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Nutritional management in
anemia
Deasy Irawati
Content
Nutritional anemia
Iron deficiency
Vitamin B deficiency
The role of other nutrients
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NUTRITIONAL ANEMIA
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Definition
Anaemia is a condition in which the number of
red blood cells or their oxygen-carrying
capacity is insufficient to meet physiologic
needs, which vary by age, sex, altitude,
smoking, and pregnancy status
Nutritional vitamin and mineral
deficiencies
Non-nutritional infection and
hemoglobinopathies
IRON DEFICIENCY
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Definiton
Iron deficiency: a state in which there is insufficient iron to maintain
the normal physiological function of tissues such as the blood,
brain, and muscles.
Iron deficiency can exist in the absence of anaemia if it has not
lasted long enough or if it has not been severe enough to cause the
haemoglobin concentration to fall below the threshold for the
specific sex and age group
Iron depletion: the state in which storage iron is absent or nearly
absent but the tissues that need iron are able to maintain normal
physiological functions.
Functional iron deficiency can develop even when iron stores are
present if the normal physiological systems for transporting iron to
target tissues are impaired cytokines due to inflammation
(hepcidin)
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Source: Gibson R. Principles of Nutritional Assessment.
2nd ed. New York: Oxford University Press, 2005
Nutritional causes
Low iron intake
poor absorption of iron from diets (Low
bioavailability of iron intake = 5%
bioavailability)
Low heme iron diet
High content of iron absorption inhibitors
(phytate, calcium, tannin and oxalates)
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Nutritional treatment
In settings where iron deficiency is the most
frequent cause
Iron supplementation continue until iron stores are
sufficient 3 months after normalization of Hb
concentration
In settings where iron deficiency is not the only
cause of anaemia
Combined treatment with other micronutrient folic
acid, vitamin A, vitamin B12, riboflavin, vitamin C,
copper
Prevention
Foodbased approaches to increase iron intake
food fortification : milk, wheat flour, soy sauce,
salt, cereals
dietary diversification
Give iron supplementation in high risk group
(low birth age baby, weaning children,
pregnancy, lactation)
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Food sources
High bioavailability iron sources: meat, fish,
egg
Medium bioavailability: beans, nut
Low bioavailability: most vegetables (spinach,
etc)
VITAMIN B DEFICIENCY
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Megaloblastic anemia
Dietary intake is the source of cobalamin and folate
Cobalaminmust be bound to intrinsic factor (IF) absorbed in the
terminal ileum cobalamin is bound to another protein,
transcobalamin II (TCII) transported to storage sites
Considerable amounts of cobalamin are accumulated in storage
sites years elapse before cobalamin deficiency develops in
patients who cannot take up dietary cobalamin.
Most often caused by folate dietary insufficiency
Very little folate is stored can occur within months of cessation of
folate ingestion
Vit B12 and folate maintain purine and pyrimidine biosynthesis
Vit B 12 and folate deficiency reduction in ability to synthesize
DNA and maintain cell division affect synthesis of red cells
macrocytic megaloblastic anemia
Other vitamin B
Improving Hb concentration riboflavin (B2),
pyridoxal (B6)
Niacin, thiamine (B1), panthothenic acid
insufficient evidence
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Food source
Mainly in meat, milk product, serealia, beans,
fruits
Treatment and prevention
Micronutrient supplementation
Food fortification
Dietary diversity
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THE ROLE OF OTHER NUTRIENTS
Anemia and vitamin A
Vitamin A deficiency may increase the risk of iron
deficient-erythropoiesis and anemia
iron absorption, storage, transport and delivery to
bone marrow
reduce erythrocytosis by lowering erythropoietin
production
induce iron sequestration due to increased severity of
infection
Vitamin A intervention that maintains a plasma
retinol increment 5 g/dL (0.175 mol/L) might
expect to raise hemoglobin by up to 4 g/L
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van Stuijvenberg ME, Kruger M, Badenhorst CJ, Mansvelt EP, Laubscher JA.
Response to an iron fortification programme in relation to vitamin A status in
6-12-year-old school children. Int J Food Sci Nutr 1997;48:419
In South Africa
vitamin A deficiency appeared to blunt serum
iron and transferrin saturation responses in
school children who were given a soup fortified
with iron (20 mg) and vitamin C (100 mg) for
nearly four months
Increased serum ferritin concentrations
suggested that iron had been absorbed and
stored, but not released in children with poorer
vitamin A status.
0
0.2
0.4
0.6
0.8
1
Odd ratio anemia
Placebo VA Fe VA+Fe
0.47
0.23
0.16
8 weeks of daily supplementation with vitamin A (2.4 mg), iron (60 mg) or both
vitamin A and iron relative to placebo receipt among 251 initially anemic, pregnant
Indonesian women significantly raised hemoglobin concentration by 3.7 g/L over
that of placebo recipients, an effect that explained 35% of pregnancy-related anemia
Suharno D, West CE, Muhilal, Karyadi D, Hautvast JG. Supplementation with vitamin
A and iron for nutritional anaemia in pregnant women in West Java, Indonesia.
Lancet 1993;342:13258
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Anemia and vitamin E
iron deficiency anemia are more susceptible to oxidative damage
in erythrocyte membranes associated with decreased production
of hemoglobin (Hb) and other iron-containing proteins such as
myoglobin, catalase, peroxidase, and cytochromes.
Iron supplementation to deficient individuals was found to increase
the oxidative stress (i.e., increased malnodialdehyde (MDA) levels
and compromised antioxidant enzyme activities)
High levels of free iron may enhance radical production via the
Fenton and Haber-Weiss reactions
Treatment of iron-deficient patients with a combination of iron and
vitamins A, C, and E proved effective in normalizing the oxidative
stress
In the absence of vitamin E, these ROO can abstract a hydrogen from PUFA (RH) and
generate both a hydroperoxide (ROOH) and another carbon-centered radical (R),
which in the presence of oxygen (O2) will form a ROO and thus a lipid peroxidation
chain reaction occurs. If a-tocopherol (a-TOH) is present it intercepts the radical 1000
times faster than the radical reacts with PUFA, and both a ROOH and an a-TO are
formed. This a-TO radical can be detoxified and a-TOH regenerated by intracellular
antioxidants including vitamin C, glutathione, and reducing equivalents (NAD(P)H)
derived fromoxidative metabolism.
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Plasma a-tocopherol concentrations less than 8 mmol/L are associated with neurologic
disease, less than 12 mmol/L with increased RBC fragility and over 32 mmol/L with
decreased risk of chronic diseases. The x-axis value is an identification number that
associates the concentrations with their corresponding publication shown in the
reference list. Some articles contain multiple values and may appear multiple times in
the referencelist.
Anemia and Cuprum
Cu reduced ceruloplasmin activity defective iron
mobilization anemia
ceruloplasmin through its ferroxidase action, is
fundamental for the transformation of the Fe2+ to Fe3+, a
step indispensable for the incorporation of iron into the
circulating transferrin iron trapped in the
reticuloendothelial system and thus unavailable for
erythropoiesis.
A reduction in the synthesis of heme due to decreased
activities of ferrochelatase, cytochrome c or both
Copper-dependent enzymes are critical for the reduction of
Fe3+ to Fe2+ in the mitochondria and for the subsequent
incorporation of iron into protoporphyrin IX.
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Defective iron mobilization
From stores
Defective iron incorporation to
protoporphyrinIX
Decreased iron absorption
Decreased iron
availability for
heme synthesis
Decreased plasma
erythropoietin levels
Shortened erythrocyte life
span due to oxidative stress
Anemia
Potential mechanisms by which copper deficiency
can induce anemia
Anemia and Selenium
Selenium could contribute to anemia
maintenance of an optimal concentration of
glutathione peroxidase, a key antioxidant
selenoenzyme, in erythrocytes
Glutathione peroxidase protects hemoglobin
against oxidation in erythrocytes
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Women aged 7079 years living in the community in the Womens Health and Aging
Studies (WHAS) I and II. In WHAS, the prevalence of anemia decreased from the
lowest to the highest quartile of serum selenium.
Serum selenium level
Semba RD, Ferrucci L, Cappola AR, Ricks MO, Ray AL, Xue QL, et al. Low serum
selenium is associated with anemia among older women living in the community.
Biol Trace ElemRes 2006;112:97108
Reference
De Benoist B, McLean E, Egli I, Cogswell M. 2008.
Worldwide prevalence of anaemia 19932005 : WHO global
database on anaemia. WHO
Gibson R. Principles of Nutritional Assessment. 2nd ed.
New York: Oxford University Press, 2005
Kraemer K, Zimmermann MB. 2007. Nutritional Anemia.
Sight and Life Press
WHO, FAO. 2004. Vitamin and mineral requirements in
human nutrition. 2 edition
WHO, UNICEF, UNU. Iron deficiency anaemia: assessment,
prevention, and control. A guide for programme managers.
Geneva, World Health Organization, 2001. WHO/NHD/01.3