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Consumption of One Egg Per Day Increases Serum Lutein and Zeaxanthin Concentrations in Older Adults without Altering Serum Lipid and Lipoprotein Cholesterol Concentrations


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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.
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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
Elizabeth F. Goodrow,
Thomas A. Wilson,
Susan Crocker Houde,
Rohini Vishwanathan,
Patrick A . Scollin,
Garry Handelman,
and Robert J. Nicolosi
Center for Health and Disease Research, Department of Clinical Laboratory and Nutritional Sciences,
Department of Nursing,
Department of Community Health and Sustainability, University of Massachusetts Lowell, MA 01854
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.
Age-related macular degeneration (AMD)
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
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
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:
0022-3166/06 $8.00 ª 2006 American Society for Nutrition.
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; Pseudomonus sp.) and triacylglycerol lipase (EC;
TABLE 1 Baseline characteristics of men and women
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
24 6 3226 2
Blood pressure, mm Hg
Systolic 139 6 9 132 6 2
Diastolic 77 6 4716 2
Values are means 6 SEM.
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
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
, 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.
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
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
). 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).
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
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*
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
No egg Egg
P-value rr
Lutein 0.200 0.040 NS 0.121 0.015 NS
Zeaxanthin 0.025 0.001 NS 0.133 0.018 NS
Lutein 0.159 0.025 NS 20.02 0.001 NS
Zeaxanthin 20.075 0.006 NS 0.015 0.001 NS
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
Lutein 20.233 0.054 NS 20.133 0.018 NS
Zeaxanthin 2 0.150 0.023 NS 20.144 0.021 NS
The r is Pearson correlation coefficient; the r
is the proportion of variance explained
uniquely by a particular variable.
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
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.
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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... After 5-wk of eating one egg per day, zeaxanthin concentrations were 38% (P<0.01) and lutein concentrations were 26% (P<0.01) higher than they were in the period before eating eggs [1]. ...
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In this study, the composition of chicken eggs from diets with various lutein levels was examined. This study involved a total of 120 laying hens. Treatments included lutein-free rations and lutein concentrations of 20, 40, 60, and 80 ppm. Each treatment was applied a total of eight times. Chickens are kept in cages with access to feeding and drinking areas. The analysis of the research data was conducted utilizing a completely random design. The parameters that were measured were the egg’s weight, its yolk, and its albumen. The components of eggs fed various dietary levels of lutein from marigold extract had not been significant (P>0.05) on all egg components stored for one day. However, the treatment had a significant impact (P<0.05) on the albumen index stored for 14 days, and the yolk to albumen ratio and albumen index for eggs stored for 21 days. This study concludes that for optimum albumen weight and index and the ratio of yolk and albumen stored for 14 and 21 days, a dose of 20 and 40 ppm in the diets is sufficient.
... Microalgal species producing high amounts of lutein can be used as animal feed and dietary sources of carotenoids for producing eggs and meat enriched with lutein (Pitargue et al., 2019). Lutein-enriched egg yolk is preferred to be included in the human diet since it has been reported to increase the plasma levels of lutein in elderly people (Goodrow et al., 2006). Microalgae such as Nannochloropsis oculata (Fredriksson et al., 2006), Chlorella (Englmaierová et al., 2013) and Chlamydomonas reinhardtii (Baek et al., 2018) are recognized as good sources of carotenoids, especially lutein and zeaxanthin for animal feed supplementation. ...
... Eggs also are excellent sources of choline and the carotenoids lutein and zeaxanthin and provide vitamin A, vitamin D, folate and iron (all shortfall nutrients), plus DHA and selenium. Lutein and zeaxanthin (252 μg/egg) (Goodrow et al., 2006) are involved in formation of HDL-C, which transports these same carotenoids to the eye where they are involved in formation of the macular pigment. That pigment protects the eye from oxidative damage and thus cataract and macular degeneration (Hobbs and Bernstein, 2014). ...
... For example, in a randomized controlled trial (RCT), cholesterol intake from eggs, with carbohydrate restriction, reduced plasma total cholesterol (TC) concentrations and increased high-density lipoprotein concentrations (HDL-C) [10]. However, another RCT reported that consuming one egg per day did not change the plasma TC or HDL-C levels [11]. ...
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Background: Studies investigating the relationship between egg consumption and the risk of cerebrovascular disease (CED) have yielded inconsistent results. This study evaluated the association between egg consumption and the risk of CED among Chinese adults. Methods: Data were obtained from China Kadoorie Biobank, Qingdao. A computerised questionnaire was used to collect information regarding egg consumption frequency. CED events were tracked through linkage with the Disease Surveillance Point System and the new national health insurance databases. Cox proportional hazards regression analyses were used to evaluate associations between egg consumption and CED risk controlling for potential confounders. Results: After a median follow-up of 9.2 years, 865 and 1083 CED events among men and women, respectively, were documented. More than 50% of participants consumed eggs daily with an average age of 52.0 (10.4) years at baseline. No association between egg consumption and CED were identified in the whole cohort and women. However, a 28% lower risk of CED was observed in those who consumed eggs at a higher frequency (HR = 0.72, 95% CI: 0.55-0.95) and a significant trend for the association (p for trend = 0.012) in a multivariable model in men. Conclusion: Higher frequency of egg consumption was associated with a lower risk of total CED events among men but not women in Chinese adults. The beneficial effect on women warrants further investigations.
... Dietary interventions have documented that whole-egg consumption increases dietary intake and improves plasma carotenoids in overweight individuals as part of a carbohydrate-restricted diet [64,65], in young men and women [66], metabolic syndrome participants [8,48], pre-menopausal women [25], elderly adults with altered lipid profile [67,68], after intake of regular, lutein-enriched and n-3 fatty-acid-enriched eggs [69] as well as in a healthy lacto-ovo-vegetarian population predominately on a plant-based diet consuming both n-3 fatty acid-enriched eggs and organic eggs [69]. In most of the above studies, plasma choline increased after consumption of eggs, whereas the choline metabolites' TMAO levels did not increase [7,67]. ...
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Plant-based (PB) diets are considered a healthy dietary pattern; however, eggs are not always included in this dietary regime. We hypothesized that the addition of two eggs per day would increase HDL cholesterol as well as plasma lutein, zeaxanthin and choline in individuals with metabolic syndrome (MetS). In this randomized controlled crossover intervention, we recruited 30 participants (49.3 ± 8 y) with MetS who followed a PB diet for 13 weeks. A registered dietitian advised all subjects on food selection and followed them through the intervention to ensure compliance. Participants underwent a 2-week washout with no eggs or spinach (a source of dietary lutein and zeaxanthin) and were randomly allocated to consume spinach (70 g) with either two eggs (EGG) or the equivalent amount of egg substitute (SUB) for breakfast for 4 weeks. After a 3-week washout, they were allocated the alternate breakfast. A total of 24 participants (13 women/11 men) finished the intervention. Plasma lipids, glucose, insulin, anthropometrics, plasma lutein, zeaxanthin, choline and trimethylamine oxide (TMAO) were assessed at baseline and the end of each intervention. When we compared individuals consuming the EGG versus the SUB breakfast, we observed a lower body weight (p < 0.02) and a higher HDL cholesterol (p < 0.025) after the EGG diet. There were no differences in plasma LDL cholesterol, triglycerides, glucose, insulin, or blood pressure. The number of large HDL particles measured by NMR was higher after EGG (p < 0.01) as compared to SUB. Plasma choline was higher in both treatments (p < 0.01) compared to baseline (8.3 ± 2.1 μmol/L). However, plasma choline values were higher in EGG (10.54 ± 2.8 μmol/L) compared to SUB (9.47 ± 2.7 μmol/L) p < 0.025. Both breakfasts increased plasma lutein compared to baseline (p < 0.01), while plasma zeaxanthin was only increased in the egg intervention (p < 0.01). These results indicate that consuming a plant-based diet in combination with whole eggs increases plasma HDL cholesterol, choline and zeaxanthin, important biomarkers in subjects with MetS.
Background: Age-related macular degeneration (AMD) is a degenerative condition of the back of the eye that occurs in people over the age of 50 years. Antioxidants may prevent cellular damage in the retina by reacting with free radicals that are produced in the process of light absorption. Higher dietary levels of antioxidant vitamins and minerals may reduce the risk of progression of AMD. This is the third update of the review. Objectives: To assess the effects of antioxidant vitamin and mineral supplements on the progression of AMD in people with AMD. Search methods: We searched CENTRAL, MEDLINE, Embase, one other database, and three trials registers, most recently on 29 November 2022. Selection criteria: We included randomised controlled trials (RCTs) that compared antioxidant vitamin or mineral supplementation to placebo or no intervention, in people with AMD. Data collection and analysis: We used standard methods expected by Cochrane. Main results: We included 26 studies conducted in the USA, Europe, China, and Australia. These studies enroled 11,952 people aged 65 to 75 years and included slightly more women (on average 56% women). We judged the studies that contributed data to the review to be at low or unclear risk of bias. Thirteen studies compared multivitamins with control in people with early and intermediate AMD. Most evidence came from the Age-Related Eye Disease Study (AREDS) in the USA. People taking antioxidant vitamins were less likely to progress to late AMD (odds ratio (OR) 0.72, 95% confidence interval (CI) 0.58 to 0.90; 3 studies, 2445 participants; moderate-certainty evidence). In people with early AMD, who are at low risk of progression, this means there would be approximately four fewer cases of progression to late AMD for every 1000 people taking vitamins (one fewer to six fewer cases). In people with intermediate AMD at higher risk of progression, this corresponds to approximately 78 fewer cases of progression for every 1000 people taking vitamins (26 fewer to 126 fewer). AREDS also provided evidence of a lower risk of progression for both neovascular AMD (OR 0.62, 95% CI 0.47 to 0.82; moderate-certainty evidence) and geographic atrophy (OR 0.75, 95% CI 0.51 to 1.10; moderate-certainty evidence), and a lower risk of losing 3 or more lines of visual acuity (OR 0.77, 95% CI 0.62 to 0.96; moderate-certainty evidence). Low-certainty evidence from one study of 110 people suggested higher quality of life scores (measured with the Visual Function Questionnaire) in treated compared with non-treated people after 24 months (mean difference (MD) 12.30, 95% CI 4.24 to 20.36). In exploratory subgroup analyses in the follow-on study to AREDS (AREDS2), replacing beta-carotene with lutein/zeaxanthin gave hazard ratios (HR) of 0.82 (95% CI 0.69 to 0.96), 0.78 (95% CI 0.64 to 0.94), 0.94 (95% CI 0.70 to 1.26), and 0.88 (95% CI 0.75 to 1.03) for progression to late AMD, neovascular AMD, geographic atrophy, and vision loss, respectively. Six studies compared lutein (with or without zeaxanthin) with placebo and one study compared a multivitamin including lutein/zeaxanthin with multivitamin alone. The duration of supplementation and follow-up ranged from six months to five years. Most evidence came from the AREDS2 study in the USA; almost all participants in AREDS2 also took the original AREDS supplementation formula. People taking lutein/zeaxanthin may have similar or slightly reduced risk of progression to late AMD (RR 0.94, 95% CI 0.87 to 1.01), neovascular AMD (RR 0.92, 95% CI 0.84 to 1.02), and geographic atrophy (RR 0.92, 95% CI 0.80 to 1.05) compared with control (1 study, 4176 participants, 6891 eyes; low-certainty evidence). A similar risk of progression to visual loss of 15 or more letters was seen in the lutein/zeaxanthin and control groups (RR 0.98, 95% CI 0.91 to 1.05; 6656 eyes; low-certainty evidence). Quality of life (Visual Function Questionnaire) was similar between groups (MD 1.21, 95% CI -2.59 to 5.01; 2 studies, 308 participants; moderate-certainty evidence). One study in Australia randomised 1204 people to vitamin E or placebo with four years of follow-up; 19% of participants had AMD. The number of late AMD events was low (N = 7) and the estimate of effect was uncertain (RR 1.36, 95% CI 0.31 to 6.05; very low-certainty evidence). There was no evidence of any effect of treatment on visual loss (RR 1.04, 95% CI 0.74 to 1.47; low-certainty evidence). There were no data on neovascular AMD, geographic atrophy, or quality of life. Five studies compared zinc with placebo. Evidence largely drawn from the largest study (AREDS) found a lower progression to late AMD over six years (OR 0.83, 95% CI 0.70 to 0.98; 3 studies, 3790 participants; moderate-certainty evidence), neovascular AMD (OR 0.76, 95% CI 0.62 to 0.93; moderate-certainty evidence), geographic atrophy (OR 0.84, 95% CI 0.64 to 1.10; moderate-certainty evidence), or visual loss (OR 0.87, 95% CI 0.75 to 1.00; 2 studies, 3791 participants; moderate-certainty evidence). There were no data on quality of life. Gastrointestinal symptoms were the main reported adverse effect. In AREDS, zinc was associated with a higher risk of genitourinary problems in men, but no difference was seen between high- and low-dose zinc groups in AREDS2. Most studies were too small to detect rare adverse effects. Data from larger studies (AREDS/AREDS2) suggested there may be little or no effect on mortality with multivitamin (HR 0.87, 95% CI 0.60 to 1.25; low-certainty evidence) or lutein/zeaxanthin supplementation (HR 1.06, 95% CI 0.87 to 1.31; very low-certainty evidence), but confirmed the increased risk of lung cancer with beta-carotene, mostly in former smokers. Authors' conclusions: Moderate-certainty evidence suggests that antioxidant vitamin and mineral supplementation (AREDS: vitamin C, E, beta-carotene, and zinc) probably slows down progression to late AMD. People with intermediate AMD have a higher chance of benefiting from antioxidant supplements because their risk of progression is higher than people with early AMD. Although low-certainty evidence suggested little effect with lutein/zeaxanthin alone compared with placebo, exploratory subgroup analyses from one large American study support the view that lutein/zeaxanthin may be a suitable replacement for the beta-carotene used in the original AREDS formula.
Background: Given China's fast-growing aging population, cognitive decline is a leading public health concern. Eggs are an affordable food rich in several shortfall nutrients that may benefit cognitive health. Aim: This study assessed the longitudinal relationship between whole egg consumption and cognition among older adults in China. Methods: Individual-level data of 4737 Chinese adults 55+ years came from the China Health and Nutrition Survey (CHNS) 1997-2006 waves. Daily egg consumption was measured using 3-day 24-h dietary recalls. Cognitive functioning was assessed with immediate and delayed recall of a 10-word list, counting backward from 20, and serial 7 subtraction. Multivariate mixed-effects regressions were performed to estimate the longitudinal associations between daily whole egg consumption and cognitive functioning in older Chinese adults. Results: Approximately 46% of CHNS participants were whole egg consumers, and their daily intake averaged 47.4 g. The overall cognitive functioning test scores, separate scores for cognitive functioning subdomains, and the prevalence of cognitive impairment at the baseline were modestly higher among whole egg consumers than nonconsumers. However, after adjusting for individual characteristics, multivariate mixed-effects regressions did not find daily whole egg consumption to be associated with cognitive functioning among CHNS participants. By contrast, several demographic and socioeconomic factors, such as age, education attainment, and health insurance coverage, were found to correlate with older Chinese adults' cognition. Conclusion: This study has measurement and design limitations. Future research should investigate the causal impact of habitual egg intake on different domains of cognition using experimental designs with an extended follow-up period.
The public and scientists remain skeptical about egg consumption, given that cardiovascular diseases (CVDs) are the leading causes of death in worldwide. This review mainly explained the recurrence of contradictory conclusions about relationships between egg consumption and CVD risk and discussed effects of egg cholesterol intake on cholesterol homeostasis. Factors including individual health status and cholesterol sensitivity, dietary pattern, region, and race should be distinguished when understanding generalized conclusions. Identified compensatory mechanisms in response to dietary cholesterol and the resulting balance in cholesterol biosynthesis, absorption, and efflux supported the view that moderate egg consumption had no substantial overall impacts on cholesterol homeostasis in healthy people. Excessive cholesterol intake is not recommended in individuals with distempered metabolism. More than cholesterol metabolism, impacts of egg consumption as a part of overall diet on CVD risk should be considered from aspects of nutrient intake, lipid metabolism, and energy supply in the future.
Cholesterol is the main sterol component in animal cells. It has a characteristic four-ring hydrophobic structure referred to as the steroid nucleus. Cholesterol is found as free cholesterol and stored as esterified cholesteryl ester. With the exception of cholesterol-rich egg yolk and shrimp, dietary cholesterol is found in food sources that are also rich in saturated fat. The 2015 Dietary Guidelines eliminated the limit of 300 mg/day of dietary cholesterol established in 1968. The 2020 Dietary Guidelines recommend the intake of eggs as part of the protein food group, intake of less than 10% from saturated fat daily, but did not set a limit for dietary cholesterol intake. Cholesterol has several functions in the body, such as a structural component of cell membranes, a precursor of all steroid hormones, bile acids, and vitamin D. Both exogenous cholesterol from the diet and endogenously synthesized cholesterol contribute to the total cholesterol pool. The rate-limiting step in endogenous cholesterol biosynthesis is the regulation by the HMG-CoA reductase enzyme. This enzyme is inhibited by statins, which are the main cholesterol-lowering drugs to prevent or control atherosclerosis, a leading cause of cardiovascular disease. Here, we will review current literature and recommendations on dietary cholesterol content and its role in cardiovascular disease.
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Background: Observational and experimental data suggest that antioxidant and/or zinc supplements may delay progression of age-related macular degeneration (AMD) and vision loss. Objective: To evaluate the effect of high-dose vitamins C and E, beta carotene, and zinc supplements on AMD progression and visual acuity. Design: The Age-Related Eye Disease Study, an 11-center double-masked clinical trial, enrolled participants in an AMD trial if they had extensive small drusen, intermediate drusen, large drusen, noncentral geographic atrophy, or pigment abnormalities in 1 or both eyes, or advanced AMD or vision loss due to AMD in 1 eye. At least 1 eye had best-corrected visual acuity of 20/32 or better. Participants were randomly assigned to receive daily oral tablets containing: (1) antioxidants (vitamin C, 500 mg; vitamin E, 400 IU; and beta carotene, 15 mg); (2) zinc, 80 mg, as zinc oxide and copper, 2 mg, as cupric oxide; (3) antioxidants plus zinc; or (4) placebo. Main outcome measures: (1) Photographic assessment of progression to or treatment for advanced AMD and (2) at least moderate visual acuity loss from baseline (> or =15 letters). Primary analyses used repeated-measures logistic regression with a significance level of.01, unadjusted for covariates. Serum level measurements, medical histories, and mortality rates were used for safety monitoring. Results: Average follow-up of the 3640 enrolled study participants, aged 55-80 years, was 6.3 years, with 2.4% lost to follow-up. Comparison with placebo demonstrated a statistically significant odds reduction for the development of advanced AMD with antioxidants plus zinc (odds ratio [OR], 0.72; 99% confidence interval [CI], 0.52-0.98). The ORs for zinc alone and antioxidants alone are 0.75 (99% CI, 0.55-1.03) and 0.80 (99% CI, 0.59-1.09), respectively. Participants with extensive small drusen, nonextensive intermediate size drusen, or pigment abnormalities had only a 1.3% 5-year probability of progression to advanced AMD. Odds reduction estimates increased when these 1063 participants were excluded (antioxidants plus zinc: OR, 0.66; 99% CI, 0.47-0.91; zinc: OR, 0.71; 99% CI, 0.52-0.99; antioxidants: OR, 0.76; 99% CI, 0.55-1.05). Both zinc and antioxidants plus zinc significantly reduced the odds of developing advanced AMD in this higher-risk group. The only statistically significant reduction in rates of at least moderate visual acuity loss occurred in persons assigned to receive antioxidants plus zinc (OR, 0.73; 99% CI, 0.54-0.99). No statistically significant serious adverse effect was associated with any of the formulations. Conclusions: Persons older than 55 years should have dilated eye examinations to determine their risk of developing advanced AMD. Those with extensive intermediate size drusen, at least 1 large druse, noncentral geographic atrophy in 1 or both eyes, or advanced AMD or vision loss due to AMD in 1 eye, and without contraindications such as smoking, should consider taking a supplement of antioxidants plus zinc such as that used in this study.
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Objective. —To evaluate the relationships between dietary intake of carotenoids and vitamins A, C, and E and the risk of neovascular age-related macular degeneration (AMD), the leading cause of irreversible blindness among adults.
Background:Adequate intake of lutein is postulated to reduce the risk of age-related macular degeneration, but kinetic information for developing a dosing regimen is sparse. Objective:The objective was to characterize lutein plasma kinetics in a multiple dosing design and to assess the effects of lutein intake on concentrations of other plasma carotenoids. Design:After a run-in period of 7 d, 19 healthy volunteers were assigned to receive daily oral doses of 4.1 mg lutein (n = 8; group 1) or 20.5 mg lutein (n = 8; group 2) for 42 d or no lutein (n = 3; control group). The supplement contained 8.3% zeaxanthin relative to lutein (100%). The time profiles of plasma xanthophyll concentrations were monitored over the dosing phase, and samples were collected frequently on day 42 and for 24 d after dosing. Results:Average plasma all-E-lutein concentrations increased from 0.14 to 0.52 ± 0.13 and 1.45 ± 0.69 μmol/L in groups 1 and 2, respectively. Dose-normalized lutein bioavailability in group 2 was ≈60% of that in group 1. Kinetic disposition half-life did not differ significantly between groups. On average, dosing for 18 d was required to reach a >90% fraction of the steady state concentration, which is consistent with an effective half-life for accumulation of ≈5.6 d. Plasma kinetics of all-E-lutein were paralleled by those of all-E-3-dehydro-lutein. Kinetic analysis indicated formation of all-E-3-dehydro-lutein from lutein. Lutein was well tolerated and did not affect the concentrations of other carotenoids. Conclusion:Long-term supplementation with 4.1 and 20.5 mg lutein as beadlets increased plasma lutein concentrations ≈3.5- and 10-fold, respectively.
Lutein may be protective against diseases such as age-related macular degeneration (ARMD). At present, data regarding bioavailability of lutein from various sources are insufficient. Healthy men (n = 10) participated in an intervention study with a crossover design. After a 2-wk washout period during which they consumed a low-carotenoid diet, the men were administered 1 of 4 lutein doses (lutein supplement, lutein ester supplement, spinach, and lutein-enriched egg) for 9 d. All lutein doses provided 6 mg lutein except for the lutein ester dose, which provided 5.5 mg lutein equivalents. Serum samples were collected from fasting subjects on d –14, 1 (baseline), 2, 3, and 10 and analyzed for changes in lutein concentration. Triacylglycerol-rich lipoproteins (TRL) were separated from postprandial blood samples (0–24 h) after the first lutein dose and analyzed for lutein concentration. Subjects completed all 4 treatments of the study in random order. Results from repeated-measures 1-way ANOVA showed that the baseline and dose-adjusted lutein response in serum was significantly higher after egg consumption than after lutein, lutein ester, and spinach consumption on d 10. There was no significant difference in TRL response. In conclusion, the lutein bioavailability from egg is higher than that from other sources such as lutein, lutein ester supplements, and spinach. The lutein bioavailability from lutein, lutein ester supplements, and spinach did not differ. This finding may have implications for dietary recommendations that may decrease the risk of certain diseases, e.g., ARMD.
Background: Information on concentrations of retinal carotenoids (macular pigment, or MP) is of particular interest because MP protects against age-related macular degeneration, the leading cause of irreversible blindness in the United States. Objective: This study was designed to evaluate the relation between dietary intake, blood concentrations, and retinal concentrations of carotenoids in a large group of volunteers. Design: Two hundred eighty volunteers in the Indianapolis area completed health and diet questionnaires, donated a blood sample, and participated in MP density assessment to determine retinal carotenoid status. Dietary intake was assessed by food-frequency questionnaire. Serum concentrations of lutein, zeaxanthin, and β-carotene were measured by HPLC. MP optical density (MPOD) was determined psychophysically with a 460-nm, 1° test stimulus. Results: Average MPOD was 0.21 ± 0.13. Average intakes of lutein + zeaxanthin and β-carotene were 1101 ± 838 and 2935 ± 2698 μg/d, respectively. Although several key dietary intake variables (eg, lutein + zeaxanthin and β-carotene) differed by sex, no significant sex differences were found in either serum concentrations of lutein and zeaxanthin or MPOD. Serum β-carotene concentrations were significantly higher in women than in men. Serum lutein + zeaxanthin and dietary intake of lutein + zeaxanthin were significantly correlated and significantly related to variations in MPOD (r = 0.21, P < 0.001, and r = 0.25, P < 0.001, respectively). Conclusions: Retinal carotenoids can be measured in epidemiologic studies. In this study, MPOD was associated with lutein + zeaxanthin in the diet and the serum. Retinal concentrations, however, were influenced by other factors as well. To understand the effect of dietary lutein + zeaxanthin intake on the retina and risk of age-related eye disease, future studies should include measures of macular concentrations of these pigments.
Background: The food matrix in which carotenoids are found affects their bioavailability. Lutein and zeaxanthin are abundant in egg yolks and accumulate in the macular region of the retina, where they may affect visual function. Objective: We sought to determine whether plasma lutein and zeaxanthin concentrations are elevated after dietary supplementation with egg yolk. Design: Eleven moderately hypercholesterolemic men and women consumed 2 separate baseline diets, which contained 29–33% of energy as total fat, with 20% of energy as either beef tallow or corn oil. These diets were supplemented with cooked chicken egg yolks (1.3 egg yolks/d for an intake of 10.4 MJ). Each subject consumed all 4 diets. Each diet was consumed for 4.5 wk, with a washout period of ≥2 wk between diet phases. At the end of each diet phase, fasting morning plasma samples were collected and stored for carotenoid analysis by HPLC. Commercial chicken egg yolks were analyzed for carotenoids and cholesterol. Results: Egg yolk supplementation of the beef tallow diet increased plasma lutein by 28% (P < 0.05) and zeaxanthin by 142% (P < 0.001); supplementation of the corn oil diet increased plasma lutein by 50% (P < 0.05) and zeaxanthin by 114% (P < 0.001). Changes in plasma lycopene and β-carotene were variable, with no consistent trend. Egg yolk supplementation increased plasma LDL-cholesterol concentrations by 8–11% (P < 0.05). Conclusions: Egg yolk is a highly bioavailable source of lutein and zeaxanthin. The benefit of introducing these carotenoids into the diet with egg yolk is counterbalanced by potential LDL-cholesterol elevation from the added dietary cholesterol.
Purpose. Alteration of macular pigment optical density (MPOD) is a potential therapeutic approach to preventing retinal degenerative diseases. This study demonstrates that MPOD can be altered by adding carotenoid-rich foods to the diet. Methods. MPOD was measured psychophysically with a 1-deg stimulus. Plasma concentrations of lutein (L), zeaxanthin (Z), and beta-carotene (BC) were obtained by HPLC with a C30 column. Measurements of MPOD and plasma carotenoids were obtained for the following time periods: two baseline measurements; 4-wks; 8-wks; and 12-wks. At the time of the 2nd baseline measurement, 10 subjects added to their regular diets daily supplements of 60 g of spinach (11 mg L, 0.3 mg Z, 5 mg BC) and 150 g of corn (0.4 mg L, 0.3 mg Z); 1 subject was given only spinach and 2 subjects only corn; 3 subjects had missing data. Results. At 4-wks both MPOD (0.51 +/- 0.21) and plasma concentrations of L (35.0 +/- 14.7 μg/dL) increased significantly from baseline (MPOD = 0.43 +/- 0.17 and L = 20.5 +/- 8.4) (p<.02 and p<.001, respectively; matched pairs t test). At eight weeks, MPOD was not significantly different from baseline, but at 12 wks, MPOD was again elevated. Examination of individual records suggests three types of responses to dietary supplementation. 1) Nonresponders in both blood and retina. 2) Responders in blood but not retina. and 3) Responders in both blood and retina. Conclusions. The rapidity with which the retina responded to dietary modification was unexpected. Further, the magnitude of the response for some individuals was considerable (∼ 50%). Alteration of MPOD for both experimental study and therapeutic intervention may represent an important tool for future work.