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The stress response has been linked to the expression of anxiety and depression, but the mechanisms for these connections are under continued consideration. The activation and expression of glucocorticoids and CRH are variable and may hold important clues to individual experiences of mood disorders. This paper explores the interactions of glucocorticoids and CRH in the presentation of anxiety and depressive disorders in an effort to better describe their differing roles in each of these clinical presentations. In addition, it focuses on ways in which extra-hypothalamic glucocorticoids and CRH, often overlooked, may play important roles in the presentation of clinical disorders.

Elliott A Beaton1, Louis A Schmidt2, Andrea R Ashbaugh2,5, Diane L Santesso2, Martin M Antony1,3,4, Randi E McCabe1,31Department of Psychiatry and Behavioural Neurosciences, McMaster University, Hamilton, Ontario, Canada; 2Department of Psychology, Neuroscience and Behaviour, McMaster University, Hamilton, Ontario, Canada; 3Anxiety Treatment and Research Centre, St. Joseph’s Healthcare, Hamilton, Ontario, Canada; 4Department of Psychology, Ryerson University, Toronto, Ontario, Canada; 5Concordia University, Montreal, Quebec, CanadaAbstract: A number of studies have noted that the pattern of resting frontal brain electrical activity (EEG) is related to individual differences in affective style in healthy infants, children, and adults and some clinical populations when symptoms are reduced or in remission. We measured self-reported trait shyness and sociability, concurrent depressive mood, and frontal brain electrical activity (EEG) at rest and in anticipation of a speech task in a non-clinical sample of healthy young adults selected for high and low social anxiety. Although the patterns of resting and reactive frontal EEG asymmetry did not distinguish among individual differences in social anxiety, the pattern of resting frontal EEG asymmetry was related to trait shyness after controlling for concurrent depressive mood. Individuals who reported a higher degree of shyness were likely to exhibit greater relative right frontal EEG activity at rest. However, trait shyness was not related to frontal EEG asymmetry measured during the speech-preparation task, even after controlling for concurrent depressive mood. These findings replicate and extend prior work on resting frontal EEG asymmetry and individual differences in affective style in adults. Findings also highlight the importance of considering concurrent emotional states of participants when examining psychophysiological correlates of personality.Keywords: social anxiety, shyness, sociability, depression, mood, frontal EEG alpha asymmetry

Christina A Brook, Louis A SchmidtDepartment of Psychology, Neuroscience and Behaviour, McMaster University, Hamilton, Ontario, CanadaAbstract: Social anxiety disorder (SAD) is a debilitating and chronic illness characterized by persistent fear of one or more social or performance situations, with a relatively high lifetime prevalence of 7% to 13% in the general population. Although the last two decades have witnessed enormous growth in the study of biological and dispositional factors underlying SAD, comparatively little attention has been directed towards environmental factors in SAD, even though there has been much ongoing work in the area. In this paper, we provide a recent review and critique of proposed environmental risk factors for SAD, focusing on traditional as well as some understudied and overlooked environmental risk factors: parenting and family environment, adverse life events, cultural and societal factors, and gender roles. We also discuss the need for research design improvements and considerations for future directions.