Academic journal article Journal of Mental Health Counseling

The Inflammatory Hypothesis of Depression: Implications for Diagnosis and Practice

Academic journal article Journal of Mental Health Counseling

The Inflammatory Hypothesis of Depression: Implications for Diagnosis and Practice

Article excerpt

Research is beginning to offer new insights into the physiological mechanisms that underlie the complexities of major depressive disorder (MDD). Additionally, several lines of research have begun to link stress and inflammation to symptoms of depression (Lotrich, 2015; Slavich O Irwin, 2014). This manuscript will summarize the existing literature from medicine, public health, and neuroscience to review the neural, physiological, and molecular pathways that underlie the relationship between stress, inflammation, and depressive symptoms. Implications for counseling will be discussed.

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The National Institute of Mental Health (NIMH) recently launched the Research Domain Criteria (RDoC; Insel et al., 2010) with the aim of enhancing the validity of mental health diagnosis by linking mental illness to genetic and neural substrates. The RDoC initiative may represent a paradigm shift in mental health, as NIMH leaders are calling for a new approach toward diagnosing mental illness and encouraging the development of modern treatments specifically aligned to neural targets. Within this context, new findings are beginning to offer insight into the physiological mechanisms that underlie the complexities of major depressive disorder (MDD), as several lines of research have reliably replicated a link between stress, inflammation (an adaptive immune response that protects individual from illness or injury), and symptoms of depression (Lotrich, 2015; Slavich & Irwin, 2014). However, because inflammation does not consistently precede the onset of MDD, nor do all subjects with MDD show elevated inflammatory activity, these data have led some to consider a new cytokine (chemical messengers that aid communication between cells in the immune system)-related subtype, theoretically separable from other manifestations of depression (Lotrich, 2015). Such findings may carry implications for clinical outcomes considering evidence that suggests elevated inflammatory markers may promote resistance to pharmacologic treatment (Raison et al., 2013; Strawbridge et al., 2015). For clinical mental health counselors (CMHCs), these findings underscore a growing need for precise counseling interventions, specifically linked to the underlying pathoetiology of depressive symptoms. This manuscript will summarize the existing literature to review the neural, physiological, and molecular pathways that mediate the relationship between stress, inflammation, and depressive symptomatology. Implications for counseling practice will be discussed.

INFLAMMATORY HYPOTHESIS OF DEPRESSION

The inflammatory hypothesis of depression described the immunological mechanisms thought to underlie symptoms of major depressive disorder (Maes, 2010). This line of research emerged when investigators noticed an increase in depressive-like symptoms among clients receiving cytokine therapy for chronic diseases and cancer (Capuron & Miller, 2011; Ceretta et al., 2012; Hoyo-Becerra, Schlaak, & Hermann, 2014). Conversely, data from challenge studies (intentionally administering a pharmacologic or pathogenic agent known to induce a physiological response) appeared to suggest that the administration of anti-inflammatory cytokines might suppress depressive symptoms triggered by proinflammatory agonists (Capuron & Miller, 2011; O'Connor et al., 2009). Moreover, both clinical trials and meta-analysis have consistently demonstrated increased serum levels of proinflammatory cytokines among depressed clients presenting with a history of childhood maltreatment, obesity, and/or refractory (treatment resistant) symptoms (Coelho, Viola, Walss-Bass, Brietzke, & Grassi-Oliveira, 2014; Dahl et al., 2014; Haapakoski, Mathieu, Ebmeier, Alenius, & Kivimaki, 2015; Shelton & Miller, 2010). These data appear to suggest that, for some, the risk of developing depression may increase under chronic pro-inflammatory conditions (Maes et al., 2012). …

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