关键词: Adverse effects Anxiety Cannabis Endocannabinoids Tetrahydrocannabinol

来  源:   DOI:10.1159/000534855   PDF(Pubmed)

Abstract:
UNASSIGNED: Cannabis has been reported to have both anxiogenic and anxiolytic effects. Habitual cannabis use has been associated with anxiety disorders (AD). The causal pathways and mechanisms underlying the association between cannabis use (CU)/cannabis use disorder (CUD) and anxiety remain unclear. We examined the literature via a systematic review to investigate the link between cannabis and anxiety. The hypotheses studied include causality, the common factor theory, and the self-medication hypothesis.
UNASSIGNED: Critical systematic review of published literature examining the relationship of CU/CUD to AD or state-anxiety, including case reports, literature reviews, observational studies, and preclinical and clinical studies. A systematic MEDline search was conducted of terms including: [anxiety], [anxiogenic], [anxiolytic], [PTSD], [OCD], [GAD], [cannabis], [marijuana], [tetrahydrocannabinol], [THC].
UNASSIGNED: While several case-control and cohort studies have reported no correlation between CU/CUD and AD or state anxiety (N = 5), other cross-sectional, and longitudinal studies report significant relationships (N = 20). Meta-analysis supports anxiety correlating with CU (N = 15 studies, OR = 1.24, 95% CI: 1.06-1.45, p = 0.006) or CUD (N = 13 studies, OR = 1.68, 95% CI: 1.23-2.31, p = 0.001). PATH analysis identifies the self-medication hypothesis (N = 8) as the model that best explains the association between CU/CUD and AD or state-anxiety. Despite the support of multiple large cohort studies, causal interpretations (N = 17) are less plausible, while the common factor theory (N = 5), stress-misattribution hypothesis, and reciprocal feedback theory lack substantial evidential support.
UNASSIGNED: The association between cannabis and anxiety is best explained by anxiety predisposing individuals toward CU as a method of self-medication. A causal relationship in which CU causes AD incidence is less likely despite multiple longitudinal studies suggesting so.
摘要:
据报道,大麻具有抗焦虑和抗焦虑作用。习惯性使用大麻与焦虑症(AD)有关。大麻使用(CU)/大麻使用障碍(CUD)与焦虑之间关联的因果途径和机制尚不清楚。我们通过系统综述研究了大麻与焦虑之间的联系。研究的假设包括因果关系,共同因素理论,和自我药疗假说。
对已发表文献的批判性系统评价,研究CU/CUD与AD或状态焦虑的关系,包括病例报告,文献综述,观察性研究,以及临床前和临床研究。对术语进行了系统的MEDline搜索,包括:[焦虑],[焦虑],[抗焦虑],[PTSD],[强迫症],[GAD],[大麻],[大麻],[四氢大麻酚],[THC]。
虽然一些病例对照和队列研究报告CU/CUD与AD或状态焦虑之间没有相关性(N=5),其他横截面,纵向研究报告了显著的关系(N=20)。荟萃分析支持与CU相关的焦虑(N=15项研究,OR=1.24,95%CI:1.06-1.45,p=0.006)或CUD(N=13项研究,OR=1.68,95%CI:1.23-2.31,p=0.001)。PATH分析将自我治疗假设(N=8)确定为最能解释CU/CUD与AD或状态焦虑之间关联的模型。尽管有多个大型队列研究的支持,因果解释(N=17)不太合理,而公因子理论(N=5),压力-错误归因假说,互惠反馈理论缺乏实质性的证据支持。
大麻与焦虑之间的关联最好的解释是焦虑使个体倾向于CU作为一种自我治疗的方法。尽管多项纵向研究表明,CU引起AD发病率的因果关系不太可能发生。
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