Cannabinoid receptors in human astroglial tumors.

“…cannabinoids are reported to inhibit the growth of tumors, including gliomas. These effects have been claimed to be mediated via cannabinoid receptors 1 and 2 (CB1, CB2).

We conclude that cannabinoid therapy of human gliomas targets not only receptors on tumor, but also on other cell types…”

http://www.ncbi.nlm.nih.gov/pubmed/16893424

Cannabinoid system and neuroinflammation: implications for multiple sclerosis.

“There is a growing amount of evidence suggesting that cannabinoids may be neuroprotective in central nervous system inflammatory conditions.

Advances in the understanding of the physiology and pharmacology of the cannabinoid system have potentiated the interest in cannabinoids as potential therapeutic targets.

…The effects of cannabinoids on cytokine brain work and on the regulation of neuroinflammatory processes may affect chronic inflammatory demyelinating diseases such as multiple sclerosis.”

http://www.ncbi.nlm.nih.gov/pubmed/18073512

Use of Dronabinol for Cannabis Dependence: Two Case Reports and Review

“Based on recent laboratory studies, dronabinol (delta-9-tetrahydrocannabinol) has been shown to reduce cannabis withdrawal symptoms and the subjective effects of marijuana.

Given that agonist agents have been found to be effective for opiate and nicotine dependence, the clinical utility of dronabinol for cannabis dependence is a reasonable approach…

It is clear from the two cases that both patients found the induction onto dronabinol helpful.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2733248/

Cannabinoids induce glioma stem-like cell differentiation and inhibit gliomagenesis.

“Glioma stem-like cells constitute one of the potential origins of gliomas, and therefore, their elimination is an essential factor for the development of efficient therapeutic strategies.

Cannabinoids are known to exert an antitumoral action on gliomas that relies on at least two mechanisms: induction of apoptosis of transformed cells and inhibition of tumor angiogenesis…

The discovery of an endogenous cannabinoid system, together with the great improvement in our understanding of the signaling mechanisms responsible for cannabinoid actions, has fostered the interest in the potential therapeutic applications of cannabinoids.

Several studies have demonstrated a significant antitumoral action of cannabinoid ligands in animal models. Thus, cannabinoid administration to nude mice curbs the growth of different tumors, including gliomas…

Cannabinoids are known to exert an antitumoral action against gliomas…

Overall, our results demonstrate that cannabinoids target glioma stem-like cells, promote their differentiation, and inhibit gliomagenesis, thus giving further support to their potential use in the management of malignant gliomas.

In conclusion, our results demonstrate the action of cannabinoids on glioma stem-like cells and thus may open new avenues for cannabinoid-based antitumoral strategies.”

http://www.jbc.org/content/282/9/6854.long

Cannabinoids inhibit peptidoglycan-induced phosphorylation of NF-κB and cell growth in U87MG human malignant glioma cells.

“Nuclear factor (NF)-κB is the key transcription factor involved in the inflammatory responses, and its activation aggravates tumors. Peptidoglycan (PGN), a main cell wall component of Gram-positive bacteria, stimulates Toll-like receptor 2 (TLR-2) and activates a number of inflammatory pathways, including NF-κB…

Cannabinoids have been reported to exert anti-inflammatory and antitumor effects…

Our finding that cannabinoids suppress the NF-κB inflammatory pathway and cell growth via CB1 receptors in glioma cells provides evidence for the therapeutic potential of targeting cannabinoid receptors for the treatment of inflammation-dependent tumor progression.”

http://www.ncbi.nlm.nih.gov/pubmed/22842590

Medical marijuana as protection against the H1N1 swine flu virus?

“When the immune system attacks a flu virus, it causes widespread inflammation throughout the body. This inflammation presents itself in runny noses, soar throats, and body aches that accompany influenza. Runaway inflammation can cause the immune system to destroy the body it was meant to protect and lead to death.

 “When inflammation goes off the handle, the body releases endocannabinoids, which are natural chemicals that suppress the immune system, taking down the inflammation before it does more harm than good. This endocannabinoid system, as it’s called, is one of the many systems responsible for maintaining balance and health in the body,” ABC News reported.

If the endocannabinoid system cannot keep up – which often happens in very severe influenza infections – organ failure, particularly lung failure, may result.

 “They die not from the virus itself but from their own immune response,” Melamede told ABC News.
Cannabis Science intends to solve this threat. Marijuana contains natural, plant-based cannabinoids, called phytocannabinoids. A medical marijuana lozenge provides the body with a boost of endocannabinoids and helps to relieve the dangerous inflammation.
While viruses like the H1N1 swine flu bug are clever in their ability to mutate and outsmart even the latest vaccines, the human body’s response – with regard to inflammation management – does not change. Cannabis Science may be on to something here.”

http://digitaljournal.com/article/276928

Obesity and cannabis use: results from 2 representative national surveys.

“We hypothesized that the prevalence of obesity would be higher in cannabis users than in nonusers… this analysis showed that even if cannabis consumption increases appetite, people using cannabis are less likely to be obese than people who do not use cannabis…

The authors conclude that the prevalence of obesity is lower in cannabis users than in nonusers.”

http://www.ncbi.nlm.nih.gov/pubmed/21868374
http://aje.oxfordjournals.org/content/174/8/929.long

Medical Marijuana Laws and Suicides by Gender and Age.

:American Journal of Public Health Logo

 

“We estimated the association between legalizing medical marijuana and suicides.

Legalization was associated with a 10.8%  and 9.4% reduction in the suicide rate of men aged 20 through 29 years and 30 through 39 years, respectively.

Suicides among men aged 20 through 39 years fell after medical marijuana legalization compared with those in states that did not legalize.

The negative relationship between legalization and suicides among young men is consistent with the hypothesis that marijuana can be used to cope with stressful life events.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4232164/

http://www.ncbi.nlm.nih.gov/pubmed/24432945

http://ajph.aphapublications.org/doi/10.2105/AJPH.2013.301612

“Legalizing Medical Marijuana May Lead To Fewer Suicides”  https://www.huffingtonpost.com/2014/02/04/marijuana-legalization-suicide_n_4726390.html

“Medical Marijuana Cuts Suicide Rates By 10% In Years Following Legalization”  http://www.medicaldaily.com/medical-marijuana-cuts-suicide-rates-10-years-following-legalization-268472

THC:CBD Spray and MS Spasticity Symptoms: Data from Latest Studies.

“New clinical experience with 9-delta-tetrahydocannabinol (THC) and cannabidiol (CBD) oromucosal spray (Sativex®)…

A randomized, placebo controlled long-term follow-up clinical trial with THC:CBD spray versus placebo demonstrated that it was not associated with cognitive decline, depression or significant mood changes…

THC:CBD oromucosal spray did not adversely influence standard driving ability in patients with moderate to severe MS spasticity…

Findings to date reinforce the efficacy and safety observed in Phase III clinical trials…

Importantly, no additional safety concerns were identified…

Thus, these new data support a positive benefit-risk relationship for THC:CBD oromucosal spray during longer-term use.”

http://www.ncbi.nlm.nih.gov/pubmed/24457846

Pre- and postsynaptic type-1 cannabinoid receptors control the alterations of glutamate transmission in experimental autoimmune encephalomyelitis.

“Type-1 cannabinoid receptors (CB1R) are important regulators of the neurodegenerative damage in multiple sclerosis (MS) and in experimental autoimmune encephalomyelitis (EAE). In GABAergic striatal neurons, CB1R stimulation exerts protective effects by limiting inflammation…

Our results provide further evidence that CB1R are involved in EAE pathophysiology, and suggest that both pre- and postsynaptic alterations of glutamate transmission are important to drive excitotoxic neurodegeneration typical of this disorder.”

http://www.ncbi.nlm.nih.gov/pubmed/24440366