2011
DOI: 10.1111/j.1369-1600.2011.00320.x
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Abstract: While there is solid evidence that cannabis use is heritable, attempts to identify genetic influences at the molecular level have yielded mixed results. Here, a large twin family sample (N=7452) was used to test for association between ten previously reported candidate genes and lifetime frequency of cannabis use using a gene-based association test. None of the candidate genes reached even nominal significance (p<.05). The lack of replication may point to our limited understanding of the neurobiology of cannab… Show more

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Cited by 21 publications
(20 citation statements)
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References 8 publications
(12 reference statements)
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“…Results are inconsistent for CNR1 , GABRA2 , FAAH , and ABCB1 (Benyamina et al, 2009; Haughey, Marshall, Schacht, Louis, & Hutchison, 2008a; Lind et al, 2008b; Verweij et al, 2012) and as such require additional investigation. Both CNR1 and FAAH have been associated with phenotypes related to reward sensitivity, impulsivity, and negative affect.…”
Section: Genetic Association Studiesmentioning
confidence: 97%
“…Results are inconsistent for CNR1 , GABRA2 , FAAH , and ABCB1 (Benyamina et al, 2009; Haughey, Marshall, Schacht, Louis, & Hutchison, 2008a; Lind et al, 2008b; Verweij et al, 2012) and as such require additional investigation. Both CNR1 and FAAH have been associated with phenotypes related to reward sensitivity, impulsivity, and negative affect.…”
Section: Genetic Association Studiesmentioning
confidence: 97%
“…Another longitudinal study of children and adolescents demonstrated support for a particular developmental pathway to adolescent cannabis use disorders; whereby severity of early childhood maltreatment potentiated less adaptive childhood personality functioning, followed by externalizing problems in preadolescence, and ultimately, adolescent cannabis abuse and dependence symptoms (Oshri, Rogosch, Burnette, & Cicchetti, 2011). Interestingly, a developmental pathway from child maltreatment to adolescent cannabis use disorder symptoms via personality and preadolescent internalizing problems was not supported (Oshri et al, 2011 (Agrawal et al, 2011;Verweij et al, 2012). It is clear that in order to further our understanding of the etiology of cannabis use disorders, continued development and validation of etiological models of cannabis use disorders will be required, which will necessarily involve the continued use of longitudinal studies and the integration of biopsychosocial areas of research.…”
Section: Etiology Of Cannabis Use Disordersmentioning
confidence: 99%
“…The fact that treatment-assisted participants more readily identified genetics/predisposition as an etiological category also might suggest that they were taught this treatment, but it is also possible that their cannabis use disorders were relatively and genuinely more influenced by genetics factors in light of their more frequent reports of family addiction problems. There is indeed solid evidence that cannabis use and cannabis use disorders have heritable components (Agrawal et al, 2011;Verweij et al, 2012).…”
Section: Recovery Advice and Reflectionsmentioning
confidence: 99%
“…Problems with the replicability of candidate-gene associations for behavioural traits are well documented (e.g. Bosker et al 2011;Verweij et al 2012), and high-powered direct replications are of paramount importance (Duncan and Keller 2011). Our AVPR1A association is neither a direct nor high-powered replication, and so should be regarded as tentative until subjected to rigorous replication, with publication of both positive and negative findings.…”
Section: Accepted M Manuscriptmentioning
confidence: 99%