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The brain-gut axis: a target for treating stress-related disorders. 脑肠轴:治疗压力相关疾病的目标。
Pub Date : 2013-01-01 Epub Date: 2013-02-27 DOI: 10.1159/000343971
Lucinda V Scott, Gerard Clarke, Timothy G Dinan

The brain-gut axis provides a bidirectional means of communication between the microbiota within the gut and the brain. Stress acting via the brain can result in alteration of the microbial composition of the gut, but increasing evidence indicates that bacteria within the gut can influence brain neurochemistry and behaviour. It is clear that post-natal colonisation of the gut plays a key role in regulating the development of the hypothalamic-pituitary-adrenal axis and the development of pivotal neurotransmitter systems. Probiotics are defined as live bacteria which confer a health benefit. Recent studies in rodents have demonstrated the capacity of a probiotic, Lactobacillus rhamnosus, to alter the expression of GABA receptors centrally whilst producing anxiolytic type effects. Preliminary studies in humans are yielding encouraging findings. It may in the future be possible to use probiotic bacteria to treat depression and other stress-related disorder but we await the results of appropriately designed placebo-controlled trials.

脑肠轴在肠道和大脑内的微生物群之间提供了一种双向的交流方式。通过大脑施加的压力会导致肠道微生物组成的改变,但越来越多的证据表明,肠道内的细菌可以影响大脑的神经化学和行为。很明显,产后肠道的定植在调节下丘脑-垂体-肾上腺轴的发育和关键神经递质系统的发育中起着关键作用。益生菌被定义为对健康有益的活细菌。最近对啮齿动物的研究表明,一种名为鼠李糖乳杆菌的益生菌能够改变GABA受体的表达,同时产生抗焦虑作用。对人类的初步研究取得了令人鼓舞的发现。将来可能会使用益生菌来治疗抑郁症和其他与压力相关的疾病,但我们还在等待适当设计的安慰剂对照试验的结果。
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引用次数: 37
Genetic factors in anxiety disorders. 焦虑症的遗传因素。
Pub Date : 2013-01-01 Epub Date: 2013-09-20 DOI: 10.1159/000351932
Katharina Domschke, Eduard Maron

Presently available clinical genetic studies point to a considerable heritability of anxiety disorders (30-67%), with multiple vulnerability genes such as 5-HT1A, 5-HTT, MAO-A, COMT, CCK-B, ADORA2A, CRHR1, FKBP5, ACE, RGS2/7 and NPSR1 suggested by molecular genetic association studies. These genes have been shown to partially interact with each other as well as with environmental factors to shape the overall disease risk in a complex genetic model. Additionally, recent studies have pointed out the crucial role of epigenetic signatures such as methylation patterns in modifying environmental influences as well as in driving the functional impact of anxiety disorder risk genes. On a systems level, vulnerability genes of anxiety disorders seem to confer some of the disease risk via intermediate phenotypes like behavioral inhibition, anxiety sensitivity or several neurobiological traits such as increased startle reactivity or dysfunctional corticolimbic activity during emotional processing. Finally, first pharmaco- and psychotherapy-genetic studies provide evidence for certain risk genes to confer interindividual variability in response to a pharmacological or psychotherapeutic intervention in anxiety disorders. Genetic research in anxiety disorders will be discussed regarding its potential to foster innovative and individually tailored therapeutic approaches for patients with anxiety disorders.

在一个复杂的遗传模型中,这些基因部分地相互作用,并与环境因素相互作用,从而形成整体疾病风险。此外,最近的研究指出了表观遗传特征(如甲基化模式)在改变环境影响以及驱动焦虑障碍风险基因的功能影响方面的关键作用。在系统层面上,焦虑症的易感基因似乎通过中间表型(如行为抑制、焦虑敏感性)或一些神经生物学特征(如增加的惊吓反应性或情绪处理过程中的皮质边缘活动功能障碍)赋予了一些疾病风险。最后,第一项药物和心理治疗遗传学研究提供了证据,证明某些风险基因在对焦虑症的药物或心理治疗干预的反应中具有个体间变异性。焦虑症的基因研究将讨论其促进焦虑症患者创新和个性化治疗方法的潜力。
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引用次数: 17
Pharmacotherapy of generalized anxiety disorder. 广泛性焦虑障碍的药物治疗。
Pub Date : 2013-01-01 Epub Date: 2013-09-20 DOI: 10.1159/000351955
Christer Allgulander, David S Baldwin

Generalized anxiety disorder (GAD) is chiefly characterized by a cognitive focus on threats and risks towards the individual and/or the immediate family. It is accompanied by a sense of tension, worry, muscle pain, disturbed sleep and irritability. The condition impairs work capacity, relations, and leisure activities, and aggravates concurrent somatic diseases. Due to its chronic course, GAD increases costs for the individual, the family, and health care services, and reduces work and educational performance. In cardiovascular or cerebrovascular disease, pulmonary disease, diabetes and neurological diseases, GAD is a risk factor for somatic complications and for lowered adherence to somatic treatments. There is evidence that GAD can be treated with cognitive behavioural therapy (CBT), and/or with medications. First-line pharmacotherapies are selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs) and pregabalin. If such therapies fail, one may reconsider the diagnosis, question adherence with the prescribed schedule, and determine the adverse influence of comorbidity (such as depression, substance use, and physical ill-health) as well as the influence of social stressors. Second-line pharmacotherapies are largely not supported by controlled trials, and so leave much to clinical judgment and careful monitoring. One may attempt treatments with benzodiazepine anxiolytics, with quetiapine, or with pregabalin as an adjunct therapy in patients with partial response to SSRI or SNRI treatment. CBT is a valid alternative to pharmacotherapy, depending on patient preference.

广泛性焦虑障碍(GAD)的主要特征是对个人和/或直系亲属的威胁和风险的认知关注。它伴随着紧张感、担忧感、肌肉疼痛感、睡眠不安感和易怒感。这种情况损害了工作能力、人际关系和休闲活动,并加重了并发的躯体疾病。由于其慢性病程,广泛性焦虑症增加了个人、家庭和卫生保健服务的成本,并降低了工作和教育表现。在心脑血管疾病、肺病、糖尿病和神经系统疾病中,广泛性焦虑症是躯体并发症和降低对躯体治疗依从性的危险因素。有证据表明广泛性焦虑症可以通过认知行为疗法(CBT)和/或药物治疗。一线药物治疗是选择性5 -羟色胺再摄取抑制剂(SSRIs), 5 -羟色胺-去甲肾上腺素再摄取抑制剂(SNRIs)和普瑞巴林。如果这些治疗失败,人们可以重新考虑诊断,质疑是否遵守规定的时间表,并确定合并症的不利影响(如抑郁、药物使用和身体不健康)以及社会压力源的影响。二线药物治疗在很大程度上没有对照试验的支持,因此留给临床判断和仔细监测的余地很大。对于对SSRI或SNRI治疗有部分反应的患者,可以尝试使用苯二氮卓类抗焦虑药、喹硫平或普瑞巴林作为辅助治疗。CBT是药物治疗的有效替代,取决于患者的偏好。
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引用次数: 2
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Modern trends in pharmacopsychiatry
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