SEPTEMBER 2012 • BRIEF NO. 7
THE J iVit A JOURNAL
Maternal Iodine Deficiency
in Rural Bangladesh
Despite a national salt iodization strategy, evidence of insufficiency
during pregnancy and subsequent consequences for offspring exists.
Severe iodine deficiency in pregnant women has long been recog-
nized to increase the risk of miscarriage and stillbirth, and is associated with mental retardation and developmental delays in the
offspring of women affected during their pregnancies. Consequences
of mild to moderate iodine deficiency for mothers and their offspring
are less well established but remain a concern. Adverse effects of
iodine deficiency are mediated through the reduced production of
thyroid hormones, with the most visible consequence of persistent
iodine deficiency being goiter, which results from the expansion of the
thyroid gland to capture any available circulating iodine. Thyroid
hormone production is the only known role for iodine in the body, but
these hormones are permissive for a myriad of body functions.
Appropriate fetal development in early pregnancy is dependent on
thyroid hormone (thyroxine) produced by the mother, and once the
fetal thyroid gland itself has matured in later gestation, the offspring
depends on a maternal supply of iodide across the placenta and
through breast milk in the postpartum period. Thus, the timing of
iodine deficiency during pregnancy may be related to the type or
extent of consequences for the offspring.
Unlike many other micronutrients which are concentrated in certain
food sources, iodine content of locally-procured foods reflects the
amount of iodine in soil, which then accumulates in plant and animal
products in the food chain. Iodine depletion of soil is likely to occur
where leaching or loss of topsoil is common, resulting in iodine-poor
foods. Under such conditions, a typical approach for ensuring the
availability of iodine to a population is to enact universal salt iodization, such that salt fortified with iodate is distributed through local
markets. Bangladesh adopted universal salt iodization in 1989, and
while this has improved iodine status in Bangladesh as assessed by
national surveys,1 iodine insufficiency remains a concern.
To ensure the nutritional
health
of
pregnant
women with respect to
iodine status, a World
Health
Organization
(WHO)
Technical
Consultation in 2007
proposed increasing the
recommendations
for
iodine intake of pregnant
women from 200 to 250 µg/day.2 Correspondingly, new guidelines
for the assessment of iodine status using urinary iodine (UI)
excretion, which reflects recent intake of iodine, have been made
specifically for pregnant women. These recommendations increase the
cutoff for the population median UI that indicates adequacy of intake
from 100 µg/L to a range of 150–249 µg/L among pregnant women.2
The new focus on pregnant women reflect the concern for iodine
adequacy specifically during this life stage and a recent recognition
that pregnant women may remain iodine insufficient due to the
increased demands for iodine during pregnancy even when other
members of a household have achieved iodine adequacy.
To determine the extent and consequences of iodine deficiency among
pregnant women of rural Bangladesh, the JiVitA Project, in collaboration with the Institute of Nutrition and Food Science, Dhaka University, measured household salt iodine content and UI among women
participating in the JiVitA-1 trial substudy in early (N=1376; <16 wk
gestation) and late (N= 1114; >32 wk gestation) pregnancy to
determine whether current levels of salt iodization were sufficient to
support adequate iodine status.3 In fact, we found that over 80% of
women had urinary iodine concentrations below 150 µg/L (Figure),
with an early pregnancy median UI of 65 µg/L, demonstrating that
women of the region were typically moderately iodine deficient as
they entered their pregnancies.
When plotted against the content of iodine in household salt,
JiVitA-1 data showed that during pregnancy median UI did not reach
150 µg/L until the iodine content of household salt was at least 32
and 51 ppm during early and late pregnancy, respectively.3 These
levels are far above the 15 ppm currently considered to be adequate
salt iodine content at the household level. We then sought to
determine whether maternal factors associated with the presence of
salt containing at least 30 ppm in households could be ascertained.
Age, nutritional status, and socioeconomic variables were not associated with the content of iodine of salt in households.3 These findings
suggest that all women in this region are at risk of iodine deficiency
and that more targeted means of reaching pregnant women may be
needed to ensure iodine
adequacy during pregnancy.
We have begun to examine the
consequences of maternal iodine
deficiency on outcomes for
B
A
N
G
L
A
D
E
S
H
50
Percent (%)
Early pregnancy
Iodine
deficient
40
Late pregnancy
30
20
10
0
<50
50 99.9
100 149.9
150 249.9
250 499.9
≥500
Urinary Iodine (µg L)
infants and children of JiVitA-1 study participants. Among a subset of
infants in whose mothers UI data were available during both early and late
pregnancy, being born low birth weight was over twice as likely when mothers were persistently iodine deficient during pregnancy (Table; unpublished
data). Some differences in anthropometry persisted when children were
revisited at 5 years of age: children whose mothers were most severely
iodine deficient in the third trimester of pregnancy weighed less, were
shorter, and had smaller chest circumferences than children with mothers
who had adequate iodine status in pregnancy.4
The extent to which in utero iodine deficiency affects cognitive outcomes in
offspring is not well described. To determine the consequences of iodine
insufficiency on cognitive and motor development of children, we assessed
these conditions in 381 5 year old children who were born to mildly,
moderately, or severely iodine deficient mothers—ie. prior to their entry
into any formal schooling.4 We found trends toward poorer performance
on tests of verbal scale, vocabulary, matrix reasoning, block design, and
overall performance in unadjusted analyses with maternal iodine deficiency.
Adjusting for other household factors, including current levels of iodine in
household salt as well as socioeconomic status, home environment,
mother’s cognition, and child nutritional status, we found that children of
mothers who were iodine deficient during pregnancy did poorer on tests of
vocabulary and verbal scale. Additionally, among children whose mothers
were severely deficient in early pregnancy, balance and motor skills were
more compromised than those of mothers with adequate status. These
findings again support the contention that micronutrient sufficiency in
utero has long-term consequences for the offspring of undernourished
mothers.
Iodine deficiency remains a nutritional problem in Bangladesh, with consequences that persist from pregnancy exposure at least into the early
childhood years. Children born to iodine deficiency mothers may be at risk
of adverse health and developmental outcomes that may be mediated
through compromised growth and cognitive function. Longer-term consequences remain to be determined, but attention should be focused on the
prevention of iodine deficiency in women of reproductive age in rural
Bangladesh.
OR (95%CI)1
Maternal Iodine
Status
N
Low Birth
Weight, N (%)
Sufficient
39
15 (38.5%)
–
Sufficient
1st TM only
90
47 (52.2%)
1.45 (0.63, 3.43)
Sufficient
3rd TM only
57
33 (60.0%)
2.20 (0.88, 5.70)
344
209 (61.5%)
2.54 (1.21, 5.50)
Insufficient
1st and 3rd TM
Abbreviation: TM, trimester
1Adjusted for parity, gestational age, maternal education, and height
Table. Association of maternal iodine status during pregnancy with
low birth weight.
JiVitA is a project of the Center for Human Nutrition of Johns Hopkins University, spanning 19 unions of Gaibandha and
Rangpur Districts in rural Northwestern Bangladesh. JiVitA has been conducting community trials, supported by epidemiologic,
ethnographic, and laboratory research since 2000, to reveal the impact of public health interventions in order to guide nutrition
and health programs and policies in Bangladesh and elsewhere in South Asia.
References
1) Dhaka University, BSCIC, IPHN, UNICEF & ICCIDD. National survey on iodine deficiency disorders and universal salt iodization in Bangladesh 2004-05. Dhaka University, BSCIC
IPHN, UNICEF, ICCIDD: Dhaka, 2007.
2) WHO, UNICEF & ICCIDD. Assessment of iodine deficiency disorders and monitoring their elimination. A guide for program managers, 3rd edn, World Health Organization:
Geneva, 2007
3) Shamim AA, Christian P, Schulze KJ, Ali H, Kabir A, Rashid M, Labrique A, Salamatullah Q, West Jr KP. Iodine status in pregnancy and household salt iodine content in rural
Bangladesh. Maternal and Child Nutrition, Oct 26, 2010.
4) Jing H. Maternal iodine deficiency during pregnancy and child cognition, motor skills and growth at age five years in rural Bangladesh. PhD dissertation, Johns Hopkins Bloomberg
School of Public Health, 2011.
Funding Agencies
For Further Information Contact
Center for Human Nutrition
Department of International Health
Johns Hopkins Bloomberg School
of Public Health
Baltimore, MD 21205
Telephone: 1-410-955-2061
http://www.jhsph.edu/chn
The JiVitA Project
Johns Hopkins University
Ji
Road 25, Block A, House 48,
Flat C-1
Banani, Dhaka, Bangladesh
NEW Telephone: (+88-02) 9840091
https://www.jivita.org
VitA
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•
•
•
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The Bill & Melinda Gates Foundation
The United States Agency for International Development
The United States Department of Agriculture
The Canadian International Development Agency
The Sight and Life Research Institute
The Ministry of Health and Family Welfare,
The Government of the People's Republic of Bangladesh
MATERNAL
MATERNAL IODINE
IODINE DEFICIENCY
DIFICIENCY IN
IN RURAL
RURAL BANGLADESH
BANGLADESH