Effect of Lutein and Zeaxanthin on Macular Pigment and Visual Function in Patients with Early Age-Related Macular Degeneration.

Department of Nutrition and Food Hygiene, School of Public Health, Peking University, Beijing, China.
Ophthalmology (Impact Factor: 6.14). 08/2012; 119(11). DOI: 10.1016/j.ophtha.2012.06.014
Source: PubMed


PURPOSE: To determine whether supplementation with lutein and zeaxanthin improves macular pigment and visual function in patients with early age-related macular degeneration (AMD). DESIGN: Randomized, double-masked, placebo-controlled trial. PARTICIPANTS: Participants with probable AMD who were 50 to 79 years of age were screened for study eligibility from the local communities. One hundred eight subjects with early AMD were recruited. INTERVENTION: Early AMD patients were assigned randomly to receive 10 mg/day lutein (n = 27), 20 mg/day lutein (n = 27), 10 mg/day lutein plus 10 mg/day zeaxanthin (n = 27); or placebo (n = 27) for 48 weeks. Macular pigment optical density (MPOD) and visual function variables were assessed at baseline, 24 weeks, and 48 weeks. MAIN OUTCOME MEASURES: The primary outcome was MPOD. Secondary outcomes were visual function variables including best-corrected visual acuity (BCVA), contrast sensitivity (CS), photorecovery time, and Amsler grid testing results. RESULTS: Macular pigment optical density increased significantly by a mean±standard error of 0.076±0.022 density unit in the 20-mg lutein group and 0.058±0.027 density unit in the lutein and zeaxanthin group during 48 weeks. There was a significant dose-response effect for lutein supplementation, and the changes in MPOD from baseline to 48 weeks were correlated negatively with baseline MPOD in all active treatment groups (r = -0.56; P<0.001). At 48 weeks, a trend toward improvement was seen in BCVA, and there was a significant between-group difference in CS at 3 and 6 cycles/degree between the 20-mg lutein group and the placebo group. The increase in MPOD related positively to the reduction in the logarithm of the minimum angle of resolution BCVA (r = -0.31; P<0.01) and the increases in CS at 4 spatial frequencies (r ranging from 0.26 to 0.38; all P<0.05). CONCLUSIONS: Among patients with early AMD, supplementation with lutein and zeaxanthin improved macular pigment, which played a causative role in boosting visual function and might prevent the progression of AMD. Future studies are required to evaluate the effect of these carotenoids on the incidence of late AMD. FINANCIAL DISCLOSURE(S): The author(s) have no proprietary or commercial interest in any materials discussed in this article.

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    • "Research to date has demonstrated the importance of MP for protecting against AMD progression [11] [12] [13] [14], and has also established that MP plays an important role in enhancing visual function in both diseased [15] [16] [17] [18] [19] and non-diseased [20] eyes, via the optical (light-filtering) properties of this pigment [21] [22]. Of note, it has been shown that supplementation [23] [24] [25] [26], and in particular supplementation with all three carotenoids (MZ, L, and Z) in a mg ratio of 10:10:2 may offer the best means of enriching MP across its spatial profile [27–29], and impacts positively on visual function (e.g., contrast sensitivity and glare disability) in human subjects [20]. "
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    ABSTRACT: Background: Macular pigment (MP) levels correlate with brain concentrations of lutein (L) and zeaxanthin (Z), and have also been shown to correlate with cognitive performance in the young and elderly. Objective: To investigate the relationship between MP, serum concentrations of L and Z, and cognitive function in subjects free of retinal disease with low MP (Group 1, n = 105) and in subjects with AMD (Group 2, n = 121). Methods: MP was measured using customized heterochromatic flicker photometry and dual-wavelength autofluorescence; cognitive function was assessed using a battery of validated cognition tests; serum L and Z concentrations were determined by HPLC. Results: Significant correlations were evident between MP and various measures of cognitive function in both groups (r = -0.273 to 0.261, p≤0.05, for all). Both serum L and Z concentrations correlated significantly (r = 0.187, p≤0.05 and r = 0.197, p≤0.05, respectively) with semantic (animal) fluency cognitive scores in Group 2 (the AMD study group), while serum L concentrations also correlated significantly with Verbal Recognition Memory learning slope scores in the AMD study group (r = 0.200, p = 0.031). Most of the correlations with MP, but not serum L or Z, remained significant after controlling for age, gender, diet, and education level. Conclusion: MP offers potential as a non-invasive clinical biomarker of cognitive health, and appears more successful in this role than serum concentrations of L or Z.
    Journal of Alzheimer's disease: JAD 08/2015; 48(1):261-277. DOI:10.3233/JAD-150199 · 4.15 Impact Factor
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    • "However, ageing and oxidative stress seem to be major determinants in pathogenesis. Many epidemiological studies suggest that the higher consumption of lutein and zeaxanthin is associated with lower risk of AMD [13–15]. Such a protective role is attributed to an action of these xanthophylls as antioxidants. "
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    ABSTRACT: Age-related macular degeneration (AMD) is associated with a low level of macular carotenoids in the eye retina. Only two carotenoids, namely lutein and zeaxanthin are selectively accumulated in the human eye retina from blood plasma where more than twenty other carotenoids are available. The third carotenoid which is found in the human retina, meso-zeaxanthin is formed directly in the retina from lutein. All these carotenoids, named also macular xanthophylls, play key roles in eye health and retinal disease. Macular xanthophylls are thought to combat light-induced damage mediated by reactive oxygen species by absorbing the most damaging incoming wavelength of light prior to the formation of reactive oxygen species (a function expected of carotenoids in nerve fibers) and by chemically and physically quenching reactive oxygen species once they are formed (a function expected of carotenoids in photoreceptor outer segments). There are two major hypotheses about the precise location of macular xanthophylls in the nerve fiber layer of photoreceptor axons and in photoreceptor outer segments. According to the first, macular xanthophylls transversely incorporate in the lipid-bilayer portion of membranes of the human retina. According to the second, macular xanthophylls are protein-bound by membrane-associated, xanthophyll-binding proteins. In this review we indicate specific properties of macular xanthophylls that could help explain their selective accumulation in the primate retina with special attention paid to xanthophyll-membrane interactions.
    02/2014; 5(1):326. DOI:10.4172/2155-9570.1000326
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    • "Macular pigment carotenoids lutein (L), zeaxanthin (Z) and meso-zeaxanthin (MZ) have numerous proposed roles within the eye and brain. These include protection from photochemical damage and oxidative stress [1] and improving visual and cognitive function [2], [3], [4], [5], [6], [7], [8], [9]. A standard clinical protocol for measuring macular pigment optical density (MPOD) using heterochromatic flicker photometry (HFP) has been developed [10]. "
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    ABSTRACT: Recent evidence indicates that gene variants related to carotenoid metabolism play a role in the uptake of macular pigments lutein (L) and zeaxanthin (Z). Moreover, these pigments are proposed to reduce the risk for advanced age-related macular degeneration (AMD). This study provides the initial examination of the relationship between the gene variants related to carotenoid metabolism, macular pigment optical density (MPOD) and their combined expression in healthy humans and patients with AMD. Forty-four participants were enrolled from a general population and a private practice including 20 healthy participants and 24 patients with advanced (neovascular) AMD. Participants were genotyped for the three single nucleotide polymorphisms (SNPs) upstream from BCMO1, rs11645428, rs6420424 and rs6564851 that have been shown to either up or down regulate beta-carotene conversion efficiency in the plasma. MPOD was determined by heterochromatic flicker photometry. Healthy participants with the rs11645428 GG genotype, rs6420424 AA genotype and rs6564851 GG genotype all had on average significantly lower MPOD compared to those with the other genotypes (p<0.01 for all three comparisons). When combining BCMO1 genotypes reported to have "high" (rs11645428 AA/rs6420424 GG/rs6564851 TT) and "low" (rs11645428 GG/rs6420424 AA/rs6564851 GG) beta-carotene conversion efficiency, we demonstrate clear differences in MPOD values (p<0.01). In patients with AMD there were no significant differences in MPOD for any of the three BCMO1 gene variants. In healthy participants MPOD levels can be related to high and low beta-carotene conversion BCMO1 genotypes. Such relationships were not found in patients with advanced neovascular AMD, indicative of additional processes influencing carotenoid uptake, possibly related to other AMD susceptibility genes. Our findings indicate that specific BCMO1 SNPs should be determined when assessing the effects of carotenoid supplementation on macular pigment and that their expression may be influenced by retinal disease.
    PLoS ONE 02/2014; 9(2):e89069. DOI:10.1371/journal.pone.0089069 · 3.23 Impact Factor
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