nutritional epidemiology: micronutrient malnutrition

Nutritional Epidemiology: Micronutrient malnutritionAsst. Prof. Dr.

Sumattana Glangkarn

sumattana glangkarn 2

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


Nutrition problems in Thailand include;- Protein energy malnutrition (PEM)- MNM; Iron deficiency anemia (IDA)

Iodine deficiency disorder (IDD)

Vitamin A deficiency.


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


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


องค์�ประกอบของฮี�โมโกลบ�น


Iron nutritional status

Biochemical and hematological tests

Serum iron concentration Total iron binding capacity Transferrin saturation Protoporphyrin Serum ferritin Transferrin receptors


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


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


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


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


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.


Hemoglobin (Hgb)

ค์�าปกติ� (g/dl)ชาย -1418

หญิ�ง -1216

เด็�ก -1116

ทารก -1015

แรกค์ลอด็ -1424


Hematocrit : Hct

3Hct. = (Hgb)ค์�าปกติ� 100(/ ml.)

ชาย -4252

หญิ�ง -3747

เด็�ก -3143

ทารก -3040

แรกค์ลอด็ -4464


Centrifuge


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


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


Conjunctiva

Normal appearing conjunctiva


Spoon finger


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


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


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


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.


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


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


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


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


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


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


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


Management of iodine deficiency

Use of iodized salt Iodination of drinking water Fortification of infant

formulas Fortification of other food


Xerophthalmia

Vitamin A Deficiency


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


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


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


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


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


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


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


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


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


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


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


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


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


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

nutritional epidemiology: micronutrient malnutrition

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