Abstract: Vitamin D is very important for overall health and wellbeing. A major source of vitamin D comes from exposure to sunlight. Measurement of 25-hydroxyvitamin D in the blood and not 1,25-dihydroxyvitamin D is used to determine vitamin D status. A blood level of 25-hydroxyvitamin D of at least 20 ng/mL is considered to be vitamin D sufficient. Vitamin D deficiency increases the risk of many common cancers, multiple sclerosis, rheumatoid arthritis, hypertension, cardiovascular heart disease, and type 1 diabetes.
Key Words: cardiovascular heart disease, disease prevention, type I diabetes, vitamin D
Vitamin D is recognized as the sunshine vitamin for good reason. During exposure to sunlight, the ultraviolet B portion of the solar spectrum, with energies between 290 to 315 nm, penetrates into the epidermis. This ultraviolet radiation is absorbed by 7-dehydrocholesterol in the skin, which results in its transformation into previtamin [D.sub.3] (see Fig. 1). (1) Previtamin [D.sub.3] is rapidly transformed into vitamin [D.sub.3] by a temperature-dependent process. Vitamin [D.sub.3] enters the circulation and is metabolized sequentially first in the liver to 25-hydroxyvitamin D [25(OH)D] and then in the kidney to 1,25-dihydroxyvitamin D [1,25(OH)[.sub.2]D]. Once formed, 1,25(OH)[.sub.2]D interacts with its specific nuclear vitamin D receptor (VDR) in the small intestine to enhance the efficiency of intestinal calcium absorption. (1) It also maintains serum calcium within the normal range by interacting with its VDR in the osteoblast, which results in the expression of receptor activator of NF-[kappa][beta] ligand (RANKL). (1,2) This plasma membrane ligand is recognized by its corresponding receptor RANK on the preosteoclast. The intimate interaction between the RANKL on the osteoblast with the preosteoclast's RANK results in signal transduction inducing the preosteoclast to become a mature osteoclast (Fig. 2). The mature osteoclast releases both proteolytic and hydrolytic enzymes and hydrochloric acid to destroy the bone's protein matrix-releasing calcium and other minerals as well as hydrolytic collagen fragments; including N-terminal telopeptide (NTX) and C-terminal peptides (CTX) into the circulation. (3)
Consequences for the Skeleton of Vitamin D Deficiency
Vitamin D deficiency during the first 2 years of life results in rickets. In adults, vitamin D deficiency can cause or exacerbate osteoporosis and induce osteomalacia. Vitamin D deficiency results in a decrease in the efficiency of intestinal calcium absorption, which results in a decrease in ionized blood calcium. The calcium sensor in the parathyroid glands respond by increasing the production of parathyroid hormone (PTH). (4) PTH interacts with its receptor on the osteoblasts to increase the RANKL. This signal induces preosteoclasts to become mature osteoclasts. The action of osteoclasts dissolving bone matrix and releasing calcium into the extracellular space increases the porosity of the skeleton. PTH stimulates tubular reabsorption of calcium in the kidney, but also causes phosphorus loss into the urine. It is this PTH-induced phosphaturia that causes the serum phosphorus levels to be low or low-normal. This subtle effect on serum phosphorus levels has serious consequences for the skeleton because there is an inadequate calcium-phosphate product to sustain normal bone mineralization. Thus, although the osteoblasts are functioning...