Abstract
Ninety percent of vitamin D comes in nature from sun exposure. With aging, the skin's ability to produce vitamin D gradually decreases by up to 75 %.
After hydroxylation in the liver to calcidiol, the end product of vitamin D production is calcitriol, which is formed in the kidney and is the only one active at receptors on target tissues. Lack of vitamin D and its active metabolite is a risk factor for osteoporosis and reduces muscle strength. and limits neuromuscular coordination.
The main effect of the active vitamin D metabolite calcitriol is to stimulate the absorption of calcium from the gut. The consequences of vitamin D deficiency are secondary hyperparathyroidism and bone loss, leading to osteoporosis and fractures.
On the bone calcitriol acts directly and indirectly. Directly acts on osteoblasts, osteocytes, osteoclasts and production of type I collagen a numerous non-collagenous protein.
Randomized clinical trials have demonstrated that vitamin D with or without calcium can increase bone mineral density (BMD), decrease bone turnover and decrease fracture incidence. Calcitriol regulates not only calcium and phosphate homeostasis but also cell proliferation and differentiation and has a role to play in the responses of immune and nervous systems.
For the treatment of osteoporosis we recommend 800 IU vitamin D in combination with calcium. In general, the dose of vitamin D should be so high that the plasma level of the active metabolite (calcitriol) suppresses parathyroid hormone secretion.
Calcium and vitamin D are essential drugs for the treatment of senile osteoporosis, and when administered, teriparatide, bisphosphonates, elective estrogen receptor modulator (SERM), hormone replacement therapy (HRT), estrogen replacement therapy (ERT), and denosumab.
