Iron is used metabolically in the formation of haemoglobin and is necessary for the oxidative processes of living tissue. Ferrous bisglycinate is absorbed intact into the mucosal cells of the intestine, and is subsequently hydrolysed into its iron and glycine components. The iron component of ferrous bisglycinate is metabolised like any other source of iron.
The solubility of iron from ferrous bisglycinate is not affected by changes in pH. The bioavailability of the ferrous bisglycinate chelate is approximately 91 % compared to that of ferrous sulphate which is approximately 27 %. Tannins and oxalates are commonly found in food and these usually inhibit the absorption of iron, whereas they do not significantly affect the absorption of ferrous bisglycinate at all. Folic acid reduces damage to DNA and prevents replication errors. A deficiency of folic acid induces cell apoptosis, disturbs cell cycling and increases the rate of cell death. Folic acid deficiency also causes abnormal cell maturation and division in the bone marrow, which results in abnormal megaloblasts which are the precursors to red blood cells. Megaloblasts are then unable to mature into red blood cells. Vitamin B12 contributes to the health of the nervous system and is involved in the production of red blood cells.
Vitamin B12 can be converted to coenzyme B12 in tissues and, as such, is essential for conversion of methylmalonate to succinate and synthesis of methionine from homocystine, a reaction that also requires folate. Without coenzyme B12, folate deficiency occurs. Vitamin B12 also facilitates fat and carbohydrate metabolism and protein synthesis. Cells characterized by rapid division (epithelial cells, bone marrow, and myeloid cells) appear to have the greatest requirement for vitamin B12. Vitamin B12 deficiency may cause megaloblastic anemia, GI lesions, and neurologic damage; it begins with an inability to produce myelin followed by gradual degeneration of the axon and nerve. Parenteral administration of vitamin B12 completely reverses the megaloblastic anemia and GI symptoms of vitamin B12 deficiency.