a b s t r a c tBackground: The use of amphetamines is a global public health concern. We summarise global data on use of amphetamines and mental health outcomes. Methods: A systematic review and meta-analysis (CRD 42017081893). We searched Medline, EMBASE, PsycInfo for methamphetamine or amphetamine combined with psychosis, violence, suicidality, depression or anxiety. Included studies were human empirical cross-sectional surveys, case-control studies, cohort studies and randomised controlled trials that assessed the association between methamphetamine and one of the mental health outcomes. Random effects meta-analysis was used to pool results for any use of amphetamines and amphetamine use disorders. Findings: 149 studies were eligible and 59 were included in meta-analyses. There was significant heterogeneity in effects. Evidence came mostly from cross-sectional studies. Any use of amphetamines was associated with higher odds of psychosis (odds ratio [OR] = 2.0, 95%CI 1.3-3.3), violence (OR = 2.2, 95%CI 1.2-4.1; adjusted OR [AOR] = 1.4, 95%CI 0.8-2.4), suicidality OR = 4.4, 95%CI 2.4-8.2; AOR = 1.7, 95%CI 1.0-2.9) and depression (OR = 1.6, 95%CI 1.1-2.2; AOR = 1.3, 95%CI 1.2-1.4). Having an amphetamine use disorder was associated with higher odds of psychosis (OR = 3.0, 95%CI 1.9-4.8; AOR = 2.4, 95%CI 1.6-3.5), violence (OR = 6.2, 95%CI 3.1-12.3), and suicidality (OR = 2.3, 95%CI 1.8-2.9; AOR = 1.5, 95%CI 1.3-1.8). Interpretation: Methamphetamine use is an important risk factor for poor mental health. High quality population-level studies are needed to more accurately quantify this risk. Clinical responses to methamphetamine use need to address mental health harms.

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The most consistent correlates of psychotic symptoms were increased frequency of methamphetamine use and dependence on methamphetamine. The findings of this review highlight the need for targeted assessment and treatment of methamphetamine use in individuals presenting with psychosis.

Background and aimsLittle is known about how cannabis use over the life-course relates to harms in adulthood.The present study aimed to identify trajectories of cannabis use from adolescence to adulthood and examine both the predictors of these trajectories and adverse adult outcomes associated with those trajectories. Design A latent trajectory analysis of a longitudinal birth cohort (from birth to age 35 years). Setting and participants General community sample (n = 1065) from New Zealand. Measurement Annual frequency of cannabis use (ages 15-35 years); childhood family and individual characteristics (birth to age 16 years); measures of adult outcomes (substance use disorders, ages 30-35 years; mental health disorders, ages 30-35 years; socio-economic outcomes at age 35 years; social/family outcomes at age 35 years). Findings A six-class solution was the best fit to the data. Individuals assigned to trajectories with higher levels of cannabis use were more likely to have experienced adverse childhood family and individual circumstances. Membership of trajectories with higher levels of use was associated with increased risk of adverse outcomes at ages 30-35 years. Adjustment of these associations for the childhood family and individual predictors largely did not reduce the magnitude of the associations. Conclusions In New Zealand, long-term frequent cannabis use, or transition to such use, appears to be robustly associated with diverse harms in adulthood. 12]. This progression also relates to multiple individual and environmental factors, including parental factors, peer influences and personality attributes [8,10,11,13,14]. Frequent cannabis use peaks by late adolescence to early adulthood [5,15] before tapering off in early adulthood [16,17] and becoming uncommon in old age [18]. Most people who are exposed to cannabis do not become regular or dependent users. However, a substantial minority of people exposed to cannabis will develop persisting heavy use into mid-adulthood [16].Longitudinal studies have shown that long-term heavy cannabis use is associated with a range of adverse outcomes. These include dependence on the drug, poorer education and work outcomes [19][20][21][22][23], impaired cognitive functioning [16,24], structural and functional brain changes [25] and higher rates of other substance disorders and mental disorders [15,26,27] including psychosis [28].

BackgroundThe extent to which exposure to childhood sexual and physical abuse increases the risk of psychotic experiences in adulthood is currently unclear.AimsTo examine the relationship between childhood sexual and physical abuse and psychotic experiences in adulthood taking into account potential confounding and time-dynamic covariate factors.MethodData were from a cohort of 1265 participants studied from birth to 35 years. At ages 18 and 21, cohort members were questioned about childhood sexual and physical abuse. At ages 30 and 35, they were questioned about psychotic experiences (symptoms of abnormal thought and perception). Generalised estimating equation models investigated covariation of the association between abuse exposure and psychotic experiences including potential confounding factors in childhood (socioeconomic disadvantage, adverse family functioning) and time-dynamic covariate factors (mental health, substance use and life stress).ResultsData were available for 962 participants; 6.3% had been exposed to severe sexual abuse and 6.4% to severe physical abuse in childhood. After adjustment for confounding and time-dynamic covariate factors, those exposed to severe sexual abuse had rates of abnormal thought and abnormal perception symptoms that were 2.25 and 4.08 times higher, respectively than the ‘no exposure’ group. There were no significant associations between exposure to severe physical abuse and psychotic experiences.ConclusionsFindings indicate that exposure to severe childhood sexual (but not physical) abuse is independently associated with an increased risk of psychotic experiences in adulthood (particularly symptoms of abnormal perception) and this association could not be fully accounted for by confounding or time-dynamic covariate factors.Declaration of interestNone.