Quilty LC, Meusel LA, Bagby RM. Neuroticism as a mediator of treatment response to SSRIs in major depressive disorder. J Affect Disord 111: 67-73

University of Toronto, Canada.
Journal of Affective Disorders (Impact Factor: 3.38). 04/2008; 111(1):67-73. DOI: 10.1016/j.jad.2008.02.006
Source: PubMed


Serotonin function has been implicated in both major depressive disorder and neuroticism. In the current investigation, we examined the hypothesis that any change in depression severity is mediated through the reduction of neuroticism, but only for those compounds which target serotonin receptors.
Ninety-three outpatients in the midst of a major depressive episode received one of three antidepressant medications, classified into two broad types: selective serotonin reuptake inhibitors (SSRIs) and non-SSRIs (i.e. reversible monoamine oxidase inhibitors [RIMAs] and noradrenergic and dopaminergic reuptake blockers [NDMs]). Patients completed the Hamilton Rating Scale for Depression, Beck Depression Inventory II and Revised NEO Personality Inventory prior to and following approximately 16 weeks of treatment. Structural equation modeling was used to test two models: a mediation model, in which neuroticism change is the mechanism by which SSRIs exert a therapeutic effect upon depressive symptoms, and a complication model, in which neuroticism change is a mere epiphenomenon of depression reduction in response to SSRIs.
The mediation model provided a good fit to the data; the complication model did not. Patients treated with SSRIs demonstrated greater neuroticism change than those treated with non-SSRIs, and greater neuroticism change was associated with greater depressive symptom change. These effects held for both self-reported and clinician-rated depressive symptom severity.
Replication within a randomized control trial with multiple assessment periods is required.
Neuroticism mediates changes in depression in response to treatment with SSRIs, such that any treatment effect of SSRIs occurs through neuroticism reduction.

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    • "There have been several reports on the influence of personality traits on health [17, 18]. For example, neuroticism or harm avoidance were found to mediate antidepressant response [19, 20], while anxiety alters immunity related to upper respiratory infection [21], natural killer cell activity [22], and functional gastrointestinal disorder [23]. Such association between disease, emotional state, and personality highlights the interplay between biological, psychological, and social factors in determining health status. "
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    ABSTRACT: Objective. Sasang typology is a traditional Korean medicine based on the biopsychosocial perspectives of Neo-Confucianism and utilizes medical herbs and acupuncture for type-specific treatment. This study was designed to develop and validate the Sasang Personality Questionnaire (SPQ) for future use in the assessment of personality based on Sasang typology. Design and Methods. We selected questionnaire items using internal consistency analysis and examined construct validity with explorative factor analysis using 245 healthy participants. Test-retest reliability as well as convergent validity were examined. Results. The 14-item SPQ showed acceptable internal consistency (Cronbach's alpha = .817) and test-retest reliability (r = .837). Three extracted subscales, SPQ-behavior, SPQ-emotionality, and SPQ-cognition, were found, explaining 55.77% of the total variance. The SPQ significantly correlated with Temperament and Character Inventory novelty seeking (r = .462), harm avoidance (r = −.390), and NEO Personality Inventory extraversion (r = .629). The SPQ score of the So-Eum (24.43 ± 4.93), Tae-Eum (27.33 ± 5.88), and So-Yang (30.90 ± 5.23) types were significantly different from each other (P < .01). Conclusion. Current results demonstrated the reliability and validity of the SPQ and its subscales that can be utilized as an objective instrument for conducting personalized medicine research incorporating the biopsychosocial perspective.
    Evidence-based Complementary and Alternative Medicine 04/2012; 2012(6):657013. DOI:10.1155/2012/657013 · 1.88 Impact Factor
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    • "Our results are also consistent with previous reports that demonstrated that low central serotonergic function is characterized by negative affective experience and lesser affiliative behavior (Knutson et al., 1998; Moskowitz et al., 2001; Tse and Bond, 2002; Young and Leyton, 2002). Furthermore, individuals with low sociotropic personality traits, who are concerned with rejection from others, showed a better response to antidepressants (Peselow et al., 1992), especially to SSRIs (Joyce et al., 2004; Quilty et al., 2008; Fiedorowicz et al., 2010). In contrast to our expectations, the majority of the pretreatment scales of the MMPI-2 could not predict response to SSRIs. "
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    ABSTRACT: There is growing evidence that individual differences among patients with major depressive disorder (MDD) on psychological and demographic measures may predict the therapeutic response to selective serotonin reuptake inhibitors (SSRIs). In this retrospective chart review, 108 outpatients with current major depressive episodes were treated with citalopram, paroxetine, or fluvoxamine. The Hamilton Depression Rating Scale and the Minnesota Multiphasic Personality Inventory-2 were administered before and after 8 weeks of SSRIs treatment. Clinical response was defined as a 50% or greater decrease in the 17-item Hamilton Depression Rating Scale total score (final visit minus baseline). This naturalistic short-term follow-up outcome study demonstrates that among depressive outpatients who responded to an 8-week trial, 57.4% achieved a good response to SSRIs. Statistical analysis showed that SSRI treatment may be 3.03 times more advantageous for MDD outpatients who are younger than 39 years. The patients with an elevated score of above 66T on the Social Introversion Minnesota Multiphasic Personality Inventory-2 scale are approximately 0.37 times as likely to be SSRI responders as are patients with a Social Introversion score less than 66T. Thus, it seems that in MDD outpatient age is the strongest predictor of response to SSRIs.
    International clinical psychopharmacology 03/2012; 27(3):134-41. DOI:10.1097/YIC.0b013e3283524d5c · 2.46 Impact Factor
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    • "Therefore, neuroticism is a vulnerability factor to both anxiety and depressive disorders. Quilty et al (2008) evaluated two models of the relationship between neuroticism and response to antidepressant therapy, a 'mediation' model (ie, SSRI-Neuroticism Change-Depression Change) and a 'complication' model (ie, SSRI-Depression Change- Neuroticism Change), by using a maximum likelihood of estimation approach. The 'mediation' model best fit the SSRI response data, indicating that overall neuroticism change is associated with change in depression severity. "
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    ABSTRACT: Major depressive disorder (MDD) is a heterogeneous illness for which there are currently no effective methods to objectively assess severity, endophenotypes, or response to treatment. Increasing evidence suggests that circulating levels of peripheral/serum growth factors and cytokines are altered in patients with MDD, and that antidepressant treatments reverse or normalize these effects. Furthermore, there is a large body of literature demonstrating that MDD is associated with changes in endocrine and metabolic factors. Here we provide a brief overview of the evidence that peripheral growth factors, pro-inflammatory cytokines, endocrine factors, and metabolic markers contribute to the pathophysiology of MDD and antidepressant response. Recent preclinical studies demonstrating that peripheral growth factors and cytokines influence brain function and behavior are also discussed along with their implications for diagnosing and treating patients with MDD. Together, these studies highlight the need to develop a biomarker panel for depression that aims to profile diverse peripheral factors that together provide a biological signature of MDD subtypes as well as treatment response.
    Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology 08/2011; 36(12):2375-94. DOI:10.1038/npp.2011.151 · 7.05 Impact Factor
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