Lutein supplementation benefits AMD patients with low macular pigment A new study finds that lutein supplementation increases MPOD, and a correlation was found between the change in MPOD and the change in VA and MDLT such that patients who show a pronounced increase in MPOD also benefit in terms of visual function.

Genetic and environmental risk factors for age-related macular degeneration (AMD) have been identified. On the basis of the risk factor profile, oxidative stress has been implicated in the pathogenesis of the disease related to low-grade inflammation and hypoxia in the outer retina. This notion is compatible with the idea that low macular pigment optical density (MPOD) is a risk factor for the disease, because the natural components of the macular pigment, lutein and zeaxanthin, show potent antioxidative properties.

Indeed, data from several large-scale studies indicate that low dietary intake of the carotenoids lutein and zeaxanthin is related to the risk of AMD.

Measurement of MPOD is difficult, and up to now, no gold standard method for the objective measurement of MPOD has been developed. Most of the studies that investigated whether the intake of lutein and/or zeaxanthin increases MPOD were based on measurements using flicker photometry. Flicker photometry, however, is a subjective method and several limitations of this technique have been identified.

In the present study, an objective spectroscopic technique is used to assess the effects of a 6-month lutein supplementation on MPOD in patients with AMD. In addition, an investigation was conducted into whether lutein supplementation improves visual acuity (VA) and macular function (mean differential light threshold; MDLT), as assessed with microperimetry.

Methods & Results

One hundred twenty-six patients with AMD (AREDS [Age-related Eye Disease Study] stages 2, 3, and 4) were included in this randomized (2:1), placebo-controlled, double-masked parallel group study. Lutein or placebo was administered for 6 months. MPOD was measured with a custom-built reflectometer. VA was assessed with ETDRS (Early Treatment Diabetic Retinopathy Study) charts, and MDLT was assessed with a microperimeter.

Lutein significantly increased MPOD by 27.9%. No significant effect of lutein supplementation on MDLT or VA was seen, although a tendency toward an increase was seen for both parameters. A significant correlation was found, however, between the increase in MPOD after 6 months and the increase in MDLT after 6 months, as well as between the increase in MPOD after 6 months and the increase in VA after 6 months.

Discussion & Conclusions

The present study confirms previous reports that supplementation with lutein increases MPOD in patients with AMD (FIGURE). In the present study, however, no significant improvement in VA was seen after lutein intake for 6 months, which is in keeping with some but not all previous studies. The present study was the first in which macular visual function was examined with a microperimeter, and a tendency toward improvement was seen, although the effect did not reach the level of significance. Nevertheless, a significant association between the change in MPOD and the change in both VA and MDLT was found (FIGURE). This result indicates that patients with a pronounced increase in MPOD also improved in their visual function.

In recent years, evidence has accumulated that AMD patients have reduced MPOD, although not all studies have found a significant difference between patients and healthy controls.

• In the AREDS it was shown that low dietary intake of lutein and zeaxanthin is associated with an increased likelihood of having large or extensive intermediate drusen, neovascular AMD, and geographic atrophy.
  
• In addition, reduced MPOD has been linked to several risk factors for AMD, including increased age, smoking, family history of AMD, light iris color, and obesity.
  
• No study so far, however, has proven that supplementation with lutein and/or zeaxanthin is capable of reducing the incidence or progression of AMD.

The current study cannot elucidate this question, because neither the sample size nor the observation period was sufficient to obtain such data. The effects of lutein on visual performance have been attributed to a reduction of chromatic aberration as well as to a preferential absorption of blue haze through the atmosphere.

In the present study, subjects who had lower MPODs at baseline showed a more pronounced increase in MPOD. This result is in keeping with data from the LUNA study, where MPOD was measured using autofluorescence. The reason for this remains unclear, but may simply be related to the usual dietary intake of these subjects. Since in the present study no food intake questionnaire was used, we cannot answer this question conclusively. In fact the data indicate that patients who had baseline MPODs of 0.5 or higher showed almost no increase in MPOD during lutein supplementation, although the scattering of data was high. The data do indicate that lutein incorporation in the retina is saturable. This finding is in good agreement with the recent discovery of a member of the steroidogenic acute regulatory domain (StARD) family as a lutein-binding protein, which is saturable.

In conclusion, the present study demonstrates that lutein supplementation increases MPOD, as assessed with an objective method in patients with nonexudative AMD. Compared with placebo, no effect was seen on VA or visual function. Nevertheless, there was a significant correlation between the lutein-induced increase in MPOD and the change in VA and MDLT, indicating that patients who have pronounced increase in MPOD during lutein administration also benefit in terms of visual function.


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Invest Ophthalmol Vis Sci. 2011 Oct 17;52(11):8174-8