Maternal exposure to childhood maltreatment and risk of stillbirth.
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ABSTRACT:
SUBMITTER: Freedman AA
PROVIDER: S-EPMC5610090 | biostudies-literature | 2017 Aug
REPOSITORIES: biostudies-literature
Publications
Maternal exposure to childhood maltreatment and risk of stillbirth.
Freedman Alexa A AA Cammack Alison L AL Temple Jeff R JR Silver Robert M RM Dudley Donald J DJ Stoll Barbara J BJ Varner Michael W MW Saade George R GR Conway Deborah D Goldenberg Robert L RL Hogue Carol J CJ
Annals of epidemiology 20170713 8
<h4>Purpose</h4>To determine the association between maternal exposure to childhood maltreatment (CM) and risk of stillbirth (fetal death at or after 20 weeks' gestation).<h4>Methods</h4>Population-based case-control study from the Stillbirth Collaborative Research Network (SCRN) conducted in 2006-2008, and the follow-up study, SCRN-Outcomes after Study Index Stillbirth (SCRN-OASIS), conducted in 2009 in the United States. Cases (n = 133) included women who experienced a stillbirth, excluding st ...[more]
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Project description:BackgroundChildhood maltreatment (CM) confers deleterious long-term consequences, and growing evidence suggests some of these effects may be transmitted across generations. We examined the intergenerational effect of maternal CM exposure on child brain structure and also addressed the hypothesis that this effect may start during the child's intrauterine period of life.MethodsA prospective longitudinal study was conducted in a clinical convenience sample of 80 mother-child dyads. Maternal CM exposure was assessed using the Childhood Trauma Questionnaire. Structural magnetic resonance imaging was employed to characterize newborn global and regional brain (tissue) volumes near the time of birth.ResultsCM exposure was reported by 35% of the women. Maternal CM exposure was associated with lower child intracranial volume (F1,70 = 6.84, p = .011), which was primarily due to a global difference in cortical gray matter (F1,70 = 9.10, p = .004). The effect was independent of potential confounding variables, including maternal socioeconomic status, obstetric complications, obesity, recent interpersonal violence, pre- and early postpartum stress, gestational age at birth, infant sex, and postnatal age at magnetic resonance imaging scan. The observed group difference between offspring of CM-exposed mothers versus nonexposed mothers was 6%.ConclusionsThese findings represent the first report to date associating maternal CM exposure with variation in newborn brain structure. These observations support our hypothesis of intergenerational transmission of the effects of maternal CM exposure on child brain development and suggest this effect may originate during the child's intrauterine period of life, which may have downstream neurodevelopmental consequences.
| S-EPMC5723537 | biostudies-literature
Project description:Face processing in mothers is linked to mother-infant social communication, which is critical for parenting and in turn for child development. Neuroimaging studies of child maltreatment-exposed (CME) mothers are sparse compared to studies of mothers with postpartum depression, which have suggested blunted amygdala reactivity to infant stimuli. We expected to see a similar pattern in CME mothers. Based on broader studies in trauma-exposed populations, we anticipated increased amygdala reactivity to negative adult face stimuli in a comparison task in CME mothers given heightened evaluation of potential threat. We examined Neuroimaging studies of mothers with childhood maltreatment exposure (CME) (18-37 years old), who performed infant (N = 45) and/or adult (N = 46) face processing tasks. CME mothers exhibited blunted bilateral amygdala reactivity to infant faces. There was no between-group difference in amygdala reactivity to adult faces. In infant and adult face processing tasks regardless of CME, superior temporal gyrus activation was increased for negative-valence stimuli. Our preliminary findings suggest that childhood maltreatment alters maternal processing of infant social cues, a critical skill impacting infant socioemotional development.
| S-EPMC7058929 | biostudies-literature
Project description:ImportancePrenatal smoking is a known modifiable risk factor for stillbirth; however, the contribution of prenatal drinking or the combination of smoking and drinking is uncertain.ObjectiveTo examine whether prenatal exposure to alcohol and tobacco cigarettes is associated with the risk of stillbirth.Design, setting, and participantsThe Safe Passage Study was a longitudinal, prospective cohort study with data collection conducted between August 1, 2007, and January 31, 2015. Pregnant women from Cape Town, South Africa, and the Northern Plains region of the US were recruited and followed up throughout pregnancy. Data analysis was performed from November 1, 2018, to November 20, 2020.ExposureMaternal consumption of alcohol and tobacco cigarettes in the prenatal period.Main outcomes and measuresThe main outcomes were stillbirth, defined as fetal death at 20 or more weeks' gestation, and late stillbirth, defined as fetal death at 28 or more weeks' gestation. Self-reported alcohol and tobacco cigarette consumption was captured at the recruitment interview and up to 3 scheduled visits during pregnancy. Participants were followed up during pregnancy to obtain delivery outcome.ResultsOf 11663 pregnancies (mean [SD] gestational age at enrollment, 18.6 [6.6] weeks) in 8506 women for whom the pregnancy outcome was known by 20 weeks' gestation or later and who did not terminate their pregnancies, there were 145 stillbirths (12.4 per 1000 pregnancies) and 82 late stillbirths (7.1 per 1000 pregnancies). A total of 59% of pregnancies were in women from South Africa, 59% were in multiracial women, 23% were in White women, 17% were in American Indian women, and 0.9% were in women of other races. A total of 8% were older than 35 years. In 51% of pregnancies, women reported no alcohol or tobacco cigarette exposure (risk of stillbirth, 4 per 1000 pregnancies). After the first trimester, 18% drank and smoked (risk of stillbirth, 15 per 1000 births), 9% drank only (risk of stillbirth, 10 per 1000 pregnancies), and 22% smoked only (risk of stillbirth, 8 per 1000 pregnancies). Compared with the reference group (pregnancies not prenatally exposed or without any exposure after the first trimester), the adjusted relative risk of late stillbirth was 2.78 (98.3% CI, 1.12-6.67) for pregnancies prenatally exposed to drinking and smoking, 2.22 (98.3% CI, 0.78-6.18) for pregnancies prenatally exposed to drinking only after the first trimester, and 1.60 (98.3% CI, 0.64-3.98) for pregnancies prenatally exposed to smoking only after the first trimester. The adjusted relative risk for all stillbirths was 1.75 (98.3% CI, 0.96-3.18) for dual exposure, 1.26 (98.3% CI, 0.58-2.74) for drinking only, and 1.27 (98.3% CI, 0.69-2.35) for smoking only compared with the reference group.Conclusions and relevanceThese results suggest that combined drinking and smoking after the first trimester of pregnancy, compared with no exposure or quitting before the end of the first trimester, may be associated with a significantly increased risk of late stillbirth.
| S-EPMC8383134 | biostudies-literature
Project description:BackgroundChildhood maltreatment is associated with adverse health outcomes and this risk can be transmitted to the next generation. We aimed to investigate the association between exposure to maternal childhood maltreatment and common childhood physical and mental health problems, neurodevelopmental disorders, and related comorbidity patterns in offspring.MethodsWe conducted a retrospective cohort study using data from the Environmental influences on Child Health Outcomes (ECHO) Program, which was launched to investigate the influence of early life exposures on child health and development in 69 cohorts across the USA. Eligible mother-child dyads were those with available data on maternal childhood maltreatment exposure and at least one child health outcome measure (autism spectrum disorder, attention-deficit hyperactivity disorder [ADHD], internalising problems, obesity, allergy, and asthma diagnoses). Maternal history of childhood maltreatment was obtained retrospectively from the Adverse Childhood Experiences or Life Stressor Checklist questionnaires. We derived the prevalence of the specified child health outcome measures in offspring across childhood and adolescence by harmonising caregiver reports and other relevant sources (such as medical records) across cohorts. Child internalising symptoms were assessed using the Child Behavior Checklist. Associations between maternal childhood maltreatment and childhood health outcomes were measured using a series of mixed-effects logistic regression models. Covariates included child sex (male or female), race, and ethnicity; maternal and paternal age; maternal education; combined annual household income; maternal diagnosis of depression, asthma, ADHD, allergy, or autism spectrum disorder; and maternal obesity. Two latent class analyses were conducted: to characterise patterns of comorbidity of child health outcomes; and to characterise patterns of co-occurrence of childhood maltreatment subtypes. We then investigated the association between latent class membership and maternal childhood maltreatment and child health outcomes, respectively.FindingsOur sample included 4337 mother-child dyads from 21 longitudinal cohorts (with data collection initiated between 1999 and 2016). Of 3954 mothers in the study, 1742 (44%) had experienced exposure to abuse or neglect during their childhood. After adjustment for confounding, mothers who experienced childhood maltreatment were more likely to have children with internalising problems in the clinical range (odds ratio [OR] 2·70 [95% CI 1·95-3·72], p<0·0001), autism spectrum disorder (1·70 [1·13-2·55], p=0·01), ADHD (2·09 [1·63-2·67], p<0·0001), and asthma (1·54 [1·34-1·77], p<0·0001). In female offspring, maternal childhood maltreatment was associated with a higher prevalence of obesity (1·69 [1·17-2·44], p=0·005). Children of mothers exposed to childhood maltreatment were more likely to exhibit a diagnostic pattern characterised by higher risk for multimorbidity. Exposure to multiple forms of maltreatment across all subtypes of maternal childhood maltreatment was associated with the highest risk increases for most offspring health outcomes, suggesting a dose-response relationship.InterpretationOur findings suggest that maternal childhood maltreatment experiences can be a risk factor for disease susceptibility in offspring across a variety of outcomes and emphasise the need for policies focusing on breaking the intergenerational transmission of adversity.FundingEnvironmental influences on Child Health Outcomes Program, Office of the Director, National Institutes of Health.
| S-EPMC9982823 | biostudies-literature
Project description:Although a growing literature describes the effects of negative childhood experiences on biological outcomes, it is difficult to compare results across studies because of differences in measures of childhood experiences, biological markers, sample characteristics, and included covariates. To ensure comparability across its analyses, this study used a single national survey of adults in the United States-the Midlife in the United States (MIDUS) study-to examine comprehensively the association between adverse childhood experiences, operationalized as childhood maltreatment (CM), and biological markers of risk for poor health and to assess whether these associations differ by type of maltreatment, sex, or race. The sample included 1254, mostly White (78%), adults aged 34-86 years (mean age 57 years), 57% of whom were female. We present incidence rate ratios (IRR) from negative binomial and Poisson regressions to examine the relationships between exposure to CM (emotional, physical, and sexual abuse; emotional and physical neglect; and a CM-index reflecting frequency across all five types of maltreatment) and four biological risk summary scores (overall physiological dysregulation, cardiometabolic risk, inflammation, and hypothalamic pituitary axis/sympathetic nervous system (HPA/SNS) function). We also tested whether the effect of each type of CM varied by sex and by race. The CM-index was associated with higher overall physiological dysregulation and inflammation, but the associations were weaker and not statistically significant for cardiometabolic risk and HPA/SNS function. With the exception of a possible sex difference in the association between sexual abuse and overall physiological dysregulation, there was little evidence that the associations varied systematically by type of CM or by sex or race. We conclude that exposure to CM predicts adult biological risk, particularly inflammation. Inconsistency with previous research suggests that additional research is needed to confirm findings regarding sex and race differences.
| S-EPMC10688890 | biostudies-literature
Project description:The reports regarding the associations between childhood maltreatment (CM) and body fat composition remain heterogeneous in humans although they are indicated in preclinical studies. In addition, the effects of CM subtypes on different types of body fat are unclear. Thus, in this study, the associations between CM and its subtypes with body fat were determined and the potential pathways were explored.The participants were assessed for a history of CM by the Childhood Trauma Questionnaire and were divided into the CM group (with CM exposures) and non-CM group (without CM exposures). Body composition was measured by dual-energy X-ray absorptiometry. Salivary and blood samples were provided by the subjects.Compared with the non-CM group, subjects with a history of CM had greater visceral fat mass (1,136?±?160 vs. 836?±?116 g, P?<?0.05) but not total body fat, android fat, body mass index, or waist-to-hip ratio. In addition, subjects with CM had a blunted cortisol awakening response and elevated inflammatory factors. Correlation analysis indicated that CM subtypes had differential effects on visceral adiposity and cortisol awakening response.It is suggested by our results that CM exposure is linked with increased visceral fat deposition, and the perturbation of the hypothalamic-pituitary-adrenal axis activity and activation of the immune system may be two potential pathways through which this relationship is explained.
| S-EPMC4509989 | biostudies-literature
Project description:BackgroundThe number of women who delay childbirth to their late 30s and beyond has increased significantly over the past several decades. Studies regarding the relation between older maternal age and the risk of stillbirth have yielded inconsistent conclusions. In this systematic review we explored whether older maternal age is associated with an increased risk of stillbirth.MethodsWe searched MEDLINE, EMBASE and the Cochrane Database of Systematic Reviews for all relevant articles (original studies and systematic reviews) published up to Dec. 31, 2006. We included all cohort and case-control studies that measured the association between maternal age and risk of stillbirth. Two reviewers independently abstracted data from all included studies using a standardized data abstraction form. Methodologic and statistical heterogeneities were reviewed and tested.ResultsWe identified 913 unique citations, of which 31 retrospective cohort and 6 case-control studies met our inclusion criteria. In 24 (77%) of the 31 cohort studies and all 6 of the case-control studies, we found that greater maternal age was significantly associated with an increased risk of stillbirth; relative risks varied from 1.20 to 4.53 for older versus younger women. In the 14 studies that presented adjusted relative risk, we found no extensive change in the direction or magnitude of the relative risk after adjustment. We did not calculate a pooled relative risk because of the extreme methodologic heterogeneity among the individual studies.InterpretationWomen with advanced maternal age have an increased risk of stillbirth. However, the magnitude and mechanisms of the increased risk are not clear, and prospective studies are warranted.
| S-EPMC2175002 | biostudies-literature
Project description:BACKGROUND: It has been suggested that prenatal stress contributes to the risk of obesity later in life. In a population-based cohort study, we examined whether prenatal stress related to maternal bereavement during pregnancy was associated with the risk of overweight in offspring during school age. METHODOLOGY/PRINCIPAL FINDINGS: We followed 65,212 children born in Denmark from 1970-1989 who underwent health examinations from 7 to 13 years of age in public or private schools in Copenhagen. We identified 459 children as exposed to prenatal stress, defined by being born to mothers who were bereaved by death of a close family member from one year before pregnancy until birth of the child. We compared the prevalence of overweight between the exposed and the unexposed. Body mass index (BMI) values and prevalence of overweight were higher in the exposed children, but not significantly so until from 10 years of age and onwards, as compared with the unexposed children. For example, the adjusted odds ratio (OR) for overweight was 1.68 (95% confidence interval [CI] 1.08-2.61) at 12 years of age and 1.63 (95% CI 1.00-2.61) at 13 years of age. The highest ORs were observed when the death occurred in the period from 6 to 0 month before pregnancy (OR 3.31, 95% CI 1.71-6.42 at age 12, and OR 2.31, 95% CI 1.08-4.97 at age 13). CONCLUSIONS/SIGNIFICANCE: Our results suggest that severe pre-pregnancy stress is associated with an increased risk of overweight in the offspring in later childhood.
| S-EPMC2912844 | biostudies-literature
Project description:ObjectiveThe objective of this study was to evaluate the effect of maternal hyperglycemia during pregnancy on cardiometabolic risk in offspring during early childhood.Research design and methodsA total of 970 mothers who had joined the Hyperglycemia and Adverse Pregnancy Outcome study were reevaluated, together with their child born during the study period, 7 years after delivery.ResultsOffspring born to mothers diagnosed with gestational diabetes mellitus (GDM), as defined by the World Health Organization 2013 GDM criteria, had higher rates of abnormal glucose tolerance (4.7% vs. 1.7%; P = 0.04), higher rates of overweight or obesity, greater BMI, higher blood pressure (BP), lower oral disposition index, and a trend toward reduced β-cell function compared with those born to mothers without GDM. For each SD increase in maternal fasting, 1-h, and 2-h glucose levels on oral glucose tolerance tests (OGTTs) between 24 and 32 weeks of the index pregnancy, the risk of abnormal glucose tolerance in the offspring showed a corresponding increase (adjusted odds ratio [OR] 1.85-2.00). The associations were independent of BMI before pregnancy, childhood obesity, or being born large for gestational age. The area under the curve for glucose levels during the five-point OGTT increased to a similar extent in boys and girls with each SD increase in maternal 1-h and 2-h plasma glucose on OGTTs during pregnancy. All three maternal glucose levels were also associated with increased adjusted ORs for childhood overweight or obesity and adiposity among girls, but not boys.ConclusionsMaternal hyperglycemia in pregnancy is independently associated with offsprings' risk of abnormal glucose tolerance, obesity, and higher BP at 7 years of age. Its effect on childhood adiposity was apparent only in girls, not boys.
| S-EPMC5399651 | biostudies-literature
Project description:ObjectiveTo assess the main risk factors associated with stillbirth in a multiethnic English maternity population.DesignCohort study.SettingNational Health Service region in England.Population92,218 normally formed singletons including 389 stillbirths from 24 weeks of gestation, delivered during 2009-11.Main outcome measureRisk of stillbirth.ResultsMultivariable analysis identified a significant risk of stillbirth for parity (para 0 and para ≥ 3), ethnicity (African, African-Caribbean, Indian, and Pakistani), maternal obesity (body mass index ≥ 30), smoking, pre-existing diabetes, and history of mental health problems, antepartum haemorrhage, and fetal growth restriction (birth weight below 10th customised birthweight centile). As potentially modifiable risk factors, maternal obesity, smoking in pregnancy, and fetal growth restriction together accounted for 56.1% of the stillbirths. Presence of fetal growth restriction constituted the highest risk, and this applied to pregnancies where mothers did not smoke (adjusted relative risk 7.8, 95% confidence interval 6.6 to 10.9), did smoke (5.7, 3.6 to 10.9), and were exposed to passive smoke only (10.0, 6.6 to 15.8). Fetal growth restriction also had the largest population attributable risk for stillbirth and was fivefold greater if it was not detected antenatally than when it was (32.0% v 6.2%). In total, 195 of the 389 stillbirths in this cohort had fetal growth restriction, but in 160 (82%) it had not been detected antenatally. Antenatal recognition of fetal growth restriction resulted in delivery 10 days earlier than when it was not detected: median 270 (interquartile range 261-279) days v 280 (interquartile range 273-287) days. The overall stillbirth rate (per 1000 births) was 4.2, but only 2.4 in pregnancies without fetal growth restriction, increasing to 9.7 with antenatally detected fetal growth restriction and 19.8 when it was not detected.ConclusionMost normally formed singleton stillbirths are potentially avoidable. The single largest risk factor is unrecognised fetal growth restriction, and preventive strategies need to focus on improving antenatal detection.
| S-EPMC3554866 | biostudies-literature