Cannabis-induced dysphoria/paranoia mediates the link between childhood trauma and psychotic-like experiences in young cannabis users

Carlyle, Molly; Constable, Toby; Walter, Zoe; Wilson, Joanna; Newland, Grace; Hides, Leanne

doi:10.1016/j.schres.2021.10.011

Cited by 8 publications

(10 citation statements)

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“…Out of 41 studies, 28 of them investigated the interplay between childhood trauma (CT) and cannabis use (CU) in conferring psychosis risk or exacerbating psychosis symptoms among both healthy individuals and patients (Tables 1 and 2 ). The review identified similar but not overlapping methodologies (Table 3 ) in terms of study population (schizophrenia/schizoaffective disorder [ 36 - 39 ], bipolar affective disorder [ 37 , 39 , 40 ], ROP patients [ 41 , 42 ], FEP patients [ 37 , 43 ], CHR individuals [ 44 ], general population [ 45 - 59 ], healthy subjects [ 43 , 60 - 62 ], cannabis-using subjects [ 37 , 63 ]), sample size (range: 112-7403 subjects), type of CT (sexual [ 36 - 38 , 40 - 57 , 59 - 63 ], physical/violence [ 36 , 38 , 41 - 44 , 46 , 47 , 49 , 50 , 53 - 56 , 60 - 63 ], emotional [ 36 , 38 , 41 , 42 , 44 , 47 , 49 , 50 , 53 , 56 , 57 , 60 - 63 ], domestic violence [ 46 ], peer victimization/bullyism [ 56 , 57 ]), cannabinoid exposure (use [ 37 - 63 ], disorder/dependence [ 36 , 40 ]), cannabinoid period of exposure (lifetime [ 36 -…”

Section: Resultsmentioning

confidence: 99%

“…Among studies investigating the independent effect of CT on psychosis risk, evidence tips the scale towards a deleterious effect of CT in terms of increasing the risk of getting a psychosis diagnosis and experiencing psychotic symptoms [ 38 , 42 , 44 , 46 - 48 , 53 , 54 , 57 , 61 , 63 ] among different study samples, including schizophrenia/schizoaffective disorder [ 38 ] and ROP patients [ 42 ], CHR individuals [ 44 ], general population [ 46 - 48 , 53 , 54 , 57 ], healthy subjects [ 61 ], and cannabis-using subjects [ 63 ]. Also, CT has been found to anticipate psychosis onset [ 39 ] and predict a poorer clinical course [ 36 ] among patient samples.…”

Section: Resultsmentioning

confidence: 99%

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Biobehavioral Interactions between Endocannabinoid and Hypothalamicpituitary- adrenal Systems in Psychosis: A Systematic Review

Colizzi

Bortoletto

Antolini

et al. 2024

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Background: The diathesis-stress paradigm and the cannabinoid-hypothesis have been proposed as possible pathophysiological models of schizophrenia. However, they have historically been studied independently of each other. Objective: This PRISMA 2020-compliant systematic review aimed at reappraising the interplay be- tween the hypothalamic-pituitary-adrenal (HPA) axis and the endocannabinoid (eCB) system in psy- chosis-spectrum disorder risk and outcome. Methods: All pathophysiological and outcome clinical studies, concomitantly evaluating the two sys- tems in psychosis-spectrum disorder risk and different stages of illness, were gathered from electronic databases (Pubmed, Web of Science, and Scopus), and discussed. Results: 41 eligible outputs were extracted, focusing on at least a biological measure (9 HPA-related studies: 4 eCB-interventional, 1 HPA-interventional, 1 both HPA-interventional and non-interventional, 3 non-interventional; 2 eCB-related studies: non-interventional), environmental measures only (29 studies: 1 eCB- interventional, 28 non-interventional), and genetic measures (1 study: non-interventional). In- dependent contributions of aberrancies in the two systems to the physiopathology and outcome of psy- chosis were confirmed. Also, concomitant alterations in the two systems, either genetically defined (e.g., CNR1 genetic variation), biologically determined (e.g., dysfunctional HPA axis or endocanna- binoid signaling), or behaviorally imputed (e.g., cannabis use, stress exposure, and response), were consistently reported in psychosis. Further, a complex biobehavioral perturbation was revealed not on- ly within each system (e.g., cannabis use affecting the eCB tone, stress exposure affecting the HPA ax- is), but also across the two systems (e.g., THC affecting the HPA axis, childhood trauma affecting the endocannabinoid signaling). Conclusion: There is a need to concomitantly study the two systems’ mechanistic contribution to psychosis in order to establish more refined biological relevance.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Biobehavioral Interactions between Endocannabinoid and Hypothalamicpituitary- adrenal Systems in Psychosis: A Systematic Review

Colizzi

Bortoletto

Antolini

et al. 2024

View full text Add to dashboard Cite

show abstract

“…A similar relationship was also with childhood trauma, such that the relationship between PRS-SZ and childhood trauma showed significant dependence on the concomitant presence of affective dysregulation, and was particularly evident for delusional ideation (van Os et al, 2020 ). Cannabis-induced dysphoria was also shown to mediate the relationship between childhood trauma and psychotic experiences (Carlyle et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

Bidirectional relationships between cannabis use, anxiety and depressive symptoms in the mediation of the association with psychotic experience: further support for an affective pathway to psychosis

et al. 2022

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Background Empirical evidence suggests that people use cannabis to ameliorate anxiety and depressive symptoms, yet cannabis also acutely worsens psychosis and affective symptoms. However, the temporal relationship between cannabis use, anxiety and depressive symptoms and psychotic experiences (PE) in longitudinal studies is unclear. This may be informed by examination of mutually mediating roles of cannabis, anxiety and depressive symptoms in the emergence of PE. Methods Data were derived from the second longitudinal Netherlands Mental Health Survey and Incidence Study. Mediation analysis was performed to examine the relationship between cannabis use, anxiety/depressive symptoms and PE, using KHB logit in STATA while adjusting for age, sex and education status. Results Cannabis use was found to mediate the relationship between preceding anxiety, depressive symptoms and later PE incidence, but the indirect contribution of cannabis use was small (for anxiety: % of total effect attributable to cannabis use = 1.00%; for depression: % of total effect attributable to cannabis use = 1.4%). Interestingly, anxiety and depressive symptoms were found to mediate the relationship between preceding cannabis use and later PE incidence to a greater degree (% of total effect attributable to anxiety = 17%; % of total effect attributable to depression = 37%). Conclusion This first longitudinal cohort study examining the mediational relationship between cannabis use, anxiety/depressive symptoms and PE, shows that there is a bidirectional relationship between cannabis use, anxiety/depressive symptoms and PE. However, the contribution of anxiety/depressive symptoms as a mediator was greater than that of cannabis.

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“…While some of the variability in risk may be explained by age at first use, frequency of use, and genetic factors [ 122 , 127 ], psychosocial stress exposure may also influence the extent to which substance use contributes to emerging psychopathological states [ 128 , 129 ]. For example, evidence suggests that childhood trauma and cannabis use interact to increase the risk and frequency of PLEs in adolescents and young adults [ 130 , 131 ].…”

Section: Psychosocial Stressorsmentioning

confidence: 99%

The Translational Future of Stress Neurobiology and Psychosis Vulnerability: A Review of the Evidence

Cullen

Labad

Oliver

et al. 2024

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Psychosocial stress is a well-established risk factor for psychosis, yet the neurobiological mechanisms underlying this relationship have yet to be fully elucidated. Much of the research in this field has investigated hypothalamic-pituitary-adrenal (HPA) axis function and immuno-inflammatory processes among individuals with established psychotic disorders. However, as such studies are limited in their ability to provide knowledge that can be used to develop preventative interventions, it is important to shift the focus to individuals with increased vulnerability for psychosis (i.e., high-risk groups). In the present article, we provide an overview of the current methods for identifying individuals at high-risk for psychosis and review the psychosocial stressors that have been most consistently associated with psychosis risk. We then describe a network of interacting physiological systems that are hypothesised to mediate the relationship between psychosocial stress and the manifestation of psychotic illness and critically review evidence that abnormalities within these systems characterise high risk populations. We found that studies of high-risk groups have yielded highly variable findings, likely due to (i) the heterogeneity both within and across high-risk samples, (ii) the diversity of psychosocial stressors implicated in psychosis, and (iii) that most studies examine single markers of isolated neurobiological systems. We propose that to move the field forward, we require well-designed, large- scale translational studies that integrate multi-domain, putative stress-related biomarkers to determine their prognostic value in high-risk samples. We advocate that such investigations are highly warranted, given that psychosocial stress is undoubtedly a relevant risk factor for psychotic disorders.

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Cannabis-induced dysphoria/paranoia mediates the link between childhood trauma and psychotic-like experiences in young cannabis users

Cited by 8 publications

References 45 publications

Biobehavioral Interactions between Endocannabinoid and Hypothalamicpituitary- adrenal Systems in Psychosis: A Systematic Review

Biobehavioral Interactions between Endocannabinoid and Hypothalamicpituitary- adrenal Systems in Psychosis: A Systematic Review

Bidirectional relationships between cannabis use, anxiety and depressive symptoms in the mediation of the association with psychotic experience: further support for an affective pathway to psychosis

The Translational Future of Stress Neurobiology and Psychosis Vulnerability: A Review of the Evidence

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