The purpose of these studies was to examine mediation and moderation processes for the influence of early adversity and current stressful circumstances on maternal sensitivity. Evidence of mediation was found in Study 1 where maternal depression and mothers’ negative appraisal of their infant mediated the influence of early adversity and low family income on maternal sensitivity. Study 1 also examined the influence of the neighborhood. A moderate-mediation model was tested where the mediating influence afore-stated was hypothesized to vary across levels of neighborhood quality. Partial evidence of moderation was found. In the context of a high quality neighborhood, mothers’ early adversity was not associated with maternal depression. Across levels of neighborhood quality, complex relationships emerged between the variables low family income, maternal depression and mothers’ appraisal of infant temperament. In a context of low neighborhood quality, there was no evidence of a direct association between low family income and maternal sensitivity, rather, low family income operated indirectly through maternal depression. In a context of high neighborhood quality, there was evidence for a direct and indirect association between low family income and maternal sensitivity. Study 2 examined associations between variation in the Arginine Vasopressin 1a receptor gene (AVPR1a) and maternal sensitivity, and whether variation in this gene moderated the influence of mothers’ early adversity on sensitivity. Mothers homozygous for the long alleles of the RS3 microsatellite were significantly less sensitive than mothers heterozygous for the long alleles and those homozygous for the short alleles. Homozygosity for the RS3 long alleles moderated the influence of mothers’ early adversity on their sensitivity; the influence of early adversity on maternal sensitivity was most pronounced for mothers with the RS3 long/long genotype. These results suggest that variation in the AVPR1a gene may be important not only for human maternal behavior, but also for stress reactivity.

The purpose of these studies was to examine mediation and moderation processes for the influence of early adversity and current stressful circumstances on maternal sensitivity. Evidence of mediation was found in Study 1 where maternal depression and mothers’ negative appraisal of their infant mediated the influence of early adversity and low family income on maternal sensitivity. Study 1 also examined the influence of the neighborhood. A moderate-mediation model was tested where the mediating influence afore-stated was hypothesized to vary across levels of neighborhood quality. Partial evidence of moderation was found. In the context of a high quality neighborhood, mothers’ early adversity was not associated with maternal depression. Across levels of neighborhood quality, complex relationships emerged between the variables low family income, maternal depression and mothers’ appraisal of infant temperament. In a context of low neighborhood quality, there was no evidence of a direct association between low family income and maternal sensitivity, rather, low family income operated indirectly through maternal depression. In a context of high neighborhood quality, there was evidence for a direct and indirect association between low family income and maternal sensitivity. Study 2 examined associations between variation in the Arginine Vasopressin 1a receptor gene (AVPR1a) and maternal sensitivity, and whether variation in this gene moderated the influence of mothers’ early adversity on sensitivity. Mothers homozygous for the long alleles of the RS3 microsatellite were significantly less sensitive than mothers heterozygous for the long alleles and those homozygous for the short alleles. Homozygosity for the RS3 long alleles moderated the influence of mothers’ early adversity on their sensitivity; the influence of early adversity on maternal sensitivity was most pronounced for mothers with the RS3 long/long genotype. These results suggest that variation in the AVPR1a gene may be important not only for human maternal behavior, but also for stress reactivity.

abstract: Several decades of research have concluded that child social functioning is a critical predictor of wellbeing across various developmental domains. Most scientists agree that both genetic and environmental influences play defining roles in social behavior; the processes by which they concurrently affect child development, however, has been the subject of less research. This work examines distinct mechanisms that shape child prosociality by examining genetic and environmental influences on development, via two empirical studies. The first study analyzed the evocative-reactive and the evocative-socially-mediated hypotheses as gene-environment correlation (rGE) mechanisms connecting the arginine vasopressin receptor 1a (AVPR1a) and dopamine receptor D2 (DRD2) genes, child prosocial behavior, and parent differential treatment (PDT). Findings present modest evidence for the evocative-reactive rGE hypothesis; specifically, AVPR1a marginally influenced child prosociality, which subsequently predicted mother preference in adolescence. The second study examined several gene-environment interactions (GxEs) in exploring how social environmental variables- positive and negative parenting- predicted child prosociality, as moderated by socially-implicated child genes, DRD2 and dopamine receptor D4 (DRD4). Findings indicated that while positive parenting was predictive of child prosociality regardless of genetic variants, the effects of negative parenting on child prosociality were dependent on child genetic variants. Together, findings from these studies suggest modest genetic and environmental influences on child behavior in middle childhood and adolescence, consistent with previous research and theory. Directions for future research are offered, and intervention and policy implications are discussed. / Dissertation/Thesis / Ph.D. Family and Human Development 2013

abstract: The main objective of this study was to use a genetically-informative design to examine the putative influences of maternal perceived prenatal stress, obstetrical complications, and gestational age on infant dysregulation, competence, and developmental maturity. Specifically, whether or not prenatal and obstetrical environmental conditions modified the heritability of infant outcomes was examined. A total of 291 mothers were interviewed when their twin infants were 12 months of age. Pregnancy and twin birth medical records were obtained to code obstetrical data. Utilizing behavioral genetic models, results indicated maternal perceived prenatal stress moderated genetic and environmental influences on developmental maturity whereas obstetrical complications moderated shared environmental influences on infant competence and nonshared environmental influences on developmental maturity. Gestational age moderated the heritability and nonshared environment of infant dysregulation, shared and nonshared environmental influences on competence, and nonshared environmental influences on developmental maturity. Taken together, prenatal and obstetric conditions were important nonlinear influences on infant outcomes. An evolutionary perspective may provide a framework for these findings, such that the prenatal environment programs the fetus to be adaptive to current environmental contexts. Specifically, prenatal stress governs gene expression through epigenetic processes. Findings highlight the utility of a genetically informative design for elucidating the role of prenatal and obstetric conditions in the etiology of infant developmental outcomes. / Dissertation/Thesis / Ph.D. Psychology 2011

Contexte : Bien qu’il ait été proposé que l’exposition à un faible statut socioéconomique (SSE) familial altère l’activité de l’axe hypothalamo-pituito-surrénalien et sa production de l’hormone cortisol, les résultats actuels sont incohérents et suggèrent la présence de facteurs supplémentaires susceptibles de modifier ces associations. Pourtant, peu d’études à ce jour ont adopté une approche développementale sensible au timing, à la stabilité et aux changements au sein du SSE familial lors de l’étude de l’association liant le SSE au cortisol. En outre, peu de travaux empiriques ont évalué si cette association est non linéaire ou si elle est modulée par le soutien social. Enfin, rares sont les études qui ont examiné dans quelle mesure cette association est affectée par les facteurs génétiques et par les processus gène-environnement, notamment à l’adolescence. Objectifs : Ancré dans une perspective de psychopathologie développementale, l’objectif principal de cette thèse est d’examiner les processus gène-environnement impliqués dans les associations entre le SSE et divers indicateurs de sécrétion cortisolaire mesurés à l’adolescence. Cette thèse a également examiné dans quelle mesure ces associations sont affectées par le timing, la chronicité et les changements au sein du SSE familial et sont atténuées par le soutien social. Méthodes : Les participants proviennent de l’Étude des jumeaux nouveau-nés du Québec, un échantillon populationnel de jumeaux recrutés à la naissance. Le SSE familial a été recueilli au cours de la petite enfance (0-5 ans) et à la mi-adolescence (14 ans). Le soutien social a été rapporté par les jumeaux à l’âge de 14 et de 19 ans. Le cortisol diurne (n=569) a été mesuré à l’âge de 14 ans au réveil, 30 minutes plus tard, l’après-midi et le soir pendant quatre jours non consécutifs. Le cortisol capillaire (n=704) a été mesuré à l’âge de 19 ans. Résultats : Cette thèse est composée de trois articles. Les résultats des deux premiers articles indiquent que l’étiologie génétique du cortisol au réveil et capillaire fluctuent au long du continuum du SSE mesuré à la petite enfance. Les formes que prennent ces interactions gène-environnement sont toutefois distinctes pour ces indicateurs. De plus, nos résultats révèlent la présence d’associations uniques entre le SSE familial mesuré à la mi-adolescence et la plupart des indicateurs cortisolaire, soit suivant une relation linéaire, ou non linéaire. Nous avons également trouvé que l’association liant le SSE au cortisol capillaire n’est pas expliquée par une étiologie génétique commune, mais semble refléter les effets de l’environnement partagé par les jumeaux. Enfin, les résultats du troisième article suggèrent que l’effet synergique du SES familial mesuré à la petite enfance et à la mi-adolescence prédisent la sécrétion cortisolaire. De plus, l’association concomitante entre le SSE et le cortisol au réveil est modulée par le soutien social. Conclusions : Collectivement, ces résultats soulignent l’importance d’adopter une approche développementale et génétiquement informative lors de l’étude de l’association liant l’adversité aux systèmes physiologiques de stress. Un tel examen pourrait contribuer à une meilleure compréhension des mécanismes sous-tendant les disparités socioéconomiques précoces documentées en matière de santé, d’apprentissage et de comportements. / Background: While exposure to lower family socioeconomic status (SES) has been proposed to induce alterations in hypothalamic-pituitary-adrenal (HPA) axis activity and its production of the hormone cortisol, existing findings are inconsistent and suggest the presence of additional factors that may modify these associations. Yet, few of the past studies have taken a developmental approach sensitive to the timing, stability, and change within family SES when investigating the association between SES and cortisol secretion. Furthermore, little empirical attention has been devoted to assessing the possibility that this association might be nonlinear or is modulated by youth’s perceived availability of social support. Lastly, the extent to which this association is affected by genetic factors as well as gene-environmental interplays has seldom been investigated, particularly in adolescence. Objectives: Rooted in a developmental psychopathology perspective, the present thesis’s main objective is to examine the gene-environment processes implicated in the associations of family SES with multiple indicators of cortisol secretion during adolescence. This thesis also investigated to what extent these associations are affected by the timing, chronicity and change in SES and buffered by perceived social support. Methods: Participants are from the Québec Newborn Twin Study, a population-based sample of twin pairs recruited at birth. Family SES was collected in early childhood (ages 0–5) and mid-adolescence (age 14). Perceived social support was reported by twins at aged 14 and 19. Diurnal cortisol (n=569) was measured at age 14 at awakening, 30 min later, in the afternoon and evening over four non-consecutive days. Hair cortisol (n=704) was measured at age 19. Results: This thesis is comprised of three articles. The results of the first two papers indicate that the genetic etiology of adolescence awakening cortisol and HCC fluctuated along the continuum of early childhood family SES. The patterns of these gene-environment interactions were, however, distinct for these indicators. Furthermore, our results pointed to unique associations between mid-adolescence family SES and most of the diurnal and hair cortisol indicators, either according to a linear or nonlinear function. We also found that the association linking mid-adolescence family SES to HCC is not explained by a common genetic etiology but appears to reflect shared environmental effects. Finally, the results of the third paper revealed that the synergistic effect of early childhood and mid-adolescence SES predicted cortisol secretion. Moreover, the concomitant association between SES and awakening cortisol was found to be modulated by mid-adolescence social support. Conclusions: Collectively, these findings underscore the necessity of espousing a developmental and genetically sensitive approach in studies investigating the impact of adversity on stress physiological systems. Such investigations may pave the way to a fuller understanding of the mechanisms underlying the early roots of socioeconomic disparities in health, learning and behaviours.