This study was conducted to investigate whether augmentation of macular pigment (MP) enhances visual performance (VP). 121 normal subjects were recruited. The active (A) group consumed 12 mg of lutein (L) and 1mg of zeaxanthin (Z) daily. MP optical density (MPOD) was assessed by customized heterochromatic flicker photometry. VP was assessed as best corrected visual acuity (BCVA), mesopic and photopic contrast sensitivity (CS), glare disability, photostress, and subjective visual function. Subjects were assessed at baseline; 3; 6; 12 months (V1, V2, V3 and V4, respectively). Central MPOD increased significantly in the A group (p < 0.05) but not in the placebo group (p > 0.05). This statistically significant increase in MPOD in the A group was not, in general, associated with a corresponding improvement in VP (p>0.05, for all variables), with the exception of a statistically significant time/treatment effect in "daily tasks comparative analysis" (p = 0.03). At V4, we report statistically significant differences in mesopic CS at 20.7 cpd, mesopic CS at 1.5 cpd under high glare conditions, and light/dark adaptation comparative analysis between the lower and the upper MP tertile groups (p < 0.05) Further study into the relationship between MP and VP is warranted, with particular attention directed towards individuals with low MP and suboptimal VP.

This study was designed to assess whether macular pigment optical density (MPOD) is associated with visual performance. One hundred and forty-two young healthy subjects were recruited. Macular pigment optical density and visual performance were assessed by psychophysical tests including best corrected visual acuity (BCVA), mesopic and photopic contrast sensitivity, glare sensitivity, photostress recovery time (PRT). Measures of central visual function, including BCVA and contrast sensitivity, were positively associated with MPOD (p<0.05, for all). Photostress recovery and glare sensitivity were unrelated to MPOD (p>0.05). A longitudinal, placebo-controlled and randomized supplementation trial will be required to ascertain whether augmentation of MPOD can influence visual performance.

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. Purpose:  Of the antioxidants found in the human retina, only the macular carotenoid quantities can be estimated noninvasively (albeit in a collective fashion), thus facilitating study of their role in that tissue. The aim of this study was to evaluate concordance between macular pigment optical density (MPOD) values recorded on a commercially available instrument, the MPS 9000, with those of an already validated heterochromatic flicker photometry instrument. Also, we assessed and compared test–retest variability for each instrument. Methods:  Macular pigment optical density at 0.5 retinal eccentricity was measured using two different heterochromatic flicker photometers, the MPS 9000 and the Macular DensitometerTM, in 39 healthy subjects. Test–retest variability was evaluated separately for each instrument by taking three readings over a 1‐week period in 25 subjects. Results:  There was a moderate positive correlation for MPOD at 0.5° of retinal eccentricity between the MPS 9000 and the Macular Densitometer described by the linear equation y = 0.763x + 0.172 (r = 0.68, p < 0.001, r2 = 0.46); however, a paired‐samples t‐test showed a significant difference in terms of mean values, with a bias of lower MPOD values being yielded by the MPS 9000 (t = −4.103, p < 0.001). Bland–Altman analysis indicated only moderate agreement between the two instruments, reflected in 95% limits of agreement of 0.1 ± 0.27. Inter‐sessional repeatability, expressed as a coefficient of repeatability, ranged from 0.18 to 0.21 [mean (±SD): 0.19 (0.02)] for the MPS 9000 and from 0.11 to 0.12 [mean (±SD): 0.12 (0.01)] for the Macular Densitometer. Conclusion:  The results demonstrate that the MPS 9000 consistently yields MPOD readings, which are lower than that found with the Macular Densitometer, and exhibits substantial test–retest variability.

Macular pigment (MP) confers potent antioxidant and anti-inflammatory effects at the macula, and may therefore protect retinal tissue from the oxidative stress and inflammation associated with ocular disease and ageing. There is a body of evidence implicating oxidative damage and inflammation as underlying pathological processes in diabetic retinopathy. MP has therefore become a focus of research in diabetes, with recent evidence suggesting that individuals with diabetes, particularly type 2 diabetes, have lower MP relative to healthy controls. The present review explores the currently available evidence to illuminate the metabolic perturbations that may possibly be involved in MP's depletion. Metabolic co-morbidities commonly associated with type 2 diabetes, such as overweight/obesity, dyslipidaemia, hyperglycaemia and insulin resistance, may have related and independent relationships with MP. Increased adiposity and dyslipidaemia may adversely affect MP by compromising the availability, transport and assimilation of these dietary carotenoids in the retina. Furthermore, carotenoid intake may be compromised by the dietary deficiencies characteristic of type 2 diabetes, thereby further compromising redox homeostasis. Candidate causal mechanisms to explain the lower MP levels reported in diabetes include increased oxidative stress, inflammation, hyperglycaemia, insulin resistance, overweight/ obesity and dyslipidaemia; factors that may negatively affect redox status, and the availability, transport and stabilisation of carotenoids in the retina. Further study in diabetic populations is warranted to fully elucidate these relationships.