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1.
Psychoneuroendocrinology ; 107: 9-18, 2019 09.
Article in English | MEDLINE | ID: mdl-31059979

ABSTRACT

The cortisol awakening response (CAR) has been shown to prospectively predict depression, but it remains unresolved whether a greater CAR predicts risk independently of subsequent acute stress, or whether greater CAR indicates increased vulnerability to subsequent acute stress. Further, no prior work has evaluated whether the CAR increases vulnerability to certain types of acute stress, but not others, in predicting depression. To address these gaps, we investigated whether the CAR predicted depressive symptoms alone and in interaction with acute interpersonal stress in a one-year longitudinal study of 86 early adolescent girls with no history of diagnosable depression. To index the CAR, adolescents collected saliva at waking and 30-minutes past waking for 3 days; compliance with the sampling protocol was electronically monitored. Diagnostic and objective contextual stress interviews were used to quantify acute stress in the 2-months prior to worst depressive symptom onset during the follow-up. Supporting hypotheses, results indicated that greater CAR predicted greater depressive symptoms, and interacted with acute interpersonal stress in predicting depressive symptoms. Further, the CAR interacted with acute dependent (i.e., at least partially arising from the person's behavior) interpersonal stress in predicting depressive symptoms. In contrast, the CAR did not interact with acute non-interpersonal stress nor acute interpersonal independent (i.e., fateful) stress in predicting depressive symptoms. These results further refine circumstances in which the CAR is predictive of depressive symptoms among early adolescent girls, and highlight the importance of focusing on etiologically relevant stress when testing interactions between physiological stress indicators and environmental stress.


Subject(s)
Depression/etiology , Hydrocortisone/analysis , Stress, Psychological/metabolism , Adolescent , Child , Circadian Rhythm/physiology , Depression/metabolism , Depressive Disorder/etiology , Depressive Disorder/metabolism , Female , Humans , Hydrocortisone/metabolism , Hypothalamo-Hypophyseal System/metabolism , Longitudinal Studies , Pituitary-Adrenal System/metabolism , Prognosis , Risk Factors , Saliva/chemistry
2.
Psychiatry Res ; 253: 99-106, 2017 07.
Article in English | MEDLINE | ID: mdl-28364592

ABSTRACT

Individuals with 22q11.2 deletion syndrome (22q11DS) exhibit a broad array of physical and psychiatric features, of which impaired social cognition and poor social functioning are common. This review seeks to (1) characterize the current understanding of impairment across social cognitive domains in the context of 22q11DS, and (2) synthesize the relevant literature on social cognition and psychosis, given that the prevalence of psychosis in 22q11DS is especially high compared to the general population. A total of 16 papers examining social cognition in 22q11DS were identified through a comprehensive literature search conducted using electronic databases such as PubMed and PSYCInfo. Results suggest that individuals with 22q11DS exhibit impaired emotion processing and complex theory of mind relative to their typically developing peers, though some findings were accounted for by neurocognitive and intellectual abilities. Further, no studies have examined the domains of attribution bias or social perception in 22q11DS, highlighting a critical gap in the extant literature. More research is needed to better elucidate the trajectory of how and why social cognitive impairment develops in 22q11DS, and to explore possible relationships to psychiatric comorbidities like psychosis. Treatment implications and future steps are considered.


Subject(s)
Cognitive Dysfunction/genetics , DiGeorge Syndrome/psychology , Social Behavior Disorders/genetics , Adolescent , Adult , Cognitive Dysfunction/psychology , Comorbidity , Emotions , Female , Humans , Male , Social Behavior , Social Behavior Disorders/psychology , Social Perception
3.
Harv Rev Psychiatry ; 25(1): 4-14, 2017.
Article in English | MEDLINE | ID: mdl-28059932

ABSTRACT

LEARNING OBJECTIVES: After participating in this activity, learners should be better able to:• Evaluate the evolution of social cognitive abilities as a developmental process• Assess the evidence regarding social cognition difficulties in youth at clinical high risk for psychosisIndividuals at clinical high risk (CHR) for psychosis exhibit a broad range of difficulties, including impaired social cognition, which may represent a target for early identification and intervention. Several studies have examined various domains of social cognition in CHR individuals. Most focus on adolescent and young adult populations, but given the accumulating evidence that impairment exists before the onset of psychotic disorders, it is critically important to begin to look for these risk markers in younger children. The present article reviews 25 studies on CHR that examine any of the following four domains of social cognition: emotion processing, theory of mind, social perception, or attribution bias. Eligible studies were identified through a comprehensive literature search, conducted using electronic databases, including PubMed/MEDLINE and PsycINFO, and combinations of key social-cognition and CHR search terms. Despite some mixed results, the existing literature establishes that CHR individuals display social-cognitive impairment, though it remains unclear as to how and when that impairment develops. Thus, by using the literature on social cognition in typically developing children as a model and reference, and by looking at the evolution of social-cognitive abilities as a developmental process, our review presents a valuable new perspective that indicates the necessity of further investigation in younger, at-risk populations. Implications for treatment and future research are discussed.


Subject(s)
Child Development/physiology , Emotions/physiology , Psychotic Disorders/physiopathology , Social Perception , Theory of Mind/physiology , Child , Humans
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