Effect of iron supplementation during pregnancy on the intelligence
quotient and behavior of children at 4 y of age: long-term follow-up
of a randomized controlled trial1–3
Shao J Zhou, Robert A Gibson, Caroline A Crowther, Peter Baghurst, and Maria Makrides
ABSTRACT
Background: Iron supplements are often prescribed during preg-
nancy despite the lack of intervention trials that have assessed the
effects of supplementation in pregnancy on childhood development.
Objective: The objective was to determine whether iron supple-
mentation during pregnancy influences childhood intelligence quo-
tient (IQ) in an industrialized country.
Design: Pregnant women (n ҃ 430) were randomly allocated to
receive iron (20 mg/d) or placebo from 20 wk gestation until deliv-
ery, and the women and their children were followed up over the long
term (4 y). Seventy percent of these families participated in the
follow-up. The proportion of women with iron deficiency anemia at
the end of pregnancy was 1% (2 of 146) in the iron group and 11%
(15 of 141) in the placebo group. The primary outcome was the IQ
of the children at 4 y of age, as assessed by the Stanford-Binet
Intelligence Scale. Secondary outcomes included child behavior and
the general health of the mothers.
Results: The mean IQ was not significantly different (P ҃ 0.980)
between the children of the iron-supplemented mothers (109 앐 11;
n ҃ 153) and the children of the mothers in the placebo group
(109 앐 11; n ҃ 149). However, the percentage of children with an
abnormal behavior score was higher in the iron group (24 of 151, or
16%) than in the placebo group (12 of 149, or 8%); the relative risk
was 1.97 (95% CI: 1.03, 3.80; P ҃ 0.037). There was no significant
difference in the health of the mothers between groups, as assessed
by the SF-36 Health Survey.
Conclusions: Prenatal iron supplementation that reduces the inci-
dence of iron deficiency anemia from 11% to 1% has no effect on the
IQ of the offspring at 4 y of age. Am J Clin Nutr 2006;83:
1112–7.
KEY WORDS Iron supplementation, pregnancy, child devel-
opment, intelligence quotient, IQ, behavior, industrialized country
INTRODUCTION
Routine iron supplementation is a common practice for pre-
venting iron deficiency (ID) and iron deficiency anemia (IDA) in
pregnancy, because the dietary iron intake of pregnant women
often does not meet the recommended dietary intake. However,
expert opinion on whether iron should be given routinely to
pregnant women is divided. In countries such as the United States
and France, pregnant women are often advised to routinely take
iron supplements of 30 to 60 mg/d, whereas the policy in Aus-
tralia and the United Kingdom is to screen and treat pregnant
1112 Am J Clin Nutr 2006;83:1112–7. Printed in USA. © 2006 American Society for Nutrition
Downloaded from https://academic.oup.com/ajcn/article-abstract/83/5/1112/4649549 by guest on 09 December 2018
women with IDA. The Cochrane systematic review (1) and the
review conducted by the US Preventive Task Force (2) both
concluded that, although iron supplementation in pregnancy im-
proves maternal iron status, there is a lack of evidence of benefit
in terms of clinical outcome measures. In particular, the US
Preventive Task Force has highlighted the need to assess the
long-term effects of iron supplementation on child development
as an area of priority for research (3).
Evidence from animal studies has consistently shown that
inadequate iron nutrition during pregnancy leads to permanent
structural and functional changes in the brain of offspring (4 – 6).
Although the degree of ID induced in experimental animals is
often more severe than in pregnant women, no human interven-
tion trials have been specifically designed to investigate the ef-
fect of iron nutrition in pregnancy on child development. The aim
of our study was to assess whether improved iron nutrition in
pregnancy, through routine iron supplementation, influences the
development of the children and the long-term health of mothers.
SUBJECTS AND METHODS
Participants
Mothers and children who participated in a double-blind ran-
domized controlled trial of iron supplementation in pregnancy
called the Australian Mothers’ and Babies’ Iron Trial (7) were
eligible for follow-up. In summary, 430 pregnant women receiv-
ing antenatal care at the Women’s & Children’s Hospital in
Adelaide, Australia, were recruited to participate in the original
trial during 1997–1999 (7). The participants were randomly al-
located to receive either iron or placebo from 20 wk of gestation
1
From the Child Nutrition Research Centre and the Department of Pedi-
atrics (SJZ, RAG, and MM), the Department of Obstetrics & Gynaecology
(CAC and MM), and the Departments of Paediatrics and Public Health (PB),
Women’s & Children’s Hospital, University of Adelaide, North Adelaide,
Australia.
2
Supported by the National Health & Medical Research Council (ID:
250431) and Channel 7 Children’s Medical Research Foundation. The iron
and placebo tablets used in the original trial were manufactured and donated
by Soul Pattinson Manufacturing, Kingsgrove, NSW, Australia.
3
Reprints not available. Address correspondence to MM, Child Nutrition
Research Centre, Level 1, Rieger Building, Women’s & Children’s Hospital,
72 King William Road, North Adelaide, SA 5006, Australia. E-mail:
maria.makrides@cywhs.sa.gov.au.
Received October 26, 2005.
Accepted for publication January 17, 2006.
 IRON IN PREGNANCY AND CHILD DEVELOPMENT 1113
TABLE 1
Demographic characteristics of the participating families1

Mother’s group assignment in AMBIT

Iron Placebo
(n ҃ 153) (n ҃ 149) P

Maternal characteristics
Age at enrollment in AMBIT (y) 28.4 앐 4.72 28.4 앐 5.1 0.983
Education level [n (%)] 0.397
울 12 y 116 (76) 119 (80)
Diploma or degree 37 (24) 30 (20)
Smoked in pregnancy [n (%)] 25 (16) 25 (17) 0.918
Iron status at birth

Downloaded from https://academic.oup.com/ajcn/article-abstract/83/5/1112/4649549 by guest on 09 December 2018

Hemoglobin (g/L) 129 앐 13 120 앐 11 쏝0.001
Serum ferritin (␮g/L) 17 앐 2 11 앐 2 쏝0.001
ID [n (%)] 45/142 (32) 78/136 (57) 쏝0.001
IDA [n (%)] 2/146 (1) 15/141 (11) 0.001
Characteristics of children
Age (y) 4.2 앐 0.2 4.2 앐 0.2 0.190
Male sex [n (%)] 80 (52) 70 (47) 0.356
Birth order [n (%)] 0.789
1 75 (49) 68 (46)
2 55 (36) 55 (37)
욷3 23 (15) 26 (17)
Gestational age at birth (wk) 39.5 앐 1.4 39.4 앐 1.7 0.745
Duration of breastfeeding (wk) 32.1 앐 35 27.1 앐 29 0.183
Breastfed [n (%)] 125 (82) 128 (86) 0.322
Breastfed 욷 6 mo [n (%)] 73 (48) 67 (45) 0.632
Weight at 4-y follow-up (kg) 18.0 앐 2.4 17.9 앐 2.5 0.650
Height at 4-y follow-up (cm) 105.0 앐 4.5 104.5 앐 3.5 0.470
Suboptimal home environment [n (%)]3 21 (14) 30 (20) 0.218
1
AMBIT, Australian Mothers’ and Babies’ Iron Trial; ID, iron deficiency (defined as ferritin 쏝 12 ␮g/L); IDA, iron deficiency anemia (defined as
hemoglobin 쏝 110 g/L and ferritin 쏝 12 ␮g/L).
2
x៮ 앐 SD (all such values).
3
Defined as a Home Screening Questionnaire score 쏝 41.

until birth. The dose of iron used in the trial was 20 mg/d, which
was intended to increase the women’s usual iron intake from 앒12
mg/d (8) to the Recommended Dietary Intake for iron during
pregnancy in Australia (22–36 mg/d) (9). The compliance rate
was 86% for both groups based on tablet back-count and monthly
phone calls (7). Women in the iron group had higher concentra-
tions of hemoglobin and serum ferritin and lower incidences of
ID and IDA at the end of pregnancy (Table 1). The follow-up was
conducted from May 2002 to January 2004, 4 y after birth. The
4-y follow up was chosen because developmental assessment at
preschool age is considered a better predictor of school achieve-
ment than is the developmental assessment in the first 2 y of
life—the time when most studies investigating the relation be-
tween ID or IDA and child development have been conducted.
For the remainder of the report, the children are referred to as the
iron group or the placebo group based on the group allocation of
their mothers’ in the original trial. This study was approved by
the Human Research Ethics Committee at the Women’s & Chil-
dren’s Hospital. Informed consent was obtained from all partic-
ipants.
Assessments
The primary outcome was childhood intelligence quotient
(IQ), assessed by using the Stanford-Binet Intelligence Scale
(10), which was administered by qualified experienced psychol-
ogists. The Stanford-Binet Intelligence Scale is an internation-
ally standardized tool for global developmental assessment,
which has 4 subscales of IQ (verbal reasoning, visual reasoning,
quantitative reasoning, and short-term memory) as well as a
combined composite IQ (10). This scale has high internal con-
sistency and test-retest reliability (10), and it has been used to
assess the effect of IDA on child development for children aged
쏜3 y (11) rather than the Bayley Scales (12), which are more
often used in younger children. Most of the IQ assessments were
conducted in a clinic room at the Women’s & Children’s Hos-
pital. For a small number of families (n ҃ 47) who were unable
to attend the hospital clinic, the assessment took place in a private
room of a child care center or preschool where the child was
attending. Child behavior was assessed by using the Strength and
Difficulties Questionnaire (SDQ) parent report form (13), which
is a behavior-screening questionnaire used to assess behavioral
problems such as emotion, conduct, hyperactivity, peer relation,
and social behavior. The SDQ has been shown to have moderate-
to-strong internal reliability, test-retest reliability, and external
validity (14, 15). A total difficulties score of 욷17 indicates ab-
normal behavior (16). The weight and height of the children were
measured with an electronic scale and a stadiometer, respec-
tively, by using standardized techniques. Information was also
1114 ZHOU ET AL
FIGURE 1. Flow diagram for AMBIT and the follow-up. IQ, intelligence quotient.
collected regarding sex, gestational age at birth, birth order, du-
ration of breastfeeding, parental education, and quality of home
environment with the Home Screening Questionnaire (HSQ)
(17), which is a screening tool used to identify home environ-
ments likely to be suboptimal for the development of children.
The HSQ has high internal reliability and test-retest reliability
(18). These variables were assessed as potential confounders of
the relation between iron supplementation and IQ and child be-
havior. Attendance at preschool was not considered to be a po-
tential confounding variable because all Australian children at-
tend preschool.
In addition, the general health of women was assessed by using
the SF-36 (19), a self-administrated questionnaire that assesses 8
concepts of health and has been used in studies that examine the
effect of ID and the general health of women (20, 21). Informa-
tion on nonpregnancy-related health problems or hospital admis-
sions since the completion of the original trial was also collected.
If the women had any subsequent pregnancies, outcomes of the
subsequent pregnancies were collected from medical records.
Families and research staff involved in data collection were
blinded to the group assignment until all primary analyses of the
4-y data had been completed.
Downloaded from https://academic.oup.com/ajcn/article-abstract/83/5/1112/4649549 by guest on 09 December 2018
Statistical analysis and sample size estimation
The data were analyzed by using SPSS software (version10.0;
SPSS Inc, Chicago, IL). The primary analyses were based on
intention to treat. Childhood IQ, behavior, and health of the
women were compared between the iron and placebo groups by
using independent-sample t tests. Differences between categor-
ical variables were compared using chi-square tests. Multiple
regression analyses were conducted for continuous outcomes,
and logistic regression was conducted for dichotomous out-
comes as secondary analyses to examine the effect of interven-
tion on childhood IQ and behavior when potential IQ covariates
were controlled. Statistical significance was set at a P value 쏝
0.05 for all statistical tests. Our sample size estimation was based
on IQ with an assumed SD of 16 (10). We initially estimated that
186 children in each group were needed to detect a minimum
difference of 5 IQ points between the iron and placebo groups
with 85% power. A 5-IQ point difference was considered clini-
cally significant because it is of the order of magnitude associated
with IQ differences in children who were fed breast milk rather
than formula as infants (22) or were exposed to high lead con-
centrations (23). Differences of this magnitude have prompted
 IRON IN PREGNANCY AND CHILD DEVELOPMENT 1115
TABLE 2
Intelligence quotient (IQ) and behavior of the children1

Mother’s group assignment in AMBIT

Iron (n ҃ 153) Placebo (n ҃ 149) MD (95% CI) RR (95% CI) P

IQ score
Composite 109 앐 112 109 앐 11 Ҁ0.03 (Ҁ2.47, 2.40) — 0.980
Verbal reasoning 109 앐 12 109 앐 11 Ҁ0.22 (Ҁ2.88, 2.44) — 0.869
Visual reasoning 103 앐 10 104 앐 11 Ҁ0.64 (Ҁ3.00, 1.72) — 0.593
Quantitative reasoning 114 앐 12 114 앐 12 Ҁ0.37 (Ҁ3.09, 2.35) — 0.790
Short-term memory 104 앐 12 104 앐 12 0.64 (Ҁ2.15, 3.44) — 0.651
Composite IQ 쏝 1 SD [n (%)] 19 (12) 20 (13) — 0.91 (0.47, 1.79) 0.795
Composite IQ 쏝 2 SD [n (%)] 4 (3) 3 (2) — 1.31 (0.29, 5.94) 0.728

Downloaded from https://academic.oup.com/ajcn/article-abstract/83/5/1112/4649549 by guest on 09 December 2018

Behavior
Emotion 1.8 앐 1.8 1.7 앐 1.8 0.10 (Ҁ0.31, 0.51) — 0.643
Conduct 2.9 앐 2.0 2.8 앐 1.9 0.02 (Ҁ0.42, 0.46) — 0.922
Hyperactivity 3.7 앐 2.3 3.7 앐 2.1 Ҁ0.02 (Ҁ0.51, 0.48) — 0.949
Peer relations 1.8 앐 1.7 1.4 앐 1.5 0.35 (Ҁ0.01, 0.71) — 0.056
Total difficulties score 10.1 앐 5.6 9.7 앐 4.9 0.45 (Ҁ0.74, 1.65) — 0.651
Abnormal, total score 욷 17 [n (%)] 24 (16) 12 (8) — 1.97 (1.03, 3.80) 0.037
1
AMBIT, Australian Mothers’ and Babies’ Iron Trial; MD, mean difference; RR, relative risk.
2
x៮ 앐 SD (all such values).

public health authorities to promote human milk feeding and to
guard against lead exposure. Halfway through the study, we
reevaluated the sample size estimate using an SD of 12, which
was typical of our study sample. One hundred six children in each
group were required to achieve an equivalent difference with the
same power.
RESULTS
Characteristics of the participants
Seventy percent of the mothers and children from the original
trial were assessed 4 y after birth (Figure 1). At follow-up, there
were no differences in the social and demographic characteristics
between families from the iron and placebo groups (Table 1). The
key difference between the iron and placebo groups was the
higher iron status of the iron-supplemented women than of
the placebo group at the end of pregnancy. Although 30% of
families did not participate in the follow-up, there were no sig-
nificant differences in the sociodemographic characteristics be-
tween participants and nonparticipants, except that more women
who did not attend the 4-y follow-up smoked during pregnancy
[35 of 128 (27%) compared with 50 of 302 (17%); P ҃ 0.012].
However, the proportion of mothers who smoked during preg-
nancy did not differ between the iron and placebo groups [25 of
153 (16%) compared with 25 of 149 (17%); Table 1].
Adjustment for covariates (including maternal age, parental ed-
ucation levels, quality of home environment, duration of breast-
feeding, gestational age at birth, birth order, and sex of the child)
did not change the outcomes for either IQ or behavior.
In an exploratory analysis, the composite IQ of the children
was negatively correlated with the total behavior score (r ҃
Ҁ0.237, P 쏝 0.0001), and children with abnormal behavior
scores had a lower mean IQ than did children whose behavior
scores were in the normal range (104 앐 11 compared with 110 앐
11; 95% CI: 2, 10; P ҃ 0.001).
General health of the mothers and outcomes of
subsequent pregnancies
There were no significant differences in any of the 8 health
concepts assessed with the use of the SF-36 between the iron and
placebo groups (Table 3). The proportion of women who had
health problems requiring medical treatment or hospital admis-
sion since the completion of the original trial (6 mo postpartum)
did not differ significantly between the iron and placebo groups
(Table 3). The proportion of women who had at least one sub-
sequent pregnancy was 76 of 152 (50%) in the iron group and was
81 of 148 (55%) in the placebo group (P ҃ 0.696). There were no
significant differences in the outcomes of subsequent pregnan-
cies in terms of gestational age at birth, birth weight, birth length,
birth head circumference, or proportion of women with IDA in
subsequent pregnancies (data not shown).

IQ and behavior of the children DISCUSSION

The mean IQ of the children at 4 y was 109 앐 11. There were
no significant differences between the iron and placebo groups in
either composite IQ or any subscales of IQ or in the proportion of
children whose IQ fell 1 or 2 SD below the mean (Table 2). The
mean scores for behavioral difficulties did not differ significantly
between the groups. However, more children in the iron group
than in the placebo group had an abnormal total behavior score
[24 of 151 (16%) compared with 12 of 148 (8%); Table 2].
To the best of our knowledge, this is the first human interven-
tion trial to evaluate the effect of iron nutrition in pregnancy on
early child development. The major finding in this sample taken
from an industrialized country is that routine iron supplementa-
tion in pregnancy had no benefit on childhood IQ, despite the
clear benefit of iron therapy on iron status in the mothers at birth.
Our finding is in contrast with the results from the cohort study
of Tamura et al (24), which was designed to investigate the
1116 ZHOU ET AL

TABLE 3
General health of the mothers1

Mother’s group assignment in AMBIT

Iron Placebo
(n ҃ 151) (n ҃ 148) MD (95% CI) P

SF-36 (19)
Physical functioning 88 앐 17 89 앐 15 Ҁ0.48 (Ҁ4.17, 3.22) 0.800
Role functioning, physical 82 앐 33 84 앐 30 Ҁ1.83 (Ҁ0.06, 5.39) 0.618
Role functioning, emotion 85 앐 31 84 앐 32 Ҁ1.43 (Ҁ5.62, 8.48) 0.690
Social functioning 85 앐 21 86 앐 19 Ҁ1.12 (Ҁ5.58, 3.34) 0.621
Bodily pain 82 앐 21 83 앐 19 Ҁ0.57 (Ҁ5.06, 3.92) 0.803
Mental health 76 앐 14 77 앐 14 1.02 (Ҁ2.21, 4.24) 0.535

Downloaded from https://academic.oup.com/ajcn/article-abstract/83/5/1112/4649549 by guest on 09 December 2018

Vitality 59 앐 19 61 앐 19 2.83 (Ҁ1.52, 7.17) 0.202
General health perceptions 78 앐 18 79 앐 18 1.82 (Ҁ2.33, 5.97) 0.388
Health problems at follow-up [n (%)] 18 of 152 (12) 21 of 148 (14) 0.84 (0.46, 1.50) 0.546
Hospital admissions at follow-up [n (%)] 22 of 151 (15) 26 of 147 (18) 0.85 (0.50, 1.44) 0.547
1
AMBIT, Australian Mothers’ and Babies’ Iron Trial; MD, mean difference.

developmental outcomes of children born small for gestational
age. They showed that children with cord ferritin concentrations
in the lowest quartile scored lower on some mental and psy-
chomotor tests at 5 y than did children with cord ferritin concen-
trations in the 2 middle quartiles (24). However, children with
cord ferritin in the highest quartile also scored lower on some
tests. Although the authors suggested that the children with cord
ferritin in the highest quartile might have a falsely elevated fer-
ritin concentration because of possible maternal infections (24),
the possibility that a high cord ferritin concentration itself may
adversely affect child development cannot be excluded. The
differences in results between the 2 studies may be explained by
the fact that the cohort study included a high proportion of small-
for-gestational-age infants or by methodologic differences in-
herent in cohort studies and randomized trials. Our study was a
randomized comparison that included women and children that
were representative of the Australian population (7, 25). The
dose of supplemental iron used in our original trial (7) was low
compared with common iron supplements used in pregnancy (1).
However, the 3-fold differences in iron intake between the iron
and placebo mothers in our original trial resulted in changes in
maternal hemoglobin and ferritin that were similar to the differ-
ences in trials in which women were supplemented with 앒100
mg Fe/d (1). Although we cannot be sure that low-dose iron
supplements increased the supply of iron to the fetus or neonate,
the maternal iron-status data indicate that a higher iron dose
would be unlikely to result in increased benefit.
The composite IQ of the children in our study was higher than
the standardized norm (10), but it is consistent with the validation
study that showed a higher IQ in Australian children, particularly
at younger ages (26). Our findings are applicable to those of other
industrialized countries because the dietary iron intake of preg-
nant women and the prevalence of IDA in pregnancy in our study
population are similar to those of pregnant women in other in-
dustrialized countries (27, 28). However, our results may not be
generalized to other populations in whom ID and anemia are
more prevalent and more severe or undernutrition is common.
The higher frequency of children with abnormal behavior
scores in the iron group than in the placebo group was unex-
pected, especially because the mean scores for behavioral diffi-
culties between groups were not significantly different and were
comparable with normative values for Australian children (15).
We are aware that the effect may have been due to chance be-
cause behavior was a secondary outcome and there were only a
small number of children with abnormal scores. Therefore, this
result needs to be interpreted with caution. Although there are no
other data regarding the effect of prenatal iron supplementation on
behavior of children, iron supplementation in infancy in a develop-
ing country has been shown to result in a more positive social in-
teraction compared with placebo (29). The need for a balanced
evaluation of safety and efficacy in iron-supplementation trials is
clearly warranted.
Routine iron supplementation in pregnancy in otherwise well-
nourished women in industrialized countries had no beneficial
effects on the long-term general health of mothers consistent with
the only other published report by Hemminki and Merilinen (30),
although routine iron supplementation in pregnancy was linked
with a higher risk of stillbirth and convulsion in infants than was
selective iron supplementation in the Finish trial (30).
Currently, accidental iron overdose from iron tablets remains
a common cause of childhood poisoning (3). From a public health
perspective, the lack of apparent clinical benefit and the potential
hazards associated with routine iron supplementation in preg-
nancy suggest that the risks may outweigh the benefits in well-
nourished populations in whom the incidence of IDA at the end
of pregnancy is 앒11%. Further research is required to clearly
delineate the population subgroups in industrialized countries
that may benefit from iron supplementation in pregnancy.
We thank Jacinda Fisher for conducting the Stanford-Binet Intelligence
tests and Mandy O’Grady, Heather Garreffa, and Jo Collins for administra-
tive and clinical support. The funding organizations and Soul Pattison Man-
ufacturing had no role in the design and conduct of the study, the analysis and
interpretation of the data, or the preparation, review, and approval of the
manuscript.
All authors contributed to the study design. SJZ collected and analyzed the
data under the supervision of MM, RAG, and CAC. SJZ wrote the manuscript
with contributions from all coauthors. PB provided statistical support for part
of the data analysis. None of the authors had a conflict of interest.
REFERENCES
1. Mahomed K. Iron supplementation in pregnancy. Cochrane Database
Syst Rev 2003;2:CD000117.
 IRON IN PREGNANCY AND CHILD DEVELOPMENT
2. US Preventive Services Task Force. Routine iron supplementation dur-
ing pregnancy. Review article. JAMA 1993;270:2848 –54.
3. US Preventive Services Task Force. Routine iron supplementation dur-
ing pregnancy. Policy statement. US Preventive Services Task Force.
JAMA 1993;270:2846 – 8.
4. Kwik-Uribe CL, Golub MS, Keen CL. Chronic marginal iron intakes
during early development in mice alter brain iron concentrations and
behavior despite postnatal iron supplementation. J Nutr
2000;130:2040 – 8.
5. Taneja V, Mishra KP, Agarwal KN. Effect of maternal iron deficiency on
GABA shunt pathway of developing rat brain. Indian J Exp Biol 1990;
28:466 –9.
6. de Deungria M, Rao R, Wobken JD, Luciana M, Nelson CA, Georgieff
MK. Perinatal iron deficiency decreases cytochrome c oxidase (CytOx)
activity in selected regions of neonatal rat brain. Pediatr Res 2000;48:
169 –76.
7. Makrides M, Crowther CA, Gibson RA, Gibson RS, Skeaff CM. Effi-
cacy and tolerability of low-dose iron supplements during pregnancy: a
randomized controlled trial. Am J Clin Nutr 2003;78:145–53.
8. McLennan W, Podger A. National Nutrition Survey Australia 1995.
Canberra, Australia: Australian Government Publishing Service, 1998.
9. National Health and Medical Research Council. Recommended Detary
Intakes for use in Australia. Canberra, Australia: Australian Government
Publishing Service, 1991.
10. Thorndike RL, Hagen EP, Sattler JM. Stanford-Binet Intelligence Scale:
Technical Manual. 4th ed. Itasca, IL: The Riverside Publishing Com-
pany, 1986.
11. Pollitt E, Saco-Pollitt C, Leibel RL, Viteri FE. Iron deficiency and
behavioral development in infants and preschool children. Am J Clin
Nutr 1986;43:555– 65.
12. Bayley N. Bayley scales of infant development. 2nd ed. San Antonio,
TX: Harcourt Brace & Company, 1993.
13. Goodman R. Strengths and difficulties questionnaire. 1999. Internet:
http://www.sdqinfo.com/questionniares/english/c2.pdf (accessed Feb-
ruary 2002).
14. Goodman R. Psychometric properties of the strengths and difficulties
questionnaire. J Am Acad Child Adolesc Psychiatry 2001;40:1337– 45.
15. Hawes DJ, Dadds MR. Australian data and psychometric properties of
the Strengths and Difficulties Questionnaire. Aust N Z J Psychiatry
2004;38:644 –51.
1117
16. Goodman R. Scoring the informant-rated strengths and difficulties ques-
tionnaire. 1999. Internet: http://www.sdqinfo.com/ScoreSheets/el.pdf
(accessed February 2002).
17. Coons C, Gay E, Fandal A, Frankenburg W. The home screening ques-
tionnaire reference manual. Denver, CO: JF Kennedy Child Develop-
ment Centre, University of Colorado Health Science Centre, 1981.
18. Frankenburg WK, Coons CE. Home screening questionnaire: its validity
in assessing home environment. J Pediatr 1986;108:624 – 6.
19. Ware J. SF-36 health survey: a manual and interpretation guide. Boston,
MA: The Health Institute, New England Medical Centre, 1993.
20. Patterson AJ, Brown WJ, Powers JR, Roberts DC. Iron deficiency,
general health and fatigue: results from the Australian Longitudinal
Study on Women’s Health. Qual Life Res 2000;9:491–7.
21. Patterson AJ, Brown WJ, Roberts DC. Dietary and supplement treatment
of iron deficiency results in improvements in general health and fatigue
Downloaded from https://academic.oup.com/ajcn/article-abstract/83/5/1112/4649549 by guest on 09 December 2018
in Australian women of childbearing age. J Am Coll Nutr 2001;20:337–
42.
22. Anderson JW, Johnstone BM, Remley DT. Breast-feeding and cognitive
development: a meta-analysis. Am J Clin Nutr 1999;70:525–35.
23. Carpenter DO. Effects of metals on the nervous system of humans and
animals. Int J Occup Med Environ Health 2001;14:209 –18.
24. Tamura T, Goldenberg RL, Hou J, et al. Cord serum ferritin concentra-
tions and mental and psychomotor development of children at five years
of age. J Pediatr 2002;140:165–70.
25. Chan A, Scott J, McCaul K, Keane R. Pregnancy outcome in South
Australia 1997 Adelaide. Adelaide, Australia: South Australia Health
Commission, 1998.
26. de Lemos M. Results of the trial testing. The use of the Stanford - Binet
Intelligence Scale in Australia. Melbourne, Victoria, Australia: The
Australian Council for Education Research Ltd, 1994:4 –7.
27. Schofield C, Stewart J, Wheeler E. The diets of pregnant and post-
pregnant women in different social groups in London and Edinburgh:
calcium, iron, retinol, ascorbic acid and folic acid. Br J Nutr 1989;62:
363–77.
28. WHO. Iron deficiency anaemia: assessment, prevention and control—a
guide for programme managers. Geneva, Switzerland: WHO, 2001.
29. Lozoff B, De Andraca I, Castillo M, Smith JB, Walter T, Pino P. Be-
havioral and developmental effects of preventing iron-deficiency ane-
mia in healthy full-term infants. Pediatrics 2003;112:846 –54.
30. Hemminki E, Merilinen J. Long-term follow-up of mothers and their
infants in a randomized trial on iron prophylaxis during pregnancy. Am J
Obstet Gynecol 1995;173:205–9.