Introduction. Night blindness is one of the early warning signs of a deficiency in Vitamin A. Each year, between 250,000 and 500,000 children lose their sight because they do not consume enough Vitamin A, and half of those will die within twelve months of losing their sight. Also, many pregnant women in developing countries suffer from night blindness as a symptom of Vitamin A deficiency, a problem compounded by mortality during pregnancy and childbirth, as well as difficulties in birth and in performing lactation (Rahi, et al., 1995, p. 332). In addition to night blindness, Vitamin A deficiency can impair one’s ability to fight off infections. This means that in parts of the world in which children do not receive immunizations, diseases such as measles still have comparatively high fatality rates. Vitamin A deficiency can become a significant problem even when the level is somewhat mild, as the problems that can ensue early on for children include a decreased growth rate, retarded blone development, and infections of a diarrheal or respiratory nature (WHO, 2005). Overall, this deficiency affects one of every three children in the world under the age of five, with the highest concentrations in Africa and Southeast Asia.
Night blindness refers to an inability in the eyes to adjust to changes in light levels. When illumination levels are low, people who suffer from night blindness cannot differentiate between images easily. When there is enough light to see, these people do not have any difficulties, but when the area dims, quality of vision plummets. The specific reason for this is an inhibited production of a particular eye pigment that works best in situations with low light called rhodopsin. It occurs in the retina and combines retinal, which is a form of Vitamin A) and a protein called opsin. The body does not generate enough retinal on its own to maintain vision, and so it is necessary to consume enough Vitamin A to maintain rhodopsin levels (Rahi et al., 1995, p. 333).
Structure, Specific Sources, and Properties of Vitamin A. The retina requires Vitamin A in the form of retinal, which is a metabolite that absorbs sunlight. People receive Vitamin A from several sources. One is food that comes from animals, in which case the substance retinyl palmitate, an ester, is converted into retinol inside the small intestine. The retinol will store the vitamin until it converts into retinal, the aldehyde form that is visually active. At that point it can aid the eye. When it comes from vegetable foods containing beta-carotene, such as carrots, the pigment turns into a pair of retinyl groups, which can also enhance levels of vitamin A in the body (Bjelakovic G., 2008).
As far as structure goes, all of the various forms of Vitamin A feature an isoprenoid chain, which is known as a retinyl group, connected to a beta-ionone ring. Both the ring and the chain are required for optimal vitamin absorption (Berdanier, 1997, p. 25).
The vegetable sources of Vitamin A are all referred to as carotenoids, while the animal sources of Vitamin A are referred to as retinoids, as referenced in the above introduction. Some significant research has gone into ways to determine how much of each different type of source is necessary for optimal health. Before 2001, a microgram of retinol was considered to be equivalent to 2 micrograms of beta-carotene when dissolved within oil, or 6 micrograms of beta-carotene when found in vegetable sources of food, because of problems that accompany absorption from food. Alpha- and gamma-carotene and cryptoxanthin also have the ability to convert into retinal, but only at an efficiency of 12 micrograms to 1 microgram of retinol. However, since that time, further research has indicated that the absorption of carotene from vegetable sources and subsequent conversion into retinal is only half as efficient as had been thought, so 12 micrograms of beta-carotene are now considered equivalent to 1 microgram of retinol, as are 24 micrograms of alpha- or gamma-carotene or cryptoxanthin (USDA, 2008). In developed countries, this is particularly important for vegetarians, because while night blindness generally strikes people who live in countries where there is not much meat or other foods that have been fortified with Vitamin A available for consumption. For general consumption, the recommended consumption for adult males is 900 micrograms or 3000 IU of retinol; for adult females, it is 700 micrograms or 2800 IU (USDA, 2008).
Meat and dairy sources include various types of liver, milk, egg, butter and cheddar cheese. Fruit and vegetable sources include carrots, sweet potatoes, apricots, cantaloupe and pumpkin (not the orange pigment), as well as spinach, collard greens, broccoli leaves (not florets), peas, mangos, papayas, and kale (USDA, 2008).
It is possible to encounter significant health issues with the overconsumption of Vitamin A. Toxicity requires fairly high level of consumption, with liver issues beginning for some people at 15,000 IU per day, although the mean value is 120,000 IU per day. If you already have renal failure, though, even consuming as much as 4,000 IU per day can cause problems. Vitamin A is fat-soluble, which means that it is much more difficult to get rid of excesses than it is for water-soluble vitamins such as B and C. Symptoms of Vitamin A toxicity include reduced appetite, irritability, nausea, muscle weakness and pain, hair loss, headaches, and vomiting. Chronic cases can also include fatigue, dried mucus membranes and skin, insomnia, anemia, diarrhea and bone fractures. In extreme cases, pseudotumor cerebri can manifest, which brings confusion, blurred vision, headaches, and a sense of increased pressure inside the skull. All that has to happen for the symptoms to abate, though, is for the patient to stop taking in Vitamin A (Penniston and Tanumihardjo, 2006, p. 193-194). With regard to the bone fractures, it is not clear how the toxicity affects bone structure, but current research has hypothesized that taking in too much Vitamin A can keep proteins also rely on Vitamin K from appearing, which makes Vitamin D less effective in the body (Masterjohn, 2006, p. 1028). Tests on animals have indicated that spontaneous bone fracture can coincide with high intake of Vitamin A, and studies on cell cultures have also found higher levels of bone resorption and diminished formation of bone with high levels of intake. Another theory for this correlation is that Vitamins A and D may fight over the same receptor, affecting the parathyroid hormone, which controls distribution of calcium (Penniston and Tanumihardjo, 2006, p. 195). This has all been confirmed by a study showing that an excessively high intake of Vitamin A can lead to low density of bone minerals (Forsmo, et al., 2008, p. 409). People who smoke or drink chronically can develop a higher risk of liver injury when they take Vitamin A or beta-carotene supplements in high dosages (Crabb, 2001, p. 209S).
Vitamin A and Vision. Vitamin A is crucial in helping the eye retain its retinal form. 11-cis-reitinal joins to the eye’s rods and cones (rhodopsin and iodopsin, respectively) at specific lysine residues. When light comes into the eye, the retinal changes to the all-“trans” variety. This form of retinal disconnects from the rods and cones in a process known as “photo-bleaching.” As this occurs, the optic nerve sends a message to the brain’s visual center. Once the newly all-“trans” retinal separates from the rods and cones, it undergoes enzymatic reactions that convert it back to its original 11-cis-retinal state. However, not all of the all-“trans” retinal returns to its original state, as some switches to all-“trans” retinol (not available for use in the eye), which means that the body also needs to be able to generate new sources, and this is where Vitamin A deficiency can cause blindness. A drop in rhodopsin levels will reduce the eye’s ability to see in low levels of light, which is one of the early warning signs of night blindness (McGuire and Beerman, 2007, p. 208).
Risk Factors for Vitamin A Deficiency and Night Blindness. As has been mentioned earlier, this is particularly a problem in developing countries, where people may not have access to the sorts of foods and supplements necessary to maintain healthy levels of Vitamin A. Researchers have identified several groups within the population that are particularly at risk; the first of these is young children and women who are pregnant (West and Mehra, 2010). Another group is all women who are of the age when they can reproduce, particularly during lactation. For all of the people at risk for this deficiency, though, a common denominator (besides those who choose a vegan diet for health reasons) is socioeconomic status. One of these metrics, maternal education, is particularly revealing; in Bangladesh and Indonesia, for example, mothers are much more likely to consume eggs in a manner to ingest enough Vitamin A, the more maternal training they have had (de Pee, et al., 1998, p. 392). Government and agency based programs of nutritional education have abated the problem, though, as mothers have adjusted their consumption appropriately after taking classes designed to help them escape the deficiency. Another metric is household income; the higher the income, the more likely that children, mothers and whole households are to consume foods that are rich in Vitamin A at a rate that will keep them from contracting the deficiency (Guo et al., 1999, p. 999). The implication is that those people who live in households with sufficient access either to Vitamin A-fortified foods or to resources that can be exchanged for those foods are much more likely to avoid night blindness and other problems associated with this vitamin deficiency.
Of course, food prices are one major component of a family’s access to foods that have any important nutrients. When prices go up, the poor try to save as much money as possible, buying less food that is dense in nutrients, such as produce, nuts, meat, fish and dairy, focusing instead on maintaining adequate consumption of the staple grains – even though it is the grains that tend to fluctuate the most in price (West and Mehra, 2010). This can have a significant effect on individual susceptibility to Vitamin A deficiency, depending on the amount of time the family’s shopping priorities are adjusted. The more that liver, eggs, dairy foods and other items that are fortified with Vitamin A are omitted from the diets, the more the risk for deficiency will increase. The speed with which a family will return to its traditional shopping habits will vary depending on the length of time that the economy is in recession, as well as such cultural factors as the fears of continued recession and typical response to those fears. Cultures that have regular issues when it comes to economic stability will generally have families that are more cautious about returning to more liberal spending habits, and so the likelihood of Vitamin A deficiency and night blindness occurring are higher in those cultures. A study conducted in Bangladesh from 1992 to 2000 found that, even though the price of rice would fluctuate by as much as 50 percent, the consumption of rice remained at a constant rate. Because the purchase of rice had such a dramatic effect on the rest of the family’s budget, though, when prices were higher, less money was spent on foods that would provide higher levels of Vitamin A, and even when prices receded, families were more likely to save money than to go back to prior shopping trends, which meant that the danger of Vitamin A deficiency had not passed (Torlesse, et al., 2003, p. 1323).
There are several steps that governments and agencies can undertake in order to help alleviate the effects of Vitamin A deficiency, including night blindness, on people in impoverished or developing countries. Breast feeding is something that mothers can do in just about any socioeconomic setting, and in developing countries, it is just about the only source of Vitamin A that infants can rely on through the first six months of life. By providing mothers with sufficient nutrition, it is possible to protect children from night blindness for the first three years of life, even if breast feeding ends well within the first year (West and Mehra, 2010). Also, providing Vitamin A supplements that are extremely high in potency can help reverse the problem. Taking oral supplements of 200,000 IU twice a year can not only help cut down on night blindness, but also childhood mortality (West and Mehra, 2010). By including these supplements with immunizations and other interventions for family health, governments and agencies can ensure that their most vulnerable citizens receive adequate levels of Vitamin A.
Summary. Night blindness is an early warning sign of later, more significant, health effects that coincide with a Vitamin A deficiency. These effects can lead to mortality in infants and young children, and can lead to liver and renal ailments in adults, which can have major detrimental effects on individual health. This is a problem that can have implications for major sections of the population in the developing world, but it will require a commitment from developed nations and charitable organizations within those countries to take the lead in providing assistance to people on the other side of the globe.
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