Smoked Cannabis Reduces Some Symptoms of Multiple Sclerosis

“Controlled trial shows improved spasticity, reduced pain after smoking medical marijuana

A clinical study of 30 adult patients with multiple sclerosis (MS) at the University of California, San Diego School of Medicine has shown that smoked cannabis may be an effective treatment for spasticity – a common and disabling symptom of this neurological disease.”

http://health.ucsd.edu/news/releases/Pages/2012-05-14-smoked-cannabis-reduces-symptoms-of-multiple-sclerosis.aspx

Medical marijuana

“Medical marijuana eases some MS symptoms, neurologists report” http://www.latimes.com/science/sciencenow/la-sci-sn-treating-ms-with-cannabis-20140324,0,2596095.story

Medical Marijuana Pills May Ease Some MS Symptoms: Review

Medical Marijuana Pills May Ease Some MS Symptoms: Review

“Medical marijuana pills and sprays might ease the symptoms of multiple sclerosis, but most other alternative therapies do little to lessen the pain and muscle rigidity that often accompanies the disease, according to new guidelines.

To reach that conclusion, an expert panel from the American Academy of Neurology reviewed more than 40 years of research on alternative medicine treatments for multiple sclerosis (MS)…

The guidelines are published in the March 25 issue of the journal Neurology.”

http://consumer.healthday.com/public-health-information-30/marijuana-news-759/guideline-medical-marijuana-may-ease-some-ms-symptoms-686096.html#.UzDKXsAnP9M.twitter

“Marijuana May Ease Some Symptoms of MS, New Guidelines Find. Medical marijuana pills or an oral spray made from cannabis may help ease some of the painful spasms caused by multiple sclerosis that make day-to-day life hard for patients, according to new guidelines from the American Academy of Neurology.” http://www.nbcnews.com/health/health-news/marijuana-may-ease-some-symptoms-ms-new-guidelines-find-n60626


Control by the endogenous cannabinoid system of ras oncogene-dependent tumor growth.

“Because THC-like compounds are used to inhibit nausea and induce appetite in cancer patients, and anandamide appears to be an endogenous orexigenic mediator, the finding of possible antitumor effect for these substances might have a tremendous potential for therapeutic intervention in preventing the progression of cancer and, at the same time, in alleviating its symptoms.

Because multiple pathways are important for the proliferation of tumor cells and because combination therapies are often more effective than single-drug administration, cannabimimetic substances may complement other anticancer agents…”

http://www.fasebj.org/content/early/2001/12/02/fj.01-0320fje.long

“[Targeting the RAS signalling pathway in cancer].”  http://www.ncbi.nlm.nih.gov/pubmed/21715253

“Targeting the RAS oncogene.”  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3804031/

Novel hexahydrocannabinol analogs as potential anti-cancer agents inhibit cell proliferation and tumor angiogenesis.

“Both natural and synthetic cannabinoids have been shown to suppress the growth of tumor cells in culture and in animal models by affecting key signaling pathways including angiogenesis, a pivotal step in tumor growth, invasion, and metastasis.

In our search for cannabinoid-like anticancer agents devoid of psychoactive side effects, we synthesized and evaluated the anti-angiogenic effects of a novel series of hexahydrocannabinol analogs.

…two analogs LYR-7 [(9S)-3,6,6,9-tetramethyl-6a,7,8,9,10,10a-hexahydro-6H-benzo[c]chromen-1-ol] and LYR-8 [(1-((9S)-1-hydroxy-6,6,9-trimethyl-6a,7,8,9,10,10a-hexahydro-6H-benzo[c]chromen-2-yl)ethanone)]…

…these results suggest that novel synthetic hexahydrocannabinol analogs, LYR-7 and LYR-8, inhibit tumor growth by targeting VEGF-mediated angiogenesis signaling in endothelial cells and suppressing VEGF production and cancer cell growth.”

http://www.ncbi.nlm.nih.gov/pubmed/20950604

 

Anti-tumor activity of the novel hexahydrocannabinol analog LYR-8 in Human colorectal tumor xenograft is mediated through the inhibition of Akt and hypoxia-inducible factor-1α activation.

“Cannabinoid compounds have been shown to exert anti-tumor effects by affecting angiogenesis, invasion, and metastasis.

 

In the present study, we examined the action mechanism by which a novel hexahydrocannabinol analog, exerts anti-angiogenic and anti-tumor activity in human cancer xenografts.

These results indicate a novel function of cannabinoid-like compound as an anti-tumor agent.”

http://www.ncbi.nlm.nih.gov/pubmed/22687485

Analgesic effects of 1′,1′ dimethylheptyl-delta8-THC-11-oic acid (CT3) in mice.

“The metabolic pathway leading to carboxylic acid derivatives of cannabinoids was discovered more than twenty years ago. While these compounds showed no cannabimimetic activity, subsequent work documented several biological responses both in vitro and in vivo for the THC acids.

 

These include inhibition of eicosanoid synthesis, antiedema effects, antagonism to PAF actions, inhibition of leucocyte adhesion and anti nociception.

In this report we present data further characterizing the analgesic properties of the title substance which is a potent synthetic member of this group. CT3 was effective in the mouse…”

 http://www.ncbi.nlm.nih.gov/pubmed/9698045

Antinociceptive activity of Delta9-tetrahydrocannabinol non-ionic microemulsions.

“Delta(9)-Tetrahydrocannabinol (Delta(9)-THC), the major psychoactive constituent of Cannabis sativa L., has been widely studied for its potential pharmaceutical application in the treatment of various diseases and disturbs.

The aim of this work was to develop a stable aqueous Delta(9)-THC formulation acceptable for different ways of administration, and to evaluate the therapeutic properties of the new Delta(9)-THC based preparation for pain treatment.

Significant antinociceptive activity has been detected by both intraperitoneal and intragastric administration of the new Delta(9)-THC pharmaceutical preparation.”

http://www.ncbi.nlm.nih.gov/pubmed/20399844

Therapeutic utility of cannabinoid receptor type 2 (CB(2)) selective agonists.

“The cannabinoid receptor type 2 (CB2) is a class A GPCR that was cloned in 1993 while looking for an alternative receptor that could explain the pharmacological properties of Δ(9)-tetrahydrocannabinol.

CB2 was identified among cDNAs based on its similarity in amino acid sequence to the CB1receptor and helped provide an explanation for the established effects of cannabinoids on the immune system.

In addition to the immune system, CB2 has widespread tissue expression and has been found in brain, peripheral nervous system, and gastrointestinal tract.

Several “mixed” cannabinoid agonists are currently in clinical use primarily for controlling pain, and it is believed that selective CB2 agonism may afford a superior analgesic agent devoid of the centrally mediated CB1 effects.

Thus, selective CB2 receptor agonists represent high value putative therapeutics for treating pain and other disease states. In this Perspective, we seek to provide a concise update of progress in the field.”

http://www.ncbi.nlm.nih.gov/pubmed/23865723

Activation of CB2 receptors as a potential therapeutic target for migraine: evaluation in an animal model.

“Experimental animal models of migraine have suggested the existence of interactions between the endocannabinoid system and pain mediation in migraine.

Extensive evidence has demonstrated a role for the cannabinoid-1 (CB1) receptor in antinociception.

…recent research suggests that also CB2 receptors, especially located outside the central nervous system, play a role in the perception of pain…

In this study we evaluated the role of CB2 receptors in two animal models of pain that may be relevant for migraine…

CONCLUSION:

These findings suggest that the pharmacological manipulation of the CB2 receptor may represent a potential therapeutic tool for the treatment of migraine.”

http://www.ncbi.nlm.nih.gov/pubmed/24636539