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Depression is the world's most devastating health condition, not just because it extracts so high a price in health, well-being, and ability to function, but because it is so common, especially in the industrialized world, where rates of depression have increased significantly in recent decades. Yet despite how common it is, we hear repeatedly that the causes of depression remain a mystery despite years of research. The New Mind-Body Science of Depression challenges the prevailing wisdom that we don't really understand the disorder. This groundbreaking book brings together a new perspective on major depression: it simply does not exist as we have been characterizing it. It is not a separate, distinct illness, and the DSM criteria, although helpful doesn't describe it effectively. Co-authors Maletic and Raison start their exploration of depression as a mind-body disorder by showing how, despite best intentions, mental health research went astray by conceptualizing depression as a discreet disease state that could be diagnosed and understood the way we understand many other medical conditions. By viewing depression as a discreet medical illness, psychiatric research encouraged an overly-reductionist understanding of the disorder that was deprived of input from a range of scientific disciplines - such as evolutionary psychology and anthropology - that provide key insights into the pathophysiology of the disease. Major depressive disorder is a highly heterogeneous diagnostic and biological entity and studying and understanding it requires a broad, interdisciplinary approach. That's what this book offers scientific disciplines, the authors present depression as a highly conserved emotional, cognitive, and behavioral response to environmental adversity, with a biology that extends from interactions between the environment and genetic risk factors, through bodily pathways such as the immune system and hypothalamic-pituitary-adrenal axis to specific patterns of brain functioning. From genetics to environmental adversity to inflammation and the immune system, the authors provide a comprehensive and full-bodied understanding of this condition. Although much remains to be learned, The New Mind-Body Science of Depression provides evidence that most of what we will eventually know about depression we know already. While the full therapeutic implications of these findings will take time to come to clinical fruition, viewing depression in ways consistent with the best current science is imperative for all researchers and clinicians. Better understanding of these pathophysiological pathways shared by many, but definitely not all, depressed patients may yield novel, more effective treatment approaches. This book explains many of them, offering hope for patients and doctors alike. One thing is sure: after reading this book you'll never look at depression the same way again. -- from dust jacket.

This randomized, noninferiority trial compared ketamine with electroconvulsive therapy in treatment-resistant depression. Ketamine was noninferior to ECT for treatment-resistant depression without psychosis.

The antidepressant effects of ketamine are thought to depend on brain-derived neurotrophic factor (BDNF) genotype and dose. The purpose of this study was to characterize the dose-related antidepressant effects of ketamine in patients with treatment-resistant depression drawn from a Chinese population predominately possessing lower activity BDNF genotypes (Val/Met, Met/Met). We conducted a double-blind, randomized, parallel-group, placebo-controlled trial of a single ketamine infusion (saline, 0.2 mg/kg, 0.5 mg/kg). Patients (N=71; BDNF genotype: Val/Val (N=12, 17%), Val/Met (N=40, 56.3%), and Met/Met (N=19, 26.8%)) received mood ratings before infusion, after infusion, and for the subsequent 14 days. Plasma ketamine levels and BDNF genotypes were assessed. This study found a significant dose-related ketamine effect on scores on the Hamilton Depression Rating Scale (HAMD). The responder analysis (>50% reduction from baseline HAMD on at least 2 days between days 2 and 5) also revealed a significant dose-related effect (saline: 12.5%, 0.2 mg/kg: 39.1%; 0.5 mg/kg: 45.8%). This is the first report to our knowledge to demonstrate the dose-related efficacy of R/S-ketamine for treatment-resistant depression and the first to characterize ketamine effects in a genotyped Chinese population in which most (83%) patients possessed at least one copy of the lower functioning Met allele of the BDNF gene.

Psilocybin is being studied for use in treatment-resistant depression. In this phase 2 double-blind trial, we randomly assigned adults with treatment-resistant depression to receive a single dose of a proprietary, synthetic formulation of psilocybin at a dose of 25 mg, 10 mg, or 1 mg (control), along with psychological support. The primary end point was the change from baseline to week 3 in the total score on the Montgomery-Åsberg Depression Rating Scale (MADRS; range, 0 to 60, with higher scores indicating more severe depression). Secondary end points included response at week 3 (≥50% decrease from baseline in the MADRS total score), remission at week 3 (MADRS total score ≤10), and sustained response at 12 weeks (meeting response criteria at week 3 and all subsequent visits). A total of 79 participants were in the 25-mg group, 75 in the 10-mg group, and 79 in the 1-mg group. The mean MADRS total score at baseline was 32 or 33 in each group. Least-squares mean changes from baseline to week 3 in the score were -12.0 for 25 mg, -7.9 for 10 mg, and -5.4 for 1 mg; the difference between the 25-mg group and 1-mg group was -6.6 (95% confidence interval [CI], -10.2 to -2.9; P<0.001) and between the 10-mg group and 1-mg group was -2.5 (95% CI, -6.2 to 1.2; P = 0.18). In the 25-mg group, the incidences of response and remission at 3 weeks, but not sustained response at 12 weeks, were generally supportive of the primary results. Adverse events occurred in 179 of 233 participants (77%) and included headache, nausea, and dizziness. Suicidal ideation or behavior or self-injury occurred in all dose groups. In this phase 2 trial involving participants with treatment-resistant depression, psilocybin at a single dose of 25 mg, but not 10 mg, reduced depression scores significantly more than a 1-mg dose over a period of 3 weeks but was associated with adverse effects. Larger and longer trials, including comparison with existing treatments, are required to determine the efficacy and safety of psilocybin for this disorder. (Funded by COMPASS Pathfinder; EudraCT number, 2017-003288-36; ClinicalTrials.gov number, NCT03775200.).

What is depression? What is bipolar disorder? How are they diagnosed and how are they treated? Can a small child be diagnosed with depression and treated with antidepressants - and should they be? Covering depression, manic depression, and bipolar disorder, this Very Short Introduction gives a brief account of the history of these concepts, before focussing on the descriptions and understanding of these disorders today.

About 20% of major depressive episodes become chronic and medication-refractory and also appear to be less responsive to standard cognitive-behavioural therapy (CBT). To test whether CBT developed from behavioural activation principles that explicitly and exclusively targets depressive rumination enhances treatment as usual (TAU) in reducing residual depression. Forty-two consecutively recruited participants meeting criteria for medication-refractory residual depression were randomly allocated to TAU v. TAU plus up to 12 sessions of individual rumination-focused CBT. The trial has been registered (ISRCTN22782150). Adding rumination-focused CBT to TAU significantly improved residual symptoms and remission rates. Treatment effects were mediated by change in rumination. This is the first randomised controlled trial providing evidence of benefits of rumination-focused CBT in persistent depression. Although suggesting the internal validity of rumination-focused CBT for residual depression, the trial lacked an attentional control group so cannot test whether the effects were as a result of the specific content of rumination-focused CBT v. non-specific therapy effects.

Cognitive dysfunction in depression and bipolar disorder (BD) is insufficiently targeted by available treatments. Erythropoietin (EPO) increases neuroplasticity and may improve cognition in mood disorders, but the neuronal mechanisms of these effects are unknown. This functional magnetic resonance imaging (fMRI) study investigated the effects of EPO on neural circuitry activity during working memory (WM) performance. Patients with treatment-resistant major depression, who were moderately depressed, or with BD in partial remission, were randomized to eight weekly infusions of EPO (40 000 IU) (N = 30) or saline (N = 26) in a double-blind, parallel-group design. Patients underwent fMRI, mood ratings and blood tests at baseline and week 14. During fMRI patients performed an n-back WM task. EPO improved WM accuracy compared with saline (p = 0.045). Whole-brain analyses revealed that EPO increased WM load-related activity in the right superior frontal gyrus (SFG) compared with saline (p = 0.01). There was also enhanced WM load-related deactivation of the left hippocampus in EPO-treated compared to saline-treated patients (p = 0.03). Across the entire sample, baseline to follow-up changes in WM performance correlated positively with changes in WM-related SFG activity and negatively with hippocampal response (r = 0.28-0.30, p < 0.05). The effects of EPO were not associated with changes in mood or red blood cells (p ⩾0.08). The present findings associate changes in WM-load related activity in the right SFG and left hippocampus with improved executive function in EPO-treated patients. clinicaltrials.gov: NCT00916552.