Vitamin D (vit. D) occurs as D-2 (ergocalciferol) and D-3 (cholecalciferol) and they are bioidentical*. Vitamin D deficiency causes rickets in infants and osteomalacia in adults by bone demineralization. With sufficient sunlight, the skin produces enough vit. D in the presence of UV light. Vitamin D-3 appears in some animal foods, such as deep-sea fish, egg yolks and liver. Vitamin D-2 is in some plants and is produced by irradiation of yeast. Both forms of vit. D can be measured by testing for 25-hydroxyvitamin D {25(OH)D} in the blood. 25(OH)D has properties of a hormone (making vit. D a prohormone), which has a half-life in the body of around 3 weeks.
Vit. D increases calcium absorption in the duodenum and mobilizes calcium in the body. Maximal calcium absorption occurs when 25(OH)D levels are 32 ng/mL and greater. Production of vit. D is controlled by the parathyroid hormone (PTH) and by serum calcium and phosphorus levels. One definition “of optimal vitamin D status is the 25(OH)D level that maximally suppresses PTH secretion…”
In 1650, childhood rickets was the first vitamin D recognized deficiency illness. The incidence of childhood rickets during the industrial revolution rose dramatically, and the association of rickets with lack of sunlight was made. Cod liver oil was the treatment of choice in the 1800’s, and from that information vit. D was discovered. Rickets is still a problem around the world, especially in children under 30 months of age. The legs, wrists and rib cage can be deformed, and rickets can even cause hypocalcemic (low calcium) seizures in infants. In tropical countries rickets is more likely to be caused by low calcium than by low vit. Of special significance, “Dark-skinned infants who are exclusively breast-fed are at greater risk of rickets and should receive 400 IU/d of supplemental vit. D.”
Supplementation of adults with vit. D reduces the risk of fractures. Osteomalacia is due to the failure of mineralization of bone with calcium and phosphorus, and is due to vit. D deficiency in adults. Osteomalacia causes pain of bones, muscles and soft tissues, and the patients have high PTH levels with low serum calcium and phosphorus. Osteomalacia in adults is like rickets in children. Vit. D supplementation has previously been shown to increase bone mineral density of the neck of the femoral bone (hip), which is subject to fracture. Of importance vit. D reduces the risk of nonvertebral fractures at the 400 IU/d dose and reduces the risk of falling at the 700 IU/d dose.
Low levels of blood 25(OH)D can cause other problems before bone disease develops and alters the course of a wide variety of illnesses. There is concern that ordinary doses of vit. D may worsen blood vessel disease, such as atherosclerosis. Low 25(OH)D levels are associated with risk factors for cardiovascular disease, such as diabetes, hypertension, obesity and elevated triglycerides.
Adequate vit. D and calcium intake reduces the risk of colon cancer. Breast cancer is associated with low vit. D intake, while calcium intake reduces breast cancer risk. Overall, vit. D deficiency is associated with increased risk of many types of cancer. Additionally, low levels of vit. D in pregnant women increase the risk of their children having allergic problems. Patients with fibromyalgia show improvement on vit. D therapy, also.
CONCLUSION: “.. it seems prudent for persons older than 50 years to take a vit. D supplement of 800 to 2000 IU/d to reduce the risk of falls and fractures.”
NOTE: *Bioidentical means that the structure of a hormone (in this case a prohormone) is identical to the hormone produced by the body.
Read about vitamin D deficiency in youths and diabetes.
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PMID: 21193656.
Summary #544.
