Lutein, zeaxanthin, macular pigment, and visual function in adult cystic fibrosis patients

Abstract

The macular pigment, thought to be a postmortem artifact less than 100 years ago by Gullstrand, has been the subject of intense research in recent years. The macular pigment is derived from dietary carotinoids, lutein, and zeaxanthin, which endow it with a yellow-orange color that absorbs short-wavelength light en route to the photoreceptors. This filtering of high-energy photons, together with scavenging of free radicals, is thought to be a mechanism of major health significance for the human retina. Decreased plasma concentrations of the pigments from which macular pigment has been derived have been associated with an increased incidence of macular degeneration, although it is unclear that levels of these carotinoids in the eye directly relate to the risk of retinal disease. More subtle than frank macular degeneration are the losses in sensitivity of cone photoreceptors associated with normal aging. A high amount of macular pigment might protect the retina from age-related loss in cone sensitivity, but other interpretations are plausible. If macular pigment does forestall the effects of normal aging, one might expect that patients with cystic fibrosis (CF) may display accelerated retinal aging. This hypothesis is based on the pancreatic insufficiency in CF, even with replacement pancreatic enzyme therapy, that results in decreased carotenoid uptake. While a few reports indicate some compromised visual function in CF patients (that may be because of nutritional deficiencies other than carotinoids), the hypothesis that CF patients may display accelerated retinal aging due to reduced macular pigment levels has not been tested. This study investigated CF patients and age-matched controls for: (1) plasma carotenoid levels; (2) optical density and distribution of macular pigment in the retina; and (3) visual performance including photopic contrast sensitivity, color discrimination and multifocal electroretinograms. Compared to age-matched controls, both serum levels of lutein and zeaxanthin and macular pigment in the retina were significantly reduced in CF patients. Despite dramatic low levels in serum and macular carotinoids (lutein and zeaxanthin) that are likely to have affected the study group for decades, CF patients did not have deficits of vision as might be expected from the hypothesis that macular pigment protects the retina against factors contributing to normal aging.—John L. Keltner The macular pigment, thought to be a postmortem artifact less than 100 years ago by Gullstrand, has been the subject of intense research in recent years. The macular pigment is derived from dietary carotinoids, lutein, and zeaxanthin, which endow it with a yellow-orange color that absorbs short-wavelength light en route to the photoreceptors. This filtering of high-energy photons, together with scavenging of free radicals, is thought to be a mechanism of major health significance for the human retina. Decreased plasma concentrations of the pigments from which macular pigment has been derived have been associated with an increased incidence of macular degeneration, although it is unclear that levels of these carotinoids in the eye directly relate to the risk of retinal disease. More subtle than frank macular degeneration are the losses in sensitivity of cone photoreceptors associated with normal aging. A high amount of macular pigment might protect the retina from age-related loss in cone sensitivity, but other interpretations are plausible. If macular pigment does forestall the effects of normal aging, one might expect that patients with cystic fibrosis (CF) may display accelerated retinal aging. This hypothesis is based on the pancreatic insufficiency in CF, even with replacement pancreatic enzyme therapy, that results in decreased carotenoid uptake. While a few reports indicate some compromised visual function in CF patients (that may be because of nutritional deficiencies other than carotinoids), the hypothesis that CF patients may display accelerated retinal aging due to reduced macular pigment levels has not been tested. This study investigated CF patients and age-matched controls for: (1) plasma carotenoid levels; (2) optical density and distribution of macular pigment in the retina; and (3) visual performance including photopic contrast sensitivity, color discrimination and multifocal electroretinograms. Compared to age-matched controls, both serum levels of lutein and zeaxanthin and macular pigment in the retina were significantly reduced in CF patients. Despite dramatic low levels in serum and macular carotinoids (lutein and zeaxanthin) that are likely to have affected the study group for decades, CF patients did not have deficits of vision as might be expected from the hypothesis that macular pigment protects the retina against factors contributing to normal aging.—John L. Keltner