Age-related macular degeneration (AMD) is the leading cause of blindness among the elderly in industrialized countries, and oxidative stress is likely to contribute to its pathogenesis.
1,2 Macular pigment (MP) represents an accumulation in the central retina of three carotenoids, lutein (L), zeaxanthin (Z), and meso-zeaxanthin (m-Z), which give the macula its characteristic yellow color.
3 There is a biologically plausible rationale for the protective role of MP in the retina: it absorbs blue light, thus reducing light-induced oxidative stress, and it has direct antioxidant properties by quenching reactive oxygen species.
1,4,5 Furthermore, there is a growing body of evidence that the blue-light filtering properties of this pigment optimize contrast sensitivity and protect against glare disability because of the impact on chromatic aberration and light scatter,
6,7 although this has been questioned.
8 L and Z cannot be synthesized de novo in mammals, and are entirely of dietary origin, predominantly derived from fruits and vegetables.
9 However, m-Z is not found in a typical diet, and is the result of conversion from retinal L.
10 Given the potentially beneficial impact of appropriate supplementation on AMD prevalence and progression, there is considerable interest among researchers, clinicians, and the general public regarding the role of supplementation with the macular carotenoids.
Several clinical studies have investigated whether MP density can be modified either through dietary modification (for example, consumption of spinach/corn) or supplementation. Supplement studies in healthy subjects and subjects with retinal degeneration generally have been small (
n = 2–108, reviewed by Connolly et al.
11), and many have not been randomized, placebo-controlled in design. Their results suggest that there is considerable variability in the MP response to dietary modification/supplementation, ranging from “non-responders” to reports of increases up to 40%.
12 Given this variation, the purpose of our study was to determine to what extent variation in response is determined by genes or environment, by establishing a classic twin study to estimate the heritability of MP response to supplemental L and Z.