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Vitamin D

Vitamin D

Description

Vitamin D, also known as calciferol, is essential for strong teeth and bones. There are two major forms of vitamin D: D2 or ergocalciferol and D3 or cholecarciferol. Vitamin D can be synthesized by the body in the presence of sunlight, as opposed to being required in the diet. It is the only vitamin whose biologically active formula is a hormone. It is fat-soluble, and regulates the body's absorption and use of the minerals calcium and phosphorus . Vitamin D is important not only to the maintenance of proper bone density, but to the many calcium-driven neurologic and cellular functions, as well as normal growth and development. It also assists the immune system by playing a part in the production of a type of white blood cell called the monocyte. White blood cells are infection fighters. There are many chemical forms of vitamin D, which have varying amounts of biological activity.

General use

The needed amount of vitamin D is expressed as an Adequate Intake (AI) rather than an Required Daily Amount (RDA). This is due to a difficulty in quantifying the amount of the vitamin that is produced by the body with exposure to sunlight. Instead, the AI estimates the amount needed to be eaten in order to maintain normal function. It is measured in International Units (IU) and there are 40 IU in a microgram (mcg). The AI for vitamin D in the form of cholecarciferol or ergocalciferol for everyone under 50 years of age, including pregnant and lactating women, is 200 IU. It goes up to 400 IU for people 51-70 years old, and to 600 IU for those over age 70. A slightly higher dose of vitamin D, even as little as a total of 700 IU for those over age 65, can significantly reduce age-related fractures when taken with 500 mg of calcium per day.

One of the major uses of vitamin D is to prevent and treat osteoporosis . This disease is essentially the result of depleted calcium, but calcium supplements alone will not prevent it since vitamin D is required to properly absorb and utilize calcium. Taking vitamin D without the calcium is also ineffective. Taking both together may actually increase bone density in postmenopausal women, who are most susceptible to bone loss and complications such as fractures.

Osteomalacia and rickets are also effectively prevented and treated through adequate vitamin D supplementation. Osteomalacia refers to the softening of the bones that occurs in adults that are vitamin D deficient. Rickets is the syndrome that affect deficient children, causing bowed legs, joint deformities, and poor growth and development.

Vitamin D also has a part in cancer prevention, at least for colon cancer. A deficiency increases the risk of this type of cancer, but there is no advantage to taking more than the AI level. There may also be a protective effect against breast and prostate cancer , but this is not as well established. Studies are in progress to see if it can help to treat leukemia and lymphoma. The action of at least one chemotherapeutic drug, tamoxifen, appears to be improved with small added doses of vitamin D. Tamoxifen is commonly used to treat ovarian, uterine, and breast cancers.

Many older adults are deficient in vitamin D. This can affect hearing by causing poor function of the small bones in the ear that transmit sound. If this is the cause of the hearing loss , it is possible that supplementation of vitamin D can act to reverse the situation.

Some metabolic diseases are responsive to treatment with specific doses and forms of vitamin D. These include Fanconi syndrome and familial hypophosphatemia, both of which result in low levels of phosphate. For these conditions, the vitamin is given in conjunction with a phosphate supplement to aid in absorption.

A topical form of vitamin D is available, and can be helpful in the treatment of plaque-type psoriasis . It may also be beneficial for those with vitiligo or scleroderma. This cream, in the form of calcitriol, is not thought to affect internal calcium and phosphorus levels. Oral supplements of vitamin D are not effective for psoriasis. The cream is obtainable by prescription only.

Evidence does not support the use of vitamin D to treat alcoholism, acne , arthritis, cystic fibrosis, or herpes.

Preparations

Natural sources

Exposure to sunlight is the primary method of obtaining vitamin D. In clear summer weather, approximately ten minutes per day in the sun will produce adequate amounts, even when only the face is exposed. In the winter, it may require as much as two hours. Many people don't get that amount of winter exposure, but are able to utilize the vitamin that was stored during extra time in the sun over the summer. Sunscreen blocks the ability of the sun to produce vitamin D, but should be applied as soon as the minimum exposure requirement has passed, in order to reduce the risk of skin cancer . The chemical 7-dehydrocholesterol in the skin is converted to vitamin D3 by sunlight. Further processing by first the liver, and then the kidneys, makes D3 more biologically active. Since it is fat-soluble, extra can be stored in the liver and fatty tissues for future use. Vitamin D is naturally found in fish liver oils, butter, eggs, and fortified milk and cereals in the form of vitamin D2. Milk products are the main dietary source for most people. Other dairy products are not a good supply of vitamin D, as they are made from unfortified milk. Plant foods are also poor sources of vitamin D.

Supplemental sources

Most oral supplements of vitamin D are in the form of ergocalciferol. It is also available in topical (calcitriol or calcipotriene), intravenous (calcitriol), or intramuscular (ergocalciferol) formulations. Products designed to be given by other than oral routes are by prescription only. As with all supplements, vitamin D should be stored in a cool, dry place, away from direct light, and out of the reach of children.

Deficiency

In adults, a mild deficiency of vitamin D may be manifested as loss of appetite and weight, difficulty sleeping, and diarrhea . A more major deficiency causes osteomalacia and muscle spasm. The bones become soft, fragile, and painful as a result of the calcium depletion. This is due to an inability to properly absorb and utilize calcium in the absence of vitamin D. In children, a severe lack of vitamin D causes rickets.

Risk factors for deficiency

The most likely cause of vitamin D deficiency is inadequate exposure to sunlight. This can occur with people who don't go outside much, those in areas of the world where pollution blocks ultraviolet (UV) light or where the weather prohibits spending much time outdoors. Glass filters out the rays necessary for vitamin formation, as does sunscreen. Those with dark skin may also absorb smaller amounts of the UV light necessary to effect conversion of the vitamin. In climates far to the north, the angle of the sun in winter may not allow adequate UV penetration of the atmosphere to create D3 Getting enough sun in the summer, and a good dietary source, should supply enough vitamin D to last through the winter. Vegans, or anyone who doesn't consume dairy products in combination with not getting much sun is also at higher risk, as are the elderly, who have a decreased ability to synthesize vitamin D.

Babies are usually born with about a nine-month supply of the vitamin, but breast milk is a poor source. Those born prematurely are at an increased risk for deficiency of vitamin D and calcium, and may be prone to tetany. Infants past around nine months old who are not getting vitamin D fortified milk or adequate sun exposure are at risk of deficiency.

People with certain intestinal, liver and kidney diseases may not be able to convert vitamin D3 to active forms, and may need at activated type of supplemental vitamin D.

Those taking certain medications may require supplements, including anticonvulsants, corticosteroids, or the cholesterol-lowering medications cholestyramine or colestipol. This means that people who are on medication for arthritis, asthma, allergies , autoimmune conditions, high cholesterol, epilepsy , or other seizure problems should consult with a healthcare practitioner about the advisability of taking supplemental vitamin D. As with some other vitamins, the abuse of alcohol also has a negative effect. In the case of vitamin D, the ability to absorb and store it is diminished by chronic overuse of alcohol products.

Populations with poor nutritional status may tend to be low on vitamin D, as well as other vitamins. This can be an effect of poor sun exposure, poor intake, or poor absorption. A decreased ability to absorb oral forms of vitamin D may result from cystic fibrosis or removal of portions of the digestive tract. Other groups who may need higher than average amounts of vitamin D include those who have recently had surgery, major injuries, or burns . High levels of stress and chronic wasting illnesses also tend to increase vitamin requirements.

Precautions

The body will not make too much vitamin D from overexposure to sun, but since vitamin D is stored in fat, toxicity from supplemental overdose is a possibility. Symptoms are largely those of hypercalcemia, and may include high blood pressure, headache , weakness, fatigue , heart arrhythmia, loss of appetite, nausea, vomiting , diarrhea, constipation, dizziness , irritability, seizures, kidney damage, poor growth, premature hardening of the arteries, and pain in the abdomen, muscles, and bones. If the toxicity progresses, itching and symptoms referable to renal disease may develop, such as thirst, frequent urination, proteinuria, and inability to concentrate urine. Overdoses during pregnancy may cause fetal abnormalities. Problems in the infant can include tetany, seizures, heart valve malformation, retinal damage, growth suppression, and mental retardation. Pregnant women should not exceed the AI, and all others over one year of age should not exceed a daily dose of 2000 IU. Infants should not exceed 1000 IU. These upper level doses should not be used except under the advice and supervision of a healthcare provider due to the potential for toxicity.

Individuals with hypercalcemia, sarcoidosis, or hypoparathyroidism should not use supplemental calciferol. Those with kidney disease, arteriosclerosis, or heart disease should use ergocalciferol only with extreme caution and medical guidance.

Side effects

Minor side effects may include poor appetite, constipation, dry mouth , increased thirst, metallic taste, or fatigue. Other reactions, which should prompt a call to a healthcare provider, can include headache, nausea, vomiting, diarrhea, or confusion.

Interactions

The absorption of vitamin D is improved by calcium, choline, fats, phosphorus, and vitamins A and C. Supplements should be taken with a meal to optimize absorption.

There are a number of medications that can interfere with vitamin D levels, absorption, and metabolism. Rifampin, H2 blockers, barbiturates, heparin, isoniazid, colestipol, cholestyramine, carbamazepine, phenytoin, fosphenytoin, and phenobarbital reduce serum levels of vitamin D and increase metabolism of it. Anyone who is on medication for epilepsy or another seizure disorder should check with a healthcare provider to see whether it is advisable to take supplements of vitamin D. Overuse of mineral oil, Olestra, and stimulant laxatives may also deplete vitamin D. Osteoporosis and hypocalcemia can result from long-term use of corticosteroids. It may be necessary to take supplements of calcium and vitamin D together with this medication. The use of thiazide diuretics in conjunction with vitamin D can cause hypercalcemia in individuals with hypoparathyroidism. Concomitant use of digoxin or other cardiac glycosides with vitamin D supplements may lead to hypercalcemia and heart irregularities. The same caution should be used with herbs containing cardiac glycosides, including black hellebore, Canadian hemp, digitalis, hedge mustard, figwort, lily of the valley, motherwort , oleander, pheasant's eye, pleurisy , squill, and strophanthus.

Resources

BOOKS

Bratman, Steven, and David Kroll. Natural Health Bible. CA Prima Publishing, 1999.

Feinstein, Alice. Prevention's Healing with Vitamins. PA: Rodale Press, 1996.

Griffith, H. Winter. Vitamins, Herbs, Minerals & Supplements: The Complete Guide. AZ: Fisher Books, 1998.

Jellin, Jeff, Forrest Batz, and Kathy Hitchens. Pharmacist's letter/Prescriber's Letter Natural Medicines Comprehensive Database. CA: Therapeutic Research Faculty, 1999.

Pressman, Alan H., and Sheila Buff. The Complete Idiot's Guide to Vitamins and Minerals. New York: Alpha Books, 1997.

Judith Turner

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Turner, Judith. "Vitamin D." Gale Encyclopedia of Alternative Medicine. 2005. Encyclopedia.com. 25 Sep. 2016 <http://www.encyclopedia.com>.

Turner, Judith. "Vitamin D." Gale Encyclopedia of Alternative Medicine. 2005. Encyclopedia.com. (September 25, 2016). http://www.encyclopedia.com/doc/1G2-3435100814.html

Turner, Judith. "Vitamin D." Gale Encyclopedia of Alternative Medicine. 2005. Retrieved September 25, 2016 from Encyclopedia.com: http://www.encyclopedia.com/doc/1G2-3435100814.html

Vitamin D Deficiency

Vitamin D deficiency

Definition

Vitamin D deficiency exists when the concentration of 25-hydroxy-vitamin D (25-OH-D) in the blood serum occurs at 12 nanograms/milliliter (ng/ml) or less. This is one-half to one-fourth the amount normally present. When vitamin D deficiency continues for many months in growing children, the disease commonly referred to as rickets occurs.

Description

Vitamin D is a fat-soluble vitamin, meaning it can be dissolved in fat. While some vitamin D is supplied by the diet, most of it is made in the body. To make vitamin D, cholesterol, a substance widely distributed in animal tissues, the yolk of eggs, and various oils and fats, is necessary. Once cholesterol enters the body, a slight alteration in the cholesterol molecule occurs, with one change taking place in the skin. This alteration requires ultraviolet light, a component of sunlight. Vitamin D deficiency and rickets tend to occur in children who do not get enough sunlight and who do not eat foods that are rich in vitamin D.

Once consumed or made in the body, vitamin D is further altered to produce a substance called 1,25-dihydroxy-vitamin D (1,25-diOH-D). The conversion of vitamin D to 1,25-diOH-D occurs in the liver and kidney. The role of 1,25-diOH-D in the body is to keep the concentration of calcium at a constant level in the bloodstream. Maintaining calcium at a constant level is absolutely required for human life, since dissolved calcium is required for nerves and muscles to work. One of the ways in which 1,25-diOH-D accomplishes this is by stimulating the absorption of dietary calcium by the intestines.

The sequence of events that can lead to vitamin D deficiency and later to bone disease, is as follows: a lack of vitamin D in the body creates an inability to manufacture 1,25-diOH-D. This results in decreased absorption of dietary calcium and an increased loss of calcium in the feces. When this happens, the bones are affected. Vitamin D deficiency results in a lack of bone mineralization (calcification) in growing children.

Demographics

Vitamin D deficiency is not common in the United States and other industrialized countries because of the wide availability of vitamin D fortified infant formulas and milks. It is somewhat more common in northern areas where there is not as much sunlight present during many parts of the year. Vitamin D deficiency is also slightly more common in inner city areas, because environmental factors, such as smog, can block the necessary ultraviolet (UV) component of sunlight. Children with darkly pigmented skin are more likely to be vitamin D deficient than light skinned children. Children who are exclusively breast-fed without vitamin D supplementation, particularly if they are not exposed to sunlight, are at higher risk of vitamin D deficiency.

Causes and symptoms

Vitamin D deficiency can be caused by conditions that result in little exposure to sunlight. These conditions include: living in northern regions, having dark skin, and having little chance to go outside. Children whose faces and bodies remain covered when outside can develop vitamin D deficiency even while living in a sunny climate. In-born errors of vitamin D metabolism can also cause vitamin D deficiency and rickets; these children cannot convert inactive vitamin D to active vitamin D and suffer the same symptoms as children with a nutritional deficiency.

Most foods contain little or no vitamin D. As a result, sunshine is often a deciding factor in whether vitamin D deficiency occurs. Although fortified milk and fortified infant formula contain high levels of vitamin D, human breast milk is rather low in the vitamin. (The term fortified means that vitamins are added to the food by the manufacturer.)

The Recommended Dietary Allowance (RDA) of vitamin D for both children and adults is 200 International Units (IU) per day. Saltwater fish such as salmon, herring, and sardines are naturally rich in vitamin D. Vitamin D fortified milk contains 400 IU per quart (liter), so half a quart (liter) of milk provides the RDA. For comparison, human breast milk contains only 4 to 60 IU per quart.

No harm is likely to result from vitamin D deficiency that occurs only a few days a year. If the deficiency occurs for a period of many months or years, however, rickets may develop. The symptoms of rickets include bowed legs and bowed arms. The bowed appearance is due to the softening of bones, and their bending if the bones are weight-bearing. Bone growth occurs through the creation of new cartilage, a soft substance at the ends of bones. When the mineral calcium phosphate is deposited onto the cartilage, a hard structure is created. In vitamin D deficiency, though, calcium is not available to create hardened bone, and the result is soft bone. Other symptoms of rickets include bony bumps on the ribs called rachitic rosary (beadlike prominences at the junction of the ribs with their cartilages) and knock-knees. Seizures may also occasionally occur in a child with rickets, because of reduced levels of dissolved calcium in the bloodstream.

When to call the doctor

The doctor should be called if the parent notices that the child has any signs of vitamin D deficiency or rickets. Such signs include skeletal pain , bowed limbs, and impaired growth. If there are lifestyle factors that make the child at risk for vitamin D deficiency, such as low milk or formula intake, a doctor should be consulted about the possibility of using vitamin D supplements.

Diagnosis

Vitamin D deficiency is diagnosed by measuring the level of 25-hydroxy-vitamin D in the blood serum. The normal concentration of this form of vitamin D ranges from 25 to 50 ng/ml. Deficiency occurs when this level decreases to about 12 ng/ml or less.

Rickets is diagnosed by x-ray examination of the leg bones. A distinct pattern of irregularities, abnormalities, and a coarse appearance can be clearly seen if a child has rickets. Measurements of blood plasma 25-OH-D, blood plasma calcium, and blood plasma parathyroid hormone must also be obtained for the diagnosis of this disease. Parathyroid hormone and 1,25-diOH-D work together in the body to regulate the levels of calcium in the blood.

Treatment

Rickets heals promptly with large doses vitamin D administered orally each day for approximately one month. During this treatment, the doctor should monitor the levels of 25-OH-D in the plasma to make sure that they are raised to a normal level. The bone abnormalities (visible by x ray) generally disappear gradually over a period of three to nine months. Parents are instructed to take their infants outdoors for approximately 20 minutes per day with their faces exposed. Children should be encouraged to play outside and to eat foods that are good sources of vitamin D. These foods include cod liver oil, egg yolks, butter, oily fish and also foods, including milk and breakfast cereals, that are fortified with synthetic vitamin D.

Care must be taken in treating vitamin D deficiency, since high doses of vitamin D are toxic (poisonous) and can result in the permanent deposit of minerals in the heart, lungs, and kidneys. Symptoms of toxicity are nausea , vomiting , pain in the joints, and lack of interest in eating food. In adults, vitamin D toxicity occurs with eating 50,000 IU or more per day. In infants, toxicity occurs with 1,000 IU per day. The continued intake of toxic doses results in death.

Rickets are usually treated with oral supplements of vitamin D, with the recommendation to acquire daily exposure to direct sunlight. An alternative to sunlight is the use of an ultraviolet lamp. When people use UV lamps, they need to cover their eyes to protect them against damage. Many types of sunglasses allow UV light to pass through, so only those that are opaque to UV light should be used. Attempts to acquire sunlight through glass windows fail to help the body make vitamin D because UV light does not pass through window glass.

Rickets may also occur with calcium deficiency, even when a child is regularly exposed to sunshine. This type of rickets has been found in various parts of Africa. The bone deformities are similar to, or are the same as, those that occur in typical rickets; however, calcium deficiency rickets is treated by increasing the amount of calcium in the diet. No amount of vitamin D can cure the rickets of a child with a diet that is extremely low in calcium. For this reason, it is recommended that calcium be given in conjunction with vitamin D supplementation.

Prognosis

The prognosis for correcting vitamin D deficiency and rickets is excellent. Vitamin D treatment results in the return of bone mineralization to a normal rate, the correction of low plasma calcium levels, the prevention of seizures, and a recovery from bone pain. On the other hand, already established deformities such as bowed legs and the rachitic rosary persist throughout adult life.

Prevention

Vitamin D deficiency is a very preventable. Eating foods that are high in vitamin D or foods that have been fortified with additional vitamins in combination with getting moderate amounts of exposure to direct sunlight, are usually enough to prevent vitamin D deficiency.

KEY TERMS

25-hydroxy-vitamin D The form of vitamin D that is measured in order to assess vitamin D deficiency.

Cholesterol A steroid fat found in animal foods that is also produced in the human body from saturated fat. Cholesterol is used to form cell membranes and process hormones and vitamin D. High cholesterol levels contribute to the development of atherosclerosis.

Fat-soluble vitamin A vitamin that dissolves easily in fat or oil, but not in water. The fat-soluble vitamins are vitamins D, E, A, and K.

International unit (IU) A measurement of biological activity in which one IU is equal to one mg (milligram).

Rachitic rosary Beadlike bumps present at the junction of the ribs with their cartilages. It is often seen in children with rickets.

Recommended Dietary Allowance (RDA) The Recommended Dietary Allowances (RDAs) are quantities of nutrients in the diet that are required to maintain good health in people. RDAs are established by the Food and Nutrition Board of the National Academy of Sciences, and may be revised every few years. A separate RDA value exists for each nutrient. The RDA values refer to the amount of nutrient expected to maintain good health in people. The actual amounts of each nutrient required to maintain good health in specific individuals differ from person to person.

Rickets A condition caused by the dietary deficiency of vitamin D, calcium, and usually phosphorus, seen primarily in infancy and childhood, and characterized by abnormal bone formation.

Some authorities still recommend exposure to sunshine as a way to prevent vitamin D deficiency, but early exposure to direct sunlight may be linked to a higher incidence of skin cancer later in life, so other experts recommend that infants not be taken into direct sunlight without protective coverings or sunscreen until at least six months of age. These experts recommend that supplemental drops or fortified formulas instead of direct sunlight provide infants' daily requirements of Vitamin D. Children playing in the sunlight with sunscreen on is not an effective way for them to get vitamin D because the sunscreen inhibits its production in the skin.

Nutritional concerns

Vitamin D deficiency is caused by the child not getting enough vitamin D through nutrition and exposure to sunshine. Even after a case of vitamin D deficiency has successfully been resolved special care should be taken with the child's diet, as vitamin D deficiency can reoccur.

Parental concerns

Vitamin D deficiency can cause rickets, which can lead to permanently stunted or irregular growth. Vitamin D deficiency can usually be easily corrected if it is noticed early, and if so the symptoms often resolve themselves. However, negative effects such as short stature and pelvic deformations can be permanent.

Resources

BOOKS

Hochber, Ze'ev, ed. Vitamin D and Rickets. Farmington, CT: S. Karger, 2003.

PERIODICALS

Spence, Jean, T. and Janet R. Serwint. "Secondary Prevention of Vitamin D-Deficiency Rickets" Pediatrics 113 (January 2004): 129.

Wharton, Brian, and Nick Bishop. "Rickets." The Lancet 362 (October 2003): 1389.

Tish Davidson, A.M.

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Davidson, Tish. "Vitamin D Deficiency." Gale Encyclopedia of Children's Health: Infancy through Adolescence. 2006. Encyclopedia.com. 25 Sep. 2016 <http://www.encyclopedia.com>.

Davidson, Tish. "Vitamin D Deficiency." Gale Encyclopedia of Children's Health: Infancy through Adolescence. 2006. Encyclopedia.com. (September 25, 2016). http://www.encyclopedia.com/doc/1G2-3447200601.html

Davidson, Tish. "Vitamin D Deficiency." Gale Encyclopedia of Children's Health: Infancy through Adolescence. 2006. Retrieved September 25, 2016 from Encyclopedia.com: http://www.encyclopedia.com/doc/1G2-3447200601.html

Vitamin D Deficiency

Vitamin D Deficiency

Definition

Vitamin D deficiency exists when the concentration of 25-hydroxy-vitamin D (25-OH-D) in the blood serum occurs at 12 ng/ml (nanograms/milliliter), or less. The normal concentration of 25-hydroxy-vitamin D in the blood serum is 25-50 ng/ml. When vitamin D deficiency continues for many months in growing children, the disease commonly referred to as rickets will occur. A prolonged deficiency of the vitamin in adults results in osteomalacia. Both diseases involve defects in bones.

Description

Vitamin D is a fat-soluble vitamin, meaning it is able to be dissolved in fat. While some vitamin D is supplied by the diet, most of it is made in the body. To make vitamin D, cholesterol, a sterol that is widely distributed in animal tissues and occurs in the yolk of eggs, as well as in various oils and fats, is necessary. Once cholesterol is available in the body, a slight alteration in the cholesterol molecule occurs, with one change taking place in the skin. This alteration requires the energy of sunlight (or ultraviolet light). Vitamin D deficiency, as well as rickets and osteomalacia, tends to occur in persons who do not get enough sunlight and who fail to eat foods that are rich in vitamin D.

Once consumed, or made in the body, vitamin D is further altered to produce a hormone called 1,25-dihydroxy-vitamin D (1,25-diOH-D). The conversion of vitamin D to 1,25-diOH-D does not occur in the skin, but in the liver and kidney. First, vitamin D is converted to 25-OH-D in the liver; it then enters the bloodstream, where it is taken-up by the kidneys. At this point, it is converted to 1,25-diOH-D. Therefore, the manufacture of 1,25-diOH-D requires the participation of various organs of the bodythe liver, kidney, and skin.

The purpose of 1,25-diOH-D in the body is to keep the concentration of calcium at a constant level in the bloodstream. The maintenance of calcium at a constant level is absolutely required for human life to exist, since dissolved calcium is required for nerves and muscles to work. One of the ways in which 1,25-diOH-D accomplishes this mission is by stimulating the absorption of dietary calcium by the intestines.

The sequence of events that can lead to vitamin D deficiency, then to bone disease, is as follows: a lack of vitamin D in the body creates an inability to manufacture 1,25-diOH-D, which results in decreased absorption of dietary calcium and increased loss of calcium in the feces. When this happens, the bones are affected. Vitamin D deficiency results in a lack of bone mineralization (calcification) in growing persons, or in an increased demineralization (decalcification) of bone in adults.

Causes and symptoms

Vitamin D deficiency can be caused by conditions that result in little exposure to sunlight. These conditions include: living in northern countries; having dark skin; being elderly or an infant, and having little chance to go outside; and covering one's face and body, such as for religious reasons. Many Arab women cover the entire body with black cloth, and wear a veil and black gloves when they go outside. These women may acquire vitamin D deficiency, even though they live in a sunny climate.

Most foods contain little or no vitamin D. As a result, sunshine is often a deciding factor in whether vitamin D deficiency occurs. Although fortified milk and fortified infant formula contain high levels of vitamin D, human breast milk is rather low in the vitamin. The term fortified means that vitamins are added to the food by the manufacturer.

To say that a food is high or low in vitamin D means how much of that food needs to be eaten in order to prevent vitamin deficiency and maintain good health. An exact meaning can be provided by comparing the Recommended Dietary Allowance of vitamin D with the amount of vitamin D supplied by a particular food per day. The Recommended Dietary Allowance, also referred to as RDA, is a recommendation based on data derived from different population groups and ages. The RDA for vitamin D for adults is 200 International Units (IU) per day, and can be supplied by eating approximately 1.5 kg of beef, 2.0 kg of corn oil, or 100 kg of cabbage. Few people, though, would want to eat a kilogram of beef in one day, and no human being is capable of eating 100 kg of cabbage in a day; therefore, these foods are poor sources of vitamin D. However, saltwater fish such as salmon, herring, and sardines are rich in vitamin D, supplied from the oils produced by these fish. The RDA can also be supplied by eating roughly 50 g of salmon or 2.0 g of cod liver oil, and since fortified milk contains 400 IU per quart, half a quart of milk provides the RDA. For comparison, human breast milk contains only 4 to 60 IU per quart.

No harm is likely to result from vitamin D deficiency that occurs for only a few days a year. If the deficiency occurs for a period of many months or years, however, rickets or osteomalacia may develop. The symptoms of rickets include bowed legs and bowed arms. The bowed appearance is due to the softening of bones, and their bending if the bones are weight-bearing. Bone growth occurs through the creation of new cartilage, a soft substance at the ends of bones. When the mineral calcium phosphate is deposited onto the cartilage, a hard structure is created. In vitamin D deficiency, though, calcium is not available to create hardened bone, and the result is soft bone. Other symptoms of rickets include particular bony bumps on the ribs called rachitic rosary (beadlike prominences at the junction of the ribs with their cartilages) and knock-knees. Seizures may also occasionally occur in a child with rickets, because of reduced levels of dissolved calcium in the bloodstream.

Although osteomalacia is rare in the United States, symptoms of this disease include reduced bone strength, an increase in bone fractures, and sometimes bone pain, muscle weakness, and a waddling walk.

Diagnosis

Vitamin D deficiency is diagnosed by measuring the level of 25-hydroxy-vitamin D in the blood serum. The normal level or concentration of this form of the vitamin ranges from 25-50 ng/ml. Deficiency occurs when this level decreases to about 12 ng/ml or less. As mentioned previously, 25-OH-D is not the active form of the vitamin. It must be converted to 1,25-diOH-D in order to cause responses in various organs of the body. However, the levels of vitamin D, or of 1,25-dihydroxy-vitamin D in the blood, do not give a reliable picture of whether a person is deficient in the vitamin. For this reason, they are not measured when testing for vitamin D deficiency.

Rickets is diagnosed by x-ray examination of leg bones. A distinct pattern of irregularities, abnormalities, and a coarse appearance can be clearly seen with rickets. Osteomalacia is also diagnosed with x-ray examination. Measurements of blood plasma 25-OH-D, blood plasma calcium, and blood plasma parathyroid hormone must also be obtained for the diagnosis of these diseases. Parathyroid hormone and 1,25-diOH-D work together in the body to regulate the levels of calcium in the blood.

Treatment

Rickets heals promptly with 4,000 IU of oral vitamin D per day administered for approximately one month. During this treatment, the doctor should monitor the levels of 25-OH-D in the plasma to make certain they are raised to a normal value. The bone abnormalities (visible by x ray) generally disappear gradually over a period of 3-9 months. Parents are instructed to take their infants outdoors for approximately 20 minutes per day with their faces exposed. Children should also be encouraged to play outside. Foods that are good sources of vitamin D include cod liver oil, egg yolks, butter, and oily fish. Some foods, including milk and breakfast cereals, are also fortified with synthetic vitamin D.

Osteomalacia is treated by eating 2,500 IU per day of vitamin D for about three months. Measurements of 25-OH-D, calcium, and parathyroid hormone should be obtained after the treatment period to make sure the therapy did, in fact, result in normal blood values.

Care must be taken in treating vitamin D deficiency, since high doses of vitamin D are toxic and can result in the permanent deposit of minerals in the heart, lungs, and kidneys. Symptoms of toxicity are nausea, vomiting, pain in joints, and lack of interest in eating food. In adults, vitamin D toxicity occurs with eating 50,000 IU or more per day. In infants, toxicity occurs with 1,000 IU per day. The continued intake of toxic doses results in death.

Rickets and osteomalacia are almost always treated with oral supplements of vitamin D, with the recommendation to acquire daily exposure to direct sunlight. An alternative to sunlight is the use of an ultraviolet (UV) lamp. When using UV lamps, the eyes must be covered to protect them against damage. Many types of sunglasses allow UV light to pass through, so only those that are opaque to UV light should be used. Attempts to acquire sunlight through glass windows fail to help the body make vitamin D. This is because UV light does not pass through window glass.

Rickets may also occur with calcium deficiency, even when a child is regularly exposed to sunshine. This type of rickets has been found in various parts of Africa. The bone deformities are similar to, or are the same as, those that occur in typical rickets; however, calcium deficiency rickets is treated by increasing the amount of calcium in the diet. No amount of vitamin D can cure the rickets of a child with a diet that is extremely low in calcium. For this reason, it is recommended that calcium be given in conjunction with vitamin D supplementation.

Prognosis

The prognoses for correcting vitamin D deficiency, rickets, and osteomalacia are excellent. Vitamin D treatment results in the return of bone mineralization to a normal rate, the correction of low plasma calcium levels, the prevention of seizures, and a recovery from bone pain. On the other hand, deformities such as bowed legs and the rachitic rosary persist throughout adult life.

Prevention

Food fortification has almost completely eliminated rickets in the United States. Vitamin D deficiency can be prevented by acquiring the RDA through drinking fortified milk and eating fortified cereals. For those who cannot drink milk, supplements of pills might be considered. In some older people, a 400 IU supplement may not be enough to result in the normal absorption of calcium; therefore, daily doses of 10,000 IU per day may be needed. For infants who are fed only breast milk (and rarely exposed to sunshine), a daily supplement of 200-300 IU is recommended.

Rickets continues to be a problem in Africans and Asian Indians who migrate to Canada or Great Britain, especially where these immigrants do not drink fortified milk. Prevention of rickets in these populations is attempted through educational programs sponsored by the government.

Resources

PERIODICALS

Kinyamu, H., et al. "Serum Vitamin D Metabolites and CalciumAbsorption in Normal Young and Elderly Free-Living Women and in Women Living in Nursing Homes." American Journal of Clinical Nutrition 65 (1997): 790-797.

KEY TERMS

25-hydroxy-vitamin D This is the form of vitamin D that is measured in order to assess vitamin D deficiency.

Cholesterol A fat-soluble steroid alcohol (sterol) found in animal fats and oils, and in egg yolks. The human body needs cholesterol to produce vitamin D.

Fat-soluble vitamin A vitamin that dissolves easily in fat or oil, but not in water. The fat-soluble vitamins are vitamins D, E, A, and K.

International unit (IU) A measurement of biological activity in which one IU is equal to one mg (milligram).

Osteomalacia Osteomalacia is a bone disease that occurs in adults and is caused by a prolonged period of vitamin D deficiency.

Rachitic rosary Beadlike bumps present at the junction of the ribs with their cartilagesoften seen in children with rickets.

Recommended Dietary Allowance (RDA) The amount of nutrients, including vitamins, that should be supplied by foods on a daily basis to maintain normal health. Recommendations are based on data obtained from different population groups and ages.

Rickets Rickets is a bone disease that occurs in infants and growing children and is caused by a prolonged period of vitamin D deficiency.

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Brody, Tom. "Vitamin D Deficiency." Gale Encyclopedia of Medicine, 3rd ed.. 2006. Encyclopedia.com. 25 Sep. 2016 <http://www.encyclopedia.com>.

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Vitamin D

Vitamin D

Vitamin D is one of the four fat-soluble vitamins. It is concerned with efficient calcium and phosphorus absorption. The vitamin works with various hormones to ensure that calcium and phosphorous are absorbed from the intestinal tract in the right proportions into the bloodstream. Calcium and phosphorous in the right ratio and amounts help determine normal bone growth. In addition, vitamin D stimulates the bones to accept calcium.

Vitamin D isn't just one vitamin but, a group of vitamins. All vitamins in the group are come from a parent compound structurally similar to cholesterol. The compound comes in a variety of forms, two of which are especially important from a nutritional standpoint.

Vitamin D2

Vitamin D2 (calciferol) is produced when ultraviolet radiation activates a sterol (fat-like substances in the steroid family) that is present mainly in yeasts and fungi (molds). Vitamin D2 is rarely seen in nature. It is manufactured in the laboratory and is regularly added to infant formulas and other fortified foods.

A Sunshine Vitamin

Vitamin D3 (cholecalciferol) is derived from a sterol present in animal tissues. In humans the sterol is converted into vitamin D on the skin's surface. The conversion is activated by ultraviolet rays from the sun. For this reason, healthy adults who are exposed to normal amounts of sunlight may produce enough vitamin D to avoid the need for added dietary sources.

Rickets

The need for vitamin D is greater in childhood. In infants and young children, lack of the vitamin can cause rickets (or rachitis). Rickets is a bone disorder that results in bowed legs, knock-knees, curved spines, and other abnormalities. Children with rickets have been discussed since Galen's time (a.d. 130-200). A detailed description of rickets was provided as early as the seventeenth century. The cause of rickets, however, wasn't discovered until fairly recently.

Early Research

In 1914 England's Medical Research Council asked Edward Mellanby (1884-1955) to concentrate on finding a cure for rickets. Mellanby was a brilliant young English biochemist and a student of famous researcher Frederick Gowland Hopkins (1861-1947). Mellanby spent the next seven years at Cambridge University conducting feeding experiments on dogs. He was convinced that rickets had a dietary basis.

Mellanby finally devised a diet that helped him prove he could cure rickets. He did so by adding certain fats to his animals' rations. In 1921 Mellanby wrote that the fats' effectiveness in rickets was due "to a vitamin or accessory food factor they contain."

This "food factor" was probably identical to the fat-soluble vitamin that American scientist Elmer McCollum was working with. In 1922 McCollum and his associates discovered that their fat-soluble vitamin consisted of two separate vitamins. The first was vitamin A and the second vitamin they named vitamin D.

In that same year, McCollum and his group confirmed that cod liver oil was an effective treatment for rickets. Cod liver oil had been a folk remedy used to treat rickets for many years.

Ultraviolet Light

A number of researchers went on to show that when the skin was exposed to sunlight or ultraviolet light, a substance virtually identical to vitamin D is produced.

Independent researchers like Alfred Hess (1875-1933) and Harry Steenbock (1886-1967) continued to work on vitamin D. In 1924 Hess and Steenbock found that foods exposed to ultraviolet light developed sub-stantially greater anti-rickets potency. This discovery led to the practice of irradiating certain foods (exposing them to low-level radiation) like milk to help prevent rickets.

[See also Hormone ; Ultraviolet radiation ; Vitamin A ]

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vitamin D

vitamin D Vitamin D3 is calciol or cholecalciferol; formed in the skin by the action of ultraviolet light on 7‐dehydrocholesterol, and hence not strictly a vitamin. However, in northern latitudes sunlight exposure may not be adequate to meet requirements, and a dietary source may become essential. Vitamin D2 (ercalciol or ergocalciferol) is a synthetic vitamer produced by irradiation of ergosterol. The name vitamin D1 was given originally to an impure mixture and is not used now.

The metabolic function of the vitamin is to control calcium metabolism. It stimulates the absorption of dietary calcium from the intestine and calcium turnover in bone. Deficiency causes rickets in young children, osteomalacia in adults.  It is not widely distributed in foods, but is found in egg yolk, butter, fatty fish, and enriched margarine. There are no reference intakes for adults in the UK or the EU; the US/Canadian RDA for adults is 5 μg, increasing to 10 and 15 μg with increasing age. The obsolete international unit of vitamin D = 25 ng calciol; 1 μg calciol = 40 iu.

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DAVID A. BENDER. "vitamin D." A Dictionary of Food and Nutrition. 2005. Encyclopedia.com. 25 Sep. 2016 <http://www.encyclopedia.com>.

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vitamin D

vitamin D A fat-soluble vitamin occurring in the form of two steroid derivatives: vitamin D2 (ergocalciferol, or calciferol), found in yeast; and vitamin D3 (cholecalciferol), which occurs in animals. Vitamin D2 is formed from a steroid by the action of ultraviolet light and D3 is produced by the action of sunlight on a cholesterol derivative in the skin. Fish-liver oils are the major dietary source. The active form of vitamin D is manufactured in response to the secretion of parathyroid hormone, which occurs when blood calcium levels are low. It causes increased uptake of calcium from the gut, which increases the supply of calcium for bone synthesis. Vitamin D deficiency causes rickets in growing animals and osteomalacia in mature animals. Both conditions are characterized by weak deformed bones.

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vitamin D

vitamin D n. a fat-soluble vitamin that enhances the absorption of calcium and phosphorus from the intestine and promotes their deposition in the bone. D2 (ergocalciferol, calciferol) a form obtained from the diet; good sources are fatty fish, eggs, and margarine. D3 (cholecalciferol) a form manufactured in the skin in the presence of sunlight. A deficiency of vitamin D leads to rickets and osteomalacia. Recommended daily intake: 10 μg (for a child up to five years); 2.5 μg (thereafter).

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"vitamin D." A Dictionary of Nursing. 2008. Encyclopedia.com. 25 Sep. 2016 <http://www.encyclopedia.com>.

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vitamin D toxicity

vitamin D toxicity Excessive intake of vitamin D results in disturbance of calcium metabolism, resulting in hypercalcaemia, i.e. dangerously raised blood calcium concentrations leading to raised blood pressure, brain damage, and kidney damage. Excessive exposure to sunlight does not lead to excessive formation of vitamin D.

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vitamin D

vi·ta·min D • n. any of a group of vitamins found in liver and fish oils, essential for the absorption of calcium and the prevention of rickets in children and osteomalacia in adults. They include calciferol (vitamin D2) and cholecalciferol (vitamin D3).

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vitamin D

vitamin D See CALCIFEROL.

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MICHAEL ALLABY. "vitamin D." A Dictionary of Zoology. 1999. Encyclopedia.com. 25 Sep. 2016 <http://www.encyclopedia.com>.

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