In 1650, the English physician Glisson described a disease observed in children in the counties of Dorset and Somerset. He called it rickets. At the end of the 18th century, there were reports of the successful treatment of rickets with cod-liver oil. Then, in the 19th century, there were reports of a therapeutic effect of sunlight on rickets, animal feed (rats) irradiated with ultraviolet rays also had a therapeutic effect. It was proven that animal fats after irradiation acquire antirachitic properties. In 1936, pure vitamin D was isolated from tuna liver oil.
The most important compounds are ergocalciferol (vitamin D2) and cholecalciferol (vitamin D3). The substance, which was previously called vitamin D1, is a mixture of ergocalciferol and other sterols.
The main function of vitamin D is to maintain a constant concentration of Ca+2 ion and phosphorus in the body, which is carried out due to the participation of the vitamin in the regulation of the absorption of these elements in the intestine, the mobilization of calcium from the skeleton by resorption of the transformed bone tissue and the reabsorption of calcium and phosphorus ions in the renal tubules.
The main pathomorphological consequence of vitamin D deficiency is a violation of bone mineralization. The biological activity of D2 and D3 is the same for humans and most animals.
Vitamin D deficiency in children manifests itself in the form of rickets, in adults it is in the form of osteoporosis and osteomalacia (softening of the bones). Vitamin D deficiency is especially widespread among young children. The initial symptoms are associated with damage to the nervous system (sleep disorder, irritability, sweating). Without treatment, the process involves bone tissue (delayed teething and fontanelle closure, softening and subsequent deformation of the bones of the spine, ribs, lower extremities), skeletal muscles (weakening of muscle tone, weakness), and in severe cases, internal organs (liver, spleen, etc.) [1].