Youngmee Kim1,2, Charles S Carver3,4, Joachim F Hallmayer5, Jamie M Zeitzer5,6, Oxana Palesh5, Eric Neri5, Bita Nouriani5, David Spiegel5. 1. Department of Psychology, University of Miami, 5665 Ponce de Leon Blvd., Coral Gables, FL, 33146, USA. ykim@miami.edu. 2. Center for Advanced Study in the Behavioral Sciences, Stanford University, Stanford, CA, 94305, USA. ykim@miami.edu. 3. Department of Psychology, University of Miami, 5665 Ponce de Leon Blvd., Coral Gables, FL, 33146, USA. 4. Center for Advanced Study in the Behavioral Sciences, Stanford University, Stanford, CA, 94305, USA. 5. Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, 401 Quarry Rd., Stanford, CA, 94305, USA. 6. Department of Psychiatry and Behavioral Sciences, VA Palo Alto Health Care System, Stanford University School of Medicine, 3801 Miranda Ave., Palo Alto, CA, 94304, USA.
Abstract
PURPOSE: This study tested a theory linking a marker of low serotonergic function to both depression and impulsivity in a sample of advanced breast cancer patients, among whom elevated depressive symptoms and difficulty regulating emotions are commonly reported. METHODS: A total of 95 patients provided blood samples for serotonin transporter polymorphic region of the gene (5-HTTLPR) and completed questionnaires that measured depressive symptoms and emotional impulsivity. RESULTS: Structural equation modeling revealed that the s allele of 5-HTTLPR was related to greater depressive symptoms (β = .20, p < .042) but only marginally to greater emotional impulsivity (β = .19, p < .068). Depressive symptoms and emotional impulsivity were positively related (β = .33, p < .003). Further tests explored possible mediation from genotype to one psychological variable via the other. Results suggest that depressive symptoms, particularly perceived interpersonal rejection, may be a pathway linking genotype to emotional impulsivity. CONCLUSIONS: Findings provide the first evidence that low serotonergic function contributes to both depression and impulsivity within a clinically meaningful sample. Furthermore, the link of s allele of 5-HTTLPR to emotional impulsivity was mediated by depressive symptoms, particularly perceptions of social rejection. Findings have implications for advanced breast cancer patients' treatment decision.
PURPOSE: This study tested a theory linking a marker of low serotonergic function to both depression and impulsivity in a sample of advanced breast cancerpatients, among whom elevated depressive symptoms and difficulty regulating emotions are commonly reported. METHODS: A total of 95 patients provided blood samples for serotonin transporter polymorphic region of the gene (5-HTTLPR) and completed questionnaires that measured depressive symptoms and emotional impulsivity. RESULTS: Structural equation modeling revealed that the s allele of 5-HTTLPR was related to greater depressive symptoms (β = .20, p < .042) but only marginally to greater emotional impulsivity (β = .19, p < .068). Depressive symptoms and emotional impulsivity were positively related (β = .33, p < .003). Further tests explored possible mediation from genotype to one psychological variable via the other. Results suggest that depressive symptoms, particularly perceived interpersonal rejection, may be a pathway linking genotype to emotional impulsivity. CONCLUSIONS: Findings provide the first evidence that low serotonergic function contributes to both depression and impulsivity within a clinically meaningful sample. Furthermore, the link of s allele of 5-HTTLPR to emotional impulsivity was mediated by depressive symptoms, particularly perceptions of social rejection. Findings have implications for advanced breast cancerpatients' treatment decision.