Lutein supplementation benefits AMD patients with low macular pigment
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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.
Invest Ophthalmol Vis Sci. 2011 Oct 17;52(11):8174-8
http://www.ncbi.nlm.nih.gov/pubmed/21873668
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