**6. Macular pigment**

362 Lipoproteins – Role in Health and Diseases

**Figure 6.** Neovascular AMD, showing sub-retinal haemorrhage in a left eye.

AMD has a multi-factorial pathogenesis.[30;31] Therefore, the development of AMD is dependent on a complex interaction between an individual's genetic composition (genotype) and lifestyle (or environmental) factors. This interaction is complex and incompletely understood; however, certain factors have been well established as representing risk for this condition, whereas others are known as putative risk factors, according to our current understanding of this disease. The well-established risk factors for the development of AMD are: increasing age, a positive family history of AMD (including specific genotypes), and tobacco smoking.[30;32;33] Therefore, tobacco smoking is the only proven environmental/lifestyle risk factor for this disease.[34;35] Putative risk factors include: obesity,[36;37] hypertension,[38] light iris colour,[39] cumulative sunlight exposure,[40] and a diet low in anti-oxidant fruits and vegetables,[41] particularly those

**5. Pathogenesis of AMD** 

Macular pigment (MP) is composed of the hydroxy-carotenoids lutein (L), zeaxanthin (Z), and *meso*-zeaxanthin (*meso*-Z). L and Z are of dietary origin and are not synthesized *de novo* in humans, whereas *meso*-Z is not found in a conventional western diet, but is understood to be primarily formed in the retina following conversion from L.[43;44] Interestingly, it has been shown that L is the dominant carotenoid in the diet,[45] whereas Z/*meso*-Z have been shown to be the dominant carotenoids at the central macula.[46;47] MP is found in highest concentration at the central macula, where it functions as a powerful antioxidant and acts as a filter of actinic short wavelength blue light, thus limiting (photo-)oxidative damage to retinal cells.[48] These properties of MP are believed to be the mechanism whereby it may protect against the development, and/or progression, of AMD.

Although MP is entirely of dietary origin, it is also subject to heritability, as reported in 2005 by Liew *et al.* in a classic twin study.[49] In that study of 76 monozygotic and 74 dizygotic female twin pairs, they estimated that heritability accounted for between 67% and 85% of an individual's MP level. However, to date a direct significant association between MP levels and the major risk genes for AMD has not been shown.[50]

MP can be measured *in vivo* by non-invasive psychophysical means, resulting in an MP optical density measurement.[51;52]
