Maternal prenatal anxiety and child COMT genotype predict working memory and symptoms of ADHD.
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ABSTRACT:
SUBMITTER: O'Donnell KJ
PROVIDER: S-EPMC5470664 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Objective: The current study examines how maternal depressive symptoms relate to child psychopathology when structured via the latent bifactor model of psychopathology, a new organizational structure of psychopathological symptoms consisting of a general common psychopathology factor (p-factor) and internalizing- and externalizing-specific risk.Method: Maternal report of depressive symptoms (Beck Depression Inventory - II) and child psychopathological symptoms (Child Behavior Checklist and Children's Behavior Questionnaire) were provided by 554 mother-child pairs. Children in the sample were 7.7 years old on average (SD = 1.35, range = 5-11 years), and were 49.8% female, 46% Latinx, and 67% White, 6% Black, 5% Asian/Pacific Islander, and 21% multiracial.Results: Maternal depressive symptoms were positively associated with the child p-factor but not with the internalizing- or externalizing-specific factors. We did not find evidence of sex/gender or race/ethnicity moderation when using latent factors of psychopathology. Consistent with past research, maternal depressive symptoms were positively associated with internalizing and externalizing composite scores on the Child Behavior Checklist.Conclusions: Findings suggest that maternal depressive symptoms are associated with transdiagnostic risk for broad child psychopathology (p-factor). Whereas the traditional Achenbach-style approach of psychopathological assessment suggests that maternal depressive symptoms are associated with both child internalizing and externalizing problems, the latent bifactor model suggests that these associations may be accounted for by risk pathways related to the p-factor rather than internalizing or externalizing specific risk. We discuss clinical and research implications of using a latent bifactor structure of psychopathology to understand how maternal depression may impact children's mental health.
| S-EPMC7529641 | biostudies-literature
Project description:Childhood obesity can be predicted by metabolic signaling at birth. Understanding what exposure factors, such as prenatal mental health, predict metabolic signaling at birth are important for understanding the etiology of childhood metabolic dysregulation. Drawing on data from the Born in Bradford (BiB) multi-ethnic birth cohort in the United Kingdom (N = 2962 dyads), this study examined associations between maternal prenatal mental health symptoms and infant leptin and adiponectin. We tested whether total maternal prenatal symptoms as well as specific symptom subscales forecasted infant cord blood levels of leptin and adiponectin. We found that higher total maternal mental health symptoms and somatic symptoms, specifically, predicted lower infant cord blood leptin. We did not find evidence that maternal prenatal mental health symptoms predicted adiponectin. Together, our findings suggest that maternal mental health symptoms may become biologically embedded through infant metabolic changes via leptin.
| S-EPMC8474689 | biostudies-literature
Project description:BackgroundThis study quantifies the dynamics of maternal mood focusing on unpredictability, and to assess if greater unpredictability of prenatal maternal mood predicts child temperament and internalizing symptoms through early adolescence.MethodsThe association between prenatal mood predictability and child internalizing symptoms were assessed in two longitudinal cohorts (N's = 227 and 180). Maternal mood was assessed repeatedly during pregnancy as early as 15 weeks' gestation. Predictability of maternal mood was calculated by applying Shannon's entropy to the distribution of responses on mood questionnaires. Maternal reports of child negative affectivity (a predictor of later internalizing) were collected at 6, 12, 24 months and 7 years of age. Child self-reports of anxiety symptoms were collected at 10 years and reports of depression symptoms at 13 years.ResultsFetal exposure to more elevated maternal mood entropy predicted higher levels of child negative affectivity at 12 months (r = .36; p < 01), 24 months (r = .31; p < 01) and 7 years (r = .32; p < 01) of age. In addition, children exposed to higher prenatal maternal mood entropy, reported higher levels of anxiety symptoms at 10 years (r = .24; p < 01) and elevated depressive symptoms at 13 years (r = .29; p < .01). These associations persisted after adjusting for maternal pre and postnatal mood valence (e.g. depression levels) and for other relevant demographic characteristics.ConclusionsOur findings provide strong support for the notion that patterns of maternal mood influence the developing brain. More specifically, they suggest that prenatal maternal mood predictability may be a critical predictor of developmental mental health trajectories and should be considered when assessing early life influences on lifespan mental health.
| S-EPMC10387303 | biostudies-literature
Project description:Prenatal maternal infection and anxiety have been linked, in separate lines of study, with child neurodevelopment. We extend and integrate these lines of study in a large prospective longitudinal cohort study of child neurodevelopment. Data are based on the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort; prenatal maternal anxiety was assessed from self-report questionnaire; prenatal infection was derived from reports of several conditions in pregnancy (n = 7,042). Child neurodevelopment at approximately 8 years of age was assessed by in-person testing, reports of social and communication problems associated with autism, and psychiatric evaluation. Covariates included psychosocial, demographic, and perinatal/obstetric risks. Prenatal infection was associated with increased likelihood of co-occurring prenatal risk, including anxiety. Regression analyses indicated that both prenatal infection and prenatal anxiety predicted child social and communication problems; the predictions were largely independent of each other. Comparable effects were also found for the prediction of symptoms of attention problems and anxiety symptoms. These results provide the first evidence for the independent effects of prenatal infection and anxiety on a broad set of neurodevelopmental and behavioral and emotional symptoms in children, suggesting the involvement of multiple mechanisms in the prenatal programming of child neurodevelopment. The results further underscore the importance of promoting prenatal physical and mental health for child health outcomes. (PsycInfo Database Record (c) 2022 APA, all rights reserved).
| S-EPMC9069845 | biostudies-literature
Project description:Early adversity predicts anxiety and depression but variation in response to adversity is not understood. We investigated whether association between early adversity and emotional symptoms in young children differs according to variation of the COMT gene. The main outcome measure was the emotionality subscale of the Strengths and Difficulties Questionnaire (SDQ) completed by mothers for 8,431 children aged 6-7 years old in the Avon Longitudinal Study of Parents and Children. Adversity measures included exposure to maternal postpartum depressive symptoms and adverse life events for children. DNA from the children was genotyped for five COMT polymorphisms including the COMT Val158Met locus. Maternal depression increased the odds of high emotionality in the children, (OR 1.99, 95% CI 1.73-2.29, P < 0.001) as did life events score, (OR 1.21 for each s.d. increase in life event score, 95% CI 1.15-1.27, P < 0.001). There was no main effect of Val158Met genotype on emotional symptoms (OR for effect of each copy of the methionine allele was 1.04, 95% CI 0.97-1.10, P = 0.284). The relationship between adversity and emotional symptoms did not vary by genotype (G x E for maternal depression chi(2) = 3.17, P = 0.205; G x E for life events chi(2) = 1.69, P = 0.430). There was no main effect of COMT haplotype, nor was there an interaction with adversity. Early adversity predicts emotional symptoms in children aged 6-7 years. Although some studies indicate a role for COMT in emotionality, anxiety, and depression in adults, no direct effect or interaction of COMT genotype was observed in this large sample of young children.
| S-EPMC2746034 | biostudies-literature
Project description:The purpose of the current study is to examine the moderating influence of the catechol O methyltransferase gene (COMT) on the maternal prenatal smoking/offspring externalizing disorder relationship. The sample consisted of 430 young adults born between 1981 and 1984 at the Mater Misericordiae Mother's Hospital in Brisbane, Australia, as well as their mothers and peers. Mothers reported their prenatal smoking status during pregnancy, and genetic data was obtained from the youth at a later follow-up in adulthood. The outcome measures in this study were mother and teacher reports of youth attention problems and aggression at age 15, and youth, mother and peer reports of youth attention problems and aggression at age 20 (combined to create latent factors of attention problems and aggression at each age). The COMT Val108/158Met polymorphism (rs4680) significantly interacted with maternal cigarette smoking during pregnancy to predict youth aggressive behavior at ages 15 and 20. This gene-environment interaction was not significant for youth attention problems.
| S-EPMC3081881 | biostudies-literature
Project description:BackgroundPrenatal exposure to phthalates, a group of synthetic chemicals widely used in consumer products, has previously been associated with adverse infant and child development. Studies also suggest that maternal depression and anxiety, may amplify the harmful effects of phthalates on infant and child neurodevelopment.Study designOur analysis included a subset of dyads enrolled in the Atlanta African American Maternal-Child Cohort (N = 81). We measured eight phthalate metabolites in first and second trimester (8-14 weeks and 24-32 weeks gestation) maternal urine samples to estimate prenatal exposures. Phthalate metabolite concentrations were averaged across visits and natural log-transformed for analysis. Maternal symptoms of depression and anxiety were assessed using validated questionnaires (Edinberg Postnatal Depression Scale and State Trait Anxiety Inventory, respectively) and the total score on each scale was averaged across study visits. The NICU Network Neurobehavioral Scale (NNNS) was administered at two weeks of age. Our primary outcomes included two composite NNNS scores reflecting newborn attention and arousal. Linear regression was used to estimate associations between individual phthalate exposures and newborn attention and arousal. We assessed effect modification by maternal depression and anxiety.ResultsHigher levels of urinary phthalate metabolites were not associated with higher levels of infant attention and arousal, but true associations may still exist given the limited power of this analysis. In models examining effect modification by maternal depression, we observed that an interquartile range increase in mono (2-ethlyhexyl) phthalate (MEHP), mono (2-ethyl-5-oxohexyl) phthalate (MEOHP), and mono (2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) was associated with a significant increase in newborn arousal only among those with high depressive symptoms (MEHP: β = 0.71, 95% confidence interval [CI] = 0.10, 1.32 for high, β = -0.30, 95% CI = -0.73, 0.12 for low; MEOHP: β = 0.60, 95% CI = -0.03, 1.23 for high, β = -0.12, 95% CI = -0.58, 0.33 for low; MEHHP: β = 0.54, 95% CI = -0.04, 1.11 for high, β = -0.11, 95% CI = -0.54, 0.32 for low). Similar patterns were observed in models stratified by maternal anxiety, although CIs were wide.ConclusionOur results suggest maternal anxiety and depression symptoms may exacerbate the effect of phthalates on infant neurodevelopment. Future studies are needed to determine the optimal levels of attention and arousal in early infancy.
| S-EPMC11367505 | biostudies-literature
Project description:ImportanceMaternal depression and anxiety can have deleterious and lifelong consequences on child development. However, many aspects of the association of early brain development with maternal symptoms remain unclear. Understanding the timing of potential neurobiological alterations holds inherent value for the development and evaluation of future therapies and interventions.ObjectiveTo examine the association between exposure to prenatal maternal depression and anxiety symptoms and offspring white matter microstructure at 1 month of age.Design, setting, and participantsThis cohort study of 101 mother-infant dyads used a composite of depression and anxiety symptoms measured in mothers during the third trimester of pregnancy and measures of white matter microstructure characterized in the mothers' 1-month offspring using diffusion tensor imaging and neurite orientation dispersion and density imaging performed from October 1, 2014, to November 30, 2016. Magnetic resonance imaging was performed at an academic research facility during natural, nonsedated sleep.Main outcomes and measuresBrain mapping algorithms and statistical models were used to evaluate the association between maternal depression and anxiety and 1-month infant white matter microstructure as measured by diffusion tensor imaging and neurite orientation dispersion and density imaging findings.ResultsIn the 101 mother-infant dyads (mean [SD] age of mothers, 33.22 [3.99] years; mean age of infants at magnetic resonance imaging, 33.07 days [range, 18-50 days]; 92 white mothers [91.1%]; 53 male infants [52.5%]), lower 1-month white matter microstructure (decreased neurite density and increased mean, radial, and axial diffusivity) was associated in right frontal white matter microstructure with higher prenatal maternal symptoms of depression and anxiety. Significant sex × symptom interactions with measures of white matter microstructure were also observed, suggesting that white matter development may be differentially sensitive to maternal depression and anxiety symptoms in males and females during the prenatal period.Conclusions and relevanceThese data highlight the importance of the prenatal period to early brain development and suggest that the underlying white matter microstructure is associated with the continuum of prenatal maternal depression and anxiety symptoms.
| S-EPMC6190835 | biostudies-literature
Project description:Prenatal maternal psychological distress increases risk for adverse infant outcomes. However, the biological mechanisms underlying this association remain unclear. Prenatal stress can impact fetal epigenetic regulation that could underlie changes in infant stress responses. It has been suggested that maternal glucocorticoids may mediate this epigenetic effect. We examined this hypothesis by determining the impact of maternal cortisol and depressive symptoms during pregnancy on infant NR3C1 and BDNF DNA methylation. Fifty-seven pregnant women were recruited during the second or third trimester. Participants self-reported depressive symptoms and salivary cortisol samples were collected diurnally and in response to a stressor. Buccal swabs for DNA extraction and DNA methylation analysis were collected from each infant at 2 months of age, and mothers were assessed for postnatal depressive symptoms. Prenatal depressive symptoms significantly predicted increased NR3C1 1F DNA methylation in male infants (β = 2.147, P = 0.044). Prenatal depressive symptoms also significantly predicted decreased BDNF IV DNA methylation in both male and female infants (β = -3.244, P = 0.013). No measure of maternal cortisol during pregnancy predicted infant NR3C1 1F or BDNF promoter IV DNA methylation. Our findings highlight the susceptibility of males to changes in NR3C1 DNA methylation and present novel evidence for altered BDNF IV DNA methylation in response to maternal depression during pregnancy. The lack of association between maternal cortisol and infant DNA methylation suggests that effects of maternal depression may not be mediated directly by glucocorticoids. Future studies should consider other potential mediating mechanisms in the link between maternal mood and infant outcomes.
| S-EPMC4622733 | biostudies-literature
Project description:Animal findings of long-term effects of maternal behaviors mediated via altered GR gene expression will, if translated into humans, have far reaching implications for our understanding of child and adolescent psychopathology. We have previously shown that mothers' self-reported stroking of their infants modifies associations between prenatal depression and anxiety and child outcomes at 29 weeks and 2.5 years. Here, we examine whether the effect of early maternal stroking is evident at 3.5 years, and in a much larger sample than in previous publications. A general population sample of 1233 first-time mothers completed anxiety measures at 20 weeks gestation, 865 reported on infant stroking at 9 weeks, and 813 on child symptoms at 3.5 years. Maternal stroking moderated the association between pregnancy-specific anxiety and internalizing (p = 0.010) and externalizing (p = 0.004) scores, such that an effect of PSA to increase symptoms was markedly reduced for mothers who reported high levels of stroking. There was no effect of maternal stroking on general anxiety. The findings confirm the previously reported effect of maternal stroking, and in a much larger sample. They indicate that there are long-term effects of early maternal stroking, modifying associations between prenatal anxiety and child emotional and behavioral symptoms.
| S-EPMC5323471 | biostudies-literature