Thread:Comments:US Senator Rand Paul blocks synthetic marijuana legislation/In full support of Senator Rand Paul

Sorry for the long comment, but I wanted to post something that I wrote earlier in the year after the D.E.A. announced their intention to emergency schedule JWH-018/200/250, CP-47,497, and cannabicyclcohexanol.

"At the end of 2010, the D.E.A. moved to emergency schedule five synthetic cannabinoids being used in “Spice”, which is synthetic cannabis. These compounds were JWH-018, JWH-073, JWH-200, cannabicyclohexanol, and CP 47,497. The reason the D.E.A. moved to act was due to reports from all over the United States of teenagers turning up in emergency rooms with seizures after smoking various spice blends. This is true, but the danger of the seizures was drastically overblown. Typically, seizures resulted from highly inexperienced users consuming ultra-high amounts of pure cannabinoids - cannabinoids that typically were either full CB1 or CB2 agonists. Also consider the fact that no synthetic blends contain the compounds cannabis contains to balance out some of the anxiety effects (cannabidiol, a sedative, being a perfect example).

Therefore, because OH GOD THINK OF THE CHILDREN, the D.E.A. moved to ban these 5 compounds for one year (while they “study them closer”), making them schedule one drugs along with marijuana.

Now, what were the effects of this? Well, “spice” did not disappear. John Huffman synthesized hundreds of analogues, therefore the market simply picked up a few more which were not illegal (such as JWH-122). More important in this matter is how the D.E.A.’s move affected science and research. When the D.E.A moved to act, dozens of scientific studies were being conducted with the compounds in question, with dozens more being conducted with other similar compounds. Scheduled drugs are drastically more difficult to do research with than unscheduled drugs. Therefore, the move to outlaw the 5 compounds flashed a big yellow light for cannabinoid research.

Hysteria aside, what has cannabinoid research found? The results are shocking. Here are a few studies showing the enormous potential for cancer treatment:

From a study at Harvard Medical School (http://www.ncbi.nlm.nih.gov/pubmed/21097714):

“Non-small cell lung cancer (NSCLC) is the leading cause of cancer deaths worldwide; however, only limited therapeutic treatments are available. Hence, we investigated the role of cannabinoid receptors, CB1 and CB2, as novel therapeutic targets against NSCLC. We observed expression of CB1 (24%) and CB2 (55%) in NSCLC patients. Furthermore, we have shown that the treatment of NSCLC cell lines (A549 and SW-1573) with CB1/CB2- and CB2-specific agonists Win55,212-2 and JWH-015, respectively, significantly attenuated random as well as growth factor-directed in vitro chemotaxis and chemoinvasion in these cells. We also observed significant reduction in focal adhesion complex, which plays an important role in migration, upon treatment with both JWH-015 and Win55,212-2. In addition, pretreatment with CB1/CB2 selective antagonists, AM251 and AM630, prior to JWH-015 and Win55,212-2 treatments, attenuated the agonist-mediated inhibition of in vitro chemotaxis and chemoinvasion. In addition, both CB1 and CB2 agonists Win55,212-2 and JWH-133, respectively, significantly inhibited in vivo tumor growth and lung metastasis (∼50%). These effects were receptor mediated, as pretreatment with CB1/CB2 antagonists abrogated CB1/CB2 agonist-mediated effects on tumor growth and metastasis. Reduced proliferation and vascularization, along with increased apoptosis, were observed in tumors obtained from animals treated with JWH-133 and Win55,212-2. Upon further elucidation into the molecular mechanism, we observed that both CB1 and CB2 agonists inhibited phosphorylation of AKT, a key signaling molecule controlling cell survival, migration, and apoptosis, and reduced matrix metalloproteinase 9 expression and activity. These results suggest that CB1 and CB2 could be used as novel therapeutic targets against NSCLC.”

From a study in Madrid, Spain (http://www.ncbi.nlm.nih.gov/pubmed/21475304):

“Hepatocellular carcinoma (HCC) is the third cause of cancer-related death worldwide. We found that Δ(9)-tetrahydrocannabinol (Δ(9)-THC, the main active component of Cannabis sativa) and JWH-015 (a cannabinoid receptor 2 (CB(2)) cannabinoid receptor-selective agonist) reduced the viability of the human HCC cell lines HepG2 (human hepatocellular liver carcinoma cell line) and HuH-7 (hepatocellular carcinoma cells), an effect that relied on the stimulation of CB(2) receptor. We also found that Δ(9)-THC- and JWH-015-induced autophagy relies on tribbles homolog 3 (TRB3) upregulation, and subsequent inhibition of the serine-threonine kinase Akt/mammalian target of rapamycin C1 axis and adenosine monophosphate-activated kinase (AMPK) stimulation.”

The study concludes “our findings may contribute to the design of new therapeutic strategies for the management of HCC”.

From another study in Spain:

“Our results show that both Delta9-tetrahydrocannabinol, the most abundant and potent cannabinoid in marijuana, and JWH-133, a non-psychotropic CB2 receptor-selective agonist, reduce tumor growth, tumor number, and the amount/severity of lung metastases in MMTV-neu mice. Histological analyses of the tumors revealed that cannabinoids inhibit cancer cell proliferation, induce cancer cell apoptosis, and impair tumor angiogenesis. Cannabinoid antitumoral action relies, at least partially, on the inhibition of the pro-tumorigenic Akt pathway. We also found that 91% of ErbB2-positive tumors express the non-psychotropic cannabinoid receptor CB2.

CONCLUSIONS: Taken together, these results provide a strong preclinical evidence for the use of cannabinoid-based therapies for the management of ErbB2-positive breast cancer.”"