scholarly journals Pharmacotherapy of Major Depressive Disorder: Focus on Desvenlafaxine Succinate

2010 ◽  
Vol 2 ◽  
pp. CMT.S74
Author(s):  
Antolin C. Trinidad ◽  
Benjamin Bregman

The newest antidepressant, desvenlafaxine (DVS) was approved by the FDA in early 2008 and since then, has been available in the market for general use. DVS is dual acting, a serotonin-norepinepherine reuptake inhibitor (SNRI). Like its parent compound, venlafaxine (VEN), DVS inhibits the neuronal re-uptake of both serotonin and norepinepherine while having minimal affinity for muscarinic cholinergic, H1-histaminergic, alpha1-adrenergic and opioid receptors. DVS is moderately effective for MDD at doses ranging from 100–400 milligrams per day. Its possible advantage is its lower risk of drug-drug interaction. There is no extant evidence that it is especially effective over and above the other existing antidepressants. Its niche will be defined by time but one speculation, given preliminary but un-replicated proof of its efficacy in vasomotor instability in peri-menopause, is that it may have a future utility for depressed women entering menopause.


1982 ◽  
Vol 141 (4) ◽  
pp. 372-376 ◽  
Author(s):  
Ilana B. Glass ◽  
Stuart A. Checkley ◽  
Eric Shur ◽  
Sheila Dawling

SummaryEleven drug free patients meeting Research Diagnostic Criteria for Major Depressive Disorder have been treated with desipramine and given a clonidine infusion after 0, 1 and 3 weeks of treatment. The sedative and hypotensive effects of clonidine were significantly inhibited after three weeks of treatment with desipramine: a similar interaction was seen after one week of treatment although this just failed to reach statistical significance. The growth hormone (GH) response to clonidine was initially impaired, but increased significantly after one week of treatment. A significant reduction in the GH response occurred during the second and third weeks of treatment with desipramine. This last finding is interpreted as evidence of adaptive change of α2 adrenoceptors: the other changes can be explained by the known ability of desipramine to block the re-uptake of noradrenaline.



2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Zhenhuang Zhuang ◽  
Ruotong Yang ◽  
Wenxiu Wang ◽  
Lu Qi ◽  
Tao Huang

Abstract Background Growing evidence has shown that alterations in the gut microbiota composition were associated with a variety of neuropsychiatric conditions. However, whether such associations reflect causality remains unknown. We aimed to reveal the causal relationships among gut microbiota, metabolites, and neuropsychiatric disorders including Alzheimer’s disease (AD), major depressive disorder (MDD), and schizophrenia (SCZ). Methods A two-sample bi-directional Mendelian randomization analysis was performed by using genetic variants from genome-wide association studies as instrumental variables for gut microbiota, metabolites, AD, MDD, and SCZ, respectively. Results We found suggestive associations of host-genetic-driven increase in Blautia (OR, 0.88; 95%CI, 0.79–0.99; P = 0.028) and elevated γ-aminobutyric acid (GABA) (0.96; 0.92–1.00; P = 0.034), a downstream product of Blautia-dependent arginine metabolism, with a lower risk of AD. Genetically increased Enterobacteriaceae family and Enterobacteriales order were potentially associated with a higher risk of SCZ (1.09; 1.00–1.18; P = 0.048), while Gammaproteobacteria class (0.90; 0.83–0.98; P = 0.011) was related to a lower risk for SCZ. Gut production of serotonin was potentially associated with an increased risk of SCZ (1.07; 1.00–1.15; P = 0.047). Furthermore, genetically increased Bacilli class was related to a higher risk of MDD (1.07; 1.02–1.12; P = 0.010). In the other direction, neuropsychiatric disorders altered gut microbiota composition. Conclusions These data for the first time provide evidence of potential causal links between gut microbiome and AD, MDD, and SCZ. GABA and serotonin may play an important role in gut microbiota-host crosstalk in AD and SCZ, respectively. Further investigations in understanding the underlying mechanisms of associations between gut microbiota and AD, MDD, and SCZ are required.





2010 ◽  
Vol 22 (4) ◽  
pp. 831-848 ◽  
Author(s):  
Erin C. Tully ◽  
William G. Iacono ◽  
Matt McGue

AbstractThis longitudinal study used a representative community sample of same-sex twins (485 monozygotic pairs, 271 dizygotic pairs) to study longitudinal changes in genetic and environmental influences on nicotine dependence (NicD) symptoms and major depressive disorder (MDD) symptoms and the longitudinal relationships between NicD and MDD symptoms at three relatively discrete ages spanning middle adolescence to early adulthood (ages 15, 18, and 21). Clinical interviews were used to assess NicD and MDD symptoms lifetime at age 15 and during the previous 3 years at the two subsequent assessments. Biometric models revealed similar patterns of findings for NicD and MDD. Heritability increased with age, particularly between ages 15 and 18. Shared environmental influences were small, and the proportion of variance attributed to shared environmental influences decreased with age. Nonshared environmental influences were moderate to large in magnitude and were entirely age specific. Both NicD and MDD symptoms showed considerable stability from age 15 to 21, and at each age those with one disorder showed elevated rates of the other. However, a cross-lagged model revealed no longitudinal predictive relationships between MDD symptoms and NicD symptoms after accounting for stability of symptoms within disorders. In summary, the transition between middle and late adolescence is a critical period for developmental shifts in the magnitudes of genetic and environmental influences on both MDD and NicD symptoms. Despite similarities in the development of genetic and environmental influences for the two phenotypes, the association between NicD and MDD reflects concurrent covariation rather than one phenotype being an antecedent influence on the subsequent development of the other.



2016 ◽  
Vol 89 (2) ◽  
pp. 212-215 ◽  
Author(s):  
Bogdan Nemes ◽  
Doina Cozman

The study of the relationship between the psychobiological model of temperament and character on one side and the development and evolution of major depressive disorder on the other side has drawn some attention in the past two decades, especially since a diagnosis model based on fewer diagnostic categories and a more phenomenological and person oriented approach seems to be supported other research and current state-of-the art therapeutic practices, which are based more on descriptive clinical data than on the current diagnostic categories.The aim of this paper was to review the latest developments in this area, but in the context of the initial development of the psychobiological model of temperament and character, i.e. as a tool for the comprehensive diagnosis of depressed individuals.Data published so far supports the following observations: (1) high harm avoidance and low self-directedness are risk factors for the development of major depressive disorder, but further research is needed to clearly establish the role of the other dimensions or their facets as predictors for the development of a depressive episode; (2) although some evidence has been obtained so far regarding the use of harm avoidance, novelty seeking, reward dependence and cooperativeness in predicting treatment response in major depressive disorder, further research is needed to clarify and/or to replicate these findings; and (3) data on temperament and character dimensions related to relapse in major depressive disorder are insufficient, although some evidence has been brought to support the hypothesis that high harm avoidance scores, and low self-directedness and novelty seeking scores might serve as predictors, further prospective studies need to be carried out to establish their utility in this respect.



10.2196/17071 ◽  
2020 ◽  
Vol 7 (4) ◽  
pp. e17071
Author(s):  
Noah Lorenz ◽  
Christian Sander ◽  
Galina Ivanova ◽  
Ulrich Hegerl

Background There is a strong link between sleep and major depression; however, the causal relationship remains unclear. In particular, it is unknown whether changes in depression core symptoms precede or follow changes in sleep, and whether a longer or shorter sleep duration is related to improvements of depression core symptoms. Objective The aim of this study was to investigate temporal associations between sleep and depression in patients suffering from major depressive disorder using an idiographic research approach. Methods Time-series data of daily sleep assessments (time in bed and total sleep time) and self-rated depression core symptoms for an average of 173 days per patient were analyzed in 22 patients diagnosed with recurrent major depressive disorder using a vector autoregression model. Granger causality tests were conducted to test for possible causality. Impulse response analysis and forecast error variance decomposition were performed to quantify the temporal mutual impact of sleep and depression. Results Overall, 11 positive and 5 negative associations were identified between time in bed/total sleep time and depression core symptoms. Granger analysis showed that time in bed/total sleep time caused depression core symptoms in 9 associations, whereas this temporal order was reversed for the other 7 associations. Most of the variance (10%) concerning depression core symptoms could be explained by time in bed. Changes in sleep or depressive symptoms of 1 SD had the greatest impact on the other variable in the following 2 to 4 days. Conclusions Longer rather than shorter bedtimes were associated with more depression core symptoms. However, the temporal orders of the associations were heterogeneous.



2020 ◽  
Author(s):  
Shusuke Numata ◽  
Masahito Nakataki ◽  
Naomi Hasegawa ◽  
Yoshikazu Takaesu ◽  
Masahiro Takeshima ◽  
...  

Abstract Background: To implement clinical practice guidelines (CPGs), it is necessary for psychiatrists to deepen their understanding of existing CPGs. The Effectiveness of Guidelines for Dissemination and Education in Psychiatric Treatment (EGUIDE) project is a nationwide dissemination and implementation study of two sets of CPGs, including one for schizophrenia and one for major depressive disorder (MDD).Methods: A total of 413 psychiatrists (n=212 in 2016; n=201 in 2017) learned the two CPGs in the education program of the EGUIDE project over two days, and clinical knowledge of the two CPGs was evaluated by two 37-item questionnaires at baseline and after the EGUIDE programs. To improve the correct answer rate for clinical knowledge after the EGUIDE programs, we revised the lecture materials associated with items that had a low correct answer rate in 2016 and used the revised lecture materials with the CPGs in 2017. The rates of correct answers for each item after the EGUIDE programs were compared between the 2016 and 2017 groups.Results: The total clinical knowledge scores significantly increased after the EGUIDE program in both the 2016 groups and the 2017 groups. We revised lecture materials related to two items in the schizophrenia CPG and five items in the MDD CPG that had low correct answer rates after the EGUIDE programs. The correct answer rate of one item on the schizophrenia CPG and one item on the MDD CPG were increased (S-D5, p=0.038; D-C6, p=0.033) and that of one item on the MDD CPG was significantly improved (D-D3, p=0.00080) in the 2017 group compared to the rates of the 2016 group. The correct response rates of the other four items were not significantly improved.Conclusions: We reported improvements in clinical knowledge of CPGs after the EGUIDE program in the 2017 group following revisions of the lecture materials based on the results from the 2016 group. These attempts to improve the degree of understanding of CPGs may facilitate the successful dissemination and implementation of psychiatric guidelines in everyday practice.Trial registration: Effectiveness of Guideline for Dissemination and Education in Psychiatric Treatment, UMIN000022645, Registered 15 June 2016, https://upload.umin.ac.jp/cgi-open-bin/ctr/ctr.cgi?function=brows&action=brows&recptno=R000026044&type=summary&language=J



2020 ◽  
Author(s):  
Shusuke Numata ◽  
Masahito Nakataki ◽  
Naomi Hasegawa ◽  
Yoshikazu Takaesu ◽  
Masahiro Takeshima ◽  
...  

Abstract Background: To implement clinical practice guidelines (CPGs), it is necessary for psychiatrists to deepen their understanding of the CPGs. The Effectiveness of Guidelines for Dissemination and Education in Psychiatric Treatment (EGUIDE) project is a nationwide dissemination and implementation study of two sets of CPGs for schizophrenia and major depressive disorder (MDD).Methods: A total of 413 psychiatrists (n=212 in 2016; n=201 in 2017) learned the two CPGs in the education program of the EGUIDE project over two days, and clinical knowledge of the two CPGs was evaluated by two 37-item questionnaires at baseline and after the EGUIDE programs. To improve the correct answer rate for clinical knowledge after the EGUIDE programs, we revised the lecture materials associated with items that had a low correct answer rate in 2016 and used the revised lecture materials with the CPGs in 2017. The rates of correct answers after the EGUIDE programs for each item between the 2016 and 2017 groups were compared.Results: The total clinical knowledge scores after the EGUIDE program significantly increased in both the 2016 groups and the 2017 groups. We revised lecture materials related to two items in the schizophrenia CPG and five items in the MDD CPG that had low correct answer rates after the EGUIDE programs. The correct answer rate of one item on the schizophrenia CPG and one item on the MDD CPG tended to be improved (S-D5, p=0.038; D-C6, p=0.033) and that of one on the MDD CPG was significantly improved (D-D3, p=0.00080) in the 2017 group compared to those in the 2016 group. The other four items were not significantly improved.Conclusions: We reported improvements in clinical knowledge of CPGs after the EGUIDE program in the 2017 group following revision of the lecture materials based on results from the 2016 group. These attempts to improve the degree of understanding of CPGs may facilitate the successful dissemination and implementation of psychiatric guidelines in everyday practice.Trial registration: Effectiveness of Guideline for Dissemination and Education in Psychiatric Treatment, UMIN000022645, Registered 15 June 2016, https://upload.umin.ac.jp/cgi-open-bin/ctr/ctr.cgi?function=brows&action=brows&recptno=R000026044&type=summary&language=J



2011 ◽  
Vol 108 (3) ◽  
pp. 874-882 ◽  
Author(s):  
Roberta Steer

To ascertain whether self-reported inability to cry would be associated with symptoms of anhedonic depression, the 21-item Beck Depression Inventory-II was administered to 1,050 outpatients diagnosed with a DSM-IV-TR major depressive disorder. 219 (21%) patients reported on the BDI-II Crying item that they were unable to cry, and 831 (79%) patients reported they were able to cry. Only BDI-II Loss of Interest was significantly associated with the inability to cry after the other BDI-II symptoms were controlled for using a multiple logistic-regression analysis. The inability to cry was discussed as an indicator of anhedonic depression.



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