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Pope C.J.,Lakehead University | Mazmanian D.,Lakehead University | Bedard M.,Lakehead University | Sharma V.,Mood and Anxiety Program | Sharma V.,University of Western Ontario
Journal of Affective Disorders | Year: 2016

Background Risk and protective factors for postpartum depression have been extensively studied, and in recent studies an association between breastfeeding and maternal mood has been reported. The present retrospective, cross-sectional study was conducted to evaluate the association between breastfeeding-related variables and postpartum depression (based on Edinburgh Postnatal Depression Scale threshold criteria) within the context of other known risk factors. Method Breastfeeding information, demographic information, and scores on the Edinburgh Postnatal Depression Scale were examined from the Canadian Maternity Experience Survey. This survey contains data collected from 6421 Canadian mothers between October 2006 and January 2007, and 2848 women between five and seven months postpartum were included in the current analyses. Results In contrast to previous research, logistic regression analyses revealed that when considered within the context of other risk factors, breastfeeding attempt and duration were not associated with postpartum depression at five to seven months postpartum. Although a relationship between the prenatal intention to combination feed and postpartum depression was observed, these variables were no longer related once other potential risk factors were controlled for. Factors that were associated with postpartum depression included lower income, higher perceived stress, lower perceived social support, no history of depression, or no recent history of abuse. Limitations A clinical diagnostic instrument was not used and variable selection was restricted to data collected as part of this survey. Conclusion These findings suggest that the association between breastfeeding and postpartum depression reported by previous researchers may in fact be due to alternative risk factors. © 2016 Elsevier B.V. All rights reserved. Source

Byrne E.M.,University of Queensland | Byrne E.M.,Queensland Institute of Medical Research | Raheja U.K.,Mood and Anxiety Program | Stephens S.H.,Diabetes and Nutrition | And 19 more authors.
Journal of Clinical Psychiatry | Year: 2015

Objective: To test common genetic variants for association with seasonality (seasonal changes in mood and behavior) and to investigate whether there are shared genetic risk factors between psychiatric disorders and seasonality. Method: Genome-wide association studies (GWASs) were conducted in Australian (between 1988 and 1990 and between 2010 and 2013) and Amish (between May 2010 and December 2011) samples in whom the Seasonal Pattern Assessment Questionnaire (SPAQ) had been administered, and the results were meta-analyzed in a total sample of 4,156 individuals. Genetic risk scores based on results from prior large GWAS studies of bipolar disorder, major depressive disorder (MDD), and schizophrenia were calculated to test for overlap in risk between psychiatric disorders and seasonality. Results: The most significant association was with rs11825064 (P = 1.7 × 10-6, β = 0.64, standard error = 0.13), an intergenic single nucleotide polymorphism (SNP) found on chromosome 11. The evidence for overlap in risk factors was strongest for schizophrenia and seasonality, with the schizophrenia genetic profile scores explaining 3% of the variance in logtransformed global seasonality scores. Bipolar disorder genetic profile scores were also associated with seasonality, although at much weaker levels (minimum P value = 3.4 × 10-3), and no evidence for overlap in risk was detected between MDD and seasonality. Conclusions: Common SNPs of large effect most likely do not exist for seasonality in the populations examined. As expected, there were overlapping genetic risk factors for bipolar disorder (but not MDD) with seasonality. Unexpectedly, the risk for schizophrenia and seasonality had the largest overlap, an unprecedented finding that requires replication in other populations and has potential clinical implications considering overlapping cognitive deficits in seasonal affective disorders and schizophrenia. © Copyright 2014 Physicians Postgraduate Press, Inc. Source

Blair K.S.,Mood and Anxiety Program | Geraci M.,Mood and Anxiety Program | Hollon N.,Mood and Anxiety Program | Otero M.,Mood and Anxiety Program | And 5 more authors.
American Journal of Psychiatry | Year: 2010

Objective: Little is known about the neural underpinnings of generalized social phobia, which is defined by a persistent heightened fear of social disapproval. Using event-related functional MRI (fMRI), the authors examined whether the intent of an event, which mediates the neural response to social disapproval in healthy individuals, differentially affects response in generalized social phobia. Method: Sixteen patients with generalized social phobia and 16 healthy comparison subjects group-matched on age, gender, and IQ underwent fMRI scans while reading stories that involved neutral social events, unintentional social transgressions (e.g., choking on food at a party and coughing it up), or intentional social transgressions (e.g., disliking food at a party and spitting it out). Results: Significant group-by-transgression interactions were observed in ventral regions of the medial prefrontal cortex. Healthy individuals tended to show increased blood-oxygen-level-dependent responses to intentional relative to unintentional transgressions. Patients with generalized social phobia, however, showed significantly increased responses to the unintentional transgressions. They also rated the unintentional transgressions as significantly more embarrassing than did the comparison subjects. Results also revealed significant group main effects in the amygdala and insula bilaterally, reflecting elevated generalized social phobia responses in these regions to all event types. Conclusions: These results further implicate the medial prefrontal cortex in the pathophysiology of generalized social phobia, specifically through its involvement in distorted self-referential processing. These results also further underscore the extended role of the amygdala and insula in the processing of social stimuli more generally in generalized social phobia. Source

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