nutritional epidemiology: micronutrient malnutrition
DESCRIPTION
Nutritional Epidemiology: Micronutrient malnutrition. Asst. Prof. Dr. Sumattana Glangkarn. Micronutrient malnutrition: a public health problem. Micronutrient malnutrition (MNM) is widespread in the industrialized nations, but more in the developing regions - PowerPoint PPT PresentationTRANSCRIPT
Nutritional Epidemiology: Micronutrient malnutritionAsst. Prof. Dr.
Sumattana Glangkarn
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Micronutrient malnutrition (MNM) is widespread in the industrialized nations, but more in the developing regions
Can affect all age groups, but young children and women of reproductive age tend to be among those most at risk of developing micronutrient deficiencies
MNM has many adverse effects on human health, even moderate levels of deficiency (detected by biochemical or clinical measurement)
Micronutrient malnutrition: a public
health problem
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Nutrition problems in Thailand include;- Protein energy malnutrition (PEM)- MNM; Iron deficiency anemia (IDA)
Iodine deficiency disorder (IDD)
Vitamin A deficiency.
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Iron-deficiency anemia Iron-deficiency anemia (IDA) is the most
common nutritional disorder in the world Women in the reproductive age group and
young children in tropical and subtropical regions
IDA affects over 2 billion people in the world Average prevalence is higher in pregnant
women (51%) than non-pregnant women High prevalence in south and south-east
Asia
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Stage of iron depletion
Stage I
Stage II
Stage III
Decrease in iron
storesBiochemical
indicators of low
iron storesIron-
deficiency anemia
Ferriti
nTransferrin saturation
Erythrocyte protoporphyrin
Hemogl
obin
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องค์�ประกอบของฮี�โมโกลบ�น
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Iron nutritional status
Biochemical and hematological tests
Serum iron concentration Total iron binding capacity Transferrin saturation Protoporphyrin Serum ferritin Transferrin receptors
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Serum iron concentration In IDA, serum iron may either be low or
even normal The normal value between 50 and 175 µg/dl There is a considerable diurnal variation;
the levels are highest in the morning and lowest during the night
It is reduced in inflammation, malignancy and during menstruation
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Total iron binding capacity Total iron binding capacity (TIBC) and
transferrin saturation indicate iron supply to issues
The normal value is about 300 µg/dl TIBC is lowered in chronic disease and
raised in iron deficiencyTransferrin saturation This is a ratio of serum iron and TIBC, normal
value is 33% In iron deficiency, there is a decreased
saturation, while in chronic diseases the saturation is normal
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Protoporphyrin Protoporphyrin is the precursor of heme Free red blood cell (RBC) protoporphyrin
is raised when there is an insufficient supply of iron for heme synthesis
It is high in IDA, caused by lead toxicity and other sideroblastic anemia
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Serum ferritin Serum ferritin reflects the status of total
body iron stores A value below about 10 ng/ml is considered
as diagnostic of iron deficiency Its levels are raised in inflammation,
infections and liver disease Serum ferritin is a sensitive indicator of iron
stores, particularly in areas where the incidence of infections is very high; the developing countries of south-east Asia
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Transferrin receptors Transferrin receptors become elevated on
cell surfaces and in plasma whenever there is insufficient iron supply to cells or iron depletion.
Because of the cost implications for multiple biochemical tests, the parameter used to indicate iron status in population studies of IDA is measured by hemoglobin.
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Hemoglobin (Hgb)
ค์�าปกติ� (g/dl)ชาย -1418
หญิ�ง -1216
เด็�ก -1116
ทารก -1015
แรกค์ลอด็ -1424
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Hematocrit : Hct
3Hct. = (Hgb)ค์�าปกติ� 100(/ ml.)
ชาย -4252
หญิ�ง -3747
เด็�ก -3143
ทารก -3040
แรกค์ลอด็ -4464
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Centrifuge
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Clinical features of iron-deficiency anemia The symptoms of IDA depend on the rate at
which anemia develops in an individual Symptoms may relate to rate of fall in
hemoglobin Lowering of hemoglobin affects oxygen carrying
capacity; in IDA, any physical exertion leads to shortness of breath
Initially, most patients complain of increasing lethargy and fatigue
More unusual symptoms are headache, tinnitus and disturbance in test
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As the severity of deficiency increases, the patients develop pallor of conjunctiva, tongue, nailbeds and soft palate
In IDA of longer duration, there may be papillary atrophy of the tongue and, the nail may become spoon shaped (koilnychia)
In children, chronic IDA may lead to behavioral changes; they may have impairment of cognitive function and short attention spans and appear withdrawn
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Conjunctiva
Normal appearing conjunctiva
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Spoon finger
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Iron metabolism Human body requires iron for the synthesis of the
oxygen transport proteins, hemoglobin and myoglobin in the body
Total body iron in men ~ 3.8 g, in women ~ 2.3 g. Approximately 2/3 of total iron is functional,
serving either a metabolic or an enzymic function; in the form of hemoglobin, circulating with in RBC
The factor influencing iron balance are intake of iron, iron stores and iron loss
Adult males require ~ 1 mg of absorbed iron daily to replace the losses in gut secretions, epithelial cells, urine and skin
In menstruating females this can increase to 1.4
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Factor influencing iron absorption Type of food consumed; meat, eggs
Interactions between foods; iron absorption enhancers (vitamin C), iron absorption inhibitors (i.e. calcium phosphate, bran)
Regulatory mechanisms in the intestinal mucosa
Bioavailability; utilization of ingested iron for metabolic functions
Amount of iron stores: liver, reticuloendothelial, bone marrow
Rate of production of red blood cells
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Iron losses In healthy individuals occur primarily in
feces (0.6 mg/day), bile and desquamated mucosal cells, and in minute quantities of blood
Urinary losses are small Women of reproductive age, in addition
to the basal losses; lose iron in menstruation
The median menstrual blood loss is about 30ml/day, an additional requirement of 0.5 mg of iron per day
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In the tropical countries, hookworm infestation is a major cause of gastrointestinal blood loss contributing to iron deficiency in older children and adults.
In the developed world, among adults, chronic use of drugs such as aspirin, bleeding tumors and ulcers contribute to iron losses.
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Risk factors for anemia
Poor iron stores Dietary inadequacy Increased demands Malabsorption and increased losses Hemoglobinopathies; thalassemia,
sickle cell anemia (non-nutritional factor)
Drug and other factors; anticancer drug, radiation therapy
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Prevention and control of iron-deficiency anemia Provision of iron supplements
Fortification of commonly consumed food with iron
Nutrition education Horticulture-based approaches to
improving the iron bioavailability of common foods
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Iodine and Iodine-deficiency Disorders The epidemiology of iodine deficiency disorders (IDD)
is currently in a transitional phase because of the great progress seen during the 1990s in the battle against IDD
Mainly in the form of national salt iodization programs The diagnosis of iodine deficiency should be seen as
a group, community or population diagnosis rather than an assessment on the individual level; interpretation of IDD status
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Definition of iodine status of a population Iodine status Median urinary
iodine concentration
(µg/l)Severe iodine deficiency
<20
Moderate iodine deficiency
20-49
Mild iodine deficiency 50-99
Ideal iodine intake 100-200
More than adequate iodine intake; increased risk hyperthyroidism
201-299
Excessive iodine intake >300
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Thyroid size by palpation Grade 0: no palpable or visible goiter Grade 1: a mass in the neck that is
consistent with an enlarged thyroid that is palpable but not visible when the neck is in the normal position (Ia), but move upwards in the neck as the subject swallows and visible when neck fully extended (Ib)
Grade 2: a swelling in the neck that is visible when the neck is in a normal position and is consistent with an enlarged thyroid when the neck is palpated
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Thyroid size by ultrasonography is a safe, noninvasive, specialized technique, which provides a more accurate measurement of thyroid volume than palpation
Thyroid-stimulating hormone (TSH) and thyroglobulin can be used as indicators to assess IDD, or as surveillance indicators
Thyroid hormones thyroxine (T4) and triiodothyronine (T3) tests are cumbersome, more expensive and less sensitive than other indicators
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WHO/UNICEF/ICCIDD recommended dietary intake for iodine (2001)Category Intake
(µg/day)Infants, 0-59 months
90
Schoolchildren, 6-12 years
120
Children > 12 years and adults
150
Pregnant and lactating women
200
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Management of iodine deficiency
Use of iodized salt Iodination of drinking water Fortification of infant
formulas Fortification of other food
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Xerophthalmia
Vitamin A Deficiency
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Vitamin A Deficiency Vitamin A deficiency is the most
common cause of childhood blindness Causing 250,000-500,000 children to go
blind every year, half of whom will die within the year
Vitamin A deficiency disorders occur when body reserves are depleted to the limit at which physiological functions are impaired
Xerophthalmia; the pathological eye signs of Vitamin A deficiency
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Sources of vitamin A Common dietary sources of performed
vitamin A are liver, milk and milk products, eggs and fish
The richest sources are liver oils of fish, such as shark, halibut and cod, and of marine mammals, such as polar bear
The livers of ox, sheep, calves or chicken also contain vitamin A at concentrations comparable to cod liver oil
Eggs, milk and other dairy products: butter and cheese, are all moderate sources
Provitamin A carotenoids are found in yellow and orange fruit and vegetables, and in dark green leafy vegetables
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Consequences of vitamin A deficiency Xerophthalmia represents the
ocular consequences of vitamin A deficiency that include night blindness (XN), conjunctival xerosis (X1A), Bitot’s spots (X1B), corneal xerosis (X2), ulceration (X3A) or necrosis/keratomalacia (X3B)
Immunocompetence: effects on the immune system, infection
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Epidemiology
Magnitude of the problem Vitamin A deficiency is, after PEM and
iron-deficiency anemia, the most widespread and serious nutritional disease among young children
In 1994, global estimate indicated that 2.8 million preschool children are clinically affected by vitamin A deficiency
Asia and Africa account for nearly 90% of the global problem
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Risk factors As a public health problem, vitamin A
deficiency occurs within an environment of social, economic and ecological deprivations in which people live in the transitional and developing economics of the world
It is imperative to understand the local conditions when designing appropriate and effective intervention programs to improve the situation
Some underlying factors: age, gender, physiological status, diet, disease patterns, socioeconomic conditions
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Age Varying levels of vitamin A deficiency, from
subclinical forms to the severe form of blinding malnutrition (keratomalacia), can occur at any age
However, vitamin A deficiency, particularly severe deficiency, affects children of preschool age
The requirements for growth are high, while the dietary intake of vitamin A is often low
Children under 12 months of age, corneal disease is relatively rare event, largely because breast-feeding is protective
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Gender In healthy human adults, both plasma
retinol and RBP (retinol binding protein) are found at levels 20% higher in males than females
Nevertheless, males have generally been found to be at higher risk of night blindness and Bitot’s spot than female during the preschool and early school-age years
Less gender difference in severe xerophthalmia
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Physiological status Vitamin A needs are increased during
periods of rapid growth, younger children are the most vulnerable group
The demands for vitamin A are also increased during the period of gestation and lactation
Night blindness during pregnancy and lactation is especially common in south Asia (15-20% of all pregnancies)
Studies have shown, breast milk of women with poor vitamin A could subsequently contribute to increased susceptibility of the infants
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Diet The basic underlying cause of vitamin A
deficiency is a diet lacking adequate amounts of vitamin A, either preformed or provitamin A carotenoids, to meet the requirement
Vitamin A deficiency is common wherever diets are of relatively low quality
Breast-feeding, the quality of complementary feeding and the quality of the children diet are all important factors in maintain vitamin A status ; xerophthalmia protective
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Diet Epidemiological studies support a
progressive of appropriate complementary feeding that has been shown to guard children from xerophthalmia through the preschool year
Intake of yellow fruit (mango and papaya) is strongly protective in the second and third years of life
Dark green leafy vegetables play a more important role from the third year onwards
After infancy, routine consumption of animal foods with preformed vitamin A (eggs, dairy products, fish and liver) is highly protective
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Disease patterns Vitamin A deficiency increase the risk
of infectious morbidity; diarrhea, respiratory infection, measles
Intestinal worms such as Giardia and Ascaris have been reported to lead to reduced absorption of vitamin A
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Socioeconomic conditions Vitamin A deficiency is confined
largely to relatively impoverished countries
Studies have shown that households with mildly xerophthalmic children have smaller landholdings, poorer housing conditions, fewer draft and grazing animals, and lower economic standing
Low education levels of the father or mother are a further risk factor
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Prevention Food-based approaches, including dietary diversification, nutrition education and fortification of staple and value-added food
Supplementation with vitamin A capsules
Breast-feeding, treatment of infectious diseases
Modification of the political, socioeconomic, physical environment
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Food fortification Food fortification refers to the addition of
micronutrients to processed foods. Salt iodization was introduced in the early
1920s in both Switzerland and the USA. From the early 1940s onwards, the
fortification of cereal products with thiamine, riboflavin and niacin became common practice
Margarine was fortified with vitamin A in Denmark.
Milk with vitamin D in the United States