Antidepressants; what’s the beef?

Abstract:
Do antidepressants, and specifically SSRIs, do more harm than good? The acrimonious debate between colleagues in the wake of yet another meta-analysis, this time by Jakobsen et al. (1), suggests we don’t know (2,3). Or rather, we don’t know how to interpret the facts that randomised clinical trials provide for us to reach a conclusion that everyone can and perhaps should accept. What are the facts? Jacobsen et al. demonstrated that the effect at the end of treatment (usually 6–8 weeks) was a mean difference of −1.94 HDRS points (95% CI −2.50 to −1.37; p< 0.00001) in favour of antidepressants compared with placebo. This confirms what others have reported from similar analyses, of various selections of the same and other trials, published and unpublished. They appear to have made a number of errors in extracting and analysing the data (2), but with little impact on the central result (4). So the question is not whether antidepressants do any good at all, it is what this difference means? NICE suggested in 2006 that ,in clinical trials comparing antidepressant and placebo, a difference on the 17-item Hamilton rating scale should be 3 for an effect to be clinically meaningful. Jakobsen et al. make much of this. Unfortunately, how that number was derived is a mystery. It is not based on a correlation between this symptomatic improvement and some superior measure of ecological benefit. Indeed, there are no convincing data which directly relate the change on a rating scale to some agreed gold standard measure of recovery. Most psychiatrists are happy, in principle, with the extrapolation of early reductions in symptoms to eventual recovery because they see it in their patients. However, a difference of 3 points at 6 weeks has no intuitive meaning. In fact, the mean change in symptom scores, while it is the usual metric, is itself potentially misleading because a more detailed examination of response profiles suggests that the distribution of HRSD scores after 6 weeks is better described as bimodal; there are already responders and non-responders. In five trials of escitalopram versus placebo, Michael Thase et al. (5) showed that a bimodal model captured over 60% of the variance, a unimodal only 6%! This suggests that a more intelligent analysis of individual patient data would give a more useful prediction of treatment response and the argument about 3, the magic number, would probably evaporate. In the case of the escitalopram trials, the mean change in HRSD was 3.23, but the probability of response (50% reduction in baseline symptom score) was increased by 19%. This approach had also been taken in a reassessment by the European regulators of their database (1984–2003). They found around an average 16% greater response rate following active treatment than placebo for newer antidepressants (which included SSRIs) (6). Another approach offers an alternative to worrying about the HRSD scales. It suggests that many items on these scales are insensitive to short term changes and/or not present at baseline. In either case, scoring them adds nothing to our understanding of drug action. A meta-analysis of the effect of SSRIs on HRSD items in regulatory trials, showed that depressed mood itself was the most sensitive. The effect size for the whole scale was 0.27, while that for mood per se was 0.4 (7). The bottom line is that SSRIs improve symptoms in major depression and that there can be little doubt around that conclusion. The number needed to treat (NNT) in studies with a mean drug–placebo difference on the HDRS scale of around 3 is between 5 and 7 and this effect size compares reasonably with most drugs used in medicine (8). Finally, analysis of the long-term efficacy of antidepressants shows that in terms of protecting patients against a subsequent relapse to depression these medicines have an NNT of less than 3 (9), which is a remarkable efficacy for any form of treatment. The key issue is how this trades off against ‘harms’. Jacobsen et al make much of the ‘serious adverse effects’ recorded in trials comparing antidepressants with placebo. In total, 239/8242 (2.7%) participants prescribed an antidepressant experienced a ‘serious adverse event’ compared with 106/4956 (2.1%) for placebo. This difference does not correct for increased exposure times in active treatment arms (patients tend to drop out of placebo arms due to lack of efficacy), so the absolute increase in risk may be substantially less than 0.6%. Indeed, a 23% reduction in the exposure in the placebo compared with active arms would obliterate the difference completely. We suspect that such an effect explains the difference in the clinical trials, although we should not be complacent about rare complications in vulnerable Acta Neuropsychiatrica
Author Listing: Guy M Goodwin;David Nutt
Volume: 31
Pages: 59 - 60
DOI: 10.1017/neu.2019.4
Language: English
Journal: Acta Neuropsychiatrica

ACTA NEUROPSYCHIATRICA

ACTA NEUROPSYCHIATR

影响因子:2.6 是否综述期刊:否 是否OA:否 是否预警:不在预警名单内 发行时间:1989 ISSN:0924-2708 发刊频率:Bimonthly 收录数据库:SCIE/Scopus收录 出版国家/地区:DENMARK 出版社:Cambridge University Press

期刊介绍

Acta Neuropsychiatrica is an international journal focussing on translational neuropsychiatry. It publishes high-quality original research papers and reviews. The Journal's scope specifically highlights the pathway from discovery to clinical applications, healthcare and global health that can be viewed broadly as the spectrum of work that marks the pathway from discovery to global health.

《神经精神病学学报》(Acta Neuropsychiatrica)是一份专注于转化神经精神病学的国际期刊。它发表高质量的原创研究论文和评论。该杂志的范围特别强调了从发现到临床应用、医疗保健和全球健康的路径,可以广泛地视为标志着从发现到全球健康的路径的工作范围。

年发文量 48
国人发稿量 5
国人发文占比 10.42%
自引率 3.8%
平均录取率 容易
平均审稿周期 较慢,6-12周
版面费 US$3255
偏重研究方向 医学-精神病学
期刊官网 http://onlinelibrary.wiley.com/journal/10.1111/%28ISSN%291601-5215
投稿链接 -

质量指标占比

研究类文章占比 OA被引用占比 撤稿占比 出版后修正文章占比
83.33% 37.86% 0.00% 0.00%

相关指数

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具体而言,就是通过综合评判期刊载文量、作者国际化程度、拒稿率、论文处理费(APC)、期刊超越指数、自引率、撤稿信息等,找出那些具备风险特征、具有潜在质量问题的学术期刊。最后,依据各刊数据差异,将预警级别分为高、中、低三档,风险指数依次减弱。

《国际期刊预警名单(试行)》确定原则是客观、审慎、开放。期刊分区表团队期待与科研界、学术出版机构一起,夯实科学精神,打造气正风清的学术诚信环境!真诚欢迎各界就预警名单的分析维度、使用方案、值得关切的期刊等提出建议!

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JCR分区 WOS分区等级:Q3区

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WOS期刊SCI分区
WOS期刊SCI分区是指SCI官方(Web of Science)为每个学科内的期刊按照IF数值排 序,将期刊按照四等分的方法划分的Q1-Q4等级,Q1代表质量最高,即常说的1区期刊。
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关于2019年中科院分区升级版(试行)

分区表升级版(试行)旨在解决期刊学科体系划分与学科发展以及融合趋势的不相容问题。由于学科交叉在当代科研活动的趋势愈发显著,学科体系构建容易引发争议。为了打破学科体系给期刊评价带来的桎梏,“升级版方案”首先构建了论文层级的主题体系,然后分别计算每篇论文在所属主题的影响力,最后汇总各期刊每篇论文分值,得到“期刊超越指数”,作为分区依据。

分区表升级版(试行)的优势:一是论文层级的主题体系既能体现学科交叉特点,又可以精准揭示期刊载文的多学科性;二是采用“期刊超越指数”替代影响因子指标,解决了影响因子数学性质缺陷对评价结果的干扰。整体而言,分区表升级版(试行)突破了期刊评价中学科体系构建、评价指标选择等瓶颈问题,能够更为全面地揭示学术期刊的影响力,为科研评价“去四唯”提供解决思路。相关研究成果经过国际同行的认可,已经发表在科学计量学领域国际重要期刊。

《2019年中国科学院文献情报中心期刊分区表升级版(试行)》首次将社会科学引文数据库(SSCI)期刊纳入到分区评估中。升级版分区表(试行)设置了包括自然科学和社会科学在内的18个大类学科。基础版和升级版(试行)将过渡共存三年时间,推测在此期间各大高校和科研院所仍可能会以基础版为考核参考标准。 提示:中科院分区官方微信公众号“fenqubiao”仅提供基础版数据查询,暂无升级版数据,请注意区分。

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版本 大类学科 小类学科 Top期刊 综述期刊
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4区
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2021年12月
升级版
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PSYCHIATRY
精神病学
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NEUROSCIENCES
神经科学
4区
2020年12月
旧的升级版
医学
3区
PSYCHIATRY
精神病学
3区
NEUROSCIENCES
神经科学
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2022年12月
最新升级版
医学
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PSYCHIATRY
精神病学
4区
NEUROSCIENCES
神经科学
4区