Iron absorption
The iron present in the body derives from the dietary intake, which allows to maintain a balance between absorption and daily losses.
A "common" diet involves the intake of 10-20 mg of iron per day, but under normal conditions only 5-10% (about 1-2 mg) is absorbed. If the requirement is increased it can even reach 20-30%.
Absorption regulation
The maintenance of homeostasis (balance between income and losses) of iron is ensured by the regulation of intestinal absorption, which is increased for the needs of erythropoiesis and reduced when iron deposits are abundant.
Foods rich in iron include liver, red meat, oysters and legumes.
Its absorption is reduced in the cases of:
- Poor iron diet (in absolute terms, but increases in percentage terms)
- Changes in gastric pH: a reduction in gastric acidity reduces its absorption
- Chelating agents in the diet: substances that bind it, reducing the amount available
- The possible decrease of absorbent intestinal surface or the alterations of the absorbent cells that constitute it
- Situations of increased intestinal motility
- Hemochromatosis (hereditary disease)
- Situations that increase iron turnover, such as vitamin B12 deficiency anemias (pernicious or due to nutritional deficiencies) or folate
- Metabolic disorders
- Presence in foods of EDTA (a preservative), of Tannates (substances present in tea), of oxalates, phosphates and carbonates.
Instead, they facilitate the absorption of ascorbic acid (vitamin C), citric acid, amino acids and sugars of alimentary origin.
Iron is absorbed as eminic iron, that is linked to hemoglobin or myoglobin present in meat. Or it can be absorbed in a soluble (ferrous) form. The heme iron is much more absorbable than the inorganic one .
Absorption occurs at the level of the duodenum (the first portion of the small intestine) and in the first section of the jejunum (intermediate portion of the small intestine).
The body regulates the amount of iron to be absorbed with three mechanisms:
- Using a deposit regulator that indicates the de / repayment status of the deposits themselves.
- Using an erythropoiesis regulator, which reports the amount of iron available for erythrocyte synthesis.
- Using a renal mechanism that signals the degree of hypoxia.
Iron in Blood
The iron, once absorbed in the intestine, enters the circulatory stream linked to a protein that is called transferrin, and here it is in a closed system where it is constantly recycled between plasma and tissues.
In clinical practice it is very useful to dose:
The amount of circulating transferrin saturated in iron, a value that takes the name of sideremia, and whose normal values are between 15 and 120 milligrams per deciliter.
The total iron-binding capacity, which is called transferrinemia, and whose normal values are between 250 and 400 milligrams deciliter.
Transferrin plays a key role in hematopoiesis, as it is responsible for the transfer of iron to erythroblasts, which have a specific receptor for them on their surface.
Iron leaks
The physiological excretion of iron occurs with urine, feces, sweat, desquamation of intestinal cells, skin, urinary tract. Iron losses in men and women after menopause amount to about 1 mg a day. In women of fertile age the losses are increased in consideration of the menstrual cycle (normally up to about 25 mg / cycle) and of pregnancies, since, from conception to delivery, there is an additional iron loss of about 700 mg, if yes consider the shares transferred to the fetus, the expulsion of the placenta and the postpartum hemorrhage; the loss due to breastfeeding is about 1 mg per day.
Iron metabolism
Under normal conditions, the iron content of the whole body varies from 2 g in women to 6 g in men. The iron is divided into a functional compartment and a storage compartment. Approximately 80% of functional iron is found in hemoglobin, myoglobin and iron-containing enzymes. Approximately 15% of the total iron is found in the storage pool, consisting of hemosiderin and ferritin . It should be noted that young women, even in good health, have significantly lower iron deposits than men. Their martial balance (of iron) is therefore much more precarious and they are consequently more vulnerable to excessive losses or to the increase in demands connected to the menstrual cycle and pregnancy.
All the storage iron is accumulated in the form of ferritin or hemosiderin. Ferritin is essentially an iron-protein complex that is found in all tissues, but particularly in the liver, spleen, bone marrow and skeletal muscles.
When iron deposits are normal, only traces of hemosiderin are found in the body. It is formed by aggregates of ferritin molecules. In conditions of martial overload, most of the iron is deposited in the form of hemosiderin.
Normally very small amounts of ferritin circulate in the plasma. The plasma ferritin derives in large part from the storage pool and therefore its dosage is a good indicator of the adequacy of the body's martial reserves. In deficiency situations, serum ferritin is always less than 12 micrograms per liter, while in conditions of overload, very high values can also be found, close to 5 thousand micrograms per liter.
The physiological importance of the martial reserve pool is the ease of mobilization in the event of an increase in requests.
Under normal conditions, there is a balance between the amount of ferritin in the deposits and the quantity of plasma. This is a useful parameter to evaluate the body's martial reserves.
There are some situations where there is iron growth in deposits:
In the event of overload due to high iron intake, such as for example those who need continuous blood transfusions or those suffering from a genetic disease called hemosiderosis.
In chronic inflammatory or tumor processes, in which iron is carried from the circulating compartment (usable) to that of deposits, with a consequent picture of anemia of chronic diseases, characterized by a reduction in circulating iron (iposideremia) and an increase in that of storage (hyperferritinemia).
Important tissue destruction: leads to a release in the circulation of the iron contained in the damaged cells with a consequent increase in circulating ferritin.
