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Early Adversity, Symptoms of Depression and Breastfeeding
- W. Jonas, A. Fleming, M. Steiner, M.J. Meaney, L. Atkinson, V. Mileva, M. Sokolowski, J. Kennedy
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- Journal:
- European Psychiatry / Volume 41 / Issue S1 / April 2017
- Published online by Cambridge University Press:
- 23 March 2020, p. S30
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Backround
There 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.
Once and Again: Intergenerational Transmission of Parenting
- K. Tombeau Cost, E. Unternaehrer, W. Jonas, H. Gaudreau, A.A. Bouvette-Tourcot, M. Steiner, J. Lydon, P. Szatmari, M. Meaney, A. Fleming
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- Journal:
- European Psychiatry / Volume 41 / Issue S1 / April 2017
- Published online by Cambridge University Press:
- 23 March 2020, p. S30
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Introduction
Animal 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.
5 - Developmental Origins of Neurobiological Vulnerability for PTSD
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- By Rosemary Bagot, Graduate student Neuroscience, McGill University, Montréal, Québec, Carine Parent, Graduate student Neurological Sciences Program, McGill University, Montréal, Québec, Timothy W. Bredy, Postdoctoral Fellow Department of Psychiatry and Biobehavioral Sciences and Brain Research Institute, University of California, Los Angeles, Tieyuan Zhang, Postdoctoral Fellow Program for the Study of Behaviour, Genes and Environment, McGill University, Montréal, Québec, Alain Gratton, Associate Professor Department of Psychiatry, McGill University; Researcher, Douglas Hospital Research Centre, Montréal, Québec, Michael J. Meaney, James McGill Professor of Medicine Departments of Psychiatry and Neurology and Neurosurgery; Director Program for the Study of Behaviour, Genes and Environment, McGill University; Associate Director of Research Researcher, Douglas Hospital Research Centre, Montréal, Québec
- Edited by Laurence J. Kirmayer, McGill University, Montréal, Robert Lemelson, University of California, Los Angeles, Mark Barad, University of California, Los Angeles
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- Book:
- Understanding Trauma
- Published online:
- 27 July 2009
- Print publication:
- 15 January 2007, pp 98-117
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Summary
The question of vulnerability lies very much at the heart of research on anxiety disorders, such as PTSD (Yehuda, Schmeidler, Wainberg, Binder-Brynes, & Duvdevani, 1998). Surprisingly, only a minority (∼25–30%) of humans subjected to even such a profound trauma as rape develop PTSD (Ressnick, Kilpatrick, Dansky, Saunders, & Best, 1993), and early family life serves as a highly significant predictor of vulnerability to PTSD following trauma (Udwin, Boyle, Yule, Bolton, & O'Ryan, 2000). Moreover, many cases of PTSD derive from events that might not be considered as necessarily traumatic by the general population (Breslau et al., 1998), a finding that further underscores the importance of vulnerability. Moreover, there is evidence for the familial transmission of vulnerability to PTSD that is related to alterations in parent–offspring interactions. These findings are not surprising because anxiety reduces parental responsiveness to offspring (e.g., Fleming, 1988, 1999). These findings suggest that early life events might alter the development of neural systems that mediate cognitive and emotional responses to trauma, and thus contribute to individual differences in vulnerability to PTSD.
The question can be rendered more precise in light of the remarkable advances in human clinical studies. First, PTSD research suggests that the probability of chronic PTSD following trauma is related to the magnitude of the initial reaction to the event (Shalev, this volume). Hence, factors that influence the development of individual differences in reactivity are likely of considerable relevance.
Fine-structure molecular epidemiological analysis of Staphylococcus aureus recovered from cows
- J. R. FITZGERALD, W. J. MEANEY, P. J. HARTIGAN, C. J. SMYTH, V. KAPUR
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- Journal:
- Epidemiology & Infection / Volume 119 / Issue 2 / October 1997
- Published online by Cambridge University Press:
- 01 October 1997, pp. 261-269
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Sixty-three Staphylococcus aureus isolates recovered from bovine sources in the USA and the Republic of Ireland were characterized by multilocus enzyme electrophoresis (MLEE), ribotyping, and random amplified polymorphic DNA polymerase chain reaction (RAPD–PCR) typing at two separate laboratories. The S. aureus isolates were assigned by MLEE to 10 electrophoretic types (ETs) (Index of Discrimination, D=0·779). In contrast, the same isolates were assigned to 13 ribotypes (D=0·888), and to 12 RAPD types (D=0·898). A common clone, ET3, of worldwide distribution, was represented by six distinct combinations of ribotypes and RAPD types. S. aureus clones recovered from cows in Ireland were also associated with mastitis in dairy cows in the USA. These findings are consistent with the hypothesis that only a few specialized clones of S. aureus are responsible for the majority of cases of bovine mastitis, and that these clones have a broad geographic distribution.