Without sun exposure, 1000 IU daily of cholecalciferol (vitamin D) is required for both children and adults. A deficiency of vitamin D in children causes poor mineralization of the collagen matrix, leading to rickets. In adults, secondary hyperparathyroidism can result from a deficiency of vitamin D. This causes the loss of bone structure and mineralization with the increased risk of osteoporosis and fractures. Poor mineralization of new bone matrix in adults results in painful osteomalacia. And vitamin D deficiency can also cause muscle weakness.
Skin cells contain 7-dehydrocholesterol. Ultraviolet B photons convert it to precholecalciferol, which is unstable and becomes vitamin D, cholecalciferol. Cholecalciferol is converted to 25-(OH)D (25 hydroxy vitamin D) by the liver and, then to 1,25-(OH)2D (1,25 dihydroxy vitamin D) by the kidney.
There has never been a recorded case of vitamin D intoxication due to sunlight. Melanin in the skin is a sunscreen and reduces vitamin D production. Vitamin D-3, cholecalciferol, is of animal origin and Vitamin D-2, ergocalciferol, is of plant origin. Vitamin D receptors have been seen in nearly every tissue and cell in the body.
In rickets, bone growth is slow and the long bones become deformed. In 1900, 80% of children of large cities of North America and Europe had rickets. The major treatment was cod liver oil and eventually milk was fortified with vitamin D.
A deficiency of vitamin D leads to a reduction of serum calcium because of decreased intestinal absorption. This results in an increase in parathyroid hormone (PTH) that causes an increase in cells called osteoclasts. These cells produce hydrochloric acid (HCL) and collegenase, which destroy bone structure. Calcium stores are removed from the bone to restore serum calcium levels. The result is that vitamin D deficiency causes secondary hyperparathyroidism, which causes skeletal wasting, osteoporosis and loss of phosphorus in the urine. One sign of this is low serum phosphorus.
Bone pain is a sign of osteomalacia. Sometimes osteomalacia is wrongly diagnosed as fibromyalgia, myositis or chronic fatigue syndrome and X-Rays can’t differentiate osteoporosis from osteomalacia. With osteomalacia pressing on the sternum or mid-tibia causes pain.
African Americans who are highly pigmented may require five to ten times more sun than people with very light skins.
Vitamin D is fat soluble and stored in body fat. Good sources of vitamin D are oily fish (salmon, mackerel, herring, and cod liver oil), and sun dried mushrooms. Milk, orange juice, cereals, and some breads are fortified with vitamin D. Exposure of the skin to the sun to the point of a light pink color can be the equivalent of taking 10-20,000 IU vitamin D.
The serum PTH levels “plateau” and are highly beneficial at a blood 25(OH)D level of 32 ng/mL. The authors state that the body uses 3,000 to 5,000 IU daily of cholecalciferol. Vitamin D-2 is of vegetable source and is 20-40% as effective as D-3, which is of animal source.
Patients with malabsorption syndromes (Crohn’s disease, Whipple’s disease, cystic fibrosis and sprue) become deficient of vitamin D, which is fat soluble, because they have trouble with fat absorption. The best treatment seems to be the tanning beds.
CONCLUSION: Vitamin D deficiency increases the risk of the following diseases: type 1 diabetes mellitus, hypertension, cardiovascular heart disease and several cancers including prostate, breast, colon, lung, and brain. Vitamin D reduces the risk of developing autoimmune diseases, including multiple sclerosis, rheumatoid arthritis and type 1 diabetes mellitus. Vitamin D also protects from hypertension and cardiovascular diseases.
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