Monthly Archives: April 2014

Pot Not Linked to Poor Health

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“Marijuana use does not correlate with negative health outcomes or hospitalizations, a study has found.”

“Marijuana may not be linked to health after all, researchers from the Boston Medical Center (BMC) and Boston University School of Medicine showed in the Journal of General Internal Medicine this week (September 23). Specifically, the team found that use of the drug did not correlate with health status or health-care utilization among adults who reported to have used the drug before. The study serves to support mounting evidence that marijuana is likely less harmful than once thought.”

http://www.the-scientist.com/?articles.view/articleNo/37625/title/Pot-Not-Linked-to-Poor-Health/

“Large waist linked to poor health…” http://www.sciencedaily.com/releases/2014/03/140312114559.htm

“Studies show poverty is linked with poor health” http://articles.latimes.com/2011/sep/14/news/la-heb-poverty-health-20110914

[Therapeutic use of cannabis derivatives].

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“The therapeutic use of cannabis has generated a lot of interest in the past years, leading to a better understanding of its mechanisms of action…

Cannabinoids such as dronabinol, Sativex and nabilone have been tested for the treatment of acute and chronic pain. These agents are most promising to relieve chronic pain associated with cancer, with human immunodeficiency virus infection and with multiple sclerosis…”

http://www.ncbi.nlm.nih.gov/pubmed/24701869

WIN induces apoptotic cell death in human colon cancer cells through a block of autophagic flux dependent on PPARγ down-regulation.

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“Cannabinoids have been reported to possess anti-tumorigenic activity in cancer models…

Here, we show that the synthetic cannabinoid WIN55,212-2 (WIN)-induced apoptosis in colon cancer cell lines is accompanied by endoplasmic reticulum stress induction.

In conclusion, at our knowledge, our results are the first to show that the reduction of PPARγ levels contributes to WIN-induced colon carcinoma cell death by blocking the pro-survival autophagic response of cells.”

http://www.ncbi.nlm.nih.gov/pubmed/24696378

Can Physical Exercise or Food Deprivation Cause Release of Fat-Stored Cannabinoids in Humans?

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“The aim of this study was to evaluate whether physical exercise or food deprivation may increase cannabionoid levels in serum or urine in abstinent chronic cannabis users.

We conclude that exercise and/or food deprivation are unlikely to cause sufficient cannabinoid concentration changes to hamper correct interpretations in drug testing programmes.”

http://www.ncbi.nlm.nih.gov/pubmed/24674455

Fasting and exercise increase plasma cannabinoid levels in THC pre-treated rats: an examination of behavioural consequences.

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“Δ9-Tetrahydrocannabinol (THC), the main psychoactive constituent of cannabis, accumulates in fat tissue where it can remain for prolonged periods.

Under conditions of increased fat utilisation, blood cannabinoid concentrations can increase.

These results confirm that fasting and exercise can increase plasma cannabinoid levels…”

http://www.ncbi.nlm.nih.gov/pubmed/24696079

Cannabinoid receptor type 1 receptors on GABAergic vs. glutamatergic neurons differentially gate sex-dependent social interest in mice.

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“Abnormalities in social behavior are found in almost all psychiatric disorders, such as anxiety, depression, autism, and schizophrenia. Thus, comprehension of the neurobiological basis of social interaction is important for a better understanding of numerous pathologies and improved treatments.

Several findings have suggested that an alteration of cannabinoid receptor type 1 (CB1) receptor function could be involved in the pathophysiology of such disorders…

In conclusion, we provide evidence that CB1 receptors specifically modulate the social investigation of female mice in a neuronal subtype-specific manner.”

http://www.ncbi.nlm.nih.gov/pubmed/24698342

The detection of THC, CBD and CBN in the oral fluid of Sativex® patients using two on-site screening tests and LC-MS/MS.

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“Sativex® is an oromucosal spray used to treat spasticity in multiple sclerosis sufferers in some European countries, the United Kingdom, Canada and New Zealand. The drug has also recently been registered by the Therapeutic Goods Administration (TGA) in Australia for treatment of multiple sclerosis.

Sativex® contains high concentrations of Δ9-tetrahydrocannabinol (THC) and cannabidiol (CBD), with the former being the subject of random roadside drug tests across Australia to detect cannabis use.

This pilot study aims to determine whether or not patients taking Sativex® will test positive to THC using these roadside screening tests. Detectable levels of THC, CBD and cannabinol (CBN) in their oral fluid were also confirmed by liquid chromatography-tandem mass spectrometry (LC-MS/MS). The study was a double-blind, placebo controlled design.

In conclusion, Sativex® users may test positive for THC by roadside drug testing within 2-3h of use. Confirmatory analysis can identify Sativex® treatment through use of THC/CBD ratios, however, these ratios would unlikely be sufficient to differentiate non-medicinal cannabis use from Sativex® use if both are taken concurrently.”

http://www.ncbi.nlm.nih.gov/pubmed/24699310

Cannabinoid receptor 2 counteracts interleukin-17-induced immune and fibrogenic responses in mouse liver.

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“Interleukin (IL)-17 is a proinflammatory and fibrogenic cytokine mainly produced by T-helper (Th)17 lymphocytes, together with the hepatoprotective and antifibrogenic cytokine, IL-22.

Cannabinoid receptor 2 (CB2) is predominantly expressed in immune cells and displays anti-inflammatory and antifibrogenic effects.

In the present study, we further investigated the mechanism underlying antifibrogenic properties of CB2 receptor and explored its effect on the profibrogenic properties of IL-17.

These data demonstrate that CB2 receptor activation decreases liver fibrosis by selectively reducing IL-17 production by Th17 lymphocytes via a STAT5-dependent pathway, and by blunting the proinflammatory effects of IL-17 on its target cells, while preserving IL-22 production.”

http://www.ncbi.nlm.nih.gov/pubmed/23813495

Anandamide Attenuates Th-17 Cell-Mediated Delayed-Type Hypersensitivity Response by Triggering IL-10 Production and Consequent microRNA Induction

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“Endogenous cannabinoids [endocannabinoids] are lipid signaling molecules that have been shown to modulate immune functions..

Cannabinoids are compounds derived from the Cannabis sativa plant and exert many effects on the immune system. Cannabinoids have potential as therapeutic agents in several different disease conditions, including experimental autoimmune hepatitis, Multiple Sclerosis, and Graft vs. Host Disease…

This report suggested a role of the endogenous cannabinoid system in regulation of allergic inflammation.

These studies also suggest that endogenous cannabinoid system is one of the homeostatic mechanisms that the body employs to down-regulate immune response to foreign antigens as well as combat autoimmunity.

Targeting of this system could yield valuable therapeutics in the future.”

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0093954

Pharmacology and toxicology of Cannabis derivatives and endocannabinoid agonists.

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“For centuries Cannabis sativa and cannabis extracts have been used in natural medicine.

Delta(9)-tetrahydrocannabinol (THC) is the main active ingredient of Cannabis. THC seems to be responsible for most of the pharmacological and therapeutic actions of cannabis.

In a few countries THC extracts (i.e. Sativex) or THC derivatives such as nabilone, and dronabinol are used in the clinic for the treatment of several pathological conditions like chemotherapy-induced nausea and vomiting, multiple sclerosis and glaucoma.

Over recent years, alternative approaches using synthetic cannabinoid receptor agonists or agents acting as activators of the endocannabinoid systems are under scrutiny with the hope to develop more effective and safer clinical applications.

The present article review recent study and patents with focus on the cannabinoid system as a target for the treatment of central nervous system disorders with emphasis on agonists.”

http://www.ncbi.nlm.nih.gov/pubmed/19832688