Archive for February, 2010
Saturday, February 27th, 2010
Clara Tourino, Andreas Zimmer, and Olga Valverde published a provacative article demonstrating that THC can protect against MDMA (ecstasy) induced brain damage. The authors note that the negative effects of long term MDMA use arise from it’s metabolism. High temperatures cause “the formation and uptake of MDMA toxic metabolites that increase oxidative stress, causing nerve terminal damage…and eventually axonal degeneration.”
Basically current research suggests that taking MDMA (ecstasy) and going dancing may increase brain damage associated with long term use.
The authors also site evidence that MDMA is often consumed with cannabis (1) (2). They point out that THC has been widely reported to lower body temperature, decrease inflammation, and is a potent anti-oxidant. Interestingly, in animal models of drug abuse THC and MDMA appear to “counter balance” each other. THC is able to attenuate many effects of MDMA including hyperthermia (overheating), hyper-locomotion, and anxiety. However, these authors are the first to explore if THC can actually protect brain cells from MDMA’s toxic effects.
Below is a figure from the publication:
This image shows a vehicle or untreated brain compared to MDMA and THC treated brains. Notice the pale complexion of the MDMA brain slice? This decrease in staining indicates a reduction in important brain proteins, this unwanted protein reduction is prevented when THC is given to the mice.
They also discuss some of the implications of their findings:
“The frequent co-use of both drugs makes it particularly interesting to study the effects of their combination Indeed, previous studies describe the effects of THC and MDMA together in animal models of locomotor activity, temperature, anxiety, reward and THC-dependence. However, the neuroprotective effects of THC on MDMA neurotoxicity have never been reported. In addition, the dose of THC used in this study (3 mg/kg, i.p.) could be considered a dose consumed by regular moderate cannabis users, and for that reason similar doses are used in the previously reported animal studies.”
So what does this mean to humans?
A few clinical studies on polydrug use have shown that use of cannabis and MDMA leads to deficits in brain function. Yet, the authors point to three studies which suggest that MDMA users that also consume THC have less ‘brain problems’ than “pure MDMA users.” (1) (2) (3)
MDMA also has a therapeutic role in diseases such as PTSD. Given that THC may reduce possible negative effects associated with MDMA use, i.e., hyperthermia and listening to techno music. Future clinical studies that are examining a therapeutic role for MDMA, should consider including groups of patients that receive a measured dose of both drugs.
Posted in Contributing Author: Jahan Marcu | No Comments »
Friday, February 19th, 2010
The Los Angeles Times, Sacramento Bee, and the Associated press published articles on studies showing that Cannabis has therapeutic value. The studies were conducted through the Center for Medicinal Cannabis Research (CMCR) at the University of San Diego. The CMCR was created in 2000 to answer the question, “Does Marijuana have Therapeutic Value?”
The CMCR have submitted their report to the legislature and Governor of California, in which the authors claim to “have found reasonable evidence that cannabis is a promising treatment.”
The CMCR report is a summary of the clinical trials on smoked or vaporized cannabis that were conducted by the organization. Basically, the organization spent 10 million dollars and completed 6 clinical trials. These trials demonstrate that cannabis is an effective pain medicine for MS and HIV/AIDS patients. Notably, one study showed that ”low potency” cannabis may be effective at reducing pain with out inducing a “high”.
The CMCR had to overcome numerous setbacks. At least 5 clinical trials were canceled for various reasons. In one instance a clinical trial on chemotherapy induced nausea and vomiting had to be cancelled because not enough cancer patients could be recruited. Additionally, the approval of a study by the government typically took 18 months.
The Full Report may be downloaded here: http://www.cmcr.ucsd.edu/CMCR_REPORT_FEB17.pdf
The Press Release can be viewed here: http://health.ucsd.edu/news/2010/2-17-medical-marijuana.htm
Elsewhere, the Iowa Pharmacy Board is already expecting cannabis to available as a medicine soon. As the board has recommended to legislators that cannabis be rescheduled to allow medical use. Could Iowa potentially distribute cannabis through a pharmacy? Not unless cannabis is removed from schedule I.
Posted in Cannabination, Contributing Author: Jahan Marcu | No Comments »
Saturday, February 6th, 2010
A growing body of scientific research suggests that cannabinoid receptors or the endocannabinoid system may have a therapeutic role in major depression (MD) and/or bipolar disorder (BD). A paper published in “Pharmaceutic Research” demonstrated that certain variations or mutations associated with the Endocannabinoid system may make humans more susceptible to MD or BD. The current study found that specific mutations in both the CB1 receptor and FAAH enzyme, were found in human subjects suffering from MD and BP. Interestingly, only the CB1 receptor mutations were linked to Major Depression, while both CB1 receptor and FAAH mutations were found patients suffering from bipolar disorders
What is the Endocannabinoid system (ECS)? And why is it linked to emotion?
The ECS is comprised of two receptors, the CB1 and CB2 receptor. The CB1 receptor is perhaps one of the most abundant receptors in the human brain. It is found in high amounts in many areas of the human brain, including parts of the brain important for emotion. It is fairly common knowledge that THC, from the cannabis plant, can activate CB1 receptors. However, humans and many other animals also make a “natural THC” called Anandamide. Anandamide is synthesized by cells in our body, and can impact a variety of natural processes such as eating, sleeping, memory, energy, and mood. Once Anandamide is synthesized it will be degraded or destroyed by another protein FAAH. The enzyme activity or the rate at which FAAH destroys Anandamide will indirectly affect the level of CB1 activity.
So, if FAAH is over active there will be fewer signals in the brain telling you to eat and sleep, among other things. If there is not enough FAAH, it will make a person hungry.
Mutations in FAAH or cannabinoid receptors may underlie many diseases; in fact a “Clinical Endocannabinoid Deficiency” has already been proposed to explain some chronic diseases such as “migraines, fibromyalgia, irritable bowel syndrome, and other functional conditions alleviated by clinical cannabis“. A previous study has also linked variations in FAAH and CB1 rceptors to anorexia nervosa and bulimia nervosa.
Posted in Cannabination, Contributing Author: Jahan Marcu | 2 Comments »
