"level of 25(OH)D is the laboratory test ordered to indicate whether or not a person has vitamin D deficiency or insufficiency. It is also considered reasonable to treat at-risk persons with vitamin D supplementation without checking the level of 25(OH)D in the serum, as vitamin D toxicity has only been rarely reported to occur. Levels of 25(OH)D that are consistently above 200 ng/mL (500 nmol/L) are thought to be potentially toxic, although data from humans are sparse. Vitamin D toxicity usually results from taking supplements in excess. Hypercalcemia is often the cause of symptoms, and levels of 25(OH)D above 150"
"among older toddlers and children, it has been attributed to low dietary calcium intakes, which are characteristic of cereal-based diets with limited access to dairy products. Rickets was formerly a major public health problem among the US population; in Denver, where ultraviolet rays are about 20% stronger than at sea level on the same latitude, almost two-thirds of 500 children had mild rickets in the late 1920s. An increase in the proportion of animal protein in the 20th century American diet coupled with increased consumption of milk fortified with relatively small quantities of vitamin D coincided with a dramatic decline"
"based on blood tests finding a low calcium, low phosphorus, and a high alkaline phosphatase together with X-rays. Prevention includes vitamin D supplements for exclusively breastfed babies. Treatment depends on the underlying cause. If due to a lack of vitamin D, treatment is usually with vitamin D and calcium. This generally results in improvements within a few weeks. Bone deformities may also improve over time. Occasionally surgery may be done to fix bone deformities. Genetic forms of the disease typically require specialized treatment. Rickets occurs relatively commonly in the Middle East, Africa, and Asia. It is generally uncommon in the"
"popularity of sugary drinks and decreased time spent outside have contributed to significant rise of developing rickets. Deformities of the female pelvis related to severe rickets impair normal childbirth, which leads to higher mortality of the infant, mother, or both. Vitamin D deficiency is most common in regions with low sunlight, especially in the winter. Chronic deficiencies in vitamin D may also be linked with breast, prostate, colon, ovarian, and possibly other types of cancers. The relationship between cardiovascular disease and vitamin D deficiency also suggest link between health of cardiac and smooth muscle. Low vitamin D levels have also"
"linked to curing rickets. This discovery led to the fortification of common foods such as milk, margarine, and breakfast cereals. This took the astonishing statistics of approximately 80–90% of children showing varying degrees of bone deformations due to vitamin D deficiency to being a very rare condition. The current RDA for infants aged 0–6 months is 10 µg (400 International Units (IU))/day and for adults over 19 years of age it is 15 µg (600 IU)/day. Diseases associated with a vitamin D deficiency include rickets, osteoporosis, and certain types of cancer (breast, prostate, colon and ovaries). It has also been"
"but been eliminated in the United States. The word ""rickets"" may be from the Old English word ""wrickken"" ('to twist'), although because this is conjectured, several major dictionaries simply say ""origin unknown"". The name ""rickets"" is plural in form but usually singular in construction. The Greek word ""rachitis"" (ῥαχίτης, meaning ""in or of the spine"") was later adopted as the scientific term for rickets, due chiefly to the words' similarity in sound. Rickets Rickets is a condition that results in weak or soft bones in children. Symptoms include bowed legs, stunted growth, bone pain, large forehead, and trouble sleeping. Complications"
"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"
"chronic neonatal hepatitis will not be able to digest fats and will not be able to absorb vitamins A, D, E and K. The lack of vitamin D leads to poor bone and cartilage development (rickets). Vitamin A is also needed for normal growth and good vision. Vitamin K deficiency is associated with easy bruising and a tendency to bleed, whereas the lack of vitamin E results in poor coordination. Chronic neonatal hepatitis will lead to the inability of the liver to eliminate toxins in the bile. This causes itching, skin eruptions and irritability. In about half of all cases"
"and permanent bone damage. Vitamin D, also coined as the sunshine vitamin, is necessary within a child’s diet as it allows body tissues and in particular bone to be properly nourished and mineralized. Vitamin D3, which is gained from dietary nutrients, is also essential for calcium absorption and homeostasis, which ensures standard muscle contraction and the transport of blood throughout the body. Without adequate consumption of vitamin D, children can become predisposed to conditions such as rickets, which is the ""softening or weakening of bones"". which can only be treated with vitamin D supplements, sunlight and surgery. Vitamin D is"
"Biotin Biotin is a water-soluble B vitamin, also called vitamin B and formerly known as vitamin H or coenzyme R. It is involved in a wide range of metabolic processes, both in humans and in other organisms, primarily related to the utilization of fats, carbohydrates, and amino acids. Biotin deficiency can be caused by inadequate dietary intake or inheritance of one or more inborn genetic disorders that affect biotin metabolism. Subclinical deficiency can cause mild symptoms, such as hair thinning or skin rash typically on the face. Neonatal screening for biotinidase deficiency began in the United States in 1984, with"
"Vitamin A deficiency Vitamin A deficiency (VAD) or hypovitaminosis A is a lack of vitamin A in blood and tissues. It is common in poorer countries, but rarely is seen in more developed countries. Nyctalopia (night blindness) is one of the first signs of VAD. Xerophthalmia, keratomalacia, and complete blindness can also occur since vitamin A has a major role in phototransduction. The three forms of vitamin A include retinols, beta-carotenes, and carotenoids. Vitamin A deficiency is the leading cause of preventable childhood blindness, and is critical to achieving Millennium Development Goal 4 to reduce child mortality. About 250,000 to"
"A and vitamin C. Beta-Carotene is required to synthesize vitamin A and vitamin A is needed to synthesize retinol. A lack of retinol-binding protein is due to a lack of retinol which is required to trigger its production. The damaging effects of porphyrins interacting with iron, absorbing photons to then emit reactive oxygen species is the mechanism of action that results in the itchy, painful blisters that are common with PCT. The reactive oxygen species that are formed interact with and exhaust the antioxidants in the skin, primarily those of beta-Carotene, vitamin E, and vitamin C. Supplementation of these three"
"commonly occurs together with folate deficiency (a lack of folic acid), which also causes glossitis and megaloblastic anemia. Vitamin B3 deficiency (pellagra) is another possible cause, and in which other association conditions such as dermatitis, diarrhea, dementia and glossitis can occur. Biotin (vitamin B7) deficiency has also been reported to cause AC, along with hair loss (alopecia) and dry eyes. Zinc deficiency is known to cause AC. Other symptoms may include diarrhea, alopecia and dermatitis. Acrodermatitis enteropathica is an autosomal recessive genetic disorder causing impaired absorption of zinc, and is associated with AC. In general, these nutritional disorders may be"
"effectors may be 'mix and match.' For example, the knockout of Rab27 causes the hypopigmentation but also immunodeficiency due to deficiencies in cytotoxic killing activity in cytotoxic T cells (something that also depends on vesicle transport). While, the knockout of myosin Va does not cause immunodeficiency, but it does cause neural defects. Though some neural problems (i.e. brain damage) can be seen in Rab27A deficient children, this is thought to be a secondary effect of the immune problems, and not directly due to the lack of Rab27A. Griscelli syndrome is a disorder of melanosome transport, and divided into several types:"
"to retinol varies from person to person and bioavailability of carotene in food varies. In addition to dietary problems, other causes of VAD are known. Iron deficiency can affect vitamin A uptake; other causes include fibrosis, pancreatic insufficiency, inflammatory bowel disease, and small-bowel bypass surgery. Excess alcohol consumption can deplete vitamin A, and a stressed liver may be more susceptible to vitamin A toxicity. People who consume large amounts of alcohol should seek medical advice before taking vitamin A supplements. In general, people should also seek medical advice before taking vitamin A supplements if they have any condition associated with"
"Two bacterial species associated with periodontitis are implicated as mediators of protein citrullination in the gums of people with RA. Vitamin D deficiency is more common in people with rheumatoid arthritis than in the general population. However, whether vitamin D deficiency is a cause or a consequence of the disease remains unclear. One meta-analysis found that vitamin D levels are low in people with rheumatoid arthritis and that vitamin D status correlates inversely with prevalence of rheumatoid arthritis, suggesting that vitamin D deficiency is associated with susceptibility to rheumatoid arthritis. Rheumatoid arthritis Rheumatoid arthritis (RA) is a long-term autoimmune disorder"
"cannot synthesize vitamin A from plant beta-carotene, and therefore must be supplemented with retinol from meat. A deficiency in vitamin A will result in a poor coat, with hair loss, with scaly and thickened skin. However an excess of vitamin A, called hypervitaminosis A, can result from over feeding cod liver oil, and large amounts of liver. Signs of hypervitaminosis A are overly sensitive skin, and neck pain causing the cat to be unwilling to groom its self, resulting in a poor coat. Supplementing vitamin A with retinol to a deficient cat, and feeding a balanced diet to a cat"
"and glossitis (inflammation of the tongue). It is not completely understood how iron deficiency causes AC, but it is known that it causes a degree of immunocompromise (decreased efficiency of the immune system) which may in turn allow an opportunistic infection of candida. Vitamin B2 deficiency (ariboflavinosis) may also cause AC, and other conditions such as redness of mucous membranes, magenta colored glossitis (pink inflammation of the tongue). Vitamin B5 deficiency may also cause AC, along with glossitis, and skin changes similar to seborrhoeic dermatitis around the eyes, nose and mouth. Vitamin B12 deficiency is sometimes responsible for AC, and"
"2011 the Centers for Disease Control and Prevention applied the IOM standard to NHANES data on serum levels collected between 2001 and 2006, and determined that 32% of Americans were deficient during that period (8% at risk of deficiency, and 24% at risk of inadequacy). The role of diet in the development of rickets was determined by Edward Mellanby between 1918 and 1920. In 1921, Elmer McCollum identified an antirachitic substance found in certain fats that could prevent rickets. Because the newly discovered substance was the fourth vitamin identified, it was called vitamin D. The 1928 Nobel Prize in Chemistry"
"with hair loss. Other signs include corneal opacity, lenticular cataracts, hemorrhagic adrenals, fatty degeneration of the kidney and liver, and inflammation of the mucous membrane of the gastrointestinal tract. Post-mortem studies in rhesus monkeys fed a riboflavin-deficient diet revealed about one-third the normal amount of riboflavin was present in the liver, which is the main storage organ for riboflavin in mammals. Riboflavin deficiency in birds results in low egg hatch rates. As a chemical compound, riboflavin is a yellow-orange solid substance with poor solubility in water compared to other B vitamins. Visually, it imparts color to vitamin supplements (and bright"
"known as 1, 25-Dihydroxycholecalciferol in the Kidney upon exposure to UV ray of sun light. Deficiency in Vitamin D or renal disease contributes to bone disorder such as in Osteomalacia in adult and Rickets in children. Osteomalacia is the softening of bones due to poor bone mineralization which is in turn due to poor calcium absorption. Ultimately, these hormonal changes in body; such as function of thyroid, parathyroid, liver and kidney disrupts metabolic changes as well as function of specific organs, which in turn leads to condition that are not desirable such as bone disorders or other endocrine related diseases."
"maternal mortality. Approximately 50% of pregnant women in South Africa have anemia. Anemia causes tiredness and weakness. If left untreated for long periods of time, it can damage the heart, brain, and other vital organs. Another common nutritional problem among South Africans is hypocalcemia, a deficiency in calcium. In a study of a randomly chosen rural South African community, 13.2% of children were found to have abnormally low levels of calcium in their blood. Additional studies done on South African children show that this deficiency can lead to Rickets. Rickets causes weakness and pain in bones and dental structures, impaired"
"linear or patchy red lesions. Vitamin B1 deficiency (thiamin deficiency) can cause glossitis. Vitamin B2 deficiency (ariboflavinosis) can cause glossitis, along with angular cheilitis, cheilosis, peripheral neuropathy and other signs and symptoms. The glossitis in vitamin B2 deficiency is described as magenta. Vitamin B3 deficiency (pellagra) can cause glossitis. Vitamin B6 deficiency (pyridoxine deficiency) can cause glossitis, along with angular cheilitis, cheilosis, peripheral neuropathy and seborrheic dermatitis. Folate deficiency (vitamin B9 deficiency) can cause glossitis, along with macrocytic anemia, thrombocytopenia, leukopenia, diarrhea, fatigue and possibly neurological signs. Apart from pernicious anemia discussed above, any other cause of vitamin B12 deficiency"
"Rickettsia rickettsii Rickettsia rickettsii (abbreviated as ""R. rickettsii"") is a gram-negative, intracellular, coccobacillus bacterium that is around 0.8 to 2.0 micrometers long"""". ""R. rickettsi"" is the causative agent of Rocky Mountain spotted fever. ""R. rickettsii"" is one of the most pathogenic ""Rickettsia"" strains. It affects a large majority of the Western Hemisphere and small portions of the Eastern Hemisphere. Rocky Mountain spotted fever first emerged in the Idaho Valley in 1896. At that time, not much information was known about the disease; it was originally called Black Measles because patients had a characteristic spotted rash appearance throughout their body. The"
"fat malabsorption such as pancreatitis, cystic fibrosis, tropical sprue, and biliary obstruction. Other causes of vitamin A deficiency are inadequate intake, fat malabsorption, or liver disorders. Deficiency impairs immunity and hematopoiesis and causes rashes and typical ocular effects (e.g., xerophthalmia, night blindness). Along with poor diet, a large amount of infection and disease is present in many developing communities. Infection is very draining on vitamin A reserves and this vitamin A deficit leaves the individual more susceptible to infection; increased documentation of xerophthalmia has been seen after an outbreak of measles and the varying stages of xerophthalmia become a good"
"deficiency can result in rickets, a disease in which bones become soft and pliable. Vitamin E is a potent anti-oxidant in the body. Vitamin E deficiencies leads to neuromuscular, vascular and reproductive abnormalities. The chewable form of Flintstones Complete contains higher amounts of vitamins and minerals than the gummy version. The chewable form, unlike the gummy version, contains: Vitamins B1 (thiamin), B2 (riboflavin), Niacin, Calcium, Iron, Copper and Selenium. Flintstones with Iron has a similar vitamin profile as Flintstones Complete gummy version. The iron content meets 75% of the Daily Value of iron for children over 2 years of age."
"In severe vitamin A deficiency, lack of glycoproteins may lead to corneal ulcers or liquefaction. Vitamin A is essential to maintain intact epithelial tissues as a physical barrier to infection; it is also involved in maintaining a number of immune cell types from both the innate and acquired immune systems. These include the lymphocytes (B-cells, T-cells, and natural killer cells), as well as many myelocytes (neutrophils, macrophages, and myeloid dendritic cells). Vitamin A may be needed for normal red blood cell formation; deficiency causes abnormalities in iron metabolism. Vitamin A is needed to produce the red blood cells from stem"
"an adequate intake of provitamin A carotenoids from fruits and vegetables or preformed vitamin A from animal and dairy products. Early weaning from breastmilk can also increase the risk of vitamin A deficiency. Secondary vitamin A deficiency is associated with chronic malabsorption of lipids, impaired bile production and release, and chronic exposure to oxidants, such as cigarette smoke, and chronic alcoholism. Vitamin A is a fat-soluble vitamin and depends on micellar solubilization for dispersion into the small intestine, which results in poor use of vitamin A from low-fat diets. Zinc deficiency can also impair absorption, transport, and metabolism of vitamin"
"together with other nutrient deficiencies, particularly of other water-soluble vitamins. A deficiency of riboflavin can be primary - poor vitamin sources in one's daily diet - or secondary, which may be a result of conditions that affect absorption in the intestine, the body not being able to use the vitamin, or an increase in the excretion of the vitamin from the body. Subclinical deficiency has also been observed in women taking oral contraceptives, in the elderly, in people with eating disorders, chronic alcoholism and in diseases such as HIV, inflammatory bowel disease, diabetes and chronic heart disease. The Celiac Disease"
"Biotin deficiency Biotin deficiency is a rare nutritional disorder which can become serious, even fatal, if allowed to progress untreated. It can occur in people of any age, ancestry, or gender. Biotin is part of the B vitamin family. Biotin deficiency rarely occurs among healthy people because the daily requirement of biotin is low, many foods provide adequate amounts of it, intestinal bacteria synthesize small amounts of it, and the body effectively scavenges and recycles it from bodily waste. However, deficiencies can be caused by consuming raw egg whites over a period of months to years. Egg whites contain high"
"in the lab of Elmer McCollum. When McCollum and another assistant Marguerite Davis published their discovery of what came to be called vitamin A, Steenbock thought he deserved more credit than he received. Steenbock carried on the vitamin A work in Madison, after McCollum accepted an offer from Johns Hopkins University. In 1923, Steenbock demonstrated that irradiation by ultraviolet light increased the vitamin D content of foods and other organic materials. After irradiating rodent food, Steenbock discovered that the rodents were cured of rickets. It is now known that vitamin D deficiency is a cause of rickets. Using $300 of"
"can be represented as two connected retinyl groups, which are used in the body to contribute to vitamin A levels. Alpha-carotene and gamma-carotene also have a single retinyl group, which give them some vitamin activity. None of the other carotenes have vitamin activity. The carotenoid beta-cryptoxanthin possesses an ionone group and has vitamin activity in humans. Vitamin A can be found in two principal forms in foods: Vitamin A deficiency is estimated to affect approximately one third of children under the age of five around the world. It is estimated to claim the lives of 670,000 children under five annually."
"it was found that the retinoid receptors which help transport vitamin A were of normal function. Eating foods high in vitamin A or taking dietary supplements, retinol or retinal will prevent a deficiency. The foods highest in vitamin A are any pigmented fruits and vegetables and leafy green vegetables also provide beta-Carotene. There can be symptoms of fat loss and a reduction of any weight gain that would be considered normal for an individual, especially developmental weight gains such as in infants which would occur if the infant was deprived of vitamin A in utero and/or if it was deprived"