Artigo Psicose e Maconha

Introduction
Prospective cohort studies have found that early-onset cannabis use is associated with an increased risk of psychosis-related outcomes.^1–7 Based on these studies and a range of other lines of evidence, reviews have generally concluded that cannabis use is a risk-modifying factor for these outcomes (ie, cannabis use is causally related to psychosis-related outcomes).^8–13 However, there are lingering concerns that the association may reflect methodological biases and unmeasured residual confounding.^14–15 In a recent meta-analysis, Moore and colleagues¹¹ noted that after adjusting for various methodological issues, there were often substantial reductions in the effect size between cannabis use and later psychosis-related outcomes.

Because the pooled effect size reported by Moore and colleagues was modest (adjusted odds ratio, 1.41; 95% confidence interval [CI], 1.20-1.65), the role of residual confounding cannot be discounted. In light of the limitations of observational epidemiology,¹⁶ it is understandable that there is debate about the public health implications of these findings.^{15, 17
Original_Article_Psicose_e_maconha.pdf}