Dataset Information

Further Evidence That Cannabis Moderates Familial Correlation of Psychosis-Related Experiences.

ABSTRACT:

Background

Familial correlations underlie heritability estimates of psychosis. If gene-environment interactions are important, familial correlation will vary as a function of environmental exposure.

Methods

Associations between sibling and parental schizotypy (n = 669 pairs, n = 1222 observations), and between sibling schizotypy and patient CAPE psychosis (n = 978 pairs, n = 1723 observations) were examined as a function of sibling cannabis use. This design is based on the prediction that in unaffected siblings who are not exposed, vulnerability for psychosis will remain latent, whereas in case of exposure, latent psychosis vulnerability may become expressed, at the level of schizotypal symptoms, causing the phenotypic correlation between relatives to become "visible" under the influence of cannabis.

Results

Siblings exposed to recent cannabis use resembled their patient-relative more closely in terms of positive schizotypy (urinalysis(+):B = 0.30, P<.001; urinalysis(-):B = 0.10, p<0.001; p-interaction = 0.0135). Similarly, the familial correlation in positive schizotypy between parent and sibling was significantly greater in siblings recently exposed to cannabis (urinalysis(+):B = 0.78, P<.001; urinalysis(-):B = 0.43, p<0.001; p interaction = 0.0017). Results were comparable when using lifetime cannabis frequency of use as exposure instead of recent use. Parental schizotypy did not predict cannabis use in the healthy sibling, nor in the patient. Similarly, parental cannabis use was not associated with level of schizotypy in the sibling, nor with psychotic symptoms in the patient, making gene-environment correlation unlikely.

Conclusion

Familial correlation of psychosis-related experiences varies considerably as a function of exposure to cannabis, confirming the importance of gene-cannabis interaction in shifts of expression of psychosis-related experiences.

SUBMITTER: van Winkel R

PROVIDER: S-EPMC4575144 | biostudies-literature | 2015

REPOSITORIES: biostudies-literature

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Publications

Further Evidence That Cannabis Moderates Familial Correlation of Psychosis-Related Experiences.

van Winkel Ruud R

PloS one 20150918 9

<h4>Background</h4>Familial correlations underlie heritability estimates of psychosis. If gene-environment interactions are important, familial correlation will vary as a function of environmental exposure.<h4>Methods</h4>Associations between sibling and parental schizotypy (n = 669 pairs, n = 1222 observations), and between sibling schizotypy and patient CAPE psychosis (n = 978 pairs, n = 1723 observations) were examined as a function of sibling cannabis use. This design is based on the predict ...[more]

PMID: 26384217

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Project description:It has been found that antipsychotic-naïve patients with first-episode psychosis (FEP) present with impaired hormonal regulation of appetite in terms of low leptin and high insulin levels (the adipoinsular axis). These findings imply that certain intrinsic mechanisms might play a role in the development of metabolic dysregulation in early psychosis. However, clinical correlates of this phenomenon remain unknown. Moreover, these alterations have not been tested in individuals at familial high risk of psychosis (FHR-P). In this study we aimed to assess the levels of adiponectin, insulin, leptin, glucose, total cholesterol, lipoproteins and triglycerides in FEP patients, unaffected offspring of schizophrenia patients (FHR-P individuals) and healthy controls (HCs) with respect to cognitive performance and psychopathological manifestation. Participants were 35 FEP patients, 33 FHR-P individuals, and 32 HCs. Cognitive performance was assessed using the Repeatable Battery for Assessment of Neuropsychological Status (RBANS). The levels of leptin and high-density lipoproteins (HDL) were significantly lower (leptin: 10.7 ± 15.7 vs. 12.6 ± 10.1, p = 0.046, and HDL: 48.0 ± 16.9 vs. 59.8 ± 17.5 mg/dl, p = 0.007), while the levels of triglycerides and insulin were significantly higher (triglycerides: 137.4 ± 58.8 vs. 77.5 ± 33.2 mg/dl, p < 0.001, and insulin: 15.2 ± 13.1 vs. 9.6 ± 5.0 µIU/ml, p = 0.023) in FEP patients compared to HCs. These differences were significant after controlling for the effects of potential confounding factors. No significant differences in the levels of serum markers between FHR-P individuals and HCs were found. There was a significant negative correlation between the level of leptin and the RBANS language score after covarying for potential confounding factors in FEP patients (B = –0.226, p = 0.006) but not in other subgroups of participants. Our findings confirm impairment of adipoinsular axis in early psychosis. However, results of our study do not support the hypothesis that familial liability to psychosis might be associated with metabolic dysregulation. Leptin levels might be associated with cognitive deficits in FEP patients. Longitudinal studies of individuals at risk of psychosis are needed to provide insights into causal mechanisms underlying our results.

Dataset Information

Further Evidence That Cannabis Moderates Familial Correlation of Psychosis-Related Experiences.

Background

Methods

Results

Conclusion

Publications

Further Evidence That Cannabis Moderates Familial Correlation of Psychosis-Related Experiences.

Similar Datasets

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