Abstract
BackgroundFamilial correlations underlie heritability estimates of psychosis. If gene-environment interactions are important, familial correlation will vary as a function of environmental exposure.MethodsAssociations 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.ResultsSiblings 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.ConclusionFamilial 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.
Highlights
Brain development is driven by environmental experience [1], and genetic variation occasions individual differences in environmental response [2], a mechanism referred to as gene-environment interaction [3]
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
We wished to examine the familial correlation of psychosis-related experiences between relatives in the same family with at least one affected member, and examine the hypothesis that familial correlations of psychotic experiences are higher in the context of cannabis use
Summary
Brain development is driven by environmental experience [1], and genetic variation occasions individual differences in environmental response [2], a mechanism referred to as gene-environment interaction [3]. We wished to examine the familial correlation of psychosis-related experiences between relatives in the same family with at least one affected member, and examine the hypothesis that familial correlations of psychotic experiences are higher in the context of cannabis use To this end, we used data from an ongoing longitudinal study (Genetic Risk and Outcome in Psychosis; GROUP) in Europe, following patients, siblings and parents pertaining to 1066 families. It was hypothesized that sibling psychosis “response” would display a stronger association with psychosis in the patient with greater level of sibling environmental exposure, following the reasoning that—if gene-environment interactions are important in the development of psychosis—latent underlying genetic vulnerability would become expressed with greater level of environmental exposure, and family members would become more comparable in terms of symptom expression under the influence of cannabis. If gene-environment interactions are important, familial correlation will vary as a function of environmental exposure.
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