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Abstract
In the Medical Marihuana state of CA, marihuana was found in drivers which resulted in 1,551 fatalities in the last 5 years. Nationally, in the 23 states and D.C. with state-approved Medical Marihuana, there were more than 1,000 fatalities in the single year of 2014. In the 27 states with no legal marihuana of any kind there were 1,619 marihuana related fatalities.

If CA marihuana use increases from the 2014 level of 18.8% to the level of WA and AK (two recreational marihuana states) at 31%, we could expect an additional 223 CA fatalities each year, for about 565 fatalities a year.

Alcohol is also heavily involved in the marihuana fatalities with 46% of the marihuana drivers were also impaired by alcohol at 0.05% and 38% legally DUI at 0.08+ BAC.

Despite the heavy use of alcohol by marihuana drivers, alcohol involvement in fatal crashes has increased less than 1% in the last 5 years.

Drivers with marihuana in Medical Marihuana states had a 29% higher involvement in fatal crashes than No Medical Marihuana states. Every percent increase in CA driver marihuana involvement in crashes will results in 19 more fatalities.

The growing legalization of marihuana for recreational use, along with the present Medical Marihuana use will cause a tidal wave of motor vehicle fatalities and injuries. This has already happened in Washington State where the level of drivers with marihuana is almost equal to the level of drivers DUI, the No.1 preventable traffic safety problem.

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Abstract:
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. Variation at the rs2494732 locus of the AKT1 gene predicted acute psychotic response to cannabis along with dependence on the drug and baseline schizotypal symptoms. Working memory following cannabis acutely was worse in females, with some suggestion of an impact of COMT polymorphism on working memory when drug-free. 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.
 
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Sharon S. Kelley, MS, PhD
“The synthetic drug abuse crisis reflects a number of similarities to a viral pandemic. The disease has spread rapidly throughout multiple countries via the assistance of a global carrier (the internet), with the virus mutation (analogue production) occurring at a pace that makes it difficult for agencies to quickly identify and regulate. Therefore, as in any disease outbreak, it becomes imperative for healthcare providers, scientists and law enforcement agencies to foster a mutual relationship of information exchange…”
 
For complete article go to The Journal of Global Drug Policy & Practice! VOLUME 9, ISSUE 4 - Winter 2015 view pdf

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Research continues to confirm that cannabis use continues to accelerate, aging, obesity and metabolic dysfunction!

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