Evidence That Familial Liability for Psychosis Is Expressed as Differential Sensitivity to Cannabis

doi:10.1001/archgenpsychiatry.2010.132

Cited by 99 publications

(42 citation statements)

References 61 publications

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“…Furthermore, these types of interactions have been reported in some FHR studies, suggesting that environmental factors may synergistically combine with pre-existing psychosis liability to cause symptoms of psychosis (Mirsky et al, 1985; Cannon and Mednick, 1993; van Os et al, 2008; GROUP, 2010). Thus, if there is a combination of factors that may explain why some individuals at FHR of psychosis go on to develop the illness and some do not, it may be important to consider why some individuals at FHR develop subthreshold symptoms and why some do not.…”

Section: Introductionmentioning

confidence: 86%

Predictors of a clinical high risk status among individuals with a family history of psychosis

Stowkowy

Addington

2013

Schizophrenia Research

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Background Risk for psychosis can be assessed on the basis of genetic risk, referred to in the literature as family high risk (FHR) or through the presence of clinical high risk symptoms (CHR). Recent studies have also shown that certain risk factors (i.e. trauma, cannabis, migration) may play a role in the development of psychosis, possibly in combination with one another and in particular in combination with a family history of psychosis. It is unknown which risk factors may play a role in the prediction of CHR status among individuals whom are already genetically vulnerable. This study compared FHR individuals who also met CHR criteria to FHR individuals who did not on various risk factors, psychopathology and functioning. Method Participants were 25 who met FHR and CHR criteria (FHR + CHR) as determined by Structured Interview for Prodromal Syndromes, 25 who met only FHR criteria (FHR-non-CHR), and 25 healthy controls. A binary logistic regression was performed to determine the best predictors of belonging to the FHR + CHR group. Results FHR + CHR and FHR-non CHR were significantly different on measures of age first tried cannabis (F = 3.65, p < 0.05) and IQ (F = 3.32, p < 0.05). FHR groups also differed on self-reported anxiety (F = 11.79, p < 0.001) and current scores of social (F = 19.74, p < 0.0001) and role (F = 17.71, p < 0.0001) functioning. The most significant predictor of belonging to the FHR + CHR group was an earlier age of cannabis use (OR = 0.44, p = 0.05). Conclusion These preliminary results are promising in determining potential risk factors for the development of psychosis in those who are at risk for psychosis on the basis of a family history.

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Section: Introductionmentioning

confidence: 86%

Predictors of a clinical high risk status among individuals with a family history of psychosis

Stowkowy

Addington

2013

Schizophrenia Research

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“…Furthermore, patients with psychotic disorder as well as individuals at risk for psychosis seem to express increased sensitivity to cannabis [3], [4], [5], [6], [7], [8]. Yet very little is known about the biological underpinnings of this association [9].…”

Section: Introductionmentioning

confidence: 99%

“…Notably, patients with psychotic disorder have been shown to be more sensitive to the behavioral and cognitive effects of cannabis [3] and individual differences in sensitivity to cannabis seem to be in part mediated by genetic risk for psychotic disorder, siblings displaying more sensitivity than well controls in a recent large prospective study [6]. Yet, the biological mechanisms underlying differential sensitivity to cannabis associated with genetic risk for psychosis remain elusive, as existing imaging studies have focused on healthy controls with minimal exposure to cannabis.…”

Section: Introductionmentioning

confidence: 99%

Delta-9-Tetrahydrocannabinol-Induced Dopamine Release as a Function of Psychosis Risk: 18F-Fallypride Positron Emission Tomography Study

et al. 2013

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Cannabis use is associated with psychosis, particularly in those with expression of, or vulnerability for, psychotic illness. The biological underpinnings of these differential associations, however, remain largely unknown. We used Positron Emission Tomography and 18F-fallypride to test the hypothesis that genetic risk for psychosis is expressed by differential induction of dopamine release by Δ9-THC (delta-9-tetrahydrocannabinol, the main psychoactive ingredient of cannabis). In a single dynamic PET scanning session, striatal dopamine release after pulmonary administration of Δ9-THC was measured in 9 healthy cannabis users (average risk psychotic disorder), 8 patients with psychotic disorder (high risk psychotic disorder) and 7 un-related first-degree relatives (intermediate risk psychotic disorder). PET data were analyzed applying the linear extension of the simplified reference region model (LSRRM), which accounts for time-dependent changes in 18F-fallypride displacement. Voxel-based statistical maps, representing specific D2/3 binding changes, were computed to localize areas with increased ligand displacement after Δ9-THC administration, reflecting dopamine release. While Δ9-THC was not associated with dopamine release in the control group, significant ligand displacement induced by Δ9-THC in striatal subregions, indicative of dopamine release, was detected in both patients and relatives. This was most pronounced in caudate nucleus. This is the first study to demonstrate differential sensitivity to Δ9-THC in terms of increased endogenous dopamine release in individuals at risk for psychosis.

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“…Data were collected from the Genetic Risk and Outcome in Psychosis study (GROUP) [25] (data are available upon request) . In representative geographical areas in the Netherlands and Belgium, patients were identified through clinicians working in regional psychotic disorder services, whose caseload was screened for inclusion criteria.…”

Section: Methodsmentioning

confidence: 99%

Evidence for a Shared Etiological Mechanism of Psychotic Symptoms and Obsessive-Compulsive Symptoms in Patients with Psychotic Disorders and Their Siblings

et al. 2015

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The prevalence of obsessive-compulsive disorder in subjects with psychotic disorder is much higher than in the general population. The higher than chance co-occurrence has also been demonstrated at the level of subclinical expression of both phenotypes. Both extended phenotypes have been shown to cluster in families. However, little is known about the origins of their elevated co-occurrence. In the present study, evidence for a shared etiological mechanism was investigated in 3 samples with decreasing levels of familial psychosis liability: 987 patients, 973 of their unaffected siblings and 566 healthy controls. The association between the obsessive-compulsive phenotype and the psychosis phenotype c.q. psychosis liability was investigated. First, the association was assessed between (subclinical) obsessive-compulsive symptoms and psychosis liability. Second, in a cross-sib cross-trait analysis, it was examined whether (subclinical) obsessive-compulsive symptoms in the patient were associated with (subclinical) psychotic symptoms in the related unaffected sibling. Evidence was found for both associations, which is compatible with a partially shared etiological pathway underlying obsessive-compulsive and psychotic disorder. This is the first study that used a cross-sib cross-trait design in patients and unaffected siblings, thus circumventing confounding by disease-related factors present in clinical samples.

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Evidence That Familial Liability for Psychosis Is Expressed as Differential Sensitivity to Cannabis

Abstract: Genetic risk for psychotic disorder may be expressed in part as sensitivity to the psychotomimetic effect of cannabis. Cannabis use may synergistically combine with preexisting psychosis liability to cause positive and negative symptoms of psychosis.

Cited by 99 publications

References 61 publications

Predictors of a clinical high risk status among individuals with a family history of psychosis

Predictors of a clinical high risk status among individuals with a family history of psychosis

Delta-9-Tetrahydrocannabinol-Induced Dopamine Release as a Function of Psychosis Risk: 18F-Fallypride Positron Emission Tomography Study

Evidence for a Shared Etiological Mechanism of Psychotic Symptoms and Obsessive-Compulsive Symptoms in Patients with Psychotic Disorders and Their Siblings

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