Dr. Mechoulam is the Israeli scientist who identified THC as the psychoactive compound in marijuana, and decades later he discovered the brain’s endocannabinoid system and the endogenous neurotransmitter anandamide. He is one of the most respected Israeli neuroscientists and has been a senior advisor to the Israeli government on marijuana policy and the ethics of research with human subjects. He discussed his experiments demonstrating the neuroprotective effects of the endocannabinoid system in mice that have had traumatic injuries to the brain. He believes the neuroprotective effects of marijuana may eventually have applications for other neurological and psychiatric conditions, including Alzheimer’s and Parkinson’s disease.
Another fascinating discovery, one with implications for PTSD, is that the cannabinoid system is integrally related to memory, specifically to memory extinction. Memory extinction is the normal, healthy process of removing associations from stimuli. Dr. Mechoulam explained that an animal which has been administered an electric shock after a certain noise will eventually forget about the shock after the noise appears alone for a few days. Mice without cannabinoid systems simply never forget – they continue to cringe at the noise indefinitely.
This has implications for patients with PTSD, who respond to stimuli that remind them of their initial trauma even when it is no longer appropriate. By aiding in memory extinction, marijuana could help patients reduce their association between stimuli (perhaps loud noises or stress) and the traumatic situations in their past. Working with Army psychiatrists, Dr. Mechoulam has obtained the necessary approvals for a study on PTSD in Israeli veterans, and hopes to begin the study soon.
The Alternative Medical Journal: General use of cannabis for PTSD Symptoms.
Despite the anecdotal evidence to the contrary, most of the experimental studies that have been conducted so far indicate that by and large the administration of exogenous cannabinoids such as vaporizing therapeutic cannabis may not be the most reliable nor effective means of utilizing the eCB system to treat anxiety and aversive memories such as those formed in PTSD. For reliable and truly effective treatment of these conditions it appears that restricting eCB breakdown by way of FAAH inhibition is the best target discovered so far within the eCB system. (The other eCB targets include the two primary receptors CB1/CB2, vanilloid receptors, eCB reuptake, as well as eCB production.) To this end, Kadmus Pharmaceuticals, Inc. has started to express serious interest in marketing a new FAAH inhibitor they have developed, currently code-named KDS-4103. KDS-4103 appears to have a lot of potential from a pharmacological perspective. Even though it produces analgesic, anxiolitic, and anti-depressant effects it otherwise does not produce a classic cannabis-like effect profile and animals easily discriminate between THC and KDS-4103. All this indicates that KDS-4103 does not produce a â€œhighâ€ like THC and other direct CB1 agonists. KDS-4103 is orally active in mammals and fails to elicit a systemic toxicity even at repeated dosages of 1,500mg/kg body mass. All other available evidence to date also suggests a very high therapeutic margin for KDS-4103. All in all, considering that the kinds of events which usually precipitate PTSD in most individuals often also involve pain, KDS-4103 seems like it may be just about the perfect medication.
So what should all this mean to the individual? Anecdotal evidence says by and large the use of therapeutic cannabis provides a significant improvement in quality of life both for those suffering from this malady and for their family and friends. Whether or not this is taking the fullest advantage possible of the eCB system in the treatment of PTSD is yet to be seen. Mostly the use of cannabis and THC to treat PTSD in humans appears to provide symptomological relief at best. In and of itself, there is nothing wrong with symptomological relief. That’s what taking aspirin for a headache, a diuretic for high blood pressure, opiates to control severe pain, or olanzapine for rapid-cycling mania is all about. We do have the potential, however, to do better than just treating symptoms of PTSD via activation of the cannabinoid receptors. With the right combination of extinction/habituation therapy and the judicious administration of a FAAH inhibitor like KDS-4103 we have the potential to actually cure many cases of PTSD. For the time being though, symptomological treatments are all we have for more generalized anxiety and depression disorders.
If an individual were to want to get the most out of using therapeutic cannabis to improve a PTSD condition they should try to use low to moderate doses with as stable a blood level as possible for general anxiety and depression symptoms. Oral cannabis produces more stable blood levels. Since peak levels will produce the most soporific effect, administration of oral cannabis right before bed should produce the most benefits for improving sleep patterns. If the goal is to use cannabis to facilitate extinction of the response to PTSD triggers than small to moderate doses of cannabis vapors should be administered shortly before planned exposure to the trigger. A series of regular extinction sessions will produce better results than a single session. If cannabis appears to make aversion, fear, or aversive memories worse then the dosage should be lowered. If feelings of fear do not improve with lower dose then discontinue use of cannabis as fear-extinction aide.
In light of all evidence currently available, it is striking that the FDA refuses to investigate cannabinoids for the treatment of anxiety disorders like PTSD yet they have approved studies of MDMA, the club drug Ecstasy, for the treatment of PTSD (Doblin, 2002). Even if you do not accept cannabis as the answer itself, it should be hard to accept that by and large we still have not found effective and reliable ways to utilize the eCB system in modern western medicine. After all, the most potent (meaning it takes the least amount to produce a threshold effect) substance know to humans is not LSD as many still assume but is instead a derivative of fentanyl, know as Carfentanil. The threshold dosages for LSD and Carfentanil are 20-30Âµg (micrograms) and 1Âµg, respectively (Wikipedia, 2 & 3). This makes Carfentanil 10,000 times more potent than morphine, 100 times more potent than fentanyl, and 20-30 times more potent than LSD. At least up until 2005 and unlike LSD, Carfentanil was(is?) regulated as a Schedule II substance in the US (Erowid). For those that do not know, this means that despite perceived extreme dangers from use or abuse of this drug it is still assumed to have medical value. With the lives and well being of so many veterans AND private citizens at stake, those in the scientific community and police makers alike cannot afford to miss the wake up call. Even a child should be able to see the hypocrisy evident in the relative policies concerning cannabinoids and opiates. It is time to fix this appalling imbalance in our policies concerning the pharmacopia or else be the laughing stock of future generations.