Age-Related Macular Degeneration (AMD)

Introduction Age-related Macular Degeneration (AMD) is the leading cause of blindness among the elderly population in North America. In 2004, 1.75 million United States citizens were afflicted with age-related macular degeneration – a debilitating disease of the eye. This number is projected to reach 3 million in the United States alone by the year 2020. Age-related macular degeneration presents itself in two major clinical manifestations, dry (non-exudative) and wet (exudative) age-related macular degeneration. Each type of AMD is defined by its own set of clinical diagnostic tools. Dry AMD is indicated by the development of drusen – extracellular debris present as yellow lesions on the surface of the macula – on the exterior surface of the

With over 600 carotenoids known to humankind, only 60 carotenoids are known to demonstrate vitamin A activity. When discussing AMD, the carotenoids of particular interest are known as xanthophylls – specifically lutein and zeaxanthin. Carotenoids are lipophilic and as a result they are absorbed via a similar mechanism to fat absorption. Similarly, carotenoids are integrated into chylomicrons and are transported throughout the body via the lipoprotein cycle. High-density lipoprotein is the primary transporter for xanthophylls, accounting for 53 percent of their transport to the retina.2, 6 Additionally, low-density lipoprotein and very-low-density lipoprotein account for 31 and 16 percent of xanthophyll transport respectively.2Lutein and zeaxanthin function as antioxidants; thus, they are capable of providing the Bruch’s membrane with a coping mechanism preventing ROS from damaging the RPE. Additionally, lutein and zeaxanthin are capable of filtering blue light and preventing excessive oxidative

Therefore, low intakes of lutein may promote the progression of AMD. To determine the effect of lutein on the progression of AMD, Richer et al.4 conducted a 12-month prospective, randomized, double-blind, placebo-controlled study that consisted of 90 subjects who expressed symptoms of AMD in one or both eyes. The participants were randomly assigned to one of three experimental groups: 29 participants were assigned to Group 1(10 mg non-esterified lutein), 30 participants were assigned to Group 2(10 mg non-esterified lutein plus additional antioxidants and nutrients in the form of a multivitamin), and 31 participants were assigned to Group 3 and received the placebo. Ophthalmic testing measured MPOD, BCVA, and CS at baseline, 4 months, 8 months, and 12 months. The three groups were controlled for age, years diagnosed with AMD, smoking, caffeine/alcohol use, iris color, multivitamin use, as well as dietary intake of lutein and iron. The results indicated that between the time baseline measurements were conducted and the final study visit: MPOD increased approximately 36 percent (0.09 log units) in Group 1, 43 percent (0.08 log units) in Group 2, and decreased 0.03 log units in Group 3. BCVA increased 5.4 and 3.5 Snellen letters for Group 1 and 2 respectively as well a decrease of 0.2 Snellen letters for Group 3. The results indicated that over the course of the study CS increased