Dear colleagues,
It is my great pleasure to introduce to you the first issue of 2017 featuring the first part of the WFSBP Consensus Statement on genetics in major depressive disorder as well as a proposal to a psychopharmacology-pharmacotherapy curriculum along with original research on treatment options and biological markers in depressive disorders.
In a commentary, Erfurth discusses the recently published WFSBP Consensus statement on the assessment and management of agitation in psychiatry. The author states that the consensus gives the right perspective to the importance in clinical practice of over-excitement, restlessness, irritability, as well as heightened responsiveness to internal and external stimuli. Furthermore, he states it to be a milestone for acknowledging agitation as a central challenge in clinical psychiatry.
The WFSBP Consensus on genetics reviews the current literature on genetics, epigenetics and gene expression markers in major depressive disorder (MDD) and antidepressant response. Results of pharmacogenetic assays that have been tested for clinical applicability have been promising in regards to the patient-outcome improvement. Additionally, serum biomarkers have shown good sensitivity and specificity in differentiating between MDD and healthy controls. Future research should include combinations of different types of biomarkers for MDD subtypes and pathological dimensions.
Baumann and colleagues review the current situation of teaching and training of psychopharmacotherapy in Europe. By analysing the situation, the authors point out the need and propose a psychopharmacology-psychopharmacotherapy curriculum for specialists in psychiatry. As the current number of hours of theoretical teaching and practical training is insufficient, the authors conclude that a catalogue of learning objectives should be established that in turn will be a part of a comprehensive curriculum at a European level.
Sonei and associates investigated mitochondrial dysfunction and its contribution to depression–cardiovascular comorbidity. It emerged that socially isolated rats had impaired respiratory chain complex and administration of fluoxetine attenuated the effects of isolation on brain mitochondria dysfunction but not in cardiac tissue. The results suggest that juvenile isolation predisposes to comorbidity of depression and cardiovascular disease and that the therapeutic effect of fluoxetine is partly mediated by its effect on mitochondrial function.
Ferensztajn-Rochowiak et al. examined the effect of long-term lithium treatment on stem cells circulating in the peripheral blood in bipolar disorder (BD). By comparing lithium treated BD patients to lithium naïve BD patients as well as healthy controls the authors found that the number of very small embryonic-like stem cells (VSELs) were higher in naïve BD patients while being similar in lithium treated BD patients and controls. Long-term lithium treatment may suppress the activation of regenerative processes by reducing the number of VSELs in the blood. These cells in lithium naïve BD patients may provide a new potential biomarker for BD.
Chang and colleagues investigated whether C-reactive protein (CRP) level could be used to differentiate between major depression (MDD) and bipolar disorder II (BD II). It emerged that at baseline the CRP levels were significantly different and remained so after treatment. The authors suggest that the level of CRP may play a role as a biomarker to differentiate between MDD and BD II.
In a letter to the Editor, Fond et al., discuss several points in regards to the paper of Chang et al. about C-reactive protein. They believe that CRP levels cannot serve as an effective biomarker to distinguish MDD from BD.
In a letter to the Editor, Chang and associates clarify a few points regarding their article as a response to the comments raised by Fond et al.
In a brief report, Bousman et al. assessed the phenotypic plasticity in a depression cohort with and without history of childhood abuse. They found that a higher plasticity allelic load (PAL) conferred greater depression symptom severity to those with a history of abuse while in those without it, it was significantly lower. As a conclusion, depression severity was dependent on the interaction between PAL and history of childhood abuse.
In his letter to the Editor, Kemp raises a few issues in regards to article of Chang et al., published previously about distinguishing bipolar from unipolar disorders on the basis of heart rate variability. The author remains unconvinced that BD-II could be differentiated from unipolar disorders based on heart rate variability.
Yours sincerely,
Siegfried Kasper, MD
Chief Editor