Rickets: MedlinePlus Medical Encyclopedia Work indoors during the daylight hours You may not get enough vitamin D from your diet if you: Are lactose intolerant (have trouble digesting milk products) Do not drink milk products Follow a vegetarian diet Infants who are breastfed only may develop vitamin D deficiency. Human breast milk does not supply the proper amount of vitamin D. This can be a particular problem for darker-skinned children in winter months (when there are lower levels of sunlight). Not getting enough calcium and phosphorous in your diet can also lead to rickets. Rickets caused by a lack of these minerals in diet is rare in developed countries, because calcium and phosphorous are found in milk and green vegetables. Your genes may increase your risk of rickets. Hereditary rickets is a form of the disease that is passed down through families. It occurs when the kidneys are unable to hold onto the mineral phosphate. Rickets may also be caused by kidney disorders that involve renal tubular acidosis . Disorders that reduce the digestion or absorption of fats will make it more difficult for vitamin D to be absorbed into the body. Occasionally, rickets may occur in children who have disorders of the liver, or who cannot convert vitamin D to its active form.

Rickets is rare in the United States. It is most likely to occur in children during periods of rapid growth, when the body needs high levels of calcium and phosphate. Rickets may be seen in children ages 6 to 24 months. It is uncommon in newborns. Symptoms Urine calcium Treatment The goals of treatment are to relieve symptoms and correct the cause of the condition. The cause must be treated to prevent the disease from returning. Replacing calcium, phosphorus, or vitamin D that is lacking will eliminate most symptoms of rickets. Dietary sources of vitamin D include fish, liver, and processed milk. Exposure to moderate amounts of sunlight is encouraged. If rickets is caused by a metabolic problem, a prescription for vitamin D supplements may be needed. Positioning or bracing may be used to reduce or prevent deformities. Some skeletal deformities may require corrective surgery. Outlook (Prognosis) The disorder may be corrected by replacing vitamin D and minerals. Laboratory values and x-rays usually improve after about 1 week, although some cases may require large doses of minerals and vitamin D. If rickets is not corrected while the child is still growing, skeletal deformities and short stature may be permanent.

If it is corrected while the child is young, skeletal deformities often improve or disappear with time. Possible Complications Skeletal fractures, may occur without cause When to Contact a Medical Professional Call your child's health care provider if you notice symptoms of rickets. Prevention You can prevent rickets by making sure that your child gets enough calcium, phosphorus, and vitamin D in the diet. People who have gastrointestinal or other disorders may need to take supplements. Ask your child's health care provider. Kidney (renal) causes of poor vitamin D absorption should be treated right away. People who have renal disorders should have their calcium and phosphorus levels monitored regularly. Genetic counseling may help people who have a family history of inherited disorders that can cause rickets. Alternative Names Osteomalacia in children; Vitamin D deficiency; Renal rickets; Hepatic rickets Images X-ray References Greenbaum LA. Rickets and hypervitaminosis D. In: Kliegman RM, Behrman RE, Jenson HB, Stanton BF, eds. Nelson Textbook of Pediatrics. 19th ed. Philadelphia, PA: Elsevier Saunders; 2011:chap 48.

Read More Rickets: Causes, Symptoms and Treatments - Medical News Today Rickets: Causes, Symptoms and Treatments Written by Stephanie Brunner B.A. 4 16 Rickets is a childhood bone disorder in which bones soften and become prone to fractures and deformity. Although rare in industrialized nations, it is still fairly common in some developing countries. The main cause of rickets is a lack of vitamin D . Not having enough calcium in one's diet may also be a cause of rickets, as may vomiting and diarrhea . Some childhood kidney and liver diseases can cause rickets, as may a digestive disorder complication that affects calcium and phosphorous absorption. Rickets affects mainly children, although the disorder may also affect adults (osteomalacia). In most cases, the child suffers from severe and long-term malnutrition , usually during early childhood. The term rickets comes from the Old English word "wrickken", meaning to twist or bend. Rickets was common in the UK and USA during the 19th century. For proper absorption of calcium and phosphorous from the gut, we need vitamin D. If vitamin D levels in a child are low, he/she may have inadequate calcium and phosphorous bone levels.

A study published in JAMA in 2013 suggested that babies should be given a daily dose of vitamin D of 400 IU (international units) to help them stay healthy . Providing a child with extra vitamin D and some minerals usually resolves the rickets problem. Symptoms of rickets A symptom is something the patient feels and reports, while a sign is something other people, such as the doctor detect. For example, pain may be a symptom while a rash may be a sign. Symptoms of rickets may include: Baby is floppy Causes of rickets Some of the conditions that can be caused by vitamin D deficiency. Lack of vitamin D - the main cause of rickets. Our bodies need vitamin D in order to absorb calcium from the intestines. Ultraviolet light (from sunlight) helps our skin cells convert vitamin D from an inactive into an active state. If we do not have enough vitamin D, calcium that we get from the food we eat is not absorbed properly, causing hypocalcemia (lower-than-normal blood calcium) to develop. Hypocalcemia results in deformities of bones and teeth, as well as neuromuscular problems.

The following foods are known to be rich on vitamin D: eggs, fish oils , margarine, some fortified milks and juices, some oily fishes, and some soymilk products that have vitamin D added. Genetic defect - hypophosphatemic rickets is a rare genetic fault that undermines the way the kidneys process phosphates. Phosphate blood levels are too low, leading to weak and soft bones. Some diseases - some renal (kidney), hepatic (liver) and intestinal diseases can interfere with the way the body absorbs and metabolizes minerals and vitamins, resulting in rickets. Risk factors for rickets Vitamin D is described as the sunshine vitamin. A study published in the journal Pharmacology and Pharmacotherapeutics in 2012 suggested that 50% of the worldwide population may be deficient in vitamin D ( source ). A risk factor is something which increases the likelihood of developing a condition or disease. For example, obesity significantly raises the risk of developing diabetes type 2. Therefore, obesity is a risk factor for diabetes type 2. Risk factors for rickets include: Poverty - rickets is more likely to occur among children who are poor.

Sunlight - children who do not get enough sunlight are more dependent on excellent nutrition to make sure they are getting enough vitamin D. Malnutrition - rickets is more common in areas of the world where severe droughts and starvation occur. On the next page we look at the diagnosis of rickets, complications caused by the condition and the available treatments for rickets. Rickets and osteomalacia - Causes - NHS Choices Rickets and osteomalacia - Causes Rickets Prevention Causes of rickets Rickets usually occurs because of a lack of vitamin D or calcium, although it can also be caused by a genetic defect or another health condition. Lack of vitamin D and calcium The most common cause of rickets is a lack of vitamin D or calcium in a child's diet. Both are essential for children to develop strong and healthy bones. Sources of vitamin D are: sunlight – your skin produces vitamin D when it's exposed to the sun, and we get most of our vitamin D this way food – vitamin D is also found in some foods, such as oily fish, eggs and fortified breakfast cereals dietary supplements Calcium is commonly found in dairy products, such as milk, cheese and yoghurt, and green vegetables, such as broccoli and cabbage.

Over time, a vitamin D or calcium deficiency will cause rickets in children and soft bones (osteomalacia) in adults. See preventing rickets for more information and advice about ensuring your child gets enough vitamin D and calcium. Who's at risk? Any child who doesn't get enough vitamin D or calcium can develop rickets, but there are certain groups of children who are more at risk. For example, rickets is more common in children of Asian, African-Caribbean and Middle Eastern origin because their skin is darker and needs more sunlight to get enough vitamin D. Babies born prematurely are also at risk of developing rickets because they build up stores of vitamin D while they're in the womb. Babies who are exclusively breastfed, especially for longer than six months, may also be at risk of vitamin D deficiency.

This is why the Department of Health recommends that: pregnant and breastfeeding women should consider taking a daily supplement containing 10 micrograms (mcg) of vitamin D babies from birth to one year of age, whether exclusively or partially breastfed, should be given a daily supplement containing 8.5 to 10mcg of vitamin D, to make sure they get enough babies fed infant formula do not need a vitamin D supplement until they are receiving less than 500ml (about a pint) of infant formula a day, because infant formula is fortified with vitamin D children aged 1 to 4 years old should be given a daily supplement containing 10mcg of vitamin D For more information, read who should take vitamin D supplements . Genetic defect Rare forms of rickets can also occur in some inherited (genetic) disorders. For example, hypophosphatemic rickets is a genetic disorder where the kidneys and bones deal abnormally with phosphate. Phosphate binds to calcium and is what makes bones and teeth hard. This leaves too little phosphate in the blood and bones, leading to weak and soft bones. Other types of genetic rickets affect certain proteins in the body that are used by vitamin D.

Underlying conditions Occasionally, rickets develops in children with rare forms of kidney, liver and intestinal conditions. These can affect the absorption of vitamins and minerals. Page last reviewed: 21/12/2015 Rickets, Vitamin D Deficiency Rickets, Vitamin D Deficiency Important It is possible that the main title of the report Rickets, Vitamin D Deficiency is not the name you expected. Please check the synonyms listing to find the alternate name(s) and disorder subdivision(s) covered by this report. Synonyms None General Discussion Vitamin-D deficiency rickets, a disorder that becomes apparent during infancy or childhood, is the result of insufficient amounts of vitamin D in the body. The vitamin deficiency may be caused by poor nutrition , a lack of exposure to the sun, or malabsorption syndromes in which the intestines do not adequately absorb nutrients from foods. Vitamin D is needed for the metabolism of calcium and phosphorus in the body, which, in turn affects how calcium is deposited in the bones; thus it is considered essential for proper bone development and growth. Major symptoms of vitamin D deficiency rickets include bone disease, restlessness, and slow growth.

This disorder is rare in the United States but is not uncommon in certain areas of the world. Resources NIH/National Institute of Diabetes , Digestive & Kidney Diseases Office of Communications & Public Liaison Bldg 31, Rm 9A06 31 Center Drive, MSC 2560 Bethesda, MD 20892-2560 Internet: For a Complete Report This is an abstract of a report from the National Organization for Rare Disorders (NORD). A copy of the complete report can be downloaded free from the NORD website for registered users. The complete report contains additional information including symptoms, causes, affected population, related disorders, standard and investigational therapies (if available), and references from medical literature. For a full-text version of this topic, go to and click on Rare Disease Database under "Rare Disease Information". The information provided in this report is not intended for diagnostic purposes. It is provided for informational purposes only. NORD recommends that affected individuals seek the advice or counsel of their own personal physicians. It is possible that the title of this topic is not the name you selected.

Please check the Synonyms listing to find the alternate name(s) and Disorder Subdivision(s) covered by this report This disease entry is based upon medical information available through the date at the end of the topic. Since NORD's resources are limited, it is not possible to keep every entry in the Rare Disease Database completely current and accurate. Please check with the agencies listed in the Resources section for the most current information about this disorder. For additional information and assistance about rare disorders, please contact the National Organization for Rare Disorders at P.O.

Box 1968, Danbury, CT 06813-1968; phone (203) 744-0100; web site or email orphan@rarediseases.org Last Updated: 4/25/2008 Rickets | Definition of Rickets by Merriam-Webster noun plural but singular in construction rick·ets \ˈrik-əts\ Medical Definition of rickets : a deficiency disease that affects the young during the period of skeletal growth, is characterized especially by soft and deformed bones, and is caused by failure to assimilate and use calcium and phosphorus normally due to inadequate sunlight or vitamin D—called also rachitis; see osteomalacia Learn More about rickets Rickets, Vitamin D Deficiency - NORD (National Organization for Rare Disorders) Rickets, Vitamin D Deficiency Synonyms of Rickets, Vitamin D Deficiency Nutritional Rickets Vitamin-D Deficiency Rickets General Discussion Vitamin-D deficiency rickets, a disorder that becomes apparent during infancy or childhood, is the result of insufficient amounts of vitamin D in the body.

The vitamin deficiency may be caused by poor nutrition, a lack of exposure to the sun, or malabsorption syndromes in which the intestines do not adequately absorb nutrients from foods. Vitamin D is needed for the metabolism of calcium and phosphorus in the body, which, in turn affects how calcium is deposited in the bones; thus it is considered essential for proper bone development and growth. Major symptoms of vitamin D deficiency rickets include bone disease, restlessness, and slow growth. This disorder is rare in the United States but is not uncommon in certain areas of the world. Signs & Symptoms Symptoms of vitamin D deficiency rickets in infants may be restlessness, lack of sleep, slow growth, a delay in crawling, sitting or walking, thinness of the top and back of the skull (craniotabes), swelling of the skull (bossing), bead-like nodules where the ribs and their cartilages join due to the rapid growth of the arms and the rib cage (rachitic rosary), and a delay in the closing of the skull bone. Some doctors describe the symptoms of rickets as aches and pains and possible enlarged bones along with swelling at the joints such as wrists and ankles.

If vitamin D deficiency rickets is not treated, the ends of the long bones may become enlarged, the legs may become bowed and knock-knees may result. Muscles can become weak and the chest may become deformed due to the pull of the diaphragm on the ribs that have been weakened by rickets (Harrison’s groove). Abnormal development and decay of teeth may also occur. In more severe, untreated cases of this disorder the bones may become fragile and fractures may easily occur. Convulsions, muscle twitching and sharp bending of the wrist and ankle joints (tetany spasms) may also be present. Occasionally, when there is too little calcium in the blood due to the lack of vitamin D (hypocalcemia), mental retardation may occur. Causes Vitamin D deficiency rickets can be caused by a lack of vitamin D in the diet, a lack of exposure to the sun, or malabsorption syndromes in which there is an inability of the intestines to adequately absorb nutrients from foods. Nursing mothers who have a diet deficient in vitamin D may get rickets themselves and pass this condition on to the newborn child.

In areas of the world where cultural habits limit exposure to sun, or the amount of sun in a day or season is limited, Vitamin D deficiency rickets tends to be more prevalent. Affected Populations Vitamin D deficiency rickets affects males and females in equal numbers. Babies of nursing mothers whose diet is deficient in vitamin D can be affected with this disorder. Although vitamin D deficiency rickets is rare in the United States, children who are dark skinned and living in cloudy northern cities as well as children on restricted diets due to cultural or religious beliefs are more likely to develop this disorder. Rickets is more common in regions of Asia where there is a lack of daylight and/or low intake of meat due to a vegetarian diet. Northern Yemen and Kuwait are also areas where Vitamin D deficiency rickets are prevalent due to lack of exposure to the sun because of cultural practices. Related Disorders Symptoms of the following disorders can be similar to those of vitamin D deficiency rickets. Comparisons may be useful for a differential diagnosis: Fanconi’s syndrome is a rare disorder characterized by kidney dysfunction and bone abnormalities similar to those of vitamin D deficiency rickets. Excess amounts of phosphate, amino acids (usually bicarbonate), glucose, and uric acid are eliminated in the urine.

This disorder may be acquired through various causes or inherited as an autosomal recessive or, when associated with Lowe’s syndrome, an x-linked recessive genetic trait. Bone symptoms include rickets in children and softening of the bones (osteomalacia) in adults. Fanconi’s syndrome may be associated with a variety of inherited metabolic disorders such as cystinosis, Lowe’s syndrome, a form of ryrosinemia, hereditary fructose intolerance, Wilson’s disease, galactosemia and glycogen storage disorders. (For more information on this disorder choose “Fanconi” as your search term in the Rare Disease Database.) Infantile scurvy is a disease that is caused by a lack of vitamin C in the diet. Symptoms of this disorder may be anemia, weakness, sores in the mouth, loosening of the teeth, irritability, loss of appetite, failure to gain weight and bleeding under the tissue layer covering the bones. Scurvy is treated with large amounts of vitamin C . Lowe’s syndrome is a rare inherited, metabolic disorder characterized by eye abnormalities such as congenital cataracts and glaucoma, bone malformations caused by vitamin D resistant rickets, mental retardation and impairment of kidney function.

This disorder affects only males and is most common in those with fair coloring. Lowe’s Syndrome is transmitted through x-linked recessive genes. (For more information on this disorder choose “Lowe” as your search term in the Rare Disease Database.) Osteomalacia is a disorder characterized by a gradual softening and bending of the bones. Pain may occur in various degrees of severity. Softening occurs because solid bones have failed to form properly (calcify) due to the lack of vitamin D or a kidney dysfunction. This disorder is more common in females than males, and often begins during pregnancy. It can exist alone or in association with other disorders. Hypophosphatemic rickets is a rare genetic form of rickets characterized by impaired transport of phosphate and diminished vitamin D metabolism in the kidneys. Calcium and phosphate are not absorbed properly in the intestines which can lead to softening of bones. Major symptoms of this disorder include skeletal changes, weakness and slow growth. Cases affecting females are usually less severe than those affecting males. One rare acquired form of this disorder may be associated with a benign tumor.

(For more information on this disorder choose “Hypophosphatemic Rickets” as your search term in the Rare Disease Database.) Pseudovitamin D deficiency rickets (vitamin D dependent rickets, type I) is characterized by more severe skeletal changes and weakness than those of hypophosphatemic rickets. This disorder is caused by abnormal vitamin D metabolism and is inherited as an autosomal recessive trait. This type of rickets often begins earlier than hypophosphatemic rickets. Blood levels of calcium are severely diminished in patients with vitamin D dependent rickets. Amino acids become lost in the urine due to abnormal kidney function. Intermittent muscle cramps may occur. Convulsions and abnormalities of the spine and pelvis may also develop. Diagnosis In children, the suspected joints are X-rayed and characteristic changes in the bone may be detected. Blood tests to determine the levels of calcium and phosphorus will be undertaken as well. A bone biopsy is performed in difficult cases. Vitamin D deficiency rickets can be prevented by providing a normal balanced diet to infants and children, assuming that they are exposed to adequate amounts of sun.

Standard Therapies Treatment Treatment of vitamin D deficiency rickets is accomplished with doses of vitamin D given daily until the bone disease is cured. The dose of vitamin D can then be reduced to the daily recommended requirement. In more severe cases of vitamin D deficiency rickets when cramps, convulsions, muscle twitching and sharp bending of the ankle and wrist joints (tetany) is present the treatment with vitamin D is supplemented with calcium salts intravenously. In some instances surgery may be required to correct distortions of bone and muscle. Investigational Therapies Information on current clinical trials is posted on the Internet at All studies receiving U.S. government funding, and some supported by private industry, are posted on this government web site. For information about clinical trials being conducted at the NIH Clinical Center in Bethesda, MD, contact the NIH Patient Recruitment Office: Tollfree: (800) 411-1222 References TEXTBOOKS Beers MH, Berkow R., eds. The Merck Manual, 17th ed. Whitehouse Station, NJ: Merck Research Laboratories; 1999:35-38. Berkow R., ed.

The Merck Manual-Home Edition.2nd ed. Whitehouse Station, NJ: Merck Research Laboratories; 2003:894. Larson DE. ed. Mayo Clinic Family Health Book. New York, NY: William Morrow and Company, Inc; 1996:896-97. Bennett JC, Plum F. Eds. Cecil Textbook of Medicine. 20th ed. W.B. Saunders Co., Philadelphia, PA; 1996:1359-65. REVIEW ARTICLES Collier S, Fulhan J, Duggan C. Nutrition for the pediatric office: update on vitamins, infant feeding, and food allergies. Curr Opin Pediatr. 2004;16:314-20. Reginato AJ, Coquia JA. Musculoskeletal manifestations of osteomalacia and rickets. Best Pract Res Clin Rheumatol. 2003;17:1063-80. Hollis BW, Wagner CL. Assessment of dietary vitamin D requirements during pregnancy and lactation. Am J Clin Nutr.

2004;79:717-26. Molgaard C, Michaelsen KF. Vitamin D and bone health in early life. Proc Nutr Soc. 2003;62:823-28. Berg EE. Rickets. Orthop Nurs. 2004;23:53-55. Specker B. Nutrition influences bone development from infancy through toddler years. J Nutr. 2004;134:691S-695S. Heaney RP. Long-latency deficiency disease: insights from calcium and vitamin D. Am J Clin Nutr. 2003;78:912-19. Wharton B, Bishop N. Rickets. Lancet. 2003;362:1389-400. Gartner LM, Greer FR, et al. Prevention of Rickets and Vitamin D Deficiency: New Guidelines for Vitamin D Intake. Pediatrics. 2003;111:908-10.

FROM THE INTERNET Years Published 1992, 1995, 2005 The information in NORD’s Rare Disease Database is for educational purposes only and is not intended to replace the advice of a physician or other qualified medical professional. The content of the website and databases of the National Organization for Rare Disorders (NORD) is copyrighted and may not be reproduced, copied, downloaded or disseminated, in any way, for any commercial or public purpose, without prior written authorization and approval from NORD. Individuals may print one hard copy of an individual disease for personal use, provided that content is unmodified and includes NORD’s copyright. National Organization for Rare Disorders (NORD) 55 Kenosia Ave., Danbury CT 06810 • (203)744-0100 Report Index Rickets - Better Health Channel Rickets Bones muscles and joints - Bone and bone marrow conditions Summary Rickets is a preventable bone disease that affects infants and young children and causes soft and weakened bones. Rickets is caused by a lack of vitamin D, calcium or phosphorus.

Vitamin D deficiency can occur as a result of having dark skin, lack of exposure of the skin to sunlight, nutritional deficiencies and disorders of the liver, kidney or small intestine. Treatment options include improved sunlight exposure, diet, vitamin D and mineral supplements. Rickets is a bone disease that affects infants and young children. The child’s growing bones fail to develop properly due to a lack of vitamin D. This can result in soft and weakened bones, fractures, bone and muscle pain, and bony deformities. You can help protect your child from the effects of rickets by understanding their risk factors for vitamin D deficiency and taking steps to prevent it. Children with naturally dark skin or inadequate exposure to sunlight are among those most commonly affected. Having a mother with vitamin D deficiency also increases a child’s risk. Other causes may be nutritional deficiencies and disorders of the liver, kidney or small intestine. A similar condition can occur in adults, but this is called osteomalacia. Although rare, rickets is on the increase among Australian children. Overuse of sun protection, due to increased concerns about skin cancer risks, is thought to be one reason for the increase.

If you think your child has rickets or is at risk of vitamin D deficiency, it is important to consult your family doctor or health care provider. They can help you decide on an appropriate treatment plan for your child. Signs and symptoms Signs and symptoms of rickets can include: Painful bones, muscle weakness, cramps and spasms Slowed growth and development Increased risk of broken bones, including spontaneous breaks that occur by themselves without pressure or trauma Dental problems such as teeth failing to form or being slow to emerge, deformed teeth or soft tooth enamel Prominent forehead and a large front fontanelle (soft spot) in infants Deformities of the skeleton such as bowed legs, kyphosis (‘hunch-back’), scoliosis (sideways curves of the spine), outward jutting breastbone or abnormal skull shape.

A range of causes Some of the contributing factors and causes of rickets include: Not enough exposure of the skin to sunlight Skin colour – the skin pigment in children with naturally dark skin tends to absorb less sunlight than fair skin Lack of vitamin D or calcium in the diet Exclusive breastfeeding (without vitamin D supplements) of infants whose mothers have vitamin D deficiency Disorders of the intestine, liver or kidneys that prevent the body from absorbing vitamin D or converting it into its active form Disorders that reduce digestion or absorption of fats, as vitamin D is a fat-soluble vitamin. The role of vitamin D Our body needs vitamin D to help it absorb calcium and phosphorus. These minerals are essential for the growth and development of strong, healthy bones. Lack of vitamin D reduces the body’s ability to control the levels of these vital minerals and increases a child’s risk of developing rickets. About 80 per cent of our vitamin D comes from exposure to the sun. When direct sunlight hits our skin, the ultraviolet radiation converts a skin substance called 7-dehydrocholesterol into vitamin D. There are also very small amounts of vitamin D in some foods. However, food sources alone are usually not enough to maintain the levels of Vitamin D that our body needs.

Once vitamin D is made in the skin or absorbed from food through the intestine, it is changed into its active form – a hormone – by the liver and kidneys. It is then available to help our body build strong bones and teeth, through the process of ‘mineralisation’. High-risk groups Children who may be at increased risk of rickets due to vitamin D deficiency include children who: Are born to women with a vitamin D deficiency Cover most of their body for religious or cultural reasons Are sick, disabled or unable to spend time outdoors for other reasons Never go outside without sunscreen Have naturally very dark skin Have some medical conditions such as certain bowel diseases Are on vegetarian, dairy-free or lactose-free diets. Diagnosis Rickets may be diagnosed using a number of tests including: Physical examination Treatment options for rickets include: Improved sunlight exposure Improved diet that includes adequate intake of calcium and vitamin D Oral vitamin D supplements – these may need to be taken for about three months Special forms of vitamin D supplements – for people whose bodies can’t convert vitamin D into its active form Treatment for any underlying disorder Surgery to correct bone deformities. High-dose supplements of vitamin D are available in Australia. These require special prescription by a doctor.

The use of this special form of vitamin D supplement may be the most effective option for the treatment of rickets. Your doctor can advise you about this. Long-term outlook Bones that are poorly mineralised respond very quickly to dietary supplementation with calcium and vitamin D. Improvements can be seen on x-ray after only a few days of treatment. If rickets is treated when the child is young, there is every chance that the skeletal deformities will disappear as the child matures. However, the deformities and reduced height will be permanent if the child goes through puberty without treatment. Prevention You can help protect your child from the effects of rickets by understanding their risk factors for vitamin D deficiency and taking steps to prevent it. Suggestions include: Sunlight – a sensible balance of sun exposure and sun protection can protect against vitamin D deficiency without putting your child at risk of skin cancer. The recommended amount of sunlight each day is a few minutes of sunlight exposure before 10am and after 3pm each day (from September to April) and two to three hours of sunlight exposure over the week (from May to August). Always protect your child’s skin from the sun during peak UV times with clothing, shade and/or sunscreen.

Diet – include food rich in vitamin D and calcium in your child’s diet. Foods naturally containing vitamin D include oily fish (especially sardines, salmon, herring and mackerel), liver and egg yolks. Foods ‘fortified’ with vitamin D include some margarines and some milks (including fortified baby formula milk). Supplements – consult with your child’s doctor or health provider about whether your child should be prescribed supplements. Be SunSmart UV radiation levels vary depending on location, time of year, time of day, cloud coverage and the environment. Babies and young children need extra protection due to their sensitive skin. Australia’s high UV radiation levels mean that most children get more than enough Vitamin D, even when outdoors for very short periods with small amounts of skin exposed. People with very dark skin may need three to four times longer in the sun than people with fair skin. This is because the pigments in dark skin slow down the chemical reaction that leads to the production of vitamin D. Children who are outdoors for prolonged periods of time, have very fair skin or have a family history of skin cancer may need to use sunscreen outside the recommended hours. Talk to your doctor for further information.

Where to get help Rickets - Symptoms, Diagnosis, Treatment of Rickets - NY Times Health Information Back to Top Causes Vitamin D helps the body control calcium and phosphate levels. If the blood levels of these minerals become too low, the body may produce hormones that cause calcium and phosphate to be released from the bones. This leads to weak and soft bones. Vitamin D is absorbed from food or produced by the skin when exposed to sunlight. Lack of vitamin D production by the skin may occur in people who: Live in climates with little exposure to sunlight Must stay indoors Work indoors during the daylight hours You may not get enough vitamin D from your diet if you: Are lactose intolerant (have trouble digesting milk products) Do not drink milk products Follow a vegetarian diet Infants who are breastfed only may develop vitamin D deficiency. Human breast milk does not supply the proper amount of vitamin D. This can be a particular problem for darker-skinned children in winter months (when there are lower levels of sunlight). Not getting enough calcium and phosphorous in your diet can also lead to rickets. Rickets caused by a lack of these minerals in diet is rare in developed countries, because calcium and phosphorous are found in milk and green vegetables.

Your genes may increase your risk of rickets. Hereditary rickets is a form of the disease that is passed down through families. It occurs when the kidneys are unable to hold onto the mineral phosphate. Rickets may also be caused by kidney disorders that involve renal tubular acidosis . Disorders that reduce the digestion or absorption of fats will make it more difficult for vitamin D to be absorbed into the body. Occasionally, rickets may occur in children who have disorders of the liver, or who cannot convert vitamin D to its active form. Rickets is rare in the United States. It is most likely to occur in children during periods of rapid growth, when the body needs high levels of calcium and phosphate. Rickets may be seen in children ages 6 - 24 months. It is uncommon in newborns. Back to Top Treatment The goals of treatment are to relieve symptoms and correct the cause of the condition. The cause must be treated to prevent the disease from returning. Replacing calcium, phosphorus, or vitamin D that is lacking will eliminate most symptoms of rickets. Dietary sources of vitamin D include fish, liver, and processed milk. Exposure to moderate amounts of sunlight is encouraged.

If rickets is caused by a metabolic problem, a prescription for vitamin D supplements may be needed. Positioning or bracing may be used to reduce or prevent deformities. Some skeletal deformities may require corrective surgery. Back to Top Outlook (Prognosis) The disorder may be corrected by replacing vitamin D and minerals. Laboratory values and x-rays usually improve after about 1 week, although some cases may require large doses of minerals and vitamin D. If rickets is not corrected while the child is still growing, skeletal deformities and short stature may be permanent. If it is corrected while the child is young, skeletal deformities often improve or disappear with time. Back to Top When to Contact a Medical Professional Call your child's health care provider if you notice symptoms of rickets. Back to Top Prevention You can prevent rickets by making sure that your child gets enough calcium, phosphorus, and vitamin D in the diet. People who have gastrointestinal or other disorders may need to take supplements. Ask your child's health care provider. Kidney (renal) causes of poor vitamin D absorption should be treated right away. People who have renal disorders should have their calcium and phosphorus levels monitored regularly.

Genetic counseling may help people who have a family history of inherited disorders that can cause rickets. Greenbaum LA. Rickets and hypervitaminosis D. In: KliegmanRM, Behrman RE, Jenson HB, Stanton BF, eds. Nelson Textbook of Pediatrics . 19th ed. Philadelphia, Pa: Saunders Elsevier; 2011:chap 48. More Information on This Topic News & Features Review Date: 8/1/2012 Reviewed By: Neil K. Kaneshiro, MD, MHA, Clinical Assistant Professor of Pediatrics, University of Washington School of Medicine. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M. Health Solutions, Ebix, Inc. A.D.A.M., Inc. is accredited by URAC, also known as the American Accreditation HealthCare Commission ( URAC's accreditation program is an independent audit to verify that A.D.A.M. follows rigorous standards of quality and accountability. A.D.A.M. is among the first to achieve this important distinction for online health information and services. Learn more about A.D.A.M.'s editorial policy, editorial process and privacy policy.

A.D.A.M. is also a founding member of Hi-Ethics and subscribes to the principles of the Health on the Net Foundation ( A.D.A.M. Copyright The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed medical professional should be consulted for diagnosis and treatment of any and all medical conditions. Call 911 for all medical emergencies. Links to other sites are provided for information only -- they do not constitute endorsements of those other sites. © 1997- 2008 A.D.A.M., Inc. Any duplication or distribution of the information contained herein is strictly prohibited. 4 Diseases Caused by a Lack of Essential Vitamins and Minerals | Mental Floss 4 Diseases Caused by a Lack of Essential Vitamins and Minerals Retronaut.com Like us on Facebook Companies pushing products with added vitamins and minerals can fool people into thinking that they’re eating a “healthy” food when they’re not—but it’s not like those vitamins and minerals are there for no reason. For much of human history, diseases of nutrient deficiency were the norm, and in some parts of the world, they still persist.

Even into the 20th century, conditions caused by a lack of certain vitamins or minerals were endemic to North America and Europe. Artificially added nutrients may not make a food “healthy,” but they do stave off several debilitating, and sometimes fatal, diseases of malnutrition. Here are a few of those maladies. 1. Scurvy Courtesy of The Diseases of Infancy and Childhood The disease of pirates: the grey-death. Scurvy is caused by a lack of vitamin C, whose chemical name, ascorbic acid, is derived from the Latin term for scurvy, scorbutus. Even though the disease was known since ancient times (described by Hippocrates around 400 BCE), it was not a scourge to those who were largely land-bound. Even though its causes were unknown, many cultures realized that eating certain herbs could reverse the symptoms, and as long as there was access to fresh food, it was generally kept under control. Scurvy didn’t become a significant problem until the Age of Discovery (beginning in the 15th century), when people at sea were not able to access that much-needed fresh food for months at a time.

Preserved meats and carbohydrates contained no vitamin C, and unlike most animals, the human body is not able to create vitamin C on its own. The early symptoms of scurvy include spongy gums, pain in the joints, and blood spots appearing under the skin. As the disease progressed, the teeth would become loose, extreme halitosis (bad breath) would develop, the afflicted would become too weak to walk or work, be in too much pain to eat, and would die “mid-sentence,” often from a burst blood vessel. Many of the early explorers lost great numbers of men to scurvy : Vasco de Gama lost 116 out of 170 men in 1499, and in 1520, Magellan lost 208 out of 230. A few deaths were attributable to other causes, but the vast majority were due to scurvy.

Courtesy of TaussMarine.com Despite not being able to pinpoint the exact cause of scurvy, in the 18th century, Naval physician James Lind was able to prove , in what’s considered to be the first controlled scientific experiment, that scurvy could be prevented (and cured) by incorporating citrus fruits such as limes and oranges into the diet of sailors. Although his findings weren’t widely accepted at first, the British Navy eventually began issuing standard rations of lemon juice, and later, limes, to their sailors—which gave rise to the term “limey” in reference to the British. These days, scurvy is an extremely rare condition, almost exclusively caused by someone eating a completely unvaried diet . In most cases, high levels of oral supplementation of vitamin C are enough to reverse the condition in a matter of weeks, and death by scurvy is almost unheard of. 2. Rickets Courtesy of Blatner.com This condition is brought on by a lack of vitamin D, which causes the body to be unable to absorb or deposit calcium. Less commonly, it can also be caused by a lack of calcium or phosphorus, but vitamin D deficiency is by far the most common cause.

Unlike vitamin C, the human body is able to produce vitamin D, but only if it has the metabolic precursors available to it. When the skin is exposed to ultraviolet light (such as from the sun), cholesterol in the skin reacts and forms cholecalciferol, which is then processed in the liver and kidneys to create the active form of vitamin D. Even with a nominally healthy diet, without enough sun exposure, the body can’t produce the vitamin D precursors on its own. This is actually re-emerging as a health concern among some increasingly-indoor groups of people, and is one of the few hypovitaminosis (lack of vitamin) conditions not considered to be a “disease of the past.” Luckily, when the deficiency is recognized, cholecalciferol can be directly taken as a vitamin supplement or acquired from eating organ meats and oils, such as cod liver oil, allowing the body to resume producing vitamin D. Rickets is a condition of children, as the deficiency’s most severe effects are on developing bones; in adults, “bone-softening,” or osteomalacia, can be caused by the same vitamin deficiency.

But in adults, it both takes significantly longer to develop and tends to cause tip-off signs that something is wrong before bone warping sets in, such as extreme pain in the bones, and unexplained muscle weakness. In children, especially those that don’t or can’t receive regular check-ups, deformity and debilitation by the deficiency is often only noticed after significant damage has been done to their developing skeletons. The most telling symptoms of rickets are at the epiphyses (growth plates) of bones: The body is unable to lengthen bones by depositing calcium, and ends up with bones that flare outward in a “cupping” appearance. This leads to costochondral swelling, or what’s known as the “rachitic rosary” along the ribcage of the child, as well as widened wrists and “thick” joints. Before widened wrists or rachitic rosary appears, the softening of the skull bones can lead to “Caput Quadratum”—a square-headed appearance, and often the first sign of skeletal growth problems. If left untreated, rickets also can cause an extremely curved back, stunted growth, and frequent fractures—all of which can lead to permanent and debilitating deformity. 3.

Beriberi Courtesy of Wikimedia Commons This condition is largely confined to Asia, especially in countries where boiled rice is a staple. The Sinhalese term “beri-beri” means, “I cannot, I cannot,” and derives from the inability to perform even the simplest of tasks once the polyneuritis (nerve inflammation) caused by the deficiency of vitamin B1 (thiamine) has permanently damaged the neurons, when the condition has progressed to the end-stage. Although beriberi was known to exist in rice-eating countries several centuries back , its prevalence boomed with the introduction of steam-driven rice-polishing mills from Europe. The superior taste of the milled white rice led many locals to abandon the local (unpolished) brown rice, and in doing so, abandon their primary source of thiamine. From the 1860s to the turn of the 20th century, people whose plant consumption was limited to the polished white rice would often come down with weakness, pain, weight loss, difficulty walking, and emotional disturbances. Beriberi became one of the leading causes of mortality in the region.

In the 1880s, a doctor named Christiaan Eijkman began researching the causes of this epidemic at a laboratory in the Dutch East Indies (now Jakarta, Indonesia), and initially believed that the condition was caused by a bacterial infection. However, after years of study, he came to the conclusion that “white rice is poisonous.” He discovered this by feeding a group of chickens solely white rice, and another group unpolished brown rice. The chickens that ate the white rice came down with beriberi-like symptoms, while the others stayed healthy. Eijkman also discovered that when the chickens fed white rice were subsequently fed brown rice, they recovered from their illness! Later dietary testing on prisoners confirmed his results. Even though he didn’t know the cause of the condition, Eijkman proved that white rice was the culprit, and shared the 1929 Nobel Prize in Medicine for his discovery. Beriberi is occasionally seen in the modern world, but its primary cause is chronic alcoholism —the poor diets of some chronic alcoholics, combined with the decreased absorption of what thiamine is consumed, leads to symptoms that unfortunately are sometimes left undiagnosed until it’s too late.

Recently, beriberi was also seen in Haitian prisons , when the prison system began buying imported polished rice from the United States, and stopped feeding their inmates the local brown rice. 4. Pellagra Courtesy of Open Library What causes blistering of the skin in the sun, pale skin, a craving for raw meat, blood dripping from the mouth, aggression, and insanity? If you answered “vampirism,” you’re close—the myth of the vampire may have its roots in the condition known as “pellagra.” Pellagra is caused by a lack of vitamin B3 (niacin). First identified and commonly diagnosed in the Asturian Empire (now Northern Spain), it was originally called “Asturian leprosy.” However, the condition was seen throughout Europe, the Middle East, and North Africa, wherever a large percentage of food energy was derived from corn, and fresh meat was not available. The area of highest prevalence was Northern Italy, where Francesco Frapoli of Milan called it “pelle agra,” meaning “sour skin.” It was initially believed that either the corn itself, or some insect associated with corn, was causing pellagra.

This belief was reinforced when much of France eliminated corn as a food staple and virtually eradicated the condition. Between the era that corn was introduced to Europe (the early 16th century) and the late 19th century, pellagra was found almost everywhere that poor people subsisted on cornmeal and little else. Around the turn of the 20th century, people began to notice that despite subsisting on just as much corn as poor Europeans, poor Mesoamerican natives didn’t come down with the condition. It was eventually discovered that this was because the traditional processing of corn in the Americas involved “ nixtamalization ,” in which the kernels were soaked in limewater before hulling them. The alkali solution freed up the niacin that was present in the grain, but previously inaccessible. Despite the extensive work of Dr. Joseph Goldberger in the 1910s and 1920s , which proved that pellagra wasn’t caused by a germ but by a dietary deficiency, the condition was occurring in epidemic proportions in the rural Southern US until the 1940s.

Today, pellagra is most common in the poorest regions of the world, especially places that rely upon food aid programmes. Some countries still ship unfortified cornmeal rather than corn masa (nixtamalized corn) or fortified cornmeal to developing countries or to their own impoverished populations. China, parts of Africa, Indonesia, and North Korea all have endemic pellagra among their lowest classes. ******* The discovery of important vitamins and how to produce them has been so significant to human health that many of those who were integral to the discoveries have been awarded the Nobel Prize in Medicine; more than 10 Nobel Prizes have been divided among almost 20 eminent scientists for the discovery or isolation of vitamins A, B1, B12, C, D, E, and K. Over the second half of the 20th century, after the beginning of widespread supplementation to everyday food items, the incidences of the conditions covered here went down dramatically across much of the world. Of course, the minerals essential to the human body play similarly important roles in maintaining health. However, humans have not historically had a widespread significant problem acquiring these nutrients, as most plants absorb many minerals from the soil.

With the increased processing of our food throughout the 20th century, however, some of these minerals have been lost, and have had to be re-added to the average Western diet through supplementation. In the rest of the world, displacement due to war, and unfortified food from aid programmes, has left survivors with enough calories, but not enough nutrients. Supplementation of assistance food and local fortification of salt and flour is beginning to help give displaced people (especially displaced children) a new chance at life without these and other nutritional diseases. In the developed world, you won’t be the healthiest bloke on the block if you eat nothing but breakfast cereal and cartons of juice—but the food industry has ensured that you at least won’t die of malnutrition. Even people with healthy diets benefit from the supplementation of vitamins and minerals in common foodstuffs, and adding the nutrients costs next to nothing. Doctors and nutritionists still agree that the healthiest way to acquire your necessary vitamins and minerals is by eating a balanced diet and spending time outdoors each day, but in the course of modern life, that’s not always possible, and if people are going to eat poorly either way, we may as well keep them from dropping dead of scurvy!

Question: The disease rickets is caused by the lack of which vitamin?
Answer: Vitamin D