Unless you were hiking in the Amazon River jungles, with no access to the internet or American TV, you probably have heard that CNN’s chief medical correspondent, Dr. Sanjay Gupta, changed his mind about marijuana (or “weed” as he keeps saying). Of course, this has become big news, because he’s such a “respected doctor” (why is that? Because he’s on TV?), and because a few years ago he was vociferously anti-cannabis.
I have no doubt that Dr. Gupta’s “conversion” to being pro-weed is genuine (and that his previous stance of anti-weed was similarly authentic), but we need to weed out what is real and what’s just smoke about his comments. His first major point about cannabis* was that the United States Drug Enforcement Agency (DEA) considers marijuana to be a Schedule 1 drug, which is defined as “drugs with no currently accepted medical use and a high potential for abuse.”
Dr. Gupta thinks this classification is ridiculous, and on the surface, many people, even those who are not devoted pot smokers, would probably agree. However, this is a political discussion, at least in the USA, and it is hardly a medical/scientific one. The chances of any political party having the fortitude to correct this classification is about as close to 0 as you can get, without actually stating that there is a 0 chance. But if Gupta wants to make a big deal of this, or that he’s so self-centered that he thinks he’ll change the mind of politicians, more power to him. But for me as a skeptic, it is not the most important thing he says.
In his article, he mentions a young girl who “started having seizures soon after birth. By age 3, she was having 300 a week, despite being on seven different medications. Medical marijuana has calmed her brain, limiting her seizures to 2 or 3 per month.” This is simply an anecdote of no quality whatsoever. Did he thoroughly investigate her case to determine if the number of seizures actually went down? Do we know that cannabis has anything to do with the change? Is this nothing more than a Post hoc ergo propter hoc fallacy, that just because she consumed cannabis and the seizures decreased does not mean anything about cannabis’ causative properties with regards to this type of seizure. And then, Dr. Gupta continues with the anecdotes by stating, “I have seen more patients like Charlotte first hand, spent time with them and come to the realization that it is irresponsible not to provide the best care we can as a medical community, care that could involve marijuana.” Why do these TV doctors (like Dr. Oz) think that their anecdotes are better than anyone else’s.
Anecdotes are useless because they aren’t controlled, because they are subject to all levels of bias, and because these stories aren’t peer-reviewed. In other words, anecdotes have no value in science-based medicine. Anecdotes do have value in formulating testable scientific hypotheses, but assuming that anecdote=data, and more anecdotes=more data is simply pseudoscientific. I don’t care what Sanjay Gupta writes or says publicly, but providing these stories as “evidence” that marijuana has a medical benefit is essential like telling me that he observed homeopathy (which is just water) working. It’s laughable.
However, the most important part of Dr. Gupta’s statements appears to be his belief that marijuana can be used in treating cancer. If you spend any amount of time on Twitter, Facebook, or just researching cancer treatments on the internet, you will run across someone claiming that smoking or eating marijuana, or injecting hemp oil (which is manufactured from the seeds of cannabis plants and don’t contain much THC, or tetrahydrocannabinol, the active hallucinogenic agent of cannabis) will cure or prevent cancer.
There is a common belief, again based on a boatload of anecdotes, that cannabis is effective in reducing nausea and vomiting in chemotherapy. In a large scale systematic review of the peer-reviewed literature, which included 30 randomized clinical trials and nearly 1800 patients, there was not much positive evidence that the use of marijuana reduced the incidence of vomiting. In fact, cannabis was only 1.38X better than other types of anti-emetics (medications that inhibit vomiting), which isn’t that much more than unity. However, patients who use cannabis are 4.67X more likely to suspend the use of the drug as a result of the side effects. The authors of the British Medical Journal article (one of the top medical journals) concluded that, “In selected patients, the cannabinoids tested in these trials may be useful as mood enhancing adjuvants for controlling chemotherapy related sickness. Potentially serious adverse effects, even when taken short term orally or intramuscularly, are likely to limit their widespread use.”
In a more recent meta-review of cannabis’ effectiveness in reducing nausea and vomiting in HIV/AIDS patients, published by Cochrane Reviews, the leading publisher of high quality meta-reviews of medical literature, the authors could find no evidence that cannabis had any effect on nausea and vomiting. The best study they could find in their analysis showed only a slight improvement in HIV/AIDS patients, and even then, the error was so large that it could be argued that cannabis might actually have a negative effect, causing more nausea (and less weight gain). The Cochrane authors concluded that:
Despite dronabinol (editor’s note: this is the pure form of THC, the active ingredient of cannabis) in being registered by at least some medicines regulatory authorities for the treatment of AIDS-associated anorexia, and some jurisdictions making allowances for the “medical” use of marijuana by patients with HIV/AIDS, evidence for the efficacy and safety of cannabis and cannabinoids in this setting is lacking. Such studies as have been performed have been of short duration, in small numbers of patients, and have focused on short-term measures of efficacy. Long-term data, showing a sustained effect on AIDS-related morbidity and mortality and safety in patients on effective antiretroviral therapy, has yet to be presented. Whether the available evidence is sufficient to justify a wide-ranging revisiting of medicines regulatory practice remains unclear.
Since cannabis’ big claim to medical fame is that it is useful as an anti-nausea treatment, it’s surprising that the literature is so lacking in supporting evidence, even when we go looking for it. But this happens a lot in junk medicine. People make claims that are so-often repeated that people accept it as a fact. Then when real scientific studies are performed, especially high quality meta-reviews, we find nothing.** However, because this claim is so profoundly accepted, there will undoubtedly be more data to review in the near and distant future.
However, Dr. Gupta’s most egregious belief is that he appears to be convinced that cannabis has a role in treating cancer. But, is there any evidence out there that actual cannabis or its byproducts have any effect on cancers? Before we start, let’s remember that there are 100 to over 200 different types of cancer (the actual number depends on how some researchers subdivide some cancers) in humans. And each of these different cancers have different pathophysiologies, different genetics, different prognoses, different causes, and different treatments. In other words, it is not one singular disease with one unified course of treatment. Always be skeptical when someone makes some claim that “XYZ cures or prevents cancer”, because that’s going to be nearly impossible. Every cancer is so different with such different physiology, there is just never going to be a magic pill.
Let’s see what’s going on recently in cannabis and cancer research.***
- Breast cancer. A recent review of the relevant research regarding the use of cannabinoids (the essential active compounds of marijuana) in the war on breast cancer concludes that “our current knowledge on the anti-tumor potential of cannabinoids in breast cancer, which suggests that cannabinoid-based medicines may be useful for the treatment of most breast tumor subtypes.” All of this research is based on rodent studies, and the joke in scientific research circles is that we’ve cured cancer in mice for decades. It’s important to understand that only a tiny percentage of therapeutic cancer drugs make it from an animal study clinical trial (about 5%), and even then, only about less than 8% (pdf) of oncology drugs that enter clinical trials actually end up being approved for use in humans. In other words, there’s only a 0.4% chance of any drug that’s being tested on cells or mice is ever going to end up being approved for human use. There is no nefarious conspiracy going on to block these drugs, it’s that in clinical trials the vast majority of these compounds fail to show effectiveness beyond their safety issues. And in cancer therapy, sometimes drugs that have a 51:49 benefit to risk ratio, and only keep a person alive for a few months get approved. So, the ones that don’t make are remarkably ineffective or unsafe. There is just no evidence that cannabis will treat or prevent breast cancer in humans. None. But let’s hope that it will fall in the 0.4% category.
- Colon cancer. In a recent article, researchers examined the effect of cannabidiol, a non-psychotropic ingredient of cannabis, on chemically induced cancerous colon cells in cell culture. The authors concluded that it could prevent colon cancer. Now, if I was harsh about mouse research as being an indicator of clinical success, I’d be harsher about cell cultures. This was tested on chemically induced colon cancers, which may or may not have the same pathophysiology of in situ colon carcinomas. And once again, we lack any clinical evidence that it might work in humans, but I guess this is another bet into the 0.4% chance column.
- Glioma. Junk medicine hawkers have been pushing hash oil to “cure” gliomas, a type of malignant brain and central nervous system cancer. It is based upon some preliminary research on just 9 patients in Spain. Only two of the patients survived more than a year, while the seven others had a course of the disease not different than what is experienced in typical treatments of gliomas. In fact, in the two patients who survived the longest (yet still died), the effect can be attributable to spontaneous (but temporary) regression of the disease, a fairly common event. In a review of these studies and claims, the author stated, “I didn’t find anything I would call “earth-shattering” or even anything that could be considered credible evidence that hash oil can cure advanced gliomas.” At this point, there is no supporting evidence that hash oil should be considered the first, second, third, or fourth line of treatment for gliomas. Right now, we have observations (which are just barely above anecdotes on the scale of scientific evidence) that hash oil might work. And maybe those observations can be used to create an hypothesis which can be tested in a controlled clinical trial. But until that point, there is no evidence that hash oil works to treat glioma. None.
- Lung cancer. In this case, it’s not about whether cannabis can treat lung cancer, but whether it actually causes it. In a recent retrospective epidemiological study, the authors stated, “in conclusion, the results of the present study indicate that long-term cannabis use increases the risk of lung cancer in young adults.” There is a “belief” that smoking pot is less problematic than smoking other types of plant material, such as tobacco. That is a false assertion, because the reason why smoking is so tied to lung cancer is that the epithelial lining of the lung is susceptible to carcinogens; moreover, as the authors state, part of gaining effects of the pot is to inhale deeply and hold the smoke in the lungs for a greater period of time than in cigarettes (and certain cigars), it might actually increase the exposure of lung cells to the smoke and any associated carcinogens. To be fair, the evidence is conflicting, but even in one large study that shows no conclusive evidence that there is an increased risk of lung cancer in non-cigarette smoking individuals, there appears to be increased risks for some types of cancer amongst marijuana smokers, including prostate cancer.
- Clinical trials involving cannabis and cancer. There are currently 8000 clinical trials that are recruiting patients for anti-cancer drugs (and over 19000 that are closed to patients), and as far as I can tell, there are none registered for marijuana, or isolated cannibinoids, dronabinol and nabilone. On the clinicaltrials.gov website, which tracks every clinical trial registered across the world (and in case you’re going to ask, no one would have a real clinical trial and not register it, since it shows you have regulatory approval to begin a trial), there is precisely one cannibinoid being used to treat cancer, and that is Sativex, which is a patented drug of nabixomols isolated from the marijuana plant. This study is just a Phase 1 trial, it hasn’t recruited any patients, and is years from providing us with any meaningful results. There might appear to be a lot of research into cannabis using cell culture and animal models, but none have been transferred over to human clinical trials. This is not unusual, because even though it seems that there is a lot of research into cannabis and cancer, the total mass of research into other compounds with respect to cancer is substantially larger, because the evidence for both mechanisms of the treatment and clinical successes for these other products are much higher. Look at it this way–there are currently over . Cannabis research is a tiny speck (though not an insignificant speck) of the cancer research world, compared to the vast body of research currently ongoing. Cancer research isn’t randomly throwing compounds at cells and seeing if they work or not, it’s a logical process to determine if a compound has a reasonable chance of inhibiting some part of the cancer growth or development. There is some potential for cannabis, but it probably doesn’t compare to what is currently in the 27,000 compounds in current clinical research, and, in a business sense, the return on investment for researching compounds that have better understood pharmacologic mechanisms of action on cancer are higher.
- Aldington S, Harwood M, Cox B, Weatherall M, Beckert L, Hansell A, Pritchard A, Robinson G, Beasley R; Cannabis and Respiratory Disease Research Group. Cannabis use and risk of lung cancer: a case-control study. Eur Respir J. 2008 Feb;31(2):280-6. doi: 10.1183/09031936.00065707. PubMed PMID: 18238947; PubMed Central PMCID: PMC2516340.
- Aviello G, Romano B, Borrelli F, Capasso R, Gallo L, Piscitelli F, Di Marzo V, Izzo AA. Chemopreventive effect of the non-psychotropic phytocannabinoid cannabidiol on experimental colon cancer. J Mol Med (Berl). 2012 Aug;90(8):925-34. doi: 10.1007/s00109-011-0856-x. Epub 2012 Jan 10. PubMed PMID: 22231745.
- Caffarel MM, Andradas C, Pérez-Gómez E, Guzmán M, Sánchez C. Cannabinoids: a new hope for breast cancer therapy? Cancer Treat Rev. 2012 Nov;38(7):911-8. doi: 10.1016/j.ctrv.2012.06.005. Epub 2012 Jul 7. Review. PubMed PMID: 22776349.
- Guzmán M, Duarte MJ, Blázquez C, Ravina J, Rosa MC, Galve-Roperh I, Sánchez C, Velasco G, González-Feria L. A pilot clinical study of Delta9-tetrahydrocannabinol in patients with recurrent glioblastoma multiforme. Br J Cancer. 2006 Jul 17;95(2):197-203. Epub 2006 Jun 27. PubMed PMID: 16804518; PubMed Central PMCID: PMC2360617.
- Lutge EE, Gray A, Siegfried N. The medical use of cannabis for reducing morbidity and mortality in patients with HIV/AIDS. Cochrane Database Syst Rev. 2013 Apr 30;4:CD005175. doi: 10.1002/14651858.CD005175.pub3. PubMed PMID: 23633327.
- Parsa CF, Hoyt CS, Lesser RL, Weinstein JM, Strother CM, Muci-Mendoza R, Ramella M, Manor RS, Fletcher WA, Repka MX, Garrity JA, Ebner RN, Monteiro ML, McFadzean RM, Rubtsova IV, Hoyt WF. Spontaneous regression of optic gliomas: thirteen cases documented by serial neuroimaging. Arch Ophthalmol. 2001 Apr;119(4):516-29. PubMed PMID: 11296017.
- Shrivastava A, Kuzontkoski PM, Groopman JE, Prasad A. Cannabidiol induces programmed cell death in breast cancer cells by coordinating the cross-talk between apoptosis and autophagy. Mol Cancer Ther. 2011 Jul;10(7):1161-72. doi: 10.1158/1535-7163.MCT-10-1100. Epub 2011 May 12. PubMed PMID: 21566064.
- Sidney S, Quesenberry CP Jr, Friedman GD, Tekawa IS. Marijuana use and cancer incidence (California, United States). Cancer Causes Control. 1997 Sep;8(5):722-8. PubMed PMID: 9328194.
- Skopp G, Richter B, Pötsch L. [Serum cannabinoid levels 24 to 48 hours after cannabis smoking]. Arch Kriminol. 2003 Sep-Oct;212(3-4):83-95. German. PubMed PMID: 14639811.
- Tramèr MR, Carroll D, Campbell FA, Reynolds DJ, Moore RA, McQuay HJ. Cannabinoids for control of chemotherapy induced nausea and vomiting: quantitative systematic review. BMJ. 2001 Jul 7;323(7303):16-21. Review. PubMed PMID: 11440936; PubMed Central PMCID: PMC34325.
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