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The Journal of Nutrition
Nutrition and Disease
Consumption of One Egg Per Day Increases
Serum Lutein and Zeaxanthin Concentrations
in Older Adults without Altering Serum Lipid
and Lipoprotein Cholesterol Concentrations
1
Elizabeth F. Goodrow,
2
Thomas A. Wilson,
2
Susan Crocker Houde,
3
Rohini Vishwanathan,
2
Patrick A . Scollin,
4
Garry Handelman,
2
and Robert J. Nicolosi
2
*
2
Center for Health and Disease Research, Department of Clinical Laboratory and Nutritional Sciences,
3
Department of Nursing,
4
Department of Community Health and Sustainability, University of Massachusetts Lowell, MA 01854
Abstract
Lutein and zeaxanthin accumulate in the macular pigment of the retina, and are reported to be associated with a reduced
incidence of age-related macular degeneration. A rich source of lutein and zeaxanthin in the American diet is the yolk of
chicken eggs. Thus, the objective of the study was to investigate the effect of consuming 1 egg/d for 5 wk on the serum
concentrations of lutein, zeaxanthin, lipids, and lipoprotein cholesterol in individuals .60 y of age. In a randomized cross-
over design, 33 men and women participated in the 18-wk study, which included one run-in and one washout period
of no eggs prior to and between two 5-wk interventions of either consuming 1 egg or egg substitute/d. Serum lutein 26%
(P , 0.001) and zeaxanthin 38% (P , 0.001) concentrations increased after 5-wk of 1 egg/d compared with the phase prior
to consuming eggs. Serum concentrations of total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides were
not affected. These findings indicate that in older adults, 5 wk of consuming 1 egg/d significantly increases serum lutein
and zeaxanthin concentrations without elevating serum lipids and lipoprotein cholesterol concentrations. J. Nutr. 136:
2519–2524, 2006.
Introduction
Age-related macular degeneration (AMD)
5
is a progressive eye
condition that affects .13 million Americans or 5% of people
age 65 and older. This disease attacks the macula of the eye, the
area responsible for the sharpest central vision. There are two
forms of AMD: dry AMD and wet AMD (1). Although
investigators are uncertain of the direct causes of dry AMD,
studies suggest that the area of the retina becomes diseased
coincident with the accumulation of yellow pigments called
drusen leading to the slow breakdown of the light-sensing cells
in the macula and gradual loss of central vision (2). Whereas the
wet form of AMD is not considered to be influenced by dietary
manipulation, the dry form is responsive to nutrients such as
vitamins and minerals (3,4).
In addition to vitamins and minerals, evidence is now
accumulating that dietary and blood concentrations of lutein
and zeaxanthin, 2 oxygenated carotenoids that concentrate in
the macula of the eye, are associated with reduced risk of AMD
(5–8). There are several studies that suggest that certain fruits
and vegetables are good sources of lutein and zeaxanthin, and
their consumption has been associated with increased blood
concentrations and macular pigment concentration of these
carotenoids (6–9). These findings are important insofar as
preliminary evidence (10,11) and a more recent clinical trial (12)
suggest that lutein supplementation may also slow the progres-
sion of AMD.
Lutein and zeaxanthin play a role in the prevention of AMD
by aiding in the filtering of damaging blue light and sunlight
(13). Because AMD is thought to be associated with long-term
oxidative damage to the retina (14,15), the reported findings,
that lutein and zeaxanthin are 2 very powerful antioxidants,
absorb ultraviolet light, and serve to protect the lens from
oxidative damage, would suggest an important role for these
nutrients in preventing or treating this disease (14). Human trials
with lutein and zeaxanthin supplements indicate that these
dietary carotenoids, in addition to fruits and vegetables, can be
used to elevate macular pigment concentration (16–20). The
chicken egg yolk, a matrix composed of digestible lipids, i.e.,
cholesterol, triglycerides, and phospholipids, also contains
lutein and zeaxanthin dispersed in the matrix along with other
fat-soluble micronutrients such as vitamin A, vitamin D, and
vitamin E. The lipid matrix of the yolk of chicken eggs provides a
readily bioavailable dietary source of lutein and zeaxanthin that
is even more bioavailable than lutein supplements and spinach
1
Supported by the American Egg Board, Egg Nutrition Center, Wash ington, DC
(R.J.N.) and the Massachusetts Lions Eye Research Fund, New Bedford, MA
(R.J.N.).
5
Abbreviations used: AMD, age-related macular degeneration; HDL-C, HDL
cholesterol; LDL-C, LDL cholesterol; TC, total cholesterol; TG, triglyceride.
* To whom correspondence should be addressed. E-mail: robert_nicolosi@uml.edu.
0022-3166/06 $8.00 ª 2006 American Society for Nutrition.
2519
Manuscript received 15 March 2006. Initial review completed 6 April 2006. Revision accepted 3 July 2006.
by guest on June 7, 2013jn.nutrition.orgDownloaded from
(21). Two other reports (22,23) examined the same human
subjects (mean age 62 y, range: 46–78 y) and showed a 28–50%
increase in plasma lutein and a 114–142% increase in plasma
zeaxanthin concentrations (22) following a diet supplemented
with 1.3 eggs/d for 4.5 wk. However, this increase was as-
sociated with an 8–11% increase in plasma LDL cholesterol
(LDL-C) concentrations (23). These observations suggest that
eggs can be used by individuals who want to increase their
circulating concentrations of these carotenoids.
Thus, one of the objectives of this study was to investigate, in
an elderly population with a mean age of 79 y, whether the
serum concentrations of both lutein and zeaxanthin respond in a
similar manner to previous reports (22,23) when consuming
1 egg/d or increased cholesterol. Most studies either do not
include a source of dietary zeaxanthin or do not analyze serum
lutein and zeaxanthin concentrations separately. A second ob-
jective was to determine whether the changes in serum lutein and
zeaxanthin concentrations are associated with any of the var-
iables measured. A third objective was to determine whether egg
consumption in this elderly age group would result in significant
increases in serum LDL-C concentrations as reported in younger
populations (22).
Subjects and Methods
Subjects. The effects of consuming 1 egg/d on serum lutein and
zeaxanthin concentrations, as well as serum lipid and lipoprotein
cholesterol concentrations, was examined in 33 subjects (7 men and 26
women) with a mean age of 79 y (range: 60–96 y) who were currently
not taking lutein and/or zeaxanthin supplements or cholesterol-lowering
medication and who spoke English comfortably. The baseline charac-
teristics of the study participants are described in Table 1. A total of 65
individuals were recruited for the study. Nineteen were excluded from
the study due to the onset of illness, death, or nonadherence to protocol.
In addition, the data from 13 other subjects who were identified (during
the baseline period) as having taken a lutein and/or zeaxanthin
supplement prior to baseline were also excluded from the final data
analysis because their baseline values of lutein and zeaxanthin were 80%
greater than the remaining 33 participants not taking supplements. The
data from this group of 13 people who took supplemental lutein and/or
zeaxanthin were analyzed separately. Of the 33 participants that
completed the study, 22 were recruited from 4 nursing homes, and 11
were from 4 senior citizen centers of the Merrimack Valley and from the
University of Massachusetts faculty and staff in Lowell. All but one
subject (Asian or Pacific Islander) were Caucasian. Twenty-nine of the 33
graduated from high school or college. Most of the subjects had been
diagnosed with at least 1 medical condition, including 22 subjects with
hypertension and 6 with diabetes. All subjects were interviewed at
baseline using a structured medical medication history and demographic
questionnaire. Blood pressure, height, and weight were recorded by a
registered nurse upon enrollment into the study. A Mini-Mental State
Examination (24) was administered by the registered nurse to each
subject to verify mental competence. A 7-d diet record was obtained
from each subject once during each of the 4 phases of the study. Nutrient
analysis was performed using EvaluEat, version 1.2 dietary analysis tool
(Pearson Education, Benjamin Cummings, 2004). Dietary intakes of
energy, protein, carbohydrate, dietary fiber, total fat, monounsaturated
fat, polyunsaturated fat, saturated fat, cholesterol, and percent energy
from protein, fat, carbohydrate, and alcohol were all assessed. The
protocol for the ethical treatment of human subjects was approved by the
University of Massachusetts Lowell Institutional Review Board and the
Commonwealth of Massachusetts, Executive Office of Elder Affairs,
Elder Rights Review Committee, Boston, MA.
Experimental design. This 18-wk randomized, cross-over study
consisted of 4 phases. Phase I consisted of a 4-wk baseline period during
which 11 senior citizen center and university subjects were instructed to
limit their consumption of foods containing lutein and zeaxanthin and to
not eat eggs or high egg-content foods. In contrast, the intake of the
background diet and the intervention treatments (eggs or egg substitute)
of the 22 nursing home subjects were strictly controlled by the nursing
home staff. Phase II consisted of a 5-wk intervention period during which
subjects consumed either no egg or egg substitute (referred to as no egg)
or 1 egg/d in addition to their normal diet. Either a daily visit or phone
call to the nursing home facility or to the subject’s home by study
personnel were used to verify consumption of all interventions. Phase III
consisted of a 4-wk washout period similar to phase I. Phase IV consisted
of a 5-wk cross-over intervention period during which those subjects
who consumed the no-egg or egg-substitute regiment (referred to as no
egg) during phase II were switched to 1 egg/d in addition to their normal
diet. Those subjects who consumed 1 egg/d during phase II were
switched to the no egg or egg substitute in addition to their normal diet.
Analysis of serum lipids and lipoprotein cholesterol measure-
ments. During each phase, morning 12-h fasting blood samples were
collected from all subjects at wk 2 and wk 4 for phases I and III and wk 3
and wk 5 for phases II and IV. Serum was harvested after centrifugation
at 1500 3 g at 4C for 20 min. Serum lipid and lipoprotein cholesterol
concentrations were measured using a Cobas Mira Plus Clinical
Chemistry Autoanalyzer. Serum total cholesterol (TC) (25) and triglyc-
eride (TG) (26) concentrations were measured enzymatically using
the Infinity Cholesterol Reagent (procedure 401) and Triglyceride (GPO-
Trinder) Reagent (procedure 337) from Sigma Diagnostics (Sigma-
Aldrich). Serum HDL cholesterol (HDL-C) was measured using the EZ
HDL Cholesterol Reagent (procedure 354L, Sigma Diagnostics, Sigma-
Aldrich). The concentration of serum LDL-C was calculated via the
Friedewald equation. The accuracy and precision of the procedures used
for the measurements of serum TC, HDL-C, and TG were maintained by
participation in the Lipid Standardization Program of the Centers for
Disease Control and the National Heart, Blood, and Lung Institute
(Atlanta, GA).
Although the results of phases I, III, and the no-egg or egg-substitute
intervention of phases II and IV during randomization were not
statistically different, the period just before the 1 egg/d was used as the
no-egg treatment for comparison with the egg-eating phase. Therefore,
results for each subject are reported as egg vs. no egg for serum lutein,
zeaxanthin, and lipid and lipoprotein cholesterol concentration.
Analysis of serum lutein and zeaxanthin. Serum aliquots were
archived in sealed 1.0 mL cryovials and stored at 280C for no .6mo
before analysis of serum carotenoids, a duration that has shown carot-
enoids to remain stable (27). Lutein and zeaxanthin standards were
provided by Hoffman-La Roche. The internal standard was b-apo-
12#-carotenol-O-t-ethyl-oxime. Cholesterol esterase (sterol esterase, EC
3.1.1.13; Pseudomonus sp.) and triacylglycerol lipase (EC 3.1.1.3;
TABLE 1 Baseline characteristics of men and women
1
Men Women
n 726
Age, y 77 6 4816 2
Weight, kg 78 6 4.5 70 6 2.7
Height, m 1.7 6 0.03 1.6 6 0.01
BMI 26 6 6276 6
TC, mmol/L 5.0 6 0.3 5.2 6 0.2
HDL-C, mmol/L 1.4 6 0.2 1.3 6 0.1
LDL-C, mmol/L 3.0 6 0.3 3.2 6 0.2
TG, mmol/L 1.5 6 0.2 1.5 6 0.2
MMSE
2
24 6 3226 2
Blood pressure, mm Hg
Systolic 139 6 9 132 6 2
Diastolic 77 6 4716 2
1
Values are means 6 SEM.
2
MMSE, Mini-Mental State Exam.
2520 Goodrow et al.
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Rhizopus) were obtained from Calbiochem. High performance liquid
chromatography (HPLC) grade solvents were used (Pharmco and Fisher
Chemical).
Serum samples (100 mL) were mixed with 900 mL of reagent,
containing 1 International Unit (IU) cholesterol esterase (Calbiochem)
and 160 IU triglyceride lipase (Calbiochem). The enzyme reagent was
prepared in a 0.1 mol/L sodium phosphate buffer, pH 7.0, with 0.1%
Triton X100. Samples were prepared according to the procedures
described by Handelman et al. (27). Calibration was achieved by
carrying the standards through the entire protocol parallel to those of the
serum samples.
HPLC separation and quantification of lutein and zeaxanthin were
carried out using a procedure adapted from Handelman et al. (27). This
HPLC assay separates the 2 carotenoids, lutein and zeaxanthin, which
were then identified and quantitated as distinct peaks in the chromato-
gram. Analyses were achieved using an Agilent model 1100 gradient
HPLC apparatus with diode array detection. The column used was a 300
mm 3 4.6 mm Adsorbosphere-HS C18 (20% carbon load) (Alltech) with
3 mm particle size coupled with an identically packed guard column. The
flow rate was 1.0 mL/min. The initial mobile phase concentration was
80% acetonitrile:20% methanol:0.4% ammonium acetate (w:v), with a
step gradient at 20 min to 30% isopropanol, returning to initial conditions
at 40 min, and then finishing with an additional 20 min equilibration
period. The column temperature was maintained at 19.5C.
Measurement of egg yolk cholesterol and carotenoid composi-
tion. For cholesterol analysis, commercial large white chicken eggs were
provided by the nursing home facilities or donated by the Aramark
Corporation, which is the food service entity for the University of
Massachusetts, Lowell. Initially, 12 randomly chosen egg yolks were
separated manually from the egg white and placed in a preweighed petri
dish to determine weight of yolk. Five hundred mL of yolk was added to
20 mL of buffer solution and vigorously mixed for 3 min. Two-hundred
mL of the yolk-buffer solution was collected and analyzed for cholesterol
content on the Cobas Mira Plus Clinical Chemistry Autoanalyzer using
the same methods described for the analysis of serum lipids and
lipoprotein cholesterol.
For carotenoid analyses from the same 12 eggs, 250 mL of yolk was
added to 20 mL 0.15 mol/L phosphate buffer, pH 7.0, with 1 mmol/L
EDTA and 0.25% Triton 3 100. For analysis, 200 mL of dilute yolk was
mixed with 0.8 mL distilled water, 1 mL 6 mol/L potassium hydroxide,
and 2 mL ethanol. After vigorous mixing, the mixture was heated at
60C for 30 min to saponify the lipids and hydrolyze the carotenoid
esters. After saponification, 60 mL of internal standard was added,
mixed, and extracted similarly to serum. For HPLC analysis, the
supernatant was collected, dried under N
2
, and redissolved in 60 mL
methanol and 25 mL was injected onto the HPLC.
Statistical analysis. Differences between the 4 phases were determined
by repeated measures 1-way ANOVA (SigmaStat, Jandel Scientific).
When differences were observed, a Student-Newman-Keuls test was
used. A paired t test was used to examine the effect of the egg vs. no-egg
phases on the different variables measured. All values were expressed as
means 6 SEM and significance was set at P , 0.05. Pearson correlation
coefficient was used to determine significant associations among the
variables measured.
Power calculation indicated that a minimum size of 30 was needed to
detect a 5% change in LDL-C with a cross-over design at an error rate
(alpha) of 0.001 with a desired power (beta) of 80.
Results
Dietary analysis. Using the 7-d diet record for a 1-wk analysis
of dietary intake per phase, no significant changes in dietary
intake between the nursing home and senior citizen center
subjects were observed despite the differences (free-living vs.
institutionalized) in the degree of background dietary control
(Table 2). The only macronutrient that increased was dietary
cholesterol during the egg intervention compared with the no-
egg/egg substitute period (P , 0.001). Although the diet analysis
database did not provide the carotenoid content of the various
foods, the frequency (number of times carotenoid-containing
foods were consumed each wk) did not differ during the egg
(10.9 6 1.8) vs. no-egg (11.1 6 2.0) interventions. These data
also showed that the background diet of the participants
consisted of only 5 carotenoid-containing foods (orange juice,
lettuce, yellow corn, broccoli, and onions) (28) and at mean
intakes of 113 g, contributed negligible amounts of dietary
carotenoids.
Egg yolk lutein, zeaxanthin, and cholesterol contents. The
cholesterol content for the 12 randomly sampled egg yolks was
210 6 9 mg/yolk (individual data not shown). Analyses of the
lutein and zeaxanthin content of the 12 egg yolks randomly
sampled were 143 6 28 and 94 6 18 mg/yolk, respectively
(individual data not shown).
Serum carotenoids and lipids. Serum lutein (Fig. 1A) and
zeaxanthin (Fig 1B) concentrations during the 4-wk phase prior
to consuming 1 egg/d increased 26 and 38%, respectively, by the
end of 5 wk of 1 egg/d intervention (P , 0.05).
Serum TC, LDL-C, HDL-C, and TG concentrations during
the no-egg and egg interventions did not differ. (Fig. 2).
Association between serum carotenoids, lipids, and lipo-
protein cholesterol. Serum lutein and zeaxanthin concentra-
tions during the no-egg and egg interventions were only
significantly associated (r) with HDL-C (Table 3). However,
these correlations, although significant, only explained #21% of
the variability (r
2
). Absent from the table are the elevated values
of serum lutein and zeaxanthin after egg consumption (r ¼
0.835, P , 0.001), which were associated with their values
before egg consumption (r ¼ 0.850, P , 0.001).
Discussion
There appear to be only 4 published studies that have used egg
yolks as a bioavailable source of the oxygenated carotenoids,
lutein and zeaxanthin. Three of these studies used carotenoid-
enriched eggs (21,29,30) and only 1 of these studies measured
lutein and zeaxanthin separately (22). In this present study,
consumption of 1 noncarotenoid-enriched egg/d for 5 wk
significantly increased serum lutein and zeaxanthin concentra-
tions by 26 and 38%, respectively, in this population with a
mean age of 79 y consuming dietary egg yolk lutein and
zeaxanthin concentrations of 143 and 94 mg/yolk, respectively.
TABLE 2 Seven-day diet record analysis of 33 subjects
consuming egg vs. no-egg diet
1
Egg No egg
Energy intake, kJ/d 6690 6 351 6489 6 268
Protein, g/d 70 6 4786 16
Carbohydrate, g/d 199 6 14 293 6 77
Dietary fiber, g/d 12 6 2146 3
Total fat, g/d 57 6 3686 16
Monosaturated fat, g/d 20 6 1236 5
Polyunsaturated fat, g/d 10 6 1116 2
Saturated fat, g/d 19 6 1226 5
Cholesterol, mg/d 451 6 24 312 6 50*
1
Values are means 6 SEM, n ¼ 33. *Different from egg, P , 0.001.
Egg consumption and serum lutein and zeaxanthin 2521
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The degree of serum carotenoid responsiveness in this commu-
nication is similar to the study by Handelman et al. (22) in
subjects consuming 1.3 egg yolks/d but is not consistent with the
results from the study of Surai et al. (30) where only individuals
consuming the designer eggs (1910 mg of lutein/egg) and not the
control eggs (120 mg lutein/egg) increased their plasma lutein
concentrations. The reason for the discordant findings of Surai
et al. (30) compared with the studies of Handelman et al. (22)
and the present communication is not known. The studies of
Yeum et al. (29) suggest that baseline values may influence serum
carotenoid responsiveness because men ingesting controlled
diets high in fruits and vegetables, and who had higher baseline
values of lutein, did not increase their serum concentrations of
lutein in response to increased dietary lutein. With the 13 people
in the present study who consumed supplements containing
lutein, baseline serum lutein concentrations (300 6 43 nmol/L)
were ;80% higher than the 33 individuals who had not con-
sumed supplements (167 6 16 nmol/L). Similar to the findings of
Yeum et al. (29), these 13 people did not show significant serum
carotenoid increases in response to increased dietary lutein and
zeaxanthin after consuming 1 store-bought egg/d (data not
shown). Surprisingly, in the randomization process in which par-
ticipants did not consume eggs for up to 13 wk (4 wk baseline
1 5 wk of Egg Beaters 1 4 wk of washout) the baseline con-
centrations of serum lutein and zeaxanthin of the 13 individuals
taking supplements remained greater than individuals not on
supplements (286 6 40 nmol/L and 71 6 9 nmol/L vs. 210 6 21
nmol/L and 56 6 5 nmol/L). These findings suggest that 13 wk
of not taking supplemental lutein and zeaxanthin is not a
sufficient duration to reduce serum lutein and zeaxanthin to
previous concentrations. This may explain why participants
recruited into the study of Chung et al. (21) were required to stay
off of supplemental lutein for 6 mo. This observation, plus the
nonresponsive carotenoid findings of Yeum et al. (29) in in-
dividuals with high baseline lutein values, was the rationale for
analyzing separately the data from the 13 people who consumed
supplements prior to the baseline period in the present study. In
addition to baseline values of circulating carotenoids, it is also
possible that the concentrations of carotenoids consumed may
affect carotenoid responsiveness. In a study of individuals who
consumed designer eggs enriched with 1910 mg of lutein for 8
wk, plasma lutein concentrations increased 88% (240 to 450
nmol/L) (30). The .2-fold (88 vs. 26%) increase in plasma
lutein concentrations in the designer-egg study of Surai et al.
(30), compared with the present study, was probably associated
with the 12-fold greater concentrations (1910 mg/yolk vs. 143
mg/yolk) of lutein in the designer eggs than in the store-bought
eggs. The possibility that dietary fat may also influence serum
carotenoid concentration is suggested by the findings of Chung
et al. (21) in subjects that consumed comparable concentrations
Figure 2 Serum lipids and lipoprotein cholesterol concentrations in older
adults when they consumed 1 egg/d for 5 wk and when they consumed no eggs
or egg substitute. Values are means 1 SEM, n ¼ 33. *Different from no egg,
P , 0.001.
TABLE 3 Association between serum concentrations of lutein
and zeaxanthin before and after egg consumption
with serum lipids and lipoprotein cholesterol
concentrations
1
No egg Egg
rr
2
P-value rr
2
P-value
TC
Lutein 0.200 0.040 NS 0.121 0.015 NS
2
Zeaxanthin 0.025 0.001 NS 0.133 0.018 NS
LDL-C
Lutein 0.159 0.025 NS 20.02 0.001 NS
Zeaxanthin 20.075 0.006 NS 0.015 0.001 NS
HDL-C
Lutein 0.410 0.168 ,0.017 0.453 0.205 0.008
Zeaxanthin 0.325 0.106 NS 0.424 0.180 0.014
TG
Lutein 20.233 0.054 NS 20.133 0.018 NS
Zeaxanthin 2 0.150 0.023 NS 20.144 0.021 NS
1
The r is Pearson correlation coefficient; the r
2
is the proportion of variance explained
uniquely by a particular variable.
2
NS, not significant.
Figure 1 Serum lutein (A) and zeaxanthin (B) concentratio ns in older adults
when they consumed 1 egg/d for 5 wk and when they consumed no eggs or egg
substitute. Values are means 1 SEM, n ¼ 33. *Different from no egg, P , 0.001.
2522 Goodrow et al.
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of lutein in which a background diet, consisting of 60% of
energy from fat compared with 17% in the present communi-
cation, was associated with 11-fold greater increase in (323 vs.
26%) blood lutein concentrations. Their (21) dramatic increase
in plasma lutein concentrations may have also resulted from the
greater consumption of lutein (6 mg/d) compared with the
concentrations consumed (148 mg/d) in the present study. Other
factors that can influence the absorption of lutein and zeaxan-
thin include digestion of the food matrix, the formation of lipid
micelles, and uptake of the carotenoids by mucosal cells and
transport of the carotenoids to the lymphatic or portal circula-
tions (31). The substantial contribution that the digestibility of
the food matrix can make to absorption is suggested by the
studies of Chung et al. (21) in which lutein from eggs was nearly
3 times more bioavailable than spinach. Competition for
absorption from other carotenoids besides lutein and zeaxanthin
has also been suggested (31), a possibility that could not be
evaluated in the present study because other carotenoids were
not measured. It is also possible that a population’s response to
dietary lutein and zeaxanthin may be age dependent, although
the studies of Johnson et al. (18), in a population aged 33–54 y,
and Yeum et al. (29), in a population ranging in age from 20 to
80 y, did not report age-dependent differences in plasma lutein
response.
The finding that concentrations of serum lutein and zeaxan-
thin during the no-egg and egg interventions were associated
with serum HDL-C, is not unexpected, insofar as these oxygen-
ated carotenoids are predominantly transported in this lipopro-
tein fraction (32). Due to the small number of subjects (n ¼ 11)
compared with the current study (n ¼ 33), Handelman et al. (22)
were unable to determine whether the lutein concentration was
associated with any serum lipid measurements such as HDL-C.
In the current study, the carotenoid responsiveness is similar
to the findings of Handelman et al. (22), despite the differences
in the mean age of the study populations (62 vs. 79 y in the
current study), which suggests that age is not related to the
degree of diet responsiveness.
A difference between our study and the results of Handelman
et al. (22) concerning serum LDL-C changes (11 and 3.2%,
respectively), may be a result of the number of subjects in our
study (33) vs. the number (11) in the study by Handelman et al.
(22). Another possibility for the difference in serum LDL-C
response may be gender related, insofar as Handelman et al. (22)
had 54% males, vs. 21% males the current study.
Our results demonstrated that increases in serum lutein and
zeaxanthin concentrations were not significantly associated with
a similar increase in serum lipids and lipoprotein cholesterol
concentrations in this population with a mean age of 79 y. The
actual 0.6 and 3.2% increase in serum TC and LDL-C
concentrations, respectively, is consistent with the meta-analysis
of studies of dietary cholesterol effects on plasma TC and LDL-C
conducted by Clarke et al. (33), Howell et al. (34), and
Weggemans et al. (35). Greene et al. (36) showed that dietary
cholesterol concentrations from consuming 3 eggs/d significantly
increased plasma LDL-C and HDL-C in subjects 29–60 y of age,
and there were no significant alterations in the ratios of LDL-C:
HDL-C or the TC:HDL-C, which is often associated with
increased atherogenicity. Our study did not find significant
increases in serum LDL-C or HDL-C, possibly because our
participants consumed only 1 egg/d. This may also be related to
the greater age of the population in this study. There are several
studies (37–39) that indicate serum LDL-C concentrations are
reduced in older populations, and, in one study, the suggested
mechanism may be reduced.
In conclusion, compared with the study of Handelman et al.
(22), our study demonstrated that consuming only 1 store-
bought egg/d in a population with a mean age of 79 y can
significantly increase both serum lutein and zeaxanthin concen-
trations without elevating serum TC and LDL-C concentrations.
The study also revealed that the degree of carotenoid response in
an older population was similar to those reported for younger
populations (22), despite the fact that the work by Handelman
et al. (22) was a metabolic ward study (personal communica-
tion, Dr. Garry Handelman, University of Massachusetts,
Lowell), environmentally different from the relatively free-living
study reported here. Finally, this study showed a significant
association between serum concentrations of carotenoids with
only HDL-C, a finding that could not be observed in the study of
Handelman et al. (22) with only 11 participants.
Acknowledgments
The authors would like to thank several individuals who made
significant contributions to this research study: Chirstopher
Monti, Olan Horne, and Sherry Toscano from Aramark Corp.;
Priscilla Fawcet from Saints Memorial Hospital; Teresa Scuderi
from Lawrence General Hospital; Naomi Prendergast from
D’Youville Senior Care; Jeffrey Munroe and Shirley Paquin
from Sunny Acres Nursing Home; Colleen Lovering from Life
Care Center of Merrimack Valley; Marguerite Foley from Blaire
House of Tewksbury; Martin Walsh from Chelmsford Senior
Center; Deborah Drake from Billerica Council on Aging; and
Pat Becker and Kathleen Urquehart from Andover Senior
Center. We would also like to thank Maureen Faul and
Margaret Martin for the overall management and recruitment
responsibilities, and Timothy J. Kotyla, Damian A. Barbato,
Kelly Anderson, Kim Chadwell, Lori Shea, April Hunter, Laura
Saba, Susannah Goodrow, Alicia Lepore, Vanessa Canales, and
Kalene Garbarz from the Center for Health and Disease
Research, University of Massachusetts Lowell for their techni-
cal support.
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