Abstract |
The Macular Pigment, MP, is a yellow oily substance that consists of the hydroxycarotenoids
Lutein and Zeaxanthin. It is located at the posterior pole of the fundus of the eye showing
maximum concentration at the 1st central deg of the macula, that is the foveola, with
decreasing concentration as we go away from it so that after the 5‐6 deg it is undetectable. It is
exclusively of dietary derivation, with main sources the green leafy and yellow vegetables and
fruits (spinach, corn etc). The retinal levels of these carotenoids are affected by many factors
apart from diet, such as smoking, iris colour, body fat, sunlight exposure, gender and age. It
presents two major properties: it absorbs the high energy short wavelengths of the visible
spectrum (400‐500 nm, maximum: 465nm) and it scavenges the free radicals thanks to which it
is involved in the research for the pathogenesis of Age‐related Macular Degeneration (AMD).
Age‐related Macular Degeneration (AMD) is a disease of practically unknown etiology. Despite
the fact that it is the leading cause of blindness for people more than 65 years old in USA and
Europe, its pathogenesis is not elucidated yet. It is considered to be an inflammatory process
with genetic predisposition and various environmental factors. Oxidative stress is considered to
have a great contribution at the manifestation of the disease. This compromises the two forms
of the disease, the atrophic (dry) from and the exudative (wet) form of AMD. The occurrence of
wet AMD in one eye signals the advanced form of the disease and these patients have then
their fellow eye in great risk of advancing at the wet form too, something that reduces
eventually their vision dramatically.
Many studies have been made in order to clarify the potential relation between MP and the
appearance and progression of AMD as well as the factors that affect it. However, no clear
answer has been given yet for the relation between MP and the progression of AMD. The
purpose of the present study is to investigate the relation between the quantity of MP and the
advanced disease. In 2001, the first large study about the role of antioxidant supplementation
in AMD, the AREDS I demonstrated that the antioxidants slow the progression of AMD in the
fellow eye (that had the dry form of the disease) of patients with the wet form in one eye,
about 25% in 5 years. The risk of developing the wet form in the fellow eye of these patients is
43 % in 5 years. The MP of the fellow eye with the dry form of the disease of patients with
unilateral wet AMD was measured in this study.
The delay of the progression of AMD that was found in AREDS after supplementation with
antioxidants probably means decreased antioxidant protection of these retinas. Reduced MP
could have similar results. In the present study, the MP of these eyes was intended to be
measured. The MP was quantified as Macular Pigment Optical Density (MPOD) with a novel
technique using Heterochromatic Flicker Photometry (HFP). The device used is QuantifEYE® MPS
9000 (Zeavision). The eye with the dry form of AMD was measured in 34 patients unilateral wet
AMD. It was compared with the MPOD of 33 age‐matched patients with bilateral dry AMD and
the MPOD of 35 age‐ matched healthy retina subjects (control group). The statistical analysis
the factors age and gender entered the model used for regression (Generalized Linear Model,
GLM, SPSS 15.0). At this point, it should be pointed out that none of the study’s subject was
taking any dietary supplementation with the MP’s carotenoids or other antioxidants.
The model showed higher levels of MPOD for patients with wet AMD in one eye and dry AMD
in the other eye compared with patients with bilateral AMD(0,58 vs 0,48, p=0,015). Moreover,
the MPOD of the patients of the study was also higher but not significantly compared with the
control group’s when the effect of age and gender entered the model (0, 58 vs 0, 5, p=0, 08). In
any case nevertheless the MPOD of the patients of the study was not less than the controls’.
Furthermore, no age effect on MPOD was observed in this study (p=0,518), while a small but
significant gender effect was noticed, with women having higher levels of MPOD at this
population around 0, 06 times (p=0,029). Should we mark that the mean MPOD of the total
population was found to be 0, 52 (CI 95% 0, 49‐0, 55).
This is the first time that the levels of MPOD at this high risk group of patients have been
measured. The findings of the current research don’t support the hypothesis that this specific
group of patients has low levels of MPOD. The heterogeneity of lifestyle (diet, smoking) and the
time suffering from the disease could probable justify the findings. The finding of the lack of
effect of age on the MPOD is consistent with many other studies, while the increased MPOD
found in women is also remarkable. Eventually, the total levels of the mean MPOD, including
the healthy and non healthy subjects, were found quite high compared with other studies in
the US and Europe. This could reflect the genetic (dark iris colour) and cultural (Mediterranean
diet) differences of the study population; although the existence of others factors that reduce
the MPOD like sun light exposure and smoking complicate the research for the cause of our
findings.
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