A controlled family study of cannabis users with and without psychosis
Section snippets
Background
Many studies have shown an association between cannabis use and schizophrenia (Compton et al., 2009, Galvez-Buccollini et al., 2012, Zammit et al., 2002). Compton et al.'s (2009) study and Galvez-Buccollini et al.'s (2012) study both found that cannabis use during adolescence may cause an earlier age of onset of psychosis than would have occurred in the absence of cannabis use. Galvez-Buccollini found a direct association between age of onset of cannabis use and age of onset of psychosis (
Subjects
Subjects came from the New York City metropolitan area where the PI (LED) was a professor in the Department of Psychiatry, New York University, Langone School of Medicine until 2011. On her relocation to Boston and the Department of Psychiatry at Harvard Medical School, the acquisition of subjects was expanded to the Boston area. Eligible subjects in both locations were between the ages of 16 and 40 and consisted of four samples:
- Sample 1
Controls with no lifetime history of psychotic illness, cannabis,
Schizophrenia in relatives
Familial aggregation of schizophrenia in first-degree relatives (FDRs) is presented in Table 2. FDR of cannabis using patients had a significantly higher MR for schizophrenia than the cannabis using controls (p = .002). No significant differences in MR for schizophrenia in the FDR of patients who use or do not use cannabis were found (p = .43). There was also no difference in MR for schizophrenia for FDR of controls who use or do not use cannabis (p = .34) (Table 2). There were no significant changes
Discussion
This study aimed to determine whether people who use cannabis during adolescence have a greater risk for developing schizophrenia because they have an increased familial risk for the illness, and thus have a genetic predisposition for developing it regardless of cannabis use. If this is the case, we would expect to find a significantly higher morbid risk for schizophrenia in the relatives of people who develop schizophrenia compared to the relatives of non-schizophrenia controls, regardless of
Role of funding source
None.
Contributors
No other contributors other than those listed in acknowledgments.
Conflict of interest
No co-authors had any conflict of interest.
Acknowledgments
This project was funded by the National Institute of Drug Abuse (R01 DA 021576).
The authors thank Veronica Tomaselli and Melissa Trachtenberg for their work on the grant in ascertainment of subjects and study conduct during their time at New York University School of Medicine and Ashley D. Cameron, BA, and Ariella A. Camera, MS for their help in data collection at the VA Boston Healthcare System. Dr. Richard Rosenthal (Chairman, Department of Psychiatry, St. Luke's Roosevelt Hospital Center,
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2021, Schizophrenia ResearchCitation Excerpt :Different theories are discussed: First, the psychosis risk might be primarily caused by familial risk for schizophrenia and only appears to be triggered by cannabis consumption. For example, Proal et al. (2014) showed that both cannabis using and non-using relatives of patients with psychosis showed increased familial risk for psychotic-like symptoms compared with their respective non-psychotic control samples. Secondly, co-occurring genetic or environmental risk factors including stress exposure could contribute to both cannabis use and PLEs in adolescents (Shakoor et al., 2015; Arranz et al., 2018).
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2018, Schizophrenia ResearchCitation Excerpt :Subjects were between the ages of 18 and 40, and were recruited from New York City and the metropolitan Boston area. Criteria for SSD patient eligibility included a current diagnosis of schizophrenia, schizoaffective disorder, schizophreniform disorder, or psychosis not otherwise specified (see Proal et al., 2014 for details of methods). This study was approved by the institutional review boards (IRBs) for each medical center where patients originated and subjects were recruited.
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2017, International Journal of Drug PolicyCitation Excerpt :These findings have been confirmed in other cohorts studies, which have also reported that individuals with cannabis use onset before or at age 18 are at an increased risk of developing psychosis (Arseneault et al., 2002; Di Forti et al., 2014; Large, Sharma, Compton, Slade, & Nielssen, 2011). Among the factors that may contribute to this enhanced vulnerability are genetic predisposition (e.g., polymorphisms of catechol-O-methyltransferase (COMT), AKT1, and DAT1, DRD2 genes), family history, early initiation and regular use, and daily use of high THC potency products (Caspi et al., 2005; Giordano, Ohlsson, Sundquist, Sundquist, & Kendler, 2015; Proal, Fleming, Galvez-Buccollini, & DeLisi, 2014; Volkow et al., 2016). Neuroimaging results support the linkage, since there are common morphological changes in CUD and schizophrenia, which may contribute to an exacerbation of psychotic symptoms in chronic cannabis users (Smith et al., 2014; Van Erp et al., 2016; Yücel et al., 2008); and research showing altered cannabinoid receptors in patients with schizophrenia suggest a role for the ECS in vulnerability to psychosis (Volk, Eggan, Horti, Wong, & Lewis, 2014; Wong et al., 2010).