Monthly Archives: May 2014

PTSD symptom reports of patients evaluated for the New Mexico Medical Cannabis Program.

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“New Mexico was the first state to list post-traumatic stress disorder (PTSD) as a condition for the use of medical cannabis. There are no published studies, other than case reports, of the effects of cannabis on PTSD symptoms. The purpose of the study was to report and statistically analyze psychometric data on PTSD symptoms collected during 80 psychiatric evaluations of patients applying to the New Mexico Medical Cannabis Program from 2009 to 2011…

RESULTS:

Greater than 75% reduction in CAPS (Clinician Administered Posttraumatic Scale) symptom scores were reported when patients were using cannabis compared to when they were not.

CONCLUSIONS:

Cannabis is associated with reductions in PTSD symptoms in some patients, and prospective, placebo-controlled study is needed to determine efficacy of cannabis and its constituents in treating PTSD.”

http://www.ncbi.nlm.nih.gov/pubmed/24830188

http://www.thctotalhealthcare.com/category/post-traumatic-stress-disorder-ptsd/

Intrahypothalamic injection of cannabidiol increases the extracellular levels of adenosine in nucleus accumbens in rats.

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“Cannabidiol (CBD) is a constituent of Cannabis sativa that promotes wakefulness as well as enhances endogenous levels of wake-related neurotransmitters, including dopamine. However, at this date, the effects of CBD on the sleep-inducing molecules, such as adenosine (AD), are unknown. Here, we report that intrahypothalamic injection of CBD (10μg/1μL) increases the extracellular levels of AD collected from nucleus accumbens. Furthermore, the pharmacodynamic of this drug shows that effects on the contents of AD last 2h post-injection. These preliminary findings suggest that CBD promotes the endogenous accumulation of AD.”

http://www.ncbi.nlm.nih.gov/pubmed/24800644

“Cannabidiol, a constituent of Cannabis sativa, modulates sleep in rats…Since CBD induces alertness, it might be of therapeutic value in sleep disorders such as excessive somnolence.”  http://www.ncbi.nlm.nih.gov/pubmed/16844117

“The nonpsychoactive Cannabis constituent cannabidiol is a wake-inducing agent.”  http://www.ncbi.nlm.nih.gov/pubmed/19045957

http://www.thctotalhealthcare.com/category/insomnia/

Novel approaches to the development of anti-sepsis drugs.

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“Sepsis is the dysregulated systemic immune response to an infection…

The authors discuss specific pharmacological approaches with a focus on immune modulation, for example, Toll-like receptor 4 inhibition and modulation of the endocannabinoid system.”

 http://www.ncbi.nlm.nih.gov/pubmed/24697209

http://www.thctotalhealthcare.com/category/sepsis-2/

CB2 cannabinoid receptors contribute to bacterial invasion and mortality in polymicrobial sepsis.

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“Sepsis is a major healthcare problem and current estimates suggest that the incidence of sepsis is approximately 750,000 annually. Sepsis is caused by an inability of the immune system to eliminate invading pathogens.

Here we examined the role of CB(2) receptors in regulating the host’s response to sepsis…

Taken together, our results establish for the first time that CB(2) receptors are important contributors to septic immune dysfunction and mortality, indicating that CB(2) receptors may be therapeutically targeted for the benefit of patients suffering from sepsis.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2712683/

Cannabinoid receptor 1 inhibition improves the intestinal microcirculation.

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“The data supports the involvement of the CB1R signaling in leukocyte activation during sepsis. Drugs targeting the CB1R may have therapeutic potential in systemic inflammation, such as sepsis.”

http://www.ncbi.nlm.nih.gov/pubmed/23334604

“Cannabinoid receptor 1 inhibition causes seizures during anesthesia induction in experimental sepsis… The data suggest that CB1R inhibition in combination with pentobarbital may increase the incidence of anesthetic-induced seizures in the case of sepsis.”

http://www.ncbi.nlm.nih.gov/pubmed/22504215

 

Cannabinoid receptor 2 activation reduces intestinal leukocyte recruitment and systemic inflammatory mediator release in acute experimental sepsis.

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“The aim of this study was to investigate the effects of CB2R manipulation on leukocyte activation within the intestinal microcirculation in two acute experimental sepsis models…

CB2R activation reduces leukocyte activation and systemic release of inflammatory mediators in acute experimental sepsis. Drugs targeting the CB2R pathway may have therapeutic potential in sepsis.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3681373/

The cannabinoid 2 receptor as a potential therapeutic target for sepsis.

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“The sepsis syndrome represents an improper immune response to pathogens and is associated with an unacceptably high rate of mortality. Although supportive care is of benefit to the septic patient, there are no viable therapeutics available that target the immune system suitable for the whole septic population. Recently, using a physiologically relevant murine mouse model, the cannabiniod 2 receptor has been shown to play a critical role in the host response to sepsis. Here, the structure, expression, signaling, and function of the CB2 receptor on leukocytes will be reviewed. Further, the effects mediated by the CB2 receptor during sepsis will be reviewed. Altogether, alterations in inflammation and the host response during sepsis by the CB2 receptor support its use as a possible therapeutic agent.”

http://www.ncbi.nlm.nih.gov/pubmed/20509835

http://www.thctotalhealthcare.com/category/sepsis-2/

Experimental cannabinoid 2 receptor-mediated immune modulation in sepsis.

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“Sepsis is a complex condition that results from a dysregulated immune system in response to a systemic infection. Current treatments lack effectiveness in reducing the incidence and mortality associated with this disease. The endocannabinoid system offers great promise in managing sepsis pathogenesis due to its unique characteristics.

The present study explored the effect of modulating the CB2 receptor pathway in an acute sepsis mouse model.

Using various compounds we have shown different mechanisms of activating CB2 receptors to reduce leukocyte endothelial interactions in order to prevent further inflammatory damage during sepsis.”

http://www.ncbi.nlm.nih.gov/pubmed/24803745