Disadvantgaes of approached made to improve iron absorption
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To learn more about these tests visit tests to determine iron levels. ... Iron deficiency without anemia can occur when a person has a normal hemoglobin, but below normal serum ferritin and/or transferrin saturation. Iron deficiency with anemia can occur when a person has low values of both serum ferritin and hemoglobin.A lower-than-normal ferritin level can indicate that you have an iron deficiency, which can happen when you don't consume enough iron in your daily diet. Another condition that affects iron levels is anemia, which is when you don't have enough red blood cells for iron to attach to.
Over 2 billion people in both developing as well as developed countries – over 30% of the world’s population – are anaemic. With the classical preconception that oral iron administration or the intake of foods rich in iron increase haemoglobin concentration and reduce the prevalence of anaemia, specific programs have been designed, but iron supplementations have been less effective than expected. Of note, this hazardous simplification on iron status neglects its distribution in the body. The correct balance of iron, defined iron homeostasis, involves a physiological ratio of iron between tissues/secretions and blood, thus avoiding its delocalization as iron accumulation in tissues/secretions and iron deficiency in blood. Changes in iron status can affect the inflammatory response in multiple ways, particularly in the context of infection, an idea that is worth remembering when considering the value of iron supplementation in areas of the world where infections are highly prevalent. The enhanced availability of free iron can increase susceptibility and severity of microbial and parasitic infections.
The discovery of the hepcidin–ferroportin (Fpn) complex, which greatly clarified the enigmatic mechanism that supervises the iron homeostasis, should prompt to a critical review on iron supplementation, ineffective on the expression of the most important proteins of iron metabolism. Therefore, it is imperative to consider new safe and efficient therapeutic interventions to cure iron deficiency (ID) and ID anaemia (IDA) associated or not to the inflammation.
In this respect, lactoferrin (Lf) is emerging as an important regulator of both iron and inflammatory homeostasis. Oral administration of Lf in subjects suffering of ID and IDA is safe and effective in significantly increasing haematological parameters and contemporary decreasing serum IL-6 levels, thus restoring iron localization through the direct or indirect modulation of hepcidin and ferroportin synthesis. Of note, the nuclear localization of Lf suggests that this molecule may be involved in the transcriptional regulation of some genes of host inflammatory response.
We recently also reported that combined administration of oral and intravaginal Lf on ID and IDA pregnant women with preterm delivery threat, significantly increased haematological parameters, reduced IL-6 levels in both serum and cervicovaginal fluid, cervicovaginal prostaglandin PGF2α, and suppressed uterine contractility. Moreover, Lf combined administration blocked further the shortening of cervical length and the increase of foetal fibronectin, thus prolonging the length of pregnancy until the 37th–38th week of gestation.
These new Lf functions effective in curing ID and IDA through the restoring of iron and inflammatory homeostasis and in preventing preterm delivery, could have a great relevance in developing countries, where ID and IDA and inflammation-associated anaemia represent the major risk factors of preterm delivery and maternal and neonatal death.
Iron, an essential element for cell growth and proliferation, is a component of fundamental processes such as DNA replication and energy production. However, iron can also be toxic when present in excess because of its capacity to don electrons to oxygen, thus causing the generation of reactive oxygen species (ROS), such as superoxide anions and hydroxyl radicals.1 ROS are known to cause tissue injury and organ failure by damaging a number of cellular components, including DNA, proteins and membrane lipids. This dichotomy of iron, able to gain and loss electrons, has led to the evolution of tight controls on iron uptake to minimize iron deficiency as well as iron excess. Sophisticated strategies have been also developed to bind and store elemental iron in a nontoxic, readily available form.
The total body iron, about 3 g in women and 4 g in men, is mainly incorporated as haemic-iron in the haemoglobin, myoglobin and cytochromes (2–2.7 g), and as non-haemic form in various enzymes. In humans, iron absorption occurs in the proximal small intestine (duodenum) in which dietary iron is daily absorbed, ensuring iron in the bone marrow. A typical diet in developed countries provides about 15 mg of iron per day but only about 10%, corresponding to 1–2 mg, is absorbed due to its exceptionally poor bio-availability. Every day, macrophages recycle 20 mg of iron derived primarily from lyses of senescent erythrocytes for the de novo synthesis of haem. The iron released from the catabolism of senescent erythrocytes appears to be the largest source of iron in the reticuloendothelial system. Finally, few milligrams of iron are daily recovered from storage in hepatocytes and macrophages.