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Official websites use. Share sensitive information only on official, secure websites. We investigated the existence of a temporal association between age at initiation of cannabis use and age at onset of psychotic illness in participants from the Survey of High Impact Psychosis SHIP in Australia. We tested for group differences in age at onset of psychotic illness and in the duration of premorbid exposure to cannabis DPEC. The effect of age at initiation of cannabis use on DPEC was not significant mean duration of 7. A temporal direct relationship between age at initiation of cannabis use and age at onset of psychotic illness was detected with a premorbid exposure to cannabis trend of 7—8 years, modifiable by higher severity of premorbid cannabis use and a diagnosis of SSD. Cannabis may exert a cumulative toxic effect on individuals on the pathway to developing psychosis, the manifestation of which is delayed for approximately 7—8 years, regardless of age at which cannabis use was initiated. There is ongoing debate regarding the association between cannabis use and age at onset of psychosis AOP. A recent meta-analysis by Large et al. If cannabis use brings forward the AOP, then one may anticipate that a temporal relationship between age at initiation of cannabis use AIC and AOP might be observed after adjustment for confounder effects. However, few studies have specifically addressed this question within sufficiently large samples of participants with psychosis. In a sample of 99 participants with a first-psychotic episode, Leeson et al. The average duration of premorbid exposure to cannabis DPEC was reported as 6 years and 33 days. In a sample of 57 participants with a nonaffective psychotic disorder who gave a history of heavy cannabis use, Galvez-Buccollini et al. In a sample of 80 young participants with early onset schizophrenia-spectrum disorders mean AOP was Taken together, these small studies suggest a temporal relationship between AIC and AOP in nonaffective psychotic disorders. Information on participants was obtained from the Survey of High Impact Psychosis SHIP , which recruited people with psychosis from across 7 sites in 5 states of Australia in For full details of the methodology, see Morgan et al. Participants were assessed using the Diagnostic Interview for Psychosis DIP , a standardized semistructured interview for psychosis. Interrater reliability was assessed in the course of the field interviews and the level of agreement achieved among interviewers was good averaged pairwise agreement of 0. The DIP also enables the interviewer to assess family history for schizophrenia and other psychiatric disorders. In addition, the DIP includes items on current and past substance use for alcohol, tobacco, cannabis, amphetamines, lysergic acid diethylamide LSD , cocaine, ecstasy, and heroin, yielding age of first use, frequency of use in the 12 months prior to psychiatric symptoms first appearing, frequency of substance use in the 12 months prior to interview, and a lifetime diagnosis of substance dependence. AOP was determined after interviewing the participant and reviewing the hospital file if consent was given. AOP was recorded to the nearest year and defined as the earliest age at which medical advice was sought for psychiatric reasons, or age at which any psychiatric symptom diagnostic of psychotic or major affective illnesses began to cause subjective distress or impair functioning. If there were no clear symptoms described, then age at first hospital admission was recorded. Age at interview, SSD, and lifetime cannabis dependence LCD were not considered as covariates because they shared large proportion of variance with both dependent and independent variables. Figure showing mean with standard errors age at onset of psychosis according to age at initiation of cannabis use and time gap between initiation to cannabis and onset of psychosis. Furthermore, we examined potential trends in our data. In order to further ascertain whether greater presumed severity of premorbid use of cannabis, diagnosis of schizophrenia-spectrum disorder SSD , or a combination may alter mean DPEC and DPEC among AIC groups, we repeated these analyses for 3 overlapping subsets. These findings, derived retrospectively from a large population of representatively ascertained participants with psychosis in Australia, 6 , 7 extend previous reports on the association between cannabis and onset of psychosis by demonstrating that AIC is directly and linearly associated with AOP and that an average delay of 7—8 years mean 7. Our study can be seen as complementary to previous work in the general population that has established a temporal association between early cannabis use and risk for psychotic disorders 11 , 12 and with McGrath et al. Much research has focused on adolescence as a particularly vulnerable period of brain maturation for those exposed to cannabis. As noted by Moore et al. The increased risk of psychosis in people using cannabis from a younger age observed in the Dunedin cohort 11 could indicate, for instance, a greater cumulative exposure to cannabis rather than a sensitive period of exposure. We can only speculate on the reasons behind the apparent 7—8-year consistent trend of cannabis exposure in people who develop psychosis. It could be argued that both AIC and AOP tend to cluster independently of each other in particular periods in the life-span AIC in adolescence, AOP in early adulthood ; therefore, collinearity resulting in a relatively constant DPEC might be expected even if no causal link between cannabis and psychosis existed. However, this is unlikely to explain why mean DPEC is relatively constant across a wide range of AIC groups extending from 12 to over 21 years of age. Furthermore, if the observed temporal association between AIC and AOP was entirely unrelated to causal effects of cannabis exposure on psychosis onset, we would not observe a shift toward a shorter mean DPEC 7. Our findings would be consistent with the notion that cannabis exposure exerts a cumulative toxic effect, particularly in people on the pathway to developing SSD, the manifestation of which is delayed for approximately 7—8 years, regardless of the AIC. While the mechanisms by which cannabis may exert such delayed effects are unclear, several authors have suggested a mechanism involving sensitization of the mesolimbic dopaminergic system, triggered by repeated stimulation with cannabis, to which susceptible individuals may be especially vulnerable, 14 , 18 , 19 possibly due to a heightened, genetically determined sensitivity to the psychotomimetic effects of cannabis. This publication is based on data collected in the framework of the Australian National Survey of High Impact Psychosis. Morgan National Project Director , A. Jablensky Chief Scientific Advisor , A. Waterreus National Project Coordinator , R. Bush, V. Carr, D. Castle, M. Cohen, C. Galletly, C. Harvey, B. Hocking, A. Mackinnon, P. McGorry, J. McGrath, A. Neil, S. Saw, H. Ethics approvals for the study were obtained from relevant institutional human research ethics committees. This report acknowledges, with thanks, the hundreds of mental health professionals who participated in the preparation and conduct of the survey and the many Australians with psychotic disorders who gave their time and whose responses form the basis of this publication. The authors have declared that there are no conflicts of interest in relation to the subject of this study. As a library, NLM provides access to scientific literature. Schizophr Bull. Find articles by Nikos C Stefanis. Find articles by Milan Dragovic. Find articles by Brian D Power. Find articles by Assen Jablensky. Find articles by David Castle. Find articles by Vera Anne Morgan. Accepted Feb 13; Issue date Mar. All rights reserved. For permissions, please email: journals. Open in a new tab. Similar articles. Add to Collections. Create a new collection. 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Age at Initiation of Cannabis Use Predicts Age at Onset of Psychosis: The 7- to 8-Year Trend
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