Deficiency of vitamin D can over a period of months cause rickets in children and osteomalacia in adults – a skeletal demineralization especially in the spine, pelvis, and lower extremities. Signs and symptoms of osteomalacia are burning in the mouth and throat, nervousness, diarrhea, and insomnia. Vitamin D is a fat-soluble vitamin and while some is supplied by the diet, most of it is made in the body. To make vitamin D, cholesterol 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 ultraviolet light (sunlight). 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 within 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 kidneys. 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 body – the liver, kidneys, 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.
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.
Rickets continues to be a problem in Africans and Asian Indians who migrate to Canada or Great Britain, especially where these immigrants do not consume fortified products.
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.
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 through 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.
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.
Food fortification has almost completely eliminated rickets in the United States. Vitamin D deficiency can be prevented by acquiring the RDA through consuming fortified products or taking supplements in the form of pills. 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.
The sequence of events that can lead to vitamin D deficiency, and then 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.
British Medical Journal, January 2010: Those with a higher level of vitamin D in their blood are less likely to develop bowel cancer than those with low levels. A study has concluded that those with the highest levels of the vitamin were at 40% lower risk of developing the disease compared with those with the lowest levels. Researchers at the International Agency for Research on Cancer (IARC) in Lyon, France, and Imperial College London looked at vitamin D quantities in 1,248 people with bowel cancer and 1,248 controls in the largest ever study of the subject.
The body's main source of vitamin D is sunlight, but higher latitudes mean less available sunlight – especially during the winter. At most latitudes in the United States, little or no vitamin D is made in the skin in the late fall (autumn) and early winter. In the most northern regions, the vitamin D blackout lasts for about six months. As a result, it has been estimated that up to 70% of Americans (and Europeans) may be deficient in vitamin D. Only in the last several hundred years has urbanization, industrialization, glass (UVB does not penetrate glass), excessive clothes (UVB does not penetrate clothes) and sunblock greatly lowered levels.
Even if one is taking vitamin D supplements, vitamin D recommendations keep going up. It is difficult to take, for example, 1,000 IU, which may be what is needed. Ideally, sunlight exposure should be one's source.
An Alabama researcher found that lack of enough sunshine exposure may increase risk of hypertension in blacks and other dark-skinned people. Those with greater amounts of pigment in the skin require six times the amount of ultraviolet B (UVB) light to produce the same amount of vitamin D3 found in lighter-skinned people.
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.
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.
People should aim to get 10 to 15 minutes of exposure to direct sunlight each day when the weather allows, without sunscreen, to allow adequate synthesis of vitamin D. Most people achieve this simply by going about their daily activities. Those living at higher latitudes (further from the equator) should supplement their diets to ensure they are getting enough vitamin D, particularly during winter. A lack of sun during the winter months means that many people are deficient in this vitamin by December each year.
In the spring and summer, light-skinned adults can make large amounts (20,000 IU) by sunbathing on both sides, without sunblock, for a few minutes (about one-third the time it takes for the skin to begin to slightly redden). Darker-skinned persons need five to 10 times longer depending on the amount of melanin pigment in the skin.
Vitamin D production occurs within minutes and is maximized long before the skin turns red or begins to tan. One does not have to get repeated blood tests when using sun exposure to obtain vitamin D. Toxicity can not occur even with heavy and continuous sunbathing because ultraviolet light begins to degrade vitamin D after making about 20,000 IU, thus reaching a steady state.