"reference point for the extent of deficiency (with mortality increasing with severity of the eye disease). In a longitudinal study of preschool Indonesian children, susceptibility to disease increased nine times when severe VAD was present. The reason for the increased infection rate in vitamin A deficient populations is the T-killer cells require retinoids to proliferate correctly. Retinoic acid binds the promoter region of specific genes, so activates the transcription process and cell replication. A vitamin A-deficient diet will have a very limited surplus of retinol, so cell proliferation and replication will be suppressed, contributing to a reduced number of T-cells"
"This protein, found in the retina and the skin, exists in fractional percentages of the normal levels found in homozygous ""Lp/Lp"" horses and so compromises the basic chemical reaction for nerve impulse transmission. Nyctalopia Nyctalopia ( ), also called night-blindness, is a condition making it difficult or impossible to see in relatively low light. It is a symptom of several eye diseases. Night blindness may exist from birth, or be caused by injury or malnutrition (for example, vitamin A deficiency). It can be described as insufficient adaptation to darkness. The most common cause of nyctalopia is retinitis pigmentosa, a disorder"
"postnatal for an extensive period of time. The deficiency can also cause conditions such as blindness or night blindness, also known as nyctalopia. Night blindness is due to the inability to regenerate rhodopsin in the rods which is needed in dim light in order to see properly. A treatment of supplements of retinoic acid which is a part of vitamin A can help replenish levels and help bring learning to normal, but after 39 weeks this is ineffective even if the treatment is daily because it will not bring the retinoid hypo-signalling back to normal. Zinc is needed to maintain"
"Nyctalopia Nyctalopia ( ), also called night-blindness, is a condition making it difficult or impossible to see in relatively low light. It is a symptom of several eye diseases. Night blindness may exist from birth, or be caused by injury or malnutrition (for example, vitamin A deficiency). It can be described as insufficient adaptation to darkness. The most common cause of nyctalopia is retinitis pigmentosa, a disorder in which the rod cells in the retina gradually lose their ability to respond to the light. Patients suffering from this genetic condition have progressive nyctalopia and eventually their daytime vision may also"
"be affected. In X-linked congenital stationary night blindness, from birth the rods either do not work at all, or work very little, but the condition doesn't get worse. Another cause of night blindness is a deficiency of retinol, or vitamin A, found in fish oils, liver and dairy products. The opposite problem, the inability to see in bright light, is known as ""hemeralopia"" and is much rarer. Since the outer area of the retina is made up of more rods than cones, loss of peripheral vision often results in night blindness. Individuals suffering from night blindness not only see poorly"
"also the brain. The cause of this is somewhat unclear but may relate to very low levels of creatine often found in this population. Treatment may include vitamin B6, Lysine or dramatic dietary change to minimise Arginine from patients diet. Research has indicated that these treatments may be somewhat effective in lowering ornithine blood concentration levels in some patients, either in combination or individually. Vitamin B6 has been found to be very effective in a small proportion of patients. Quite often, the presenting symptom of ornithine aminotransferase (OAT) deficiency is myopia which progresses to night blindness. The onset of myopia"
"problem, known as hemeralopia, that is, inability to see clearly in bright light, is much rarer. The fovea is blind to dim light (due to its cone-only array) and the rods are more sensitive, so a dim star on a moonless night must be viewed from the side, so it stimulates the rods. This is not due to pupil width since an artificial fixed-width pupil gives the same results. Night blindness can be caused by a number of factors the most common of which being vitamin A deficiency. If detected early enough nyctalopia can be reversed and visual function can"
"supplied by vitamin A in the diet. Deficiency of all-""trans"" retinal can lead to night blindness. This is part of the bleach and recycle process of retinoids in the photoreceptors and retinal pigment epithelium. Phototransduction process in invertebrates like the fruit fly is different from the vertebrates. PI(4,5)P cycle underlies the phototransduction process. Here, light induces the conformational change into Rhodopsin and converts it into meta-rhodopsin. This helps in dissociation of G -protein complex. Alpha sub-unit of this complex activates the PLC enzyme (PLC-beta) which hydrolyze the PIP2 into DAG. This hydrolysis leads to opening of TRP channels and influx"
"also an option. To reduce the levels of ornithine in the blood, a diet restricted in arginine has been used. Some research has shown that when diet or other treatment is initiated early in life, the outcome can be improved. Ornithine aminotransferase deficiency Ornithine aminotransferase deficiency (also known as gyrate atrophy of the choroid and retina) is an inborn error of ornithine metabolism, caused by decreased activity of the enzyme ornithine aminotransferase. Biochemically, it can be detected by elevated levels of ornithine in the blood. Clinically, it presents initially with poor night vision, which slowly progresses to total blindness. It"
"reduction in best night-time acuity due to the impairment of contrast sensitivity function (CSF) which is induced by intraocular light-scatter resulting from surgical intervention in the natural structural integrity of the cornea. Aulus Cornelius Celsus, writing ca. 30 AD, described night blindness and recommended an effective dietary supplement: ""There is besides a weakness of the eyes, owing to which people see well enough indeed in the daytime but not at all at night; in women whose menstruation is regular this does not happen. But success sufferers should anoint their eyeballs with the stuff dripping from a liver whilst roasting, preferably"
"Vitamin D deficiency Vitamin D deficiency, or hypovitaminosis D, most commonly results from inadequate sunlight exposure (in particular sunlight with adequate ultraviolet B rays). Vitamin D deficiency can also be caused by inadequate nutritional intake of vitamin D, disorders limiting vitamin D absorption, and conditions impairing vitamin D conversion into active metabolites—including certain liver, kidney, and hereditary disorders. Deficiency impairs bone mineralization, leading to bone softening diseases such as rickets in children. It can also worsen osteomalacia and osteoporosis in adults, leading to an increased risk of bone fractures. Muscle weakness is also a common symptom of vitamin D deficiency,"
"becomes totally opaque, which is one of the most common reasons for blindness around the world, particularly in developing countries. Keratomalacia Keratomalacia is an eye disorder that results from vitamin A deficiency. Vitamin A is required to maintain specialized epithelia (such as in the cornea and conjunctiva). The precise mechanism is still not known, but vitamin A is necessary for the maintenance of the specialized epithelial surfaces of the body. A lack of vitamin A leads to atrophic changes in the normal mucosal surface, with loss of goblet cells, and replacement of the normal epithelium by an inappropriate keratinized stratified"
"hydroquinolones (amebicidal medications), ethambutol and isoniazid (tuberculosis treatment), and antibiotics such as linezolid and chloramphenicol. Tobacco is also a major cause of toxic optic neuropathy. The predominant cause of nutritional optic neuropathy is thought to be deficiency of B-complex vitamins, particularly thiamine (vitamin B), cyanocobalamin (vitamin B) and recently copper. Deficiency of pyridoxine (vitamin B), niacin (vitamin B), riboflavin (vitamin B), and/or folic acid also seems to play a role. Those individuals who abuse alcohol and tobacco are at greater risk because they tend to be malnourished. Those with pernicious anemia are also at risk due to an impaired ability"
"at night, but also require extra time for their eyes to adjust from brightly lit areas to dim ones. Contrast vision may also be greatly reduced. Rods contain a receptor-protein called rhodopsin. When light falls on rhodopsin, it undergoes a series of conformational changes ultimately generating electrical signals which are carried to the brain via the optic nerve. In the absence of light, rhodopsin is regenerated. The body synthesizes rhodopsin from vitamin A, which is why a deficiency in vitamin A causes poor night vision. Refractive ""vision correction"" surgery (especially PRK with the complication of ""haze"") may rarely cause a"
"dies before age 5; and 1 in 16 children in Southern Asia. Given that vitamin A is critical for proper functioning of the visual system and for maintaining immune defences, its deficiency remains a public health issue. An estimated 250,000 to 500,000 children deficient in vitamin A become blind every year, half of them dying within 12 months of losing their sight. This deficiency accounts for 350 million cases of blindness and 670,000 deaths globally (WHO, 2001). In Africa alone, it contributes to 23 per cent of child deaths. In 2009, the prevalence of low serum retinol, associated with vitamin"
"integrity due to the enzymatic defect. Lens dislocation in homocystinuria is usually bilateral and in 60% of cases occurs in the inferior or nasal direction. Deficiencies of vitamins B6, B9, and B12 can lead to high homocysteine levels. Vitamin B12, or cobalamin, acts as a cofactor for the enzyme methionine synthase (which forms part of the S-adenosylmethionine (SAM) biosynthesis and regeneration cycle). Vitamin B12 deficiency prevents the 5-methyltetrahydrofolate (5-MTHF) form of folate from being converted into THF due to the ""methyl trap"". This disrupts the folate pathway and leads to an increase in homocysteine which damages cells (for example, damage"
"Ornithine aminotransferase deficiency Ornithine aminotransferase deficiency (also known as gyrate atrophy of the choroid and retina) is an inborn error of ornithine metabolism, caused by decreased activity of the enzyme ornithine aminotransferase. Biochemically, it can be detected by elevated levels of ornithine in the blood. Clinically, it presents initially with poor night vision, which slowly progresses to total blindness. It is believed to be inherited in an autosomal recessive manner. Approximately 200 known cases have been reported in the literature. The incidence is highest in Finland, estimated at 1:50,000. Research suggests there can be some adverse effect on muscles and"
"protein rhodopsin, the visual pigment used in low light levels. This represents the first step of the visual cycle. This is why eating foods rich in vitamin A is often said to allow an individual to see in the dark, although the effect they have on one's vision is negligible. In fact, excess vitamin A intake can cause toxicity to the optic nerve and permanent vision loss. Vitamin A is essential for the correct functioning of epithelial cells. In vitamin A deficiency, mucus-secreting cells are replaced by keratin producing cells, leading to xerosis. Glycoprotein synthesis requires adequate vitamin A status."
"Vitamin B12 deficiency Vitamin B deficiency, also known as cobalamin deficiency, is the medical condition of low blood levels of vitamin B. In mild deficiency a person may feel tired and have a reduced number of red blood cells (anemia). In moderate deficiency there may be inflammation of the tongue and the beginning of neurological problems including abnormal sensations such as ""pins and needles"", while severe deficiency may include reduced heart function and greater neurological problems. Neurological problems may include changes in reflexes, poor muscle function, memory problems, decreased taste, and in extreme cases psychosis. Sometimes temporary infertility may also"
"survey for the South African Department of Health that showed that one out of three children under the age of six have a Vitamin A deficiency. Vitamin A is necessary for good vision, and a shortage of this substance can lead to visual impairments and potentially even blindness. The World Health Organization showed that half of Vitamin A-deficient blind children die within the year, due to the detrimental effects of Vitamin A on the immune system. Vitamin C deficiency also has detrimental effects on the South African population. Scurvy, a disease that develops from an extended shortage of Vitamin C,"
"– night blindness. Persistent deficiency gives rise to a series of changes, the most devastating of which occur in the eyes. Some other ocular changes are referred to as xerophthalmia. First there is dryness of the conjunctiva (xerosis) as the normal lacrimal and mucus-secreting epithelium is replaced by a keratinized epithelium. This is followed by the build-up of keratin debris in small opaque plaques (Bitot's spots) and, eventually, erosion of the roughened corneal surface with softening and destruction of the cornea (keratomalacia) and leading to total blindness. Other changes include impaired immunity (increased risk of ear infections, urinary tract infections,"
"thought to correlated with cardiovascular disease, type 1 diabetes, type 2 diabetes, and some cancers. Review studies have also seen associations between vitamin D deficiency and preeclampsia. Vitamin D deficiency Vitamin D deficiency, or hypovitaminosis D, most commonly results from inadequate sunlight exposure (in particular sunlight with adequate ultraviolet B rays). Vitamin D deficiency can also be caused by inadequate nutritional intake of vitamin D, disorders limiting vitamin D absorption, and conditions impairing vitamin D conversion into active metabolites—including certain liver, kidney, and hereditary disorders. Deficiency impairs bone mineralization, leading to bone softening diseases such as rickets in children. It"
"to truncate the protein. Nyctalopin Nyctalopin is a protein located on the surface of photoreceptor-to-ON bipolar cell synapse in the retina. It is composed of 481 amino acids. and is encoded in human by the ""NYX"" gene. This gene is found on the chromosome X and has two exons. This protein is a leucine-rich proteoglycan which is expressed in the eye, spleen and brain in mice. Mutations in this gene cause congenital stationary night blindness in humans (CSNB). which is a stable retinal disorder. The consequence of this mutation results in an abnormal night vision. Nyctalopin is critical due to"
"results from a deficiency in vitamin B which is an essential coenzyme. The aforementioned changes in mental state occur in approximately 82% of patients' symptoms of which range from confusion, apathy, inability to concentrate, and a decrease in awareness of the immediate situation they are in. If left untreated, WE can lead to coma or death. In about 29% of patients, ocular disturbances consist of nystagmus and paralysis of the lateral rectus muscles or other muscles in the eye. A smaller percentage of patients experience a decrease in reaction time of the pupils to light stimuli and swelling of the"
"located throughout the protein. As the function of the nyctalopin protein is unknown, these mutations have not been further characterized. However, many of them are predicted to lead to truncated proteins that, presumably, are non-functional. The incomplete form of X-linked congenital stationary night blindness (CSNB2) is caused by mutations in the CACNA1F gene, which encodes the voltage-gated calcium channel Ca1.4 expressed heavily in retina. One of the important properties of this channel is that it inactivates at an extremely low rate. This allows it to produce sustained Ca entry upon depolarization. As photoreceptors depolarize in the absence of light, Ca1.4"
"and antioxidants were found to be keep the vitamin A intact during storage in high humidity. Another study found that vitamin A losses would stabilize after six months and that the loss of vitamin A during cooking could be predicted. A lack of vitamin A can cause night blindness; a study in 2005 showed that 348 pregnant Nepali women who ate Ultra Rice had improvement in night vision which did not different significantly from the improvement which could come from vitamin A as liver, carrots, capsule, or green leafy vegetables. A ferric pyrophosphate in Ultra Rice was shown in a"
"is composed of the 11-cis-retinal covalently linked via a Schiff base to the opsin protein (either rod opsin or blue, red or green cone opsins). The process of vision relies on the light-induced isomerisation of the chromophore from 11-""cis"" to all-""trans"" resulting in a change of the conformation and activation of the photoreceptor molecule. One of the earliest signs of vitamin A deficiency is night-blindness followed by decreased visual acuity. George Wald won the 1967 Nobel Prize in Physiology or Medicine for his work with retina pigments (also called visual pigments), which led to the understanding of the role of"
"children who suffer from vitamin A deficiency (VAD). In 2005, 190 million children and 19 million pregnant women, in 122 countries, were estimated to be affected by VAD. VAD is responsible for 1–2 million deaths, 500,000 cases of irreversible blindness and millions of cases of xerophthalmia annually. Children and pregnant women are at highest risk. Vitamin A is supplemented orally and by injection in areas where the diet is deficient in vitamin A. , 43 countries had vitamin A supplementation programs for children under 5; in 10 of these countries, two high dose supplements are available per year, which, according"
"been linked to impaired immune system and brain functions. In addition, recent studies have linked vitamin D deficiency to autoimmune diseases, hypertension, multiple sclerosis, diabetes, and incidence of memory loss. Outside the tropics UVR has to penetrate through a thicker layer of atmosphere, which results in most of the UVB reflected or destroyed en route; because of this there is less potential for vitamin D biosynthesis in regions far from the equator. Higher amount of vitamin D intake for dark-skinned people living in regions with low levels of sunlight are advised by doctors to follow vitamin D rich diet or"
"A because it is essential for the synthesis of the vitamin A transport proteins and as the cofactor in conversion of retinol to retinal. In malnourished populations, common low intakes of vitamin A and zinc increase the severity of vitamin A deficiency and lead physiological signs and symptoms of deficiency. A study in Burkina Faso showed major reduction of malaria morbidity with combined vitamin A and zinc supplementation in young children. Due to the unique function of retinal as a visual chromophore, one of the earliest and specific manifestations of vitamin A deficiency is impaired vision, particularly in reduced light"
"anemia and weakened immunity, and increase their risk of morbidity and mortality from infectious disease. This also presents a problem for women, with WHO estimating that 9.8 million women are affected by night blindness. Clinical vitamin A deficiency is particularly common among pregnant women, with prevalence rates as high as 9.8% in South-East Asia. Estimates say that 28.5% of the global population is iodine deficient, representing 1.88 billion individuals. Although salt iodization programs have reduced the prevalence of iodine deficiency, this is still a public health concern in 32 nations. Moderate deficiencies are common in Europe and Africa, and over"
"the part of the eye that senses light. Diabetic retinopathy is the leading cause of blindness in the United States. Diabetic retinopathy is known to be associated with a number of epigenetic markers, including methylation of the Sod2 and MMP-9 genes, an increase in transcription of LSD1, a H3K4 and H3K9 demethylase, and various DNA Methyl-Transferases (DNMTs), and increased presence of miRNAs for transcription factors and VEGF. It is believed that much of the retinal vascular degeneration characteristic of diabetic retinopathy is due to impaired mitochondrial activity in the retina. Sod2 codes for a superoxide dismutase enzyme, which scavenges free"
"of damage which can also be due to lack of vitamin A, but which is caused by lack of other forms of vitamin A which work in the visual system. Xerophthalmia from ""hypovitaminosis A"" is specifically due to lack of the hormone-like vitamin A metabolite retinoic acid, since (along with certain growth-stunting effects) the condition can be reversed in vitamin A deficient rats by retinoic acid supplementation (however the retinal damage continues). Since retinoic acid cannot be reduced to retinal or retinol, these effects on the cornea must be specific to retinoic acid. This is in keeping with retinoic acid's"