No abstract

Age-related macular degeneration, the leading cause of blindness in the elderly, is a degenerative condition of the macula characterized by death or dysfunction of the photoreceptors. With the aging population growing, the incidence of age-related macular degeneration is expected to increase. This raises concern about the future of visual dysfunction related falls and the resulting injuries in the elderly population. Lutein and zeaxanthin are macular pigments that may play a role in reducing the development and progression of age-related macular degeneration. Evidence is accumulating on the consumption of lutein and zeaxanthin (in whole food or supplemental form), the resulting concentrations in the serum, and tissue distribution throughout the body, particularly in the retina. Lutein and zeaxanthin intake increases serum concentrations which in turn increases macular pigment density. Existing literature focuses on factors affecting macular pigment density, functions of lutein and zeaxanthin as blue-light filters and antioxidants, and risk factors associated with age-related macular degeneration. Few studies have focused on the impact of dietary lutein and zeaxanthin on retinal function and the potential to preserve vision and prevent further degeneration. This presents an opportunity for further research to determine an effective dose that delays the progression of age-related macular degeneration.

: The authors conclude that dietary ganglioside is absorbed in the small intestine and transported to different membrane sites, altering ganglioside levels in the intestinal mucosa, plasma and brain and thus possibly having the potential to change developing enterocyte function (and possibly that of other cell lines).

Prenatal alcohol exposure produces a multitude of detrimental alcohol-induced defects in children collectively known as fetal alcohol spectrum disorder (FASD). Children with FASD often exhibit delayed or abnormal mental, neural, and physical growth. Socioeconomic status, race, genetics, parity, gravidity, age, smoking, and alcohol consumption patterns are all factors that may influence FASD. Optimal maternal nutritional status is of utmost importance for proper fetal development, yet is often altered with alcohol consumption. It is critical to determine a means to resolve and reduce the physical and neurological malformations that develop in the fetus as a result of prenatal alcohol exposure. Because there is a lack of information on the role of nutrients and prenatal nutrition interventions for FASD, the focus of this review is to provide an overview of nutrients (vitamin A, docosahexaenoic acid, folic acid, zinc, choline, vitamin E, and selenium) that may prevent or alleviate the development of FASD. Results from various nutrient supplementation studies in animal models and FASD-related research conducted in humans provide insight into the plausibility of prenatal nutrition interventions for FASD. Further research is necessary to confirm positive results, to determine optimal amounts of nutrients needed in supplementation, and to investigate the collective effects of multiple-nutrient supplementation.

Using streptozotocin-induced diabetic Wistar rats, studies were camed out to examine the metabolic availability of vitamin A in the plasma, liver and the retina of the eye. Control and diabetic rats were fed ad lib. on a semi-puriiied diet either with or without (basal) vitamin A supplementation, or pair-fed on the basal diet for 4 weeks. Despite the fact that diabetic rats consumed 48 YO more feed, they had lower plasma concentrations of retinol (P < 0.003). The decrease in plasma retinol concentration was a response to diabetes (or diabetes-induced trauma), since neither pair-feeding ( P < 0.01) nor vitamin A supplementation altered this effect (P < 0.05). Furthermore, the hepatic concentrations of the vitamin in these animals remained elevated and this increase was greater in the supplemented diabetic group ( P < 0.001). Decreases in 1 1 4 s retinal (a component of rhodopsin) concentrations in the retina were also observed in diabetic animals. The increased hepatic and the decreased plasma and retina vitamin A levels suggest a defect in the transport of the vitamin from the liver. Diabetes: Streptozotocin: Vitamin A