood lipid concen- Selenium 15.4 mg
trations in comparison to an isocaloric, egg-free, breakfast [30]. Fluoride 0.6 mg
Vitamins
Likewise, no changes in concentrations of LDL-C or HDL-C were Vitamin C, total ascorbic acid 0.6 mg
detected in middle-aged men as well as premenopausal women Thiamin 0.020 mg
(ages 20–50 y) who consumed 3 eggs/d for 30 d [31]. Similar Riboflavin 0.228 mg
results have also been detected in other populations. In post- Niacin 0.038 mg
Pantothenic acid 0.766 mg
menopausal women (
60 y) [32] and adults ages 40 to 65 y [33],
Vitamin B-6 0.085 mg
consumption of 3 eggs/d and 1 egg/d, respectively, failed to affect Folate, total 24 mg
LDL-C or HDL-C concentrations. When evaluated together, the Folate, DFE 24 mg
evidence strongly suggests that the addition of eggs to normal Choline, total 146.9 mg
dietary intake of a wide variety of subjects fails to negatively Betaine 0.2 mg
Vitamin B-12 0.44 mg
impact the blood lipid profiles, which are risk factors CVD risk Vitamin A, RAE 80 mg
across multiple age ranges and ethnicities of apparently healthy Retinol 80 mg
individuals. Carotene, beta 0 mg
Researchers have also investigated the impacts of eggs in Carotene, alpha 0 mg
Cryptoxanthin, beta 4 mg
active individuals. The cardioprotective effects of exercise have
Vitamin A, IU 270 IU
been well-documented [34,35], and since regular exercise, Lycopene 270 IU
whether endurance and/or resistance, is promoted as a key Lutein þ Zeaxanthin 270 IU
component of a healthy lifestyle [36], evaluation of the potential Vitamin E (alpha-tocopherol) 0.52 mg
interactive effects of exercise and egg consumption is important. Tocopherol, beta 0.00 mg
Tocopherol, gamma 0.25 mg
However, relatively little has been conducted to assess the Tocopherol, delta 0.03
concomitant effects of egg consumption and exercise on lipid Vitamin D (D2þD3) 1.0 mg
profiles. We recently demonstrated that daily intake of a breakfast Vitamin D3 (cholecalciferol) 1.0 mg
providing 2 eggs/d for 12 wk did not affect TC, LDL-C, or HDL-C Vitamin D 41 IU
Vitamin K (phylloquinone) 0.2 mg
concentrations of healthy individuals during a supervised resis-
Lipids
tance training program performed three times per week [37]. Saturated fatty acids 1.563 g
Interestingly, the egg-based breakfast improved serum TG Monounsaturated fatty acids 1.829 g
concentrations, whereas an isocaloric bagel-based breakfast did Polyunsaturated fatty acids 0.956 g
not. These results are supported by previous research demon- U-3 (EPA) 0.00 g
U-3 (DHA) 0.029 g
strating that eggs did not blunt the positive lipid altering effects of
Fatty acids, total trans 0.019 g
endurance training in normolipidemic men and women [38]. Cholesterol 186 mg
Overall, the research tends to suggest that consuming eggs does Amino acids
not attenuate exercise-induced improvements in blood lipid Tryptophan 0.083 g
Threonine 0.278 g
profiles, and that eggs may be a positive addition to the diets of
Isoleucine 0.336 g
recreationally trained individuals. Leucine 0.543 g
Egg yolks are a concentrated source of dietary choline [39] Lysine 0.456 g
(Table 2), which is an essential nutrient required for normal Methionine 0.190 g
human liver and muscle function, and important for fetal Cystine 0.136 g
Phenylalanine 0.340 g
development [39]. Increased dietary choline is converted to
Tyrosine 0.250 g
trimethylamine by gut bacteria and is oxidized trimethylamine- Valine 0.429 g
N-oxide (TMAO) in the liver [40]. TMAO has been shown to Arginine 0.410 g
increase atherosclerosis in the coronary vasculature [40–43]; Histidine 0.154 g
Alanine 0.368 g
thus, studying the relationship between eggs and TMAO is
Aspartic acid 0.664 g
warranted. To date, only one study has assessed the effect of egg Glutamic acid 0.836 g
consumption on plasma TMAO and markers of CVD [44]. In a (Continued)
longitudinal, double-blind, randomized dietary intervention,
82 Z. S. Clayton et al. / Nutrition 37 (2017) 79–85
Table 2 (Continued )
Nutrient Concentration
Glycine 0.216 g
Proline 0.256 g
Serine 0.486 g
DHA, docosahexaenoic acid; EPA, eicosapentaenoic acid; RAE, retinol activity
equivalents; USDA, United States Department of Agriculture
healthy volunteers were assigned to consume zero, one, two,
four, or six egg yolks within a 24-h period. Results suggest that
consumption of more than two eggs resulted in increased
plasma TMAO; however, no differences in high-sensitivity
C-reactive protein or oxidized LDL-C (markers of CVD risk)
were observed [44]. Considering the short-term nature of this
study, long-term studies are justified to determine the
relationship between eggs, TMAO, and vasculature function.
Egg consumption by individuals at higher risk for CVD
Cardiovascular disease is progressive, slow to develop, and
various comorbidities increase risk of CVD [45]. Targeting comor-
bidities such as obesity, insulin resistance, and metabolic syndrome
(MetS) is a key avenue of research regarding CVD prevention.
Considering obesity, insulin resistance and MetS increase risk for
CVD, it would be beneficial to further evaluate the effects of egg
intake in these specific at-risk populations. Following, we present a
discussion of dietary intervention trials that have studied the
impacts of egg consumption by individuals with preexisting heart
conditions and/or who are at great risk for developing CVD.
Importantly, these studies have generally been conducted in
subjects who were also moderately restricted for carbohydrate
intake. As previously stated, carbohydrate restriction may
independently decrease plasma triacylglycerols [23], which should
be considered when interpreting the findings of these studies.
Egg intake in obese and insulin resistant individuals
Overweight and obese individuals (body mass index [BMI]
>25 and <50 kg/m2) are at greater risk for developing insulin
resistance, type 2 diabetes mellitus, and MetS, which may
independently or concomitantly lead to development of CVD
[46]. One study [47] compared the differential effects of
providing either an egg-based (two eggs) or bagel-based break-
fast to obese adults during an energy-deficit, low-fat diet
(1000 kcal). No differences in serum lipid concentrations were
detected within either group. However, subjects consuming the
egg-based breakfast displayed significantly reduced adiposity
compared to those consuming the bagel-based breakfast. These
results suggest that eating 2 eggs/d in addition to usual dietary
intake may augment the typical decrease in adiposity observed
with an energy deficit [47]. A similar study conducted in over-
weight and obese adult men showed that 12 wk of a moderate
carbohydrate restriction with simultaneously consumption of 3
eggs/d did not influence plasma LDL-C but significantly increased
plasma HDL-C relative to a cholesterol-free egg substitute [22].
Additionally, insulin sensitive, insulin-resistant, and obese
individuals completing a dose-response (zero, two, or four eggs)
crossover study all exhibited increases in plasma HDL-C
concentrations after eating 4 eggs/d for 4 wk [48]. In that
study, LDL-C also increased proportionally to HDL-C within both
insulin-sensitive and insulin-resistant individuals. Overall, the
available research indicates that eating eggs fails to negatively
alter some markers of CVD risk in individuals at high risk for
CVD, and that improvement in some risk factors may occur.
Egg intake in individuals with metabolic syndrome
A predominant contributor to the increased CVD risk coupled
with MetS is the atherogenic dyslipidemia that has frequently
been demonstrated to be associated with this condition [49] and
may ultimately lead to impaired endothelial function and
vascular stiffening [46]. Recently, the addition of 2 eggs/d to
usual dietary intake for 6 wk did not affect endothelial function
(as assessed by flow mediated dilation) in obese individuals with
coronary artery disease [50].
Some interventions have targeted improvement of serum
lipid concentrations as a means to treat MetS, thereby decreasing
CVD risk. Restriction of carbohydrate intake, primarily to
promote weight and fat loss, has also been used as a potential
strategy for decreasing CVD risk [51]. In one study, researchers
fed 3 eggs/d during carbohydrate restriction (25–30% energy) to
individuals with MetS. Elevations in plasma HDL-C, LDL-C size,
and a reduction in TG was detected over time, whereas these
changes were not detected in the group consuming a
cholesterol-free egg substitute [52]. Moreover, the same group
has shown that MetS patients consuming 3 eggs/d have signifi-
cantly reduced fasting plasma concentrations of tumor necrosis
factor-alpha and C-reactive protein relative to individuals with
MetS consuming a cholesterol-free egg substitute [53]. These
inflammatory cytokines are commonly associated with obesity,
insulin resistance, and MetS [54]; therefore, they may serve as a
prospective target for addressing the mechanism by which eggs
modulate serum lipids. Of note, in comparison to an oatmeal-
based breakfast, a breakfast including one egg per day for 5 wk
decreased fasting concentrations of tumor necrosis factor-alpha
in adults with type 2 diabetes mellitus [55].
Modulation of lipoprotein metabolism: The potential
mechanism linking eggs to heart health
HDL-C is a key biomarker for protection against cardiovascular
disease. Low circulating concentrations of HDL-C place an
individual at elevated risk for developing CVD [56]. Higher HDL-C
has been linked to cardiovascular health through the capacity of
HDL particles to facilitate acquisition of lipids from macrophage
foam cells within the arterial wall for promotion of reverse
cholesterol transport [49]. Antiinflammatory properties of HDL
particles further attenuate atherogenesis [57]. It is widely
accepted that HDL particle function is impaired under inflam-
matory conditions; however, strictly measuring steady-state
blood HDL-C concentration may fail to fully elucidate the true
antiatherogenic potential of this lipoprotein [57,58]. Therefore,
studies addressing the mechanistic role of HDLs as lipid acceptors
and antiinflammation particles may serve as a more accurate
estimate of CVD risk than static HDL-C concentrations alone.
Andersen et al. [59] co-incubated RAW 264.7 macrophage
cells with serum collected from individuals with metabolic
syndrome consuming 3 eggs/d for 12 wk. Those researchers
demonstrated an increase in the capacity of HDL particles to
accept cholesterol at week 12 in comparison to baseline relative
to serum that was acquired from individuals consuming the
equivalent portion of an egg substitute devoid of cholesterol.
Consequently, the same research group demonstrated that an
increase in lecithin-cholesterol acyltransferase activity may have
been responsible for the alterations in the cholesterol-accepting
capacity. Lecithin-cholesterol acyltransferase functions in the
 Z. S. Clayton et al. / Nutrition 37 (2017) 79–85
reverse cholesterol transport system by converting free choles-
terol to cholesteryl esters, which increases the capacity of HDL
particles to accept cholesterol [57]. The same group also revealed
that when serum from individuals consuming whole eggs was
co-incubated with a potent proinflammatory substance (lipo-
polysaccharide [LPS]), the serum elicited a protective effect on
peripheral blood mononuclear cell inflammatory cytokine
secretion (decreased secretion), relative to serum collected from
individuals consuming cholesterol-free egg substitute [60].
Egg yolks are a source of bioavailable xanthophyll caroten-
oids, specifically lutein and zeaxanthin. Significant elevation in
the plasma concentrations of carotenoids have also been
detected following egg ingestion, relative to an egg substitute
free of cholesterol [61]. Xanthophyll carotenoids have previ-
ously been shown to protect against inflammation [9], oxida-
tion [24], and atherosclerosis [62]. This research highlights a
potential mechanism by which eggs may promote cardiovas-
cular health. Although definitive mechanisms of possible
cardio-protective effects of eggs are not clear, research is
increasingly suggesting that the consumption of eggs do not
increase risk for CVD of either healthy or diseased individuals.
Furthermore, egg consumption may ultimately lead to
decreased risk for CVD.
Relationship between egg intake and glucose metabolism
Insulin resistance is an independent predictor of coronary
heart disease, hypertension, as well as stroke, and over time can
lead to type 2 diabetes mellitus (T2 DM) [7]. Insulin resistance is
defined by the inability of the hormone, within its physiological
range, to elicit its effect on target tissues (skeletal muscle,
adipose tissue, and liver) [63]. Glucose uptake is one the primary
roles of insulin across its target tissues [64]; thus, studying
glucose metabolism allows for direct and indirect assessment of
insulin resistance. Considering the effect hyperglycemia and
insulin resistance have on CVD, it is imperative to understand the
relationship between egg intake and glucose metabolism within
the context of this review.
In animal experiments, a diet rich in saturated fat is a common
way to induce hyperglycemia and hyperinsulinemia [65]. A diet
enriched with cholesterol from egg yolk (14% of total diet weight),
compared with a control diet, was shown to be associated with
hyperglycemia in 10-wk fed, male, Wistar albino rats [66].
However, limited and inconsistent human studies have examined
the potential link between eggs and glucose metabolism. Thus,
results of this animal study in which cholesterol composed an
exceedingly high portion of the diet should be interpreted with
caution.
Researchers from the Zutphen Study [67] reported a positive
association between egg consumption or dietary cholesterol and
fasting glucose. Furthermore, a prospective analysis of approxi-
mately 60 000 males and females suggested a positive associa-
tion between egg consumption and incidence of type 2 diabetes
mellitus [68]. However, in a prospective study of approximately
4000 males and females from the Cardiovascular Health Study
(1989–2007), egg consumption was not associated with
incidence of T2 DM [68].
Researchers conducting randomized trials in overweight [22]
as well as overweight and obese individuals with T2 DM [69,70],
have not observed impaired glucose metabolism after consuming
3 eggs/d for 12 wk while on a carbohydrate-restricted diet [22], 2
eggs/d for 12 wk while on an energy-restricted-high protein diet
[69], or 2 eggs/d for 6 wk while on a weight maintenance diet
[70]. Recently, we demonstrated that consuming 2 eggs/d for
83
12 wk did not alter plasma glucose or insulin concentrations in
young healthy adults during resistance training [16].
Taken together, intervention research has not detected
adverse glycemic or insulinemic responses by consuming 1 to 3
eggs/d in young healthy and obese populations. Considering the
mixed results from epidemiologic studies, future human and
animal trials, along with expanded epidemiologic research, is
warranted to clarify the relationship between egg intake and
glucose metabolism.
Egg consumption and stroke risk
In the United States, stroke is the fourth leading cause of
mortality, with an estimated stroke incidence of 795 000 [17].
Increased risk of stroke has been reported in individuals with
poor cardiovascular health, and is commonly associated with
suboptimal diet quality [17]. Risk factors are categorized as
either modifiable or non-modifiable, with diet considered a
modifiable risk factor [71]. Between 2009 and 2012, greater
than 100 million US adults ages 20 y or older were reported to
have hypercholesterolemia, which is an independent risk factor
for stroke [17]. As previously mentioned, the DASH diet and TLC
advise individuals with increased CVD risk to avoid consuming
cholesterol. Moreover, the recent Dietary Guidelines for
Americans advise individuals to consume as little dietary
cholesterol as possible, despite no apparent health risk. Taken
together, it is imperative to understand the relationship
between egg intake and stroke risk.
To evaluate the potential association between egg
consumption and risk of stroke, Qureshi et al. [72] analyzed data
from National Health and Nutrition Examination Survey
(NHANES)-I to assess a nationally representative cohort of over
9000 apparently healthy adults. Findings indicated that
consumption of >6 eggs/wk did not increase the risk for stroke.
Furthermore, Scrafford et al. [73] conducted a hazard ratio
analysis of data from NHANES-III to assess the association of egg
intake and stroke risk. No positive association between egg
consumption and increased risk of stroke was detected,
corroborating previous findings. Moreover, Rong et al. [10]
conducted a dose response meta-analysis of prospective
cohort studies and determined that consuming one egg per day
did not increase an individual’s risk for stroke.
Future directions
Future research should consider the effects of egg consumption
on CVD risk in individuals classified as hyper-responders, as this
cohort has been identified but not extensively studied. Further-
more, gene expression of ABCG5 and ABCG8 have been associated
with an individual’s ability to absorb cholesterol [74,75] and may
serve as an important target to better understand potential
genetic influences on egg metabolism in the future. To date, only 2
studies [74,75] have been conducted to assess the effects of egg
intake on individuals with a polymorphism in the ABCG5 gene.
These studies demonstrated that subjects expressing the C/C
ABCG5 polymorphism exhibit a greater increase in plasma total
cholesterol and LDL-C following egg consumption, compared to
those with the C/G or G/G genotypes. Therefore, future studies of
potential gene-egg interactions are warranted for these and other
genes that have been shown to be involved with cholesterol
handling. Moreover, with the rise of the “omics” in the sciences
provided by high-resolution mass spectrometry, investigations are
warranted to determine the effects of egg consumption on the
proteome, to follow up on the hypothesis that eggs may elicit
84 Z. S. Clayton et al. / Nutrition 37 (2017) 79–85
antiinflammatory responses due to being a concentrated source of
xanthophyll carotenoids.
Since insulin resistance is an independent risk factor for CVD,
it is crucial to conduct studies in both animal and human models
that assess glucose metabolism in response to egg intake.
Utilizing methods such as, hyperinsulinemic-euglycemic clamps,
intravenous glucose tolerance tests, oral glucose tolerance tests,
and/or insulin tolerance tests, rather than restricting assess-
ments to fasting glucose and insulin measurements, would be of
great value. Furthermore, given the interactive nature of lipid
and glucose metabolism, further studies are justified that
concomitantly assess metabolism of both substrates.
Ultimately, to better understand the health modulating
effects of eggs, it is important to utilize a variety of approaches
when designing future studies. A more comprehensive under-
standing of how eggs affect human health may guide nutrition
professionals and the community at large.
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