76 research outputs found

    Evidence-b(i)ased psychiatry

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    Evidence-b(i)ased psychiatry

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    Evidence-b(i)ased psychiatry

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    A comparison of DSM-5 and DSM-IV agoraphobia in the World Mental Health Surveys

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    BACKGROUND: The Diagnostic and Statistical Manual of Mental Disorders, version 5 (DSM-5) definition of agoraphobia (AG) as an independent diagnostic entity makes it timely to re-examine the epidemiology of AG. Study objective was to present representative data on the characteristics of individuals who meet DSM-IV criteria for AG (AG without a history of panic disorder [PD] and PD with AG) but not DSM-5 criteria, DSM-5 but not DSM-IV criteria, or both sets of criteria.METHODS: Population-based surveys from the World Mental Health Survey Initiative including adult respondents (n = 136,357) from 27 countries across the world. The Composite International Diagnostic Interview was used to assess AG and other disorders.RESULTS: Lifetime and 12-month prevalence estimates of DSM-5 AG (1.5% and 1.0%) were comparable to DSM-IV (1.4% and 0.9%). Of respondents meeting criteria in either system, 57.1% met criteria in both, while 24.2% met criteria for DSM-5 only and 18.8% for DSM-IV only. Severe role impairment due to AG was reported by a lower proportion of respondents who met criteria only for DSM-IV AG (30.4%) than those with both DSM-5 and DSM-IV AG (44.0%; χ 21  = 4.7; P = 0.031). The proportion of cases with any comorbidity was lower among respondents who met criteria only for DSM-IV AG (78.7%) than those who met both sets (92.9%; χ 21 = 14.5; P &lt; 0.001).CONCLUSIONS: This first large survey shows that, compared to the DSM-IV, the DSM-5 identifies a substantial group of new cases with AG, while the prevalence rate remains stable at 1.5%. Severity and comorbidity are higher in individuals meeting DSM-5 AG criteria compared with individuals meeting DSM-IV AG criteria only.</p

    Evidence-b(i)ased psychiatry

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    Ongeveer één op de vijf mensen krijgt gedurende het leven te maken met een depressie of angststoornis. De behandelingen hiervoor (antidepressiva en psychotherapie) zijn uitgebreid bestudeerd, maar belangrijke vragen zijn nog onbeantwoord gebleven. Dit proefschrift beantwoordt een aantal van deze vragen en toont aan dat de evidence base bedreigd wordt door vertekeningen (biases), doordat positieve bevindingen vaker gepubliceerd worden dan negatieve. Bovendien wijst dit proefschrift verschillende kenmerken aan die goede behandeluitkomsten voorspellen. Ten eerste bleek dat negatieve studies van antidepressiva en psychotherapie vaak ongepubliceerd bleven of gepubliceerd werden alsof ze positief waren, wat een misleidend beeld van effectiviteit veroorzaakte. Ernstige negatieve gebeurtenissen, zoals suïcidepogingen, die mogelijk gerelateerd zijn aan de behandeling, werden ook vaak niet (correct) gerapporteerd in gepubliceerde artikelen. Daarnaast werden negatieve studies minder vaak geciteerd dan positieve studies of negatieve studies die positief gepresenteerd waren. Ten tweede bleek dat patiënten met een lichte vorm van sommige (maar niet alle) angststoornissen, specifiek gegeneraliseerde angststoornis en paniekstoornis, weinig baat hadden bij antidepressiva vergeleken met patiënten met ernstigere klachten. In depressieve patiënten voorspelde een kleine verbetering in hun depressie tijdens de eerste twee weken van een behandeling met antidepressiva goede uitkomsten, maar welke specifieke symptomen opknapten was onbelangrijk. Samenvattend heeft dit proefschrift opgehelderd dat, hoewel behandelingen voor depressie en angst effectief zijn, hun effectiviteit en veiligheid overschat worden door biases. Het heeft daarnaast aangetoond dat patiënten met ernstige klachten van gegeneraliseerde angst of paniek en diegenen met een vlotte verbetering na het starten van de behandeling het beste reageren op antidepressiva

    Commentary:The evidence base regarding the long-term effects of childhood mental disorder treatments needs to be strengthened – reply to Dekkers et al. (2023)

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    In their reply to our editorial (Journal of Child Psychology and Psychiatry, 2023, 64, 464), Dekkers et al. (Journal of Child Psychology and Psychiatry, 2023, 64, 470) argue that treatment is the best choice for children with mental disorders because there is ‘sound evidence’ that interventions are effective, also in the long term. We agree that there is sound evidence for treatment effectiveness in the short-term and there is some evidence for longer-term effects of certain specific treatments, such as behavioral parent training in children with behavioral disorders, as acknowledged in our editorial. However, we strongly disagree that there is sound evidence for long-term effectiveness.</p

    Initial severity and antidepressant efficacy for anxiety disorders, obsessive-compulsive disorder, and posttraumatic stress disorder:An individual patient data meta-analysis

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    Background: It has been suggested that antidepressant benefits are smaller for mild than severe depression. Because antidepressants are also used for anxiety disorders, obsessive-compulsive disorder (OCD), and posttraumatic stress disorder (PTSD), we examined the influence of severity for these disorders. Methods: We used individual patient data of eight trials (3,430 participants) for generalized anxiety disorder (GAD); four trials (1,195 participants) for social anxiety disorder (SAD); four trials (1,132 participants) for OCD; three trials (1,071 participants) for PTSD; and 10 trials (2,151 participants) for panic disorder (PD). Mixed-effects models were used to investigate an interaction between severity and treatment group. Results: For GAD and PD, severity moderated antidepressant efficacy. The antidepressant-placebo difference was 1.4 (95% CI: 0.4-2.5; SMD: 0.21) Hamilton Anxiety Rating Scale (HAM-A) points for participants with mild GAD (baseline HAM-A=10), increasing to 4.0 (3.4-4.6; SMD: 0.45) or greater for severely ill participants (HAM-A >= 30). For PD, the difference was 0.4 (0.3-0.6) panic attacks/2weeks for participants with 10 panic attacks/2weeks at baseline, increasing to 4.7 (3.0-6.4) for participants with 40. For SAD, OCD, and PTSD, no interaction was found. Across severity levels, the differences were 16.1 (12.9-19.3; SMD: 0.59) Liebowitz Social Anxiety Scale points, 3.4 (2.5-4.4, SMD: 0.39) Yale-Brown Obsessive-Compulsive Scale points, and 10.3 (6.9-13.6; SMD: 0.41) Clinician-Administered PTSD Scale points. Conclusions: Antidepressants are equally effective across severity levels for SAD, OCD, and PTSD. For GAD and PD, however, benefits are small at low severity, and the benefit-risk ratio may be unfavorable for these patients

    Comparing the evidential strength for psychotropic drugs:a Bayesian meta-analysis

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    Approval and prescription of psychotropic drugs should be informed by the strength of evidence for efficacy. Using a Bayesian framework, we examined (1) whether psychotropic drugs are supported by substantial evidence (at the time of approval by the Food and Drug Administration), and (2) whether there are systematic differences across drug groups. Data from short-term, placebo-controlled phase II/III clinical trials for 15 antipsychotics, 16 antidepressants for depression, nine antidepressants for anxiety, and 20 drugs for attention deficit hyperactivity disorder (ADHD) were extracted from FDA reviews. Bayesian model-averaged meta-analysis was performed and strength of evidence was quantified (i.e. BFBMA). Strength of evidence and trialling varied between drugs. Median evidential strength was extreme for ADHD medication (BFBMA = 1820.4), moderate for antipsychotics (BFBMA = 365.4), and considerably lower and more frequently classified as weak or moderate for antidepressants for depression (BFBMA = 94.2) and anxiety (BFBMA = 49.8). Varying median effect sizes (ESschizophrenia = 0.45, ESdepression = 0.30, ESanxiety = 0.37, ESADHD = 0.72), sample sizes (Nschizophrenia = 324, Ndepression = 218, Nanxiety = 254, NADHD = 189.5), and numbers of trials (kschizophrenia = 3, kdepression = 5.5, kanxiety = 3, kADHD = 2) might account for differences. Although most drugs were supported by strong evidence at the time of approval, some only had moderate or ambiguous evidence. These results show the need for more systematic quantification and classification of statistical evidence for psychotropic drugs. Evidential strength should be communicated transparently and clearly towards clinical decision makers

    Citation bias and selective focus on positive findings in the literature on the serotonin transporter gene (5-HTTLPR), life stress and depression

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    Background Caspi et al.'s 2003 report that 5-HTTLPR genotype moderates the influence of life stress on depression has been highly influential but remains contentious. We examined whether the evidence base for the 5-HTTLPR-stress interaction has been distorted by citation bias and a selective focus on positive findings. Method A total of 73 primary studies were coded for study outcomes and focus on positive findings in the abstract. Citation rates were compared between studies with positive and negative results, both within this network of primary studies and in Web of Science. In addition, the impact of focus on citation rates was examined. Results In all, 24 (33%) studies were coded as positive, but these received 48% of within-network and 68% of Web of Science citations. The 38 (52%) negative studies received 42 and 23% of citations, respectively, while the 11 (15%) unclear studies received 10 and 9%. Of the negative studies, the 16 studies without a positive focus (42%) received 47% of within-network citations and 32% of Web of Science citations, while the 13 (34%) studies with a positive focus received 39 and 51%, respectively, and the nine (24%) studies with a partially positive focus received 14 and 17%. Conclusions Negative studies received fewer citations than positive studies. Furthermore, over half of the negative studies had a (partially) positive focus, and Web of Science citation rates were higher for these studies. Thus, discussion of the 5-HTTLPR-stress interaction is more positive than warranted. This study exemplifies how evidence-base-distorting mechanisms undermine the authenticity of research findings
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