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Review on iron and its importance for human health

  • School of Public Health
  • Child Growth and Development Research Center, Research Institute for Primordial Prevention of Non-Communicable Disease, Isfahan University of Medical Sciences

Abstract and Figures

It is well-known that deficiency or over exposure to various elements has noticeable effects on human health. The effect of an element is determined by several characteristics, including absorption, metabolism, and degree of interaction with physiological processes. Iron is an essential element for almost all living organisms as it participates in a wide variety of metabolic processes, including oxygen transport, deoxyribonucleic acid (DNA) synthesis, and electron transport. However, as iron can form free radicals, its concentration in body tissues must be tightly regulated because in excessive amounts, it can lead to tissue damage. Disorders of iron metabolism are among the most common diseases of humans and encompass a broad spectrum of diseases with diverse clinical manifestations, ranging from anemia to iron overload, and possibly to neurodegenerative diseases. In this review, we discuss the latest progress in studies of iron metabolism and bioavailability, and our current understanding of human iron requirement and consequences and causes of iron deficiency. Finally, we discuss strategies for prevention of iron deficiency.
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Journal of Research in Medical Sciences
| February 2014 | 164
Review on iron and its importance for human health
Nazanin Abbaspour, Richard Hurrell1, Roya Kelishadi2
Department of Environmental Systems Science, Institute of Terrestrial Ecosystem, Swiss Federal Institute of Technology, Zurich,
1Department of Health Sciences and Technology, Laboratory of Human Nutrition, Institute of Food, Nutrition and Health, Swiss Federal
Institute of Technology, Zurich, Switzerland, 2Child Growth and Development Research Center, Isfahan University of Medical Sciences,
Isfahan, Iran
It is well-known that defi ciency or over exposure to various elements has noticeable eff e cts on human health.  e eff ect of an element
is determined by several characteristics, including absorption, metabolism, and degree of interaction with physiological processes.
Iron is an essential element for almost all living organisms as it participates in a wide variety of metabolic processes , including oxygen
transport, deoxyribonucleic acid (DNA) synthesis, and electron transport. However, as iron can form free radicals, its concentration
in body tissues must be tightly regulated because in excessive amounts, it can lead to tissue damage. Disorders of iron metabolism
are among the most common diseases of humans and encompass a broad spectrum of diseases with diverse clinical manifestations,
ranging from anemia to iron overload, and possibly to neurodegenerative diseases. In this review, we discuss the latest progress in
studies of iron metabolism and bioavailability, and our current understanding of human iron requirement and consequences and
causes of iron defi ciency. Finally, we discuss strategies for prevention of iron defi ciency.
Key words: Anemia, human iron requirement, iron bioavailability, iron defi ciency, iron metabolism
are highly insoluble, and thus is not readily available
for uptake by organisms.[2] In response, various cellular
mechanisms have evolved to capture iron from the
environment in biologically useful forms. Examples
are siderophores secreted by microbes to capture
iron in a highly speci c complex[12] or mechanisms to
reduce iron from the insoluble ferric iron (Fe+3) to the
soluble ferrous form (Fe+2) as in yeasts.[13] Many of the
mechanisms found in lower organisms, have analogous
counterparts in higher organisms, including humans. In
the human body, iron mainly exists in complex forms
bound to protein (hemoprotein) as heme compounds
(hemoglobin or myoglobin), heme enzymes, or nonheme
compounds (flavin-iron enzymes, transferring, and
ferritin).[3] The body requires iron for the synthesis of
its oxygen transport proteins, in particular hemoglobin
and myoglobin, and for the formation of heme enzymes
and other iron-containing enzymes involved in electron
transfer and oxidation-reductions.[14,3] Almost two-thirds
of the body iron is found in the hemoglobin present in
circulating erythrocytes, 25% is contained in a readily
mobilizable iron store, and the remaining 15% is
bound to myoglobin in muscle tissue and in a variety
of enzymes involved in the oxidative metabolism and
many other cell functions.[15]
Iron is recycled and thus conserved by the body. Figure 1
shows a schematic diagram of iron cycle in the body.
From ancient times, man has recognized the special role
of iron in health and disease.[1] Iron had early medicinal
uses by Egyptians, Hindus, Greeks, and Romans.[2,3]
During the 17th century, iron was used to treat chlorosis
(green disease), a condition o en resulting from the
iron de ciency.[4] However, it was not until 1932 that the
importance of iron was nally se led by the convincing
proof that inorganic iron was needed for hemoglobin
synthesis.[5] For many years, nutritional interest in iron
focused on its role in hemoglobin formation and oxygen
transport.[6] Nowadays, although low iron intake and/
or bioavailability are responsible for most anemia in
industrialized countries, they account for only about
half of the anemia in developing countries,[7] where
infectious and inflammatory diseases (especially
malaria), blood loss from parasitic infections, and other
nutrient de ciencies (vitamin A, ribo avin, folic acid,
and vitamin B12) are also important causes.[8]
Biochemistry and physiology
In contrast to zinc, iron is an abundant element on
earth[2,9] and is a biologically essential component of
every living organism.[10,11] However, despite its geologic
abundance, iron is o en a growth limiting factor in the
environment.[9] This apparent paradox is due to the fact
that in contact with oxygen iron forms oxides, which
How to cite this article: Abbaspour N, Hurrell R, Kelishadi R. Review on iron and its importance for human health. J Res Med Sci 2014;19:164-74
Address for correspondence: Prof. Roya Kelishadi, Child Growth and Development Research Center, Isfahan University of Medical Sciences,
Isfahan, Iran. E-mail:
Received: 08-06-2013; Revised: 03-11-2013; Accepted: 27-11-2013
Abbaspour, et al.: Iron review
Journal of Research in Medical Sciences | February 2014 |
Iron is delivered to tissues by circulating transferrin, a
transporter that captures iron released into the plasma
mainly from intestinal enterocytes or reticuloendothelial
macrophages. The binding of iron-laden transferrin to
the cell-surface transferrin receptor (TfR) 1 results in
endocytosis and uptake of the metal cargo. Internalized iron
is transported to mitochondria for the synthesis of heme
or iron-sulfur clusters, which are integral parts of several
metalloproteins, and excess iron is stored and detoxi ed
in cytosolic ferritin.
The fraction of iron absorbed from the amount ingested is
typically low, but may range from 5% to 35% depending
on circumstances and type of iron.[3]
Iron absorption occurs by the enterocytes by divalent
metal transporter 1, a member of the solute carrier
group of membrane transport proteins. This takes place
predominantly in the duodenum and upper jejunum.[16] It is
then transferred across the duodenal mucosa into the blood,
where it is transported by transferrin to the cells or the
bone marrow for erythropoiesis [producing red blood cells
(RBCs)].[14,17,18] A feedback mechanism exists that enhances
iron absorption in people who are iron de cient. In contrast,
people with iron overload dampen iron absorption via
hepcidin. It is now generally accepted that iron absorption
is controlled by ferroportin which allows or does not allow
iron from the mucosal cell into the plasma.
The physical state of iron entering the duodenum greatly
in uences its absorption. At physiological pH, ferrous iron
(Fe+2) is rapidly oxidized to the insoluble ferric (Fe+3) form.
Gastric acid lowers the pH in the proximal duodenum
reducing Fe+3 in the intestinal lumen by ferric reductases,
thus allowing the subsequent transport of Fe+2 across the
apical membrane of enterocytes. This enhances the solubility
and uptake of ferric iron. When gastric acid production is
impaired (for instance by acid pump inhibitors such as the
drug, prilosec), iron absorption is reduced substantially.
Dietary heme can also be transported across the apical
membrane by a yet unknown mechanism and subsequently
metabolized in the enterocytes by heme oxygenase 1 (HO-1)
to liberate (Fe+2).[19] This process is more e cient than the
absorption of inorganic iron and is independent of duodenal
pH. It is thus not in uenced by inhibitors such as phytate and
polyphenols. Consequently, red meats high in hemoglobin
are excellent nutrient sources of iron. Directly internalized
Fe+2 is processed by the enterocytes and eventually (or
not) exported across the basolateral membrane into the
bloodstream via Fe+2 transporter ferroportin. The ferroportin-
mediated e ux of Fe+2 is coupled by its reoxidation to Fe+2,
catalyzed by the membrane-bound ferroxidase hephaestin
that physically interacts with ferroportin[20] and possibly also
by its plasma homologue ceruloplasmin. Exported iron is
scavenged by transferrin, which maintains Fe+3 in a redox-
inert state and delivers it into tissues. The total iron content
of transferrin (3 mg) corresponds to less than 0.1% of body
iron, but it is highly dynamic and undergoes more than 10
times daily turnover to sustain erythropoiesis. The transferrin
iron pool is replenished mostly by iron recycled from e ete
RBCs and, to a lesser extent, by newly absorbed dietary
iron. Senescent RBCs are cleared by reticuloendothelial
macrophages, which metabolize hemoglobin and heme,
and release iron into the bloodstream. By analogy to
intestinal enterocytes, macrophages export Fe+2 from their
plasma membrane via ferroportin, in a process coupled by
reoxidation of Fe+2 to Fe+3 by ceruloplasmin and followed by
the loading of Fe+3 to transferrin.[21]
Theil et al.,[21] recently reported that an independent
mechanism also exists for the absorption of plant ferritins
mostly present in legumes. However, the relevance of the
ferritin transporter is unclear as most ferritin seems to be
degraded during food processing and digestion, thereby
releasing inorganic iron from the ferritin shell for absorption
by the normal mechanism.[22] As one ferritin molecule
contains 1000 or more iron atoms, and should also be
una ected by iron absorption inhibitors, such a mechanism
would provide an important source of iron in the developing
world where legumes are commonly consumed.
Regulation of iron homeostasis
Since iron is required for a number of diverse cellular
functions, a constant balance between iron uptake,
transport, storage, and utilization is required to maintain
iron homeostasis.[11] As the body lacks a de ned mechanism
Figure 1: Iron is bound and transported in the body via transferrin and stored in
ferritin molecules. Once iron is absorbed, there is no physiologic mechanism for
excretion of excess iron from the body other than blood loss, that is, pregnancy,
menstruation, or other bleeding
Abbaspour, et al.: Iron review
Journal of Research in Medical Sciences
| February 2014 | 166
for the active excretion of iron, iron balance is mainly
regulated at the point of absorption.[23,24]
Hepcidin is a circulating peptide hormone secreted by
the liver that plays a central role in the regulation of
iron homeostasis. It is the master regulator of systemic
iron homeostasis, coordinating the use and storage of
iron with iron acquisition.[25] This hormone is primarily
produced by hepatocytes and is a negative regulator
of iron entry into plasma [Figure 2]. Hepcidin acts by
binding to ferroportin, an iron transporter present on
cells of the intestinal duodenum, macrophages, and cells
of the placenta. Binding of hepcidin induces ferroportin
internalization and degradation.[26] The loss of ferroportin
from the cell surface prevents iron entry into plasma
[Figure 2a]. Decreased iron entry into plasma results in
low transferrin saturation and less iron is delivered to the
developing erythroblast. Conversely, decreased expression
of hepcidin leads to increased cell surface ferroportin and
increased iron absorption[27] [Figure 2c]. In all species, the
concentration of iron in biological uids is tightly regulated
to provide iron as needed and to avoid toxicity, because
iron excess can lead to the generation of reactive oxygen
species.[28] Iron homeostasis in mammals is regulated at
the level of intestinal absorption, as there is no excretory
pathway for iron.
Plasma hepcidin levels are regulated by di erent stimuli,
including cytokines, plasma iron, anemia, and hypoxia.
Dysregulation of hepcidin expression results in iron
disorders. Overexpression of hepcidin leads to the
anemia of chronic disease, while low hepcidin production
results in hereditary hemochromatosis (HFE) with
consequent iron accumulation in vital organs [Figure 2].
Most hereditary iron disorders result from inadequate
hepcidin production relative to the degree of tissue iron
accumulation. Impaired hepcidin expression has been
shown to result from mutations in any of 4 di erent genes:
TfR2, HFE, hemochromatosis type 2 (HFE2), and hepcidin
antimicrobial peptide (HAMP). Mutations in HAMP, the
gene that encodes hepcidin, result in iron overload disease,
as the absence of hepcidin permits constitutively high iron
absorption. The role for other genes (TFR2, HFE, and HFE2)
in the regulation of hepcidin production has been unclear.[27]
Ferritin concentration together with that of hemosiderin
re ects the body iron stores. They store iron in an insoluble
form and are present primarily in the liver, spleen, and bone
marrow.[2] The majority of iron is bound to the ubiquitous
and highly conserved iron-binding protein, ferritin.[18]
Hemosiderin is an iron storage complex that less readily
releases iron for body needs. Under steady state conditions,
serum ferritin concentrations correlate well with total body
iron stores.[29] Thus, serum ferritin is the most convenient
laboratory test to estimate iron stores.
Apart from iron losses due to menstruation, other bleeding
or pregnancy, iron is highly conserved and not readily lost
from the body.[30] There are some obligatory loss of iron from
the body that results from the physiologic exfoliation of cells
from epithelial surfaces,[30] including the skin, genitourinary
tract, and gastrointestinal tract.[3] However, these losses are
estimated to be very limited (1 mg/day).[31] Iron losses through
bleeding can be substantial and excessive menstrual blood
loss is the most common cause of iron de ciency in women.
Dietary iron occurs in two forms: heme and nonheme.[23]
The primary sources of heme iron are hemoglobin and
myoglobin from consumption of meat, poultry, and sh,
whereas nonheme iron is obtained from cereals, pulses,
legumes, fruits, and vegetables.[32] Heme iron is highly
bioavailable (15%-35%) and dietary factors have little
e ect on its absorption, whereas nonheme iron absorption
is much lower (2%-20%) and strongly in uenced by the
presence of other food components.[23] On the contrary, the
quantity of nonheme iron in the diet is manyfold greater
than that of heme-iron in most meals. Thus despite its
lower bioavailability, nonheme iron generally contributes
more to iron nutrition than heme-iron.[33] Major inhibitors
of iron absorption are phytic acid, polyphenols, calcium,
and peptides from partially digested proteins.[23] Enhancers
are ascorbic acid and muscle tissue which may reduce ferric
Figure 2: Hepcidin-mediated regulation of iron homeostasis. (a) Increased
hepcidin expression by the liver results from in ammatory stimuli. High levels of
hepcidin in the bloodstream result in the internalization and degradation of the iron
exporter ferroportin. Loss of cell surface ferroportin results in macrophage iron
loading, low plasma iron levels, and decreased erythropoiesis due to decreased
transferrin-bound iron. The decreased erythropoiesis gives rise to the anemia
of chronic disease. (b) Normal hepcidin levels, in response to iron demand,
regulate the level of iron import into plasma, normal transferrin saturation, and
normal levels of erythropoiesis. (c) Hemochromatosis, or iron overload, results
from insuf cient hepcidin levels, causing increased iron import into plasma,
high transferrin saturation, and excess iron deposition in the liver. Source: De
Domenico, et al.[27]
ab c
Abbaspour, et al.: Iron review
Journal of Research in Medical Sciences | February 2014 |
iron to ferrous iron and bind it in soluble complexes which
are available for absorption[23]
Factors enhancing iron absorption
A number of dietary factors influence iron absorption.
Ascorbate and citrate increase iron uptake in part by acting
as weak chelators to help to solubilize the metal in the
duodenum [Table 1].[34] Iron is readily transferred from these
compounds into the mucosal lining cells. The dose-dependent
enhancing e ect of native or added ascorbic acid on iron
absorption has been shown by researchers.[34] The enhancing
e ect is largely due to its ability to reduce ferric to ferrous
iron but is also due to its potential to chelate iron.[35] Ascorbic
acid will overcome the negative e ect on iron absorption
of all inhibitors, which include phytate,[36] polyphenols,[37]
and the calcium and proteins in milk products,[38] and will
increase the absorption of both native and forti cation iron.
In fruit and vegetables, the enhancing e ect of ascorbic acid is
o en cancelled out by the inhibiting e ect of polyphenols.[39]
Ascorbic acid is the only absorption enhancer in vegetarian
diets, and iron absorption from vegetarian and vegan meals
can be best optimized by the inclusion of ascorbic acid-
containing vegetables.[40] Cooking, industrial processing,
and storage degrade ascorbic acid and remove its enhancing
e ect on iron absorption.[41]
The enhancing effect of meat, fish, or poultry on iron
absorption from vegetarian meals has been shown,[42] and
30 g muscle tissue is considered equivalent to 25 mg ascorbic
acid.[33] Bjorn-Rasmussen and Hallberg[43] reported that the
addition of chicken, beef, or sh to a maize meal increased
nonheme iron absorption 2-3-fold with no in uence of
the same quantity of protein added as egg albumin. As
with ascorbic acid, it has been somewhat more di cult
to demonstrate the enhancing e ect of meat in multiple
meals and complete diet studies. Reddy et al.,[44] reported
only a marginal improvement in iron absorption (35%) in
self-selected diets over 5 days when daily muscle tissue
intake was increased to 300 g/day, although, in a similar
5-day study, 60 g pork meat added to a vegetarian diet
increased iron absorption by 50%.[45]
Factors inhibiting iron absorption
In plant-based diets, phytate (myo-inositol hexakisphosphate)
is the main inhibitor of iron absorption.[23] The negative
e ect of phytate on iron absorption has been shown to be
dose dependent and starts at very low concentrations of 2-10
mg/meal.[37,46] The molar ratio of phytate to iron can be used
to estimate the e ect on absorption. The ratio should be 1:1
or preferably, 0.4:1 to signi cantly improve iron absorption
in plain cereal or legume-based meals that do not contain
any enhancers of iron absorption, or, 6:1 in composite meals
with certain vegetables that contain ascorbic acid and meat
as enhancers.[47]
Polyphenols occur in various amounts in plant foods and
beverages, such as vegetables, fruit, some cereals and
legumes, tea, co ee, and wine. The inhibiting e ect of
polyphenols on iron absorption has been shown with black
tea and to a lesser extent with herbal teas.[48,49] In cereals
and legumes, polyphenols add to the inhibitory e ect of
phytate, as was shown in a study that compared high and
low polyphenol sorghum.[23]
Calcium has been shown to have negative effects on
nonheme and heme iron absorption, which makes it
di erent from other inhibitors that a ect nonheme iron
absorption only.[50] Dose-dependent inhibitory e ects were
shown at doses of 75-300 mg when calcium was added
to bread rolls and at doses of 165 mg calcium from milk
products.[51] It is proposed that single-meal studies show
negative e ects of calcium on iron absorption, whereas
multiple-meal studies, with a wide variety of foods and
various concentrations of other inhibitors and enhancers,
indicate that calcium has only a limited e ect on iron
Animal proteins such as milk proteins, egg proteins, and
albumin, have been shown to inhibit iron absorption.[53]
The two major bovine milk protein fractions, casein and
whey, and egg white were shown to inhibit iron absorption
in humans.[54] Proteins from soybean also decrease iron
Competition with iron
Competition studies suggest that several other heavy
metals may share the iron intestinal absorption pathway.
These include lead, manganese, cobalt, and zinc [Table 1].
As iron de ciency o en coexists with lead intoxication,
this interaction can produce particularly serious medical
complications in children.[56]
Lead is a particularly pernicious element to iron
metabolism.[57] Lead is taken up by the iron absorption
machinery (DTM1), and secondarily blocks iron through
competitive inhibition. Further, lead interferes with a
number of important iron-dependent metabolic steps
such as heme biosynthesis. This multifaceted in uence
has particularly dire consequences in children, were
lead not only produces anemia, but can impair cognitive
Table 1: Factors that could in uence iron absorption
Physical state (bioavailability) Heme > Fe+2 > Fe+3
Inhibitors phytates, polyphenols, calcium,
some proteins,
Competitors; in animal studies lead, cobalt, strontium,
manganese, zinc
Facilitators ascorbate, citrate, some amino
acids, meat, fi sh, poultry
Abbaspour, et al.: Iron review
Journal of Research in Medical Sciences
| February 2014 | 168
development. Lead exists naturally at high levels in ground
water and soil in some regions, and can clandestinely a ack
children’s health. For this reason, most pediatricians in the
U.S. routinely test for lead at an early age through a simple
blood test.
During early infancy, iron requirements are met by the
li le iron contained in the human milk.[58] The need for
iron rises markedly 4-6 months a er birth and amounts to
about 0.7-0.9 mg/day during the remaining part of the rst
[58] Between 1 and 6 years of age, the body iron content
is again doubled.[58] Iron requirements are also very high in
adolescents, particularly during the period of growth spurt.
Girls usually have their growth spurt before menarche,
but growth is not nished at that time. In boys there is a
marked increase in hemoglobin mass and concentration
during puberty. In this stage, iron requirements increase to
a level above the average iron requirements in menstruating
women[58] [see Table 2].
The average adult stores about 1-3 g of iron in his or her
body. A fine balance between dietary uptake and loss
maintains this balance. About 1 mg of iron is lost each
day through sloughing of cells from skin and mucosal
surfaces, including the lining of the gastrointestinal tract.[59]
Menstruation increases the average daily iron loss to about
2 mg per day in premenopausal female adults.[60] The
augmentation of body mass during neonatal and childhood
growth spurts transiently boosts iron requirements.[61]
A dietary intake of iron is needed to replace iron lost in
the stools and urine as well as through the skin. These
basal losses represent approximately 0.9 mg of iron for an
adult male and 0.8 mg for an adult female.[62] The iron lost
in menstrual blood must be taken into consideration for
women of reproductive age [Table 2].
The highest probability of suffering iron deficiency is
found in those parts of a population that have inadequate
access to foods rich in absorbable iron during stages of
high iron demand. These groups correspond to children,
adolescents, and women of reproductive age, in particular
during pregnancy.[63,58]
In the case of infants and adolescents, the increased iron
demand is the result of rapid growth. For women of
reproductive age the principle reason is the excessive blood
loss during menstruation. During pregnancy, there is a
signi cant increase in iron requirement due to the rapid
growth of the placenta and the fetus and the expansion
of the globular mass.[63] In contrast, adult men and
postmenopausal women are at low risk of iron de ciency
and the amount of iron in a normal diet is usually su cient
to cover their physiological requirements.[63]
Consequences of iron de ciency
Iron de ciency is de ned as a condition in which there
are no mobilizable iron stores and in which signs of a
compromised supply of iron to tissues, including the
erythron, are noted.[64] Iron de ciency can exist with or
without anemia. Some functional changes may occur in
the absence of anemia, but the most functional de cits
appear to occur with the development of anemia.[2] Even
mild and moderate forms of iron de ciency anemia can be
associated with functional impairments a ecting cognitive
development,[65] immunity mechanisms,[66] and work
capacity.[67] Iron de ciency during pregnancy is associated
with a variety of adverse outcomes for both mother and
infant, including increased risk of sepsis, maternal mortality,
perinatal mortality, and low birth weight.[68] Iron de ciency
and anemia also reduce learning ability and are associated
with increased rates of morbidity.[68]
Causes of iron de ciency
Iron de ciency results from depletion of iron stores and
occurs when iron absorption cannot keep pace over an
extended period with the metabolic demands for iron
to sustain growth and to replenish iron loss, which is
primarily related to blood loss.[2] The primary causes of
iron de ciency include low intake of bioavailable iron,
increased iron requirements as a result of rapid growth,
pregnancy, menstruation, and excess blood loss caused by
pathologic infections, such as hook worm and whipworm
Table 2: Iron requirements of 97.5% of individuals in
terms of absorbed irona, by age group and sex (World
Health Organization, 1989)
Age/sex mg/dayb
4-12 months 0.96
13-24 months 0.61
2-5 years 0.70
6-11 years 1.17
12-16 years (girls) 2.02
12-16 years (boys) 1.82
Adult males
Pregnant womenc1.14
First trimester 0.8
Second and third trimester 6.3
Lactating women 1.31
Menstruating women 2.38
Postmenopausal women 0.96
a Absorbed iron is the fraction that passes from the gastrointestinal tract into the body
for further use. b Calculated on the basis of median weight for age. c Requirements
during pregnancy depend on the woman’s iron status prior to pregnancy
Abbaspour, et al.: Iron review
Journal of Research in Medical Sciences | February 2014 |
causing gastrointestinal blood loss[69-72] and impaired
absorption of iron.[73] The frequency of iron de ciency
rises in female adolescents because menstrual iron losses
are superimposed with needs for rapid growth.[74] Other
risk factors for iron de ciency in young women are high
parity, use of an intrauterine device, and vegetarian
Nutritional iron deficiency arises when physiological
requirements cannot be met by iron absorption from the
diet.[72] Dietary iron bioavailability is low in populations
consuming monotonous plant-based diets with li le meat.[72]
In many developing countries, plant-based weaning-foods
are rarely forti ed with iron, and the frequency of anemia
exceeds 50% in children younger than 4 years.[64]
When iron stores are depleted and insufficient iron is
available for erythropoiesis, hemoglobin synthesis in
erythrocyte precursors become impaired and hematologic
signs of iron de ciency anemia appear.
Iron de ciency and eventually anemia develop in stages
and can be assessed by measuring various biochemical
indices. Although some iron enzymes are sensitive to iron
de ciency,[63] their activity has not been used as a successful
routine measure of iron status.[2]
Laboratory measurements are essential for a proper
diagnosis of iron de ciency. They are most informative
when multiple measures of iron status are examined and
evaluated in the context of nutritional and medical history.
The plasma or serum pool of iron is the fraction of all iron
in the body that circulates bound primarily to transferrin.
Three ways of estimating the level of iron in the plasma or
serum include 1) measuring the total iron content per unit
volume in μg/dL; 2) measuring the total number of binding
sites for iron atoms on transferrin, known as total iron-
binding capacity in μg/dL2; and 3) estimating the percentage
of the two bindings sites on all transferrin molecules that
are occupied called the percentage transferrin saturation.[76]
However, marked biologic variation can occur in these
values as a result of diurnal variation, the presence of
infection or in ammatory conditions and recent dietary
iron intake.[76]
Zinc protoporphyrin re ects the shortage of iron supply
in the last stages of hemoglobin synthesis so that zinc is
inserted into the protoporphyrin molecule in the place
of iron. Zinc protoporphyrin can be detected in RBCs
by uorimetry and is a measure of the severity of iron
de ciency.[76]
Serum ferritin is a good indicator of body iron stores
under most circumstances. When the concentration of
serum ferritin is 15 μg/L iron stores are present; higher
concentrations re ect the size of the iron store; when the
concentration is low (<12 μg/L for <5 years of age and
<15 μg/L for >5 years of age) iron stores are depleted.[76]
However, ferritin is an acute phase reactant protein and
its serum concentrations can be elevated, irrespective of a
change in iron stores, by infection or in ammation.[76,2] This
means that it might be di cult to interpret the concentration
of ferritin where infectious diseases are common.
Another indicator of iron status is the concentration of TfR in
serum. Since TfR is mostly derived from developing RBCs,
it re ects the intensity of erythropoiesis and the demand for
iron. As iron stores are exhausted, the concentration rises in
iron de ciency anemia indicating sever iron insu ciency.
This is provided that there are no other causes of abnormal
erythropoiesis.[76] Clinical studies indicate that the serum
TfR is less a ected by in ammation than serum ferritin.[77]
The major advantage of TfR as an indicator is the possibility
of estimating the magnitude of the functional iron de cit
once iron stores are depleted.[78]
The ratio of TfR to ferritin (TfR/ferritin) was designed to
evaluate changes in both stored iron and functional iron and
was thought to be more useful than either TfR or ferritin
alone.[79] TfR/ferritin has been used to estimate body iron
stores in both children and adults.[80] However, the high cost
and the lack of standardization of the TfR assay so far have
limited the applicability of the method.[81]
Low hemoglobin concentration is a measure of anemia, the
end stage of iron de ciency.[76,2]
Anemia describes the condition in which the number
of RBCs in the blood is low, or the blood cells have less
than the normal amount of hemoglobin. A person who
has anemia is called anemic. The purpose of the RBC is
to deliver oxygen from the lungs to other parts of the
body. The hemoglobin molecule is the functional unit
of the RBCs and is a complex protein structure that is
inside the RBCs. Even though the RBCs are made within
the bone marrow, many other factors are involved in
their production. For example, iron is a very important
component of the hemoglobin molecule; erythropoietin, a
molecule secreted by the kidneys, promotes the formation
of RBCs in the bone marrow.
Having the correct number of RBCs and prevention of anemia
requires cooperation among the kidneys, the bone marrow,
and nutrients within the body. If the kidneys or bone marrow
Abbaspour, et al.: Iron review
Journal of Research in Medical Sciences
| February 2014 | 170
are not functioning, or the body is poorly nourished, then
normal RBC count and functions may be di cult to maintain.
Anemia is actually a sign of a disease process rather than
a disease itself. It is usually classi ed as either chronic or
acute. Chronic anemia occurs over a long period of time.
Acute anemia occurs quickly. Determining whether anemia
has been present for a long time or whether it is something
new, assists doctors in nding the cause. This also helps
predict how severe the symptoms of anemia may be. In
chronic anemia, symptoms typically begin slowly and
progress gradually; whereas in acute anemia symptoms
can be abrupt and more distressing.
RBCs live about 100 days, so the body is constantly trying
to replace them. In adults, RBC production occurs in the
bone marrow. Doctors try to determine if a low RBC count
is caused by increased blood loss of RBCs or from decreased
production of them in the bone marrow. Knowing whether
the number of white blood cells and/or platelets has changed
also helps determine the cause of anemia.
World Health Organization (WHO) estimates that two
billion people are anemic worldwide and attribute
approximately 50% of all anemia to iron de ciency.[64] It
occurs at all stages of the life cycle but is more prevalent in
pregnant women and young children.[82] Anemia is the result
of a wide variety of causes that can be isolated, but more
o en coexist. Some of these causes include the following:
Iron de ciency anemia
The most signi cant and common cause of anemia is iron
de ciency.[82] If iron intake is limited or inadequate due to
poor dietary intake, anemia may occur as a result. This is
called iron de ciency anemia. Iron de ciency anemia can
also occur when there are stomach ulcers or other sources
of slow, chronic bleeding (colon cancer, uterine cancer,
intestinal polyps, hemorrhoids, etc).[83]
Anemia of chronic disease
Any long-term medical condition can lead to anemia. This
type of anemia is the second most prevalent a er anemia
caused by iron de ciency and develops in patients with
acute or chronic systemic illness or in ammation.[84] The
condition has thus been termed “anemia of in ammation”
due to elevated hepcidin which blocks both the recycling of
iron from the macrophages and iron absorption.[85]
Anemia from active bleeding
Loss of blood through heavy menstrual bleeding or wounds
can cause anemia.[82] Gastrointestinal ulcers or cancers such
as cancer of the colon may slowly lose blood and can also
cause anemia.[86,87]
Anemia related to kidney disease
The kidneys releases a hormone called the erythropoietin
that helps the bone marrow make RBCs. In people with
chronic (long-standing) kidney disease, the production of
this hormone is diminished, and this in turn diminishes the
production of RBCs, causing anemia.[88] Although de ciency
of erythropoietin is the primary cause of anemia in chronic
renal failure, it is not the only cause. Therefore, a minimal
workup is necessary to rule out iron de ciency and other
cell-line abnormalities.[89]
Anemia related to pregnancy
A gain in plasma volume during pregnancy dilutes the RBCs
and may be re ected as anemia.[90] Iron de ciency anemia
accounts for 75% of all anemia in pregnancy.[90]
Anemia related to poor nutrition
Vitamins and minerals are required to make RBCs. In
addition to iron, vitamin B12, viamin A, folate, ribo avin,
and copper are required for the proper production of
hemoglobin.[82] De ciency in any of these micronutrients
may cause anemia because of inadequate production of
RBCs. Poor dietary intake is an important cause of low
vitamin levels and therefore anemia.
Obesity and anemia
Obesity is characterized by chronic, low-grade, systemic
in ammation, elevated hepcidin, which, in turn has been
associated with anemia of chronic disease. Ausk and
Ioannou[91] hypothesized that obesity may be associated
with the features of anemia of chronic disease, including
low hemoglobin concentration, low serum iron and
transferrin saturation, and elevated serum ferritin.
Overweight and obesity were associated with changes in
serum iron, transferrin saturation, and ferritin that would
be expected to occur in the se ing of chronic, systemic
in ammation. Obesity-related in ammation may increase
hepcidin concentrations and reduce iron availability.
Aeberli et al.,[92] compared iron status, dietary iron intake
and bioavailability, as well as circulating levels of hepcidin,
leptin, and interleukin-6 (IL-6), in overweight versus normal
weight children. They indicated that there is reduced iron
availability for erythropoiesis in overweight children and
that this is likely due to hepcidin-mediated reduced iron
absorption and/or increased iron sequestration rather than
low dietary iron supply.
Alcohol has numerous adverse e ects on the various types
of blood cells and their functions.[93] Alcoholics frequently
have defective RBCs that are destroyed prematurely.[93,94]
Alcohol itself may also be toxic to the bone marrow and
may slow down the RBC production.[93,94] In addition, poor
nutrition and de ciencies of vitamins and minerals are
Abbaspour, et al.: Iron review
Journal of Research in Medical Sciences | February 2014 |
associated with alcoholism.[95] The combination of these
factors may lead to anemia in alcoholics.
Sickle cell anemia
Sickle cell anemia is one of the most common inherited
diseases.[96] It is a blood-related disorder that a ects the
hemoglobin molecule and causes the entire blood cell to
change shape under stressed conditions.[97] In this condition,
the hemoglobin problem is qualitative or functional.
Abnormal hemoglobin molecules may cause problems in
the integrity of the RBC structure and they may become
crescent-shaped (sickle cells).[97] There are di erent types
of sickle cell anemia with di erent severity levels. It is
particularly common in African, Middle Eastern, and
Mediterranean ancestry.[97]
This is another group of hemoglobin-related causes of
anemia, which involves the absence of or errors in genes
responsible for production of hemoglobin.[97] A hemoglobin
molecule has subunits commonly referred to as alpha
and beta globin chains. A lack of a particular subunit
determines the type of alpha or beta thalassemia.[97,98] There
are many types of thalassemia, which vary in severity
from mild (thalassemia minor) to severe (thalassemia
major).[98] These are also hereditary, but they cause
quantitative hemoglobin abnormalities, meaning an
insufficient amount of the correct hemoglobin type
molecules is made. The alpha and beta thalassemias are
the most common-inherited single-gene disorders in the
world with the highest prevalence in areas where malaria
was or still is endemic.[97]
Aplastic anemia
Aplastic anemia is a disease in which the bone marrow
is destructed and the production of blood cells is
diminished.[99] This causes a deficiency of all three
types of blood cells (pancytopenia) including RBCs
(anemia), white blood cells (leukopenia), and platelets
(thrombocytopenia).[100,101] Many common medications can
occasionally cause this type of anemia as a side e ect in
some individuals.[99]
Hemolytic anemia
Hemolytic anemia is a type of anemia in which the RBCs
rupture, known as hemolysis, and are destroyed faster
than the bone marrow can replace them.[102] Hemolytic
anemia could happen due to a variety of reasons and is
often categorized as acquired or hereditary. Common
acquired causes of hemolytic anemia are autoimmunity,
microangiopathy, and infection. Disorders of RBC enzymes,
membranes, and hemoglobin cause hereditary hemolytic
The four principle strategies for correcting micronutrient
e ciencies in populations can be used for correcting iron
de ciency, either alone or in combination. These are education
combined with dietary modi cation, to improve iron intake
and bioavailability; iron supplementation (provision of iron,
usually in higher doses, without food), iron forti cation of
foods and the new approach of bioforti cation. However,
there are some di culties in the application of some of these
strategies when considering iron.
Food diversi cation
Dietary modi cations for reducing Indian Dental Association
involve increased intake of iron rich foods, especially esh
foods, increased consumption of fruits and vegetables rich
in ascorbic acid to enhance nonheme iron absorption, and
reduced intake of tea and co ee, which inhibit nonheme iron
absorption.[103,58] Another strategy is to reduce antinutrient
contents in order to make the iron supplied from their food
sources more available. Iron bioavailability may be increased
by techniques such as germination and fermentation, which
promote enzymatic hydrolysis of phytic acid in whole
grain cereals and legumes by enhancing the activity of
endogenous or exogenous phytase enzymes.[104] Even the
use of nonenzymatic methods, such as thermal processing,
soaking, and milling, for reducing phytic acid content in
plant-based staples has been successful in improving the
bioavailability of iron (and zinc).[105,106]
For oral iron supplementation, ferrous iron salts (ferrous
sulfate and ferrous gluconate) are preferred because of
their low cost and high bioavailability.[72] Although iron
absorption is higher when iron supplements are given on an
empty stomach, nausea, and epigastric pain might develop
due to the higher iron doses administered (usually 60 mg
Fe/day). If such side-e ects arise, lower doses between
meals should be a empted or iron should be provided
with meals, although food reduces absorption of medicinal
iron by about two-thirds.[107] Iron supplementation during
pregnancy is advisable in developing countries, where
women o en enter pregnancy with low iron stores.[108]
Although the benefits of iron supplementation have
generally been considered to outweigh the putative risks,
there is some evidence to suggest that supplementation at
levels recommended for otherwise healthy children carries
the risk of increased severity of infectious disease in the
presence of malaria.[109,110]
Forti cation
Fortification of foods with iron is more difficult than
forti cation with nutrients, such as zinc in our, iodine in
Abbaspour, et al.: Iron review
Journal of Research in Medical Sciences
| February 2014 | 172
salt, and vitamin A in cooking oil.[72] The most bioavailable
iron compounds are soluble in water or diluted acid but o en
react with other food components to cause o - avors, color
changes or fat oxidation.[103] Thus, less soluble forms of iron,
although less well absorbed, are o en chosen for forti cation
to avoid unwanted sensory changes.[72] Forti cation is usually
made with much lower iron doses than supplementation. It
is closer to the physiological environment and might be the
safest intervention in malarious areas.[111] There is no concern
over the safety of iron supplementation or iron forti cation
in nonmalarial endemic areas.[112]
Iron compounds recommended for food fortification
by the[7] include ferrous sulfate, ferrous fumarate, ferric
pyrophosphate, and electrolytic iron powder. Wheat our is
the most common iron forti ed food and it is usually forti ed
with elemental iron powders which are not recommended by
WHO.[7,113] Hurrell and Egli[23] reported that of the 78 national
wheat flour programs only eight would be expected to
improve iron status. These programs used recommended iron
compounds at the recommended levels. The other countries
used non recommended compounds or lower levels of iron
relative to our intake. Commercial infant foods, such as
formulas and cereals, are also commonly forti ed with iron.
Bioforti cation
Iron contents vary from 25 to 56 mg/kg in the di erent
of wheat and 7-23 mg/kg in rice grains. However, most of this
iron is removed during the milling process. Iron absorption
from cereals and legumes, many of which have high native
iron content, is generally low because of their high contents
of phytate and sometimes polyphenols.[48] Bioforti cation
strategies include plant breeding and genetic engineering.
Iron levels in common beans and millet have been successfully
increased by plant breeding but other staple is more di cult or
not possible (rice) due to insu cient natural genetic variation.
Lucca et al.,[114] increased the iron content in rice endosperm
to improve its absorption in the human intestine by means
of genetic engineering. They introduced a ferritin gene from
Phaseolus vulgaris into rice grains, increasing their iron
content up to twofold. To increase iron bioavailability, they
introduced a thermotolerant phytase from Aspergillus fumigatus
into the rice endosperm. They indicated that this rice, with
higher iron content and rich in phytase has a great potential
to substantially improve iron nutrition in those populations
where iron de ciency is so widely spread.[114] Unfortunately
the phytase did not resist cooking. The importance of various
minerals as zinc[115] and iron needs more a ention at individual
and public health levels.
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Source of Support: Nil, Con ict of Interest: None declared.
... Therefore, iron is indispensable for transporting and storing oxygen and for energy metabolism. 14 Iron has the ability to recycle within the body as the red blood cells are phagocytosed by reticuloendothelial macrophage and the content of iron is either taken up for hematopoiesis in case it is required or stored up for later use. ...
... 4,22 The factors responsible for CKD include increased inflammatory cytokines, reduced renal clearance, and reduced EPO levels. [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23] In CKD patients, absolute iron deficiency arise from an increased rate of blood loss during dialysis. 24 Iron loss is contributed by frequent phlebotomies and blood remaining in the dialysis tubing. ...
... Iron deficiency per se (with or without anaemia) is nearly 2.5 times more prevalent than IDA; rendering it the commonest nutritional deficiency. 13 Adolescent girls and women of childbearing age are more commonly affected in developing countries due to increased iron demand because of menstrual blood losses, poorer overall nutrition and healthcare access. IDA is also commoner in multiparous women who also show higher prevalence of GSD. ...
... IDA is also commoner in multiparous women who also show higher prevalence of GSD. 13,14 Insights into factors that contribute to gallstone formation can therefore have public health implications, and can aid institution of preventive measures. With this background, we studied the frequency of iron deficiency anaemia in GSD patients. ...
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Background: Gallstone disease (GSD) is a very common condition worldwide and the key event in the cholesterol stone formation is the supersaturation of bile with cholesterol. The role of trace elements like iron, calcium has been suggested in the pathogenesis of gallstones. Both iron deficiency and GSD are more prevalent in India. With this background, we studied the frequency of iron deficiency anaemia in GSD patients.Methods: This prospective observational study enrolled 150 adult patients undergoing laparoscopic cholecystectomy for symptomatic GSD in a north-Indian tertiary care hospital. Complete hemogram, serum ferritin, iron and unbound iron-binding capacity (TIBC) were performed in all patients. To simplify interpretation, anaemia was defined as Hb <12 gm/dl; iron deficiency was defined as either ferritin value lower than the reference range, or, if the ferritin was within the reference range, reduced % transferrin saturation with normal-or-high TIBC.Results: Anaemia was present in 66% and 77.3% were having iron deficiency; of which 84.5% were females. Iron deficiency with anaemia was present in 85.3%; therefore remaining patients had latent iron deficiency. Serum ferritin was normal or raised in 52 (68.1%) patients with iron deficiency, indicating that it is insensitive as a stand-alone test for iron deficiency.Conclusions: At a public health level, our results may suggest that addressing the problem of endemic iron deficiency may also reduce the possible development of GSD in the community. Thus, pre-operative assessment of iron status appears to be a cautious choice in all patients planned for cholecystectomy as indirectly it will address the problem of anaemia in the population.
... There are five factors that trigger significant incidence of anemia, namely perceptions of nutrition, consumption of blood booster tablets, level of protein and iron intake, and bleeding during menstruation (Gautam et al., 2019;Triharini et al., 2018;Thomson et al., 2012;Abbaspour et al., 2014;Sumarlan et al., 2018). ...
Adolescent girls are one of the groups of people who is prone to iron nutrient deficiency. Iron is required as a substitute for iron lost due to the menstrual cycle. This research aims to determine the trigger factors of anemia in adolescent girls who become participants of the prevention and control program of anemia. This type of research is an observational research with cross sectional design and using statistical test of chelstle method of Mantel Haentzel and OR value for its meaning. The results shows there are four significant triggers of anemia that is perception of adolescent about nutrition (OR = 2,24; 95% CI = 1,05 - 4,76), adherence to TTD (OR = 2,49; 95% CI = 1.11 - 5.58), protein consumption levels (OR = 3.27, 95% CI = 1.57 - 6.84), iron intake (OR = 2.81; 95% CI = 1.30 - 6.05), and duration of menstrual bleeding (OR = 8.08; 95% CI = 1.05 - 61.89). The distribution of blood booster tablets or tablet tambah darah (TTD) needs to be intensified again, accompanied by an emphasis on the benefits of TTD tablets for young women, and to continue to consume independently when the distribution of TTD is terminated. In conclusion, adolescent girls are prevalent to iron nutrient due to menstrual cycle. Therefore, nutrition counseling should also be given besides consuming fresh foods rich in protein and iron as well as vegetables and fruits, because both foods contain vitamin C which greatly helps the absorption of iron in the body.
... Fe metal is an essential metal whose existence in a certain amount is needed by living organisms, but in excessive amounts can affect living organisms. The high content of Fe metal will have an impact on human health including poisoning (vomiting), intestinal damage, premature aging to sudden death, arthritis, birth defects, bleeding gums, cancer, kidney cirrhosis, constipation, diabetes, diarrhea, dizziness, fatigue, hepatitis, hypertension, insomnia (Youdim, 2001;Abbaspour et al. 2014;Wessling-Resnick 2017 The method of monitoring the pollution of a device by heavy metals has been developed chemically, by determining the level of each pollutant in water or sediment. However, this monitoring is more effective if applied in conjunction with biological monitoring or using living organisms (Rashed, 2001). ...
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This study aims to determine the content of nickel (Ni) and iron (Fe) as well as histopathological analysis of marine fish in Obi Island waters as a bioindicator of pollution. Besides, water quality conditions were carried out in-situ and ex-situ observations. The parameters observed were temperature, brightness, salinity, pH, dissolved oxygen, nitrate, orthophosphate, ammonia, iron (Fe), and nickel (Ni). The results showed the temperature range between 26.48 ℃ to 27.99 ℃ below the quality standard or low temperature. The brightness of the relationship between 12 m and 13 m is under quality standards. The salinity range between 31.01 ppt to 32.13 ppt below the quality standard. The pH range is from 8.6 to 8.7 in high or alkaline conditions. Ammonia range between 0.4 mg / L to 0.7 mg / L exceeds the quality standard. The range of nitrate between 0.009 mg / L to 0.012 mg / L exceeds the quality standard. The range of phosphate between 0.016 mg / L to 0.019 mg / L exceeds the quality standard. The DO range between 3.68 mg / L to 3.77 mg / L lower than the quality standard. The metal range of 0.6 mg / L to 0.9 mg / L exceeds the quality standard. The range of Ni metal between 0.06 mg / L to 0.09 mg / L exceeds the quality standard. Histopathological analysis showed that the liver had a hemorrhage, degeneration of blood vessels, vacuolate degeneration, necrosis, or cell death. The muscles experience edema, degeneration of muscle fibers, atrophy of muscle bundles, vacuolar degeneration of muscle Bundles, hemorrhage, infiltration of lymphocytes, and necrosis. The intestine experience infiltration of lymphocytes, melanomacrophages, and necrosis. While P. tayenus fish ovaries showed necrosis structure oocytes. This research can be a reference for warning of heavy metal pollution in Obi Island waters, binding to the nature of heavy metals that can accumulate in fish tissue.Keywords: Water quality; Heavy Metal; Pollution; Histopathological; Obi Island.
... It is involved in a wide range of metabolic processes, including oxygen transport, DNA synthesis, and electron transport. However, the concentration in body tissues must be regulated because iron can generate free radicals and its high concentration can lead to tissue damage [47]. Iron deficiency is a very common problem in humans, usually caused by insufficient intake of this element with food or excessive menstrual bleeding. ...
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The aim of this study was to determine antioxidant activity (DPPH and phosphomolyb-denum method), polyphenols content (total polyphenols, flavonoids, and phenolic acids), mineral compounds composition (Cu, Zn, Mn, Fe, Cr, Ni, Co, Pb and Cd) and antimicrobial activity (with disc diffusion method) of medicinal herbs traditionally used in the Slovak republic. The tested plants belonged to the Primulaceae, Urticaceae, Grossulariaceae, Rosaceae, Lamiaceae, Asteraceae, Equisetaceae, Tropaeolaceae, and Plantaginaceae families. The highest antioxidant activities were found in samples of Rosa canina L. (DPPH-29.43 ± 0.11 mg TE/g; TE-Trolox equivalent) and Fragaria vesca L. (phosphomolybdenum method-679.56 ± 3.06 mg TE/g), both from the Rosaceae family. Total polyphenols (determined using the Folin-Ciocâlteu-reagent) were most abundant in a sample of Fragaria vesca L.-124.51 ± 5.05 mg GAE/g (GAE-gallic acid equivalent), total flavonoids (determined using the aluminum chloride method)-in a sample of Primula veris L.-48.35 ± 3.77 mg QE/g (QE-quercetin equivalent), and total phenolic acids (determined using Arnova reagent)-in a sample of Thymus serpyllum L.-102.31 ± 2.89 mg CAE/g (CAE-caffeic acid equivalent). Regarding mineral compounds composition, samples of Fragaria vesca L. and Thymus serpyllum L. showed the highest levels of iron. In samples of Calendula officinalis L. and Trapaeolum majus L., the highest amounts of zinc were determined, while copper was the most abundant in samples of Urtica dioica L. and Melissa officinalis L. The amounts of heavy metals were within legally acceptable limits. The extract of Equisetum arvense L. showed the strongest inhibitory activity towards Clostridium perfrin-gens CCM 4991 (6 mm), while the one from Mentha piperita L.-towards Candida glabrata CCM 8270 (4.83 mm) and Candida tropicalis CCM 8223 (4.33 mm).
... Transportation of iron is through the mucosal cells of the upper small intestine by the plasma protein transferrin. Transferrin synthesis occurs primarily in the liver and appears to be related to the level of iron storage (3) . Childhood nephrotic syndrome characterized by heavy proteinuria results in low plasma albumin and odema (4). ...
... Malnutrition from micronutrient deficiency mainly include iron deficiency anaemia, calcium deficiency and vitamin A deficiency that mostly prevalent in India as well as other developing countries resulting in lot of consequences. Iron that mostly is accessible from our diet through different vegetables, especially the leafy vegetables, is one of the most important micronutrients compulsory for survival of human beings as its essentiality to synthesise globin-proteins particularly haemoglobin and myoglobin that are involved in oxygen transport in blood and to produce heme enzymes and other iron-containing enzymes that actively participate in electron transfer and oxidation reduction reactions (Hurrell, 1997 ;Abbaspour et al., 2014). In relation to this phenomenon, a severe health problem, anaemia as a result of iron deficiency became highly violent throughout the world especially among the women and children. ...
... Fishes and other kinds of seafood are important sources of essential nutrients and minerals for human health. For instance, Fe, widely found in fish and seafood, is critical in oxygen transport, cellular respiration, and the synthesis of deoxyribonucleic acid (DNA) (Dixit et al., 2021;Abbaspour et al., 2014). However, when consumed in high concentrations, Fe can be harmful, causing organ failure, constipation, nausea, abdominal pain, convulsion, and even death (Barhum and Bull, 2022). ...
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Due to trace metals' toxicity, accumulative tendency, and non-biodegradability, we assessed their levels in six fish species: Chrysichthys nigrodigitatus (Silver Catfish), Sarotherodon melanotheron (Blackchin Tilapia), Scomber scombrus (Atlantic Mackerel, locally known as Titus), Sardinella maderensis (Sardine), Dentex canariensis (Canary dentex), and Pseudotolithus typus (Croaker) commonly available in the Lagos lagoon. Samples of various sizes and maturity were selected, and their tissues (fillets, gills, and intestines) were examined for trace metal concentrations. Fe was the most concentrated metal in all the tissues (1.64-8.61 mg/kg), albeit below the WHO permissible limits (100 mg/kg). Others were Pb (0.05-8.2 mg/kg), Zn (0.48-4.88 mg/kg), Cu (0.08-2.51 mg/kg), and Cd (0.03-1.95 mg/kg), with only Zn and Cu entirely below WHO permissible limits of 100 and 30 mg/kg, respectively. Specifically, the toxic metals were more concentrated in the intestines (mean = 4.36 ± 1.02 mg/kg), reaching 8.61 mg/kg, followed by the gills (mean = 1.50 ± 0.77 mg/kg; max = 3.17 mg/kg), while the fillet was the least toxic metal-laden (mean = 0.55 ± 0.08 mg/kg; max = 2.01 mg/kg). Further, Fulton condition factor assessment (body weight-length relationship) identified Sarotherodon melanotheron as ''good'' (1.74) and Dentex canariensis as ''moderately good'' (1.33), while others were ''poor'' Overall, Scomber Scrombus, Psuedotolithus typus, and Dentex canariensis exhibited the least toxic metal accumulations. Therefore, having considered WHO's permissible limits for the metals in edible fishes, these three species seem suitable for human consumption, provided other environmental and human conditions are favorable.
Conference Paper
The relationship of anemia as a risk factor for child mortality was analyzed by using cross-sectional, longitudinal and case-control studies, and randomized trials. Five methods of estimation were adopted: I) the proportion of child deaths attributable to anemia; 2) the proportion of anemic children who die in hospital studies; 3) the population-attributable risk of child mortality due to anemia; 4) survival analyses of mortality in anemic children; and 5) cause-specific anemia-related child mortality. Most of the data available were hospital based. For children aged 0-5 y the percentage of deaths due to anemia was comparable for reports from highly malarious areas in Africa (Sierra Leone 11.2%, Zaire 12.2%, Kenya 14.3%). Ten values available for hemoglobin values <50 g/L showed a variation in case fatality from 2 to 29.3%. The data suggested little if any dose-response relating increasing hemoglobin level (whether by mean value or selected cut-off values) with decreasing mortality. Although mortality was increased in anemic children with hemoglobin <50 g/L, the evidence for increased risk with less severe anemia was inconclusive. The wide variation for mortality with hemoglobin <50 g/L is related to methodological variation and places severe limits on causal inference; in view of this, it is premature to generate projections on population-attributable risk. A preliminary survival analysis of an infant cohort from Malawi indicated that if the hemoglobin decreases by 10 g/L at age 6 mo, the risk of dying becomes 1.72 times higher. Evidence from a number of studies suggests that mortality due to malarial severe anemia is greater than that due to iron-deficiency anemia. Data are scarce on anemia and child mortality from non-malarious regions. Primary prevention of iron-deficiency anemia and malaria in young children could have substantive effects on reducing child mortality from severe anemia in children living in malarious areas.
The effects of different polyphenol-containing beverages on Fe absorption from a bread meal were estimated in adult human subjects from the erythrocyte incorporation of radio-Fe. The test beverages contained different polyphenol structures and were rich in either phenolic acids (chlorogenic acid in coffee), monomeric flavonoids (herb teas, camomile (Matricaria recutita L.), vervain (Verbena officinalis L.), lime flower (Tilia cordata Mill.), pennyroyal (Mentha pulegium L.) and peppermint (Mentha piperita L.), or complex polyphenol polymerization products (black tea and cocoa). All beverages were potent inhibitors of Fe absorption and reduced absorption in a dose-dependent fashion depending on the content of total polyphenols. Compared with a water control meal, beverages containing 20-50 mg total polyphenols/serving reduced Fe absorption from the bread meal by 50-70%, whereas beverages containing 100-400 mg total polyphenols/serving reduced Fe absorption by 60-90%. Inhibition by black tea was 79-94%, peppermint tea 84%, pennyroyal 73%, cocoa 71%, vervain 59%, lime flower 52% and camomile 47%. At an identical concentration of total polyphenols, black tea was more inhibitory than cocoa, and more inhibitory than herb teas camomile, vervain, lime flower and pennyroyal, but was of equal inhibition to peppermint tea. Adding milk to coffee and tea had little or no influence on their inhibitory nature. Our findings demonstrate that herb teas, as well as black tea, coffee and cocoa can be potent inhibitors of Fe absorption. This property should be considered when giving dietary advice in relation to Fe nutrition.
In Brief Diabetes is one of the most common causes of chronic kidney disease (CKD). Anemia is a frequent complication of CKD. This article reviews the treatment of anemia in patients with CKD. Topics include the prevalence of anemia in this population, causes and impact of anemia in these patients, target hemoglobin goals, treatment and monitoring, and causes of hyporesponse to anemia treatment.
Since its first discovery in an Iranian male in 1961, zinc deficiency in humans is now known to be an important malnutrition problem world-wide. It is more prevalent in areas of high cereal and low animal food consumption. The diet may not necessarily be low in zinc, but its bio-availability plays a major role in its absorption. Phytic acid is the main known inhibitor of zinc. Compared to adults, infants, children, adolescents, pregnant, and lactating women have increased requirements for zinc and thus, are at increased risk of zinc depletion. Zinc deficiency during growth periods results in growth failure. Epidermal, gastrointestinal, central nervous, immune, skeletal, and reproductive systems are the organs most affected clinically by zinc deficiency. Clinical diagnosis of marginal Zn deficiency in humans remains problematic. So far, blood plasma/serum zinc concentration, dietary intake, and stunting prevalence are the best known indicators of zinc deficiency. Four main intervention strategies for combating zinc deficiency include dietary modification/diversification, supplementation, fortification, and bio-fortification. The choice of each method depends on the availability of resources, technical feasibility, target group, and social acceptance. In this paper, we provide a review on zinc biochemical and physiological functions, metabolism including, absorption, excretion, and homeostasis, zinc bio-availability (inhibitors and enhancers), human requirement, groups at high-risk, consequences and causes of zinc deficiency, evaluation of zinc status, and prevention strategies of zinc deficiency.