Published online August 31, 2007
PEDIATRICS Vol. 120 No. 3 September 2007, pp. 559-567 (doi:10.1542/peds.2007-0151)
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ARTICLE

Fetal Alcohol Exposure, Iron-Deficiency Anemia, and Infant Growth

R. Colin Carter, MDa, Sandra W. Jacobson, PhDb, Christopher D. Molteno, MDc and Joseph L. Jacobson, PhDb,d

a Division of Emergency Medicine, Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts; Departments of
b Psychiatry and Behavioral Neurosciences
d Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, Michigan
c Department of Psychiatry, University of Cape Town Faculty of Health Sciences, Cape Town, South Africa


   ABSTRACT
TOP
 ABSTRACT
METHODS
 RESULTS
 DISCUSSION
 CONCLUSIONS
 REFERENCES
 
OBJECTIVES. Our goals were to determine whether prenatal alcohol exposure is associated with an increased incidence of iron-deficiency anemia in infancy and to compare effects of fetal alcohol exposure and iron-deficiency anemia on infant growth. We also tested whether effects of fetal alcohol exposure on growth are mediated or moderated by iron-deficiency anemia.

METHODS. A total of 96 infants born to mothers from the Coloured (mixed ancestry) community in Cape Town, South Africa, were recruited prenatally; 42 mothers drank heavily during pregnancy, and 54 abstained or drank small amounts of alcohol. Growth was assessed at birth and 6.5 and 12 months, and iron-deficiency anemia was assessed at 6.5 or 12 months.

RESULTS. Infants whose mothers binge drank during pregnancy (≥4 drinks per occasion) were 3.6 times more likely to be diagnosed with iron-deficiency anemia at 12 months than were infants whose mothers did not binge drink. Prenatal alcohol exposure was associated with reduced weight at birth, 6.5 months, and 12 months and with shorter length at 6.5 and 12 months. Iron-deficiency anemia was related to reduced 12-month weight and head circumference and to slower growth velocity between 6 and 12 months. The effects of prenatal alcohol on weight were not mediated by iron-deficiency anemia; however, they were seen primarily in infants with iron-deficiency anemia.

CONCLUSIONS. The association of maternal binge drinking with an increased incidence of iron-deficiency anemia may reflect disruption of accumulation of fetal iron stores or postnatal deficiencies in iron uptake, absorption, or intake. Moreover, iron deficiency seems to exacerbate the prenatal alcohol effects on growth.

Key Words: fetal alcohol exposure • FASD • iron deficiency anemia • growth retardation • binge drinking during pregnancy • birth weight • growth velocity

Abbreviations: FAS—fetal alcohol syndrome • IDA—iron-deficiency anemia • AA—absolute alcohol • Hgb—hemoglobin concentration • MCV—mean corpuscular volume • MCH—mean corpuscular hemoglobin concentration • RDW—red cell distribution width

Fetal alcohol spectrum disorder refers to the range of alcohol-related developmental disorders from the most severely affected children with fetal alcohol syndrome (FAS) to nonsyndromal children who exhibit generally subtler neurobehavioral deficits than those seen with FAS.1,2 The effect of prenatal alcohol exposure on poorer infant growth is seen not only in children with full FAS but also in fetal alcohol-exposed children who lack the characteristic facial dysmorphology.3–5 Iron deficiency has also been linked to disruption of normal infant growth. Severe maternal iron-deficiency anemia (IDA) during the first and second trimesters is associated with lower birth weight in animal and human studies.6 However, the effects of iron deficiency on postnatal growth are controversial, with some studies linking iron deficiency in infancy to slower growth7–9 but others demonstrating increased iron deficiency in infants who grow more rapidly during the first postpartum year.10

Data from 2 previous studies suggest that prenatal alcohol exposure may lead to iron deficiency in infancy. In a generally well-nourished Seattle cohort, most pregnant women who drank alcohol during pregnancy were iron sufficient, but the heaviest drinkers developed iron deficiency.11 This iron deficiency may be significant because the fetus depends on maternal iron to accumulate iron stores during the third trimester that will be needed for growth and development during the first 6 postpartum months. In a study using a rat model, prenatal alcohol exposure led to disruption of iron homeostasis in the central nervous system with alterations in iron levels of the cerebral cortex, cerebellum, and brainstem.12 These changes persisted into adulthood.

We examined the relation between heavy prenatal alcohol exposure and IDA in infancy in a prospective, longitudinal study in which maternal drinking was ascertained during pregnancy. To achieve this aim, we documented maternal alcohol intake and measured hematologic values indicative of iron status at age 6.5 or 12 months in a cohort of infants born to Cape Coloured (mixed ancestry) women in Cape Town, South Africa.

Recent studies have reported very heavy alcohol use during pregnancy13,14 and a high prevalence of FAS in this population in the Western Cape Province of South Africa.15 This population, descendents of white Europeans, Malaysians, and Khoi (Hottentot), has historically comprised the large majority of workers in the wine-producing and fruit-growing region of the Western Cape. In a cross-sectional study of Cape Coloured infants age 6 and 12 months, anemia was found in almost two thirds and IDA in almost one third of the infants.16 The mechanisms are as yet unknown, but hemoglobinopathies were documented.17

In this study, we tested the hypothesis that prenatal alcohol exposure increases the incidence of IDA during infancy. We then compared the effects of prenatal alcohol exposure and IDA on growth and tested 2 hypotheses: (1) that the effects of alcohol exposure on growth are mediated by alcohol-related iron deficiency in infancy and (2) that the effects of prenatal alcohol exposure on growth are exacerbated by infant iron deficiency.


   METHODS
TOP
 ABSTRACT
 METHODS
RESULTS
 DISCUSSION
 CONCLUSIONS
 REFERENCES
 
Sample
The sample consisted of 96 infants born to Cape Coloured women living in Cape Town, who are participating in a prospective study on the effects of heavy prenatal alcohol exposure on neurobehavioral development. The mothers were recruited between July 1999 and January 2002 at the antenatal clinic of a midwife obstetric unit that serves an economically disadvantaged, predominantly Cape Coloured population.13

The cohort, which was recruited to overrepresent more heavily exposed infants, consisted of 42 heavy-drinking mothers and 54 light drinkers and abstainers who were recruited during the same period by our research nurse. In our study, each gravida was interviewed regarding her alcohol consumption both at the time of recruitment and at conception, using an interview derived from the time-line follow-back approach.18 Any woman who averaged ≥1.0 oz of absolute alcohol (AA) per day, the equivalent of 2 standard drinks, or reported ≥2 incidents of binge drinking (which at that time was defined as ≥5 standard drinks per occasion) during the first trimester of pregnancy was invited to participate in the study.* Women initiating antenatal care at this clinic who drank <0.5 oz of AA per day and did not binge drink during the first trimester were also invited to participate. Women <18 years of age and those with diabetes, epilepsy, or cardiac problems requiring treatment were not invited to participate. Religiously observant Muslim women were also excluded because their religious practices prohibit alcohol consumption. Infant exclusionary criteria were major chromosomal anomalies, neural tube defects, multiple births, and seizures. Informed consent was obtained from each mother at recruitment and at the first laboratory visit. Approval for human research was obtained from both the Wayne State University and University of Cape Town human investigation committees.

Procedure
For each assessment performed after recruitment, a staff driver and a research staff nurse transported the mother and infant to our laboratory at the University of Cape Town Faculty of Health Sciences in a van dedicated for use in the study. All mothers were interviewed antenatally and at 1-month postpartum regarding their alcohol and drug use during pregnancy. The interviews were conducted in Afrikaans or English, depending on the woman's preference. Infants were measured for weight and head circumference at birth and for weight, length, and head circumference at 6.5 and 12 months of age, corrected for gestational age in cases of preterm birth. The mother received a small monetary compensation, a gift for her infant, and a photograph of herself with her infant.

Hematologic Evaluation
A capillary blood sample from a fingerstick was collected by a trained nurse in a 750-µL EDTA tube and transported to the Red Cross War Memorial Children's Hospital laboratory, where an automated complete blood count analysis was performed, including white blood cell count, hemoglobin concentration (Hgb), hematocrit, platelet count, and red blood cell indices, including mean corpuscular volume (MCV), mean corpuscular hemoglobin concentration (MCH), and red cell distribution width (RDW). The analysis was conducted on the same day as collection, and the machine was standardized before each batch of samples with commercially supplied Coulter 4C control material. Samples were collected at the 12-month visit for 74 infants. Because of budgetary constraints, 22 infants were only followed through age 6.5 months, and their complete blood count data were collected at the 6.5-month visit. Statistical analyses were performed separately for the 2 groups.

Infants were determined to have IDA if they had Hgb of <10.9 g/L and RDW of ≥15.0% plus MCV of ≤70.0 fL or MCH of ≤23.0 pg. Five infants who were not anemic (Hgb: >10.9 g/L) and had borderline values (Hgb: 11–12 g/L; MCH: 20–23.4 pg; MCV: 65.1–70.7 fL, and RDW: 13.8%–18.8%) were classified as indeterminate and excluded from analysis. These infants may have had iron deficiency that was not yet manifest as anemia or was not significant enough to manifest as anemia. Infants with Hgb of <10.9 g/L who did not meet the other IDA criteria were determined to have anemia of other causes.

Alcohol, Smoking, and Drug Use
In the time-line follow-back interview administered at recruitment, the mother was asked about her drinking on a day-by-day basis during a typical 2-week period around the time of conception, with recall linked to specific times of day and activities. If her drinking had changed since conception, she was also asked about her drinking during the past 2 weeks and when her drinking had changed. At the follow-up antenatal visit, the mother was again asked about her drinking during the previous 2 weeks. If there were any weeks since the recruitment visit when she drank greater quantities, she was asked to report her drinking for those weeks as well. At the 1-month postpartum visit, the mother was asked about her drinking during a typical 2-week period during the latter part of pregnancy, as well as her drinking during any weeks during that period when she drank greater quantities. Volume was recorded for each type of alcohol beverage consumed each day and converted to ounces of AA by using multipliers proposed by Bowman et al19 (liquor: 0.4 oz; beer: 0.04 oz; wine: 0.2 oz). Six summary measures were constructed: average ounces of AA per day at conception, AA per day averaged across pregnancy, AA per drinking day (quantity per occasion) at conception and across pregnancy, and proportion drinking days (frequency) at conception and across pregnancy. In addition to the quantitative alcohol interview, alcohol abuse and/or dependence were diagnosed on the basis of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, criteria using the alcohol module of the Diagnostic Interview Schedule.20 Each mother was also asked at both the antenatal and postnatal interviews how many cigarettes she smoked per day and how often she used any illicit drugs, including cocaine, marijuana, and methaqualone ("mandrax"), during pregnancy.

Physical Growth
Birth weight and head circumference were obtained from hospital medical charts. Weight, length, and head circumference were measured at 6.5 months. Growth velocity was calculated as the change in a given growth index over a specific period of time (eg, birth to 6.5 months), divided by that period of time in weeks. Growth velocity values were calculated for birth to 6.5 months, birth to 12 months, and 6.5 to 12 months. Gestational age was calculated from early pregnancy ultrasound examination or expected date of confinement when ultrasound data were not available.

Data Analysis
Before analysis, all variables were checked for normality of distribution. Average AA per day at conception and across pregnancy were positively skewed (skew >3.0) and were normalized by means of log (x + 1) transformation. Data were obtained for the following control variables: socioeconomic status; maternal age at delivery; parity; infant gender; gestational age at birth; and prenatal exposure to marijuana, methaqualone, or cigarette smoking. Because a control variable cannot be the true cause of an observed deficit unless it is related both to exposure and outcome,21 association with either exposure or outcome can be used as the criterion for inclusion in a multivariate analysis to control for confounding. In this study, control variables were selected in relation to outcome, which has the additional advantage of increasing precision by also including covariates unrelated to exposure.22 All control variables that were even weakly related to each infant growth measure (at P < .10) were controlled statistically in all multiple regression analyses relating prenatal alcohol exposure and IDA to that growth measure. Two-tailed t tests were used to compare means of control variables and sample characteristics between maternal infant pairs in which the mothers drank at high levels and those in which mothers abstained or drank at low levels. The relation between binge drinking in pregnancy and IDA was examined by using {chi}2 analysis. Odds ratios were calculated to estimate the increased relative risk of IDA associated with pregnancy binge drinking, and {varphi} coefficients were calculated to assess the magnitude of the relation of prenatal binge exposure to IDA. Multiple regression analysis was used to examine the relation between growth and alcohol exposure, as well as growth and iron deficiency, after control for potential confounders. To examine the degree to which IDA moderates the effect of prenatal alcohol exposure on growth, the regressions were rerun separately for the infants with and without IDA.


   RESULTS
TOP
 ABSTRACT
 METHODS
 RESULTS
DISCUSSION
 CONCLUSIONS
 REFERENCES
 
Sample characteristics are summarized in Table 1. The mothers were poorly educated; only 18.8% completed high school. Heavy-drinking mothers were less educated, and fewer were married. Sixteen (16.7%) infants were born preterm (gestational age <37 weeks), but only 4 were born at <34 weeks' gestational age. Six infants were low birth weight (<2000 g), 2 of whom were very low birth weight (<1500 g). Infants born to heavy-drinking mothers weighed less at birth and tended to have smaller head circumference at birth and to weigh less at 12 months.


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  		TABLE 1 Sample Characteristics

 
Alcohol, Smoking, and Drug Use During Pregnancy
The mothers who drank at the time of conception consumed an average of 1.7 oz of AA (the equivalent of 3.4 standard drinks) per day, and alcohol consumption across pregnancy averaged 1.0 oz of AA (2.0 drinks) per day (Table 1). However, these women did not drink on a daily basis but concentrated their drinking on 1 to 2 days per week at conception and across pregnancy. The average quantity consumed per occasion was 4.7 oz of AA (9.4 drinks) at conception and 4.1 oz of AA (8.2 drinks) during pregnancy. Among the drinkers, more than half were alcohol abusing or dependent: 14.3% met criteria for alcohol abuse; 42.9% for alcohol dependence. Among the abstainers or light drinkers, 7.4% had a history of abuse, and 9.3% had been dependent. A large proportion of the women (70.8%) smoked cigarettes during pregnancy, with one fifth (19.2%) smoking an average of ≥10 cigarettes per day. As seen in Table 1, women who drank heavily smoked almost twice as much as abstainers or light drinkers during pregnancy. Ten women reported using marijuana, 5 of whom used it ≥3 days per week; 8 were in the heavy-drinking group. Three women reported using methaqualone regularly during pregnancy, and 1 used it once; all were heavy drinkers. None of the women reported cocaine use.

Hematologic Values
Thirty-four (38.3%) infants met criteria for IDA. All but 5 infants diagnosed with IDA had microcytosis (MCV: ≤70 fL), and 4 of those 5 had an MCV of <72 fL. All but 5 infants had hypochromia (MCH: ≤23 pg), and all 5 had an MCH of <24 pg. Infants with IDA were very anemic; half had Hgb of <10 g/L, and one quarter had Hgb of <9 g/L. Twenty-one (21.9%) infants who had Hgb of <10.9 g/L did not meet criteria for IDA and were classified as having anemia of other cause. The majority of these infants had mild anemia; over three quarters had Hgb of ≥10.0 g/L.

Relation of Prenatal Alcohol Exposure to IDA
Table 2 compares the prevalence of IDA among infants exposed to binge drinking in utero with that among those not exposed to binge drinking. Based on the odds ratio, infants whose mothers binge drank during pregnancy (≥4 drinks per occasion) were 3.6 times more likely to be diagnosed with IDA at 12 months than infants whose mothers abstained or drank <4 drinks per occasion. For the small group of infants with data collected at age 6.5 months, this finding was more pronounced ({varphi} = 0.36, compared with a {varphi} value of 0.29 at 12 months; odds ratio: 4.7) but fell short of conventional levels of statistical significance. By contrast to infants with IDA, there was no difference in exposure to binge drinking between those diagnosed with anemia of other causes and those who were not anemic at either age (Table 3). Among the 54 infants found to be IDA or iron sufficient at 12 months, cigarette smoking was related to both alcohol use (r = 0.50; P < .001) and IDA status (r = 0.24; P < .05). However, the finding of increased iron deficiency among infants whose mothers binge drank persisted after excluding those born to moderate-to-heavy smokers (mothers who smoked ≥4 cigarettes per day; {chi}12 = 8.37, N = 32, P = .004; {varphi} = 0.51), indicating that this finding is not attributable to prenatal exposure to cigarette smoking.


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  		TABLE 2 Relation of Prenatal Binge Drinking to IDA

 

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  		TABLE 3 Relation of Prenatal Binge Drinking to Anemia of Other Causes

 
Relation of Physical Growth to Prenatal Alcohol Exposure and IDA
Table 4 presents a series of regression analyses in which prenatal alcohol exposure and IDA were each entered simultaneously together with potential confounding variables, identified as described earlier. Prenatal alcohol exposure was associated with reduced birth weight after controlling for maternal smoking. The effect of prenatal alcohol on birth weight controlling for gestational age was also significant, indicating that reduced birth size was not a consequence of shorter gestation. Weight at 6.5 and 12 months and length at 12 months of age were associated with prenatal alcohol, with effects that fell short of statistical significance. By contrast, the effect of IDA on infant growth was not evident until 12 months. Although there was no effect of alcohol on growth velocity, IDA was related to slower growth velocity between 6.5 and 12 months. The effects of prenatal alcohol exposure and IDA seem to be independent, because the impact of both was similar in magnitude in the 12-month weight regression.


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  		TABLE 4 Relation of IDA at 12 Months and Prenatal Alcohol Exposure to Growth

 
Table 5 presents the relation of pregnancy drinking to infant growth separately for infants diagnosed with and without IDA at 12 months. The effects of alcohol on infant growth were generally stronger in infants with IDA, suggesting that IDA exacerbates the effects of prenatal alcohol exposure on prenatal and postnatal growth. The effect on length at 6.5 and 12 months was seen only in the infants with IDA. Furthermore, the effects of alcohol on growth among infants with IDA were similar to but stronger than those seen in Table 4 for the sample as a whole.


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  		TABLE 5 Comparison of the Relation of Prenatal Alcohol Exposure to Growth in IDA Versus Nonanemic Infants

 
Maternal cigarette smoking was related to lower birth weight (r = –0.27; P < .05) and tended to be associated with reduced weight and head circumference at 12 months (r = –0.22 and –0.26, respectively; both P <.10) but not to growth velocity (all P > .20). As noted earlier, the effects of fetal alcohol exposure and IDA reported in Tables 4 and 5 were adjusted for smoking during pregnancy. Marijuana use was not related to prenatal or postnatal growth (all P > .20) or growth velocity (all P > .15).


   DISCUSSION
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
CONCLUSIONS
 REFERENCES
 
To our knowledge, this study is the first to prospectively link prenatal alcohol exposure to IDA in infancy. The large numbers of infants with IDA and anemia of other causes in our cohort are consistent with a previous report of a high prevalence of anemia and IDA among the Cape Coloured population.16 Maternal binge drinking was associated with a significantly higher incidence of IDA at 12 months of age, which may reflect disruption of accumulation of fetal iron stores or postnatal deficiencies of iron intake or absorption. This pattern of binge drinking involving concentrated drinking on 1 to 2 days per week is also commonly found in nonalcoholic women in the United States and elsewhere.23 Disruption of fetal iron stores is potentially important given that infants are dependent on prenatally acquired iron for the first 6 months of life before dietary intake begins to play a more substantial role.24 Thus, IDA at 6 months may be a good marker for disruption of fetal iron stores. Although the effect of binge drinking in our sample was not statistically significant at 6.5 months, probably because of the small number of infants for whom hematologic data were available, the magnitude of the effect was actually greater than at 12 months, providing evidence of insufficient fetal accumulation of iron stores in infants exposed prenatally to alcohol.

Mechanisms that might lead to disruption of fetal iron accumulation include maternal iron deficiency during pregnancy, alcohol-induced disruption of placental iron transport to the fetus, and alcohol-induced disruption of the infant's ability to absorb or store iron. Fetal iron status is generally independent of maternal iron status unless the mother is severely iron deficient. Given that there was no evidence of severe iron deficiency or malnutrition in a subset of the mothers in this cohort whose nutritional status was evaluated,25 maternal IDA is not likely to explain the association of prenatal alcohol and infant IDA for more than a small subset of cases.

Alternatively, prenatal alcohol exposure may disrupt transport of iron across the placenta. Disruption of placental iron transport is believed to mediate the development of fetal iron deficiency in conditions such as maternal diabetes mellitus and is independent of fetal anoxia.26 Miller et al12 reported that prenatal alcohol exposure led to a disruption of iron homeostasis in the central nervous system that persisted into adulthood in their animal model. Consistent with these findings, fetal alcohol-related IDA at 12 months might also be caused by alterations in the prenatally exposed infant's ability to absorb and/or utilize iron postnatally, especially after 6 months of age, when fetal iron stores become depleted. Regardless of timing or mechanism, the clear association between prenatal alcohol exposure and increased risk of IDA suggests a need for targeted iron-deficiency screening and intervention for fetal alcohol-exposed children. This is particularly important, given the well-documented effects of IDA in infancy on cognition and behavior.27 Further research is needed to determine any overlap and/or interaction between the effects of IDA and fetal alcohol exposure on development.

Consistent with previous findings,3–5 prenatal alcohol exposure was associated with poorer prenatal and postnatal growth. In contrast to the impact of cigarette smoking,4 the effect of alcohol on growth indices persisted postnatally; the infants did not catch up. Iron deficiency was not related to smaller birth size, but infants who were iron deficient at 12 months grew more slowly from 6 to 12 months. This finding is consistent with studies of economically disadvantaged children in Indonesia and Mexico that link iron deficiency with poorer growth.7–9 This pattern is not seen in studies in the United States and Europe, where children are generally well-nourished and not severely iron deficient. In these studies, iron has been reported to relate to faster postnatal growth, a finding that has been interpreted as an increased risk of exhausting fetal iron stores among faster growing infants.10,28,29 In our study, the infants with iron deficiency may have grown more slowly as a result of inadequate iron stores, reduced postnatal iron intake, deficits in other nutrients needed to absorb and properly utilize iron, or poorer overall nutrition, of which IDA may be a marker.

Although fetal alcohol exposure was strongly associated with IDA in infancy, IDA did not mediate the effect of prenatal alcohol on infant size because prenatal alcohol exposure remained significant after controlling statistically for infant iron status. Thus, different mechanisms are apparently responsible for the adverse effects of fetal alcohol exposure and IDA on infant growth. However, the impact of prenatal alcohol on growth indices at birth, 6.5 months, and 1 year was greater in the infants with iron deficiency, suggesting that IDA exacerbates the effects of alcohol on growth. Alternatively, IDA at 12 months may provide a marker for broader malnutrition from conception onward.


   CONCLUSIONS
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 CONCLUSIONS
REFERENCES
 
Infants exposed to alcohol prenatally are at increased risk for IDA and should thus be screened and treated where indicated. Whether the exacerbation of the effect of prenatal alcohol on growth is because of iron deficiency per se or because of other nutritional deficiencies, these findings suggest that nutrition may play an important role in the impact of fetal alcohol exposure on growth that warrants attention in future studies. Moreover, additional investigation of the role of nutrition in fetal alcohol spectrum disorder may lead to the discovery of useful nutritional and/or pharmacologic interventions that could reduce the impact of fetal alcohol exposure on infant development.


   ACKNOWLEDGMENTS
 
This work was supported by administrative supplements from the National Institutes of Health National Institute on Alcohol Abuse and Alcoholism to grant RO1-AA09524 and grants from the National Institutes of Health Office of Research on Minority Health, the Foundation for Alcohol Related Research (Cape Town, South Africa) and the Joseph Young, Sr, Fund from the State of Michigan.

We acknowledge the contribution of the late Andrea Hay to this research. We thank our collaborator Denis Viljoen; our South African research staff, Anna-Susan Marais, Magdalene September, Deborah Price, and Dickie Naude for their help in collecting the data; our Wayne State University postdoctoral fellows Matthew Burden and Rinat Armony-Sivan and laboratory research staff, Julie Croxford, Neil Dodge, and Douglas Fuller for their help in data processing and analysis; and Betsy Lozoff, John Beard, James Connor, and our other collaborators on the Brain and Behavior in Early Iron Deficiency Program Project for their consultation. We also thank the Cape Town Parent Centre, Mireille Landman, and Stephen Rollnick for their contributions to the maternal pregnancy drinking and counseling program.


   FOOTNOTES
 
Accepted Apr 13, 2007.

Address correspondence to Sandra W. Jacobson, PhD, Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, 2751 E Jefferson, Room 460, Detroit, MI 48207. E-mail: sandra.jacobson{at}wayne.edu

Portions of this research were presented at the 2002 and 2004 meetings of the Research Society on Alcoholism; June 28–July 3, 2002; San Francisco, CA; and June 26–30, 2004; Vancouver, British Columbia, Canada; and the 2004 meetings of the International Conference on Infant Studies; May 5–8, 2004; Chicago, IL.

The authors have indicated they have no financial relationships relevant to this article to disclose.

* All women who reported drinking during pregnancy were advised that stopping or reducing their drinking would reduce the risk to their baby. All the mothers (drinkers and nondrinkers) were invited to participate in a home-visitor program run by the Parent Centre, a nonprofit organization in the community. The program involved meeting with a home visitor 1 to 2 times per week during pregnancy and for 6 months' postpartum. The home visitors were trained to use a motivational interviewing approach to support and encourage the mothers to talk about their use of alcohol and other stresses in their everyday life, with the aim of helping the mother find ways to reduce her alcohol intake or be referred for treatment for alcoholism. The home visitors were supervised by and met weekly with a licensed psychologist and/or a senior social worker at the Parent Centre. Arrangements were made with the psychiatry department at Groote Schuur Hospital for referral for treatment of severe depression and/or alcohol abuse or dependence if requested by the mother. Back


   REFERENCES
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 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 CONCLUSIONS
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PEDIATRICS (ISSN 1098-4275). ©2007 by the American Academy of Pediatrics




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