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2 Psychology Department and 3 Animal and Nutritional Sciences, University of New Hampshire, Durham, NH 03824; and 4 Clinical Laboratory and Nutritional Sciences, University of Massachusetts, Lowell, MA 01854
* To whom correspondence should be addressed. E-mail: awenzel{at}unh.edu.
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ABSTRACT |
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Introduction |
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TOPABSTRACTIntroductionSubjects and MethodsResultsDiscussionLITERATURE CITED |
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The macular pigment may protect the central retina from disease by attenuating photostress. Lutein and zeaxanthin are deposited primarily in the anterior layers of the retina (4). Consequently, light incident on the central retina must pass through the macular pigment before reaching the photopigments and posterior tissue. The macular carotenoids absorb wavelengths of visible light below 
520 nm. Ham et al. (5) showed that such wavelengths of light are more potentially harmful than longer wavelengths of light in that 10 times or more energy was needed to induce retinal damage at long wavelengths of visible light compared with shorter ones. The amount of light absorbed by macular pigment, measured as OD, varies among individuals (6). Relative to individuals with high macular pigment OD (MPOD),5 individuals with low MPOD may be at greater risk for retinal disease due to the greater levels of potentially harmful short-wavelength light reaching posterior ocular tissue. Bone et al. (7) found that eyes from individuals with age-related macular degeneration had significantly lower concentrations of macular carotenoids compared with eyes from individuals of similar age but free from disease.
If macular pigment protects the central retina, individuals at risk for retinal disease may benefit from lutein and zeaxanthin supplementation. Intervention studies have found changes in MPOD following lutein supplementation with doses between 2.6 mg/d (8) and 30 mg/d (9). Aleman et al. (10), for example, reported a significant mean increase of 0.08 log units after subjects consumed 20 mg of lutein supplements for 6 mo. Similar increases were observed in 3 mo using 30 mg of lutein supplements (9) or 11.2 mg of lutein and 0.6 mg of zeaxanthin from a combination of spinach and corn (11). Although the retinal loci measured in these studies were slightly different, the similar increases in MPOD with dissimilar doses of lutein suggest that lutein, and perhaps zeaxanthin, may be more bioavailable to the retina from spinach than from supplements. Recently, Chung et al. (12) observed a 33% higher serum lutein response after subjects consumed spinach compared with when they consumed an equal dose of lutein from supplements. The serum response after consuming either spinach or supplements, however, was significantly lower than the response to an equal amount of lutein from lutein-enhanced eggs. These findings suggest that lutein may be more bioavailable from a food matrix than from supplements. Further, increased consumption of eggs may increase not only serum, but macular, carotenoid concentrations. The objective of the current project was to determine whether consuming 6 eggs/wk for 12 wk could increase MPOD.
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Subjects and Methods |
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331 µg of lutein and zeaxanthin/yolk and were purchased from a local supermarket. The treatment eggs for the EGG 2 group contained 964 µg of lutein and zeaxanthin/yolk and were purchased from a local, certified organic farm. Subjects in EGG 1 and EGG 2 received 1 dozen treatment eggs every 2 wk. They were instructed to consume no more than 2 treatment eggs/d and not go >2 d without eating the eggs. Subjects in the PILL group received a 1-mo supply of pills in an unmarked bottle each month. Empty pill bottles and egg cartons were collected at each laboratory visit. All subjects were told to continue their normal diet and use of multivitamins, as no subjects were consuming supplements containing lutein or zeaxanthin. At baseline, height and weight were measured for the calculation of BMI (kg/m2). Serum lipids, serum carotenoids, and MPOD were measured at baseline and after 4, 8, and 12 wk of intervention. The use of human subjects in this study was approved by the University of New Hampshire Institutional Review Board and complied with the Helsinki Declaration.
Measurement of serum cholesterol.
Subjects fasted for 12 h prior to each laboratory visit. A trained phlebotomist collected a blood sample from the subject's antecubital vein into a lithium heparin Vacutainer tube (36–7871; Becton Dickinson). A 60-µL sample was drawn from the tube and injected into the well of a lipid test cassette (10–991) and analyzed by a Cholestech LDX instrument. In short, this system uses reflectance photometry to determine lipoprotein concentrations after 4 reagent pads react with the blood sample. In 9 subjects, 7 in EGG 1 and 2 in PILL, lipoprotein concentrations were measured using a Roche Cobas Mira Plus (Roche Instrument Center) analyzer because the Cholestech LDX was not available. With this instrument, lipoprotein concentrations were measured using selective antibody reagents. Both instruments provided total cholesterol, HDL-C, and triglyceride concentrations. LDL cholesterol (LDL-C) was calculated with the Friedewald formula (total cholesterol – HDL-C – triglyceride/2.2). Total cholesterol was divided by HDL-C to yield a ratio (TC:HDL-C) associated with heart disease risk (13). The variability in measurements obtained with the Cobas Mira Plus is ±2%, whereas the measurement variability of cholesterol for the Cholestech LDX is ±7%.
Measurement of serum carotenoids. A second blood sample was collected at each visit for carotenoid analyses. Blood was collected from the antecubital vein into a Vacutainer SST Gel and Clot Activator tube (36–6511 Becton Dickinson). After clotting for 30 min, blood was centrifuged at 3000 x g at 4°C for 15 min (Beckman Centrifuge TJ-6; Beckman Coulter). Serum was drawn off and stored in aliquots at –80°C until analyzed.
Aliquots were prepared following the technique of Handelman et al. (14). In brief, the serum samples were precipitated with ethanol containing internal standard and extracted into hexane. The extraction procedure was performed twice and the layers from both extractions were combined in amber vials. The sample was completely evaporated under nitrogen, and then resuspended in 200 µL ethanol. An aliquot of 20 µL was removed for analysis with reversed-phase HPLC. Two separate analyses of each sample were performed.
Serum concentrations of lutein, zeaxanthin, and ß-carotene were quantified with a Hewlett-Packard/Agilent Technologies 1100 Series HPLC system (Waldbronn). The photodiode array detector was set at 452 nm and a C18 analytical column (4.6- x 250-mm Bakerbond Mallinckrodt Baker) was used to separate the analytes. The mobile phase had a flow rate of 1.0 mL/min and consisted of 90% acetonitrile and 10% methanol buffered with 0.1% ammonium acetate (Solvent A). From the start of the run to min 18, 100% Solvent A was running. Beginning at min 18, the mobile phase transitioned, for 4 min, to 70% solvent A and 30% Solvent B, 100% isopropanol. This gradient was maintained for 23 min, after which transition to 100% solvent A occurred over 1 min. Quantification was performed with peak area ratios to internal standards and by simultaneously analyzing laboratory standards and external standards. Accuracy of the method to quantify carotenoids was assessed using the National Institute of Standards and Technology (NIST) Standard Reference Material SRM 986. The variability for replicate analyses of carotenoids was <±2%.
Measurement of egg yolk carotenoids. The concentration of lutein and zeaxanthin in randomly selected treatment eggs was analyzed with a technique described by Handelman et al. (15). In short, egg yolks were separated from the albumin and homogenized with 150 mL of 1x PBS. A 1-mL aliquot was collected and placed on a dry bath incubator heat block (11–718–6, Fisher Scientific) at 60°C for 60 min. Samples were then precipitated with ethanol containing internal standard and extracted into a 50:50 mixture of hexane and ethyl ether. The extraction procedure was performed twice, with layers from both extractions combined in amber vials. The sample was completely evaporated under nitrogen and then resuspended in 200 µL ethanol. An aliquot of 20 µL was removed for HPLC analysis. Two separate analyses of each sample were performed. The same reverse-phase gradient HPLC system used for serum carotenoid analyses was used for egg carotenoid analyses.
Measurement of MPOD.
Heterochromatic flicker photometry was used to measure MPOD (16). In this technique, the difference in short-wavelength sensitivity between a foveal locus, where macular pigment is present, and a parafoveal locus, where macular pigment is undetectable or negligible, is used to estimate MPOD. In the fovea, sensitivity to a short-wavelength light was measured with a centrally fixed disc that subtended 1° of visual angle. Sensitivity in the nasal parafovea was measured with a 2° disc centered at 7° eccentricity by the subject's fixation of a small point of light. Both discs were composed of a 460-nm test light that alternated in square-wave with a 540-nm reference light (1.7 log trolands), and superimposed on a 6°, 470-nm background (1.5 log trolands). The radiance of the test light, relative to the reference light, necessary to eliminate a subject's perception of flicker was determined 6 times for both targets. The mean log radiance of these measures was used to calculate MPOD. Specifically, the mean log energy of the 6 measures in the parafovea was subtracted from the mean log energy of the 6 foveal measures to yield MPOD. Two measures of MPOD were obtained for each subject at baseline, 4, 8, and 12 wk. One measure was performed on the day of the blood draw and a second was performed within 3 d. The mean of these 2 measurements was used as a subject's MPOD for the corresponding visit (e.g., baseline). The variability observed between the 2 measurements was ±0.03 log units. An optical system designed by Macular Metrics and described by Wooten et al. (17) was used to conduct the measurements.
Statistical analysis.
Subjects' serum cholesterol, serum carotenoids, and MPOD at baseline were plotted as histograms and fit with a normal curve. All data appeared to be normally distributed based on a visual inspection of the data. Pearson product-moment correlations were performed using baseline subject characteristics (i.e., age and BMI), lipoprotein concentrations, serum carotenoid concentrations, and MPOD. A 1-way ANOVA and Tukey's HSD procedure were used to compare between-group means at baseline. Within-group changes in lipoproteins, serum carotenoids, and MPOD were assessed using one-factor repeated measures ANOVA. For significant tests (P < 0.05), the strength of association was calculated with partial eta squared (
). All analyses were performed with SPSS 13.0 and Origin 7.0. Data are reported as means ± SEM.
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Results |
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TOPABSTRACTIntroductionSubjects and MethodsResultsDiscussionLITERATURE CITED |
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) but not in the EGG 1 (P = 0.83) or EGG 2 (P = 0.47) groups; the changes in the PILL group followed a cubic trend (P = 0.047, 
) (Table 2). HDL-C did not change in any treatment group (EGG 1: P = 0.22; EGG 2: P = 0.35; PILL: P = 0.35). Consequently, the ratio of total cholesterol to HDL-C (TC:HDL-C) did not change in the EGG 1 (P = 0.31) or EGG 2 (P = 0.58) treatment groups. In contrast, the increased total cholesterol in the PILL group resulted in a TC:HDL-C ratio that followed a cubic trend (P = 0.001, 
) and differed from baseline (P < 0.001, 
). Serum LDL-C concentrations did not change from baseline (EGG 1: P = 0.47; EGG 2: P = 0.75; PILL: P = 0.07). Like total cholesterol, triglycerides did not change in the EGG 1 (P = 0.33) or EGG 2 (P = 0.50) groups, but did increase in the PILL group (P = 0.02, 
) and appeared to follow a cubic trend (P = 0.04, ).
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0.83 mmol/L, representing a 17% increase. Their HDL-C concentration, likewise, increased 17%, or 0.28 mmol/L. As a result, their TC:HDL-C ratio did not change from baseline. Their ratio at baseline and after 2 mo of intervention was 3.2. Total cholesterol decreased 1 mo after cessation of treatment in all 3 subjects, and HDL-C decreased in 2 subjects. The decreases in total cholesterol and HDL-C were 0.61 mmol/L and 0.07 mmol/L, respectively.
After 12 wk of intervention, serum lutein concentration was 0.477 ± 0.06 µmol/L in EGG 1 (P = 0.014), 0.540 ± 0.01 µmol/L in EGG 2 (P = 0.52), and 0.457 ± 0.11 µmol/L in the PILL group (P = 0.56). In contrast to serum lutein, serum zeaxanthin significantly increased from baseline in both egg treatment groups (EGG 1: P = 0.04, 
; EGG 2: P = 0.01, 
) (Figure 1). Serum zeaxanthin did not change in the PILL group (P = 0.17). Serum L+Z, like serum lutein (alone), increased in the EGG 1 group (P = 0.07) but did not change in the EGG 2 (P = 0.33) and PILL (P = 0.45) groups. At wk 12, serum ß-carotene concentration was 2.16 ± 0.86 µmol/L in the EGG 1 group (P = 0.56), 0.607 ± 0.13 µmol/L in the EGG2 group (P = 0.26), and 0.859 ± 0.23 µmol/L in the PILL group (P = 0.53).
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) and EGG 2 (P = 0.04, ), MPOD significantly increased from baseline (Figure 2). The increases in MPOD followed a linear trend (EGG 1: P = 0.007, 
; EGG 2: P = 0.042, 
). No change in MPOD was observed in the PILL group (P = 0.51).
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Discussion |
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TOPABSTRACTIntroductionSubjects and MethodsResultsDiscussionLITERATURE CITED |
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In previous egg interventions, subjects were described as either hyporesponders or hyperresponders based on their change in serum cholesterol from baseline (23). Herron et al. (24), for example, defined hyperresponders as individuals whose serum total cholesterol increased >0.06 mmol/L for each additional 100 mg/d of dietary cholesterol. Individuals with an increase <0.06 mmol/L or a decrease in serum cholesterol were considered hyporesponders. Assuming the cholesterol content of the treatment eggs was similar to other eggs, about 200 mg, subjects in EGG 1 and EGG 2 could be described as hyperresponders if their change in serum cholesterol exceeded 0.102 mmol/L ([0.85 eggs/d x 200 mg/egg ÷ 100 mg] x 0.06 mmol/L). Based on this calculation, 7 of the 16 (43%) egg consumers were hyperresponders. A similar percentage of hyperresponders was reported by Herron et al. (24). Three of the 7 hyperresponders in the current project were removed from treatment after 2 mo because their serum total cholesterol exceeded 5.1 mmol/L. The other hyperresponders' total cholesterol changed similarly, increasing about 0.71 mmol/L, but did not exceed the 5.1 mmol/L threshold for discontinuation of treatment. Of note, the change in serum L+Z was 8 times greater in the 7 hyperresponders than in the 9 hyporesponders, an effect recently reported by Clark et al. (25).
Lutein and zeaxanthin are circulated through the bloodstream bound to lipoproteins. Consequently, serum concentrations of lutein and zeaxanthin may be directly related to serum lipoprotein concentrations (26–28). In the current study, serum L+Z was linearly related to both HDL-C and LDL-C at baseline. A direct relation between lipoproteins and serum L+Z suggests that changes in lipoprotein concentrations may affect serum concentrations of L+Z (28). Indeed, there was a linear relation (r = 0.523, n = 16, P = 0.03) between changes in HDL-C from baseline and changes in serum L+Z from baseline in individuals who consumed eggs. No relation was observed between changes in LDL-C and changes in serum L+Z (r = 0.350, n = 16, P = 0.18). These findings are not surprising, because lutein and zeaxanthin may be primarily transported by to HDL-C (29). Egg consumption, then, may increase the carrying capacity of carotenoids in serum by increasing HDL-C concentration. Additionally, egg consumption may increase carotenoid carrying capacity in serum by increasing the number of large HDL-C particles. Recently, Greene et al. (30) found an increase in HDL-C particle size following egg intervention. Moreover, both serum lutein and serum zeaxanthin concentrations during intervention were linearly related to HDL-C particle size.
In addition to serum lipoprotein concentrations, competition for carotenoids among body tissues may affect the amount of carotenoid available to serum and the retina (31). Compared with individuals with low BMI, individuals with high BMI may have a greater number of peripheral binding sites for carotenoids and, consequently, attenuated serum and retinal responses to intervention. In a cross-sectional study, Broekmans et al. (32) reported significant negative correlations between BMI and serum lutein concentration and between BMI and MPOD. In the current study, BMI was not related to baseline carotenoid status or changes in serum and retinal carotenoids. The influence of BMI, however, may only impact individuals with a BMI >27 (33) or 29 (34). Only 1 egg consumer had a BMI >27 and volunteers were excluded from the project if their BMI was >30.
Regardless of BMI, the dose of carotenoid obviously affects the relative amount of carotenoid absorbed and ultimately available to various tissues. In studies that measured both serum and macular carotenoids, significant increases were reported with supplement doses between 2.6 mg/d (8) and 30 mg/d (9) of lutein and in a food intervention with 11.2 mg/d of lutein and 0.6 mg/d of zeaxanthin (11). The approximate daily dose of L+Z in the current study was 283.6 µg/d from the EGG 1 treatment and 826.2 µg/d from the EGG 2 treatment. Despite these relatively small doses of carotenoids, the increases in MPOD were similar to previous carotenoid interventions (8,10,11), which suggests that the lutein and zeaxanthin in egg yolk may be more bioavailable to the macula than from other sources. Unlike vegetables and supplements, carotenoids in egg yolks are packaged in a lipid matrix that may facilitate absorption (15). No previous egg interventions measured changes in MPOD, although studies reported increases in serum lutein and zeaxanthin following interventions with 1.3 yolks/d (15), 3 liquid whole eggs/d (21,24,25,30), and 4 lutein-enhanced eggs/d (12).
As observed in other intervention studies (8,10,11), some subjects did not appear to respond to the increased consumption of carotenoids. Hammond et al. (11), in a carotenoid intervention, identified 3 different response patterns of subjects: 1) individuals who responded with increases in both serum and MPOD (i.e., retinal responders); 2) individuals who responded with an increase in serum but not the retina (i.e., retinal nonresponders); and 3) individuals who did not respond in either serum or MPOD (i.e., serum and retinal nonresponders). In the current study, 8 egg consumers could be described as retinal responders, 4 as retinal nonresponders, and 1 as a serum and retinal nonresponder. Three egg consumers, however, appeared to have a different response pattern and might be described as serum nonresponders. In these subjects, MPOD, but neither serum lutein nor zeaxanthin, increased from baseline. Four of the cholesterol hyperresponders were retinal responders, with the other 3 being retinal nonresponders. The subjects who either did not respond to treatment or showed only a change in the retina were cholesterol hyporesponders.
The mean increase in MPOD was greater in the EGG 1 group than in the EGG 2 group. One possible reason for the difference was the number of retinal responders in each group. Six subjects in the EGG 1 group (5 serum and retinal responders and 1 retina-only responder) showed an increase in MPOD, whereas 5 subjects (3 serum and retinal responders and 2 retina-only responders) showed an increase in the EGG 2 group. Another possible reason for the different retinal responses was MPOD at baseline, which significantly differed between the 2 groups. If the amount of carotenoid in the retina inversely affects the accumulation of additional carotenoids, then changes in the EGG 2 group may have been limited more than changes in the EGG 1 group. In fact, there was an inverse relation between baseline MPOD and change in MPOD among egg consumers (r = –0.590, n = 16, P = 0.016) (Figure 3). Future carotenoid interventions may benefit from pseudo-randomizing subjects to avoid the possible effects of 2 treatment groups with dissimilar MPOD at baseline.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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5 Abbreviations used: CHD, coronary heart disease; EGG 1, treatment of 6 eggs/wk for 12 wk with 331 µg of lutein and zeaxanthin/yolk; EGG 2, treatment of 6 eggs/wk for 12 wk with 964 µg of lutein and zeaxanthin/yolk; HDL-C, HDL cholesterol; L+Z, combined serum lutein and zeaxanthin; LDL-C, LDL cholesterol; MPOD, macular pigment OD; PILL, treatment of 1 sugar-filled capsule/d for 12 wk; TC:HDL-C, ratio of total cholesterol to HDL-C; , partial eta squared.
Manuscript received 1 April 2006. Initial review completed 3 May 2006. Revision accepted 19 July 2006.
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LITERATURE CITED |
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