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Prenatal depression and 5-HTTLPR interact to predict dysregulation from 3 to 36 months--a differential susceptibility model.

ABSTRACT: BACKGROUND:Childhood dysregulation, which reflects deficits in the capacity to regulate or control one's thoughts, emotions and behaviours, is associated with psychopathology throughout childhood and into adulthood. Exposures to adversity during the prenatal period, including prenatal depression, can influence the development of dysregulation, and a number of candidate genes have been suggested as moderators of prenatal exposure, including polymorphisms in the promoter region of the serotonin transporter gene (5-HTTLPR). We examined whether prenatal depression and child 5-HTTLPR interact to predict childhood dysregulation. METHOD:Sample of N = 213 mother-child pairs from the Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN) project. Mothers reported the IBQ-R at 3 and 6 months, and the ECBQ at 18 and 36 months, from which measures of dysregulation were extracted. Mothers' self-reported symptoms of depression on the CES-D at 24-36 weeks of gestation, and at 6, 12, 24 and 36 months postnatal. 5-HTTLPR genotype was extracted from buccal swabs. Mixed-model and confirmatory analyses were conducted. RESULTS:Prenatal depression and 5-HTTLPR interacted to predict dysregulation from 3 to 36 months, within a model of strong differential susceptibility. CONCLUSION:Children with S or LG alleles, when exposed to prenatal depression, have higher levels of dysregulation, and when exposed to lower or little prenatal depression, have higher capacity for regulation. Our findings support efforts to identify, support and treat prenatal depression.

SUBMITTER: Babineau V

PROVIDER: S-EPMC5398894 | biostudies-literature | 2015 Jan

REPOSITORIES: biostudies-literature

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Prenatal depression and 5-HTTLPR interact to predict dysregulation from 3 to 36 months--a differential susceptibility model.

Babineau Vanessa V Green Cathryn Gordon CG Jolicoeur-Martineau Alexis A Bouvette-Turcot Andrée-Anne AA Minde Klaus K Sassi Roberto R St-André Martin M Carrey Normand N Atkinson Leslie L Kennedy James L JL Lydon John J Steiner Meir M Gaudreau Helene H Levitan Robert R Meaney Michael M Wazana Ashley A

Journal of child psychology and psychiatry, and allied disciplines 20140515 1

<h4>Background</h4>Childhood dysregulation, which reflects deficits in the capacity to regulate or control one's thoughts, emotions and behaviours, is associated with psychopathology throughout childhood and into adulthood. Exposures to adversity during the prenatal period, including prenatal depression, can influence the development of dysregulation, and a number of candidate genes have been suggested as moderators of prenatal exposure, including polymorphisms in the promoter region of the sero ...[more]

PMID: 24827922

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Project description:Scientific enthusiasm about gene × environment interactions, spurred by the 5-HTTLPR (serotonin transporter-linked polymorphic region) × SLEs (stressful life events) interaction predicting depression, have recently been tempered by sober realizations of small effects and meta-analyses reaching opposing conclusions. These mixed findings highlight the need for further research. Converging evidence suggests that the effects of 5-HTTLPR genotype may be neurodevelopmental in origin, but we are not aware of empirical studies that have investigated whether the 5-HTTLPR genotype × SLE interaction predicts preschool-onset depression (PO-MDD), the earliest validated form of depression.Children (n = 234) aged 3-5 were recruited for a longitudinal study designed to examine PO-MDD. In a comprehensive baseline assessment, the child's primary caregivers completed questionnaires and were interviewed about their child's behaviors, psychiatric symptoms, and exposure to SLEs.A 5-HTTLPR × SLEs interaction emerged, such that children homozygous for the short allele were more susceptible to depression in the context of elevated SLE than long allele carriers. In contrast, at low SLE exposure, short allele homozygotes had fewer depressive symptoms. The data were best fit by a plasticity model with a substantial reduction in fit by diathesis-stress models.Extending studies in adult and adolescent populations, these data suggest that 5-HTTLPR genotype may provide plasticity to environmental influence, for better or worse. Specifically, children homozygous for the short allele were more susceptible to the depressogenic effects of SLEs but benefitted, in the form of reduced depressive symptoms, in the context of relatively benign environmental conditions (i.e. relatively low SLE exposure). These data highlight the importance of examining gene × environment interactions across development, environment, and outcome but should be interpreted cautiously given the small sample size.

Project description:Background Although depression is well established as an independent risk factor for cardiovascular disease (CVD) in the nonpregnant population, this association has largely not been investigated in pregnant populations. We aimed to estimate the cumulative risk of new CVD in the first 24 months postpartum among pregnant individuals diagnosed with prenatal depression compared with patients without depression diagnosed during pregnancy. Methods and Results Our longitudinal population-based study included pregnant individuals with deliveries during 2007 to 2019 in the Maine Health Data Organization's All Payer Claims Data. We excluded those with prepregnancy CVD, multifetal gestations, or no continuous health insurance during pregnancy. Prenatal depression and CVD (heart failure, ischemic heart disease, arrhythmia/cardiac arrest, cardiomyopathy, cerebrovascular disease, and chronic hypertension) were identified by International Classification of Diseases, Ninth Revision (ICD-9)/International Classification of Diseases, Tenth Revision (ICD-10) codes. Cox models were used to estimate hazard ratios (HRs), adjusting for potential confounding factors. Analyses were stratified by hypertensive disorder of pregnancy. A total of 119 422 pregnancies were examined. Pregnant individuals with prenatal depression had an increased risk of ischemic heart disease, arrhythmia/cardiac arrest, cardiomyopathy, and new hypertension (adjusted HR [aHR], 1.83 [95% CI, 1.20-2.80], aHR, 1.60 [95% CI, 1.10-2.31], aHR, 1.61 [95% CI, 1.15-2.24], and aHR, 1.32 [95% CI, 1.17-1.50], respectively). When the analyses were stratified by co-occurring hypertensive disorders of pregnancy, several of these associations persisted. Conclusions The cumulative risk of a new CVD diagnosis postpartum was elevated among individuals with prenatal depression and persists even in the absence of co-occurring hypertensive disorders of pregnancy. Further research to determine the causal pathway can inform postpartum CVD preventive measures.

Project description:BackgroundDepression is the leading cause of mental health-related morbidity and affects twice as many women as men. Hispanic/Latina women in the US have unique risk factors for depression and they have lower utilization of mental health care services. Identifying modifiable risk factors for maternal depression, such as ambient air pollution, is an urgent public health priority. We aimed to determine whether prenatal exposure to ambient air pollutants was associated with maternal depression at 12 months after childbirth.MethodsOne hundred eighty predominantly low-income Hispanic/Latina women participating in the ongoing MADRES cohort study in Los Angeles, CA were followed from early pregnancy through 12 months postpartum through a series of phone questionnaires and in-person study visits. Daily prenatal ambient pollutant estimates of nitrogen dioxide (NO2), ozone (O3), and particulate matter (PM10 and PM2.5) were assigned to participant residences using inverse-distance squared spatial interpolation from ambient monitoring data. Exposures were averaged for each trimester and across pregnancy. The primary outcome measure was maternal depression at 12 months postpartum, as reported on the 20-item Center for Epidemiologic Studies-Depression (CES-D) scale. We classified each participant as depressed (n = 29) or not depressed (n = 151) based on the suggested cutoff of 16 or above (possible scores range from 0 to 60) and fitted logistic regression models, adjusting for potential confounders.ResultsWe found over a two-fold increased odds of depression at 12 months postpartum associated with second trimester NO2 exposure (OR = 2.63, 95% CI: 1.41-4.89) and pregnancy average NO2 (OR = 2.04, 95% CI: 1.13-3.69). Higher second trimester PM2.5 exposure also was associated with increased depression at 12 months postpartum (OR = 1.56, 95% CI: 1.01-2.42). The effect for second trimester PM10 was similar and was borderline significant (OR = 1.58, 95% CI: 0.97-2.56).ConclusionsIn a low-income cohort consisting of primarily Hispanic/Latina women in urban Los Angeles, we found that prenatal ambient air pollution, especially mid-pregnancy NO2 and PM2.5, increased the risk of depression at 12 months after childbirth. These results underscore the need to better understand the contribution of modifiable environmental risk factors during potentially critical exposure periods.

Dataset Information

Prenatal depression and 5-HTTLPR interact to predict dysregulation from 3 to 36 months--a differential susceptibility model.

Publications

Prenatal depression and 5-HTTLPR interact to predict dysregulation from 3 to 36 months--a differential susceptibility model.

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