Maternal Adversity , Vulnerability And Neurodevelopment Research Articles

Variation in the mu-opioid receptor gene (OPRM1) moderates the influence of maternal sensitivity on child attachment

The endogenous opioid system is thought to play an important role in mother-infant attachment. In infant rhesus macaques, variation in the μ-opioid receptor gene (OPRM1) is related to differences in attachment behavior that emerges following repeated separation from the mother; specifically, infants carrying at least one copy of the minor G allele of the OPRM1 C77G polymorphism show heightened and more persistent separation distress, as well as a pattern of increased contact-seeking behavior directed towards the mother during reunions (at the expense of affiliation with other group members). Research in adult humans has also linked the minor G allele of the analogous OPRM1 A118G polymorphism with greater interpersonal sensitivity. Adopting an interactionist approach, we examined whether OPRM1 A118G genotype and maternal (in)sensitivity are associated with child attachment style, predicting that children carrying the G allele may be more likely to develop an ambivalent attachment pattern in response to less sensitive maternal care. The sample consisted of 191 mothers participating with their children (n = 223) in the Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN) project, a community-based, birth cohort study of Canadian mothers and their children assessed longitudinally across the child’s development. Maternal sensitivity was coded from at-home mother-child interactions videotaped when the child was 18 months of age. Child attachment was assessed at 36 months using the Strange Situation paradigm. As predicted, G allele carriers, but not AA homozygotes, showed increasing odds of being classified as ambivalently attached with decreasing levels of maternal sensitivity. Paralleling earlier non-human animal research, this work provides support for the theory that endogenous opioids contribute to the expression of attachment behaviors in humans.

Interactions between a polygenic risk score for plasma docosahexaenoic fatty acid concentration, eating behaviour, and body composition in children.

The relationship between eating behaviour and current body weight has been described. However little is known about the effect of polyunsaturated fatty acids (PUFA) in this relationship. Genetic contribution to a certain condition is derived from a combination of small effects from many genetic variants, and polygenic risk scores (PRS) summarize these effects. A PRS based on a GWAS for plasma docosahexaenoic fatty acid (DHA) has been created, based on SNPs from 9 genes. To analyze the interaction between the PRS for plasma DHA concentration, body composition and eating behaviour (using the Children Eating Behaviour Questionnaire) in childhood. We analyzed a subsample of children from the Maternal, Adversity, Vulnerability and Neurodevelopment (MAVAN) cohort with PRS and measurements of eating behaviour performed at 4 years of age (n = 210), 6 y (n = 177), and body fat determined by bioelectric impedance at 4 y and 6 y or by air displacement plethysmography and dual-energy X-ray absorptiometry at 8 y (n = 42 and n = 37). PRS was based on the GWAS from Lemaitre et al. 2011 (p threshold = p < 5*10-6), and a median split created low and high PRS groups (high PRS = higher DHA level). In ALSPAC children, we observed an association between PRS and plasma DHA concentration (β = 0.100, p < 0.01) and proportion (β = 0.107, p < 0.01). In MAVAN, there were interactions between PRS and body fat on pro-intake scores in childhood, in which low PRS and higher body fat were linked to altered behaviour. There were also interactions between PRS and pro-intake scores early in childhood on body fat later in childhood, suggesting that the genetic profile and eating behaviour influence the development of adiposity at later ages. A lower PRS (lower plasma PUFA) can be a risk factor for developing higher body fat associated with non-adaptive eating behaviour in childhood; it is possible that the higher PRS (higher plasma PUFA) is a protective feature.

Cognitive Development and Brain Gray Matter Susceptibility to Prenatal Adversities: Moderation by the Prefrontal Cortex Brain-Derived Neurotrophic Factor Gene Co-expression Network.

Background: Previous studies focused on the relationship between prenatal conditions and neurodevelopmental outcomes later in life, but few have explored the interplay between gene co-expression networks and prenatal adversity conditions on cognitive development trajectories and gray matter density.Methods: We analyzed the moderation effects of an expression polygenic score (ePRS) for the Brain-derived Neurotrophic Factor gene network (BDNF ePRS) on the association between prenatal adversity and child cognitive development. A score based on genes co-expressed with the prefrontal cortex (PFC) BDNF was created, using the effect size of the association between the individual single nucleotide polymorphisms (SNP) and the BDNF expression in the PFC. Cognitive development trajectories of 157 young children from the Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN) cohort were assessed longitudinally in 4-time points (6, 12, 18, and 36 months) using the Bayley-II mental scales.Results: Linear mixed-effects modeling indicated that BDNF ePRS moderates the effects of prenatal adversity on cognitive growth. In children with high BDNF ePRS, higher prenatal adversity was associated with slower cognitive development in comparison with those exposed to lower prenatal adversity. Parallel-Independent Component Analysis (pICA) suggested that associations of expression-based SNPs and gray matter density significantly differed between low and high prenatal adversity groups. The brain IC included areas involved in visual association processes (Brodmann area 19 and 18), reallocation of attention, and integration of information across the supramodal cortex (Brodmann area 10).Conclusion: Cognitive development trajectories and brain gray matter seem to be influenced by the interplay of prenatal environmental conditions and the expression of an important BDNF gene network that guides the growth and plasticity of neurons and synapses.

Early Life Adversity and Polygenic Risk for High Fasting Insulin Are Associated With Childhood Impulsivity.

While the co-morbidity between metabolic and psychiatric behaviors is well-established, the mechanisms are poorly understood, and exposure to early life adversity (ELA) is a common developmental risk factor. ELA is associated with altered insulin sensitivity and poor behavioral inhibition throughout life, which seems to contribute to the development of metabolic and psychiatric disturbances in the long term. We hypothesize that a genetic background associated with higher fasting insulin interacts with ELA to influence the development of executive functions (e.g., impulsivity in young children). We calculated the polygenic risk scores (PRSs) from the genome-wide association study (GWAS) of fasting insulin at different thresholds and identified the subset of single nucleotide polymorphisms (SNPs) that best predicted peripheral insulin levels in children from the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort [N = 467; pt– initial = 0.24 (10,296 SNPs), pt– refined = 0.05 (57 SNPs)]. We then calculated the refined PRS (rPRS) for fasting insulin at this specific threshold in the children from the Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN) cohort and investigated its interaction effect with adversity on an impulsivity task applied at 36 months. We found a significant effect of interaction between fasting insulin rPRS and adversity exposure predicting impulsivity measured by the Snack Delay Task at 36 months [β = −0.329, p = 0.024], such that higher PRS [β = −0.551, p = 0.009] was linked to more impulsivity in individuals exposed to more adversity. Enrichment analysis (MetaCoreTM) of the SNPs that compose the fasting insulin rPRS at this threshold was significant for certain nervous system development processes including dopamine D2 receptor signaling. Additional enrichment analysis (FUMA) of the genes mapped from the SNPs in the fasting insulin rPRS showed enrichment with the accelerated cognitive decline GWAS. Therefore, the genetic background associated with risk for adult higher fasting insulin moderates the impact of early adversity on childhood impulsivity.

597 Sleep Bruxism in Preschool Children: Associations with Emotional-Behavioral Problems

Abstract Introduction Several psychosocial factors contribute to the etiology of sleep bruxism in childhood, including emotional-behavioral problems, as well as environmental and familial factors. It is known that sleep bruxism is prevalent in preschoolers, but most etiology studies were conducted with school-aged children or adolescents. Studies focusing on younger, preschool-aged populations that consider family-related factors are lacking. This study aimed to assess the relationship between emotional-behavioral problems and the presence of sleep bruxism in preschoolers, while taking maternal depressive symptoms into consideration. Methods Three hundred eighty-three mother-child dyads from the Maternal Adversity, Vulnerability, and Neurodevelopment (MAVAN) cohort were included in the present study. Mothers completed the Child’s Sleep Habits Questionnaires (CSHQ; includes the frequency of bruxism), a questionnaire about their child’s emotional-behavioral problems (CBCL; anxiety and depressive problems), and reported their own depressive symptoms (CES-D). Measures were completed at two timepoints: when children were 4 and 5 years old. Generalized Estimating Equation (GEE) models were used to evaluate the relationship between sleep bruxism frequency and children’s emotional-behavioral problems, while controlling for maternal depressive symptoms, child’s biological sex, family socioeconomic status, and age. Results Maternal reports indicated that 12% of children experienced sleep bruxism at least sometimes at age four, and 20% did at age five. Children’s anxiety and depressive symptoms were associated with increased sleep bruxism frequency (p &amp;lt; 0.05). Associations between children’s emotional-behavioral problems and bruxism remained statistically significant when controlling for maternal depressive symptoms, child’s biological sex, family socioeconomic status, and time (p &amp;lt; 0.05). Conclusion In this normative cohort of children, sleep bruxism was associated with anxiety and depressive symptoms in children as young as age four. Furthermore, this relationship can still be observed when the severity of maternal depressive symptoms is considered. Whether anxiety and depressive symptoms contribute to sleep bruxism, or vice versa, remain to be further investigated. Nevertheless, results suggest that screening of emotional-behavioral problems should be considered in children experiencing sleep bruxism. Support (if any) Fonds de recherche du Québec - Santé

DCC gene network in the prefrontal cortex is associated with total brain volume in childhood.

BackgroundGenetic variation in the guidance cue DCC gene is linked to psychopathologies involving dysfunction in the prefrontal cortex. We created an expression-based polygenic risk score (ePRS) based on the DCC coexpression gene network in the prefrontal cortex, hypothesizing that it would be associated with individual differences in total brain volume.MethodsWe filtered single nucleotide polymorphisms (SNPs) from genes coexpressed with DCC in the prefrontal cortex obtained from an adult postmortem donors database (BrainEAC) for genes enriched in children 1.5 to 11 years old (BrainSpan). The SNPs were weighted by their effect size in predicting gene expression in the prefrontal cortex, multiplied by their allele number based on an individual’s genotype data, and then summarized into an ePRS. We evaluated associations between the DCC ePRS and total brain volume in children in 2 community-based cohorts: the Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN) and University of California, Irvine (UCI) projects. For comparison, we calculated a conventional PRS based on a genome-wide association study of total brain volume.ResultsHigher ePRS was associated with higher total brain volume in children 8 to 10 years old (β = 0.212, p = 0.043; n = 88). The conventional PRS at several different thresholds did not predict total brain volume in this cohort. A replication analysis in an independent cohort of newborns from the UCI study showed an association between the ePRS and newborn total brain volume (β = 0.101, p = 0.048; n = 80). The genes included in the ePRS demonstrated high levels of coexpression throughout the lifespan and are primarily involved in regulating cellular function.LimitationsThe relatively small sample size and age differences between the main and replication cohorts were limitations.ConclusionOur findings suggest that the DCC coexpression network in the prefrontal cortex is critically involved in whole brain development during the first decade of life. Genes comprising the ePRS are involved in gene translation control and cell adhesion, and their expression in the prefrontal cortex at different stages of life provides a snapshot of their dynamic recruitment.

General psychopathology, internalising and externalising in children and functional outcomes in late adolescence.

BackgroundInternalising and externalising problems commonly co‐occur in childhood. Yet, few developmental models describing the structure of child psychopathology appropriately account for this comorbidity. We evaluate a model of childhood psychopathology that separates the unique and shared contribution of individual psychological symptoms into specific internalising, externalising and general psychopathology factors and assess how these general and specific factors predict long‐term outcomes concerning criminal behaviour, academic achievement and affective symptoms in three independent cohorts.MethodsData were drawn from independent birth cohorts (Avon Longitudinal Study of Parents and Children (ALSPAC), N = 11,612; Generation R, N = 7,946; Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN), N = 408). Child psychopathology was assessed between 4 and 8 years using a range of diagnostic and questionnaire‐based measures, and multiple informants. First, structural equation models were used to assess the fit of hypothesised models of shared and unique components of psychopathology in all cohorts. Once the model was chosen, linear/logistic regressions were used to investigate whether these factors were associated with important outcomes such as criminal behaviour, academic achievement and well‐being from late adolescence/early adulthood.ResultsThe model that included specific factors for internalising/externalising and a general psychopathology factor capturing variance shared between symptoms regardless of their classification fits well for all of the cohorts. As hypothesised, general psychopathology factor scores were predictive of all outcomes of later functioning, while specific internalising factor scores predicted later internalising outcomes. Specific externalising factor scores, capturing variance not shared by any other psychological symptoms, were not predictive of later outcomes.ConclusionsEarly symptoms of psychopathology carry information that is syndrome‐specific as well as indicative of general vulnerability and the informant reporting on the child. The ‘general psychopathology factor' might be more relevant for long‐term outcomes than specific symptoms. These findings emphasise the importance of considering the co‐occurrence of common internalising and externalising problems in childhood when considering long‐term impact.

Alternating optimization for G × E modelling with weighted genetic and environmental scores: Examples from the MAVAN study.

Motivated by the goal of expanding currently existing Genotype × Environment interaction (G × E) models to simultaneously include multiple genetic variants and environmental exposures in a parsimonious way, we developed a novel method to estimate the parameters in a G × E model, where G is a weighted sum of genetic variants (genetic score) and E is a weighted sum of environments (environmental score). The approach uses alternating optimization, an iterative process where the genetic score weights, the environmental score weights, and the main model parameters are estimated in turn, assuming the other parameters are constant. This technique can be used to construct relatively complex interaction models that are constrained to a particular structure, and hence contain fewer parameters. We present the model as a 2-way interaction longitudinal mixed model, for which ordinary linear regression is a special case, but it can easily be extended to be compatible with k-way interaction models and generalized linear mixed models. The model is implemented in R (LEGIT package) and using SAS macros (LEGIT_SAS). Through simulations, we demonstrate the power and validity of this approach even with small sample sizes. Furthermore, we present examples from the Maternal Adversity, Vulnerability, and Neurodevelopment (MAVAN) study where we improve significantly upon already existing models using alternating optimization. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Association Between Repeated Episodes of Gastroenteritis and Mental Health Problems in Childhood and Adolescence.

The Avon Longitudinal Study of Parents and Children (ALSPAC) and Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN) cohorts were used to determine whether repeated exposure to gastroenteritis in early life could predict risk for psychiatric problems in childhood and in ALSPAC adolescents. We determined whether inflammatory biomarkers moderated the association between repeated gastroenteritis and mental health in adolescents from ALSPAC. Episodes of gastroenteritis from birth to 30 and 36 months were reported by mothers. Psychological problems were assessed using the total difficulties and subscale scores on the Revised Rutter Parent Scale for Preschool Children at 42 months and the Strengths and Difficulties Questionnaire (SDQ) at 81 months in ALSPAC. Presence of psychiatric disorders at 15.5 years was assessed using the Development and Well-Being Assessment (DAWBA) in ALSPAC. In the MAVAN replication cohort, total difficulties were assessed on the SDQ at 60 and 72 months. Serum interleukin-6 (IL-6) and C-reactive protein (CRP) at 9.5 years and CRP at 15.5 years were measured in ALSPAC participants. Repeated gastroenteritis associated with the total difficulties score in ALSPAC and MAVAN children. The β values were small, indicating that the clinical relevance of these findings requires further investigation. Repeated gastroenteritis was significantly associated with an increased prevalence of externalizing disorders at age 15.5 years, but odds ratios were small. CRP or IL-6 at 9.5 years or CRP at 15.5 years did not significantly moderate the association between repeated gastroenteritis and prevalence of psychiatric disorders. Identifying factors associated with vulnerability to psychopathology is key to early identification of individuals at risk.

The early care environment and DNA methylome variation in childhood.

Prenatal adversity shapes child neurodevelopment and risk for later mental health problems. The quality of the early care environment can buffer some of the negative effects of prenatal adversity on child development. Retrospective studies, in adult samples, highlight epigenetic modifications as sentinel markers of the quality of the early care environment; however, comparable data from pediatric cohorts are lacking. Participants were drawn from the Maternal Adversity Vulnerability and Neurodevelopment (MAVAN) study, a longitudinal cohort with measures of infant attachment, infant development, and child mental health. Children provided buccal epithelial samples (mean age = 6.99, SD = 1.33 years, n = 226), which were used for analyses of genome-wide DNA methylation and genetic variation. We used a series of linear models to describe the association between infant attachment and (a) measures of child outcome and (b) DNA methylation across the genome. Paired genetic data was used to determine the genetic contribution to DNA methylation at attachment-associated sites. Infant attachment style was associated with infant cognitive development (Mental Development Index) and behavior (Behavior Rating Scale) assessed with the Bayley Scales of Infant Development at 36 months. Infant attachment style moderated the effects of prenatal adversity on Behavior Rating Scale scores at 36 months. Infant attachment was also significantly associated with a principal component that accounted for 11.9% of the variation in genome-wide DNA methylation. These effects were most apparent when comparing children with a secure versus a disorganized attachment style and most pronounced in females. The availability of paired genetic data revealed that DNA methylation at approximately half of all infant attachment-associated sites was best explained by considering both infant attachment and child genetic variation. This study provides further evidence that infant attachment can buffer some of the negative effects of early adversity on measures of infant behavior. We also highlight the interplay between infant attachment and child genotype in shaping variation in DNA methylation. Such findings provide preliminary evidence for a molecular signature of infant attachment and may help inform attachment-focused early intervention programs.

Once and again: Intergenerational transmission of parenting

IntroductionAnimal and human studies suggest that individual differences in maternal parenting behaviour are transmitted from one generation to the next.ObjectiveThis study aimed to examine potential psychosocial mechanisms underlying an intergenerational transmission of conceptualization of parenting, including affect, cognition, and parental support.MethodsIn a subsample of 201 first-time mothers participating in the Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN) project, we assessed maternal childhood rearing experiences, using the Parental Bonding Instrument and the Childhood Trauma Questionnaire. At 6 months postpartum, mothers completed questionnaires on parenting stress, symptoms of depression, internalization of maternal care regulation and current relationship with mother and father.ResultsWe found significant direct associations of maltreatment and rearing by the grandmother with parenting stress at 6 months. These associations were mediated through distinct psychosocial pathways: the association of maltreatment on higher parenting stress was fully mediated through more maternal symptoms of depression (z = 2.297; P = 022). The association between sub-optimal rearing provided by the mother and higher parenting stress was mediated through lower internalization of maternal care regulation (z = -2.155; P = 031) and to a lesser degree through more symptoms of depression (z = -1.842; P = 065). Finally, higher quality rearing by the grandfather was indirectly related to lower parenting stress through positive current relationship with the father (z = -2.617; P = 009).ConclusionsThere are distinct pathways by which early experiences manifest in parenting stress. By understanding the structure of dysregulated parenting, clinicians will have practical information to specifically target maternal motivation, social supports, and depressed mood to disrupt maladaptive parenting cognitions and practices.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Early adversity, symptoms of depression and breastfeeding

BackroundThere is considerable variation in the prevalence of breastfeeding, which allows for investigation of factors that influence the initiation and duration of breastfeeding and its association with well being of the mother infant dyad.AimsTo better understand factors that influence (1) maternal breastfeeding status and (2) the “effects” of breastfeeding on mothers and infants.MethodsParticipants (n = 170) derive from a longitudinal Canadian study “Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN)”, a project designed to understand the pre- and postnatal influences on maternal health and child social-emotional development. Mothers provided data on breastfeeding status, early life adversity, oxytocin gene and oxytocin gene receptor polymorphisms, depression/anxiety, infant temperament and maternal sensitivity.ResultsEarly life adversity associated with a shorter breastfeeding duration and higher maternal depression levels. The relation between mothers’ early adversity and the duration of breastfeeding was mediated by mothers’ depression level, but only in women carrying one variant of the oxytocin rs2740210 gene marker (CC genotype). Mothers who breastfeed at 3 months acted more sensitively towards their infants when they were 6 months old and they in turn had infants who at 18 months showed reduced negative affectivity.ConclusionWomen who have been exposed to early adversity are “living with the past” and they are, to certain extent, protected or more vulnerable to depression, depending on their genotype. Breastfeeding associated with higher maternal sensitivity, which associated with decreased negative emotionality in the infant at 18 months. Our results help to clarify associations between early life experiences, breastfeeding, and the mother-infant relationship.Disclosure of interestThe authors have not supplied their declaration of competing interest.

A DRD4 gene by maternal sensitivity interaction predicts risk for overweight or obesity in two independent cohorts of preschool children.

Recent evidence suggests that early exposure to low maternal sensitivity is a risk factor for obesity in children and adolescents. A separate line of study shows that the seven-repeat (7R) allele of the dopamine-4 receptor gene (DRD4) increases susceptibility to environmental factors including maternal sensitivity. The current study integrates these lines of work by examining whether preschoolers carrying the 7R allele are more vulnerable to low maternal sensitivity as it relates to overweight/obesity risk. The Maternal Adversity Vulnerability and Neurodevelopment (MAVAN) project in Canada was used as the discovery cohort (N=203), while the Generation R study in the Netherlands was used as a replication sample (N=270). Regression models to predict both continuous BMI z-scores and membership in any higher BMI category based on established World Health Organization (WHO) cutoffs for 48months of age were completed. In both cohorts, there was a significant maternal sensitivity by DRD4 by sex interaction predicting higher body mass indices and/or obesity risk. As hypothesized, post hoc testing revealed an inverse relationship between maternal sensitivity and body mass indices in 7R allele carriers relative to noncarriers. This finding was strongest in girls in the Canadian cohort and in boys in the Dutch cohort. Many children who carry the 7R allele of DRD4 appear to be more influenced by maternal sensitivity as it relates to overweight/obesity risk, consistent with a plasticity effect. Given the relatively small sample sizes available for these analyses, further replications will be needed to confirm and extend these results.

Preschool Children Without 7-repeat DRD4 Gene More Likely to Develop Disorganized Attachment Style

&#x0D; &#x0D; &#x0D; &#x0D; Background: A disorganized attachment style is characterized by fearful and disoriented behaviours when a child is separated from their caregiver. Its presence is an early predictor of the later development of psychopathology, including depression. This study seeks to determine the effects of one environmental factor - the incidence of low birth weight - and one genetic factor - the presence of the long (7-repeat) polymorphism of the dopamine D4 receptor (DRD4) gene - on the development of disorganized attachment between the child and the mother.&#x0D; Methods: We sampled 251 mother-child dyads from the Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN) project. We measured birth weight and DRD4 genotype, and assessed attachment style using modified separation-reunion procedure.&#x0D; Results: Birth weight did not have a significant effect on disorganized attachment (b=-0.001, t(230)=0.006, p=0.910). Presence of DRD4 7-repeat polymorphism had a significant negative effect on presence of disorganized attachment style (b=-1.196, t(230)=0.411, p=0.004).&#x0D; Conclusion: Children without the DRD4 7-repeat allele were more likely to display a disorganized attachment style compared to children with the DRD4 7-repeat allele. This indicates that the 7-repeat allele of the DRD4 gene may serve as a protective factor against disorganized attachment.&#x0D; &#x0D; &#x0D; &#x0D;

Establishment and consolidation of the sleep-wake cycle as a function of attachment pattern

The development of sleep-wake regulation in infants depends upon brain maturation as well as various environmental factors. The aim of the present study was to evaluate sleep duration and quality as a function of child attachment to the mother. One hundred and thirty-four mother–child dyads enrolled in the Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN) project were included in this study. Attachment was assessed with the Strange Situation procedure at 36 months and maternal sleep reports were collected at 6, 12, 24 and 36 months. Differences in sleep characteristics were assessed with mixed models with one factor (attachment group) and one repeated measure (age). Children classified as disorganized had a significantly lower duration of nocturnal sleep, went to bed later, signaled more awakenings, had shorter periods of uninterrupted sleep (only at 12 months) and had shorter periods of time in bed (only at 6 months) than children classified as secure and/or ambivalent (p < 0.05). This is the first study to show that children with insecure disorganized attachment present a distinct sleep pattern in comparison with those with secure or ambivalent attachment between 6 and 36 months of age. Sleep disturbances could exacerbate difficulties in these families that are already considered vulnerable.

The maternal adversity, vulnerability and neurodevelopment project: theory and methodology.

To describe the theory and methodology of the multi-wave, prospective Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN) study. The goal of MAVAN is to examine the pre- and postnatal influences, and their interaction, in determining individual differences in mental health. MAVAN is a community-based, birth cohort study of pregnant Canadian mothers and their offspring. Dyads are assessed longitudinally, with multiple assessments of both mother and child in home and laboratory across the child's development. Study measures, including assessments of cognitive and emotional function, are described. The study uses a candidate gene approach to examine gene-environment interdependence in specific developmental outcomes. Finally, the study includes measures of both brain-based phenotypes and metabolism to explore comorbidities associated with child obesity. One of the unique features of the MAVAN protocol is the extensive measures of the mother-child interaction. The relation between these measures will be discussed. Evidence from the MAVAN project shows interesting results about maternal care, families, and child outcomes. In our review, preliminary analyses showing the correlations between measures of maternal care are reported. As predicted, early evidence suggests that maternal care measures are positively correlated, over time. This review provides evidence for the feasibility and value of laboratory-based measures embedded within a longitudinal birth cohort study. Though retention of the samples has been a challenge of MAVAN, they are within a comparable range to other studies of this nature. Indeed, the trade-off of somewhat greater participant burden has allowed for a rich database. The results yielded from the MAVAN project will not only describe typical development but also possible targets for intervention. Understanding certain endophenotypes will shed light on the pathogenesis of various mental and physical disorders, as well as their interrelation.

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

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. 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. Prenatal depression and 5-HTTLPR interacted to predict dysregulation from 3 to 36 months, within a model of strong differential susceptibility. 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.

Maternal Anxiety and Breastfeeding

Maternal anxiety and depression may impair maternal intention, motivation, and self-efficacy in multiple domains associated with child health including breastfeeding. We tested the hypothesis that mothers who experience substantial anxiety during pregnancy or the postpartum period are at increased risk for reduced initiation, exclusivity, and continuation of breastfeeding. We obtained data on 255 Canadian pregnant women from the Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN) study recruited between June 2004 and February 2009. We utilized data collected from 18 to 23 weeks gestation through 12 months postpartum. Multivariate logistic regression was used to assess whether scores on the Hamilton Anxiety Scale (HAM-A) and State-Trait Anxiety Inventory (STAI) were associated with initiation, exclusivity, and continuation of breastfeeding. Prenatal anxiety was not associated with breastfeeding outcomes. In adjusted models, a single point increase in HAM-A scores at 3 months postpartum was associated with an 11% reduction in the odds of exclusive breastfeeding at 6 months (adjusted odds ratio [aOR] = 0.89; 95% CI, 0.80-0.99). A single point increase in STAI State and STAI Trait scores at 3 months postpartum was associated with a 4% (aOR = 0.96; 95% CI, 0.92-0.99) and 7% (aOR = 0.93; 95% CI, 0.86-1.00) reduction, respectively, in the odds of any breastfeeding at 12 months. Our findings suggest a relationship between maternal anxiety and reduced exclusivity and continuation of breastfeeding. Maternal anxiety should be actively monitored and managed appropriately in the postpartum period to support optimal breastfeeding practices.

The Effect of Maternal Anxiety/Depression on Breastfeeding Outcomes: MAVAN (Maternal Adversity Vulnerability and Neurodevelopment) Study

ObjectivesWe tested the hypothesis that mothers who experience substantial anxiety or depression at different time periods are at risk for reduced initiation, exclusivity and duration of breastfeeding.MethodsLongitudinal data on mental health and infant feeding were collected on 257 Canadian women from 18–23 weeks gestation through 12 months postpartum. Multivariate logistic regression was used to assess whether scores on the Edinburgh Post‐Natal Depression Scale (EPDS), Hamilton Anxiety Scale (HAMA) and State‐Trait Anxiety Inventory (STAI) were associated with breastfeeding practices.ResultsIn adjusted models, a single point increase in HAMA scores measured at 3 months postpartum was associated with an 11% reduction in the odds of exclusively breastfeeding at 6 months [aOR= 0.89, 95% (CI 0.80, 0.99)]; also a single point increase in STAI State and STAI Trait scores measured at 3 months postpartum was associated with a 4% reduction in odds [aOR= 0.96, 95% CI (0.92, 0.99)] and an 8% reduction in the odds of any breastfeeding at 12 months [aOR= 0.929, 95% CI (0.86, 1.00) ] respectively.ConclusionOur findings support a relationship between maternal anxiety and reduced breastfeeding but do not show significant associations between maternal depression and breastfeeding practices. Small sample sizes may have limited detection of significant findings.Grant Funding Source: None