"hospital in Uganda however showed no significant difference in vitamin D levels of malnourished children compared to non-malnourished children. Because both groups were at risk due to darker skin pigmentation, both groups had vitamin D deficiency. Nutritional status did not appear to play a role in this study. There is an increased risk of vitamin D deficiency in people who are considered overweight or obese based on their body mass index (BMI) measurement. The relationship between these conditions is not well understood. There are different factors that could contribute to this relationship, particularly diet and sunlight exposure. Alternatively, vitamin D"
"Moroccan immigrants. The Middle East, despite high rates of sun-exposure, has the highest rates of rickets worldwide. This can be explained by limited sun exposure due to cultural practices and lack of vitamin D supplementation for breast-feeding women. Up to 70% and 80% of adolescent girls in Iran and Saudi Arabia, respectively, have vitamin D insufficiency. Socioeconomic factors that limit a vitamin D rich diet also plays a role. In the United States, vitamin D insufficiency varies dramatically by ethnicity. Among males aged 70 years and older, the prevalence of low serum 25(OH) D levels was 23% for non-Hispanic whites,"
"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"
"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"
"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"
"cause of rickets. He discovered that feeding caged dogs on a diet of porridge induced rickets, which could then be cured with cod liver oil and concluded that rickets was caused by a dietary factor. It was later discovered that the actual cause of rickets is lack of vitamin D due to lack of sunlight which can be prevented or remedied by ingesting food rich in vitamin D, such as cod liver oil. He worked on the detrimental effect of foods containing significant phytic acid, particularly cereals. In 1914 he married May Tweedy, a lecturer at Bedford College (London) who"
"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"
"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"
"the underlying cause. Phosphate may be given by mouth or by injection into a vein. Hypophosphatemia occurs in about 2% of people within hospital and 70% of people in the intensive care unit (ICU). Primary hypophosphatemia is the most common cause of non-nutritional rickets. Laboratory findings include low-normal serum calcium, moderately low serum phosphate, elevated serum alkaline phosphatase, and low serum 1,25 dihydroxy-vitamin D levels, hyperphosphaturia, and no evidence of hyperparathyroidism. Hypophosphatemia decreases 2,3-diphosphoglycerate (2,3-DPG) causing a left shift in the oxyhemoglobin curve. Other rarer causes include: Hypophosphatemia is caused by the following three mechanisms: Hypophosphatemia is diagnosed by measuring"
"the nutritional factor causing rickets, and proved that fat-soluble vitamins present in cod liver oil, or exposure to ultra violet light, could cure and prevent rickets in children. Chick was appointed Head of a new nutrition section at the Lister Institute and continued with her research on rickets and, additionally, pellagra. The department was relocated to the Cambridge house of the Lister director CJ Martin during the Second World War. She served as secretary of the League of Nations health section committee on the physiological bases of nutrition from 1934 to 1937. In 1941 she was a founding member of"
"fewer potatoes, and less sugar. In conversation with John Howland, a Johns Hopkins pediatrician, and later with Howland's staff doctors Edwards A. Park and Paul G. Shipley, they found that rickets could be induced through diet. McCollum's research during the early 1920s found that rats could develop rickets when fed a plain cereal diet. His group tested more than 300 diets on rats, finally finding that cod-liver oil could prevent rickets. Building on the work of Edward Mellanby, who had been inspired by the discovery of vitaminA by McCollum and Davis, McCollum fed animals with induced rickets cod liver oil"
"HIV infection, gastrectomy, malabsorptive disorders, certain cancers and their associated treatments. Since Vitamin D is a fat-soluble vitamin, it cannot be added to a wide variety of foods. Foods that it is commonly added to are margarine, vegetable oils and dairy products. During the late 1800s, after the discovery of curing conditions of scurvy and beriberi had occurred, researchers were aiming to see if the disease, later known as rickets, could also be cured by food. Their results showed that sunlight exposure and cod liver oil were the cure. It was not until the 1930s that vitamin D was actually"
"United States and Europe, except among certain minority groups. It begins in childhood, typically between the ages of 3 and 18 months old. Rates of disease are equal in males and females. Cases of what is believed to have been rickets have been described since the 1st century, and the condition was widespread in the Roman Empire. The disease was common into the 20th century. Early treatments included the use of cod liver oil. Signs and symptoms of rickets can include bone tenderness, and a susceptibility for bone fractures particularly greenstick fractures. Early skeletal deformities can arise in infants such"
"that was heated and aerated so its vitamin A was destroyed. The oil could no longer cure night blindness but did cure rickets. After his rats recovered, he named the substance for the next free letter of the alphabet, vitamin D. Then they became convinced that sunshine and cod-liver oil both protected against rickets, and tested this by carrying rats outside to the sunshine. Soon after, a generation of children grew up on cod-liver oil, and rickets was virtually wiped out. Harry Day, a colleague and McCollum biographer, writes that finding vitaminD was the work of ""a host of investigators"""
"During the late 18th and early 19th centuries, the use of deprivation studies allowed scientists to isolate and identify a number of vitamins. Lipid from fish oil was used to cure rickets in rats, and the fat-soluble nutrient was called ""antirachitic A"". Thus, the first ""vitamin"" bioactivity ever isolated, which cured rickets, was initially called ""vitamin A""; however, the bioactivity of this compound is now called vitamin D. In 1881, Russian medical doctor studied the effects of scurvy at the University of Tartu . He fed mice an artificial mixture of all the separate constituents of milk known at that"
"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."
"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"
"at the Lister Institute of Preventative Medicine. She remained in Vienna until 1922, but continued her research in the United Kingdom. Mackay was a part of a British team led by Harriette Chick whose studies displayed the importance of cod liver oil and sunlight in preventing and potentially curing rickets. While working on finding the cause of rickets, Mackay noticed all of the infants in her studies were anemic, and thus she became interested in finding the cause of anemia. Mackay returned to London and conducted the first investigation on anemia in infants with the help of medical statistician Major"
"vitamins) and named vitamin C as the then-unknown substance preventing scurvy. Lafayette Mendel and Thomas Osborne also performed pioneering work on vitamins A and B. In 1919, Sir Edward Mellanby incorrectly identified rickets as a vitamin A deficiency because he could cure it in dogs with cod liver oil. In 1922, McCollum destroyed the vitamin A in cod liver oil, but found that it still cured rickets. Also in 1922, H.M. Evans and L.S. Bishop discover vitamin E as essential for rat pregnancy, originally calling it ""food factor X"" until 1925. In 1925, Hart discovered that trace amounts of copper"
"has been shown that deficiencies of vitamin D and calcium increase the likelihood of various birth defects such as spina bifida and rickets. Natural selection has led to females with lighter skin than males in all indigenous populations because women must get enough vitamin D and calcium to support the development of fetus and nursing infant and to maintain their own health. The sexes also differ in how they change their skin color with age. Men and women are not born with different skin color, they begin to diverge during puberty with the influence of sex hormones. Women can also"
"X-linked hypophosphatemia X-linked hypophosphatemia (XLH), also called X-linked dominant hypophosphatemic rickets, or X-linked Vitamin D-resistant rickets, is an X-linked dominant form of rickets (or osteomalacia) that differs from most cases of rickets in that vitamin D supplementation does not cure it. It can cause bone deformity including short stature and genu varum (bow leggedness). It is associated with a mutation in the PHEX gene sequence (Xp.22) and subsequent inactivity of the PHEX protein. The prevalence of the disease is 1:20000. The leg deformity can be treated with Ilizarov frames and CAOS surgery. It is also treated with medications including human"
"solar radiation. Lighter skin is due to a low concentration in pigmentation, thus allowing more sunlight to trigger the production of vitamin D. In this way, high frequencies of light hair in northern latitudes are a result of the light skin adaptation to lower levels of solar radiation, which reduces the prevalence of rickets caused by vitamin D deficiency. The darker pigmentation at higher latitudes in certain ethnic groups such as the Inuit is explained by a greater proportion of seafood in their diet and by the climate which they live in, because in the polar climate there is more"
"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"
"to treat renal osteodystrophy, hypoparathyroidism, vitamin D dependent rickets type I, and osteoporosis. Furthermore, he elucidated the pathophysiology of hereditary vitamin D-dependent rickets which involves defective vitamin D metabolism, and the pathophysiological mechanisms of X-linked hypophosphatemic rickets. Holick helped develop the first clinical assays for 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D, determined how vitamin D3 is made in the skin from sun exposure, and established how season, time of day, skin pigmentation, sunscreen use, and latitude influenced this vital cutaneous process. He established that the skin was not only the organ responsible for making vitamin D3 but was also a target"
"B. In 1919 Sir Edward Mellanby incorrectly identified rickets as a vitamin A deficiency, because he could cure it in dogs with cod-liver oil. In 1922 McCollum destroyed the vitamin A in cod liver oil but found it still cured rickets, thus identifying vitamin D. Also in 1922, H.M. Evans and L.S. Bishop discovered vitamin E as essential for rat pregnancy, and originally called it ""food factor X"" until 1925. In 1925 Hart discovered that iron absorption requires trace amounts of copper. In 1927 Adolf Otto Reinhold Windaus synthesized vitamin D, for which he won the Nobel Prize in Chemistry"
"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"
"time, the only alleged symptom is chronic fatigue, while bone aches are not spontaneous but only revealed by pressure or shocks.It differs from renal osteodystrophy, where the latter shows hyperphosphatemia. The causes of adult osteomalacia are varied, but ultimately result in a vitamin D deficiency: Biochemical features are similar to those of rickets. The major factor is an abnormally low vitamin D concentration in blood serum.Major typical biochemical findings include: Furthermore, a technetium bone scan will show increased activity (also due to increased osteoblasts). Radiological appearances include: Prevention of osteomalacia rests on having an adequate intake of vitamin D and"
"December 1940 from malignant hyperthermia after a minor operation to deal with a thrombosis. Kurt Huldschinsky Kurt Huldschinsky (1883 in Berlin – 15 December 1940 in Alexandria, Egypt) was a German Pediatrician of Polish heritage (Prussian). He served in the Wehrmacht as a field medic in World War I. Later, as a medical doctor and research scientist, he successfully demonstrated in the winter of 1918/1919 how rickets could be treated with Ultra-violet lamps. At that time perhaps half of all German children suffered from rickets. It was already understood that this disease was caused by Calcium deficiency. Up to that"
"mineralization-inhibiting proteins and peptides (such as osteopontin and ASARM peptides) occurs in the extracellular matrix of bones and teeth, likely contributing locally to cause matrix hypomineralization (osteomalacia). The most common cause of osteomalacia is a deficiency of vitamin D, which is normally derived from sunlight exposure and, to a lesser extent, from the diet. The most specific screening test for vitamin D deficiency in otherwise healthy individuals is a serum 25(OH)D level. Less common causes of osteomalacia can include hereditary deficiencies of vitamin D or phosphate (which would typically be identified in childhood) or malignancy. Vitamin D and calcium supplements"
"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"
"Goodpasture and his colleagues at Vanderbilt University in the early 1930s. ""Rickettsia"" species are transmitted by numerous types of arthropod, including chigger, ticks, fleas, and lice, and are associated with both human and plant disease. Most notably, ""Rickettsia"" species are the pathogens responsible for typhus, rickettsialpox, Boutonneuse fever, African tick bite fever, Rocky Mountain spotted fever, Flinders Island spotted fever and Queensland tick typhus (Australian tick typhus). Despite the similar name, ""Rickettsia"" bacteria do not cause rickets, which is a result of vitamin D deficiency. The majority of ""Rickettsia"" bacteria are susceptible to antibiotics of the tetracycline group. The classification"
"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"
"Autosomal dominant hypophosphatemic rickets Autosomal dominant hypophosphatemic rickets (ADHR) is a rare hereditary disease in which excessive loss of phosphate in the urine leads to poorly formed bones (rickets), bone pain, and tooth abscesses. ADHR is caused by a mutation in the fibroblast growth factor 23 (FGF23). ADHR affects men and women equally; symptoms may become apparent at any point from childhood through early adulthood. Blood tests reveal low levels of phosphate (hypophosphatemia) and inappropriately normal levels of vitamin D. Occasionally, hypophosphatemia may improve over time as urine losses of phosphate partially correct. ADHR may be lumped in with X-linked"