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1.  The Combined Association of Psychosocial Stress and Chronic Hypertension with Preeclampsia 
American journal of obstetrics and gynecology  2013;209(5):10.1016/j.ajog.2013.07.003.
This study aims to evaluate perceived lifetime stress (LS), perceived stress during pregnancy (PS), chronic hypertension (CH) and their joint association with preeclampsia risk.
This study includes 4,314 women who delivered a singleton live birth at the Boston Medical Center from October 1998 through February 2008. CH is defined as hypertension diagnosed before pregnancy. Information regarding LS and SP was collected by questionnaire. Preeclampsia was diagnosed by clinical criteria.
LS, SP and CH were each associated with an increased risk of preeclampsia (OR(95%CI)=2.1(1.6–2.8) for LS; 1.7(1.3–2.1) for SP; 11.1(8.1–15.4) for CH). Compared with normotensive pregnancy with low LS, both normotensive pregnancy with high LS (2.1(1.5–2.9)) and pregnancy with CH and low LS (10.6(7.5–15.1)) showed an increased risk of preeclampsia, while pregnancy with high LS and CH yielded the highest risk of preeclampsia (21.3(10.3–44.3)). The joint association of SP and CH on preeclampsia was very similar to that of the joint association of LS and CH.
This finding indicates that high psychosocial stress and CH can act in combination to increase the risk of preeclampsia up to 20-fold. This finding underscores the importance of efforts to prevent, screen and manage CH, along with reducing psychosocial stress, particularly among women with CH.
PMCID: PMC3825759  PMID: 23850528
Psychosocial stress; chronic hypertension; combined effect; preeclampsia
2.  Prepregnancy body mass index and risk of preterm birth: association heterogeneity by preterm subgroups 
To evaluate the association between prepregnancy body mass index (BMI) is associated with early vs. late and medically-induced vs. spontaneous preterm birth (PTB) subtypes.
Using data from the Boston Birth Cohort, we examined associations of prepregnancy BMI with 189 early (<34 completed weeks) and 277 late (34–36 completed weeks) medically-induced PTBs and 320 early and 610 late spontaneous PTBs vs. 3281 term births (37–44 weeks) in multinomial regression. To assess for mediation by important pregnancy complications, we performed sequential models with and without hypertensive disorders of pregnancy, chorioamnionitis, and gestational diabetes.
Prevalence of prepregnancy obesity (BMI ≥ 30.0 kg/m2) was 28% among mothers with medically-induced PTBs, 18% among mothers with spontaneous PTBs, and 18% among mothers with term births (p = <0.001). After adjustment for demographic and known risk factors for PTB, prepregnancy obesity was associated with higher odds of both early [OR 1.78 (1.19, 2.66)] and late [OR 1.49 (1.09, 2.04)] medically-induced PTB. These effect estimates were attenuated with inclusion of hypertensive disorders of pregnancy and gestational diabetes. For spontaneous deliveries, prepregnancy obesity was associated with decreased odds of PTB (0.76 [0.58, 0.98]) and underweight was nearly associated with increased odds of PTB (1.46 [0.99, 2.16]).
Prepregnancy obesity is associated with higher risk of medically-induced, but not spontaneous PTB. Hypertensive disorders of pregnancy and gestational diabetes appear to partially explain the association between prepregnancy obesity and early and late medically-induced PTB.
PMCID: PMC4022544  PMID: 24779674
Maternal obesity; Prepregnancy BMI; Medically-induced preterm birth; Spontaneous preterm birth; Late preterm birth
3.  Placental Weight Mediates the Effects of Prenatal Factors on Fetal Growth: the Extent Differs by Preterm Status 
Obesity (Silver Spring, Md.)  2013;21(3):10.1002/oby.20254.
Elevated pre-pregnancy body mass index (BMI), excessive gestational weight gain (GWG), and gestational diabetes (GDM) are known determinants of fetal growth. The role of placental weight is unclear. We aimed to examine the extent to which placental weight mediates the associations of pre-pregnancy BMI, GWG, and GDM with birthweight-for-gestational age, and whether the relationships differ by preterm status. We examined 1035 mother-infant pairs at birth from the Boston Birth Cohort. Data were collected by questionnaire and clinical measures. Placentas were weighed without membranes or umbilical cords. We performed sequential models excluding and including placental weight, stratified by preterm status. We found that 21% of mothers were obese, 42% had excessive GWG, and 5% had GDM. 41% were preterm. Among term births, after adjustment for sex, gestational age, maternal age, race, parity, education, smoking and stress during pregnancy, birthweight-for-gestational age z-score was 0.55 (0.30, 0.80) units higher for pre-pregnancy obesity vs. normal weight. It was 0.34 (0.13, 0.55) higher for excessive vs. adequate GWG, 0.67 (0.24, 1.10) for GDM vs. no DM, with additional adjustment for pre-pregnancy BMI. Adding placental weight to the models attenuated the estimates for pre-pregnancy obesity by 20%, excessive GWG by 32%, and GDM by 21%. Among preterm infants, GDM was associated with 0.67 (0.34, 1.00) higher birthweight-for-gestational age z-score, but pre-pregnancy obesity and excessive GWG were not. Attenuation by placental weight was 36% for GDM. These results suggest that placental weight partially mediates the effects of pre-pregnancy obesity, GDM and excessive GWG on fetal growth among term infants.
PMCID: PMC3418379  PMID: 23592670
pre-pregnancy BMI; gestational weight gain; gestational diabetes; placental weight; fetal growth; birth weight z-score
4.  Role of African Ancestry and Gene-Environment Interactions in Predicting Preterm Birth 
Obstetrics and gynecology  2011;118(5):1081-1089.
To estimate whether African ancestry, specific gene polymorphisms, and gene-environment interactions could account for some of the unexplained preterm birth variance within blacks.
We genotyped 1,509 African ancestry informative markers, cytochrome P-450 1A1 (CYP1A1) and glutathione S-transferases Theta 1 (GSTT1) variants in 1,030 self-reported black mothers. We estimated the African ancestral proportion using the ancestry informative markers for all 1,030 self-reported black mothers. We examined the effect of African ancestry and CYP1A1 and GSTT1 smoking interactions on preterm birth cases as a whole and within its subgroups: very preterm birth (gestational age less than 34 weeks); and late preterm birth (gestational age greater than 34 and less than 37 weeks). We applied logistic regression and receiver operating characteristic (ROC) curve analysis, separately, to evaluate if African ancestry and CYP1A1- and GSTT1-smoking interactions could make additional contributions to preterm birth beyond epidemiological factors.
We found significant associations of African ancestry with preterm birth (22% vs. 31%, OR=1.11; 95%CI: 1.02–1.20) and very preterm birth (23% vs. 33%, OR=1.17; 95%CI: 1.03–1.33), but not with late preterm birth (22% vs. 29%, OR=1.06; 95%CI: 0.97–1.16). In addition, the ROC curve analysis suggested that African ancestry and CYP1A1- and GSTT1-smoking interactions made substantial contributions to very preterm birth beyond epidemiologic factors.
Our data underscore the importance of simultaneously considering epidemiological factors, African ancestry, specific gene polymorphisms and gene-environment interactions to better understand preterm birth racial disparity and to improve our ability to predict preterm birth, especially very preterm birth.
PMCID: PMC3218119  PMID: 22015876
5.  Association of genetic ancestry with preterm delivery and related traits among African American mothers 
In the United States, the rate of preterm delivery (PTD) is higher in African Americans (17.8%) than non-Hispanic whites (11.5%). Such disparity cannot be fully explained by differences in socioenvironmental factors.
We genotyped 812 mothers in a case-control PTD study at Boston Medical Center who self-reported their ethnicity as “black.” Regression analysis and Wilcoxon rank-sum test were applied to evaluate ancestral distribution and the association between genetic ancestry and PTD-related traits, as well as the potential confounding effect of population stratification.
The estimated African ancestral proportion was 0.90 ± 0.13. We found significant associations of ancestral proportion with PTD as a whole and PTD subgrouped by the presence of maternal hypertensive disorders. We did not observe significant confounding as a result of population stratification in this case-control PTD study.
Our data underline the need for more intensive investigation of genetic admixture in African Americans to identify novel susceptibility genes of PTD.
PMCID: PMC2859981  PMID: 19446788
admixture; genetic ancestry; population stratification
6.  Maternal cigarette smoking, metabolic gene polymorphisms, and preterm delivery: new insights on G×E interactions and pathogenic pathways 
Human genetics  2008;123(4):359-369.
Preterm delivery (PTD, <37 weeks of gestation) is a significant clinical and public health problem. Previously, we reported that maternal smoking and metabolic gene polymorphisms of CYP1A1 MspI and GSTT1 synergistically increase the risk of low birth weight. This study investigates the relationship between maternal smoking and metabolic gene polymorphisms of CYP1A1 MspI and GSTT1 with preterm delivery (PTD) as a whole and pre-term subgroups. This case–control study included 1,749 multi-ethnic mothers (571 with PTD and 1,178 controls) enrolled at Boston Medical Center. After adjusting covariates, regression analyses were performed to identify individual and joint associations of maternal smoking, two functional variants of CYP1A1 and GSTT1 with PTD. We observed a moderate effect of maternal smoking on PTD (OR = 1.6; 95% CI: 1.1–2.2). We found that compared to non-smoking mothers with low-risk genotypes, there was a significant joint association of maternal smoking, CYP1A1 (Aa/aa) and GSTT1 (absent) genotypes with gestational age (β = −3.37; SE = 0.86; P = 9 × 10−5) and with PTD (OR = 5.8; 95% CI: 2.0–21.1), respectively. Such joint association was particularly strong in certain preterm subgroups, including spontaneous PTD (OR = 8.3; 95% CI: 2.7–30.6), PTD < 32 weeks (OR = 11.1; 95% CI: 2.9–47.7), and PTD accompanied by histologic chorioamnionitis (OR = 15.6; 95% CI: 4.1–76.7). Similar patterns were observed across ethnic groups. Taken together, maternal smoking significantly increased the risk of PTD among women with high-risk CYP1A1 and GSTT1 genotypes. Such joint associations were strongest among PTD accompanied by histologic chorioamnionitis.
PMCID: PMC2852624  PMID: 18320229
7.  From mother's mouth to infant's brain 
Perspective on the paper by Saito et al (see page 113)
PMCID: PMC2675477  PMID: 17337671
8.  The Relationship Between Maternal Depression, In-Home Violence, And Use Of Physical Punishment: What Is The Role Of Child Behavior? 
Archives of disease in childhood  2008;94(2):138-143.
Maternal depression and in-home violence are independently associated with the use of physical punishment on children; however, the combined impact of these factors on the practice of physical punishment is unknown, as is the extent to which their relationship to physical punishment varies with child behavior.
1) Determine the combined impact of maternal depression and violence exposure on one physical punishment practice, smacking; 2) Explore the role of child behaviors in this relationship.
Multivariable regression analysis of a nationally representative sample of US kindergarten children. Maternal depressive symptoms, violence exposure, and use of smacking as a discipline technique were measured by parent interview. Child behaviors were reported by teachers.
12,764 mother-child dyads were included in the analysis. The adjusted odds ratio (aOR) for smacking among mothers with depressive symptoms was 1.59 (95% CI 1.40, 1.80); among mothers exposed to in-home violence, 1.48 (95% CI 1.18, 1.85); among dually exposed mothers, 2.51 (95% CI 1.87, 3.37). Adjusting these models for child self-control or externalizing behavior yielded no change in these associations, and no effect modification by child behavior was detected. Among mothers reporting to smack their children, depression was associated with an increased smacking frequency (aIRR 1.12; 95% CI 1.01, 1.24); however, this association was reduced to borderline significance when adjusting the models for child self-control or externalizing behavior (aIRRs 1.10; 95% CI 1.00, 1.21). Depressed mothers who were also exposed to violence demonstrated higher rates of smacking (aIRR 1.29; 95% CI 1.09, 1.53); this remained stable when adjusting for child behaviors.
Maternal depression and violence exposure are associated with smacking as a means of punishment. The magnitude of this association is increased when depression and violence occur together. When coexistent, they also appear associated with the frequency of smacking. Child self-control and externalizing behavior do not appear to impact substantially the association between maternal depressive symptoms, violence exposure, and smacking.
PMCID: PMC2829298  PMID: 18786952
Maternal Depression; Violence; Corporal Punishment; Spanking; Smacking; Child Behavior
9.  From principle to practice: moving from human rights to legal rights to ensure child health 
Archives of Disease in Childhood  2007;92(2):100-101.
Perspective on the paper by Waterston and Goldenhagen (see page 176)
PMCID: PMC2083336  PMID: 17264280
12.  Growth, Development, and Behavior in Early Childhood Following Prenatal Cocaine Exposure 
Despite recent studies that failed to show catastrophic effects of prenatal cocaine exposure, popular attitudes and public policies still reflect the belief that cocaine is a uniquely dangerous teratogen.
To critically review outcomes in early childhood after prenatal cocaine exposure in 5 domains: physical growth; cognition; language skills; motor skills; and behavior, attention, affect, and neurophysiology.
Data Sources
Search of MEDLINE and Psychological Abstracts from 1984 to October 2000.
Study Selection
Studies selected for detailed review (1) were published in a peerreviewed English-language journal; (2) included a comparison group; (3) recruited samples prospectively in the perinatal period; (4) used masked assessment; and (5) did not include a substantial proportion of subjects exposed in utero to opiates, amphetamines, phencyclidine, or maternal human immunodeficiency virus infection.
Data Extraction
Thirty-six of 74 articles met criteria and were reviewed by 3 authors. Disagreements were resolved by consensus.
Data Synthesis
After controlling for confounders, there was no consistent negative association between prenatal cocaine exposure and physical growth, developmental test scores, or receptive or expressive language. Less optimal motor scores have been found up to age 7 months but not thereafter, and may reflect heavy tobacco exposure. No independent cocaine effects have been shown on standardized parent and teacher reports of child behavior scored by accepted criteria. Experimental paradigms and novel statistical manipulations of standard instruments suggest an association between prenatal cocaine exposure and decreased attentiveness and emotional expressivity, as well as differences on neurophysiologic and attentional/affective findings.
Among children aged 6 years or younger, there is no convincing evidence that prenatal cocaine exposure is associated with developmental toxic effects that are different in severity, scope, or kind from the sequelae of multiple other risk factors. Many findings once thought to be specific effects of in utero cocaine exposure are correlated with other factors, including prenatal exposure to tobacco, marijuana, or alcohol, and the quality of the child’s environment. Further replication is required of preliminary neurologic findings.
PMCID: PMC2504866  PMID: 11268270
13.  Neonatal Neurobehavioral and Neuroanatomic Correlates of Prenatal Cocaine Exposure 
Complex methodologic challenges face researchers studying the effects of prenatal cocaine exposure on infant outcome. These include unavoidable imprecision in ascertaining the gestational timing and dose of cocaine to which the fetus was exposed and difficulties in identifying and quantifying the confounding, mediating, and moderating variables. Review of research on neonatal behavioral and cranial ultrasound findings following in utero cocaine exposure is used to illustrate these issues. We conclude that there are measurable but not dramatic dose-related effects of prenatal cocaine exposure on infant central nervous system structure and function. The effects of dose of prenatal cocaine exposure on later child development remain to be determined. Such research would be facilitated by a scientific consensus delineating relative doses of prenatal cocaine exposure.
PMCID: PMC2423320  PMID: 9668396
14.  Late Dose-Response Effects of Prenatal Cocaine Exposure on Newborn Neurobehavioral Performance 
Pediatrics  1996;98(1):76-83.
To determine in a representative sample of full-term urban newborns of English-speaking mothers whether an immediate or late dose-response effect could be demonstrated between prenatal cocaine exposure and newborn neurobehavioral performance, controlling for confounding factors.
The Neonatal Behavioral Assessment Scale (NBAS) was administered by masked examiners to a total sample of 251 clinically healthy, full-term infants at 2 days and/or 17 days. Three in utero cocaine exposure groups were defined: heavily exposed (n = 44, >75th percentile self-reported days of use during pregnancy and/or >75th percentile of meconium benzoylecognine concentration); lightly exposed (n = 79, less than both 75th percentiles); and unexposed (n = 101, no positive biological or self-report marker). At the 3-week examination there were 38 heavily exposed, 73 lightly exposed, and 94 unexposed infants. Controlling for infant birth weight, gestational age, infant age at the time of examination, mothers’ age, perinatal risk, obstetric medication, and alcohol, marijuana, and cigarette use, a regression analysis evaluated the effects of levels of cocaine exposure on NBAS performance.
No neurobehavioral effects of exposure on the newborn NBAS cluster scores or on the qualifier scores were found when confounders were controlled for at 2 to 3 days of age. At 3 weeks, after controlling for covariates, a significant dose effect was observed, with heavily exposed infants showing poorer state regulation and greater excitability.
These findings demonstrate specific dose-related effects of cocaine on 3-week neurobehavioral performance, particularly for the regulation of arousal, which was not observed in the first few days of life.
PMCID: PMC2373273  PMID: 8668416
cocaine exposure and newborn neurobehavior; neurobehavioral effects of prenatal cocaine exposure; dose-related cocaine effects on newborn neurobehavior; prenatal cocaine impairment of newborn regulation of arousal; Brazelton Scale; behavior of cocaine-exposed newborns
15.  Children Who Witness Violence, and Parent Report of Children’s Behavior 
To examine how much distress children report in response to violence that they have witnessed and how this is associated with parental reports of children’s behavior.
As part of a study of in utero exposure to cocaine, children completed the Levonn interview for assessing children’s symptoms of distress in response to witnessing violence. The children’s care givers completed the Exposure to Violence Interview (EVI), a caretaker-report measure of the child’s exposure to violent events during the last 12 months. The EVI was analyzed as a 3-level variable: no exposure, low exposure, and high exposure. The caregivers also completed the Children’s Behavior Checklist (CBCL).
Of 94 six-year-old children, 58% had no exposure to violence, 36% had low exposure to violence, and 6% had high exposure to violence, according to caretaker reports. The children’s median ±SD Levonn score was 64 (SD ± 19.3). The mean (SD ± CBCL total T-score was 53 (SD ± 10.2). In multiple regression analyses with gender, low and high exposure on EVI, Levonn, and prenatal cocaine exposure status as predictors, the Levonn score explained 4.8% of total variance in children’s CBCL internalizing scores, 9.1% of the total variance in CBCL externalizing score, and 12.2% of the total variance in CBCL total score (P = .04, P = .004, and P <.001, respectively).
After accounting for the caretaker’s report of the level of the child’s exposure to violence, the child’s own report significantly increased the amount of variance in predicting child behavior problems with the CBCL. These findings indicate that clinicians and researchers should elicit children’s own accounts of exposure to violence in addition to the caretakers’ when attempting to understand children’s behavior.
PMCID: PMC2366171  PMID: 12144371
16.  Level of In Utero Cocaine Exposure and Neonatal Ultrasound Findings 
Pediatrics  1999;104(5 Pt 1):1101-1105.
To assess whether there is an association between the level of in utero cocaine exposure and findings on neonatal cranial ultrasound, controlling for potentially confounding variables.
Study Design
In a prospective longitudinal study, three cocaine exposure groups were defined by maternal report and infant meconium assay: unexposed, heavier cocaine exposure (>75th percentile self-reported days of use or of meconium benzoylecogonine concentration) or lighter cocaine exposure (all others). Neonatal ultrasounds from 241 well, term infants were read by a single radiologist who was masked to the exposure group.
Infants with lighter cocaine exposure did not differ from the unexposed infants on any ultrasound findings. After controlling for infant gender, gestational age, and birth weight z scores and for maternal parity, blood pressure in labor, ethnicity, and use of cigarettes, alcohol, and marijuana during pregnancy, the more heavily cocaine-exposed infants were more likely than the unexposed infants to show subependymal hemorrhage in the caudothalamic groove (covariate adjusted odds ratio: 3.88; 95% confidence interval: 1.45, 10.35).
This is the first study to demonstrate that ultrasound findings suggestive of vascular injury to the neonatal central nervous system are related to the level of prenatal cocaine exposure. Inconsistency in previous research in identifying an association between prenatal cocaine exposure and neonatal cranial ultrasound findings may reflect failure to consider dose effects.
PMCID: PMC2365465  PMID: 10545554
17.  Elevated Plasma Norepinephrine After In Utero Exposure to Cocaine and Marijuana 
Pediatrics  1997;99(4):555-559.
To compare plasma catecholamine concentrations between cocaine-exposed and unexposed term newborns and to determine the relationship between plasma catecholamines and newborn behavior.
Forty-six newborn infants participating in a prospective study of the neonatal and long-term effects of prenatal cocaine exposure were studied. Based on maternal self-report, maternal urine screening, and infant meconium analysis, 24 infants were classified as cocaine-exposed and 22 as unexposed. Between 24 and 72 hours postpartum, plasma samples for norepinephrine (NE), epinephrine, dopamine, and dihydroxyphenylalanine analysis were obtained. The Neonatal Behavioral Assessment Scale was administered at 1 to 3 days of age and at 2 weeks of age by examiners masked to the drug exposure status of the newborns.
The cocaine-exposed newborns had increased plasma NE concentrations when compared to the unexposed infants (geometric mean, 923 pg/mL vs 667 pg/mL). There were no significant differences in plasma epinephrine, dopamine, or dihydroxyphenylalanine concentrations. Analysis for the effect of potential confounding variables revealed that maternal marijuana use was also associated with increased plasma NE, although birth weight, gender, and maternal use of alcohol or cigarettes were not. Geometric mean plasma NE was 1164 pg/mL in those infants with in utero exposure to both cocaine and marijuana compared to 812 pg/mL in those exposed to only cocaine and 667 pg/mL in those exposed to neither. Among the cocaine-exposed infants, plasma NE concentration correlated with an increased score for the depressed cluster (r = .53) and a decreased score for the orientation cluster (r = −.43) of the Neonatal Behavioral Assessment Scale administered at 1 to 3 days of age. Adjusting for marijuana exposure had no effect on these relationships between plasma NE and the depressed and orientation clusters.
Plasma NE is increased in newborns exposed to cocaine and marijuana. Increased plasma NE is associated with selected neurobehavioral disturbances among cocaine exposed infants at 1 to 3 days of life but not at 2 weeks.
PMCID: PMC2365460  PMID: 9093298
18.  The parent-provider relationship: Does race/ethnicity concordance or discordance influence parent reports of the receipt of high quality basic pediatric preventive services? 
Recent research among adults suggests that having a provider of the same race/ethnicity may enhance the quality of health care above and beyond just having any regular source of care. It is not known whether such relationships exist in pediatric care. The purpose of this study is to identify the distribution and methods by which families have a race/ethnicity concordant provider of well-child care and examine whether differences exist in the receipt of basic preventive services (BPS) and familycentered care (FCC) among those with concordant, discordant, and no regular providers. Analyses are stratified by geography to assess whether urban versus nonurban setting moderates these differences. This study uses publicly available data from the 2000 National Survey of Early Childbood Health (NSECH), a nationally representative, cross-sectional telephone survey of parents of children ages 4–35 months (n=1,996). African Americans and Latinos were more likely than whites to lack a regular provider of well-child care (60.9% and 65.7% vs. 50.6%) and less likely to have a concordant provider (9.8% and 5.7% vs. 38.5%) (P<.0011). African Americans with a regular provider were about three times more likely to establish a concordant relationship in urban versus nonurban settings (32.4% vs. 12.5%, P<.011), No statistically significant differences in BPS or FCC were found by concordance versus discordance for any group, a finding that held regardless of geographic setting. White children with no regular provider received better BPS than those with a discordant provider (e.g., excellent BPS of 37.2% vs. 27.1%, P<..05), but children with no regular provider were more likely than those with either concordant or discordant providers to have lower FCC in one (Latinos, whites) or three domains (African Americans). Despite racial/ethnic differences in the likelihood of having a concordant regular provider of well-child care, no disparities were found in BPS or FCC associated with discordance, even after stratification by urban/nonurban setting. Lacking a regular provider was associated with lower FCC versus having either a concordant or discordant provider, suggesting that efforts to improve these aspects of well-child care might focus less on linking children with a race/ethnicity concordant provider and more on social, cultural, and linguistic factors that impact having any regular provider.
PMCID: PMC3456673  PMID: 16221918
Children; Patient-provider relationship; Primary care; Racial/ethnic disparities

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