Vitamin D3 and vitamin D2 can be ingested from the diet and from supplements. Very few foods contain vitamin D. Dermal synthesis of vitamin D from cholesterol is dependent on sun exposure (specifically UVB radiation).
Vitamin D from the diet or dermal synthesis from sunlight is biologically inactive; activation requires enzymatic conversion in the liver and kidney. Evidence indicates the synthesis of vitamin D from sun exposure is regulated by a negative feedback loop that prevents toxicity, but because of uncertainty about the cancer risk from sunlight, no recommendations are issued by the Institute of Medicine for the amount of sun exposure required to meet vitamin D requirements.
Vitamin D has a significant role in calcium homeostasis and metabolism. Its discovery was due to effort to finding the dietary substance lacking in rickets, the childhood form of osteomalacia. Beyond its use to prevent osteomalacia or rickets, the evidence for other health effects of vitamin D supplementation in the general population is inconsistent.
In the liver, cholecalciferol (vitamin D3) is converted to calcidiol, which is also known as calcifediol . Ergocalciferol (vitamin D2) is converted in the liver to 25-hydroxyergocalciferol. These two specific vitamin D metabolites are measured in serum to determine a person's vitamin D status. Part of the calcidiol is converted by the kidneys to calcitriol, the biologically active form of vitamin D. Calcitriol circulates as a hormone in the blood, regulating the concentration of calcium and phosphate in the bloodstream and promoting the healthy growth and remodeling of bone. Calcitriol also affects neuromuscular and immune function.
Deficiency in Vitamin D
A diet deficient in vitamin D or inadequate sun exposure causes osteomalacia or rickets when it occurs in children, which softens the bones. vitamin D deficiency has become a worldwide issue in the elderly and remains common in children and adults. Low blood calcidiol can result from avoiding the sun. Deficiency results in impaired bone mineralization and bone damage which leads to bone-softening diseases.
Rickets is a childhood disease, is characterized by impeded growth and soft, weak, deformed long bones that bend and bow under their weight as children start to walk. This condition is characterized by bow legs, which can be caused by calcium or phosphorus deficiency, as well as a lack of vitamin D. Today, it is largely found in low income countries.
Vitamin D deficiency remains the main cause of rickets among young infants in most under developed countries, like the third world countries.
Vitamin D is carried in the bloodstream to the liver, where it is converted into the prohormone calcidiol. Circulating calcidiol may then be converted into calcitriol, the biologically active form of vitamin D, in the kidneys. Following the final converting step in the kidney, calcitriol is released into the circulation. By binding to vitamin D-binding protein, a carrier protein in the plasma, calcitriol is transported to various target organs.
One of the most important roles of vitamin D is to maintain skeletal calcium balance by promoting calcium absorption in the intestines, promoting bone resorption by increasing osteoclast number, maintaining calcium and phosphate levels for bone formation, and allowing proper functioning of parathyroid hormone to maintain serum calcium levels.
10 Ways to Get Your Daily Vitamin D
- Fortified Cereal
- Certain Mushrooms
- Sunlight
- Some types of Orange Juice
- Beef Liver
- Fortified Milk
- Cold Liver Oil
- Supplements
- Egg Yolks
- Fatty Fish
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