Iodine deficiency disorders (IDDs)
refer to the spectrum of consequences of iodine deficiency in a population resulting from its deficit in soil
and water. Consumption of crops and plants grown on iodine-deficient soils
leads to IDD in populations solely dependent on this vegetation for their
iodine requirements. When iodine intake falls below the recommended
levels, the thyroid may no longer be able to synthesize sufficient amounts
of thyroid hormones.
Iodine deficiency (ID) causes its impact right from the
development of fetus to people of all age groups. It results in abortion,
stillbirth, mental retardation, deaf-mutism, squint, dwarfism, goiter at
all ages, neuromotor defects, etc. People living in areas affected by
severe ID may have an intelligence quotient (IQ) of up to 13.5 points
below that of those from comparable communities in areas where there is no
ID. Currently, ID is the single most important preventable cause of brain
damage [1].
In India, out of 582 districts in the country, surveys
conducted in 324 districts have revealed that IDD is a public health
problem in 263 districts, with a goiter prevalence rate of more than 10%
[2]. The Government of India under the Prevention of Food Adulteration Act
(PFA) stipulated that iodized salts should have a minimum of 30 ppm iodine
at the production level and 15 ppm at the retail level. This level of salt
iodization provides physiological needs of 100-150 µg/day which is
reflected in the median urinary iodine excretion (UIE) levels of 100-200
µg/L. The status of UIE levels in different regions of country has been
extensively assessed by surveys over the last decade. Out 223 districts
surveyed, 194 (86%) had median UIE levels of 100 mcg/L. Similarly, out of
330 districts from which salt samples were collected and analyzed, 191
(58%) districts had an iodine content of salt of 15 ppm and more at
beneficiary level, indicating successful implementation of National Iodine
Deficiency Control Program (NIDDCP) [3].
In the current issue of the Indian Pediatrics, a
study has been published from Kutch District of Gujarat [4] in
which authors have found Goiter prevalence of 11.2% among primary school
children in spite of presence of (i) median urinary iodine
excretion level of 110 µg/L and (ii) 92% salts samples with iodine
content of 15 ppm and more. The authors have concluded that IDD was a mild
public health problem in the district. The reported continuation of high
goiter prevalence in children in spite of adequate salt iodization in the
region needs to be discussed. This could be due to following reasons:
1. Misclassification of goiter: According to
WHO, ultrasonography provides a more precise measurement of thyroid
volume compared with palpation. The specificity and sensitivity of
palpation of goiter are low in grades 0 and 1 due to a high
inter-observer variation [1]. Studies conducted amongst experienced
examiners have revealed that the misclassification of goiter can be as
high as 40%. A recent study found discrepancy between palpation and
ultrasound up to a level of 23.9% amongst goitrous children [5].
2. Persistence of goiter after adequate salt
iodization: Elevated goiter prevalence for up to 4 years in
school-aged children after successful introduction of iodized salt has
been reported, primarily because of persistent goiter in older children
[6].
3. Concomitant presence of anemia: The
therapeutic response to oral iodine in goitrous children with iron
deficiency anemia is impaired [7]. In Gujarat the prevalence of anemia
amongst children (6-59 months) has been documented as 69.7% [8]. This
could be another reason for lack of impact of iodized salt in study
population.
Once a salt iodization program has been initiated, the
principal impact indicator recommended in the population is the median
urinary iodine level. The changes in goiter prevalence lag behind changes
in iodine status, and therefore cannot be relied upon to accurately
reflect current iodine intake. The thyroid size reflects iodine nutrition
over months or years. Therefore, even though populations may have attained
iodine sufficiency on the basis of median urinary iodine concentration,
high prevalence of goiter may persist in children [9]. Also, as most
iodine consumed is excreted in the urine, urinary iodine excretion level
is a valid marker of a previous day’s dietary iodine intake. Therefore, we
must use the urinary iodine excretion levels as a biochemical marker for
iodine nutritional status in a community .
Competing interests: None.
Funding: None.
References
1. WHO/UNICEF/ICCIDD: Assessment of iodine deficiency
disorders and monitoring their elimination: A guide for programme
managers. Third edition. Geneva: WHO; 2007. Available at
www.who.int/entity/nutrition/publications/micronutrients/iodine_deficiency/en/
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8. International Institute for Population Sciences (IIPS)
and ORC Macro National Family Health Survey (NFHS 3) 2005-2006, Mumbai
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