Remember how I wanted to figure out why different variables can cause somewhat psycho/schizo reactions to Cannabis?
Well, this research in the UK touches on that, and partly Isolates the psychological response to being caused from a Genotype - "AKT1".
I posted the link earlier and just now really had the time to look into it - I've also taken the liberty of pasting the most relevant sections of the paper and highlighting the key parts (at least to me).
In Isolating what causes this less than ideal response, they've essentially identified a possibility for stopping it.
However, part of the research team was compensated for their efforts. "CJAM" has consulted for Janssen and GlaxoSmithKline and received compensation. The remaining authors declare no conflict of interest.
Everything cited below is taken from the following link and it's Authors, respectively.
http://www.nature.com/tp/journal/v6/n2/full/tp2015219a.html
These findings are the first to demonstrate that AKT1 mediates the acute response to cannabis in otherwise healthy individuals and implicate the AKT1 pathway as a possible target for prevention and treatment of cannabis psychosis.
The current study, therefore, set out to examine the gene × cannabis use interaction in a group of healthy young cannabis users, with no family history of schizophrenia, assessed both at the time of smoking cannabis and when non-intoxicated. We assessed the impact of the two loci that have been previously demonstrated to have an interaction between psychotic symptoms and cannabis: the functional Valine158Methionine (Val158Met) polymorphism of the COMT gene and AKT1 rs2494732. Given these genotypes have been shown to interact with working memory,
11,
12 we included a measure of this in our study. Our novel naturalistic design allowed us to assess (1) acute psychotic symptoms, (2) cognitive function and (3) level of THC, the main active ingredient in the cannabis smoked at the time of ingestion.
Smoking cannabis daily doubles an individual’s risk of developing a psychotic disorder, yet indicators of specific vulnerability have proved largely elusive. Genetic variation is one potential risk modifier. Single-nucleotide polymorphisms in the AKT1 and catechol-O-methyltransferase (COMT) genes have been implicated in the interaction between cannabis, psychosis and cognition, but no studies have examined their impact on an individual’s acute response to smoked cannabis. A total 442 healthy young cannabis users were tested while intoxicated with their own cannabis—which was analysed for delta-9-tetrahydrocannbinol (THC) and cannabidiol content—and also ±7 days apart when drug-free.
Psychotomimetic symptoms and working memory were assessed on both the sessions.
In summary, we found that the AKT1 rs2494732 C allele was associated with increased psychotomimetic symptoms after The other factor impacting on acute psychotomimetic response to cannabis was baseline schizotypy. Gender was the only factor to predict acute working memory impairment, with poorer performance in females. When drug free, cannabis dependence weakly predicted schizotypal symptoms and COMT genotype had a marginal impact on working memory, along with ethnicity. The findings of this study contribute to a recent and growing body of evidence suggesting that variation at the AKT1 locus confers details of the risk of cannabis smoking for schizophrenia. This is likely to be in the context of numerous other genetic variants, so the clinical utility at the moment is unclear. It is nonetheless encouraging that there is concordance between genetic influences on acute effects of cannabis and those mediating risk of psychosis.smoking cannabis.
However, the fact that AKT1 is relevant to the biology of psychotic symptoms suggests that this might be a promising direction for novel therapeutics for cannabis-induced psychosis.
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