2006 - 2007 Publications > Genetics of Cannabinoid System

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Genetics of Cannabinoid System

Tyndale et al (2007) reported that a genetic variation in fatty acid amide hydrolase (FAAH), C385A (P129T), a mammalian enzyme that inactivates neuromodulatory-signaling lipids including the endogenous cannabinoid 1 receptor agonist anandamide, altered the risk for trying, regular use of or dependence on cannabis, but not alcohol or nicotine. Subjects with the A/A genotype (with reduced FAAH expression and activity) were less likely to be THC dependent than subjects with either a C/C or C/A genotype (11% vs. 26%, P < 0.05). However, there was an increased risk for regular use of sedatives among the A/A genotype group. Am J Med Genet B Neuropsychiatr Genet. 2007 Jul 5;144(5):660-6

Hopfer et al (2007) found an evidence for suggestive linkage for cannabis dependence symptoms on chromosome 3q21 near marker D3S1267 (LOD=2.61), and on chromosome 9q34 near marker D9S1826 (LOD=2.57) in a study of 324 sibling pairs from 192 families. Other reports of linkage regions for illicit substance dependence have been reported near 3q21, suggesting that this region may contain a quantitative trait loci influencing cannabis dependence and other substance use disorders. Drug Alcohol Depend. 2007 Jun 15;89(1):34-41. Epub 2006 Dec 13.

Hopfer et al (2006) reports that that SNP rs806380, located in intron 2 of the CNR1 gene,is significantly associated with developing one or more cannabis dependence symptoms, with the G allele having a protective effect.  Am J Med Genet B Neuropsychiatr Genet. 2006 Aug 17; 141B(8), Pages 895-901

Hopfer et al (2006) reports evidence for suggestive linkage for cannabis dependence on found on chromosome 3q21 near marker D3S1267 (LOD=2.61), and on chromosome 9q34 near marker D9S1826 (LOD=2.57). Drug Alcohol Depend. 2006 Dec 12.

Agrawal et al 2006 report results in adult Australian twins suggesting that overlapping genetic and environmental factors probably play a significant role in the co-occurrence of cannabis and OID use and misuse. However, strong evidence, across males and females, was also found for a model where the liability to experiment with cannabis, or use of it at an early age or repeatedly, had a causal influence on the liability to experiment with OIDs. Further studies are needed to evaluate the correlated vulnerabilities model and the gateway hypothesis. Psychol Med. 2006 Nov 1;:1-12 [Epub ahead of print]

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