Vitamin D promotes the reabsorption of soccer at the renal level, intestinal absorption of of phosphorus and calcium and bone mineralization processes. Obtained from sun exposure or through diet, it is present in a biologically inactive form and must undergo two hydroxylation reactions. Few foods contain it in appreciable quantities. A particularly rich food is liver oil cod. They follow, Then, fatty fish (like the salmon and the herring), il latte and its derivatives, the egg, liver and green vegetables.
The first alterations, in case of vitamin D deficiency, consist of: resulting decrease in serum calcium and phosphorus levels iperparathyroidism secondary and increased concentration of alkaline phosphatase. Subsequently, there is an alteration of the mineralization processes with rickets (in bambino) ed osteoporosis (nell’adult) and muscle weakness, bone deformation e pains. Some Studies of 2006 have brought to light how vitamin D deficiency may be linked to flu syndrome.
Vitamin D is metabolically activated through sequential hydroxylations in the liver and kidney producing 1,25-dihydroxyvitamin, a steroid hormone ligand that binds with high affinity to the vitamin D receptor (VDR) in target tissues where it acts as a mediator or “signal transducer”.
There are multiple common polymorphic variants of the VDR gene, including:
FokI polymorphism, BsmI polymorphism, Polimerifism all of all.
The combination of these polymorphisms can be associated with:
- to a predisposition to a low level of bone mass,
- to a reduced absorption of calcium at the intestinal level
- to poor bone mineralization.
Through genetic testing it is possible to highlight the presence of these polymorphisms which can alter the individual ability to assimilate and use the vitamin D contained in foods, influencing the biological processes it controls. In these cases it is possible to restore the correct metabolic balance by modifying one's diet, balancing the deficiencies induced by one's genetic constitution
