Andrée-Anne Bouvette-Turcot

Maternal childhood adversity and child temperament: An association moderated by child 5-HTTLPR genotype

We examined transgenerational effects of maternal childhood adversity on child temperament and a functional promoter polymorphism, 5‐HTTLPR, in the serotonin‐transporter gene (SLC6A4) as potential moderators of such maternal influences in 154 mother–child dyads, recruited into a longitudinal birth cohort study. We examined the interactive effects of maternal childhood experience using an integrated measure derived from Childhood Trauma Questionnaire (CTQ) and Parental Bonding Index (PBI). Triallelic genotyping of 5‐HTTLPR was performed. A measure of ‘negative emotionality/behavioural dysregulation’ was derived from the Early Childhood Behaviour Questionnaire at 18 and 36 months. Negative emotionality/behavioural dysregulation was highly stable between 18 and 36 months and predicted psychosocial problems at 60 months. After controlling multiple demographics as well as both previous and concurrent maternal depression there was a significant interaction effect of maternal childhood adversity and offspring 5‐HTTLPR genotype on child negative emotionality/behavioural dysregulation (β = 1.03, t11,115 = 2.71, P < .01). The results suggest a transgenerational effect of maternal developmental history on emotional function in the offspring, describing a pathway that likely contributes to the familial transmission of vulnerability for psychopathology.

Attachment disorganization among children in Neonatal Intensive Care Unit: Preliminary results

BACKGROUND Preterm children have been reported to be at higher risk to develop attachment insecurity. AIMS The present study aimed to investigate potential differences in attachment security between newborns who were sent to Neonatal Intensive Care Unit (NICU) and those who were not, in a population of full-term children. STUDY DESIGN Participants (162 mother-child dyads) were part of a longitudinal study (MAVAN). Twenty-three of these children received special care at birth (NICU group). Attachment security was assessed at 36 months with the Strange Situation Procedure. Socio-economic status (SES), birth weight, maternal mood, maternal sensitivity, mental/psychomotor developmental indexes, Apgar scores, presence of complications during delivery and infant general health were assessed. RESULTS In the No-NICU group, 55.4% of children were securely attached, 24.5% were insecure and 20.1% were disorganized. However, in the NICU group, 43.5% of children were securely attached, 8.7% were insecure and 47.8% were disorganized (χ(2)=9.0; p=.01). The only differences between the 2 groups were a lower Apgar, more respiratory infections and more visits to walk-in clinic/hospital (ps<.05) and a trend for lower SES and more ear infections in the NICU group. Logistic regressions revealed an odds ratio of 6.1 (p=.003) of developing a disorganized attachment after a stay in NICU, when controlling for these confounding variables. CONCLUSION Newborns who were admitted to NICU have an odds ratio of about 6 to develop a disorganized attachment at 36 months. These preliminary results support the importance of supportive parental proximity and contact with the infant in the NICU and possible after-care.

Effects of Genotype and Sleep on Temperament.

BACKGROUND AND OBJECTIVES: Sleep problems are frequent in young children; however, children vary in the degree to which they are affected by poor sleep quality. We investigated whether a polymorphism in the serotonin transporter gene, which is linked to emotional function, is a potential moderator of the influences of sleep duration on infant temperament using longitudinal data. METHODS: We examined the interactive effects of average sleep duration between 6 and 36 months of age and the 5-HTTLPR genotype on negative emotionality/behavioral dysregulation at 36 months in 209 children recruited into a longitudinal birth cohort study. Triallelic genotyping of 5-HTTLPR was performed by looking at SLC6A4 genotype, focusing on the serotonin transporter-linked polymorphic region (5-HTTLPR) including the SNP polymorphism (rs23351). Child sleep habits were assessed with a maternal self-report questionnaire. RESULTS: After controlling for demographics and both previous and concurrent maternal depression, multiple linear regression analyses revealed a significant interaction effect of average sleep duration for the first 3 years of life and 5-HTTLPR genotype on child negative emotionality/behavioral dysregulation such that the effects were exclusive to those with low-expressing 5-HTTLPR genotypes. CONCLUSIONS: The results suggest differential susceptibility to the effect of sleep duration early in life, which reiterates that the short allele of the 5-HTTLPR represents a marker of increased environmental sensitivity regarding emotional development. Differential susceptibility theory posits that certain factors may increase an individual’s susceptibility to the environment, in either a positive or negative fashion.

The joint contribution of maternal history of early adversity and adulthood depression to socioeconomic status and potential relevance for offspring development

BACKGROUND We examined the interactive effects of maternal childhood adversity and later adulthood depression on subsequent socioeconomic status (SES). METHODS Our community sample ranged from 230 to 243 mothers (across measures) drawn from a prospective, longitudinal cohort study. Maternal childhood adversity scores were derived using an integrated measure derived from the Childhood Trauma Questionnaire (CTQ) and the Parental Bonding Index (PBI). Maternal depression was measured in the prenatal period with the Center for Epidemiologic Studies Depression Scale (CES-D). SES measures included maternal highest level of education and family income as obtained prenatally. RESULTS The analyses yielded significant interaction effects between maternal childhood adversity and prenatal depression that predicted income, prenatally. Women who reported higher levels of childhood adversity combined with higher levels of self-reported depressive symptoms were significantly more likely to live in low SES environments. Results also showed that level of education was predicted by childhood adversity independent of maternal symptoms of depression. CONCLUSION The results suggest that SES is influenced by a life course pathway that begins in childhood and includes adversity-related mental health outcomes. Since child health and development is influenced by both maternal mental health and SES, this pathway may also contribute to the intergenerational transmission of the risk for psychopathology in the offspring. The results also emphasize the importance of studying potential precursors of low SES, a well-documented environmental risk factor for poor developmental outcomes in the offspring.

Prenatal maternal depression and child serotonin transporter linked polymorphic region (5-HTTLPR) and dopamine receptor D4 (DRD4) genotype predict negative emotionality from 3 to 36 months.

Prenatal maternal depression and a multilocus genetic profile of two susceptibility genes implicated in the stress response were examined in an interaction model predicting negative emotionality in the first 3 years. In 179 mother-infant dyads from the Maternal Adversity, Vulnerability, and Neurodevelopment cohort, prenatal depression (Center for Epidemiologic Studies Depressions Scale) was assessed at 24 to 36 weeks. The multilocus genetic profile score consisted of the number of susceptibility alleles from the serotonin transporter linked polymorphic region gene (5-HTTLPR): no long-rs25531(A) (LA: short/short, short/long-rs25531(G) [LG], or LG/LG] vs. any LA) and the dopamine receptor D4 gene (six to eight repeats vs. two to five repeats). Negative emotionality was extracted from the Infant Behaviour Questionnaire-Revised at 3 and 6 months and the Early Child Behavior Questionnaire at 18 and 36 months. Mixed and confirmatory regression analyses indicated that prenatal depression and the multilocus genetic profile interacted to predict negative emotionality from 3 to 36 months. The results were characterized by a differential susceptibility model at 3 and 6 months and by a diathesis-stress model at 36 months.

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.

Examining the Interface of Children’s Sleep, Executive Functioning, and Caregiving Relationships: A Plea Against Silos in the Study of Biology, Cognition, and Relationships

Research in developmental psychology is increasingly showing that children’s biology, cognition, and social relationships, which have often been studied separately, are in fact closely tied and influence each other in complex ways. This article summarizes work by our team and others on the connections among young children’s sleep, their executive functioning, and the quality of their caregiving relationships. Overall, children exposed to higher-quality parenting perform better on executive tasks and get sleep of higher quality or duration. In turn, sleep relates to subsequent executive performance, while also modulating the links between parenting and child outcomes. We propose directions for future research to address causal relations and to better pinpoint the direction and magnitude of the associations between these areas of child development.

Epigenetics and Early Life Adversity: Current Evidence and Considerations for Epigenetic Studies in the Context of Child Maltreatment

The association between early childhood adversity and later risk of mental disorders is well established. The mechanisms by which signals from the early environment are transmitted to the neonate and shape mental health are beginning to be understood. Chemically stable, epigenetic modifications, such as DNA methylation, have emerged as putative mechanisms for the enduring effects of the early social environment on neural development and function. In this chapter, we review data from both preclinical models and clinical studies of early adversity and epigenetic mechanisms. Specifically, we examine the mechanism of DNA methylation, which may mediate the lasting effects of early adversity on later mental health.

Maternal early life adversities and the offspring's epigenome: A M.A.V.A.N. project

Overexposure of the developing fetus to glucocorticoids is a key mechanism linking early development with later life disease. In humans low birthweight, a marker of an adverse in utero environment, associates with increased fasting cortisol, increased hypothalamic-pituitary-adrenal (HPA) axis reactivity and with cardiovascular risk factors, cardiovascular disease and poorer cognitive function. Animal models suggest the HPA axis of female offspring is more susceptible to programming insults. We hypothesised that there would be similar sex differences in humans. We carried out a systematic review, searching Embase, Medline and Web of Science up to June 2014. Two independent researchers screenedarticles for eligibility. The29 includedstudies investigated the consequences of maternal stressors of asthma, psychosocial stress and glucocorticoid medications on HPA axis outcomes of placental glucocorticoid biology, and HPA axis function in earlyand later-life. Overall, the studies reported sex differences such that female offspring were more responsive to stress both in earlyand later-life: females had lower birthweight, increased therapeutic responsiveness to glucocorticoids, increased diurnal cortisol secretion and HPA axis reactivity, compared to males. Further, in comparison to males, the female placenta increased its permeability to maternal glucocorticoids following maternal stress with downregulation of the enzyme 11-beta-hydroxysteroid dehydrogenase (which converts active cortisol to inactive cortisone) in response to maternal glucocorticoid exposure or maternal asthma. Theobservationsof increasedprogrammedvulnerabilityof theHPA axis in females is consistentwith data fromanimalmodels andmay be a mechanism underlying sex differences in later life diseases including depression and cardiometabolic disease.