Feeling fatigued & dizzy with poor memory? You could be low in iron
Iron is a vital element necessary for the manufacture of the oxygen carrying molecule, haemoglobin. Ferritin is one of the major storage sources of iron & can be used as a therapeutic iron supplement without the usual side effects, such as constipation.
Ferritin as a medicinal source of iron
Of all the indispensable trace elements required by higher animals, iron is by far the most important, on account of its presence as a structural component of haemoglobin. 70% of the total iron in the human body is present as haemoglobin and about 3 percent in the muscles as myoglobin, however most of the remainder is found in ferritin, which together with hemosiderin, forms the major storage sources of iron.
The mean value of storage iron for men is about 1 gm and for women about 500 mg. Iron is rigidly conserved. Only small amounts are lost through sloughing of epithelial cells from the skin and gastrointestinal, genitourinary and respiratory systems. Homeostasis is maintained by controlled absorption of iron by the gut.
Menstruation is the most common cause of blood loss in women and they require a greater intake than men. In women who lose more than 80 ml of blood during menstruation, or who have suffered losses through child bearing, iron stores may be considerably reduced or may even be entirely absent.
An iron deficiency can develop easily, especially for those individuals who are commonly considered to be in a high-risk group. Among these, infants, adolescents, old people and pregnant women constitute the most exposed groups, even in industrialized countries such as New Zealand, United States, France and Italy.
It is known that iron deficiency not only manifests itself in the classical condition of sideropenic anaemia, but also in a series of events not directly related to haemo-pathological patterns. These conditions of "tissular anaemia" must be taken into consideration, in order to prevent more marked damages, due to iron deficiency.
Ferritin - bioavailability iron
Ferritin is a high molecular weight iron-binding protein, which is currently used as a therapeutic iron supplement in Europe. Physicians in Italy, who have faced the widespread problem of Mediterranean anaemia, have used ferritin for numerous clinical conditions involving iron depletion.
This unique iron supplement has numerous advantages over other inorganic sources of iron. Ferritin is rapid acting and is exceptionally well tolerated by sensitive individuals. Other iron salts, such as ferrous sulphate, commonly cause gastrointestinal upset and other side effects. The tendency of ferrous sulphate to cause gastrointestinal bleeding may result in a net negative iron balance in some individuals given the salt.
Ferritin can be given in very large doses, resulting in a much higher percentage extraction of iron by the gut than with other iron supplements, without causing significant gastrointestinal distress. Ferritin is also a weaker oxidation catalyst than inorganic iron salts and does not deplete endogenous antioxidant defences. The gentle, physiological character of ferritin as an iron source is especially useful in fragile clinical situations such as pregnancy, infancy and old age.
Physiological role of ferritin
Ferritin is a ubiquitous, water-soluble, iron storage protein present within cells. It is widely distributed in both plant and animal species, which signifies an essential biological role. In addition, ferritin occurs in normal mammalian plasma. Ferritin provides a readily accessible store of the metal essential for the synthesis of haemoglobin and the iron metalloenzymes. On the other hand, ferritin sequesters potentially toxic ionic iron. Duodenal ferritin acts to inhibit iron absorption when excesses of iron are administered.
The capacity of cells to synthesize ferritin appears to have developed early in evolution. Although bacteria contain a variety of iron-chelating compounds, including peptides involved in iron transport, ferritin first emerges as an identifiable characteristic entity in fungi.
Ferritin has been firmly established as a component of plant cells, where it shows responsiveness to the iron available to the plant. Among animals, ferritin has been identified in the tissues of annelid worms, shellfish, insects, fish, amphibians and mammals. In the mammal, the liver, spleen and bone marrow have the largest deposits of stored iron but ferritin can be detected in all tissues.
The capacity to make ferritin, presumably, is universally distributed as part of the equipment of cells for utilizing iron, which in more than minimal concentrations, can lead to denaturation of cell proteins.
Ferritin appears to have many important roles in the organism but is mainly related with iron absorption and transport and with iron storage within the cell. An utmost important role for ferritin has been proposed in the duodenal cellular mechanism for iron transfer from the brush border to the vascular lumen of the enterocyte.
Tissue ferritin has two major functions:
(1) To store iron and
(2) To prevent the accumulation of high concentrations of free toxic iron in the cells.
Unlike tissue ferritin, serum ferritin has a low iron content and the protein is glycosilated. Serum ferritin is produced by the reticuloendothelial cells and its concentration reflects the amount of storage iron.
Evidence has been obtained that the serum ferritin level in normal subjects is proportional to the size of body iron stores. The serum ferritin level is three times higher in males than in females, a finding consistent with the known sex difference in storage iron.
Pathologic disturbances in iron balance have a marked effect on the serum ferritin level. In iron deficiency, a mean of 5 mg per ml is reported. Similarly, in patients with iron overload due to either hemochromatosis or excess transfusion, the serum ferritin is invariably elevated. High serum ferritin levels are found also in patients with hepatocellular necrosis, acute & chronic infection and inflammation and in malignancy.
Serum ferritin may be of value as a marker of hypothyroidism and thyroid hormone resistance. Synovial fluid ferritin determination in the arthritides may not have as much diagnostic value as was originally suggested. High serum ferritin predicts persistence of hepatitis infection.
Ferritin and ascorbic acid
In iron overload, optimal rates of iron chelation are possible only in the presence of approximately normal levels of tissue ascorbic acid. Ascorbic acid administration enhances deferoxamine-induced urinary iron excretion in thalassemia and for this reason, the treatment of iron overload by chelation therapy has been accompanied by simultaneous administration of ascorbic acid in order to produce a negative iron balance. The mechanism for this increase in chelation remains unclear but it is unlikely that ascorbic acid in some way increases the low molecular weight labile iron pool.
Ascorbic acid appears to have an important physiological role in storage iron metabolism, but its exact function is unclear. Most of the current evidence points to the fact that removal of iron from ferritin may involve reaction with the flavin nucleotides. The function of ascorbic acid may be related to redox potentials within the cell. These factors are of relevance to the management of iron-storage diseases.
Physicians routinely use ascorbic acid in conjunction with ferritin, since it enhances iron absorption. Increased ferritin absorption is noted when taken together with 100mg of ascorbic acid. However, the two ingredients should not be combined in the same capsule, or oxidation reactions may occur.
Ferritin binds more than iron. Copper, cadmium and beryllium are also chelated. Ferritin may act to regulate and detoxify various metal ions.
Evidence of absorption
On the basis of sedimentation characteristics, X-ray crystallography, light scattering and quantitative polyacrylamide gel electrophoresis, it is agreed that the protein shell of ferritin has a molecular weight between 430,000 and 490,000 Daltons; up to 4,500 atoms of iron can be stored as ferric oxyhydroxide. The structure is very compact, which may explain its unusual stability to heat.
It is known that epithelial cells are able to uptake the ferritin macromolecule by pinocytosis. Using the "bloodless rat", a new model for macromolecular transport, some investigators have seen that ferritin, enclosed in vesicles, is transported through the cytoplasm of the absorptive cells to the basal membrane.
According to Modesti, ferritin is absorbed directly by the cell membrane of the apical surface. Using electro-microscopic procedures, he successfully demonstrated that there is a passage of ferritin from the lumen into the intracellular spaces and lymphatics. Employing different techniques, Williams and Hemings were able to confirm similar findings.
Clinical use of ferritin
In 1952, E. Antonini first proposed the clinical use of purified horse spleen ferritin as a source of iron for treatment of sideropenic syndromes. The clinical use of ferritin as an iron supplement has been widely accepted with complete adherence of all patients to therapy, due to its perfect tolerability. The drug is well tolerated, also when administered in the fasting state.
Administration of high dose ferritin may be used as an iron supplement in cases of iron deficiency. Ferritin may also be used in the prevention of anaemia in pregnant women who have reduced iron reserves in the last trimester. In severe iron deficiency anaemia, a greater amount of ferritin iron may be used to produce an increase of 2 gm% of haemoglobin every 21 days, as has been recommended in previous studies.
Ciccone and co-workers studied the pattern of the curve of serum iron values after massive oral administration of a preparation containing ferritin. There was a statistically significant rise in sideremia values by the first hour after administration, reaching peak at the second to third hour.
An investigation of the treatment of 30 children, 17 boys and 13 girls aged from 2 months to 13 years, all presenting with symptoms of iron deficiency in the form of hypochromic sideropenic anaemia were treated with ferritin for 90 days. Excellent improvement was noted in 11 patients and generally satisfactory results in 18 of the patients. In only one child was no improvement in symptoms noted. The absence of side effects and high tolerability of the preparation enabled treatment to continue over an extended period of time.
Fochi and co-workers conducted a clinical investigation on 69 pregnant women, anaemic and non-anaemic. The purpose of the study was to assess the effect of 50 days of treatment with four different medicinal iron preparations, namely ferrous sulphate, iron chondroitinsulfuric acid complex, ferritin alone or associated with folinic acid and cobamamide on various haematological parameters (Hb, RCC, Ht, CV, Iron and Transferrin IBC). The four products demonstrated a similar efficacy in maintaining anaemic conditions under control. Ferrous sulphate caused side effects. Ferrous sulphate has caused severe side effects, especially if administrated during pregnancy and in childhood and despite its high rating in AMA Drug Evaluations, is not the treatment of choice worldwide.
Comparative studies between ferrous sulphate and ferritin on two groups of 15 pregnant women, each suffering from pregnancy sideropenia, demonstrated equal effectiveness in reducing anaemic sideropenia. Ferritin tolerance was very good, but ferrous sulphate tolerance was not good (nausea, vomiting and gastric pain were common symptoms).
In the second trial, 40 children under 12 affected by "anaemia without anaemia" were treated for a period of 60 days with ferritin or placebo. Ferritin improved the hematochemical parameters while the placebo had no effect. In another clinical study, Fochi and co-workers studied 79 pregnant women, 48 of whom were anaemic. Ferritin iron induced an improvement superior to other forms of iron.
The clinical data after oral administration of ferritin generally does not demonstrate an increase in serum ferritin. On the contrary, an immediate increase of serum iron is reported. Consequently, one can safely assume that the role of orally administered ferritin is completely different from that of endogenous ferritin, at least when one considers the immunosuppressive effects sometimes attributed to the latter. Orally administered ferritin, as a protein, slowly liberates iron in the digestive tract. While the amount of iron absorbed from ferritin is relatively low, this iron is better tolerated than other iron salts.
Each capsule of Ferritin (CVR, mol.weight. 455,000) contains 5 mg of elemental iron and is derived from purified New Zealand bovine splenic ferritin. The ferritin contained in this product is an individually-resolved, high molecular weight compound and not a crude ferritin complex. Ferritin is absorbed best when taken between meals.
Take 1 to 6 capsules daily, as recommend by your health care professional. The hematologic response becomes fully evident after two weeks of supplementation. To replenish depleted iron stores: oral therapy should be continued for approximately 4 to 6 months after the haemoglobin level has returned to normal.
Iron replacement therapy
Chronic fatigue of known etiology
Other causes of iron deficiency anaemia
NOTE: Differential diagnosis is essential to establish and, if possible, to treat the underlying cause of anaemia.
As an iron donor, ferritin is not indicated in anaemia derived from conditions different from iron deficiency (e.g. aplastic or hemolytic anaemias).
All iron compounds are contra-indicated in patients with primary hemochromatosis and transfusion siderosis.
Excessive iron storage is rare following oral administration, except in patients with increased iron absorption (e.g. thalassemia, chronic haemolytic states, Laennec's cirrhosis, side-roachrestic anaemia).
Ferritin is contraindicated in cases of acute pancreatitis due to the fact that one of the most frequent causes of this condition is hemochromatosis.
At Ideal Health we stock one of the only supplement forms of Ferritin available, sourced from New Zealand bovine.