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Medical marijuana as the new herbalism, part 2: Cannabis does not cure cancer

marijuana-cancer

About a month ago, I finally wrote the post I had been promising to write for months before about medical marijuana. At the time, I also promised that there would be follow-up posts. Like Dug the Dog seeing a squirrel, I kept running into other topics that kept me from revisiting the topic. However, over the past couple of weeks, the New York Times gave me just the little nudge I needed to come back and revisit the topic, first by openly advocating the legalization of marijuana, then by vastly overstating the potential medical benefits of pot (compare the NYT coverage with my post from a month ago), and finally this weekend by running a story lamenting the federal law that makes research into medical marijuana difficult in this country.

I stated my position on marijuana last time, which is that marijuana should be at least decriminalized or, preferably, legalized, taxed, and regulated, just like tobacco and alcohol. I also likened the cult of medical marijuana to the “new herbalism,” because it (1) vastly inflates the potential of medicinal uses of marijuana and (2) ascribes near-mystical powers to smoking or making extracts out of marijuana, rather than identifying and isolating constituents of the plant that might have medicinal value. All of this is very much like herbalism in alternative medicine. Indeed, promoting laws legalizing medicinal marijuana is such an obvious ploy to open the door to full legalization that some advocates don’t even bother to disingenuously deny it any more. Given that I tend to support legalization, as a physician this sort of deception irritates me. It also has consequences, particularly when overblown claims are made for what cannabis can do. Perhaps the best example of this is the claim that cannabis cures cancer, which pops up all over the Internet in memes such as the one in the image above.

Don’t believe me? Just Google “cannabis cures cancer” or “marijuana cures cancer.” To my relief, you’ll find the National Cancer Institute’s page on cannabis and cannabinoids, which, as I discussed last time, dwells more on whether cannabinoids are useful for pain relief, nausea, and cancer cachexia than on whether they can be used to treat cancer directly. However, you’ll also find pages like 20 Medical Studies That Prove Cannabis Can Cure Cancer, a Facebook page Cannabis Cures Cancers!, and articles like Rick Simpson’s Hemp Oil Medicine, which resembles a lot of articles for various alternative medicine and quackery in terms of providing lots of testimonials of cures for skin cancer, diabetic ulcers, and other skin diseases and conspiracy mongering but no hard evidence. Indeed, a commenter by the ‘nym of “Danman” showed up at another blog many of you are familiar with and proceeded to make hilariously bad arguments for the healing power of cannabis and how a post at that blog was a “prohibitionist hit piece,” even though it expressed the opinion that marijuana should be legalized over the course of over 150 comments. Meanwhile, others are recommending hash oil for gliomas with a near-religious fervor, touting the same sort of evidence that Stanislaw Burzynski uses to claim he can cure gliomas with antineoplastons.

So what is the story, really?

Cannabinoids versus cancer: Hype versus science

The first problem one encounters when examining the evidence concerning the effect of cannabinoids on cancer is that the vast majority of studies touted by advocates claiming that “cannabis cures cancer” are either in vitro or animal studies. In vitro and animal studies are what we in the biz call “preclinical data,” meaning data obtained before trying a treatment in the clinic. As the American Cancer Society put it:

More recently, scientists reported that THC and other cannabinoids such as CBD (cannabidiol) slow growth and/or cause death in certain types of cancer cells growing in laboratory dishes. Some animal studies also suggest certain cannabinoids may slow growth and reduce spread of some forms of cancer. However, these substances have not been tested in humans to find out if they can lower cancer risk. There is no available scientific evidence from controlled studies in humans that cannabinoids can cure or treat cancer.

This basically says it all, and it’s tempting to wind up this post right there, but, as Han Solo said after being urged to be quiet while taking out some storm troopers, “Hey, it’s me.” Besides, you, our SBM readers, expect science in addition to my self-absorbed blather, as amusing as it might sometimes be. So you shall have it. As good a place as any to start is, as you might imagine, 20 Medical Studies That Prove Cannabis Can Cure Cancer. After all, I assume that Arjun Walia, the person who put this list together, wanted to provide the very best evidence that could be found, particularly given the emphasis that “this is a short list.” I perused the papers in the list and was—shall we say?—underwhelmed. I’ll divide my discussion into tumor types, the way the list does. First, you have to understand that CBD, one of the cannabinoids found in marijuana, is viewed as particularly promising because it does not produce the same psychotropic effects as Δ9-tetrahydrocannabinol (THC), making it a particularly attractive for developing treatments whose side effects don’t involve being stoned all the time.

Glioma. The first thing that jumped out at me is that one of these papers has nothing to do with cancer, specifically this study that suggested that cannabinoids could protect the brain against neurodegeneration in neonatal rats caused by the toxin ouabain (an Na+/K+-ATPase inhibitor). The vast majority of the other studies were in human cell lines, such as this one studying the effect of cannabidiol, a nonpsychoactive cannabinoid, on glioma cell lines. As a cancer researcher, I noted that the IC50 (the concentration that produces 50% of maximal inhibition of the parameter being measured), was 25 μM, which is a bit higher than we like for an anticancer compound. I was thus not particularly impressed, although in fairness subcutaneous injection of CBD was able to inhibit the growth of glioma xenografts implanted subcutaneously in athymic nude mice, although no dose-response was demonstrated, and a dose of 0.5 mg per mouse is a pretty generous dose (25 mg/kg for a typical 20 g mouse). So while there does appear to be antitumor effect against the glioma cell lines tested, it was, at best, modest. Certainly it wasn’t the sort that would knock my socks off as a cancer researcher. A different study, which combined THC and temozolomide, produced more impressive results, not for the THC, which produced at best modest antitumor effect, but for the combination, which looked a bit more promising. Of course, one also must note that this is not hash oil or smoked pot, but the purified THC component. That THC might be useful against glioma does not tell us that hemp oil or smoking the weed will be useful against glioma any more than the fact that digoxin works in congestive heart failure tells us that it would be a good idea to ingest foxglove leaves.

Skeptical Raptor puts it in perspective:

In one study, the researchers determined that it would take a concentration of cannabinoids of approximately 10 µmol/L to cause the death breast cancer cells in cell culture. This converts to around 3.14mg/L of THC. So, you’d have to assume that to kill any breast cancer cells, you’d need at least a blood level of 3.14 mg/L to achieve breast cancer cell death. So how close to that 3.14 mg/L can we get by just smoking a joint or two? According to research, smoking one joint will give you a blood level of THC of around 1.3-6.4 ng/mL serum, or about .00013-.00064 mg/L. In other words, to get an anti-cancer effect, you need to light up around 1000 joints per day.

The IC50 values in these studies were higher than 10 μM.

Finally, there was one human study in the list of glioma papers. Basically, this was a phase I trial testing a method of administering THC. This was also some strange science in that nine patients with recurrent glioma had their tumors resected, but a catheter was left in the cavity left behind after surgery, and then:

Each day an aliquot of the THC solution (100 mg ml−1 in ethanol) was dissolved in 30 ml of physiological saline solution supplemented with 0.5% (w v−1) human serum albumin, and the resulting solution was filtered and transferred to an opaque syringe. This process was performed at the Department of Pharmacy of the Hospital Universitario de Canarias. Owing to the high hydrophobicity of THC, we controlled by gas chromatography/mass spectrometry (see below) the actual concentration of THC in the final solution. The THC solution was administered to the patients for different times starting at days 3–6 after surgery at a rate of 0.3 ml min−1 with a syringe pump connected to the subcutaneous reservoir. In the case of Patients 1 and 2, who received THC for 30 and 26 days, respectively, biopsies were also taken after the THC-treatment period and various tumour-cell parameters were evaluated.

As you can see, this is very different from smoking marijuana or ingesting hash oil. It involves directly infusing THC solution at a high concentration directly into the brain cavity where the tumor had been, in the hope of killing off any remaining tumor cells surrounding the cavity. Let’s just put it this way. There’s a reason why direct intratumoral injection of any drug is generally frowned upon, and that’s because it’s invasive and rarely works. Moreover, no one generally bothers with intratumoral infusion of a drug unless it requires a very high concentration to work. Mean survival was 24 weeks, and two patients survived approximately a year. The authors try (rather like Stanislaw Burzynski, actually) to argue that this is better than would be expected based on other studies and controls, and to claim that some patients responded. I find no convincing evidence of this in the paper, and in a cohort of nine patients though, it’s pretty darned hard to conclude this. I agree with Harriet. There is nothing “earth shattering” about these results. They could be consistent with an antitumor effect, but they could just as easily be consistent with no effect. Worse, this was not simply ingesting, smoking, or being injected with cannabinoids. The study involved having catheters sticking out of the subjects’s heads and having THC infused directly into the brain.

Breast cancer. I’m a breast cancer surgeon; so I’m going to go out of order here. There are four breast cancer studies listed. The first study examines CBD activity against a mouse breast cancer cell line 4T1 (another cell line I’m quite familiar with, having used it in my lab and because it was a cell line developed by a now retired investigator whom I know), and the breast cancer cell line MDA-MB-231 (which I’m more familiar with than I’d like to be). Basically, the study showed a modest effect against these two cell lines in vitro and in mouse models using 1 mg/kg and 5 mg/kg CBD. The second study looked at five different cannabinoids and found that CBD was the most potent inhibitor of breast cancer cell growth in vitro (IC50 between 6.0 and 10.5 μM) and that CBD and “CBD-rich oil” could inhibit the growth of MDA-MB-231 tumor xenografts. In this study, the effects of THC on cancer cell growth were weak (IC50 between 14.2 and over 25 μM, depending on the cell line). The third study showed similar results for HER2/neu(+) tumor cell lines using THC and specific synthetic agonists (activators) of cannabinoid receptors CB1 and CB2 (Win55,212-2 and JWH-015, which activate CB1 and CB, respectively) except that THC was not as weak. The fourth study didn’t look at marijuana cannabinoids at all, but rather the endogenous cannabinoid anandamine, with similar results.

Lung cancer. The next set of three studies look at lung cancer. The first study used a cell line with which I’m quite familiar, A549 lung cancer cells, using both cell culture and mouse xenograft models. I must say that I was singularly unimpressed with the effect sizes, at least in the in vitro studies, which also required fairly high concentrations (15 μM) of THC. In a mouse tail vein injection model of lung metastases, 5 mg/kg of THC decreased metastases by 50%, which is not bad, and in a straightforward xenograft model resulted in a 50% growth delay of the tumors, which is also not bad. The next study found similar results testing CBD against lung cancer cell lines and tumor cells from a patient in cell culture and mouse models. The third study showed that stimulation of cannabinoid receptors (CB1 and CB2) with synthetic agonists, Win55,212-2 and JWH-015, which activate CB1 and CB2, respectively, inhibited the growth and invasion of A549 lung cancer cells in vitro and their growth and metastases in mouse models.

And so it goes. Nearly all of these studies look at purified cannabinoids, usually either THC or CBD, but sometimes the endogenous cannabinoid anandamine (which isn’t even in marijuana), as with the breast cancer study above and this prostate cancer study. Some use synthetic agonists, such as the breast cancer and lung cancer studies above, or this study of mantle cell lymphoma that tested R(+)-methanandamide in addition to Win55,212-2, or this study of non-Hodgkin’s lymphoma, which also used R(+)-methanandamide. With the exception of the glioma study, all were preclinical studies looking at cell culture models and mouse models. One was a review article. One, as I pointed out above, had nothing to do with cancer, and I suspect the author included it to round up his list of studies to 20.

Unfortunately, it’s a highly intellectually dishonest list of studies if your goal is to provide evidence that “cannabis” (as in the plant or extracts from the plant) can cure cancer. Unfortunately, this is not the first time Arjun Walia has constructed such a list. Last year, Liz Ditz nailed him for constructing a similarly intellectually dishonest list of studies that “show vaccines cause autism.” Let’s just put it this way. In 2013, Walia was still citing some highly discredited studies, such as studies by Mark and David Geier.

The intellectual dishonest of representing this list of studies as evidence that cannabis cures cancer aside, it is a group of moderately interesting papers that suggest that purified cannabinoid receptor agonists can produce reasonable, albeit by no means spectacular, antitumor effects in preclinical models. As a whole, they suggest that some of these purified cannabinoid agonists, whether naturally occurring, such as THC, CBD, or synthetic, such as R(+)-methanandamide, or specific to CB1 or CB2, such as Win55,212-2 and JWH-015, might be worth investigating further. Again, we’re talking about pharmacology, isolating active substances and purifying or chemically modifying them to improve their activity and safety profile, not smoking weed or using hash oil. Cancer Research UK concludes:

But claims that this body of preclinical research is solid “proof” that cannabis or cannabinoids can cure cancer is highly misleading to patients and their families, and builds a false picture of the state of progress in this area.

It’s also noted that the best results in the lab have come from using a combination of highly purified THC and CBD, but that there have also been positive results with synthetic cannabinoids, such as a molecule called JWH-133, just as I’ve described, through mechanisms that include:

  • Triggering cell death, through a mechanism called apoptosis
  • Stopping cells from dividing
  • Preventing new blood vessels from growing into tumors
  • Reducing the chances of cancer cells spreading through the body, by stopping cells from moving or invading neighbouring tissue
  • Speeding up the cell’s internal ‘waste disposal machine’ – a process known as autophagy – which can lead to cell death

Unfortunately, as good as that sounds, it’s not all good. There is also evidence that cannabinoids, under some circumstances, can stimulate cancer cell growth and possibly contribute to tumor progression. They can also have different effects depending on dose and the level of cannabinoid receptors on the tumor cells being treated. For instance, this study suggests that cannabinoids only induce apoptosis in cells that express low levels of receptors that couple to a signaling pathway called ERK1/2 but don’t induce apoptosis in cells that have high levels of receptors because they then couple through a survival pathway known as AKT. Interestingly, cannabinoids also seem able to induce cell death through pathways that don’t involve cannabinoid receptors. In other words, it’s complicated, because cancer is complicated, and cancer drugs tend to work only against certain cancers. If cannabinoids do have anticancer effects in humans, it will likely only be against certain cancers, most likely combined with existing chemotherapy and targeted drugs. We also know from the preclinical work that has been done that it will take purified THC and/or CBD and/or synthetic cannabinoid receptor agonists to produce even the modest effects observed thus far, effects that are too modest to expect cannabinoids to be any sort of cure for cancer on their own. Smoking weed or using hash oil just isn’t going to cut it.

But what about the anecdotes?

On that other blog that you all hopefully know and love, one of the commenters, Justin Kander, cited a case report that’s been going around social media as “proof” that cannabis cures cancer. This case report describes a 14-year-old girl, PK, who presented with symptoms of “weakness, shortness of breath and bruising when she was taken to the Hospital for Sick Children, Toronto, Canada, on the 10th March 2006.” She was diagnosed with acute lymphoblastic leukemia (ALL) and underwent standard chemotherapy for ALL for six months. Upon analysis, she was found to be positive for a mutation in the Philadelphia chromosome, which is found in 2-10% of pediatric ALL cases. Philadelphia chromosome-positive ALL tends to have a poorer prognosis than other ALL. PK underwent a bone marrow transplant but was noted to have blast cells six months after treatment and therefore underwent aggressive chemotherapy along with a tyrosine kinase inhibitor. After more recurrences and more treatment (such as radiation therapy to the brain for a presumed, but never completely documented, infiltration of the brain by leukemia, it was stated in the case report:

On the 4th February 2009, blood was noted in the patient’s stools and a blood cell count revealed the presence of blast cells. As a result, all treatment including the disatinib was suspended and the patient’s medical staff acknowledged failure in treating her cancer. It was charted by the patient’s hematologist/oncologist that the patient ‘suffers from terminal malignant disease. She has been treated to the limits of available therapy… no further active intervention will be undertaken’. She was placed in palliative home care and told to prepare for her disease to overwhelm her body and from which she would suffer a stroke within the next 2 months.

The family found articles on how cannabis supposedly cures cancer, and found their way to Rick Simpson, who has been featured in utterly credulous articles in High Times and SF Weekly (the latter of whose editors really should have known better) as the man who can cure cancer with hemp oil, who provided her with hemp oil mixed with honey (because of the bitter taste and viscous nature of hemp oil). This was administered in daily doses. It is claimed in this case report that there was a strong correlation between increasing dose of the hemp oil and decreases in PK’s blast count (a measure of leukemia cells in the blood), but looking at Figures 1, 2, 3, and 4, I have a hard time seeing it. Figure 1 shows increasing doses of hemp oil from what was called the “chronic” strain. That’s the closest we see to decreasing blast counts correlating with hemp oil dose. By day 15, the chronic strain was gone, and PK started taking Hemp Oil #2 from an outside source. In actuality in Figure 2, we see the blast count increasing with increasing dose until day 27, when it starts falling. Figure #3 shows Hemp Oil #3 (Afghan/Thai strain) from days 44 to 49. Given that the blast count stayed the same one can’t say much about this. Then Hemp Oil #4 was tried from day 50 to day 67, and her blast counts started rising. Finally, Hemp Oil #5 was tried and PK’s blast count fell between days 69 and 78. During that time, PK suffered the psychotropic effects of the hemp oil, including euphoria, disoriented memory, and the like.

Unfortunately, PK developed gastrointestinal bleeding and bowel perforation with peritonitis on day 78 and passed away. So, basically, she lived two and a half months after being placed on hospice. The authors assert that a dose-response curve was achieved, but to my eye I really don’t see it, except perhaps at the beginning, nor do I really buy the claim that the bumps in blast counts correlate with using “lower potency” strains. They also assert because PK was treated for tumor lysis syndrome (a syndrome in which the waste products of tumor breakdown, often seen after intense chemotherapy in hematopoietic malignancies, injure organs such as the kidneys), it must mean that the hemp oil was effective.
Unfortunately, even if a mild dose-response effect was observed that would not rule out spontaneous remission. Spontaneous remission is known to occur in ALL, although it is usually temporary, and spontaneous tumor lysis syndrome has been reported, although it is rare. In any case, one has to wonder whether the patient’s bone marrow was petering out near the end, something that is hard to determine because almost no laboratory values other than blast counts are presented, except at the end, when she had a very low platelet count (8K; normal 150K to 450K), a low white blood cell count (1.4, normal 4.5-13.0), and severe anemia (hemoglobin 8.2; normal: 13 to 16). It wasn’t established how the diagnosis of tumor lysis syndrome was made other than that the patient had elevated urate levels. Indeed, the entire case report seemed to have been written with the belief that it was the hemp oil that accounted for the decrease in blasts. A lot of information has been left out about the patient’s clinical course. All we know is that, after being placed in hospice, she was fortunate to have her blast count fall, developed a central line infection, and was treated for tumor lysis syndrome. We can also infer that she was still having considerable issues with her gut because she was on total parenteral nutrition (being fed by vein) and had trouble when they started to try to feed her orally again.

It should also be remembered that, whether or not hemp oil was responsible for the decline in blasts (which is possible but not convincingly demonstrated by this case study) or whether it was “burnout” of the bone marrow in the terminal phase of the disease or even spontaneous remission, the patient still died. She still developed GI bleeding and a GI perforation with peritonitis and died of it only 78 days after going on hospice. There’s no way of knowing whether hemp oil prolonged her life. Probably it did not, as a two to three month survival after going into hospice after being declared terminal for leukemia is well within what is expected. In other words, this case report is mighty thin gruel indeed.

Of course, the sad story of PK and the treatment of her terminal relapsed ALL with hemp oil is probably the highest quality cancer cure testimonial out there, and unfortunately its quality is not that high at all. The rest of the anecdotes I ran into tended to be about as convincing to someone familiar with cancer as nearly all the other alternative cancer cure testimonials I’ve found; i.e., not very. If you don’t believe me, take a look at this article, in which Rick Simpson claims his success rate for patients with terminal cancer is around 70% and says:

“The ones that can’t be saved are usually the ones who’ve had the most chemotherapy and radiation, or wait too long to start the treatment,” he says. “They have to be able to stay alive long enough for the oil to start to work.” In fact, most patients who undergo chemotherapy die from the treatment, not the disease.

No, it is not a “fact” that most patients who undergo chemotherapy die from the treatment, not the disease. It’s a lie. In any case, Rick Simpson is just like cancer quacks the world over, who have no firm evidence to back up their miraculous-sounding cure rates and excuse their failures by claiming that the treatment patients had before prevented the quackery from working. Quacks like Rick Simpson do those who think that cannabinoids have promise in treating cancer no favors.

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Conclusions

There’s a lot of interesting research about the role of cannabinoid receptors in cancer and whether targeting them with cannabinoid agonists from marijuana or other natural sources, synthetic agonists, or endocannibinoids will be a useful tool to add to the armamentarium of anticancer therapies. From what we know now, it is quite clear that cannabis does not cure cancer, at least not by itself and certainly not ingested or smoked as marijuana or ingested or applied topically as hemp oil. Even in purified form, naturally-derived or synthetic cannabinoid agonists show relatively modest antitumor activity in preclinical models, which means that they will have to be combined with existing chemotherapeutic regimens. If they do find their way into the routine clinical treatment of cancer, it will be through rigorous pharmacological studies and rigorous clinical trials, the latter of which, in particular, are painfully lacking. Indeed, if you search ClinicalTrials.gov, you’ll quickly find lots of trials of cannabinoids to treat cancer-related symptoms and side effects, but precious few to treat cancer itself. There’s this phase I trial of Dexanabinol in Patients With Advanced Solid Tumors, which has been open two years and is still accruing patients, as well as this one of Dexanabinol against brain cancers. It’s not a lot, and suggests that there is not much interest in even synthetic cannabinoids as a treatment for cancer. After all, there are so many other promising avenues that a class of drugs that show the modest effects that the cannabinoids I’ve discussed do just don’t excite researchers that much.

In any event, the claims of advocates that “cannabis cures cancer” are nothing more than herbalism infused with the magical thinking of the naturalistic fallacy. Just because it’s “natural” does not make it better. In the case of cannabis for cancer, the only potentially promising way forward is to isolate the active components and figure out which of the hundreds of different cancers in which these components have activity against.

Finally, I have no objection to lobbying for the legalization of marijuana for recreational use. I would support such measures myself. However, trying to use hugely exaggerated claims of medicinal benefit as a back door path to legalization gets my skeptical antennae all a’twitchin’ about all the other claims made by advocates and provides ammunition for critics whose real goal is prohibition.

Next installment: More testimonials analyzed.

Posted in: Cancer, Herbs & Supplements, Politics and Regulation

Leave a Comment (343) ↓

343 thoughts on “Medical marijuana as the new herbalism, part 2: Cannabis does not cure cancer

  1. Fred de Vries says:

    You would like to see that marijuana should be at least decriminalized or, preferably, legalized, taxed, and regulated. That’s a view that probably takes into account a THC content of about 5%, which will deliver a mildly sedative effect.

    In The Netherlands however the THC content of cannabis is much, much higher and can reach more than 15%. An official study found that (Het gemiddelde THC-
    percentage in nederwiet was significant lager dan in de vorige meting (13,5% in
    2012/2013 versus 15,5% in 2011/2012
    ). The average THC-content in nederwiet was significantly lower versus the previous survey: 13,5% in
    2012/2013 versus 15,5% in 2011/2012.

    In The Netherlands cannabis has become so potent that law makers are considering reclassifying it to a hard drug. We see quite a few serious addicts that simply cannot function normally anymore.

    Nobody is suggesting anymore to legalize it anymore, but we do see a user more as a patient than as a criminal.

    1. Renate says:

      I don’t think nobody in The Netherlands is suggesting legalising cannabis anymore. Besides, legalising also means one can set standart for the product and the amount of THC it contains.

    2. Sean Duggan says:

      Although, honestly, I think that we can probably accommodate that in the legal system as well. There are laws in place that restrict alcohol content, albeit on a state-by-state level. When I lived in Ohio and New Jersey, the stores all carried Everclear ™, a form of grain alcohol that was sold in 190 proof form (95% alcohol). Some states don’t allow the 190 proof form which has led to the manufacturers making a 151 proof form. Similarly, I could see regulating the level of THC allowed in commercial marijuana, which would likely have to be tested on a random or periodic basis to ensure people are holding to the standard.

      1. Windriven says:

        Mrs. Windriven is forced to ankle on down to Portland to purchase Everclear for the making of limoncello. It is not for sale at 190 in WA. I’ve no idea what the final concentration of alcohol in our homebrew limoncello is but it is not something one drinks from a tumbler.

    3. Thor says:

      In 2008, the US national average was 8.5%. Today, typical medical marijuana in California has at least 15% THC, but goes higher. Hash with 20% is available like candy, as is oil, which can contain 60% THC.

      “We see quite a few serious addicts that simply cannot function normally anymore”.

      citation needed

      1. Windriven says:

        Here in WA state we’ve had a number of reports of kitchen chemists blowing themselves up extracting hash oil. I’m not sure what the draw is for making one’s own – maybe its like brewing one’s own beer? But some of the stories have been pretty funny and thankfully, while damage has occasionally been significant, injuries so far, have not. There must be a PNW version of a deep South ejaculation that should always cause foreboding: Hey Bubba, watch this!

        1. n brownlee says:

          And it’s so dumb. Middle-eastern and Asian processing has used enfleurage successfully for a long, long time. Extremely high-quality product, safe, easy, and effective. Or, so I hear.

          1. Windriven says:

            “Or so I hear.” ;-)

            “Extremely high-quality product, safe, easy, and effective.”

            But it lacks the entertainment value of blowing the windows out of your kitchen.

    4. LJames says:

      It will be like alcohol. It will end up going through the same population statistical experiments on how much is too much THC and then creating tools to test THC levels in the blood when pulled over and laws will pass to give DUI’s for being to sedate while driving a vehicle, which is potentially a death machine if you’re high while driving.

      1. Joe Hockey says:

        A car is a potential death machine whether the driver is high or not. Most people driving high are going to be fully capable of doing so because, unlike alcohol, their decision making ability isn’t as impaired and their reaction speed shouldn’t be much different. We share the roads with everyone and there are a plethora of drivers out there who have demonstratively poor judgement as well as atrociously slow reaction speeds. Get these people off the roads before you take me out, because I get high to put up with this shit. Road rage is more dangerous than putting yourself in a chilled out state with heightened levels of concentration. So I choose the latter where appropriate.

        Also, another 2c I’d like to throw down, if your weed has more active chemicals in it, say 3x the amount whatever ditch weed people reminisce about had however many years ago, then wouldn’t you just use a third of it? Or at the very least, less of it?
        I’ve been in the game ages, smoked a good selection of nug, and if I get some quality bud that takes a single hit to get offa, then mate, I’m probably not going to have another just to whitey up all my lunch.

        One day I’d like to be able to live as a person instead of feeling like a confused entity inside of a weirdly restrained system, but I accept that this will probably never happen because everyone is the latter and the sense of importance derived from directing someone else in a direction is that much easier than finding your own. People are so intelligently stupid.
        Don’t believe what you read, hear or see until you know what it is you’re looking at. And don’t falsify what you’re presenting to a point you can manipulate lazy people. Everyone is lazy, and that behaviour is the route of all evil.
        Also, stay off drugs, it will make you think like a person! They are also potentially dangerous, hence why they’re ‘controlled’. But you can’t control things that aren’t you. The longer we continue to try this the worse we will become. The world can’t be 6 families playground for too much longer, start living for yourself.
        Sorry for the abundance of unrelated banter, but if you’re reading this then it was worth it.

        1. Andrey Pavlov says:

          Most people driving high are going to be fully capable of doing so because, unlike alcohol, their decision making ability isn’t as impaired and their reaction speed shouldn’t be much different… Road rage is more dangerous than putting yourself in a chilled out state with heightened levels of concentration.

          This is actually completely untrue. I can’t find the reference at the moment but I know Dr. Novella has written about this. Suffice to say the evidence is actually rather clear – driving while smoking increases your risk of an accident by around 6-10 fold. And it is because your decision making capacity is impaired, your reaction speed is impaired, and your concentration is impaired.

          The interesting part of the data is that those under the influence of marijuana tend to have fewer accidents than those under the influence of alcohol. That is because marijuana smokers take on different behaviors and tend to drive more slowly and defensively… to make up for their impairments. However, while they are less dangerous than drunk drivers they are still vastly more dangerous than a sober driver.

          1. Simplexion says:

            Please present evidence to back up these claims of certainty.
            You sound like someone who has never experienced cannabis.

            1. Andrey Pavlov says:

              Please present evidence to back up these claims of certainty.

              Easy enough.

              Detrimental effects of cannabis use vary in a dose-related fashion, and are more pronounced with highly automatic driving functions than with more complex tasks that require conscious control, whereas with alcohol produces an opposite pattern of impairment. Because of both this and an increased awareness that they are impaired, marijuana smokers tend to compensate effectively while driving by utilizing a variety of behavioral strategies.

              Reference

              The takeaway message is that there is cognitive impairment but that marijuana users overestimate their impairment and try to compensate. Alcohol users do not. Plus the impairment pattern is (understandably) different. Some studies show no increase in crash risk, others do.

              Meta-analyses of over 120 studies have found that in general, the higher the estimated concentration of THC in blood, the greater the driving impairment, but that more frequent users of marijuana show less impairment than infrequent users at the same dose, either because of physiological tolerance or learned compensatory behavior.

              As for the actual increase in traffic accidents:

              One weakness of driving studies is that subjects are aware of being observed and assessed, so such studies are generally a better measure of what drivers are capable of doing rather than what they actually do. Epidemiological studies attempt to assess the actual risk that a driver may cause an accident under the influence of a drug, relative to that of a sober person driving under similar conditions. The relative risk is expressed in the form of an “odds ratio” (OR), which is the multiplier for the increased accident risk from driving under the influence of marijuana.

              Some studies show no increased risk, some do. In this paper the odds ratios for traffic accident under the influence of THC are all over the place, ranging from 1.7 to around 4 depending on the method used and the location.

              But I will concede one point – my specific numbers of 6 – 10 fold are not correct. As I said, I couldn’t find the reference I was looking for and made a mistake in my recollection. It should have been more like 2 – 4 fold. Which is certainly better, but it is still essentially unquestionable that driving stoned increases your risk of accident.

              You sound like someone who has never experienced cannabis.

              What is the emoticon for a really hearty belly laugh?

              I am from California and one of my good friends happens to have invented, developed, and currently sits on the board of directors for Weedmaps.com. I can assure you my friend, not only have I experienced cannabis in the past, but I have experienced better cannabis than you have.

              1. n brownlee says:

                “marijuana users overestimate their impairment and try to compensate.”

                Once, while driving under the influence, I saw a red light on Doheney. I braked smoothly and stopped promptly, but I was a block and a half away from it.

                It was a long, long time ago.

              2. Andrey Pavlov says:

                Once, while driving under the influence, I saw a red light on Doheney

                Doheny? As in California? By Dana Point? Home is San Clemente for me.

              3. n brownlee says:

                Yes- I lived in LA in ’67, part of ’68, off and on, and went back often through about 1974. Friends there, and in San Francisco.

                long, long before your time. Whisky-A-GoGo, the Doors, Etc. It was a pretty good time to be in your ‘twenties.

              4. Andrey Pavlov says:

                Yes- I lived in LA in ’67, part of ’68, off and on, and went back often through about 1974. Friends there, and in San Francisco.

                Oh man! That means you were there before they ruined Killer Dana! Please tell me you surfed it before they built that damned jetty and harbor and ruined one of the worlds best surf breaks!

              5. n brownlee says:

                @Andrey
                No… I do not and did not surf; I can barely swim. I walked the beach in a crouch, looking at stuff and dragging stuff out of tide pools.

              6. Andrey Pavlov says:

                @n brownlee:

                well… at least you saw it back then. I’ve been surfing out in Doheny and down by Old Man’s at San O and heard the old timers talk about Killer Dana.

              7. Volteric says:

                Andrey! San Clemente homie!? Lived and surfed there daily! Mommy and Daddy still live there so we are around the hood at least once a month. I assume you are not the Russian Ant Photographer?? :-)

              8. Beavis says:

                “The takeaway message is that there is cognitive impairment but that marijuana users overestimate their impairment and try to compensate.”

                Wow. Sorry to say this, but your reading comprehension is atrocious. Try reading that again. They don’t “try to” compensate. It clearly says they “compensate effectively”.

                You also gloss over a lot of important statements such as this one: “Experienced smokers who drive on a set course show almost no functional impairment under the influence of marijuana, except when it is combined with alcohol.”

                If you read this part of the study you linked to:

                “Cannabis users perceive their driving under the influence as impaired and more cautious,40 and given a dose of 7 mg THC (about a third of a joint), drivers rated themselves as impaired even though their driving performance was not; in contrast, at a BAC 0.04% (slightly less than two “standard drinks” of a can of beer or small 5 oz. glass of wine; half the legal limit in most US states), driving performance was impaired even though drivers rated themselves as unimpaired.”

                you will clearly see why worries about driving stoned are greatly overblown. People who THINK they are too impaired by cannabis to drive are actually NOT, so people who ARE too impaired to drive DEFINITELY KNOW IT. They also then contrast that with the effects of alcohol where one can consume a LEGAL amount, feel like they are not too impaired drive when they actually ARE! Yikes!

                More quotes from your study:

                “This awareness of impairment has behavioral consequences. Several reviews of driving and simulator studies have concluded that marijuana use by drivers is likely to result in decreased speed and fewer attempts to overtake, as well as increased “following distance”. The opposite is true of alcohol.”

                Hmm… It causes them to practice safer driving procedures. Speed kills. Passing kills. Following too close kills.

                “Other studies have found no adverse effects of marijuana use on sign detection,49 a sudden lane-changing task,43 or the detection of and response to hazardous events.48″

                You mention the epidemiological studies (the ones that showed risk), but ignore the CONCLUSION about those studies presented in the paper (deciding instead to draw your own):

                “Overall, though, case-control and culpability studies have been inconclusive, a determination reached by several other recent reviewers.101, 102 Similar disagreement has never existed in the literature on alcohol use and crash risk.103″

                Those epidemiological studies are also fraught with problems, which the authors go into some detail about.

                You may not know this but the NHTSA has extensively studied the effects of cannabis use on ACTUAL DRIVING performance and concluded there was little adverse effect. They found impairment in just one category (lane retention) but that impairment did not exceed that of a LEGAL level of alcohol (BAC 0.04%).

                http://ntl.bts.gov/lib/25000/25800/25867/DOT-HS-808-078.pdf

              9. Andrey Pavlov says:

                @volteric:

                <blockquote.Andrey! San Clemente homie!? Lived and surfed there daily! Mommy and Daddy still live there so we are around the hood at least once a month. I assume you are not the Russian Ant Photographer?? :-)

                Somehow I missed this. Well, I know how – my RSS reader randomly omits certain comments. The reason I found this is because Beavis’s comment came up and brought me back here and I happened to scan across yours.

                My parents still live there as well, but I typically end up going back home only a couple of times per year. When I am home I surf T-street as I can see the break from my bedroom window :-)

                And no, I am not the ant photographer. LOL. Though his stuff is pretty cool – very strange, innovative, and well done.

              10. Andrey Pavlov says:

                @beavis:

                What an apropos ‘nym given your level of ability to understand and hold discourse.

                Wow. Sorry to say this, but your reading comprehension is atrocious. Try reading that again. They don’t “try to” compensate. It clearly says they “compensate effectively”.

                O RLY?

                In this paper the odds ratios for traffic accident under the influence of THC are all over the place, ranging from 1.7 to around 4 depending on the method used and the location.

                When the minimum OR for traffic accidents under the influence of marijuana is 1.7 that means, by definition, that they are not compensating effectively. Compensating effectively means that the OR would be 1. Meaning that the odds of a stoned person getting into a car accident is equal to that of a non-stoned person. An OR of 1.7 means that a stoned person is 1.7 times more likely to be involved in an accident than a non-stoned person. Which shows that they do compensate… but not fully. And that is the best case scenario and the most generous data. The median clusters more around 2-3, which means at least a double risk of accident associated with smoking vs not.

                you will clearly see why worries about driving stoned are greatly overblown.

                Yes, actually I agree that they are overblown. In fact, that sort of was the take away from my comment. What is not true, however, is that there is zero increased risk and that, as you are attempting to claim, marijuana smokers completely compensate for their impairment.

                You then continue to focus on why driving stoned is safer than driving drunk. I agree. But that does not mean it is actually safe to drive stoned. There is still more risk associated with it. Period. The fact that the risk is less than that of driving drunk and that the general media coverage on the topic is overblown does not mean there is no additional risk when driving stoned.

                Which is, yet again, why people like you piss me off. Marijuana is safer than alcohol on pretty much all fronts. The evidence clearly points us to that conclusion. But when Beavis’s like you come around and try and claim that marijuana is completely safe it makes it really easy for those who would like to demonize marijuana to point out how incredibly stupid your arguments are.

                Stick with the facts, admit the truth that marijuana is harmful, it does impair driving ability, and it does increase risk, but that it does so much less than other drugs (particularly alcohol). It is not only the evidence based position, but makes it tougher to argue against because anyone with half a brain can see that being intoxicated on anything must have some effect on outcomes, which makes arguments like yours too easy to dismiss.

              11. Beavis says:

                @Andrey

                “What an apropos ‘nym given your level of ability to understand and hold discourse.”

                Fabulous display of debating skills, starting off with an ad hominem attack (typical deflection technique used by those with a weak argument). https://yourlogicalfallacyis.com/ad-hominem

                “When the minimum OR for traffic accidents under the influence of marijuana is 1.7 that means, by definition, that they are not compensating effectively. Compensating effectively means that the OR would be 1.”

                I’m sorry, but can you please tell me what section of the study you are referencing here (the section #)? In MY reading of it, some studies found increased risk and some found either no increased risk or even a DECREASED risk.

                After you answer this and I understand where you are coming from, I will respond to the rest of your reply.

              12. Beavis says:

                Oops, I just realized that I pasted the wrong quote from your reply. Sorry for any confusion. I was curious about this part:

                “In this paper the odds ratios for traffic accident under the influence of THC are all over the place, ranging from 1.7 to around 4 depending on the method used and the location.”

                What section number are you referencing?

              13. Andrey Pavlov says:

                @beavis:

                Fabulous display of debating skills, starting off with an ad hominem attack

                Says the guy who started out by saying:

                Wow. Sorry to say this, but your reading comprehension is atrocious. Try reading that again.

                Tit for tat, mon amie. And BTW, if you are going to bandy about terms like ad hominem you should learn what they actually mean. An ad hominem is a logical fallacy if and only if the personal attack is used to dismiss the argument in question. I didn’t dismiss your entire argument by saying you are a Beavis and leaving it at that. I made the comment and then followed it up with an actual argument.

                I’m sorry, but can you please tell me what section of the study you are referencing here (the section #)? In MY reading of it, some studies found increased risk and some found either no increased risk or even a DECREASED risk.

                Yes, some studies show a decreased risk but most don’t. And if you want to find the section it really is as simple as doing a search for “1.7″ and it comes right up:

                Several studies have found that cannabis users are more likely to be responsible for crashes (OR 1.7).80–82 Crouch found that marijuana use contributed to the demise of 168 fatally-injured truckers in all cases in which the serum concentration of THC exceeded 1 ng/mL.83 Terhune’s study of 497 road traffic accidents found that cannabis users had a responsibility rate of 76% versus 42.5% for the control group.84 A later, larger study by the same author on 1882 drivers killed in seven US states found no difference between responsibility rates, however,68 and it is unclear why the conclusions of the two studies differed.

                (section 3.3.1.2)

                When discussing the idea of a decreased risk it is important to note that:

                Because of these difficulties, epidemiological studies have also shown inconsistent effects, some finding decreased or no risk from driving while smoking marijuana, and others increased risk. Most studies are fraught with methodological problems that could lead to underreporting of drug use or misclassification of experimental subjects into or out of the marijuana-using category, confounding results.

                In section 3.3.1 there is the discussion of the studies that purport to show decreased risk of traffic accidents. Of which the above quote is the paper’s take away.

                That section demonstrates that the studies showing no difference or a protective effect are methodologically flawed. For example:

                Terhune’s study of 1882 motor vehicle deaths calculated an OR of 0.7 for cannabis use, 7.4 for alcohol use, and 8.4 for cannabis and alcohol use combined

                Cannabis alone is protective, but when combined with alcohol it makes it even worse? That seems counter intuitive, no?

                The key issue is that unlike alcohol, there is no way to actually determine if the person in question was acutely intoxicated with cannabis at the time of the accident:

                Drummer’s later and more extensive ten-year study of 3400 traffic fatalities in three Australian states found that drivers with blood THC levels less than 5 ng/mL, and those with only carboxy-THC present (THC-COOH, a metabolite that is excreted in the urine for weeks and is thus more likely to indicate past use than current use), had an OR of 1.0, but those with serum levels greater than 5 ng/mL had an OR of 6.6, the same as that for a BAC of 0.15%

                and

                Laumon’s study of 10,748 French motor vehicle fatalities found that although rates of alcohol and cannabis intoxication were similar (nearly 3%), ten times as many crashes were associated with alcohol as with cannabis; however, investigators noted a dose-dependent effect on OR with increasing THC serum levels, confirming Drummer’s observation by calculating an OR of 4.72 for THC levels greater than 5 ng/mL

                So when you take it all together, one finds that the plurality of studies show an increase in risk, with only a few which have methodological problems showing a decrease in risk. Combined with studies showing a dose-response curve of cannabis and traffic accidents along with a little Bayesian prior (it should make sense that any intoxication of any kind should impair a person’s ability to perform complex tasks that require a time sensitive response) means that yes, indeed, cannabis use does increase the risk of traffic accidents.

                The data do also clearly show us that, for the most part, it is safe to conclude that this increased risk is not as high as alcohol use.

                What remains to be answered is how much higher the risk of traffic accidents is under the influence of cannabis, hence the wide range.

                What you are doing is cherry picking a few studies that show a decreased risk and not only ignoring their methodological limitations, but also ignoring literally everything else that not only shows an increased risk but also why it makes sense that there would be an increased risk.

                After you answer this and I understand where you are coming from, I will respond to the rest of your reply.

                I’m not particularly confident in your ability to read the paper since you seemingly couldn’t find the plainly obvious sections of the paper in question in the first place. But I’ll admit I am curious as to what you may have to say.

              14. Beavis says:

                No, not tit for tat, my friend.

                You started out by quoting this passage: “Because of both this and an increased awareness that they are impaired, marijuana smokers tend to compensate EFFECTIVELY (emphasis mine) while driving by utilizing a variety of behavioral strategies.”

                and then proceeded to pervert its meaning by saying: “The takeaway message is that there is cognitive impairment but that marijuana users overestimate their impairment and TRY TO (emphasis mine) compensate.” so that it fits your own biased narrative.

                When I pointed this out by questioning your reading comprehension (perhaps I should have questioned your honesty and/or motive instead?), you responded with your ad hominem attack. As you can see my point was justified, yours was not. Is my handle really relevant to this discussion?

                “An ad hominem is a logical fallacy if and only if the personal attack is used to dismiss the argument in question.”

                Okay…

                “I didn’t dismiss your entire argument by saying you are a Beavis and leaving it at that.”

                Oh… I see. If you insert the word “entire”, that changes everything…

                “I made the comment and then followed it up with an actual argument. ” which consisted of you quoting this “In this paper the odds ratios for traffic accident under the influence of THC are all over the place, ranging from 1.7 to around 4 depending on the method used and the location.

                When the minimum OR for traffic accidents under the influence of marijuana is 1.7 that means, by definition, that they are not compensating effectively. ”

                So, you attempted to back up your claim that those under the influence only TRY to compensate by focusing exclusively on the studies that found increased risk, while completely ignoring those that did not.

                You then go on to quote some of the problems involving epidemiological studies (sorry, but ALL of these studies have problems not just the ones that contradict your narrative, which means these studies, in general, are of limited use), which supports what I’ve already said in my prior reply: “Those epidemiological studies are also fraught with problems, which the authors go into some detail about.”

                Now, contrary to your idea that “That section demonstrates that the studies showing no difference or a protective effect are methodologically flawed.” the paper mentions problems with ALL of these studies, including in the sections that you use to support your claim:

                3.3.1.2: “Terhune’s study of 497 road traffic accidents found that cannabis users had a responsibility rate of 76% versus 42.5% for the control group.84 A later, larger study by the same author on 1882 drivers killed in seven US states found no difference between responsibility rates, however,68 and it is unclear why the conclusions of the two studies differed.

                Unfortunately, many positive studies fail to take into consideration interactions with other drugs,80–82 and since alcohol and cannabis in combination cause more impairment than either drug alone, failure to control for concurrent alcohol use represents a significant limitation. Lack of blinding can also be a problem, as knowledge by the raters of drug use influences assignment of culpability. This was likely a confound in Crouch’s study.83″

                3.3.1.3 “Summary of culpability studies

                Although the results of culpability studies have therefore been somewhat contradictory, all find that the combination of alcohol and cannabis has worse consequences than use of cannabis alone.68, 71, 73, 85 In general, culpability studies suffer from two main confounds. The first is delay to sampling, which classifies some THC users who were impaired at the time of the accident into the non-use group, and the second is use of the metabolite carboxy-THC to identify marijuana-users, which can mistakenly classify some non-impaired drivers in the impaired group.”

                3.3.3: “Dussault and Breault’s study also only measured carboxy-THC, so the calculated OR was really for the risk of accidents given marijuana use at all rather than for marijuana use while driving. In addition, 15.4% of their roadside survey control group refused testing, and since this was the subset of the group that was more than likely to have been using illicit drugs, the refusals probably depressed the incidence of marijuana use in the control group and artificially increased the OR. The control group in Mura’s study was comprised of non-trauma patients at the hospital, rather than drivers who had not crashed, making the odds ratio an incorrect calculation. In addition, non-trauma hospital patients are not representative of the population and arguably may have had a lower rate of marijuana smoking, again distorting the OR.

                Because of these difficulties, epidemiological studies have also shown inconsistent effects, some finding decreased or no risk from driving while smoking marijuana, and others increased risk. Most studies are fraught with methodological problems that could lead to underreporting of drug use or misclassification of experimental subjects into or out of the marijuana-using category, confounding results.

                In contrast, epidemiological studies on the relationship between alcohol consumption and accident have been clear-cut and consistent, demonstrating that the risk of a motor vehicle accident increases significantly with BAC > 0.05%.95″

                4: “Epidemiological studies have themselves been inconsistent, and thus have not resolved the question. One possibility is that people who smoke marijuana share qualities—being young, male, and risk-taking—that would increase their risk of road traffic accidents even in the absence of marijuana use. It has been suggested that there is a single factor that underlies adolescent “problem behaviors” such as illicit drug use, precocious sexual intercourse, and problem drinking.96 Two epidemiological studies in New Zealand that attempted to address this hypothesis found that the significant relationship that existed between self-reported cannabis use and self-reported accidents (OR 1.6 and 3.9, respectively) disappeared after risky driver behaviors and unsafe driver attitudes were controlled for.97, 98″

                So, unlike your narrative, we see they go into pretty extensive detail about the problems with ALL of these epidemiological studies, not just the ones that did not find increased risk. This leads us to the conclusion that experimental studies seem to carry more weight than those mixed epidemiological studies.

                “Terhune’s study of 1882 motor vehicle deaths calculated an OR of 0.7 for cannabis use, 7.4 for alcohol use, and 8.4 for cannabis and alcohol use combined

                Cannabis alone is protective, but when combined with alcohol it makes it even worse? That seems counter intuitive, no?”

                No, it does not. If you had actually fully read this and other studies on the subject, you would have noted what is repeated in them: that cannabis users effectively compensate for their impairment by adopting safer driving techniques (slowing down, not passing, increasing following distance) and generally being more cautious and paying more attention. However, when you add alcohol into the equation, this eliminates the compensation ability and the intoxicating effects of the two drugs become additive. This is not only mentioned in section 4 of this paper, but repeated in other literature, including the NHTSA study I linked to. Why is it so hard for you to admit the POSSIBILITY that users ARE able to effectively compensate for their slight impairment by the fact that they do adopt safer driving techniques and pay closer attention than the control groups?

                “What you are doing is cherry picking a few studies that show a decreased risk and not only ignoring their methodological limitations, but also ignoring literally everything else that not only shows an increased risk but also why it makes sense that there would be an increased risk. ”

                Ahem. Pot. Kettle. Black. What you are doing is cherry picking a few studies that show an INCREASED risk and not only ignoring their methodological limitations, but also ignoring literally everything else that not only shows EITHER NO OR DECREASED risk but also why it makes sense that there MIGHT NOT BE an increased risk.

                You tell me to “Stick with the facts”, yet YOU cherry pick parts of the paper that support your narrative and ignore the parts that do not, including the authors CONCLUSION (!!!) about the studies you cling to:

                3.3.3 Summary of epidemiological studies (SUMMARY!)

                “Because of these difficulties, epidemiological studies have also shown inconsistent effects, some finding decreased or no risk from driving while smoking marijuana, and others increased risk.”

                I am not ignoring the studies that show increased risk (like you claim I am), I agree with the authors that the studies’ results are mixed, and that these epidemiological studies are inherently flawed and unreliable, meaning we cannot make the determination that you have made. The totality of evidence does not support your conclusion and multiple analyses by experts back this up.

              15. Andrey Pavlov says:

                @ beavis:

                Continue believing what you wish. I have no problem admitting that in some people in some circumstances marijuana may provide a protective effect. However it is ludicrous to think that on a population level that would hold true.

                The data overall show that marijuana does impair driving ability and increase risk of traffic accidents. Multiple lines of evidence plus prior plausibility all point to that. As I said, we can quibble about just how much, but it is simply not at all in line with the evidence to argue that marijuana doesn’t effect accident risk.

                Why do I focus on the “few” studies that show an increased risk? For multiple reasons. The first is prior plausibility. Impairment of cognitive and motor function is most plausibly going to lead to impairment of complex tasks like driving. The second is that the preponderance of data show an increased risk. It is not an even 50-50 split in data giving us absolutely no direction to point to. The third is the difference in effect sizes seen by the different data. For those in the preponderance, which show increased risk, the effect size is large with the smallest noted to be 1.7. In the minority of data that show no increased risk or protective effect the effect size is small, which is consistent with statistical noise.

                SInce you like summaries, how about the overall one?

                In summary, laboratory tests and driving studies show that cannabis may acutely impair several driving-related skills in a dose-related fashion, but that the effects between individuals vary more than they do with alcohol because of tolerance, differences in smoking technique, and different absorptions of THC. Driving and simulator studies show that detrimental effects vary in a dose-related fashion, and are more pronounced with highly automatic driving functions, but more complex tasks that require conscious control are less affected, which is the opposite pattern from that seen with alcohol. Because of both this and an increased awareness that they are impaired, marijuana smokers tend to compensate effectively for their impairment by utilizing a variety of behavioral strategies such as driving more slowly, passing less, and leaving more space between themselves and cars in front of them… serum concentrations of THC higher than 5 ng/mL are associated with an increased risk of accidents… In the meantime, patients who smoke marijuana should be counseled to have a designated driver if possible, to wait at least three hours after smoking before driving if not, that marijuana is particularly likely to impair monotonous or prolonged driving, and that mixing marijuana with alcohol will produce much more impairment than either drug used alone.

                So yes, I’ll re-iterate quite clearly that I do believe that marijuana is much less impairing than alcohol in terms of driving and that indeed people can develop both physiological tolerance and compensatory behaviours that will further decrease the risk. In some people under some circumstances the risk can be reduced to a close approximation of zero. But overall it is simply asinine to try and claim that any intoxication can possibly have zero effect on driving ability and not raise the risk of traffic accidents. And that is indeed what the data show. Which is why the authors of the paper say quite clearly that after consuming marijuana a designated driver should be had. You don’t have a similar caution for driving after consumption of milk, now do you?

              16. Beavis says:

                @andrey Since you have already made several blatantly false claims in this discussion and also intentionally altered the meaning of quotes from studies, perhaps you will forgive me if I do not take your word on this claim:

                “The data overall show that marijuana does impair driving ability and increase risk of traffic accidents”

                and this:

                “the preponderance of data show an increased risk. It is not an even 50-50 split in data giving us absolutely no direction to point to. ”

                In order for you to make these claims, which unless I’m mistaken, appear nowhere in the study, you clearly MUST have added up the total number of studies and the total population size of both the pro- and anti- increased accident study groups.

                Can you please share the numbers you came up with for the total number of studies and the total study population of both groups (for studies from the following sections: 3.3.1.1, 3.3.1.2, 3.3.2.1, and 3.3.2.2)?

                “I have no problem admitting that in some people in some circumstances marijuana may provide a protective effect. However it is ludicrous to think that on a population level that would hold true. ”

                No, it is not ludicrous by any means. Why are you SO CERTAIN that group A (slightly impaired in the ability to maintain constant lane position, but also simultaneously practicing numerous safer driving strategies) is in general more likely to cause a fatal accident than group B (supposedly unimpaired control group who tend to speed, follow too close, pass frequently, pay less attention, etc.)? It just makes no logical sense to claim that.

                Keep in mind that your entire argument is based on epidemiological studies, which we have already determined (A) have mixed and inconsistent results and (B) have inherent problems, flaws and limitations that call into question their results.

                These studies are so flawed that repeating the same study on a different population can demonstrably yield opposite results:

                “Terhune’s study of 497 road traffic accidents found that cannabis users had a responsibility rate of 76% versus 42.5% for the control group.84 A later, larger study by the same author on 1882 drivers killed in seven US states found no difference between responsibility rates, however,68 and it is unclear why the conclusions of the two studies differed.”

                How do you explain this, other than that those studies and their results are questionable? One plausible explanation is that since the first study was much smaller, it is more error-prone and more likely to achieve incorrect results and more statistical variability.

                Another explanation that shows that the studies you use to come to your conclusion are flawed is this: “One possibility is that people who smoke marijuana share qualities—being young, male, and risk-taking—that would increase their risk of road traffic accidents even in the absence of marijuana use. It has been suggested that there is a single factor that underlies adolescent “problem behaviors” such as illicit drug use, precocious sexual intercourse, and problem drinking.96 Two epidemiological studies in New Zealand that attempted to address this hypothesis found that the significant relationship that existed between self-reported cannabis use and self-reported accidents (OR 1.6 and 3.9, respectively) disappeared after risky driver behaviors and unsafe driver attitudes were controlled for.97, 98″

                Those studies, which are among the ones you use to support your conclusion, were clearly flawed and came to the WRONG conclusion because the authors made a mistake (at least I’d like to think so, rather than it being a case of them manipulating the data to achieve the results they wanted – which certainly does happen in some studies) and did not adequately control for confounding factors. This same inadequate controlling of confounders and inadequate control group matching is rampant among such studies, putting into question their results.

                Obviously you are also aware that all studies that relied on metabolites (such as urine testing) instead of active THC are completely useless as they only measure prior use, not recent use (and CERTAINLY NOT intoxication), so they must be discarded.

              17. MadisonMD says:

                Those studies, which are among the ones you use to support your conclusion, were clearly flawed and came to the WRONG conclusion because the authors made a mistake (at least I’d like to think so, rather than it being a case of them manipulating the data to achieve the results they wanted – which certainly does happen in some studies) and did not adequately control for confounding factors. This same inadequate controlling of confounders and inadequate control group matching is rampant among such studies, putting into question their results.

                Wow. Was just following this discussion. But you are saying:
                (1) Andrey’s conclusions are supported by studies.
                (2) That you believe that the studies are wrong because either:
                (a) They made a mistake (but you don’t say which one or how you know they made a mistake)
                (b) They manipulated the data (Wow. But you don’t say how you know the books were cooked)
                (3) Moreover, you go on to say that additionally, the controls were inadequate (didn’t control for confounders).

                Sure, #3 might be legit for any epidemiologic study attempting to assess cause-effect. But your other reasons to dismiss data that doesn’t fit with your beliefs are a bit over-the-top. It is fairly plausible to imagine that being high on any drug could impair driving. So you have two Bradford Hill criteria here.

                Show objectively better epidemiological data studies which do have better controls, no mistakes, and unmanipulated data (how would you know?), and then you take the point in other peoples minds (as well as your own).

              18. Beavis says:

                @MadisonMD

                “Wow. Was just following this discussion. But you are saying:
                (1) Andrey’s conclusions are supported by studies.”

                Yikes! You haven’t been following very well then, as I (and the authors of the study Andrey referenced, and the authors of two other studies) said the studies results are INCONSISTENT and do not resolve the question. Andrey somehow took this as being proof of his theory.

                “(2) That you believe that the studies are wrong because either:
                (a) They made a mistake (but you don’t say which one or how you know they made a mistake)”

                Actually, I did say (rather I quoted the authors, who did). They did not control for risky driver behaviors and unsafe driver attitudes.

                (b) They manipulated the data (Wow. But you don’t say how you know the books were cooked)”

                If you care to read it again I did not claim they did this, but did mention that it is possible. Do you think it doesn’t happen? I do think there may be a somewhat higher likelihood of this happening particularly in studies dealing with cannabis as many people have VERY strong personal feelings about it (some having been taught to hate and fear it their entire lives) and sometimes universities may even have political pressure put on them because this is such a touchy subject.

                “(3) Moreover, you go on to say that additionally, the controls were inadequate (didn’t control for confounders).

                Sure, #3 might be legit for any epidemiologic study attempting to assess cause-effect. But your other reasons to dismiss data that doesn’t fit with your beliefs are a bit over-the-top. ”

                I’m not dismissing the data. I’m merely saying it is inconclusive.

                “It is fairly plausible to imagine that being high on any drug could impair driving.”

                Right. It is ALSO plausible that being under the influence of cannabis alone does not increase (or even decreases) the risk of being in a fatal accident.

              19. Andrey Pavlov says:

                @ beavis:

                Whatever man. If you want to believe that being high doesn’t have an overall net negative effect on a person’s ability to drive, then go on living in your fantasy world. I just finished my 15 hour overnight shift in the ICU by telling the mother of my 25 year old patient that there is nothing more we can do and that his death is inevitable on a timecourse of a few hours. So forgive me if I don’t have the energy or desire to have any further “discourse” with you on this topic beyond saying that you are pretty damned stupid if you really think it is at all reasonable to argue that getting high either makes you a better driver or doesn’t make you a worse one. You are hiding behind uncertainty in the data and making scientifically stupid arguments in the process. I have very little patience for people like you even on a good day. There are plenty of legitimate reasons to decrease the demonization of marijuana for both recreational and medicinal purposes. But dumbass arguments like yours only serve to sabotage that because anyone with two brain cells and no agenda can see how patently absurd it is to try and argue that drivers who are high on any substance can be anything but more risky. People like you give the right wing nutters easy fodder to blow things out of proportion.

                Marijuana is a pretty darned safe drug, it certainly poses less risks across the board and in just about every facet of life than the vast majority of other drugs, including and most notably alcohol. But it is still a drug, it is still harmful to one’s health, and it still increases risk of adverse events such as traffic accidents.

                If you feel the need to respond go right ahead. I won’t be wasting my very limited time on it during my week of nights on a busy ICU service. But you won’t get any traction here with bad arguments like yours. Enjoy pissing in the wind if you must.

              20. Beavis says:

                @andrey: (sorry, I responded to your comment yesterday, but my reply was posted way down below in an unrelated section. Perhaps I clicked the wrong “reply” button. The comment format on this site is a bit hard to follow sometimes. I will repost it here with a few minor modifications, and moderators can feel free to delete the duplicate of this below)

                ” If you want to believe that being high doesn’t have an overall net negative effect on a person’s ability to drive”

                I never made such a claim. Do you understand that “overall net negative effect on a person’s ability to drive” is saying something completely different than “statistically significant increased risk of a fatal accident”?

                “I just finished my 15 hour overnight shift in the ICU”

                Of course I am very grateful to doctors and the wonderful and important (often thankless) work they do. I come from a family of doctors. However, I wonder if you drove home after your shift? If you did, you should probably be aware that fatigued driving can be even MORE risky than drunk driving (!), which could make your many comments warning about the dangers of stoned driving appear slightly hypocritical. But, seeing how very concerned you are about public safety, I’m guessing you probably did not drive yourself.

                “beyond saying that you are pretty damned stupid if you really think it is at all reasonable to argue that getting high either makes you a better driver or doesn’t make you a worse one.”

                I made neither of those claims although the second one of those statements is certainly plausible. My hypothesis, which lines up with the results of experimental studies, is that cannabis alone, while producing a small degree of impairment, allows users to effectively compensate and may not increase (or may even decrease) one’s risk of being involved in a fatal accident. Another possibility to consider is that it does slightly increase one’s risk, but not to the degree of statistical significance.

                “You are hiding behind uncertainty in the data and making scientifically stupid arguments in the process.”

                No, I am not. You are attributing arguments to me that I never made.
                It is YOU who claims that the clearly inconclusive (which we both seem to now agree on) epidemiological data demonstrates a clearly increased risk of fatal accidents.

                “But dumbass arguments like yours only serve to sabotage that because anyone with two brain cells and no agenda can see how patently absurd it is to try and argue that drivers who are high on any substance can be anything but more risky.”

                The problem here is that you apparently cannot tell the difference between the disparate concepts of “slight impairment” and “statistically significant increased fatal crash risk”. After extensively studying the effects of cannabis on actual driving performance, the NHTSA concluded “THC’s adverse effects on driving performance appear relatively small. ”

                http://ntl.bts.gov/lib/25000/25800/25867/DOT-HS-808-078.pdf

                With this in mind, I think the insults you are hurling my way for merely AGREEING with the NHTSA study findings are a bit excessive and uncalled for.

                You seem to be implying that ANY impairment, NO MATTER HOW SMALL OR SIGNIFICANT, definitely increases the risk of fatal accidents. Would someone drinking 1 ml of beer have an increased risk? What about 0.1 ml?

                In reality, a statistically-significant increased risk depends on the DEGREE of impairment AND the TYPE of impairment AND upon lack of adequate compensatory behavior.

              21. Andrey Pavlov says:

                I never made such a claim. Do you understand that “overall net negative effect on a person’s ability to drive” is saying something completely different than “statistically significant increased risk of a fatal accident”?

                True. And do you understand that hiding behind such semantic games is nothing more than a means to obfuscate? It is perfectly rational and reasonable to assume the causal relation between “negative effect on driving ability” and “increase in the risk of traffic accident.” You will also note that I never said fatal accidents. You are adding yet another weasel word to make the stats even harder to demonstrate to continue hiding behind the uncertainty. It increases the risk of all accidents. And by hiding behind the phrase “statistically significant” and adding the word “fatal” you are setting up a very narrow interpretation with a long goalpost in order to try and sound like you are making a valid point. The former is something expected at an undergrad level understanding of science and the latter is merely shifting goalposts.

                However, I wonder if you drove home after your shift? If you did, you should probably be aware that fatigued driving can be even MORE risky than drunk driving (!), which could make your many comments warning about the dangers of stoned driving appear slightly hypocritical.

                Yes, I am aware. And yes I did drive home. And no it is not hypocritical. And even if it were hypocritical that doesn’t matter as it has no bearing on the argument. I could be driving home stoned and drunk and it would still have no bearing on the argument of whether cannabis use increases the risk of all traffic accidents.

                And the reason it is not hypocritical is because I am not driving home stoned, which is a very avoidable activity, but instead driving home tired after a shift which is unavoidable, but I take precautions as best I can.

                Another possibility to consider is that it does slightly increase one’s risk, but not to the degree of statistical significance.

                See my first comment about a pedestrian understanding of science and hiding behind ambiguity in data. Just because there is nothing to show a statistically significant finding doesn’t mean the finding isn’t there. There are other means by which to assess that and come to a conclusion with a confidence in concordance with the level of evidence.

                It is YOU who claims that the clearly inconclusive (which we both seem to now agree on) epidemiological data demonstrates a clearly increased risk of fatal accidents.

                No, the data is not inconclusive it is conflicting. And there is more data and knowledge to bring to bear than just a handful of epidemiological studies. And the preponderance of data, within an appropriate Bayesian framework, allows for the conclusion that cannabis does increase risk of traffic accidents and is an overall negative influence on the ability to drive. There are plenty of ways to actually prove that this is wrong and, if they existed, I would amend my views accordingly. However it is difficult to do so (as the evidence we’ve discussed explicitly notes) so the data isn’t there. Given what data we have, I am not 100% firmly and definitively stating that cannabis does increase risk of traffic accidents. What I am saying is that it almost certainly does to some degree, that it does so less than alcohol, and that the question that remains is by how much. Which is a perfectly reasonable conclusion to come to based on the actual evidence.

                After extensively studying the effects of cannabis on actual driving performance, the NHTSA concluded “THC’s adverse effects on driving performance appear relatively small. ”… With this in mind, I think the insults you are hurling my way for merely AGREEING with the NHTSA study findings are a bit excessive and uncalled for

                The problem is you are agreeing with what you think the NHTSA findings are by fitting it into your narrative. Let’s take that sentence for a second and note something important:

                “THC’s adverse effects on driving performance appear relatively small. ”

                You are taking this word in the colloquial layman sense rather than the actual scientific sense intended in the report. You are also, seemingly, only reading the abstract when even a quick read (when you know what you are looking for) will actually show your interpretation of the meaning is false:

                “In summary, this program of research has shown that marijuana, when taken alone, produces a moderate degree of driving impairment which is -related to the consumed THC dose. The impairment manifests itself mainly in the ability to-maintain a steady lateral position on the road, but its magnitude is not exceptional in comparison with changes produced by many medicinal drugs and alcohol. Drivers under the influence of marijuana retain insight in their performance and will compensate where they can, for example, by slowing down or increasing effort. As a consequence, THC’s adverse effects on driving performance appear relatively small. Still we can easily imagine situations where the influence of marijuana smoking might have an exceedingly dangerous effect; i.e., emergency situations which put high demands on the driver’s information processing capacity, prolonged monotonous driving, and after THC has been taken with other drugs, especially alcohol. We therefore agree with Moskowitz’ conclusion that “any situation in which safety both for self and others depends upon alertness and capability of control of man-machine interaction precludes the use of marihuana”. However, the magnitude of marijuana’s, relative to many other drugs‘, effects also justify Gieringer’s (1988) .conclusion that “marijuana impairment presents a real, but secondary, safety risk; and that alcohol is the leading drug-related accident risk factor”.

                Which is precisely in concordance with my conclusions which I have been stating rather consistently: that marijuana does impair overall driving ability, that it does increase risk in driving, and that yes, it does so less than alcohol and other drugs, but – and here is the key – it still does increase risk in driving and decrease overall driving ability.

                You are merely hiding behind the term “relatively” as if that means that the effects are negligible when the study clearly does not conclude that.

                You seem to be implying that ANY impairment, NO MATTER HOW SMALL OR SIGNIFICANT, definitely increases the risk of fatal accidents. Would someone drinking 1 ml of beer have an increased risk? What about 0.1 ml,/blockquote>

                No, not at all. And your analogy is simply absurd. I am saying that intoxication by marijuana produces impairment in a dose dependent manner and that it increases the risk of all accidents, not just moved goalposts of your fatal ones. If you take a tiny toke and aren’t as high, then of course your risk will be lower, same as having only a half a beer. That’s what “dose dependent” means. My contention has been consistently and explicitly that once you are intoxicated on marijuana the risk is there. If you aren’t high, but still had a hit off a J, then no, you don’t apply to the discussion at hand.

              22. MadisonMD says:

                I wonder what Beavis would think about doctors using cannabis before or during duty? We know that alcohol could impair judgement and that is completely unacceptable. Narcotics the same. However, cannabis impairs judgement to much less extent, apparently. Lets even imagine there were some studies that showed that cannabis did not cloud a physicians judgement whereas others showed there was a slight impairment.

                So, Beavis, I’m wondering if you would be OK with your physician practicing medicine– actually admitting you to the hospital or operating on you– after a joint or two? (Hell, those shifts are long, Beavis!)

              23. Beavis says:

                @MadisonMD

                “I wonder what Beavis would think about doctors using cannabis before or during duty? We know that alcohol could impair judgement and that is completely unacceptable. Narcotics the same. However, cannabis impairs judgement to much less extent, apparently. Lets even imagine there were some studies that showed that cannabis did not cloud a physicians judgement whereas others showed there was a slight impairment.

                So, Beavis, I’m wondering if you would be OK with your physician practicing medicine– actually admitting you to the hospital or operating on you– after a joint or two? (Hell, those shifts are long, Beavis!)”

                My views are as follows: I would prefer that my doctors not use ANY recreational drugs either before or during their shift (as likely would anyone). I would put forth that any doctor that uses recreational drugs before or during their shift is most likely an irresponsible BAD DOCTOR. However, if I did indeed have such a bad doctor, I would probably also prefer they were using cannabis rather than alcohol or a multitude of other drugs, including many legal ones. As for my doctors responsibly using cannabis on their own time, even recreationally, I have NO PROBLEM with that whatsoever. Do you? If so, why? My standards for surgeons would likely be much higher, and I would prefer they not use any drugs that could potentially impair them, legal or not, before or during their shift, including not just alcohol, but also nicotine, caffeine, and any other potentially impairing drugs .

                Now, if the doctor were using it for valid MEDICAL reasons, then I would certainly evaluate it along the lines of other potentially-impairing medications. I have no idea what the rules are for doctors taking necessary, yet potentially-impairing medications on duty. Perhaps you can enlighten me on this.

            2. Andrey Pavlov says:

              @simplexion:

              BTW, another good reference on cannabis and driving impairment.

              Experimental studies have repeatedly shown that THC impairs cognition, psychomotor function and actual driving performance in a dose related manner. The degree of performance impairment observed in experimental studies after doses up to 300 μg/kg THC were equivalent to the impairing effect of an alcohol dose producing a blood alcohol concentration (BAC) ≥0.05 g/dl… Case-control studies generally confirmed experimental data, but culpability surveys showed little evidence that crashed drivers who only used cannabis are more likely to cause accidents than drug free drivers. However, most culpability surveys have established cannabis use among crashed drivers by determining the presence of an inactive metabolite of THC in blood or urine that can be detected for days after smoking and can only be taken as evidence for past use of cannabis. Surveys that established recent use of cannabis by directly measuring THC in blood showed that THC positives, particularly at higher doses, are about three to seven times more likely to be responsible for their crash as compared to drivers that had not used drugs or alcohol. Together these epidemiological data suggests that recent use of cannabis may increase crash risk, whereas past use of cannabis does not.

              In other words, damned skippy that THC impairs your ability to drive and increases your risk of crashing. Some data in the past were flawed because they used evidence of recent past use rather than current intoxication which of course does not impair you.

              But it is people like you that drive me absolutely batty. You are making it harder to have a rational and reasonable discussion about cannabis because you (and people like you) make patently stupid claims that somehow, magically, marijuana can get you high but somehow not affect complex motor skills like driving. It makes discussions about how it ends up having less harmful effects than alcohol impossible because anybody with half a brain can see that you are a nitwit for suggesting it doesn’t affect you at all and can just dismiss your argument entirely.

              If you want to actually do something positive and appropriately stop the demonization of marijuana in a society that embraces alcohol, you need to make rational and reasoned arguments. Not stupid ones like the one you did.

              Oh, and don’t try and pull out unfounded assumptions like your interlocutor never having tried cannabis as a means by which to attempt and discredit him or her. Because you never know who you are talking to. And you will inevitably run into someone like me who can school you hard in pretty much every single word that comes out of you.

            3. WilliamLawrenceUtridge says:

              A car is a potential death machine whether the driver is high or not. Most people driving high are going to be fully capable of doing so because, unlike alcohol, their decision making ability isn’t as impaired and their reaction speed shouldn’t be much different. We share the roads with everyone and there are a plethora of drivers out there who have demonstratively poor judgement as well as atrociously slow reaction speeds. Get these people off the roads before you take me out, because I get high to put up with this shit. Road rage is more dangerous than putting yourself in a chilled out state with heightened levels of concentration. So I choose the latter where appropriate.

              And

              Please present evidence to back up these claims of certainty.
              You sound like someone who has never experienced cannabis.

              May I just point out that this is the exact rationalizations used by people who have drunk too much to justify driving home drunk?

              Intoxicants not only impair your reflexes, they impair your ability to recognize your impairment. There’s a reason why people swear they won’t drive home while drunk, right up until they’ve had their second glass of wine.

            4. Andrey Pavlov says:

              I wonder what Beavis would think about doctors using cannabis before or during duty?

              Deeeaaamn son. That was a solid way to put it.

              Yes Beavis, please do tell us your thoughts on that matter. And let me know if I should find a dealer to pick up a J on my way to the ICU tonight.

          2. Beavis says:

            ” If you want to believe that being high doesn’t have an overall net negative effect on a person’s ability to drive”

            I never made such a claim. Do you understand that “overall net negative effect on a person’s ability to drive” is saying something completely different than “statistically significant increased risk of a fatal accident”?

            “I just finished my 15 hour overnight shift in the ICU”

            Of course I am very grateful to doctors and the wonderful and important (often thankless) work they do. I come from a family of doctors. However, I wonder if you drove home after your shift? If you did, you should probably be aware that fatigued driving can be even MORE risky than drunk driving (!), which could make your many comments warning about the dangers of stoned driving appear slightly hypocritical. But, seeing how very concerned you are about public safety, I’m guessing you probably did not drive yourself.

            “beyond saying that you are pretty damned stupid if you really think it is at all reasonable to argue that getting high either makes you a better driver or doesn’t make you a worse one.”

            I made neither of those claims although the second one of those statements is certainly plausible. My hypothesis, which lines up with the results of experimental studies, is that cannabis alone may not increase (or may even decrease) one’s risk of being involved in a fatal accident. Another possibility to consider is that it does slightly increase one’s risk, but not to the degree of statistical significance.

            “You are hiding behind uncertainty in the data and making scientifically stupid arguments in the process.”

            No, I am not. You are attributing arguments to me that I never made.
            It is YOU who claims that the clearly inconclusive (which we both seem to now agree on) epidemiological data demonstrates a clearly increased risk of fatal accidents.

            “But dumbass arguments like yours only serve to sabotage that because anyone with two brain cells and no agenda can see how patently absurd it is to try and argue that drivers who are high on any substance can be anything but more risky.”

            The problem here is that you apparently cannot tell the difference between the disparate concepts of “slight impairment” and “statistically significant increased fatal crash risk”. After extensively studying the effects of cannabis on actual driving performance, the NHTSA concluded “THC’s adverse effects on driving performance appear relatively small. ”

            http://ntl.bts.gov/lib/25000/25800/25867/DOT-HS-808-078.pdf

            With this in mind, I think the insults you are hurling my way for merely AGREEING with the NHTSA study findings are a bit excessive and uncalled for.

        2. KayMarie says:

          Road rage is more dangerous than putting yourself in a chilled out state with heightened levels of concentration. So I choose the latter where appropriate.

          I agree that people with uncontrolled rage disorders should be kept off the road until such time as a psychiatrist can determine they are not a danger to others without taking medications that impair driving ability.

          I also like how there was an assumption that all the impaired drivers are stone cold sober and not under the influence. Because they’d be better drivers when impaired than when they are sober?

          Anywho, (warning anecdote ahead) I had a number of friends in college who were new to pot smoking. They didn’t do it in high school. At least a few thought the pot smoking increased their concentration so usually toked up right after class and before starting on their homework and studying.. Based on their grades their impression of increased concentration and cognitive ability was incorrect. Most had to do a lot of make up work to get back on track and they all changed the timing of their smoking to after their studying and homework was done.

          The data tend to show that my friends experience of less concentration even when their perception of greater ability to think is generally more common than pot makes you much more capable.

          I mean other than you are so rageful and it interferes with your abilities so much that any amount of sedation/relaxing medications is going to be better than your normal state of being.

    5. Beavis says:

      OMG! Have you actually heard that vodka is like 8 times more potent than beer?! 8 times (!!!) and they actually freely sell it in stores to anyone!

      In Whocareswhatcountry, alcohol has become so potent that law makers are considering reclassifying it to a hard drug. We see quite a few serious addicts that simply cannot function normally anymore.

      Your hysteria is somewhat amusing. Think about how silly you sound and try to relax.

  2. Angora Rabbit says:

    “(T)here have also been positive results with synthetic cannabinoids, such as a molecule called JWH-133, just as I’ve described, through mechanisms that include:

    Triggering cell death, through a mechanism called apoptosis
    Stopping cells from dividing
    Preventing new blood vessels from growing into tumors
    Reducing the chances of cancer cells spreading through the body, by stopping cells from moving or invading neighbouring tissue
    Speeding up the cell’s internal ‘waste disposal machine’ – a process known as autophagy – which can lead to cell death

    Unfortunately, as good as that sounds, it’s not all good. ”

    You got that right. And ethanol, good old ethanol, does exactly the same thing, both in cell culture and in animal models. And in humans. And yet we don’t run around saying “booze it up ’cause ethanol will cause apoptosis and autophagy.” * Rather the contrary – ethanol and its metabolites are considered carcinogens and tumor promoters.

    There is a combination of messianic hype and greedy monetizing going on with the legalization of marijuana, which is going to be sad to watch as more innocents are ripped off and taken advantage of.

    * Note to self: doubtless some dimwit will, having misread this.

    1. David Gorski says:

      In all fairness, cannabinoids do show a lot more specificity in terms of cell type than alcohol does.

    2. Angora Rabbit says:

      Totally agree with you. CB1 and CB2 are much cleaner than trying to map ethanol binding sites, although the latter is feasible. What frosts my kidneys are the plethora of studies that throw compound X onto cell lines and measure cell death, without consideration of dose, bioavailabilty, or science-based mechanism. What cell population would we expect to have, for example, CB1 or CB2 receptors (liver, neuronal subtypes…). If the cell line lacks an appropriate receptor, then what is really being shown? (Allowing that the oil gimish could have compounds operating through other mechanisms.)

      Coming down to Volteric’s comments, this is why I personally can’t get excited. Making cultured cells miserable doesn’t buy much more than a cup a coffee and a bad abstract. I get a lot of “lets make neurons apoptose” manuscripts to review, and I’ve reached a point where I won’t review them unless there’s also an underlying mechanism being tested.

      1. WilliamLawrenceUtridge says:

        “What frosts my kidneys” is henceforth beings appropriated for disseminated use throughout my life. I thank you, the world thanks you.

      2. CHotel says:

        Rather than bothering with a long-winded, scientific explanation of why mechanism-free in vitro studies like there are useless, I pretty much exclusively respond to people bringing them up for discussion with “You know what else kills cancer cells well? Setting the petri dish on fire.”

        1. KayMarie says:

          Reminds me of an old saying from my days associating with people screening things to see if they were anti-carcinogens (so anti-mutagenic properties with the idea of stopping cancer before it starts, and so much of that research feeds into the woo).

          Dead cells don’t mutate. Just because you get the numbers you want on a specific petri plate doesn’t mean you are getting the effects you are looking for.

          Although I haven’t heard of anyone using bleach enemas to prevent cancer (as plates treated with bleach have no mutant cells on them so look, no cancer–oh no, surely they are not going to try this at home now, right??), just autism of all things.

          Great, now I want my favorite anti-mutagens. Vanillin and cinnamonaldehyde. I need a cinnamon roll with vanilla icing, stat! http://www.ncbi.nlm.nih.gov/pubmed/17178418 (because I know y’all are going to request the citation)

    3. LBSquirrel says:

      Almost anything will stop or slow down cancer cell growth on a dish. Coffee, milk, water.

      1. KayMarie says:

        Great now I’m craving a latte with my cinnamon roll with vanilla icing.

  3. rork says:

    Work on CB1 and 2 might lead somewhere, as well as some other basic research on other effects of some cannabis compounds. Parts of the usual slow development cycle are to understand the mechanisms, and then starting from a poorly working bicycle (CBD) that usually has off-target effects you don’t like (and I don’t just mean being stoned), with time and hard work maybe you can design a Ferrari, based on what gets learned. We didn’t inhibit SHH for cancer fights by injecting people with cyclopamine, or making them eat Corn Lily.

    1. David Gorski says:

      Or, as I like to say, we don’t ask cancer patients to chew on the leaves of the Happy tree to dose themselves with amptothecin, irinotecan, or topotecan, to eat leaves from the periwinkle plant to get vinca alkaloids, or to eat the bark of the Pacific Yew tree to get taxol.

  4. Ed Whitney says:

    “Punish crime and discourage vice” is sound public policy. Recreational marijuana is a vice which no court of law should punish. Beyond that, there is nothing wrong with tight regulation of its marketing, especially to the young. Ditto for fraudulent health claims.

  5. Max says:

    I’m curious about patent US 6630507, “Cannabinoids as antioxidants and neuroprotectants”
    Original Assignee: The United States Of America As Represented By The Department Of Health And Human Services
    Filed in 1999, granted in 2003.

    I don’t see anything engineered or synthesized about it. It looks like they patented an application for a natural substance. Is that allowed? It seems to be in a gray area between invention and scientific discovery.

    1. Derek Freyberg says:

      Max, at a quick look the claims of that patent seem to fall afoul of the new US PTO guidelines on patenting of natural products. But the claims are “method of treatment” claims, and many comments on the new guidelines suggest that the PTO is overreaching.

  6. Max says:

    “In any event, the claims of advocates that “cannabis cures cancer” are nothing more than herbalism infused with the magical thinking of the naturalistic fallacy.”

    Would they claim that tobacco cures cancer?
    Why does tobacco cause cancer and cannabis doesn’t?

  7. Derek Freyberg says:

    I recall that for some brain cancers (and I don’t recall whether it’s gliomas), after resection of as much of the tumor as possible, biodegradable plastic wafers releasing BCNU (an anticancer nitrogen mustard) have been implanted in the surgical site. If THC were all that effective, surely it would be better to implant THC-containing wafers than just syringe in solution (with the consequent risk of infection, etc.). And I don’t hear of anyone doing that. Moreover, the potency of the compounds – even the “active ingredients” let alone the whole gemisch that is hemp oil – seems pretty low: the best anticancer therapeutics have activities in cell culture at well below micromolar, sometimes down to single digit nanomolar.

  8. qetzal says:

    I wish the ACS statement had included one more sentence (bold):

    More recently, scientists reported that THC and other cannabinoids such as CBD (cannabidiol) slow growth and/or cause death in certain types of cancer cells growing in laboratory dishes. Some animal studies also suggest certain cannabinoids may slow growth and reduce spread of some forms of cancer. However, these substances have not been tested in humans to find out if they can lower cancer risk. There is no available scientific evidence from controlled studies in humans that cannabinoids can cure or treat cancer. In fact, when compounds that show anti-cancer activity in isolated cells or in animals are subsequently tested in humans, the vast majority turn out NOT to be safe and effective.

    I think that’s a critical point. It’s not just that we haven’t confirmed activity in humans yet. It’s that by itself, activity in vitro or in animal models has very little value in predicting efficacy in humans. It’s barely better than picking chemicals at random.

    @Max:

    If you read the claims of that patent, you’ll see that they did not actually patent any of the relevant substances. They patented methods of using those substances for treating certain diseases. So, yes, that’s allowed, even if the substances themselves are natural. At least in the US; I think other places may have different rules about such “method of use” patents.

    1. Volteric says:

      I would forego your last sentence and replace it with: While some modest effects have been demonstrated, more well designed, controlled human studies are needed to prove whether or not Cannabinoids are useful in treating XYZ cancer(s) or not.

      1. qetzal says:

        I disagree on two counts.

        First of all, people who don’t do this for a living deserve to understand that activity against cancer cells in a dish or in a mouse model is NOT a very good reason to think something will work in humans. Not by itself, anyway. Way too many things have failed in humans after showing promise in vitro and in animals. In fact, as I said, the great majority of things that worked in vitro &/or in animals turn out NOT to work in humans.

        Second, it’s not at all clear that human studies are “needed” for these compounds. The modest activity outlined in the OP does not sound too promising to me. It’s not physically possible to conduct clinical trials on every compound that shows modest preclinical activity.

        I absolutely agree that US federal laws have unnecessarily hampered research into the effects of cannabis and its components, and I would certainly like to see those barriers eliminated. But even then, clinical studies should only be conducted when there is sufficiently robust justification. As Dr. Gorski has outlined, that doesn’t seem to be the case here.

        1. Volteric says:

          I am still perplexed by statements like: “…clinical studies should only be conducted when there is sufficiently robust justification”

          How can there be “robust justification” if so few human studies exist? What is objectionable to finding out? There were “modest effects” NOT just in cell culture and animals, but in a few human studies as well. And it’s not just the effects. There is some understanding as to what pathways and mechanisms are probably at play here so I am befuddled as to why anybody would not advocate more science around this issue? In short, it seems justifiable and warranted to further human studies.

          1. Windriven says:

            “What is objectionable to finding out?”

            Nothing. The problem is that medical research is a scarce commodity. There are only so many research dollars and only so many competent scientists. Competition for research funding is brutal. So the money goes where the funders expect the greatest likelihood of positive results.

            There is nothing to stop you or anyone else from setting up a foundation, amassing a huge pot of research money, and parceling it out to fund whatever studies you think have merit.

            1. Beavis says:

              “There is nothing to stop you or anyone else from setting up a foundation, amassing a huge pot of research money, and parceling it out to fund whatever studies you think have merit.”

              LOL. I think you mean nothing BESIDES the fact that the US government will basically refuse to allow any study on the beneficial medical use of cannabis in humans to actually go forward?

              1. Windriven says:

                So collect your money and do the research in The Netherlands. There are scientists there too. Or do it here in WA or in CO.

              2. Andrey Pavlov says:

                LOL. I think you mean nothing BESIDES the fact that the US government will basically refuse to allow any study on the beneficial medical use of cannabis in humans to actually go forward?

                You are kidding right? Geez Beavis! I know you say you are a layman and to excuse some of your scientific naivete, but the problem is you make completely and utterly false statements as if you actually knew what you were talking about, without doing even the slightest due diligence. Go to clinicaltrials.gov and do a search for cannabis. 522 results. Only open trials? 201 trials. That means that there are currently 201 clinical trials on cannabis (which means in humans) that are actively recruiting participants. If you want to be very narrow and include only trials with a known active and open status that is still 161 trials.

                At least get your basic facts straight. Otherwise it becomes painfully obvious to anyone who does know what they are talking about that you already have a narrative in your head and are merely spouting off whatever “facts” support that narrative.

          2. AdamG says:

            Investing in clinical trials is extremely expensive. Why invest time, money, and effort into a compound showing only modest effects when there are others that show greater preclinical promise?

            1. David Gorski says:

              Exactly. Cannabinoids, both natural and synthetic, seem to show relatively modest activity against the cancers I’ve seen them tested against. That’s nice, but doesn’t vault them to the top of list of compounds I want to see developed to the point that they are ready for clinical trials. In other words, as in herbalism, the hype outweighs the actual promise, especially as a cancer treatment.

              1. Volteric says:

                Can you please share which drugs you have in mind that you feel should top cannabinoids?

              2. WilliamLawrenceUtridge says:

                Can you please share which drugs you have in mind that you feel should top cannabinoids?

                For which type of cancer? For which sub-type of cancer? For which stage of cancer? For the primary tumor, or for possible metastases? For which body part any metastases has settled into? For which specific tumor section expressing which specific genetic derangements? For which set of proteomic expressions within which part of the tumor within which part of the body?

                Cancer isn’t “one thing”. Cancer is a generic term for a generic process that, once you get down to the details, is incredibly diverse. Think of “cancer” the way you would think of “types of transportation”. There’s walking and running (four-legged or two-legged; bear walking, bipedalism, mixed; sprint, gallop, trot, jog, mosey, meander, stroll). There’s flight (animal, mechanical, hovering, powered, gliding, helicopter, plane, glider, flight suit, jetpack, space shuttle, rocket, catapult, BASE diving, jumping, explosive). There’s aquatic (swimming, hydraulic propulsion, undersea crawling, drifting). There’s supra-aquatic (sail, motor, raft, drifting, swimming, surfing). There’s space (inertia, solar sail, gravitational slingshot, atomic rocket, space laser, surfing a supernova).

                Asking for better examples of drugs that cure cancer than cannabinoids, much like asking if cannabinoids can cure “cancer”, is the wrong question. There’s a reason we will never find a “cure” for cancer. Instead, there will be a multitude of “cures” depending on the unique characteristics of the individual cells, some of which we may never find a cure for. And as genetic testing and profiling of individual tumors become more and more of a reality, we can get ever-more-specific, treating not merely the specific stage of a paticular tumor from a particular original tissue, but the specific genetic rearrangements of that particular tumor from that partiuclar original tissue.

              3. CHotel says:

                Cancer isn’t “one thing”. Cancer is a generic term for a generic process that, once you get down to the details, is incredibly diverse. Think of “cancer” the way you would think of “types of transportation”. There’s walking and running (four-legged or two-legged; bear walking, bipedalism, mixed; sprint, gallop, trot, jog, mosey, meander, stroll). There’s flight (animal, mechanical, hovering, powered, gliding, helicopter, plane, glider, flight suit, jetpack, space shuttle, rocket, catapult, BASE diving, jumping, explosive). There’s aquatic (swimming, hydraulic propulsion, undersea crawling, drifting). There’s supra-aquatic (sail, motor, raft, drifting, swimming, surfing). There’s space (inertia, solar sail, gravitational slingshot, atomic rocket, space laser, surfing a supernova).

                Stealing this. Just wonderful.

              4. Volteric says:

                Thank you William. That was very helpful!

              5. WilliamLawrenceUtridge says:

                Stealing this. Just wonderful.

                Delightful, I enjoy being quoted to an unhealthy and narcissistic degree.

                Thank you William. That was very helpful!

                If you found that interesting, I highly recommend The Emperor of all Maladies. It’s very readable, very interesting, and gives some amazing historical context on the treatment of cancer, as well as why current treatment options are sub-optimal.

          3. Volteric says:

            Since the Federal Government feels it’s their place to tell me what I can and cannot ingest I’ll leave it to them to pay for the research that supports their idiotic claim that Cannabis has absolutely no medical value and is as dangerous heroin addiction and overdose. To date they haven’t done that or listened to the very commissions they assembled to demonstrate it’s danger. (Schafer Commission, etc)

            1. Windriven says:

              They don’t have to prove it. The so-called war on drugs isn’t going away. MJ may enjoy broader decriminalization or even legalization but the war will go on. No war on drugs, no need for an army of DEA agents and their little black PJs and really cool automatic weapons and flash-bangs and body armor. Its a 14 year old’s wet dream and if you’ve ever talked to any of those guys* …

              Truth is, I’d probably rather have them under some sort of semi-adult supervision than running around loose or working the sheriff’s department in East Jesus, AZ or somewhere.

              *Calm yourself. I’m not saying all of them. But a disturbing fraction.

              1. Beavis says:

                “The so-called war on drugs isn’t going away.”

                I wouldn’t be so sure about this if I were you. Once it becomes painfully apparent in the case of cannabis that legalization and regulation is far superior to prohibition (just like we learned with alcohol), a much more serious investigation into the drug war at large will likely occur. We already have real-world proof out of Portugal that drug criminalization is in fact counterproductive and leads to HIGHER rates of use and addiction than does removing criminalization and simply offering voluntary treatment for addicts instead.

              2. Windriven says:

                Don’t confuse facts with politics. The war on drugs may someday end – at least for pot. But someday won’t be tomorrow and it won’t be a year from tomorrow.

            2. WilliamLawrenceUtridge says:

              You’re tilting at a windmill here – most would agree the prohibition on marijuana is dramatically out of step with its potential for harm. I think it’s only illegal because it happens to be “foreign” to the historical roots of European civilization. If pot were indigenous to Paris or Rome or London, I’m sure it would be legal.

              The claim that marijuana has no medicinal value or has medicinal value are equally idiotic – in the absence of evidence, there is no reason to assume or promote it as being a panacea or worthless. But don’t blame the medical community for prohibition of it – blame politics and the legal system. Few doctors think pot is a significant health problem in and of itself.

              1. Volteric says:

                Agreed. I don’t blame the medical community whatsoever. My criticism was against the Federal prohibition and their reluctance to make science on this issue front and center.

          4. Vicki says:

            The other angle is, suppose you are (or your parent, spouse, sibling, or child is) a cancer patient. The doctor says that none of the existing standard treatments will cure you, and would you be interested in a clinical trial.

            If you say yes, they tell you that there are three drugs being looked at for your kind of cancer, but you can only try one at a time. Drugs A and B are most promising. Here are the side effects of each. Oh, and there’s also Drug C, which has the same side effects as Drug A, and is less promising, but we’ve got funding from the Volteric Foundation, so we’re offering you this option as well.

            Put that way, not many people are likely to choose Drug C, nor should they. It’s not like choosing between blueberry and peach pie, where I can have blueberry today and peach tomorrow, or a half slice of each.

            1. Volteric says:

              That’s helpful somewhat. I suppose I am having trouble with the analogy. Drugs A and B are, I assume, the drugs that look to be more promising than Cannabinoids or the drugs that are showing more pre-clinical promise than the modest effects of Cannabinoids?

              If so, I need to follow through on ADAM’s link he provided when I asked what other compounds/drugs look more promising as anti-tumorous. I trust that there are and I need to understand what makes them better than ‘modest”

              The obstacle I believe I am having is in thinking that Cannabinoids have shown more promising effects against tumors and metastasis than other pre-clinical compounds. In all fairness, if they exist why aren’t they getting the media attention that Cannabis has? (I guess the obvious answer is more people will read or watch something on a controversial compound versus some ho-hum other drug. I take responsibility for my own ignorance of the “ho-hum” drugs as well)

              1. Andrey Pavlov says:

                In all fairness, if they exist why aren’t they getting the media attention that Cannabis has? (I guess the obvious answer is more people will read or watch something on a controversial compound versus some ho-hum other drug. I take responsibility for my own ignorance of the “ho-hum” drugs as well)

                Well, you answered your own question here Volteric. Media attention is an extremely bad proxy to use for determining the scientific promise of anything.

              2. KayMarie says:

                Almost nothing gets a lot of media attention in the pre-clinical stage.

                Unless, of course, it happens to be from a fruit not usually eaten in the USA so you can easily create an MLM company by putting a tiny amount of the juice from the fruit in a bottle and then the only one releasing press release after press release is involved in selling it…but I digress.

                That and you have to test a lot of chemicals in the pre-clinical stage, and since most disappoint they don’t get a lot of attention unless there is something about it the lay public has some knowledge of. Most people have heard of weed. Most people don’t want to hear about long complex name of something synthesized for some reason they can’t understand out of lord only knows what and it’s the 10th one of these published about this month.

                Usually once it gets to the testing in humans stage and there is some major result then, and only then will you read about it in the press. And then often not in the mainstream but more of the news section of a science journal type of media attention.

                But people know what weed is, so you’ve crossed that barrier, there is controversy about pot, so that gets eyes on the page, so you report on that rather than Dr. John Doe isolated yet another moderately active compound from a series of similar compounds she is testing.

                And you say if as if no other compounds in all the world are being tested. Lots of things get tested because if you find one that is really effective there are big rewards for that. If you want proof that someone in all the world is looking for other potential chemotherapy agents try pubmed rather than your local or national news outlet.

              3. Volteric says:

                @ Kay & Andrey, I embarrassed to say I started on PUBMED. Well, that’s true for Cannabidiol. My interest in that had everything to do with it being used as an anxiolytic. The cancer claims were primarily popular science news outlets/websites. In my defense I don’t frequent CAM sites, etc. nor am I a defender of anything non-EBM. I consider myself a part of the Skeptic community (why I am familiar with SBM) BUT I am obviously not well versed in the medical sciences and it’s language. (If you want to argue about your god belief you might find me very well versed:-)

              4. KayMarie says:

                Well if you include cannabis related terms in all your searches you won’t find the same things you would with broader search terms.

                How many drugs has NCI tested?

                DTP has over 400,000 drugs in its repository that have gone through some kind of screening process at NCI. About 80,000 compounds have been screened since 1990, using the current screening system.

                http://www.cancer.gov/cancertopics/factsheet/NCI/drugdiscovery

                So hard to think that other potential chemotherapy agents are just ifs that the SBM crowd imagined might exist. :-)

              5. Andrey Pavlov says:

                @ Kay & Andrey, I embarrassed to say I started on PUBMED…

                Yes, that stuff is very dense. And difficult to parse. But it is a truism that not everything can be reduced to pithy sound bites and little factoids. The devil is in the details, particularly with medical claims.

                BUT I am obviously not well versed in the medical sciences and it’s language. (If you want to argue about your god belief you might find me very well versed:-)

                No shame in that. I am ignorant of the language and sciences of other fields as well. I follow cosmology and quantum physics as a hobby of interest, just to understand the general gist and salient points. I’d say I’m better than your average ursine at it. But I recently tried to read an actual paper from the field and it may as well have been in Aramaic.

                And I also am very well versed in god belief rhetoric. In no small part because I have found stunning similarities between CAM belief and god belief.

              6. Andrey Pavlov says:

                @kay:

                An excellent and accurate description. Well said.

                (in response to why pot gets so much media play and other compounds don’t)

              7. WilliamLawrenceUtridge says:

                I consider myself a part of the Skeptic community (why I am familiar with SBM) BUT I am obviously not well versed in the medical sciences and it’s language. (If you want to argue about your god belief you might find me very well versed:-)

                Mazel Tov for recognizing this fact, you’ve just dodged Dunning-Kruger. Frequenting the SBM comments is a good way, as is checking out the back catalog. Two good books are Snake Oil Science and Bad Science (the Goldacre book, not the Taubes book). They’ll go into the basics of clinical trials and why each step is necessary. Trick or Treatment is good for addressing specific SCAMS. And anything by Steven Barrett.

                And actually, Flat Earth News, though not specific to medicine, is also a good introduction to the systematic distortions brought about by mass market news.

          5. MadisonMD says:

            I am still perplexed by statements like: “…clinical studies should only be conducted when there is sufficiently robust justification” How can there be “robust justification” if so few human studies exist?

            Resources are only one issue. A larger issue is type I error. Lets do a simple thought experiment:
            (1) Imagine you dream up 100 possible cancer therapies.
            (2) You say, hell, lets try ‘em. Run 100 RCTs with standard alpha=0.05.
            (3) You will get 5 false positives. i.e. 5 “proven effective therapy” that are in reality useless. If your guesses were quite bad (0-1/100), then you are condemning future patients to worse outcomes than present (new ineffective therapies with side effects accepted as standard of care).

            If, on the other hand, you have strong preliminary data supporting the use in a specific cancer type/genetic subtype and you know the mechanism by which it works, you have improved prior plausibility (remember the difference between EBM and SBM?), making a false positive less likely.

            Additionally, if you know mechanism you can do much cooler things in your clinical trial and learn a great deal more. For example, you could monitor whether you are actually inhibiting your drug target at the desired times. That could be very important as you might have the right target, but learn, say, that just prior to the next dose the target is reactivated because the drug was cleared a bit. If this occurs you might want to change the dosing interval, dosing amount, or modify the molecule to improve the pharmacology. Or, equally important, you may discover that you are inactivating the molecular target effectively but yet the drug lacks a therapeutic effect. This is crucial information as it will then allow early curtailment of future drug development directed a this target (which is then known to be ineffective).

            Finally, if you know mechanism, you might be able to do a very very cool thing in your clinical trial: identify the mechanisms of resistance. This has double value:
            (a) It may confirm the direct therapeutic target in an actual human cancer through genetic rescue.* e.g. Bcr-Abl T315I mutation and imatinib resistance.
            (b) It is a necessary step in developing therapeutic strategies towards overcoming or preventing resistance (as also has been done for T315I.

            *You cannot imagine how difficult and uncommon it is to prove the direct molecular target of a drug in oncology, and how often drugs have multiple targets which can cloud the issue and impede progress for decades.

            1. Andrey Pavlov says:

              An excellent point that I certainly missed in my own comments.

              Thank you for reminding us of that point. I really do need to burn that into my memory so it comes to the fore more often.

            2. KayMarie says:

              Thank you for that important point. If you rush to a human trial before enough preclinical work, you might not understand the mechanism well enough to design the treatment in a way it could work. Much like when drugs were only tested in men we missed a few that actually can work for woman as there are differences in metabolism and biochemistry that can tweak the way a drug works just enough to make it seem ineffective in a RCT even when it can be effective when properly administered.

    2. Max says:

      Would something like “Vitamin C treatment for scurvy” or “Water treatment for dehydration” be patentable?

      1. KayMarie says:

        I think there has to be something new/innovative about it, not just we’ve been doing this forever, but heck no one else bothered to file it.

        1. Max says:

          Missing the point. If I discover that some disease is caused by some vitamin deficiency, can I turn that discovery into an invention by simply patenting the treatment of that disease with that vitamin?

          1. Volteric says:

            Apparently you can. That’s what the US Patent on Cannabinoids is: method of treatment, but if you are pointing out the absurdity of that I stand bemused with you.

          2. WilliamLawrenceUtridge says:

            It probably depends what country, and specific decisions by the supreme court. Plus, you are pretending that the patent process is staffed by idiots who can’t tell the difference between truly novel ideas and ones we already know.

            And mostly I’m guessing you’re trying to make your rather unclear point as a means of claiming that pot cures cancer, which it doesn’t.

  9. Volteric says:

    Dr. Gorski- based on the modest effects you shared I am curious if you were diagnosed with cancer if you would add some form of Cannabis or Cannabinoids to your regimen? Why or why not?

    1. WilliamLawrenceUtridge says:

      I won’t claim to speak for him, but I am pretty comfortable guessing a response along the lines of “I might consume it for nausea and vomiting, but given the results shown here, it would be utterly useless to hope for unrefined cannabinoids to have a significant impact on the cancer itself.”

      Why do you believe, apparently quite strongly, that cannabinoids can cure cancer, particularly given the disappointing results discussed above?

      1. Volteric says:

        William, I don’t believe Cannabis cures cancer at all. In fact, I am often correcting those who makes these claims and many others. It appears to me that it might be useful in cancer treatments but as I continue to learn here I continue to evolve my understanding.

        The intent behind the question was to gauge if Gorski has any objections to a cancer patient taking Cannabinoids? Is there any risk or potential interference? Does he see modest effects as worthy enough to add to regimen? I’m sure thousands of people are in a situation right now where that decision is being seriously considered considering the rapidity of medical marijuana acceptance.

        1. WilliamLawrenceUtridge says:

          Few here would object to end-stage cancer patients trying various things. Mostly we, or at least I, object to the waste of resources (scientific or medical or even just insurance money) being spent on unproven treatments, patients dying earlier because they reject proven treatments due to the blandishments of greedy quacks, and patients dying in greater pain because of above. Further, those modest petri dish effects may not change the course of cancer, and can add to the already complicated complications of treatment.

          Look, marijuana is a potent psychoactive drug. That doesn’t mean it must also cure cancer. And the doses required to get you high appear to be much lower than the doses that might inhibit tumor growth. Money is better-spent elsewhere (and I’ll include “promoting legalization” as a better use of those funds).

    2. MadisonMD says:

      I wouldn’t use it if I had cancer. Nor would I recommend it to a patient for any medical purpose. However, if a patient enjoys it recreationally and chooses to use it, given existing legal risks, no problem. There drug interaction risk is unknown but likely low.

      Disclosure: (1) I’m a medical oncologist; (2) I never used marijuana; (3) I have prescribed legal THC for nausea and have reviewed the literature– it is not highly effective for nausea. Existing antiemetics including 5HT3 and bradykinin inhibitors are highly effective so there is little specific use for THC.

      One of my patient’s well-meaning son forced marijuana on her. From her telling, it was a rather miserable experience. She had never used it in her life and was on targeted therapy essentially without side effects. Some people really don’t like getting high.

      1. Andrey Pavlov says:

        One of my patient’s well-meaning son forced marijuana on her. From her telling, it was a rather miserable experience. She had never used it in her life and was on targeted therapy essentially without side effects. Some people really don’t like getting high.

        A friend of mine did something similar with his grandmother. She suffers from terrible osteoarthritis. He convinced his mother that marijuana would be a good choice since nothing else relieved her pain and she always complained about how miserable she was. His mother was reticent but ultimately agreed. They opted to give her a lollipop with some tea (it was the lollipop that had the THC). At first grandma loved it. She became happy and said she felt like she was a little drunk (it was the only feeling she could related it to). Then she said that for the first time in so long her joints not only stopped hurting they actually felt good. They became warm and she said they felt like she had a dozen masseuses working on her. My friend and his mother were quite pleased with themselves. Then grandma said she wanted a bath. So they drew her one. In the meantime she kept licking that lollipop.

        By the time the bath was drawn, grandma had become over baked. As they began to get her in the tub she became nauseated then wobbly. She almost slipped and fell in the tub. They got her in safely, but then she started moaning and complaining of vertigo. Then she became more sedated and began to slip under the water of the tub. Mom panicked and my friend did too. They managed to get her out of the tub and in a robe and then bed. The next hour was not very much fun for anyone, but after that grandma felt good again.

        So that right there is one big barrier to advising patients to try marijuana for any reason – the dosage is hard to standardize and titrate, depending on the method of consumption. This goes doubly for people naive to its effects.

        My (future) mother in law had breast cancer and had quite bad side effects from the chemo. She now says that she really wished she had tried some marijuana to see if it may have helped her since nothing else really did.

        So I personally would only suggest (rather than recommend) a patient try it as a last line drug. Certainly not 1st or 2nd or even 3rd. If the patient was naive, I would advise caution (and probably relate my anecdote about my friend’s grandma). Depending on the state would change what would be available as a means to try it. I know in California they have sublingual sprays. These would probably be a best choice for naive people since a single spray is a small dose with the onset of effect rather quick so it is much easier to titrate the dose. Now that I think of it I have actually had a patient ask me about it once and I also said that trying to smoke it for the first time is even sketchier an idea since it is extremely likely they will cough a lot and feel miserable for it. I would advise extreme caution with any means of consumption and stress that they take very small doses and wait extra time in between doses to prevent over bake (like grandma).

        For patients who have had or still do have marijuana, it is a different story. I would advise them that it is indeed possible that it could interfere with their therapy though, as MadisonMD points out, low likelihood it would.

        And, of course, tailor the recommendations as I said before – people with asthma shouldn’t smoke it. People whom I anticipate could or will need surgery also shouldn’t smoke it. And so on.

        1. mouse says:

          Hm – I’m all for good joint pain relief, but unless you can separate the high from the analgesic, I can’t say I’d be interested. If it means being stoned whenever you’re not in pain, I don’t see the point.

          Personal preference, I’m sure.

          1. Andrey Pavlov says:

            @mouse:

            As I said – not everyone would actually enjoy the high. Some people will. Some people won’t like it all the time but some will enjoy it as temporary relief (and escape) from time to time.

          2. WilliamLawrenceUtridge says:

            If it means being stoned whenever you’re not in pain, I don’t see the point.

            Agreed, I prefer my life sober, I have more fun when I can think clearly and be less of an ass.

            Yes, this is me being less of an ass. I’m painfully obnoxious when drunk. Think a shorter, uglier, more muscular Don Draper right after receiving an award.

        2. Volteric says:

          All excellent points! I know that Cannabis fell out of favor prior to prohibition because irregularity with potency and dosing. It is something I have found very difficult to navigate in my own use. I do not buy claims of differing effects with different strains. What matters, IMO, is the cannabinoid profile where the THC/CBD content is lab tested and known. 25% THC in bud is going to be a bit different (to the inexperienced) than a bud with 15% CBD/ 5% THC. Technically I don’t think the effects are different. It just takes less to feel the otherwise standard effect, but most newbies do NOT understand this and why I find 99% of budtenders to be bimbos.

          In any case, medical or not, it needs to be regulated and standardized immediately.

          As aside, a friend has ALS and was taking a good amount of Vicodin. He ate some Cannabis (50/50 THC/CBD) and felt significant pain relief and was able to walk without falling and eased his constipation. He ended up preferring the Cannabis to the Vicodin (doesn’t take anymore) and seems more in control of the little control he has over his body. Just to be clear: He is not taking Cannabis to cure his ALS. :-)

      2. Volteric says:

        Mouse-”Hm – I’m all for good joint pain relief, but unless you can separate the high from the analgesic, I can’t say I’d be interested. If it means being stoned whenever you’re not in pain, I don’t see the point.”

        That’s exactly why some prefer high CBD/low THC Cannabis. They report pain relief with no high. While I now understand the effects on Cancer(s) as being only modest, many report pain relief without the high with CBD and as well as CBD along with low THC.

        As you know, pain, like psychiatric issues, are more subjective. Whereas whether or not tumors are reduced with Cannabis is objective.

        1. Andrey Pavlov says:

          @volteric:

          I am not aware of any specific evidence on CBD and pain. If you have those references I’d be interested.

            1. mouse says:

              I think it’s nice that you presented evidence that is particularily applicable to me. This forum is usually so specist, with all it’s focus on evidence from human trials.

            2. KayMarie says:

              It isn’t “suck” as not the 100% proof in a human being it actually works the way the people who claim it is a cure-all say it does.

              http://www.ncbi.nlm.nih.gov/pubmed/24117398
              “in female C57Bl/6 mice.”

              http://www.ncbi.nlm.nih.gov/pubmed/22585736
              “dorsal horn neurons in rat spinal cord slices”

              http://www.ncbi.nlm.nih.gov/pubmed/23180178
              ” The results of the current investigation were equivocal, with conflicting findings in the two phases of the study.” At least this one was in humans

              http://www.ncbi.nlm.nih.gov/pubmed/21238581
              “This review”
              which means it isn’t a clinical trial so you have to check to see how good the studies they reviewed are.

              http://www.ncbi.nlm.nih.gov/pubmed/17157290
              “adjuvant-injected rats”

              1. Volteric says:

                So I’m assuming what applies to the claims of Cannabis and Cancer is no different than Cannabidiol and Pain, namely there is modest effects which justify more pre-clinical studies??

                Early on in my CBD and Cannabis research my B.S. detector went off immediately because of it being billed as a panacea., but then part of me thought it made sense in light of what I learned about the “Endocannabinoid System.” However, my wife is in nursing school and there is zero mention of this system in any of her textbooks and wondered if others have made more out of this than what the evidence supports??

              2. KayMarie says:

                I think you can say it is biologically active and deserves to be on the list of things we might do more pre-clinical work on. A lot depends on how it stacks up with other compounds with about the same amount of data.

                If the best we have is a few compounds with modest results and this is the close to being the best of the bunch you’ll get more research dollars than if it is just middle of the pack and there are a lot of compounds with more promising data.

                But science is a human endeavor and it isn’t always driven completely objectively so there may be other factors that drive the research dollars to it or away from it.

                FWIW a lot of things get made more of than the evidence supports. Some of which have much more comprehensive data sets.

          1. Volteric says:

            @Andrey–So I guess this is interesting because it sounds like high CBD will move to a human study on its impact on pain…

            http://abc7news.com/261437/

            1. Andrey Pavlov says:

              @volteric:

              Thanks for the link. I am in the hospital all day today. Will see if I have some time to read it and get back to you.

            2. Andrey Pavlov says:

              @volteric:

              Well, I read the news release.

              I won’t nitpick the slight sensationalism and typical journalistic fluff in the piece.

              However, it is particularly light on the science. Doesn’t really give me much of anything to go on.

              I know pubmed can be daunting and in fact I myself actually don’t use it all that much. That is because I prefer Google Scholar. You are more likely to get utter garbage on GS than PM, but not by a huge amount. Plus I can easily tell the difference and the ease of looking on GS makes it all the better. I do all my lit reviews on GS.

              But then, of course, I actually go to the primary source. Which would definitely be tough for you. Especially since much of it is behind a paywall. Like this one which seems really interesting.

              The problem is that abstracts always tell the best possible story. And in a lot of CAM or otherwise dubious research flat out lie about what the actual data show. In this case I would be very interested to see their methodology, particularly how they managed to maintain blinding and how they structured their questionnaires. In studies where there is a psychoactive compound (THC was used in this particular one, not just CBD) the question of blinding is vital. And in studies on pain how the study was conducted and the assessments done is also vital; pain is profoundly influenced by placebo and nocebo affects as well as all sorts of study artifacts. Plus statistical significance and clinical significance are less likely to correlate in studies on pain since the endpoints are subjective.

              If you are keen to try and start getting a handle on reading scientific papers, I can actually recommend this blog post by PZ Myers and there were two blog posts by a guy going by the ‘nym of Prometheus who is a friend of SBM. His blog has been taken down, but his posts were so good I saved them as PDFs for myself. You can find links to download them from my google drive here and here.

              If you go through those I think you will have a solid basis from where to begin learning how to read scientific papers.

              1. Volteric says:

                Excellent! Thank you muchly!

  10. Volteric says:

    “It’s not a lot, and suggests that there is not much interest in even synthetic cannabinoids as a treatment for cancer. After all, there are so many other promising avenues that a class of drugs that show the modest effects that the cannabinoids I’ve discussed do just don’t excite researchers that much.”

    It doesn’t excite them because of modest effects or is it because there are too many obstacles and red tape for human trials to be done? I think the evidence is that it hasn’t been easy for researchers to do human studies because of Federal prohibition. You can’t say there isn’t enough evidence, say there is some promise and then conclude that the scant evidence doesn’t excite medical researchers. You said there isn’t enough evidence. There is enough promise to do the human studies so that we can know if Cannabinoids are or are not effective anti-cancer agents.

    1. David Gorski says:

      A drug whose IC50 is above 10 μM and only exhibits relatively modest antitumor effects isn’t going to excite that many cancer researchers. (I know this from personal experience.) It would be one thing if it had an IC50 above 10 μM but had awesome anticancer effects or if it really potentiated the effect of existing anticancer therapy. Researchers would be all over it, difficulties doing the research notwithstanding, but what I see from my review of the literature is modest promise at best for some cancers. It’s probably worth investigating further, but in terms of prioritizing what sorts of drugs should be advanced to human trials, cannabinoids would be way down the list.

      1. Volteric says:

        Fair enough. Thanks for the response. I am still very curious about your response to: If you were diagnosed with cancer if you would add some form of Cannabis or Cannabinoids to your regimen? Why or why not?

        1. e canfield says:

          My father tried smoking marijuana (not around his wife and children) when he had testicular cancer in the 70s. He says he might as well have been burning dollar bills, for all the benefit he got. Mom and my sister never even tried when they developed their respective cancers; they get a whiff and they break out in hives. So, no, I personally will not be trying hemp in any form in the likely event that I get a cancer some day.

          1. Volteric says:

            I’m sure you’re aware that Cannabinoids can be had without combustion.

            1. e canfield says:

              Combustion is irrelevant. They also break out if they eat hemp seeds.

              1. Volteric says:

                Didn’t realize they were allergic. Sorry if I didn’t see that.

        2. David Gorski says:

          If you were diagnosed with cancer if you would add some form of Cannabis or Cannabinoids to your regimen

          No. There’s no good evidence that it has significant anticancer activity.

          1. Volteric says:

            Thank you.

      2. Volteric says:

        Dr. Gorski-Forgive my ignorance but are there enough studies to know that Cannabinoids are not an IC50 above 10 μM?? My point, ad nauseum, is do we know enough to dismiss the effects as modest? Or should we further human studies to to determine this very question?

        1. David Gorski says:

          Nearly every study I’ve seen on THC or CBD has shown an IC50 between 10 μM and 30 μM. There were one or two with IC50 values below 10 μM for certain tumor types, but not that much below. I’m sure I could have missed a few, but overall I was underwhelmed by the activities reported for cannabinoids against common cancers.

        2. WilliamLawrenceUtridge says:

          Volteric, you have to realize that there are a near-infinite number of potential molecules that could have anticancer properties. Your first sentence could be repeated with nearly any molecule and the answer would be almost certainly “no”. With an entire universe of potential cures for cancer that exist, to hyperfocus on cannabinoids when they haven’t shown much potential to date says more about the societal and individual preoccupation with wanting pot to be a miracle than it does about pot actually being a miracle. You can always ask the question, “what if we increase the concentration” or “what if we increase the dose” for any substance, but at some point you have to accept negative results and spend precious resources elsewhere.

          There’s a pretty strong possibility that, like most molecules, plant-derived or not, psychoactive or not, cannabinoids simply don’t have widespread anticancer activities. If these results were applied to any other molecule that people didn’t use to get high or weren’t currently illegal, you would be no more aware or interested in them as a chemotherapeutic agent than, say, table salt.

          1. Volteric says:

            This is making more sense!

            1. WilliamLawrenceUtridge says:

              And thank you for remaining civil, asking questions and obviously paying attention to the responses. It’s a rare and precious thing on the internet.

              1. Volteric says:

                I understand how painstaking it can be. I’m fairly active at debunking religion and pseudoscience claims myself. Cannabis confessedly is somewhat a sacred cow only because I have personally benefited from it and spent way to many hours studying papers I have no business examining! But I understand what works for my issues have nothing to do with Cancer(s).

                As I mentioned I have been bugging Harriett Hall, Skeptoid, SBM, Gorski, Novella for about 2 years to address this issue because I value the rigor of this community!

  11. Simon says:

    Speaking of selective evidence, what about the numerous people who claim to have successfully cured their cancers with cannabis oil ONLY? Rick Simpson’s facebook page has many contributors claiming just that. They can’t all be spontaneous remission, or liars, can they?

    Mr Simpson seems curiously disinterested in making money, too – the normal red flag with alternative medicine. He sells a book, but that’s all, his formula is free for anyone to read. He may be wrong, but I don’t doubt his sincerity myself.

    1. David Gorski says:

      @Simon: Try searching for “Burzynski AND testimonial”; “Burzynski AND ‘success story’”: or for “alternative cancer cure testimonial” and you’ll see that I’ve already addressed such issues with other claimed “miracle cures, not just once, but many, many times—just as I did with that case report. Anecdotes such as those of Rick Simpson’s and of those to whom he’s given his hemp oil are invariably dicey at best. They’re not reliable evidence for reasons I’ve explained over and over and over again on this blog over the course of nearly seven years.

    2. WilliamLawrenceUtridge says:

      1) He still sells a book, doesn’t he?

      2) One doesn’t need to be purely motivated by money to be a quack. There are many pious frauds who are interested in it for fame, or for ego, or even simply because they strongly believe in what they say. That doesn’t make them right, and that doesn’t mean their anecdotes are suddenly more convincing than the anecdotes provided by any other quack.

  12. James L says:

    I always think of this comic whenever I hear of “x” curing cancer.

    1. James L says:

      Whoops. Here it is.
      http://xkcd.com/1217/

  13. JD says:

    I cant blame you most people dont realize there are this many studys this isnt even ALL of them just the ones Ive found so far(I know this is I find more ALL the time, cannabis DOES cure cancer I dunno how much more evidence you want/need we know how & why it works, we have lab study’s, chemical study’s, animals study’s, human study’s & pseudo human trials
    http://www.ncbi.nlm.nih.gov/pubmed/12648025
    http://www.ncbi.nlm.nih.gov/pubmed/19914218
    http://www.ncbi.nlm.nih.gov/pubmed/15026328
    http://www.ncbi.nlm.nih.gov/pubmed/16893424
    http://www.ncbi.nlm.nih.gov/pubmed/15361550
    http://www.ncbi.nlm.nih.gov/pubmed/19889794
    http://www.ncbi.nlm.nih.gov/pubmed/19015962
    http://www.ncbi.nlm.nih.gov/pubmed/19608284
    http://www.ncbi.nlm.nih.gov/pubmed/17237277
    http://www.ncbi.nlm.nih.gov/pubmed/11586361
    http://www.ncbi.nlm.nih.gov/pubmed/14692532
    http://www.ncbi.nlm.nih.gov/pubmed/16571653
    http://www.ncbi.nlm.nih.gov/pubmed/18286801
    http://www.ncbi.nlm.nih.gov/pubmed/16250836
    http://www.ncbi.nlm.nih.gov/pubmed/17934890
    http://www.ncbi.nlm.nih.gov/pubmed/12052046
    http://www.ncbi.nlm.nih.gov/pubmed/19189054
    http://www.ncbi.nlm.nih.gov/pubmed/18354058
    http://www.ncbi.nlm.nih.gov/pubmed/19047095
    http://www.ncbi.nlm.nih.gov/pubmed/10913156
    http://www.ncbi.nlm.nih.gov/pubmed/9653194
    http://www.ncbi.nlm.nih.gov/pubmed/18088200
    http://www.ncbi.nlm.nih.gov/pubmed/16909207
    http://www.ncbi.nlm.nih.gov/pubmed/17342320
    http://www.ncbi.nlm.nih.gov/pubmed/19059457
    http://www.ncbi.nlm.nih.gov/pubmed/12723496
    http://www.ncbi.nlm.nih.gov/pubmed/19442536
    http://www.ncbi.nlm.nih.gov/pubmed/16728591
    http://www.ncbi.nlm.nih.gov/pubmed/19539619
    http://www.ncbi.nlm.nih.gov/pubmed/16500647
    http://www.ncbi.nlm.nih.gov/pubmed/19189659
    http://www.ncbi.nlm.nih.gov/pubmed/14617682
    http://www.ncbi.nlm.nih.gov/pubmed/18938775
    http://www.ncbi.nlm.nih.gov/pubmed/11106791
    http://www.ncbi.nlm.nih.gov/pubmed/19394652
    http://www.ncbi.nlm.nih.gov/pubmed/20336665
    http://www.ncbi.nlm.nih.gov/pubmed/19442435
    http://www.ncbi.nlm.nih.gov/pubmed/15451022
    http://www.ncbi.nlm.nih.gov/pubmed/18197164
    http://www.ncbi.nlm.nih.gov/pubmed/16835997
    http://www.ncbi.nlm.nih.gov/pubmed/11903061
    http://www.ncbi.nlm.nih.gov/pubmed/17675107
    http://www.ncbi.nlm.nih.gov/pubmed/17202146
    http://www.ncbi.nlm.nih.gov/pubmed/19425170
    http://www.ncbi.nlm.nih.gov/pubmed/18454173
    http://www.ncbi.nlm.nih.gov/pubmed/17065222
    http://www.ncbi.nlm.nih.gov/pubmed/10700234
    http://www.ncbi.nlm.nih.gov/pubmed/16787257
    http://www.ncbi.nlm.nih.gov/pubmed/15958274
    http://www.ncbi.nlm.nih.gov/pubmed/16139274
    http://www.ncbi.nlm.nih.gov/pubmed/16624285
    http://www.ncbi.nlm.nih.gov/pubmed/16616335
    http://www.ncbi.nlm.nih.gov/pubmed/11269508
    http://www.ncbi.nlm.nih.gov/pubmed/19690545
    http://www.ncbi.nlm.nih.gov/pubmed/12511587
    http://www.ncbi.nlm.nih.gov/pubmed/20307616
    http://www.ncbi.nlm.nih.gov/pubmed/16818634
    http://www.ncbi.nlm.nih.gov/pubmed/17952650
    http://www.ncbi.nlm.nih.gov/pubmed/16818650
    http://www.ncbi.nlm.nih.gov/pubmed/16596790
    http://www.ncbi.nlm.nih.gov/pubmed/15638794
    http://www.ncbi.nlm.nih.gov/pubmed/15275820
    http://www.ncbi.nlm.nih.gov/pubmed/12133838
    http://www.ncbi.nlm.nih.gov/pubmed/18339876
    http://www.ncbi.nlm.nih.gov/pubmed/9771884
    http://www.ncbi.nlm.nih.gov/pubmed/10570948
    http://www.ncbi.nlm.nih.gov/pubmed/12182964
    http://www.ncbi.nlm.nih.gov/pubmed/19229996
    http://www.ncbi.nlm.nih.gov/pubmed/19609004
    http://www.ncbi.nlm.nih.gov/pubmed/16337199
    http://www.ncbi.nlm.nih.gov/pubmed/16936228
    http://www.ncbi.nlm.nih.gov/pubmed/18546271
    http://www.ncbi.nlm.nih.gov/pubmed/15453094
    http://www.ncbi.nlm.nih.gov/pubmed/19589225
    http://www.ncbi.nlm.nih.gov/pubmed/15047233
    http://www.ncbi.nlm.nih.gov/pubmed/19509271
    http://www.ncbi.nlm.nih.gov/pubmed/19480992
    http://www.ncbi.nlm.nih.gov/pubmed/18387516
    http://www.ncbi.nlm.nih.gov/pubmed/19916793
    http://www.ncbi.nlm.nih.gov/pubmed/18438336
    http://www.ncbi.nlm.nih.gov/pubmed/15454482
    http://www.ncbi.nlm.nih.gov/pubmed/17583570
    http://www.ncbi.nlm.nih.gov/pubmed/17931597
    http://www.ncbi.nlm.nih.gov/pubmed/18615640
    http://www.ncbi.nlm.nih.gov/pubmed/14640910
    http://www.ncbi.nlm.nih.gov/pubmed/20191092
    http://www.ncbi.nlm.nih.gov/pubmed/18025276
    http://www.ncbi.nlm.nih.gov/pubmed/616322
    http://www.ncbi.nlm.nih.gov/pubmed/15753356
    http://www.ncbi.nlm.nih.gov/pubmed/12091357
    http://www.ncbi.nlm.nih.gov/pubmed/18199524
    http://www.ncbi.nlm.nih.gov/pubmed/19887554
    http://www.ncbi.nlm.nih.gov/pubmed/19457575
    http://www.ncbi.nlm.nih.gov/pubmed/16908594
    http://www.ncbi.nlm.nih.gov/pubmed/12130702
    http://www.ncbi.nlm.nih.gov/pubmed/11854771
    http://www.ncbi.nlm.nih.gov/pubmed/20053780
    http://www.ncbi.nlm.nih.gov/pubmed/16754784
    http://www.ncbi.nlm.nih.gov/pubmed/20090845
    http://www.ncbi.nlm.nih.gov/pubmed/15978942
    http://www.ncbi.nlm.nih.gov/m/pubmed/21097714/
    http://www.ncbi.nlm.nih.gov/pubmed/20516734
    http://www.ncbi.nlm.nih.gov/pubmed/21915267
    http://www.ncbi.nlm.nih.gov/pubmed/20859676
    http://www.ncbi.nlm.nih.gov/pubmed/22776349
    http://www.ncbi.nlm.nih.gov/pubmed/11479216
    https://www.ncbi.nlm.nih.gov/pubmed/1159836
    http://www.ncbi.nlm.nih.gov/pubmed/22198381?dopt=Abstract
    http://www.ncbi.nlm.nih.gov/pubmed/12746841?dopt=Abstract
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3339795/?tool=pubmed
    http://www.ncbi.nlm.nih.gov/pubmed/22594963
    http://www.ncbi.nlm.nih.gov/pubmed/22231745
    http://www.ncbi.nlm.nih.gov/pubmed/21475304
    http://www.ncbi.nlm.nih.gov/pubmed/15313899
    http://www.nature.com/bjc/journal/v95/n2/abs/6603236a.html
    http://www.jneurosci.org/content/21/17/6475.abstract
    http://mct.aacrjournals.org/content/10/1/90.abstract
    http://jpet.aspetjournals.org/content/308/3/838.abstract
    http://jpet.aspetjournals.org/content/early/2006/05/25/jpet.106.105247.full.pdf+html
    http://www.molecular-cancer.com/content/9/1/196
    http://www.pnas.org/content/95/14/8375.full.pdf+html
    http://www.nature.com/onc/journal/v27/n3/abs/1210641a.html
    http://cancerres.aacrjournals.org/content/66/13/6748.abstract
    http://www.aacrmeetingabstracts.org/cgi/content/abstract/2006/1/1084?maxtoshow&hits=80&RESULTFORMAT&fulltext=cannabinoid&searchid=1&FIRSTINDEX=560&resourcetype=HWCIT
    http://onlinelibrary.wiley.com/doi/10.1002/ijc.23584/abstract
    http://molpharm.aspetjournals.org/content/70/5/1612.abstract
    http://www.cancer.gov/cancertopics/pdq/cam/cannabis/healthprofessional/page4
    http://www.labnews.co.uk/news_archive.php/987/5/cannabis-destroys-cancer-cells/
    http://www.examiner.com/article/ca-scientists-prove-marijuana-fights-aggressive-cancers-human-trials-soon
    http://www.huffingtonpost.com/2012/09/19/marijuana-and-cancer_n_1898208.html
    http://hempvision.tv/hollywood-actor-larry-hagman-beat-cancer-with-medical-marijuana/
    http://sanfrancisco.cbslocal.com/2012/01/10/healthwatch-study-finds-pot-smoke-less-harmful-than-tobacco/
    http://phoenixtears.ca

    1. David Gorski says:

      I bet you haven’t read even half (or a quarter) of those articles and studies. More importantly, I challenge you to show me a study from that list that isn’t just like the twenty or so I discussed; i.e., preclinical cell culture and animal studies that show a fairly high IC50 even using purified cannabinoid extracts. That will require actually reading at least the abstracts (possibly more) of all of those studies.

      1. Volteric says:

        If I’m understanding IC50 properly, I recall research on Cannabidiol (CBD) that indicates high levels can be used without any toxicity or unwanted side effects.

        1. KayMarie says:

          I think you are thinking LD50, dose needed to kill 50%

          IC50 is how much drug you need to inhibit the thing you are trying to inhibit by 50%.

          Usually you want something that does a lot with very low concentrations so you don’t have to give people huge amounts of it. Even if you need to give even huger amounts to get toxicity.

          1. Volteric says:

            Thank you for clarifying this for me! As I mentioned to Dr. Gorski, I recall a multitude of studies around the Cannabinoid Cannabidiol (CBD) and it appears that you can take very very high amounts of without any toxicity or unwanted side effects and achieve “modest effects” on certain types of cancer.

            1. KayMarie says:

              One of the problems with take lots and lots and lots of it for modest effects is often in my limited understanding the best treatments for cancer kill a lot of cells at a time and you take them over a fairly short period of time so you get the cancer cells all dead before they get mutate into something worse (drug resistant, more likely to spread, etc)

              If you just want to manage the cancer as a chronic disease then I might go for low toxicity with modest effect expecting that it might ease cancer symptoms for awhile until such time as the cancer becomes resistant to the treatment and things get very much worse usually pretty rapidly.

              I also don’t know if people really get purified treatments with one chemical in it from the dispensaries. So the question is how much of all the other chemicals in the plant do you have to eat/smoke/vape and are they equally free of any unwanted effects.

              Although I think some people want those other effects so may not mind.

              Personally, if I have a cancer and it isn’t a watch and wait situation, I’m of the “kill it with fire” type of person. Get it as dead as possible as quickly as possible with the lowest chance of recurrence. If you pick a treatment where 50% of the people are cancer free at 5 years, the ones in the survivors group got the highest doses in the shortest amount of time. Those not strong enough for that, who are getting a more modest effect from lower doses of the drug over longer periods of time, usually end up in the dead at 5 years out group.

              So it seems unlikely that the modest approach for this one drug in all the world is somehow going to be wildly more effective than anything else. I think people do need to know the risks of “killing it softly” as the song goes rather than killing it thusly, “I wanna kill. Kill. I wanna, I wanna see, I wanna see blood and gore and guts and veins in my teeth. Eat dead burnt bodies. I mean kill, Kill, KILL, KILL!”

              Let that be a warning to any of my cells planing a cancerous mutiny.

              1. Volteric says:

                Haha! In all the PUBMED studies I have read on CBD (Cannabidiol) very high and pure amounts of CBD were used without any side effects/high/toxicity. I am not aware of anything at dispensaries on the magnitude of what is used in these studies which is to say that companies like Dixie Botanicals are deceptive when they publish these research papers on CBD on their website implying that their product(s) do what the research indicates. For example I saw doses of CBD in range pf 400mgs-1000mgs of pure CBD in these papers. Their highly priced product contains at best 25mgs. Not sure how you can honestly ride the coattails of research like that.

                In any case, to answer my own question (which I wish Gorski would answer) is that if I were diagnosed with cancer I would stick to evidence based methods and would include Cannabinoids in so long as I knew that it did not interfere with EBM. It appears to me thus far, one study notwithstanding, that it would not interfere with evidence based approaches, but as I have fomented here I’d like the science to be pursued so we can know. Anything short of that I’m not finding persuasive. If Gorski or SBM in general (not just the blog) are saying Hey we’ve done the human studies and we know with some certitude that Cannabinoids offer no benefits for said cancer I’d follow the evidence. I just don’t think the evidence is enough one way or another and why I’m advocating further human studies.

              2. Chris says:

                “I just don’t think the evidence is enough one way or another and why I’m advocating further human studies.”

                Now you just need to find a way to pay for them. I live in one of the two states that have decriminalized marijuana. I am sure that some of the businesses will be successful enough to provide that kind of financing.

                If it can happen with tobacco, it could happen with cannabis:
                http://www.bloomberg.com/news/2014-08-06/ebola-drug-from-tobacco-part-of-promising-therapies.html

              3. Volteric says:

                Colorado raised $9 million the first month from taxes designated for research. I would say that would be the way it could be paid for. Of course, I wish more human studies were done before they ever called it Medical Marijuana. Again, as Gorski points out there have been legitimate roadblocks and I anticipate those will be lifted soon with the needed re-scheduling of Cannabis. I’d be interested if anyone in the SBM community thinks it should be moved out of Schedule 1?

              4. Chris says:

                “Colorado raised $9 million the first month from taxes designated for research. I would say that would be the way it could be paid for.”

                That is peanuts when it comes to cancer therapy research. Plus as public funds it is legally delegated elsewhere. A quick look shows it is slated to pay for school construction, and other needs.

                Read the link I posted. The research funding to get the new drug derived from genetically modified tobacco did not come from taxes, it came from the tobacco companies.

                There are companies in Colorado that are creating edible products out of cannabis, and then there are the accessories. Add that to the legal growing operations and you will see some large high value businesses that may be willing to do research to make it even more profitable to supply cannabis to pharmaceutical products.

              5. mouse says:

                KayMarie “I think people do need to know the risks of “killing it softly” as the song goes rather than killing it thusly, “I wanna kill. Kill. I wanna, I wanna see, I wanna see blood and gore and guts and veins in my teeth. Eat dead burnt bodies. I mean kill, Kill, KILL, KILL!”

                Citation please…Oh, google to the rescue, Ha!- I wondered where those lyrics were from – thinking it was a death metal band., but Arlo Guthrie, Alice’s Restaurant. good one.

                Very nice explanation, by the way.

            2. WilliamLawrenceUtridge says:

              Thank you for clarifying this for me! As I mentioned to Dr. Gorski, I recall a multitude of studies around the Cannabinoid Cannabidiol (CBD) and it appears that you can take very very high amounts of without any toxicity or unwanted side effects and achieve “modest effects” on certain types of cancer.

              …in a petri dish. Human studies are different. Humans have livers, can express toxicities that rats and cells can’t, have different metabolisms, and much, much larger bodies (surface area to volume makes a big difference). For most molecules you need far better results than this for anyone to consider it “promising”. Why do cannabinoids get a free pass or reduced criticism? Because it might make legalization of recreational use easier? While I totally support legalization, I’m strongly against distorting medical research or diverting scarce funding money as a work-around to get there.

              1. Volteric says:

                No, I am confident that humans were given these high doses of purified CBD in the PUBMED papers I read. Doesn’t mean it works, I’m just saying that CBD is unique in that very, very high doses are tolerable with no side effects or toxicity.

              2. Volteric says:

                And I don’t think Cannabinoids should get a free pass. If I thought that I wouldn’t be here working through to a better understanding. I can’t help if it if I am bringing false interpretations to the table. I want my points to be challenged and shown for their weaknesses. My opinions are like science, tentative and self-correcting. I don’t mind being wrong but I also can’t help raising the things that seem(ed) like breakthroughs and articles left and right, that feel respectably scientific, being not the whole stories or with many caveats. I do wish that the modest effects turned out to be a cure, but I realize that the evidence is the evidence. I still think modest effects are worthy enough to do more human studies and I hope that the MMJ industry or whomever does some great studies so we can know what potential it factually has on cancer(s). You might be surprised that I have no agenda for recreational with the medical guise approach. I came across so many respectable news articles extolling it’s medical use that I stand here honestly a bit confused and a little annoyed.

              3. AdamG says:

                You might be surprised that I have no agenda for recreational with the medical guise approach.

                Sorry but I find this hard to believe when you’re going around actively recommending cannabis to people to treat anxiety and schizophrenia.

              4. Volteric says:

                Adam–Don’t ascribe motives to me when I clearly share them with you. Did I recommend Cannabis for Schizophrenia? No. I shared a study you asked me to cite. I do NOT nor would ever recommend Cannabis to a person with schizophrenic. I did share my personal experience in treating my own anxiety/panic disorder and depression, and was I surmised as to why it’s been working for me.

                I suggest you work on you’re bedside manner.

              5. AdamG says:

                I’m a scientist, not a doctor.

                Did you click the link I provided (the word ‘schizophrenia’)? This one: http://f**kcombustion.com/threads/diagnosed-schizophrenic-seeks-cannabidiol.9476/

                replace the two stars with ‘uc’.

                In that thread you are clearly enabling a self-identified schizophrenic to a) stop their meds and b) try cannabis, potentially for the first time. Do you not see how dangerous that is?

                Not only did you direct this person to places where they could find highly concentrated forms of cannabis, but you provided them with a link to the ‘research’ with only a single study seemingly supporting your point, without noting the large literature base investigating the link between cannabis use and those at UHR for psychosis, like that forum user.

                I do NOT nor would ever recommend Cannabis to a person with schizophrenic

                How exactly would you describe your behavior in that thread then?

              6. Volteric says:

                Adam-

                <>>

                If you’re a scientist then I would suggest maybe observing and examining a little better? IN any case, I mean your overall manners need a little sharpening.

                1) I did not advise them to stop taking their meds. I shared him how to get purified CBD (Cannabidiol) legally (not Cannabis!) Followed by my personal experience that it didn’t work for me and an article showing why CBD from this source may not be all it appears to be. I was learning at this time myself as I still am.

                And then I pointed him to do his own research on PUBMED.

                “Not only did you direct this person to places where they could find highly concentrated forms of cannabis, but you provided them with a link to the ‘research’ with only a single study seemingly supporting your point, without noting the large literature base investigating the link between cannabis use and those at UHR for psychosis, like that forum user.”

                Again it wasn’t Cannabis, but Cannabidiol (CBD) extracted from hemp. Not the same thing.

                “How exactly would you describe your behavior in that thread then?”

                At that time it appeared that that CBD has no known toxicity, no side effects and according to the abstract: “Either treatment was safe and led to significant clinical improvement, but cannabidiol displayed a markedly superior side-effect profile.”

              7. Volteric says:

                Adam, I just realized the links you provided were links to where I posted on another forum (I didn’t realize those were actual link. I thought they might be prompting me to search those terms like other forums)

                In the Anxiety thread, I did advocate to a user of Cannabis to seek out Cannabis high in CBD/low THC, but that is my way of offering a harm reduction approach for those who are using high THC Cannabis who may not understand that THC might be exacerbating their anxiety. I’m fine with that suggestion.

      2. Don says:

        You are a nay saying, opinionated, useful idiot.

        Trying to shrink tumours with marijuana ( proven), by smoking a joint, is like trying to cure a migraine headache by shoving a low dose aspirin up your ass.

        ” According to research, smoking one joint will give you a blood level of THC of around 1.3-6.4 ng/mL serum, or about .00013-.00064 mg/L. In other words, to get an anti-cancer effect, you need to light up around 1000 joints per day.”

        And I certainly do not need the opinion of morons you quote , that opinion which you call as “perspective”. When it is just ignorance based bunk.

        While you babble weed does nothing for cancer, how can it then have an anti cancer effect? You accept it has an anti cancer effect, yet rely on dosing issues. OR do you. I am confused, you bring so much opinionated bunk.

        Doh..

        The cannabis should be given via IV, or consumed, while in the care of a doctor.. But I don’t pretend to be an expert in how to do that, and clearly nor are you. Difference is, I do not pretend my ignorance is knowledge like you do.

        This man is a demagogue. A money whore. And the reason no human trials go on is because the US government patented the weed, and thereby made it a crime to study it.

        Your challenge to show human studies is just more bullshit.

        Tell me quack, are you saying that cannabis does NOT kill cancer cells?

        1. Windriven says:

          @Don

          First, this particular thread is nested so deeply that I’m not entirely sure who the object of your rage is. Be that as it may, let’s talk about what is certain and not dwell on what is speculative.

          ” You accept it has an anti cancer effect, yet rely on dosing issues.”

          What part of that is problematic for you, Don? It appears that some cannabinoids have some anti-cancer effects. Do you accept that all drugs have a dose-response curve? Would you expect a homeopathic dilution of, say, THC to have the same therapeutic effect as, say, 500 ug/L?

          Dosing matters whether it is an antibiotic or an anxiolytic or a chemotherapy agent.

          “The reason no human trials go on is because the US government patented the weed, and thereby made it a crime to study it.”

          Really? I thought it was because they classified marijuana as a Schedule I drug. Could you cite the patent number? I’d like to read the application.

          “Tell me quack, are you saying that cannabis does NOT kill cancer cells?”

          Bleach kills cancer cells. Intense radiation kills cancer cells. Nitric acid kills cancer cells. There are compounds in cannabis that appear to act on cancer cells. But this goes back to the issue of dosing and extends well beyond that too. Just because something impacts cancer cells does not mean that it is an effective treatment for cancer. It does not mean that in meaningful therapeutic doses it will not damage other tissues as badly or worse than the target cells. It does not mean that any dose will do.

          But hey Don, keep on truckin’. And be careful calling people quacks and money whores especially when those people have forgotten more about cancer than you will ever know about it. Develop a little depth in your approach. A little humility, too. There are deeply knowledgeable people here who will share an immense amount of information, just for the asking. But they will be considerably less generous if you introduce yourself by pissing in their morning cup of coffee.

          Continue in this tone and our next encounter will have a somewhat different character.

          1. Beavis says:

            I was just reading this, but felt compelled to respond when I read this:

            “Bleach kills cancer cells. Intense radiation kills cancer cells. Nitric acid kills cancer cells.”

            Come on, now.. That is a ridiculous comparison. All of those things kill not only cancer cells, but harm or kill the healthy cells around them. Cannabinoids do not.

            Here (I believe) is the patent he is talking about:

            United States Patent 6,630,507
            “Cannabinoids as antioxidants and neuroprotectants”
            http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.htm&r=1&f=G&l=50&s1=6630507.PN.&OS=PN/6630507&RS=PN/6630507

            ” It does not mean that in meaningful therapeutic doses it will not damage other tissues as badly or worse than the target cells. ”

            Actually, with cannabiniods large doses seem tolerable in humans without such harm. If you (or anyone) could you give us an idea of what scale (how many mg/day of CBD) would be considered a “meaningful therapeutic dose”, we could try to find evidence that that dosage is tolerable with limited side effects.

            1. Windriven says:

              “Actually, with cannabiniods large doses seem tolerable in humans without such harm.”

              How large? How large a dose is therapeutic by which delivery route for how long and for which cancer(s)?

              Without a clear handle on the answers to those questions, safety is purely speculative because dose is undefined.

              Re: patent 6,630,507 – how does this patent make “it a crime to study it?”

              1. Beavis says:

                ““Actually, with cannabiniods large doses seem tolerable in humans without such harm.”

                How large? How large a dose is therapeutic by which delivery route for how long and for which cancer(s)?”

                Would you not agree that it might be in our best interests to investigate that and answer those questions?

                “Re: patent 6,630,507 – how does this patent make “it a crime to study it?””

                I never made such a claim. It was the other poster. In my understanding, while it may not be a crime to study it (IF given proper government permissions), it is has basically not been ALLOWED (for many decades) to be studied (such permissions are not granted) for beneficial medical use in humans. The US government has intentionally added extra roadblocks to the study of cannabis that other substances do not face.

              2. Windriven says:

                “Would you not agree that it might be in our best interests to investigate that and answer those questions?”

                I have not opposed research. If there are researchers who share your enthusiasm, there is nothing preventing them from pursuing study. The US has made marijuana related research difficult but not all countries are as benighted in that regard and even here the wall is crumbling.

                “I never made such a claim (regarding a US patent on cannabinoids).”

                Fair enough. You did however provide the patent number. I thought you might also have insight into why the argument is mounted that the patent makes studying marijuana “illegal.”

              3. Beavis says:

                ‘ I thought you might also have insight into why the argument is mounted that the patent makes studying marijuana “illegal.”’

                I pretty much already answered this… It seems to mostly be a question of semantics. “illegal” and “never allowed to occur” are basically saying the same thing. For what it’s worth, I honestly do not know how the patent will affect the legality of research in the future. The patent seems to basically boil down to the government having the rights to the medical use of cannabinoids (including CBD) as antioxidants and neuroprotectants. Some company researching or attempting to sell cannabinoid medications to treat something such as Alzheimer’s disease, diabetes, stroke, or even cancer (if, for instance, oxidation plays a role in the disease) might potentially violate the patent. I am not a lawyer…

                It is interesting to note that the US government has recently licensed the commercialization rights of this patent to a NY company, which is (or soon will be) seeking FDA approval to start clinical trials in using CBM for treating CTE. Perhaps some other company trying to research the same thing might be in violation of the patent, effectively making it illegal.

                http://www.kannalife.com/kannalife-sciences-inc-signs-exclusive-license-agreement-with-national-institutes-of-health-office-of-technology-transfer-nih-ott/

                http://www.kannalife.com/kannalife-sciences-inc-signs-new-license-agreement-with-national-institutes-of-health-nih-for-treatment-of-chronic-traumatic-encephalopathy/

            2. Andrey Pavlov says:

              <blockquote.If you (or anyone) could you give us an idea of what scale (how many mg/day of CBD) would be considered a “meaningful therapeutic dose”

              MadisonMD has already done that and you completely missed the point by talking about first pass metabolism issues. The point is that the serum concentration is important. It doesn’t matter how you get it there – that is pharmacokinetics and is a reflection of how easy or hard it may be to achieve that level in actual people. But once that level is achieved, what are the actual effects? And MadisonMD showed you through simple math that the amount of cannabinoids necessary to achieve a serum level that has been shown to have (the rather modest) effect on cancer cells is many orders of magnitude more than it takes to get someone intoxicated on the cannabinoids. And once you get to that serum level, we simply don’t know what the actual effects on a human being would be* but, based on the general knowledge of biochemistry and physiology it stands to reason that there are very likely to be adverse effects. Because the levels are orders of magnitude higher than what is typically already causing some noticeable effect from other uses of cannabis. It is a general truism in biology that taking something and cranking up the levels to orders of magnitude higher than is necessary to achieve any physiological effect means that there will be some other physiological effects. The only difference in medicine between an adverse effect and a desired effect is whether it happens to be targeting what you want. So we already know that tiny doses have some effect so massively larger doses must have additional and/or significantly more pronounced effects, the majority of which almost certainly cannot be targeting only the effect we desire. Which makes it an adverse effect.

              And KayMarie’s analogy was perfectly apt. Getting overbaked and not knowing how to handle your $hit is an adverse effect. And if people can get overbaked on serum concentrations massively lower than those necessary to produce a biological response in cancer, it stands to reason that this will only be magnified and added to when you crank it up to 11.

              *which is part of why it would not be a good cancer drug – we genuinely have trouble even achieving serum levels that high in the first place

              1. Windriven says:

                “Getting overbaked and not knowing how to handle your $hit”

                Which doesn’t do squat for the cancer, but on the bright side you aren’t as bummed about having it.

              2. Andrey Pavlov says:

                Which doesn’t do squat for the cancer, but on the bright side you aren’t as bummed about having it.

                Which I genuinely think is a very important thing. And if my patient wants to toke up to take a mental vacation from his terminal cancer, I say more power to them. I certainly can’t really see myself actively recommending that to patients though. Cultural issues and the risk of being misinterpreted in a negative way make it too risky. But I could envision a patient who, after a few consultations to get to know him better, it may become a broachable topic. I guess I’ll find out some day.

              3. Windriven says:

                No arguments from me, Drey.

    2. Thor says:

      Sometimes I wonder why so many proponents of pseudo-science and unfounded medical claims display a lack of writing skills commensurate with their lack of evidence.

      1. Windriven says:

        Education. I don’t even mean college degrees. I mean basic education. Reading comprehension, composition, basic mathematics, logic, reasoning, science.

        I’m not sure what rattles in the minds of some of these dufi, that without the slightest understanding of the science involved, they feel competent to hold forth on curing cancer. Most of them couldn’t get jobs in a hospital gift shop but they’re happy to tell those who have spent a lifetime working on complex and difficult issues in science and medicine just how full of sh!t they are. It beggars the imagination.

        1. Thor says:

          Bingo – the correct answer (to my veiled rhetorical question).
          Add in the Dunning-Kruger effect as part of the “dufiness” factor and,
          voila – a bunch of predictable, over-bloated verbiage and hubris.
          “Sound and fury……”.

    3. KayMarie says:

      Pseudo human studies?

      1. Windriven says:

        Yes, pseudohumans. Some of them comment in these pages from time to time. You can identify them by their failure to pass the pseudo-Touring test: the ability to write a single comment that is both coherent and doesn’t contravene any major scientific principles. See: lowball or Steve Rodrigues (and what ever happened to Thingy?).

        1. Chris says:

          Thingy was banned.

          1. Windriven says:

            No kidding? She was a predictable annoyance but I don’t recall her ever being abusive. I’m surprised but certainly not unhappy.

            1. Chris says:

              She did become abusive to parents of kids with issues, and for general inane repetitiveness. If not here, then definitely on the other not so secret blog. Where she would try to come back with sock puppets.

              She also has the rare distinction of also being banned from the sMothering Commune and Age of Autism.

              1. Windriven says:

                Wow! Banned from sites on both sides of the sanity line. That is quite an accomplishment!

      2. Frederick says:

        Pseudo humans, could they be cyborgs? Or aliens humans hybrids? Lol I’m also wondering what he meant by that.

    4. AdamG says:

      It couldn’t be clearer that you didn’t bother to read a single one of these studies. Hint: just because it has ‘cannabinoid’ in the title doesn’t mean it says what you want it to!

      link one describes pharmacological properties of cannabinoids, but says nothing as to their medicinal properties.

      link four, hilariously, demonstrates that cannabinoids will not be useful for astroglial tumors due to low CB1 expression

      link eight reviews the presence of cannabinoid receptors in skin tissue. nothing to due with treating cancer.

      link ten involves brain injury (?) but has nothing to do with cancer.

      Most of the rest of the links consist of in vitro or animal studies of cannabinoid analogues, or decade-old reviews of these same in vitro or animal studies. Nearly all of them call for more research, specifically clinical trials.

      cannabis DOES cure cancer

      Yet not a single link you shared demonstrates that cannabis ‘cured’ cancer. In fact, not a single study you cited contradicts Orac’s conclusion that

      Even in purified form, naturally-derived or synthetic cannabinoid agonists show relatively modest antitumor activity in preclinical models, which means that they will have to be combined with existing chemotherapeutic regimens. If they do find their way into the routine clinical treatment of cancer, it will be through rigorous pharmacological studies and rigorous clinical trials, the latter of which, in particular, are painfully lacking.

      You’re going to have to better than that.

      1. qetzal says:

        I like Link 3:

        Taken together, our data show that concentrations of THC comparable with those detected in the serum of patients after THC administration accelerate proliferation of cancer cells instead of apoptosis and thereby contribute to cancer progression in patients.

        There you have it: proof that cannabis DOES cure cancer! If, by “cure cancer” you mean “make cancer worse.”

        (Yes, this is indeed the same study that Dr. Gorski already noted showing stimulation of cancer cell growth.)

    5. KayMarie says:

      Reminds me of the old joke from back in the day that the usual way to screen the applicants for an academic position was to weigh the Curriculum vitae.

    6. Egstra says:

      from the very first link: “However, its acid metabolite THC-COOH, the non-psychotropic cannabidiol (CBD), several cannabinoid analogues and newly discovered modulators of the endogenous cannabinoid system are also promising candidates for clinical research and therapeutic uses.”

      “promising candidates” — nope, no cure there.

    7. Frederick says:

      Wow, right there, you just demonstrated that your are just trolling. A kilometer of links doesn’t prove anything if they are poor quality. Write some good logical assertions, then back them up with good evidences just then we can talk.

    8. ka says:

      Well i started reading the studies and the animal testing described seemed very gross. Freaky. In any case, some humans swear by cannabis as a cure for many variants of illness. The plant is juiced and grown as a variety of vegetable. I think the idea seems to be well worth researching ALREADY. How long must these poor animals be subjected to torture. Im sure a few terminally ill cancer patients would volunteer. My question is where is the beaurocratic paperwork involved in this one? Mountains of it by the sounds of it… ai, cant life move a little faster? Im sure cannabis has many medical benefits…and this is already proven, if cannabis happens to decrease the metasis of cancer cells (or some cancers)… well it wouldnt be a big miracle. Hurry up already with these damn studies on humans… some anedocal evidence seems very promising.

      1. KayMarie says:

        And lots of people swear by certain knee surgeries that when finally tested showed to have zero benefit. As well as blood-letting and a lot of other things we now know don’t do you much good and may be harmful.

        It isn’t just about who does the paperwork (although grants are a huge investment in generating paperwork) it is do you have the evidence to justify the trial.

        If we test it with the wrong doses and the wrong way to ingest it and the wrong strains and all that and it fails because we had no idea how to design the clinical trials properly is that going to advance the cause any better than taking the time and effort to do it properly?

  14. Xplodyncow says:

    Open access = liberal spelling (“disatinib”)? If authors overlook proper spelling, what else have they missed?

    1. Missmolly says:

      My thoughts exactly! And if you read the case study in entirety, you find highly technical medical jargon such as ‘This was the outcome of stopping total parenteral nutrition too quickly and causing shock to the patient’s body’ and ‘Upon X-ray, it was noted that gastrointestinal bleeding had occurred’.
      The whole paper is grossly unscientific. It does look pretty, though- and I expect that’s convincing enough to sway desperate people without a science background.

  15. Volteric says:

    For whatever it’s worth here is my short personal experience with Cannabis:

    Seems like many illicit drugs are the pharmaceuticals of the poor. Why is that?

    Having been prescribed many drugs for anxiety/panic disorder/depression I was surprised by how well Cannabis worked. On the one hand it works well like an anti-anxiety medication (sedation and sleep!) but it offered something that no anti-depressant did for me, namely feel well! Yes, the high, albeit slight, introduced me to states of happiness and well being–not something a depressed person is currently familiar with–and something none of the antidepressants did for me. At best they made me neutral/without emotion/zombie like. Every drug has a risk/benefit profile and I think Cannabis compared to Xanax and alcohol is relatively safe. I’ll exchange short term memory loss? (What?) for sleep and well being any day of the week!

    1. AdamG says:

      Some new data you might not be aware of: http://www.ncbi.nlm.nih.gov/pubmed/25055169

      1. Volteric says:

        Thank you Adam. I have read papers that show that Cannabis alleviates psychoses in schizophrenics as well. Correlation causation issue might be going on here. Schizophrenics might be getting relief rather than it causing. Cannabis use has gone up, but schizophrenia remains around 1 percent.

        1. AdamG says:

          I have read papers that show that Cannabis alleviates psychoses in schizophrenics as well.

          Citations, please.

            1. Volteric says:

              Correction: I should have said I read papers where Cannabidiol (CBD) alliterated schizophrenic symptoms.

              1. Volteric says:

                Alleviated. Any way to edit a post?

              2. KayMarie says:

                alliterated?

                Cannabidiol cures crazy conversations?

              3. mouse says:

                Here’s the full text link.

                http://www.nature.com/tp/journal/v2/n3/full/tp201215a.html

                Just to emphasis this paper is not cannabis “Cannabidiol is a non-psychotropic component of marijuana that binds to CB1 receptors with only comparably very low affinity17, 18 and is devoid of overt cannabimimetic or pro-psychotic properties.17″

                Also it’s 42 patients randomized, so 21 recieved Cannabidiol, which is a preliminary result as far as I see.

                Please don’t irresponsibly suggest that cannabis can treat schizophrenia. As the family member of a person with schizophrenia I can tell you that misinformation like that is dangerous to schizophrenic patients and those close to them.

          1. Volteric says:

            @ Kay :-)

            Here is the abstract I was referring to:

            Cannabidiol is a component of marijuana that does not activate cannabinoid receptors, but moderately inhibits the degradation of the endocannabinoid anandamide. We previously reported that an elevation of anandamide levels in cerebrospinal fluid inversely correlated to psychotic symptoms. Furthermore, enhanced anandamide signaling let to a lower transition rate from initial prodromal states into frank psychosis as well as postponed transition. In our translational approach, we performed a double-blind, randomized clinical trial of cannabidiol vs amisulpride, a potent antipsychotic, in acute schizophrenia to evaluate the clinical relevance of our initial findings. Either treatment was safe and led to significant clinical improvement, but cannabidiol displayed a markedly superior side-effect profile. Moreover, cannabidiol treatment was accompanied by a significant increase in serum anandamide levels, which was significantly associated with clinical improvement. The results suggest that inhibition of anandamide deactivation may contribute to the antipsychotic effects of cannabidiol potentially representing a completely new mechanism in the treatment of schizophrenia.

          2. Volteric says:

            Hey Mouse I think I specifically corrected my error after I realized this point and before you probably noticed it. I understand the challenge in that my nephew has schizophrenia so calm down a bit and give people the benefit of the doubt.

            1. mouse says:

              @Volteric -What I saw was someone making claims, then only correcting their error once they were asked for a citation. I suggest you check your sources before making claims. Also – that was giving you the benefit of the doubt and being calm.

              1. Volteric says:

                @ Mouse, are you suggesting that I was lying until shown to be? I realized all by my big self I made an error before anyone pointed it out. Giving me the benefit of the doubt would’ve been asking me or seeking to clarify if I was suggesting Cannabis use for schizophrenia. The answer is absolutely not. You implied that I was suggesting it when by saying: “Please don’t irresponsibly suggest that cannabis can treat schizophrenia”

              2. mouse says:

                No – I am not suggesting you are lying. Why would you think that? I suggested that your initial comment on cannabis alleviating psychosis was irresponsible because you didn’t double check your information before posting. You had just been shown a paper suggesting that cannabis use at a young age is a risk factor in the development of schizophrenia. Why not check your source before dismissing that research and countering that cannabis can actually help?

                When you discovered your mistake, why not change your position on the possible risks of cannibis to those with a vulnerablity to psychosis? As you know, sizophrenia is a very serious disease. Wouldn’t the precautionary principle apply?

                I suspect that you are looking for information to support your conclusions rather than looking for problems with your conclusions. This is a human tendency that we all fall prey too.

                By the way, here’s a few others sources with similar conclusions to the paper AdamG linked to.

                http://www.ncbi.nlm.nih.gov/pubmed/17007222
                Conclusion “It is most plausible that cannabis use precipitates schizophrenia in individuals who are vulnerable because of a personal or family history of schizophrenia.”

                http://www.ncbi.nlm.nih.gov/pubmed/19748375
                conclusion – “The objective of this article was to examine whether cannabis use can be an independent risk factor for chronic psychotic disorders, by using established criteria of causality. Data extracted from the selected studies showed that cannabis use may be an independent risk factor for the development of psychotic disorders. Early screening of the vulnerability to psychotic disorder should permit improved focus on prevention and information about the specific risks related to cannabis use among this population.”

                http://www.ncbi.nlm.nih.gov/pubmed/15763748
                “This paper evaluates three hypotheses about the relationship between cannabis use and psychosis in the light of recent evidence from prospective epidemiological studies. These are that: (1) cannabis use causes a psychotic disorder that would not have occurred in the absence of cannabis use; (2) that cannabis use may precipitate schizophrenia or exacerbate its symptoms; and (3) that cannabis use may exacerbate the symptoms of psychosis. There is limited support for the first hypothesis. As a consequence of recent prospective studies, there is now stronger support for the second hypothesis. Four recent prospective studies in three countries have found relationships between the frequency with which cannabis had been used and the risk of receiving a diagnosis of schizophrenia or of reporting psychotic symptoms. These relationships are stronger in people with a history of psychotic symptoms and they have persisted after adjustment for potentially confounding variables.”

                Also “Giving me the benefit of the doubt would’ve been asking me or seeking to clarify if I was suggesting Cannabis use for schizophrenia. ”

                Well, no, the way I see it, giving you the benefit of the doubt is assuming that you are intelligent and compassionate enough to start checking you sources before posting, once someone has pointed out that a simple misunderstanding can lead to problems in a vulnerable person.

              3. Volteric says:

                Mouse,

                “You had just been shown a paper suggesting that cannabis use at a young age is a risk factor in the development of schizophrenia. Why not check your source before dismissing that research and countering that cannabis can actually help?”

                Because I saw a paper that said precisely that Cannabidiol (not Cannabis) did help alleviate symptoms safely: “Either treatment was safe and led to significant clinical improvement, but cannabidiol displayed a markedly superior side-effect profile.” http://www.nature.com/tp/journal/v2/n3/full/tp201215a.html

                I do NOT reject the papers that CANNABIS can trigger schizophrenia in developing teen brains. There’s a difference between CBD alleviating psychoses and Cannabis triggering schizophrenia. Moreover I do think that causation/correlation needs to be unraveled in this issue altogether in that those with Schizophrenia may be self-medicating because it works for them. It works for psychiatric problems, but I realize that my experience doesn’t equal objective evidence.

                So, allow me to declare what I say to my teenagers: Cannabis use can trigger schizophrenia and you are more vulnerable now than ever so stay away from it and all psychoactive substances including alcohol.

              4. mouse says:

                @Volteric – I am very glad you advise your teens against the use of cannibis (and other recreational drugs/alchohol) and educate them on the risks, which go beyond szizophrenia, but I will stay on the thread topic.

                “Moreover I do think that causation/correlation needs to be unraveled in this issue altogether in that those with Schizophrenia may be self-medicating because it works for them. ”

                I think you are looking at this from the wrong angle. I feel like you are saying that it must be proven that cannibis is causally linked to a worse prognosis in schizophrenia before it is considered unsafe.

                But I think we all agree that cannibis is a drug. With drugs we assume that the substance is unsafe and ineffective (especially since this one has a proven correlation to poor outcomes in patient with schizophrenia) until it is has proven/documented benefits and risks in the applicable populations.

                If there is no solid evidence for the safety and effectiveness of cannibis for schizophrenia then any experimentation outside an approved clinical trial is just unethical human experiment on a socially vunerable population.

              5. Volteric says:

                Hi Mouse-”I think you are looking at this from the wrong angle. I feel like you are saying that it must be proven that cannibis is causally linked to a worse prognosis in schizophrenia before it is considered unsafe.”

                I think there are a few things that need to be differentiated in our discussion:

                1) Those with schizophrenia
                2) those most susceptible to schizophrenia teens and younger adults)
                3) Cannabis/Marijuana
                4) Cannabidiol (CBD)

                I think what makes this difficult is that Cannabis is generally very, very low or non-existent in CBD. Generally, it is bred for the highest THC primarily for recreational use. (Audrey I’m sure can verify this or just look at Weedmap menus. I have found that 99% of dispensaries do NOT carry high CBD Cannabis) There’s been a ground swell of interest growing around breeding plants with profiles like 15% CBD/5% CBD but again it’s rare and dispensaries can knowingly or unknowingly call something known for high CBD and it contain little to no CBD.)

                In any case, as I have already stated I would never recommend Cannabis of any kind to a teen/young adult. My worry is primarily with triggering schizophrenia, based on the research I have seen. Moreover, any psychoactive substance taken while the brain is still developing is good enough reason to refrain. In short I consider Cannabis use in this case to be unsafe.

                As to those already with Schizophrenia, purified or extracted Cannabidiol (CBD) identified as safe and effective in the study I shared I have no moral objection in recommending and all I mean is that because it appears rather safe and effective one should make a judgment call for themselves.

                If they are already consuming Cannabis and have schizophrenia I would be interested to know if they are using Cannabis because it relieves symptoms or exacerbates symptoms. I can only assume that it’s the former otherwise I have a hard time believing folks seeking to exacerbate their psychoses (and I don;t think enough studies have determined which is which)

              6. mouse says:

                @Volteric – Sorry for the delay. I’ve been off the grid.

                You said “As to those already with Schizophrenia, purified or extracted Cannabidiol (CBD) identified as safe and effective in the study I shared I have no moral objection in recommending and all I mean is that because it appears rather safe and effective one should make a judgment call for themselves.”

                How is one supposed to make a judgement call for themselves with so little real information? That’s why we have the FDA, so that those of us who don’t feel like being the lab rats of anyone who has a drug to sell can find reliable accurately dosed medication that is supported by scientific evidence rather than marketing claims.

                You cite one small study. In the study they state “We planned to randomly assign 35 patients to each treatment group which would have provided 82% power to detect an effect size of 0.7 (≈9/13=Δ/σ) in the change-from-baseline PANSS/BPRS total score at a two-sided 5% significance level using an unadjusted two-sample t-test.26 Unfortunately, enrolment was significantly affected by the exclusion of cannabinoid-positive patients in urine drug screening (Figure 1), which led to a termination of the study due to expiration of funding.”

                So this is not the size sample group they wanted – that they felt would prove or disprove their hypothesis and it doesn’t sound like they did all they felt should be done.

                The trial also uses accurately dosed medication with dosing changes for individual patients in response to the side effects. You seem to be recommending inaccurately/inconsitently dosed CBD with no mechanizism for titering the dosage.

                The trial started out with 198 schizophrenic candidates, but excluded 156. (The exclusion criteria are in the full paper). The study was for 28 days of treatment. The is no follow up or data for longer treatment times.

                As far as I can make out, of the twenty one patients receiving CBD, treatment was discontinued in three patients. 1 psychogenic seizures, 1 persistent suicide ideation, 1 withdrew consent. So that’s 5% rate psychogenic seizures (what is that?) 5% rate of persistent suicide ideation, in less than 28 days of treatment. Is that suicide ideation the result of the small sample size, is it a true 5% risk or is it possibly a higher/lower risk? If it’s an increased rate of suicide ideation, what is the increased rate of suicide attempts over time or successful suicides?

                In the chart the comparison treatment had 1 withdrawal consent. 0% psychogenic seizures, 0% suicide ideation (as far as I can make out). But it says in the text, standard treatment had 5 withdrawals…I can’t find that in the tables.

                Anyone who has insights, feel free to chime in.

                So basically a large majority of patients couldn’t participate in the trial. The study is underpowered by the authors proclamation. The dosages used in the study is not available to the public in a standardize consistent form. There are no long term results. The drug is not FDA approved at all (as far as I know) and is certainly not FDA approved for the treatment of schizophrenia.

                But you have no moral objection to recommending it to a person with a life threatening illness? Even without informed consent?

                Would you be happy if a new SSRI was recommended as safe and effective by your psychiatrist based on one underpowered short term study? I wouldn’t. I would be pissed! Particularly if the medication was offered at a different or inconsistent dosage from the one studied.

                As to Cannabis (not CBD) and schizophrenia. There are many reasons people with schizophrenia may use cannabis while it is still harmful. It might have a short term pleasant effect with longer term more powerful negative effects. You still don’t seem to be getting it. A drug/medication is dangerous until proven “safe”*. But hey! I’m sure Pfizer or the other drug companies would love to start selling drugs based on a model where they advertise and sell their products, and the FDA must prove the drug is harmful to have it withdrawn.

                *by which I mean to have a proven risk/benefit.

              7. mouse says:

                Also @ Volteric – “If they are already consuming Cannabis and have schizophrenia I would be interested to know if they are using Cannabis because it relieves symptoms or exacerbates symptoms. I can only assume that it’s the former otherwise I have a hard time believing folks seeking to exacerbate their psychoses (and I don;t think enough studies have determined which is which)”

                I just wanted to add – It’s well known about half of people with schizophrenia have anosognosia* as a component of their illness. This means that they lack insight into their disease or the presence/severity of their symptoms. They do not differentiate reality from psychosis. The psychosis is their reality and they will actively resist any explanation otherwise. How does a person who does not differentiate psychosis from reality know what substances exacerbate the psychosis?

                *http://www.nami.org/Content/NavigationMenu/Mental_Illnesses/Schizophrenia9/Anosognosia_Fact_Sheet.htm

            2. Volteric says:

              Hi Mouse, I’ve been out and about as well. I only care to answer your question in this way: how and why *I* made this judgement call…As I mentioned in a previous post: I have been prescribed many FDA approved drugs to treat my condition. Most of them were failures. The ones that worked well are more dangerous than Cannabis in that the amounts that were effective were near possible overdoses. I’m not going to stress this point beyond what is obvious: Cannabis accomplished what no pharmaceutical drug has with no unwanted side effects. I am far more concerned over my benzo use than vaporizing or eating Cannabis. Have you ever experienced a withdrawal from heavy benzo use?? I used Cannabis everyday for 1.5 years before I needed to travel a week for business. When I did I did so without Cannabis and I experienced ZERO WITHDRAWAL. Until somebody shows me that there are clear and significant reasons/evidence that Cannabis is more dangerous than Xanax I’ll continue to make that judgment call. I am on deck willing to change my regimen should evidence show that the risks outweigh the benefits in this context. I can tell you I am not awaiting for the FDA or the DEA or NIDA to make this judgement call simply because I am convinced Cannabis is not outlawed due to scientific or medical reasons. It wasn’t prohibited on those grounds in 1937 and it remains prohibited for political reasons not scientific ones. I do however eagerly await sound science and research around my particular use. Should I be made aware of something new about the true hazards of Cannabis I will continue to enjoy the relief it has and continues to provide.

              1. Volteric says:

                I’d like to also say, in case anybody is wondering, I only started taking Cannabis after I was made aware of Cannabidiol as an anxiolytic. CBD and Cannabis served as last ditch attempts to treat my chronic anxiety/panic/insomnia. It was a judgment call I have yet to regret, but again I am open to being wrong.

              2. WilliamLawrenceUtridge says:

                I’ll just point out that you aren’t using cannabis to substitute for drugs – you are using cannabis as a drug. And there are some drugs that have tolerable adverse effects, low toxicity and few if any withdrawal symptoms. If you are using cannabis as an anxiolytic, then it’s euphoric effect is an adverse effect.

                Cannabis is fat soluble, which is why it doesn’t appear to have withdrawal symptoms – it trickles out of fat cells gradually over time.

                All of which underscores the importance of decriminalization/legalization and research.

    2. Thor says:

      Volteric, I placed a comment to you at #16 instead of here.

  16. Thor says:

    I’m glad to hear your condition has improved. What a relief it must be for you. Millions consider the mental effect of cannabis to be a legitimate medical use. A close friend once told me that without marijuana he would either have killed somebody, or killed himself. Brain chemistry is certainly an area of medical cannabis research that must be looked into more. Regardless of the level anxiety, or even depression, marijuana has the tendency to round out the edges with it’s mild euphoria generating properties. This is obviously vastly different than studying it’s anti-cancer effects.

    That said, a warning must be given as it is well-known that some people have substantial negative mental/emotional effects. Since THC is psychoactive, it can bring simmering dysfunctions and pathologies to the fore. For some, anxiety and depression are simply heightened. Strange personality traits can emerge, as well paranoia.

    1. Volteric says:

      I am grateful for your post! This is definitely something I have been concerned about. As I mentioned above I have seen conflicting reports around this and one reason I would love solid research around this. As aside I sit perplexed by what happened with the UOA and her being fired mysteriously. So many vets with PTSD would benefit for the reasons I shared. I don’t know what all the euphoriaphobia is for, but I think their is great value in stoking feelings of well being and present oriented thinking. I am in my mid-forties and I began taking Cannabis about 2 years ago and I can’t say that have had any experiences close psychosis/hallucinations. (Funny enough I was reading Sagan’s essay on his Cannabis use and I sat there scratching my head thinking he might be describing LSD, Peyote or Shrooms! In short, much of what he shares I’ve never experienced.) At best, I am eventually sedated, slightly feel well, a little hungry, very horny and ultimately fall sleep waking up quite refreshed and rested. There have been a few times where it’s provoked some anxiety but I believe most of that was self-provoked. I’m assuming that I would have exhibited some psychotic experience by now if I was prone to it??

      1. Volteric says:

        Sorry, I wasn’t able to edit all my typos!

      2. Thor says:

        It was apparent that you don’t fall into that category (whew…).
        Great term: euphoriaphobia. God forbid someone should be allowed to experience a really nice sensation, for a change. No, that’s too damn hedonistic.

        It’s not a secret that the hallucinogens you listed, including ayahuasca, and especially ecstasy , have been used as therapeutic modalities. E shows a real potential benefit for PTSD and other psychiatric disorders.

        1. Volteric says:

          Word. I’ve been following MAPS (Multidisciplinary Association For Psychedelic Studies) from the sidelines with great interest.

        2. Volteric says:

          Hi Thor, I’m curious as to your thoughts on research impediment. In particular this report: http://www.drugpolicy.org/sites/default/files/DPA-MAPS_DEA_Science_Final.pdf

    2. Volteric says:

      So far the strange personality traits that have emerged is I can be more playful, less prone to anger fits, more sensual, less argumentative and somewhat happier. In all fairness the only negative I have seen is every once in awhile I loose track of my point. That might be a benefit to others!

  17. Keln says:

    The same arguments are made for anything that people want to be legalized or made the standard. The truth about marijuana is, that it isn’t that horrible of a drug. I’ve never tried it and have no inclination to, but based on all available data, I don’t see it as any worse than alcohol. Perhaps it is slightly better, considering how many lives alcohol abuse has ruined. But it doesn’t cure anything. With cancer patients, it does seem to reduce the nausea and inability to eat with those on chemo. But it doesn’t do anything for the cancer. As a drug, its affects are pretty harmless. It doesn’t incite violence, nor are people generally known to go to great lengths to get the drug as is the case with narcotics. The question of it being a “gateway drug” is more a question of behavior. It is illegal, and so the same person that provides pot also provides harder drugs leading to an increased likelihood of trying those drugs. Legal and regulated marijuana would remove it from the criminal class of drugs, making it no longer a gateway to anything other than increased Cheetos consumption. Pot use should be discouraged due to its psychological affects, but it should not be illegal. Decriminalization only allows people to use it, but doesn’t remove it as a product from the criminal element. Only when it can be produced legally and regulated can marijuana be as “safe” as alcohol or tobacco. As this is a hot button issue with many people, research into marijuana use really does need to be increased. I highly doubt the medicinal claims about pot though, as they are made by people with a pro-pot agenda, not by scientists.

  18. Andrey Pavlov says:

    Phew! What a comments section. And one that I would normally like to participate in more extensively as I have my own thoughts, done some of my own research, and happen to have a friend in the industry in question.

    However, I just started a new service and am stupidly busy. I just put in a 15 hour day on call and got slammed with 12 admits in the last 4 hours (no, I didn’t do all of them, but the team was rather busy). And on this service I am on call every other day. Yay!

    Anyways, I can say that I pretty much agree with everything Dr. Gorski has said. I myself have been endlessly annoyed (as have some of my friends who are themselves educated in the relevant fields) by the stupid amounts of hype surrounding marijuana. Is it really not good enough that it is a pretty safe drug with no real reason to be illegal for recreational use plus some modest benefits and some reasonable future avenues of research? Does the rhetoric have to make it some damned super plant that cures everything and actually improves the health of otherwise healthy people? Seriously, anytime some pothead tries to say that somehow marijuana smoke is magical and actually improves lung function I want to smack him or her upside the head. Hard.

    But I digress. Volteric, if you happen to read this comment – take some time to learn from the people here. I normally would be very happy to go through your comments and reply to some of the salient points you raise, but I just don’t have the time. I have a day off on Wednesday, so perhaps then if I have the will to plow through them all.

    But let me give you a piece of advice – and I mean this very genuinely. Pull back from the perspective of trying to get people to prove to you why cannabis isn’t so great (medicinally speaking, of course) and try and learn the relevant points about what makes any substance a useful drug.

    For example, you ask why it is a big deal that the IC50 is so high, particularly given the really high LD50 of CBD. You are essentially saying, “Well it is safe, so why not just give massive doses of it?” Well two thing. Firstly, things don’t scale like that very well. Meaning that just adding more dosage doesn’t just work out to be a linear extrapolation of the lower dosage profile. It is the same way you can’t build a 1/50th scale model of a bridge and just multiply every dimension by 50 to get a full sized functional bridge. But the bigger reason is that it simply isn’t possible to achieve such high concentrations at the target tissue site. Don’t forget that all that CBD has to actually get to the tissue in question to function at all. The reality is that such a high IC50 means that to achieve that concentration in tissue is very likely nigh impossible, particularly given the fact that CBD and THC are extremely hydrophobic. Or at the very least the effort simply wouldn’t be worth it.

    Another bit of advice, as Chris already commented briefly, don’t play the tu quoque game. When Dr. Gorski takes the time from his busy 15 hour day to explain that THC/CBD is simply not that promising a cancer drug and why, it is completely irrelevant to ask what other compounds are more promising. It simply doesn’t matter. The merits of cannabis as an anti-cancer drug should stand on their own. Even if there aren’t any better candidates, there are still better places to spend research money. Now don’t get me wrong, I still think research should be done – it is a highly bioactive plant. But the avenues of research should be rationally dictated.

    Anyways, just a bit of friendly advice that if you take you will learn a lot. Now, time to eat some pizza, read some articles, and stalk my patients from home.

    1. Volteric says:

      Hey thank you very much! I sincerely appreciate your advice and I highly respect this blog and it’s community. As a laymen I want to be as informed as possible, but honestly at times the science is hard to understand and decipher.

      1. Volteric says:

        And I really look forward to more of your thoughts about my questions and points raised!

        1. Thor says:

          That’s why SBM is lucky to have people like Andrey, and others, augmenting the posts with solid professional, and thinking skills. Andrey is a treasure as an SBM commentator (and sometime poster)! Whenever he doesn’t post his customary, usually detailed, comments, I know that he must be plain too busy (or hiding from the world – ha). But, something is always missing without his input. Keep tuning in to the site and you’ll catch him for certain.

          1. Volteric says:

            Well for whatever it’s worth-you stood out as well!

            1. Thor says:

              Merci, Volteric.

      2. Andrey Pavlov says:

        Well, first off… Thor you are much too kind. But thank you for the wonderful compliments. This time I am not hiding from the world though. I really am that busy. Things should smooth out a bit once I get the hang of this new service though. The first few days are always rocky as you get used to how the team works, how patient flow works, and as you figure out how to maximize your workflow efficiency.

        As for Volteric – also kudos to you. Your response has motivated me to take some time on Wednesday to address at least some of your comments as best I can.

        As a laymen I want to be as informed as possible, but honestly at times the science is hard to understand and decipher.

        Haha, yes it is. Which is why folks like the Food Babe are such a joke. You actually have to understand a lot of background science in order to come to a reasonable conclusion about the stuff that is less clear. Most people will simply ignore that and just assume that they know what an IC50 vs LD50 really means. Those who keep insisting on that are the ones who inevitably get thrown to the wolves… namely WLU and Windriven :-P (I keed, I keed). But seriously, those are the ones who end up simply becoming irrelevant trolls.

        Your response shows you are not of that ilk and for that I thank you and welcome you. We here, myself included, are always happy to educate and explain.

        So perhaps tomorrow (not on call) I will be able to shoot off a few responses. Otherwise Wednesday when I am off.

        My patient doesn’t have an aortic dissection (at least not by my read, but I am not staying up for the radiologist to give his) and I have to be up at 4:30 tomorrow. So now, I need sleep.

        1. Volteric says:

          Very much looking forward to it!

        2. WilliamLawrenceUtridge says:

          Andrey, given your interest and relationships in this area, you might consider a guest post on the topic of marijuana and medicine, perhaps in general, perhaps for non-cancer topics (mental health for instance? Or I’d love to see a detailed post about it’s proposed use to prevent seizures).

    2. WilliamLawrenceUtridge says:

      Firstly, things don’t scale like that very well. Meaning that just adding more dosage doesn’t just work out to be a linear extrapolation of the lower dosage profile.

      One thing to keep in mind as well – there’s not really one dosage, there are multiple. Nutmeg, for instance, at low doses is merely a flavouring (which is still a form of psychoactivity). At higher doses, it because a hallucinogen. At slightly higher doses, it is an emetic. Alcohol, at low doses, is a mild anticoagulant. At higher doses, a euphoric. At higher doses, it’s lethal. Most new antidepressants are also, at lower doses, effective sleeping aides. At higher doses, lethal.

      So even if THC is an effective chemotherapeutic agent at high doses, that doesn’t mean it’s not also something else at those doses, because relatively insensitive receptors for other functions become active at these much higher doses. The body is poorly designed (not designed actually), so it’s not like there is a 1:1 receptor:function relationship. That’s why drugs have side effects (and also why sometimes the side effect is the main effect).

  19. E-rook says:

    I attended a talk recently that posited the use of compounds that inhibit endocannabinoid metabolism to treat anxiety and depression. I think that medical use is certainly more plausible than pot curing cancer.

    1. Volteric says:

      I very much agree and had to realize that while I was lead to think it may be a useful agent in Cancer(s) I think it has more promise in Psychiatry, but again my experience aside, I’d like this validated by the proper studies to confirm or deny this before I would say with any certitude about it’s efficacy.

  20. Andrey Pavlov says:

    @volteric:

    So I’ve decided to just make one comment as I scroll through the plethora of comments here, including yours. Forgive me if I end up repeating myself or someone else – please don’t view it as needlessly hammering you. It will inevitably be because I am doing this as I go in order to do my best to adequately and appropriately respond while also minimizing the time on my part necessary to do so (i.e. I will only edit parts that really need it). It is my one day off per week and while I do enjoy spend part of it this way, I would like to get other things done as well. It is a long comment and at nearly 75% the length of Dr. Gorski’s OP, I think it is long enough. LOL. To be fair, a decent chunk of that is quoting Volteric. Here is to hoping that I didn’t screw up the HTML tags.

    How can there be “robust justification” if so few human studies exist? What is objectionable to finding out?

    I think the responses by windriven and WLU (and the rest) adequately address this point. Justification for research is a complex topic and requires many lines of converging evidence, plus plausibility. At the end of the day, however, what is justifiable is essentially subjective and limited by funding (often times artificially because we’d rather spend money on stupid shit than actual research). The point being is that we also have to have some sort of rough ballpark of what reasonable effect sizes are at various stages of evidence. Does this mean it will always be the correct cutoff? Of course not. Science is still a human endeavor and mistakes will be made. Could we potentially miss out on some amazingly useful property of cannabis for the treatment of some types of cancer (or other ailments)? No doubt. Does it mean we should just throw money at it in the hopes of finding something? Well, in a world of limitless resources (which includes qualified people in addition to funding and materiel) sure. I think every one of us would advocate researching anything with even a scintilla of plausibility. But that is very far from the world we actually live in.

    The other key is that you don’t get the justification from human studies but for human studies. That comes from the preclinical work which, as I just said, is not perfect (but is the best that we have). Now me personally, I would not have been able to tell you what an appropriate IC50 is in order to get excited about the potential of a compound (though I could have looked it up of course). But I don’t have a PhD nor do I do bench research (anymore, I did as an under- and post-grad) let alone on cancer specifically (never did cancer research). But Dr. Gorski is and does. So when he says that the noted IC50′s are unimpressive I am not one to argue, let alone you. If you wish to argue that we should, as a scientific community, change our threshold for IC50′s then you need to actually be deep in that scientific community to justify your assertions, rather than just get fixated on the fact that it does have some effect. In other words, it is people like Dr. Gorski who get to say a finding is modest or not, not even I and certainly not you.

    Since the Federal Government feels it’s their place to tell me what I can and cannot ingest I’ll leave it to them to pay for the research that supports their idiotic claim that Cannabis has absolutely no medical value and is as dangerous heroin addiction and overdose. To date they haven’t done that or listened to the very commissions they assembled to demonstrate it’s danger. (Schafer Commission, etc)

    Well, you are preaching to the choir and making a non sequitur. Firstly I think we all here pretty much agree that the current legal status and scheduling of marijuana is absurd and not based in science. Hell, Dr. Gorski said it himself plain as day.

    The non sequitur is that this then means the federal government must fund research on it. Just because they have inappropriately banned the plant doesn’t give scientific justification for its study. The two are completely independent topics and the justification for research must stand on its own, also independently.

    Dr. Gorski- based on the modest effects you shared I am curious if you were diagnosed with cancer if you would add some form of Cannabis or Cannabinoids to your regimen? Why or why not?… The intent behind the question was to gauge if Gorski has any objections to a cancer patient taking Cannabinoids? Is there any risk or potential interference? Does he see modest effects as worthy enough to add to regimen? I’m sure thousands of people are in a situation right now where that decision is being seriously considered considering the rapidity of medical marijuana acceptance

    This is a personal question that ultimately has no utility to the discussion at hand or the original topic of the article. My friend (whom my fiance calls “John the Mythical Pot Smoking Monster) would undoubtedly keep using marijuana during cancer treatment unless there were very specific and well supported reasons for him not to (which, to my knowledge, don’t exist). However Dr. Gorski has never had marijuana and getting a diagnosis of cancer for him would not likely be a time to begin experimentation with the particular psychotropic effects of the drug.

    If you are asking a scientific question then the only one that can come from what you have written essentially becomes “what is the harm of adding a drug that is likely safe and might have some amount, however small, of additive anti-cancer effect to a treatment regimen.” From a scientific standpoint that is simply a non-starter. There are literally hundreds of thousands of compounds that could fit the bill and pass the same muster to be included in a chemotherapeutic regimen. Given a lack of specific necessary knowledge agnosticism with some admonishment of the precautionary principle is in order. But the real thing is that science always tries to limit variable so we can understand what is going on. If you add something that I can’t characterize to the mix, we simply have no idea of how it would affect the cancer or your own physiology. So when your cancer doesn’t respond or you have some side effect of treatment or some other issue comes up, it now becomes an unknown variable and in ambiguous cases makes clinical decision making all the more difficult.

    All that said, WLU hit the nail on the head IMHO when he said that it would be unscientific to recommend it as an adjunct to treating the cancer but I would not necessarily actively dissuade my patients from using it for symptoms of treatment they find distressing and ameliorable by marijuana. Nausea, lack of appetite, and even anxiety can benefit from cannabis use in the right people and the right circumstances. People do “freak out” from cannabis use (probably heightened by the legal status and history of fear mongering) and people do get paranoid when using it (I’ve experienced that myself). By the same token, if you have cancer and want a day to get stoned, eat a tub of ice cream and watch movies, who am I do say you cannot enjoy that even if I am not someone who would find that sort of activity pleasurable? But I would do it in the proper context and say that it is most probably safe to do so, but that we do not know what we do not know about what kind of adverse effects that may have. I may also advise my patients to use different means of consumption depending on their other morbidities. For example I would strongly advice a patient with cancer, COPD, and asthma to not smoke it but instead ingest it some other way.

    Dr. Gorski-Forgive my ignorance but are there enough studies to know that Cannabinoids are not an IC50 above 10 μM?? My point, ad nauseum, is do we know enough to dismiss the effects as modest? Or should we further human studies to to determine this very question?

    Well, WLU said it very well again. And this is where the subjectivity and human element of scientific research come into play. Dr. Gorski is absolutely correct to say that the existing evidence is not that exciting. You are also completely correct to say that it could have a profound effect on some specific type of cancer that is as of yet undiscovered. But the point is that this can be said for just about an endless number of compounds. What we are trying to say here is not that no research should be done, but that there is simply nothing special about cannabis in this regard. There is nothing that should make us chomp at the bit to keep digging. And ultimately research is done by humans. It takes a lot of effort and fortitude to commit years and years (if not decades) of your life studying a particular topic. Particularly in the bench sciences since these are notoriously extremely low yield to begin with. It is why, for example, I do not do bench science research any more nor will I ever likely do it again. I respect the bench sciences immensely and the people who do it (like my dear friend and co-author here, Igor Bussel). But it just doesn’t motivate me to spend my time doing it.

    Perhaps nobody will be motivated to research a particular topic, subject, or compound. And perhaps this will prove to be a loss to humanity… at least until it is picked up in some possible future. But this is simply the nature of being human. What we should not do, however, is unfairly elevate a topic to a higher level of scientific excitement because of personal excitement. And we also should not circumvent the proper process of science by skipping pre-clinical work in favor of clinical work without proper justification. Of course even this is nuanced and there are always exceptions, but it involves a lot of hard work to prove these rare exceptions and they should be treated as exactly that – exceptions to the rule.

    So how do we know enough to dismiss the effects as modest? Quite simple – everything we actually know so far shows the effects are modest. We do not know if there is some permutation where the effects are not modest. But then again neither do you. And it is just as possible that there are no effects that are beyond modest. What it takes now is someone interested enough in the topic to pursue it and demonstrate that. Perhaps you could get the proper education and background and actually get the grants and do the work. If you really think that this is so likely to be the way cannabis research turns out, then you should also have the motivation to put in the proper work to do it rather than just armchair quarterback the people that are and chastise others who aren’t. Just don’t confuse dismissing the effects we know as modest with dismissing the entirety of the idea of investigating cannabis for medicinal purposes. Nobody here is doing the latter. We are just arguing that, once again, there is nothing special about cannabis over countless other bioactive molecules.

    In all the PUBMED studies I have read on CBD (Cannabidiol) very high and pure amounts of CBD were used without any side effects/high/toxicity.

    Yes, but that doesn’t mean that there aren’t toxicities that we aren’t able to detect. It is also not something that can be safely extrapolated to other populations and other contexts. Particularly in the case of cancer patients who have deranged physiologies, typically other comorbid conditions, and loads of other pharmaceutical agents. Exposing people to extremely high concentrations of anything in such states (and in general, really) simple cannot be predicted. I think it is indeed safe to say that at levels that are likely to be consumable commercially it is most likely safe with minimal interactions. But we cannot say for certain and we absolutely cannot say for higher levels. Which is why we say it is irresponsible to say that it does not have toxicities and could or should be used in the manner you seem to be advocating.

    if I were diagnosed with cancer I would stick to evidence based methods and would include Cannabinoids in so long as I knew that it did not interfere with EBM. It appears to me thus far, one study notwithstanding, that it would not interfere with evidence based approaches, but as I have fomented here I’d like the science to be pursued so we can know. Anything short of that I’m not finding persuasive. If Gorski or SBM in general (not just the blog) are saying Hey we’ve done the human studies and we know with some certitude that Cannabinoids offer no benefits for said cancer I’d follow the evidence. I just don’t think the evidence is enough one way or another and why I’m advocating further human studies.

    The problem is you don’t know what you don’t know. And nobody knows if CBDs would interfere with EBM – it simply has not been tested. All you can say is that it probably doesn’t, at least at lower doses.

    You’d like the science pursued? Hey! So would we! But I hope I’ve explained enough why wishing it to be so doesn’t equate to it being so.

    Beyond that you are merely hiding in the area of the unknown unknowns and saying that this lack of knowledge is good enough to justify your use of CBDs. Fine. That is your judgment call. But you need to recognize that this is precisely what it is – a judgment call. The evidence so far does not support the usage you advocate nor a call for more human studies. It does support more pre-clinical studies. Because, once again, the same sort of position can be taken for any number of compounds out there. Your particular predilection for CBDs is just that – your particular predilection and is independent of what the science says and how rigorous scientific inquiry proceeds.

    Which is fine. On an individual basis we have to make decisions based on incomplete (and often wrong) information all the time. But that is different to saying that this then justifies (scientifically) particular usages and research.

    I’d be interested if anyone in the SBM community thinks it should be moved out of Schedule 1?

    I’ve answered this before but I’ll do it again directly: yes, I think it is ridiculous that it is a Schedule 1 drug.

    I still think modest effects are worthy enough to do more human studies

    Well, hopefully I have illustrated to you why this is not the case and why, if you are so excited and convinced by the existing data you should pursue an education and career path to do the work yourself. Otherwise it is nothing more than armchair quarterbacking and saying how the world should be, according to you. The real point being is that you don’t have the necessary knowledge and experience to actually make the claim that the modest effects are worthy enough. You even admit you don’t and yet you still make the assertion.

    Seems like many illicit drugs are the pharmaceuticals of the poor. Why is that?
    Having been prescribed many drugs for anxiety/panic disorder/depression I was surprised by how well Cannabis worked. On the one hand it works well like an anti-anxiety medication (sedation and sleep!) but it offered something that no anti-depressant did for me, namely feel well! Yes, the high, albeit slight, introduced me to states of happiness and well being–not something a depressed person is currently familiar with–and something none of the antidepressants did for me. At best they made me neutral/without emotion/zombie like. Every drug has a risk/benefit profile and I think Cannabis compared to Xanax and alcohol is relatively safe. I’ll exchange short term memory loss? (What?) for sleep and well being any day of the week!

    I actually agree that cannabis has a better safety profile than alcohol or benzos. And there are actually many other psychoactive drugs that have been used in the past and shown to have benefit in certain psychiatric conditions. Watch the documentary on Sasha Shulgin’s life if you haven’t already. There is an inappropriate stigma associated with such research which, IMHO, is primarily nothing more than moralistic control of others and their particular preferences for a good time in life. Some of it is legitimate in that there are harms associated with drug use of any kind, including marijuana. But none of that is relevant to the discussion about the scientific promise of cannabis and cancer. In fact, almost none of that has anything to do with actual science on the topic and is mostly due to political posturing. Nixon promised to reduce crime rates. The problem is that most crime at the time was on a state rather than federal level. And so now drugs are illegal. Makes it look like something is being done. Marijuana was demonized in the early 1900′s because hemp was a competitor for wood based paper products and William Randolph Hurst didn’t like that. It hurt his bottom line. Of course that isn’t the whole story, so please don’t think I am being simplistic or naive enough to think that, but it illustrates some salient points.
    The point being that your question is legitimate, but not a scientific one that can be answered by science. It is a political and cultural one.

    I am in my mid-forties and I began taking Cannabis about 2 years ago and I can’t say that have had any experiences close psychosis/hallucinations…. There have been a few times where it’s provoked some anxiety but I believe most of that was self-provoked. I’m assuming that I would have exhibited some psychotic experience by now if I was prone to it??

    Not necessarily. While you can feel comfortable that the likelihood of experiencing such problems is rather low, it is certainly not zero. Any drug can ultimately cause any problem at any time. I have seen patients on ACEi’s for a year before developing angioedema as a result. I myself was on an ACEi for a few months before I developed the “ACE cough” which most people develop within the first couple weeks of treatment. The point is that things change – both your weed and your body.
    Additionally there is good evidence to support the idea that cannabis use does indeed trigger schizophrenia in susceptible individuals. However, the data also show that this risk declines with age and comes down to roughly background levels sometime in the early to mid 20′s. So you are probably safe in that regard. Additionally triggering schizophrenia in young and developing brains that are susceptible to it is a completely different beast to the effects of cannabis once a person has overt schizophrenia. In your comments you seem to be conflating the two ideas.

    And now this comment has certainly gotten sufficiently long. Please use the Principle of Charity in reading it as I may have made some assumptions, not clarified some points as thoroughly as necessary, and possibly made a gaff or two along the way. But I hope that my point and thoughts are at least mostly intelligible.

    1. Volteric says:

      Well, you did not disappoint! I am extremely grateful for your response and there was nothing in it I found objectionable or personal (thank you!) I’ve been wanting for a very long time to subject what I know about this subject to the scrutiny of people I deeply and highly respect (and SBM tops the list!)

      I will be re-reading and studying this page until I have a deeper understanding because not everything is clear to me mostly because of own ignorance. Again I’m an only an opinionated laymen (I sure hope I haven’t come across as an medical armchair quarterback!) As I mentioned earlier, I’ve been studying the subject with great interest for about 2.5 years. I’ve read many of the abstracts that I will take the time to read through their entirety but often it feels like looking at a Chinese newspaper. I do know or pretend to know much of what I am reading.

      As I spend time examining what you wrote and everybody else I will raise my confusion or questions. These are not intended to be defensive. I can’t help it if I have a pressing thought or even misinformation that I’m confused about.

      And again, thank you for not making me feel the subject of a witch hunt!

      1. Andrey Pavlov says:

        Glad to be of help Volteric.

        Reading scientific literature is indeed difficult. It is a skill that requires years of dedicated honing to master. I do not think it is pompous of me to say that I am better at it than many of my own colleagues. You learn the basics of doing it in medical school, but unless you go above and beyond, there is still a lot to learn. SBM and my own interest pushed me to go above and beyond.

        I will be back on service for another week (until next wednesday) and will be extremely busy again. If I have the time and motivation I’ll respond to your future comments as best I can. It is also a subject that I am interested in. For no particularly good reason beyond the fact that I have non-science friends in the industry and I like to promote rational discourse on any topics and this seemed as good a one as any other.

        As for not making it like a witch hunt… well, it takes two for that. You showed some genuine interest in actually learning and that goes a long way with me specifically and around these parts in general.

    2. Volteric says:

      @Andrey, what’s dawned on me is that human studies do NOT necessarily follow from modest effects in pre-clinical studies. Being a complete novice this point escaped me entirely. I thought modest effects over no effects was much more significant than it actually is. It just means more pre-clinical studies are warranted. If I am understanding you (and others) Cannabis is a highly bioactive plant worthy of study, but the studies thus far as it relates to Cancer(s) is just simply modest. Nothing more. Can you point me to anything where I can understand how any substance or compound goes from modest effects to worthy of human studies? I’m wondering what are the tell-tale signs that truly warrant human studies?

      1. KayMarie says:

        In general the sequence goes something like this.

        Pre clinical

        1. In vitro studies. Does it do something in a test tube (problems, may be at concentrations that kill cells, or under conditions incompatible with a living cell).

        2. Cell line studies. OK, does it do the same thing in a living cell at concentrations a cell can survive and in the conditions compatible with the cell living.

        3. Animal studies. OK, how do you get it from outside a cell to where it needs to be in a whole animal (do you have to inject it, can they eat it). Also gives you the first data about toxicology in a multicellular animal. Does the liver turn it into something nasty trying to get it back out of the body. Does it destroy the kidneys on the way out, etc. Hopefully you can induce the illness you are testing for in the animal (either breeding, inserting human genes, some chemical will damage the right bits to simulate an illness)

        4. Additional mechanistic studies (so what actually does it do and how does it do that, which may be in a variety of experimental types).

        OK, now you have a compound you know what it does, you know how it does it, you know you can get it to the part of the animal it needs to get to, you know the animal can get rid of it safely. You have some idea of what kind of dose (mgs/kg) may be appropriate. you may be ready for your first in person test, so on to clinical testing.

        Generally you need a lot of testing prior to jumping right to humans because of the ethics of potentially causing harm when you have no idea what this thing does, how much to give, if it might help, etc.

        Phase I. Extremely common side effects, does it go to the same place in a person it does in a mouse, dog, rabbit, monkey, etc. Do we detox it the same way? and what testing of the dose range. Usually done in healthy humans so no or little data on does it actually treat the disease/symptoms. This is the “is it safe enough to try”.

        You may redo some of the preclinical testing and then go back to Phase I if something odd happens in humans that don’t happen in others, or if you now need more information about mechanisms based on these results.

        Phase II. Giving it to people with the problem to see if it can do anything for the problem.

        Just because you ingest it and excrete it as expected doesn’t mean it treats the disease. Especially when sometime in animal models you have to use special mice or rats because they don’t normally get this illness on their own (or the experimentally induced version of the illness may not react the same way as a naturally occurring one).

        Once you show it can work (usually in a few hundred patients) and what dose is needed to work in this population it is on to…

        Phase III. Usually something like a few thousand patients. Here you look for less common side effects as well as confirm the dose range and it actually does some good results.

        This is where the FDA will give approval or not.

        Phase IV. Post marketing testing. To study anything that is observed once the drug is on the market.

        Lots of things do not progress all the way. If the data doesn’t indicate a big enough response or something you cannot do to a person. Like if the earlier data calculate up to a dose of 10 pounds a day. Well you can’t do that to a person.

        1. Volteric says:

          Fantastic, Kay! Thank you!

          1. Andrey Pavlov says:

            @volteric:

            Sorry this will be brief. I lost a longer reply and am waiting for sign out today.

            Just wanted to say a quick kudos – you seem to be getting what we are saying. And you were already provided an excellent reply from KayMarie.

            One thing to add – to directly answer your actual question of “what are the telltale signs of promise” though. The answer is basically the hardest one in medical (and really all) research. Every field and sub-field will have its own set of signs. Many of them false. Many of them hard to discern. But all requiring deep knowledge and dedication to suss out. There isn’t simply an easy way of saying “Here, look for this stuff and when you see it about something you read on the internet you are on to something.” There are some good telltale signs of it being crap, but that is also because the Bayesian prior of anything being crap is always going to be higher than it not being crap. In other words there are only a few ways to be right and infinite ways to be wrong. So if you think something is right, you are still probably wrong. If you think something is crap… well, you have a higher chance of being correct. LOL.

            And so it is with testing these compounds. Any of a million things can go wrong at any step that Kay pointed out. And even if it doesn’t it can still fail at the end. And even if it doesn’t it can still prove to be too problematic in Phase IV. And so on.

            Which is why most things are always simply going to be “meh.” The movies that show these stunning and amazing sudden and profound breakthroughs… well, that’s Hollywood, not real life. Behind the scenes there is (damned near always) a huge line of incremental advances to get to what people then see and falsely perceive as some giant leap ahead. That’s why science is hard work that requires true dedication.

    3. WilliamLawrenceUtridge says:

      By the same token, if you have cancer and want a day to get stoned, eat a tub of ice cream and watch movies, who am I do say you cannot enjoy that even if I am not someone who would find that sort of activity pleasurable?

      It’s funny, I read this about marijuana and think “yeah, that’s reasonable”. But if you said it about alcohol, my reaction would be “yeah, that guy’s an alcoholic, he’s going to die of cirrhosis”.

      Odd.

  21. Dr Bud says:

    What a terrible article! You claim to be a “researcher” but post no “research”. You then go on to use a vague Star Wars reference to prove a pointless point. Facts are facts marijuana contains more cancer killing properties than any drug or treatment (including the daft use of radiation? Barbaric and dated) ever period. I question the reasons for writing this and moreover who do you work for and who paid you to write this blantent propaganda.

    1. Volteric says:

      Dr. Bud, You might do yourself a favor-seeing that you are hyper-zealous for the tree- by taking a step back and allowing yourself to examine what Gorski wrote and the well thought out comments that have followed. He is an experienced Oncologist who is well versed in deciphering the research. You are free to make the judgment call for yourself, if you have cancer, but it would be highly irresponsible for you or anyone to go beyond the evidence. The evidence as of now is modest. Nothing more and nothing less. I had a hard time understanding this, but you might follow my progression on this through the comments. Welcome!

      1. Volteric says:

        Well, I guess this was another drive-by??

        1. Windriven says:

          If it wasn’t illegal I’d put a bounty on these assh0les.

          A species that lets grifters slip into a lab coat and call themselves ‘doctor’ is a species that ain’t built to last.

    2. Windriven says:

      Dr. Bud, your reasoning is as pathetic as your useless (LBP excepted) playing-doctor scam.

      “Facts are facts marijuana contains more cancer killing properties than any drug or treatment (including the daft use of radiation? ”

      Facts are facts, Sparky. Where are yours? Put up or shut up, you’re embarrassing yourself and you’re littering this space with random stupidity.

      “What a terrible article!”

      What an inane comment.

      “You claim to be a “researcher” but post no “research”.”

      This is a blog, dipsh!t. Gorski publishes research in peer reviewed professional journals. He posts analysis and commentary in blogs. You poseurs should learn the difference, it would take chiropractic a step closer to something that doesn’t stink of fantasy and septic sludge. It leaves you with an awfully long way to go but, I think it was Mao who observed, “the journey of 1000 miles begins with a simple step.”

      “I question the reasons for writing this…”

      And I question why chiropractic isn’t a felony so I guess we’ll both go to bed tonight plagued with uncertainties.

      “and moreover who do you work for and who paid you to write this blantent propaganda.”

      Jesus, are you too stupid to correct words highlighted by spell check or just too lazy? We are all paid by a cabal of Jewish Illuminati Templars of the Cross of Zoroaster. I thought that was obvious.

      1. Volteric says:

        My love and respect for you deepens! :-)

    3. WilliamLawrenceUtridge says:

      What a terrible article! You claim to be a “researcher” but post no “research”.

      Are you stupid? I count fourteen primary studies, two links to clinical trials that are ongoing and two links to major national cancer research societies.

      Facts are facts marijuana contains more cancer killing properties than any drug or treatment

      That’d be great if it were a fact. If it’s so great, why doesn’t it work in petri dishes? Or mice with tumor grafts? Why aren’t cancer patients who smoke marijuana for nausea cured of their cancer? If the signal is as strong as you claim (which would be astonishing, there are some drugs that are very good at killing cancer, and surgery is pretty much curative) it would be quite trivial to show. And given the history of marijuana’s use for intoxication, chances are it would have been recognized as an anticancer panacea in Biblical times.

      I question the reasons for writing this and moreover who do you work for and who paid you to write this blantent propaganda.

      Oh, you are stupid. Or you didn’t read it. Yeah, Dr. Gorski is in favour of legalization, and your content-free comment ends with a delightful pharma shill gambit, which just shows you are too stupid to right a substantive post containing meaningful disagreements.

      Way to go champ.

  22. You tried to debunk most things positive but you did not explain why the USPTO has many PATENTS on THCV, CBD, and CBG treating CANCER? Just google USPTO cannabis cancer and you’ll see those, or just thc in the uspto search. THESE ARE PATENTS why would they patent something if it doesn’t work?

    http://appft1.uspto.gov/netacgi/nph-Parser?Sect1=PTO2&Sect2=HITOFF&p=1&u=%2Fnetahtml%2FPTO%2Fsearch-bool.html&r=1&f=G&l=50&co1=AND&d=PG01&s1=%22GW+Pharma%22&s2=cannabis&OS=%22GW+Pharma%22+AND+cannabis&RS=%22GW+Pharma%22+AND+cannabis

    1. Volteric says:

      Patents do NOT mean efficacy nor that said product does what it claims. Just peruse all the inane patents for products and “inventions” that never see the light of day. Point is, again, a patent does not mean said therapy or method works. Just like buying a domain name doesn’t make a website or a successful business. It’s just a domain and it’s just a patent. If you listen closely to the discussion here it’s the outcomes and the evidence that truly matters not just that study but all the studies done thus far on Cannabis and Cancer(s).

  23. bones says:

    “The combination of THC, CBD and essential oils in cannabis-based medicinal extracts may produce a therapeutic preparation whose benefits are greater than the sum of its parts” GW pharmaceutical website.

    Your argument that the individual components should be isolated and tested doesn’t necessarily hold in this case. Couple this to the fact that GW pharma have recently filed a patent application in the US. PHYTOCANNABINOIDS FOR USE IN THE TREATMENT OF CANCER US patent: 20140221469.

    1. MadisonMD says:

      Cool and if GW demonstrates safety and efficacy of their standardized drug for some type of cancer in a particular situation, they will be able to market their drug. However the vast majority of drugs at the patent stage do not ever pass that standard.

    2. Windriven says:

      20140221469 is not a valid US Patent number. Maybe an application. But none of that matters. There are patents for all kinds of fantasies. A patent does not prove that the treatment works.

      1. Richard Abbott says:

        That is indeed an application number, they start with a year.

    3. WilliamLawrenceUtridge says:

      Why do you monkeys wave around patents as if they were meaningful? Patents are intellectual claims made at a specific time to protect future commercialization. They have nothing to do with efficacy. Their purpose is to establish priority of claim, not defence of truth.

      I would ask why you don’t cite the scientific literature, but know the reason – the scientific literature doesn’t support cannabis or its derivatives being particularly effective as cancer treatments.

  24. Evan Harper says:

    Minor point, but, I don’t think there’s any honey involved in Rick Simpson’s “miracle cure” oil. In Canada “honey oil” is sometimes used as a name for cannabis oil extracted with butane, so called for its color and viscosity. here is a Facebook post where Rick Simpson describes giving tea with cannabis oil to someone with a honey allergy. (He claims that she accidentally mixed it up with tea that had actual honey in it as well as cannabis oil, but was unaffected because in addition to cancer his oil magically suppresses allergies.)

  25. R Miller says:

    The past couple of responses show how childish and knee-jerk the ‘cannabius as cure-all” community is:

    Somehow, Dr. Gorski is evil and obviously hired by pharmaceutical companies to discredit cannabis as a cure for cancer… at the same time, pharmaceutical companies are patenting certain cannabis compounds because they *know* it really works.

    Like seriously, you guys couldn’t spend 5 minutes together in a room to at least make sure your conspiracies were at a minimum internally consistent?

    “THESE ARE PATENTS why would they patent something if it doesn’t work?”

    Sigh. The risk-benefit of filing a patent is extremely in favor of filing for compounds that hold some promise, no matter how small. It’s a little bit of time and cost that pays off really big if they can bring something to market. It doesn’t mean they are absolutely confident it will be clinical viable, it’s a strategic gamble.

  26. Matthew Sands says:

    While this article does appear in many ways to be the voice of reason it is actually guilty of the exact type of misrepresentation that it condemns. The claim in the title that “cannabis does not cure cancer” is at best an unproven and unfounded statement and at worst an outright lie. You could say it remains unproven on a clinical level and I actually agree that many of the articles that claim that cannabis as a cancer cure has been proven clinically is a misrepresentation of the facts, but so is your claim that it does not. The fact is that the clinical data does not prove cannabis cure cancer or that it doesn’t, mostly because no studies have been made that attempted to prove that. All they have been set up to do is explore the anti tumour effects in some manner while observing other effects on nerve tissue and healthy cells. As the author actually points out, most of the clinical and pre clinical data is consistent with the claim that cannabis has anti tumour effects (which I understand is not the same as proving it as an outright cure) and what he doesn’t really point out is that the selective nature of cannabinoids as cancer killing agents sets it apart from virtually all other drugs and treatments. Cannabinoids have been shown to kill cancer cells in a selective manner and represent no toxic threat to healthy cells or organs, even at very high doses.
    All this article does is temper the claims that have been overblown about the clinical evidence for cannabis as a cancer cure with an insistence that the clinical data is more modest than that.
    I am not as zealous as people like Rick Simpson in my claims for cannabis as a cancer treatment. I have seen it fail enough to know it is not a guarantee and, unlike Rick Simpson, I don’t dismiss the failures as being just because the patients are “too damaged by chemo”.
    I’d like to point out that my comment merely states that there is sufficient evidence for cannabis oil to be a viable treatment option that should be available, especially for those who are written off as terminal.
    This author sounds like he is being fair and grounded but his claim that “cannabis does not cure cancer” is equally as unfounded and irresponsible, if not more so, than those who claim that current clinical data proves it does cure cancer.
    The clinical data does not prove cannabis cures cancer, but it is plenty sufficient to prove the potential for it to do exactly that. And is certainly sufficient to support it’s use, especially as chemo drugs have been approved for trials based on much less evidence.
    This author conveniently neglects to address the more impressive anecdotal cases (like biochemist Dennis Hill who cured his stage 4 cancer with cannabis oil, Mike Cutler who achieved similar results etc.)
    This author points out that cannabis has not been proven as a cancer cure in clinical data, but doesn’t seem to take into account that clinical studies have not actually tested such a claim. As he mentions they are all either testing single compounds like THC or CBD, sometimes both in combination, they are often administered in a fashion that is not designed to test whether it can cure cancer outright but merely to test whether anti tumour effects are observed and what effects administration has on healthy cells and nerves.
    In other words the clinical data is consistent with the claim that cannabinoids can and do kill cancer cells and inhibit tumour growth and spread. But they do not prove it to be an outright cure, largely because they are not trying to.
    But in addition to conveniently neglecting to mention the more impressive evidence this author also ignores the fact that the evidence is above and beyond what is required for other cancer drugs to at least be moved to clinical trials and he also neglects to mention that the biggest proven discovery regarding cannabis is a cancer treatment is the fact that, unlike virtually every other treatment available, cannabinoids are completely selective. They can kill certain forms of cancer with out any damage or toxicity to healthy cells, with out any risk of toxicity to any part of the body and with the only foreseeable side effect being the potential to be stoned from the THC.

    What I am saying is that cannabis should be available as a cancer treatment and trialled properly to confirm what it’s real potential is as a cancer treatment/cure and what cancers it does and doesn’t work on.
    Also I’d like to point out that while the testing of cannabis or cannabinoids in the form of natural extracts remains PROHIBITED, the patents and trials for patented or synthetic cannabis based drugs has been approved. Despite the clinical and preclinical data strongly suggesting that the anti cancer effects of cannabinoids are more impressive when administered in naturally occurring combinations (in other words cannabinoids and terpenoids have a synergistic effect on each other and increase the effects beyond what can be achieved with isolated compounds). Also the fact that patented drugs are approved for trials and trials are only approved when patents are established only supports the claim that this medicine is held back for the sake of money and profits. There is no scientific basis, for example, to use a diluted form of cannabis extract like Sativex to test its effect on brain cancer when the pure undiluted oil would surely be more effective and indicative. The only reason to use Sativex in its patented form is that it is in its patented form.
    That is where the real scandal is. The potential of cannabis as a cancer treatment is being held back from being fully explored for the sake of patents and profits.

    While this author does rightly point out that the clinical data for cannabis as a cancer treatment is exaggerated by many and anecdotal evidence alone, even the more founded and supported cases, are not outright proof either. His claims that cannabis does not cure cancer goes directly against the vast majority of available evidence.
    The claim that cannabis cures cancer may seem an over exaggerated claim but the claim that is does not cure cancer is an unfounded claim that is in conflict with a lot of the evidence.
    The truth is we do not know for sure what cannabis can do as a cancer treatment and until the law allows proper testing and trials we won’t know. But the current evidence does very much support the potential for cannabis to be both a cancer treatment and even a potential stand alone cure for many types of cancer and the fact that it remains prohibited and unavailable as such is nothing short of criminal.

    1. MadisonMD says:

      The claim in the title that “cannabis does not cure cancer” is at best an unproven and unfounded statement and at worst an outright lie.

      So, in your view, saying ‘Twinkies don’t cure cancer’ is damnable lie?

      1. Andrey Pavlov says:

        So, in your view, saying ‘Twinkies don’t cure cancer’ is damnable lie?

        Bazinga!

      2. Beavis says:

        ” The claim in the title that “cannabis does not cure cancer” is at best an unproven and unfounded statement and at worst an outright lie.

        So, in your view, saying ‘Twinkies don’t cure cancer’ is damnable lie?”

        If there existed a wealth of published evidence documenting Twinkies many anti-cancer effects, then I would agree with that statement.

        1. Windriven says:

          Proof is a positive attribute. Eating gopher toes may cure cancer. I have no compelling data either way.

          If cannabis is to be accepted as a cancer cure, its utility and safety in that role need to be clearly demonstrated. That is a difficult, but by no means insuperable, challenge. There is enough interest that money and researchers shouldn’t be a problem.

        2. MadisonMD says:

          If there existed a wealth of published evidence documenting Twinkies many anti-cancer effects, then I would agree with that statement.

          twinkies are a superfood with anticancer properties, didn’t you know? They are completely non-toxic, have been taken by millions, don’t impair your ability to drive. Their contents are magic because toxicity has never been seen. They contain polysorbate 60, closely related to polysorbate 80 which is used to formulate docetaxel. Moreover, twinkies contain diacetyl, which is known to have anticancer effects– see here.

          So don’t dis the magical non-toxic cancer-fighting properties of twinkies my friend! Do the research for yourself. You can’t really say it doesn’t cure cancer until the research is complete.

          (There is a long way between anti-cancer effects and curing cancer, Mr. Tone Troll. We’ve heard it before.)

    2. David Gorski says:

      The claim in the title that “cannabis does not cure cancer” is at best an unproven and unfounded statement and at worst an outright lie.

      No, it’s a reasonable conclusion based on the existing state of the evidence. Even if the most promising studies are true, it does not mean that “cannabis cures cancer.” Indeed, even the most promising studies show that it almost certainly does not. That doesn’t mean cannabinoids might not someday be useful tools in our armamentarium of anticancer drugs to be used in combination chemotherapy. There’s a difference. People claiming “cannabis cures cancer” either don’t understand or deny the difference. Moreover, I never said I didn’t support clinical trials. I’m just only modestly (at best) enthusiastic about them, given the relatively modest antitumor effects demonstrated in the preclinical studies I’ve reviewed and the limited resources for testing new putative anticancer compounds.

      It’s also a huge exaggeration to claim that cannabinoids are “completely selective.” There’s no such thing as “completely selective” in pharmacology. Saying something like that just reveals ignorance of basic pharmacology. Similarly, I note that no evidence has been presented that hemp oil has anticancer activity. Certainly that ridiculously badly written case report (how on earth a journal could publish such dreck, I don’t know) is not compelling evidence.

    3. qetzal says:

      @ Matthew Sands:

      Your post is simply wrong on many points.

      The claim in the title that “cannabis does not cure cancer” is at best an unproven and unfounded statement and at worst an outright lie.

      Unproven – fair enough. Unfounded – no. Dr. Gorski offered plenty of foundation for why cannabis (very probably) does not cure cancer. An outright lie? Certainly not.

      [T]he selective nature of cannabinoids as cancer killing agents sets it apart from virtually all other drugs and treatments.

      Baloney. There are lots and lots of “cancer killing agents” that are very selective. Especially if you’re only looking at cells in vitro or mouse models. If activity and selectivity in those models were predictive, we would have cured every type of cancer there is, a hundred times over, 20 years ago.

      The clinical data does not prove cannabis cures cancer, but it is plenty sufficient to prove the potential for it to do exactly that. And is certainly sufficient to support it’s use, especially as chemo drugs have been approved for trials based on much less evidence.

      No, the clinical data – as summarized by Dr. Gorski – is sufficient to suggest that cannabis might have some value in treating some cancers. It’s not sufficient to prove the potential to cure cancer. The data is adequate to support further use in clinical trials, but the data doesn’t come close to supporting routine therapeutic use. No chemo drug has ever been FDA approved for therapeutic use based on evidence as limited as that for cannabis. And most chemo drugs are supported by FAR more preclinical evidence before they ever begin even Phase I clinical studies in humans.

      This author conveniently neglects to address the more impressive anecdotal cases (like biochemist Dennis Hill who cured his stage 4 cancer with cannabis oil, Mike Cutler who achieved similar results etc.)

      The problems with these cases is that they’re rarely adequately documented. In fact, when I googled Dennis Hill, I found lots of sites claiming he had stage 4 prostate cancer. But Hill himself is quoted here as saying he had Stage 3 cancer. And the documentation provided on that page only documents localized cancer within the prostate. It doesn’t show evidence for spreading outside the prostate, which I believe is required for Stage 3. Did he really have Stage 3? Did he really take only cannabis oil – no chemo, no radiation? Does prostate cancer like his ever spontaneously regress? I don’t know, and I bet you don’t either. MAYBE his case (and others) would be intriguing IF they were adequately documented.

      [T]his author also ignores the fact that the evidence is above and beyond what is required for other cancer drugs to at least be moved to clinical trials

      And there are trials being conducted with cannabis derivatives. But Dr. Gorski, who is an actual cancer researcher, is telling you that in his opinion, the evidence so far is not very compelling. As another PhD researcher who has worked on quite a few novel cancer treatments in my career, I second his opinion. Maybe cannabis derivatives would actually work much better than he or I expect. But the current evidence is most certainly NOT “above and beyond what is required for other cancer drugs.” It’s actually much weaker than what most researchers would consider appropriate.

      Also the fact that patented drugs are approved for trials and trials are only approved when patents are established only supports the claim that this medicine is held back for the sake of money and profits.

      Wrong again. There is no requirement that patents must be established for trials to be approved. None. A pharmaceutical company may choose not to pursue drugs that they can’t protect from competitors, but that’s a different matter. Lack of patents certainly wouldn’t stop NCI from funding trials on cannabis.

      There is no scientific basis, for example, to use a diluted form of cannabis extract like Sativex to test its effect on brain cancer when the pure undiluted oil would surely be more effective and indicative.

      Really? You know, for a fact, that undiluted oil would SURELY be more effective? No, you don’t. And you have the chutzpah to accuse Dr. Gorski’s headline of being a lie?

      Basically, the only thing you get right in your whole screed is that yes, it’s at least possible that cannabis might cure some cancers. However, in the light of everything we know about cancer and everything that’s ever been tried before, the available evidence strongly suggests that cannabis will NOT cure any cancers. It might have some activity in treating cancer, but even that is quite uncertain.

    4. WilliamLawrenceUtridge says:

      The claim in the title that “cannabis does not cure cancer” is at best an unproven and unfounded statement and at worst an outright lie.

      Balls to that – cannabis will never cure cancer, but extracts might.

      And the anti-tumor effects are mild at best, certainly not promising. If you have to dope someone up to the gills to get an effect, people might not like it either. And for that matter – at the 10nL range, what does that represent in terms of the amount of hash you would have to eat? There’s a reason it’s not seen as promising, it takes a lot of pot or extract to reach that level disseminated in the tissues.

      And is certainly sufficient to support it’s use, especially as chemo drugs have been approved for trials based on much less evidence.

      Really? Which ones?

      he potential of cannabis as a cancer treatment is being held back from being fully explored for the sake of patents and profits.

      Really? You don’t think Big Pharma would love to make a fuckton of money off of a new form of effective chemotherapy? Why not?

      But the current evidence does very much support the potential for cannabis to be both a cancer treatment and even a potential stand alone cure for many types of cancer

      Re-read Dr. Gorski’s article, no it doesn’t. It’s a mildly promising treatment, at high doses. But not really that promising really.

      and the fact that it remains prohibited and unavailable as such is nothing short of criminal.

      No, it’s stupid historical chance, but it’s not criminal. It’s also not chemo.

  27. Tin Tin says:

    As you quite clearly state there is a lack of in vivo studies, as this area has been ‘limited’ to date by the unwanted psychoactive side effects and not on the relationship between CBD-induced apoptosis and autophagic cell death.
    Perhaps a better review of cannabinoids and cancer cures could take you down the signaling pathway route, especially in increasing cellular trafficking of Cytochrome C in glioma’s.

    Jones S. et al Characterization of Bioactive Cell Penetrating Peptides from Human Cytochrome c: Protein Mimicry and the Development of a Novel Apoptogenic Agent Chemistry & Biology, Volume 17, Issue 7, 30 July 2010, Pages 735–744

    McAllister SD,et al. Pathways mediating the effects of cannabidiol on the reduction of breast cancer cell proliferation, invasion, and metastasis. Breast Cancer Res Treat 2011; 129: 37–47.

    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; 10:1161–72.

    Jacobsson SO, Rongård E, Stridh M, Tiger G, Fowler CJ. Serum-dependent effects of tamoxifen and cannabinoids upon C6 glioma cell viability. Biochem Pharmacol 2000; 60:1807–13.

    Massi P, Vaccani A, Ceruti S, Colombo A, Abbracchio MP, Parolaro D. Antitumor effects of cannabidiol, a nonpsychoactive cannabinoid, on human glioma cell lines. J Pharmacol Exp Ther 2004; 308: 838–45.

  28. Velda says:

    Please check out the requirements needed to become a dispenser of Medical Marijuana in Florida. I have a M.D. degree in Family practice and an alternative medicine degree so I checked it out to see if I qualified.
    I don’t.
    To qualify you need $150,000, take an 8 week course, not be a user of marijuana and be able to have all this money to cover all the bonds and legal requirements for employees and licenses.
    Not one thing about knowledge of medical conditions or patient care.
    But you will be shut down and fined if you treat some one who does not qualify and the patient will be arrested.

    1. MadisonMD says:

      So? There are 173,025 studies going on in the U.S. right now. When one shows us convincing efficacy, clinical practice changes… but most will not. Let us know when results are available, but it is more interesting to cover only the few studies with positive results.

  29. John Baptiste says:

    I’d like to ask the author of the article why he left out the study on pancreatic cancer, also part of the list of 20 studies that he documents in this article. The study reports:

    “Pancreatic adenocarcinomas are among the most malignant forms of cancer and, therefore, it is of special interest to set new strategies aimed at improving the prognostic of this deadly disease. The present study was undertaken to investigate the action of cannabinoids, a new family of potential antitumoral agents, in pancreatic cancer. We show that cannabinoid receptors are expressed in human pancreatic tumor cell lines and tumor biopsies at much higher levels than in normal pancreatic tissue. Studies conducted with MiaPaCa2 and Panc1 cell lines showed that cannabinoid administration (a) induced apoptosis, (b) increased ceramide levels, and (c) up-regulated mRNA levels of the stress protein p8. These effects were prevented by blockade of the CB2 cannabinoid receptor or by pharmacologic inhibition of ceramide synthesis de novo. Knockdown experiments using selective small interfering RNAs showed the involvement of p8 via its downstream endoplasmic reticulum stress–related targets activating transcription factor 4 (ATF-4) and TRB3 in Δ9-tetrahydrocannabinol–induced apoptosis. Cannabinoids also reduced the growth of tumor cells in two animal models of pancreatic cancer. In addition, cannabinoid treatment inhibited the spreading of pancreatic tumor cells. Moreover, cannabinoid administration selectively increased apoptosis and TRB3 expression in pancreatic tumor cells but not in normal tissue. In conclusion, results presented here show that cannabinoids lead to apoptosis of pancreatic tumor cells via a CB2 receptor and de novo synthesized ceramide-dependent up-regulation of p8 and the endoplasmic reticulum stress–related genes ATF-4 and TRB3. These findings may contribute to set the basis for a new therapeutic approach for the treatment of pancreatic cancer.”

    That, to me, does not seem like a “mild at best” solution to pancreatic cancer, one of the most lethal out there. The fact that Dr. Gorski seems to have omitted this from his article, instead selecting the studies that show only a “mild” effect on tumours, raises suspicion for me.

    I am not a doctor, or a scientist, and I’m aware that, in matters of medicine, my opinion probably counts for very little. However, the studies that Gorksi has analysed here may show that cannabis does not cure cancer, but it is not anywhere close to be sufficient enough evidence to ‘prove’ that cannabis, in some form, does not aid in the fight against cancer. In fact, it does quite the opposite.

    I don’t know about anyone else, but I have lost relatives and friends to cancer, and if I ever contracted it myself, I would try everything in my power to defeat it, including the use of high CBD concentrated cannabis oil. All of these studies linked in this article show, at least on some level, that the components found in cannabis help with cancer, even if it is only ‘mild’ affect. To me personally, and to others that have lost people to this awful disease, ‘mild’ is better than not at all. I would never go against what a doctor prescribed me (unless of course I was too weak to survive it), but in every circumstance I could imagine, I would supplement my treatment with cannabis oil.

    I’m also of the opinion that isolating singular compounds of the cannabis plants, such as THC, or CBD, is counter-productive to studying the plant’s application medicinally. There are a variety of cannabinoids in the cannabis plants, and rather than taking specific compounds and testing them in a vacuum without any of the others, I would be intrigued to see a clinical study where subjects were given a form of cannabis medicine that contained all the active cannabinoids.

    Unfortunately, since the plant is still regarded by most governing bodies as a health hazard, I think it will be a long time yet until we can start the mass scientific evaluation needed to truly see how the cannabis plant can be used in the fight against cancer.

    On an unrelated note – to the Gorksi brigade currently patrolling this comments section like a pack of zealous hunting dogs, please spare me your nay saying founded on the blog post of one doctor. It’s not progressive and it doesn’t help anyone. The fact that doctors and scientists from around the world are all still pursuing research opportunities in regards to cannabis would suggest to me that, despite Gorski’s ‘irrefutable proof’, that cannabis plant does indeed contain some beneficial medical application towards cannabis. And yes, I can provide evidence of this if required.

    1. David Gorski says:

      I left off the pancreatic cancer study because, after slogging through in vitro and animal study after in vitro and animal study after in vitro and animal study that all show only modest anticancer activity due to purified cannabinoids, I was getting tired. So I looked at this pancreatic cancer study just now, and guess what? It’s just like the other ones, except that the animal results (which are the ones that tend to get my attention the most in preclinical studies) are even less impressive than some of the other studies, even though the IC50 values for the in vitro studies are a bit lower than some of the other papers, in the single-digit micromolar range.

      That’s the reason.

    2. WilliamLawrenceUtridge says:

      I am not a doctor, or a scientist, and I’m aware that,

      And with your comment, so are we.

      However, the studies that Gorksi has analysed here may show that cannabis does not cure cancer, but it is not anywhere close to be sufficient enough evidence to ‘prove’ that cannabis, in some form, does not aid in the fight against cancer. In fact, it does quite the opposite.

      Ok, to get it out of the way – you’ve shown only a pancreatic cell line can be inhibited by cannabis. Note that it’s easy to kill cells in a petri dish. There are thousands of studies that show promise of compounds in petri dishes. Humans aren’t petri dishes.

      Second, it’s always possible to argue that there is one more type of cancer (or stage) that X could cure. Cancers of different tissue origins are close to different species than they are different varieties of cancer. There’s a reason pancreatic cancer is terrifying, and an osteosarcoma is much less so. So if anyone claims that X can cure “cancer”, they’re probably pretty ignorant – because you must specify what type of cancer, what stage, has it metastasized, and eventually what particular genes are deranged and expressing what proteins. So great, cannabis might cure pancreatic cancer. Prove it in people and I’ll be interested, because I, a non doctor, nonscientist, can cure cancer in a dish, with a hammer. Or by taking the lid off. Or leaving it on. Get it?

      I don’t know about anyone else, but I have lost relatives and friends to cancer, and if I ever contracted it myself, I would try everything in my power to defeat it, including the use of high CBD concentrated cannabis oil.

      Great, try to do it within the context of a clinical trial. Just realize that if the numbers found above are accurate, you’re going to be bathing in it from the inside out. It takes a lot of pot to reach those levels, so much so that you are going to be injecting it, not smoking it. And that’s why pot and its derivatives isn’t very promising – you just need too much of it. Imagine it was alcohol, and showed promise only at levels equivalent to chugging two litres of vodka every day. Would you say that’s a “good” cancer drug?

      ‘mild’ is better than not at all.

      Yeah, but this is only “mild” when it’s in a dish. What happens when it’s circulating through your body, being deposited in fat cells, being processed by the liver, making you high 24/7, making you crave salty and sweet all the time? Oh, and it costs a lot of money. Are those adverse effects sufficient to make you put up with that “mild” increase? Particularly when nobody has proven it exists outside of a dish?

      but in every circumstance I could imagine, I would supplement my treatment with cannabis oil.

      Yes, and you might be totally wasting your time and money. You might have been better off enrolling in a clinical trial. Hell, it might even cure you – but you don’t know in advance so you’re basically gambling with the rest of your life. For me, I’m far more interested in possibilities that have shown more promise.

      I’m also of the opinion that isolating singular compounds of the cannabis plants, such as THC, or CBD, is counter-productive to studying the plant’s application medicinally.

      Yes, but you’re not a doctor as a scientist, so why does your opinion matter? There are people who conduct pharmacognosy research, research on plants, and they will point out that synergy is actually vanishingly rare. Also think about this – why would or should the cannabis plant evolve a specific set of proteins that selectively kill human tumors? What possible evolutionary mechanism would there be?

      You can think this all you want – doesn’t mean it’s true. Nature doesn’t exist to provide us with cures (it generally is better at providing what needs to be cured; rabies is far more natural than modern cannabis for instance).

      On an unrelated note – to the Gorksi brigade currently patrolling this comments section like a pack of zealous hunting dogs, please spare me your nay saying founded on the blog post of one doctor. It’s not progressive and it doesn’t help anyone.

      Oh go fuck yourself. You don’t want to have your comment torn apart at the seams? Don’t post it. Suck it up, buttercup – want a feedback-free cheerleading zone? Go to a blog that promotes cannabis without pointing out that a human is not a petri dish. Your treatment isn’t special either, we’re this mean to everyone.

      Also – want to help people? Stick close to the evidence and abandon your beliefs that cannabis MUST do something. About the only thing it MUST do is get us high, because that’s what it’s bred for.

      Don’t think that your comment, or the attention paid to this post, are anything particularly special. All the posts regularly get this kind of attention, as well as all the commentors who make the same errors you do.

      that cannabis plant does indeed contain some beneficial medical application towards cannabis. And yes, I can provide evidence of this if required.

      Two points:
      1) Cannabis might have some such applications, but sadly the evidence is currently lacking so your argument is about as useful as saying that someday we MUST discover an alternative to fossil fuels, so there’s no point in conserving them.

      2) Great, provide evidence. Because so far, you’ve provided none but your own opinion. Pubmed-indexed citations please.

  30. Jo says:

    Wow. Some very brainwashed trolls commenting on here..
    I had chemo almost killed me so ditched it. Took 1 grm oil in pessery anally a day and within 30 felt alive. No tumour, cannot find ANYTHING after 3 months.
    WAKE UP YOU IDIOTS.
    The billions made in killer chemo drugs is very profitable so why make a cure.
    The UK has now realised, people like me, that ordinary folk are curing their own cancer with HTC and CBD from cannabis through oil. They’ve just patented it..
    Before they banned cannabis in the early 1900s it was used IN ALL MEDICINES and cured people. 1936 cancer act came in and BOOM. BIG BUCKS, as you can only get treated by medical practitioner BY LAW.
    We are now in secret giving my uncle the oil to cure him, he is 78, for pancreatic cancer as the chemo was killing him. He is like a different man.
    WAKE UP AND SMELL THE WEED TROLLS

    1. KayMarie says:

      You use that word troll, but I don’t think you know what it means.

      People who all agree that on a website, let’s call it a metaphorical house this is the metaphorical living room and generally agree on approach and can agree to disagree without resorting to the capslock key when responding are not trolls.

      At least not in that house and living room.

      The person that bursts in screaming that this shouldn’t be a living room, we need to put a toilet in the middle of it and gosh darn the color on the wall is the wrong shade of beige…those are the trolls. Especially if they don’t want to even try to understand why we put the couch over there by that window.

      Now science-based types can be trolls on other sites in their metaphorical bathroom complaining that someone put a toilet in the living room.

      That people have a different view does not make them a troll. It is where and how they decide to express their view.

      1. weing says:

        “You use that word troll, but I don’t think you know what it means.”
        I guess I misunderstood. I thought he was referring to himself and other brainwashed, weed trolls like him.

        1. KayMarie says:

          I shudder to think what weed trolls smell like. Especially if enough to wake one from a sound sleep.

    2. WilliamLawrenceUtridge says:

      I had chemo almost killed me so ditched it.

      So…you had cancer, you got chemo, then you didn’t have cancer, then you put drugs up your but. Wow, it’s almost as if your chemo cured your cancer! Chemo is in fact curative in some cases.

      The billions made in killer chemo drugs is very profitable so why make a cure.

      Two points:

      1) Was the drug oil you put in your asshole free?

      2) Do you have any idea how profitable a true “cure for cancer” would be over the short term? You know, the short term, the kind of decision-making window that most companies use when making decisions? Also, you are aware that “cancer” isn’t one thing, it’s hundreds of diseases with one vaguely-related cause, right?

      The UK has now realised, people like me, that ordinary folk are curing their own cancer with HTC and CBD from cannabis through oil. They’ve just patented it..

      …except patents protect an idea, they don’t prove it works. And if it’s really that effective, why haven’t we seen results in the research? In non-resistant bacterial infections, antibiotics have an extremely high rate of success, to the point that you can essentially prove it works with two groups of ten people. We don’t see that with cannabis. Why not?

      Before they banned cannabis in the early 1900s it was used IN ALL MEDICINES and cured people.

      Yes, but that’s because basically all treatments at that time were palliative, and pot does get you stoned, which makes you feel better about being sick.

      We are now in secret giving my uncle the oil to cure him, he is 78, for pancreatic cancer as the chemo was killing him. He is like a different man.

      I bet, he’s probably high 24-7 now. That’ll change anyone’s perspective. If you actually have an uncle with pancreatic cancer though, he’ll probably die in a couple months. Pancreatic cancer is nasty. I hope he doesn’t die blaming you for giving him false hope of a cure – that’s the kind of thing that lingers with you for decades.

  31. Jo says:

    And one more thing.
    Dr Leonard Coldwell YouTube explains the killer Cooprations chem. then explains cannabis oil.
    Ask how many Drs would give their loved ones CHEMO RADIOTHERAPY AND OPERATION… They know better.
    Too much information and HUMAN TESTIMONIALS about to be SO IGNORANT.
    http://www.chemo-facts.com/
    YOU CANNOT EDUCATE “STUPID”

    1. Woo Fighter says:

      MR. Leonard Coldwell is not a real doctor; that’s not his real name, he’s a dangerous lunatic who is a former colleague of Kevin Trudeau, and he does NOT have a 92.3% success rate curing cancer. He is not even allowed to touch a patient these days as he has no license to practice medicine anywhere in the United States, if indeed he ever held a medical license anywhere in the world. He does appear on fringe radio shows like Coast to Coast to shill his many self-published books and DVDs, and sells tickets to expensive weekend conference packages across the US. He also takes part in all those quackalicious “Cancer Healing Alliance” workshops and webinars.

      Furthermore, he didn’t “cure Ronald Reagan” using secret suppressed cancer treatments only available in Germany.

      Mr. Coldwell espouses an amalgam of non-scientific crap like alkaline nonsense, Hulda Clark’s crazy theories, nutrition and positive thinking aka “The Secret, and he is a vocal supporter of Burzynsi (thieves and conmen have to stick together, I guess. An alliance of evil). He claims he can cure anyone of any cancer in six weeks with a 92.3% success rate. You just need to buy his books or other merchandise.

      1. Woo Fighter says:

        RE: Mr. Leonard Coldwell:

        From the introduction to one of his books:

        “Nearly everybody in the orthodox medical field disagrees with almost everything said in this book, along with the ideas, techniques and systems published herein. I, the author, don’t really care! Why? Because I have the results to show, and can reproduce cancer cures anytime I want, if I would be given the legal authority to practice my IBMS(TM).

        FTC and FDA warning: guys I do not trade or sell anything or make any direct profit from any of my suggestions. Not even my books. So don’t
        even bather (sic) to harass me because it will lead to legal action against you personally not against the agencies. http://www.instinctbasedmedicine.com (http://www.instinctbasedmedicine.com) You can get free individual advice from the http://www.goodlifefoundation.com (http://www.goodlifefoundation.com) from Dr. Hohn MD NMD just write to drhohn@goodlifefoundation.com.

        And note this disclaimer: All health statements made are based on freedom of religion and for and form (sic) the Church Of Inner Healing.

        Like Jim Humble of MMS fame, he’s hiding behind a fake church to make his ludicrous health claims. Or like $cientology.

        I just read the free preview pages of his cancer book on Amazon.com. He is truly certifiable.

        Here’s part of a discussion about Coldwell on James Randi’s site:

        http://forums.randi.org/archive/index.php/t-228730.html

  32. weing says:

    Something tells me you’ve been smoking it.

  33. Geza Csikasz says:

    Interesting read.

    The only take-away for me is that none (or very few) clinical trials exist which therefore justify the conclusion that cannabis doesn’t cure cancer. In very simple terms – it cannot be true because it cannot be proven. And so far, it has been very hard to actually test this because of all the bullshit around cannabis as a health hazard.

    What baffles me is that you move on to say that you don’t expect any clinical trials to produce any positive results in terms of curing or in some way inhibiting cancer. Wouldn’t it be a more true scientific stance to say – perform clinical trials and see what happens? Yes, you are underwhelmed and unexcited by the pre-clinical results so far. That’s observation. But for any assumption or claim beyond that is just speculation.

    You did say that the competition is fierce and given the modest potential observable so far, it would not justify clinical trials and more extensive research/testing. Well, that’s your opinion, basically a risk/reward assessment. Nothing that can be proven until it is actually tested.

    There seem to be other companies and professionals that have another risk/reward assessment and they are funding clinical and thorough research. Before I say cannabis does or doesn’t cure cancer, I’ll wait and see what results they get.

    1. WilliamLawrenceUtridge says:

      The only take-away for me is that none (or very few) clinical trials exist which therefore justify the conclusion that cannabis doesn’t cure cancer. In very simple terms – it cannot be true because it cannot be proven. And so far, it has been very hard to actually test this because of all the bullshit around cannabis as a health hazard.

      Not quite. Few clinical trials exist. More could prove that pot can’t cure cancer (more accurately – that upon controlled testing, pot did not impact longevity or progression for specific types and stages of cancers, since you can’t ever disprove anything and “cancer” isn’t really one thing). And while testing is indeed impaired by the fact that pot is a controlled substance, one must also consider the fact that there’s not really any good preliminary evidence supporting it being a cure or treatment for cancer itself.

      What baffles me is that you move on to say that you don’t expect any clinical trials to produce any positive results in terms of curing or in some way inhibiting cancer. Wouldn’t it be a more true scientific stance to say – perform clinical trials and see what happens? Yes, you are underwhelmed and unexcited by the pre-clinical results so far. That’s observation. But for any assumption or claim beyond that is just speculation.

      But evaluation of that preclinical data is very, very important – there are millions, even billions of possible treatments for different cancers. We can’t test them all. We simply don’t have the money – we don’t even have enough people with cancer to test all possible hypotheses – therefore we rely on proxy data from dish and rat studies. Because nobody has figured out a better way to discern which molecules might cure cancer (with some exceptions, Gleevec is one I think).

      You did say that the competition is fierce and given the modest potential observable so far, it would not justify clinical trials and more extensive research/testing. Well, that’s your opinion, basically a risk/reward assessment. Nothing that can be proven until it is actually tested.

      Sure, but nothing can be tested until you pony up the resources. And the agencies that dispense resources have an obligation to spend them on the most promising avenues. And basically – that’s not pot, there’s no reason to expect it to be pot, and there’s no reason for pot to magically cure cancer (particularly given how long it has existed).

      There seem to be other companies and professionals that have another risk/reward assessment and they are funding clinical and thorough research. Before I say cannabis does or doesn’t cure cancer, I’ll wait and see what results they get.

      Sure, but what you have here isa cancer researcher, a scientist-practitioner who studies cancer-treating compounds, saying the preclinical data is pretty unpromising. So for the purposes of an average citizen, pot just doesn’t seem worth hanging your hopes, or money on. While the title states quite baldly that pot doesn’t cure cancer, the body is a little more nuanced but still comes to the conclusion that there’s not really any good reason to think that pot does cure cancer.

      At this point, any belief that pot does cure cancer is essentially ignoring the evidence in favor of ungrounded hope.

    2. MadisonMD says:

      Wouldn’t it be a more true scientific stance to say – perform clinical trials and see what happens?

      Not really. Because scientists needs to triage a nearly infinite number of possibilities, by pursuing the most promising. If I were to say twinkies cure cancer, for example, would you say, ‘Yeah, maybe they do because we haven’t done clinical trials to test that idea?’

      Consider that the NCI has screened 400,000 compounds for anticancer activity. Beyond this, there exists an estimated possible 10^60 compounds that could be tested. Why should scientists prioritize chemicals merely because they originate from cannabis? It is scientific to prioritize the most promising compounds with the best preclinical activity coupled with good pharmacology and toxicology. It costs $ hundreds of millions to adequately test a new drug, so with the limited resources available, the future is brightest if we test the most promising. This is the scientific stance.

      There seem to be other companies and professionals that have another risk/reward assessment and they are funding clinical and thorough research.

      Yeah great. If others deem this the most promising opportunity, then hell yes, they should invest in it. If they have the data to convince their investors and or scientific funding sources, then they get the resources to do the study. Until then, it is best to refrain from telling granny that marijuana will cure her cancer.

  34. Bill Syrjala says:

    This author is clueless. The science does exist, he chooses to ignore it. Cannabis oil *does* cure cancer. I know dozens of people told to go home and die by the “best” oncologists in the world. 5, 10, 15 years later they are all alive and well and cancer free.

    The author also does not understand the ‘entourage effect’ and why it is important, and why isolating compounds from the plant is the wrong approach.

    1. WilliamLawrenceUtridge says:

      This author is clueless. The science does exist, he chooses to ignore it. Cannabis oil *does* cure cancer. I know dozens of people told to go home and die by the “best” oncologists in the world. 5, 10, 15 years later they are all alive and well and cancer free.

      That’s great. You should put those case series together and examine them against the recognized standard for determining if an anecdote represents quality data or something else. Peter Moran’s website is probably a good starting point for background knowledge. From there, a hypothesis can be generated and tested, which might then show why actual tests of cannabis have consistently failed to show significant promise as a chemotherapeutic agent. You’ve got a lot of work ahead of you, so go ahead, get to it!

      The author also does not understand the ‘entourage effect’ and why it is important, and why isolating compounds from the plant is the wrong approach.

      Well, you’ve even got a preliminary hypothesis then! Great, while synergistic effects are rare, they do occur in biology. So – go out and test then! If cannabis is as effective as you claim and the survivors aren’t merely statistical anomalies or people who misunderstood their doctors, then the world will welcome your work, and we can rejoice in a new way of curing cancer!

    2. Andrey Pavlov says:

      The author also does not understand the ‘entourage effect’ and why it is important, and why isolating compounds from the plant is the wrong approach.

      You can ask MadisonMD but I am probably the biggest proponent of cannabis around here and think it has a higher than average likelihood of having synergistic properties.

      But the reality is that there is really no evidence that cannabis is clinically useful in the treatment of cancer (and only some evidence it is useful for treating some of the symptoms of cancer and chemotherapy, in some people, and as a 3rd line option at best, probably 4th line) and, as Madison and Gorski have pointed out evidence against its future clinical utility.

      To my mind that doesn’t close the door on it and I do think that more research is justifiable, but nothing even remotely approaching the claims you make nor the common claims we see are justifiable. And I certainly do not even remotely expect it to be the next Gleevec.

      And, of course, isolating compounds from the plant is indeed the best approach. Otherwise one cannot characterize them well nor have any chance of actually discovering and maximizing any synergistic effects.

  35. Beavis says:

    Dr. Gorksi, for us laypeople can you please explain this comment in further detail:

    “I noted that the IC50 (the concentration that produces 50% of maximal inhibition of the parameter being measured), was 25 μM, which is a bit higher than we like for an anticancer compound”

  36. MadisonMD says:

    Few drugs require concentrations this high. In humans, it is difficult to achieve such high concentrations (except for the very smallest molecules, say <150-200 Da) and the risk of off-target effects and toxicity are typically greater. For these reasons, drugs are typically developed to more potently inhibit the target of interest– in the 1-50 nM range for IC50.

    In laboratory cell culture experiments it is easy to achieve very high concentrations, but they are not usually relevant to actual use in humans where metabolism, absorption, etc. limit the maximal concentration that can be achieved pharmacologically. It is a common and classic problem with preclinical drug research in cell culture– findings that are actually not applicable to humans.

    1. Beavis says:

      @MadisonMD Thank you for the explanation. The reason I asked is that the IC50 seems to be the main reason Dr. Gorski dismisses CBD and other cannabanoids as potential cures. I certainly understand why in general this matters with most compounds for the reasons you explained. However, I do wonder how much this really matters where cannabinoids are concerned.

      As a fairly well-informed layman, I’m fairly confident that toxicity is not much of an issue as cannabinoids are known to be remarkably non-toxic and safe. So I guess the remaining concerns would be off-target effects and difficulty reaching the required concentration in the body through either ingestion of concentrates or injections. Perhaps Dr. Gorski or someone else knowledgeable can address those issues as they relate to CBD and other cannabinoids.

  37. MadisonMD says:

    I certainly understand why in general this matters with most compounds for the reasons you explained. However, I do wonder how much this really matters where cannabinoids are concerned.

    There is nothing magical about compounds from cannabinoids versus compounds from other sources. I have no reason to think these compounds are privileged in any way.

    I’m fairly confident that toxicity is not much of an issue as cannabinoids are known to be remarkably non-toxic and safe.

    At the concentrations achieved by cannabis users these may be relatively non-toxic and safe. But at pharmacologic concentrations required to achieve an anticancer effect, the story could be completely different.

    1. Beavis says:

      “There is nothing magical about compounds from cannabinoids versus compounds from other sources.”

      Actually, there is. Cannabinoids seem to be among the least toxic of pretty much anything we call a drug. This is why I asked if someone knowledgeable on the subject could respond.

      “At the concentrations achieved by cannabis users these may be relatively non-toxic and safe. But at pharmacologic concentrations required to achieve an anticancer effect, the story could be completely different.”

      I’m not talking about “concentrations achieved by cannabis users”. I’m talking about medical use (pharmacologic concentrations). May be… Could… Lets be more specific here… Are the levels of CBD in the cancer studies that Dr. Gorksi mentioned achievable in humans without toxic and other serious negative side effects? (I’m guessing the answer to this question is “yes”, however as I said before, I’m just a fairly well informed layman, not an expert)

      1. n brownlee says:

        Magic? Really? I don’t think so, though it may sometimes feel that way.

        ” Cannabinoids seem to be among the least toxic of pretty much anything we call a drug”

        This statement is so qualified (- may? among the least? pretty much?) that it’s entirely meaningless.

        1. Beavis says:

          @n brownlee

          ” ” Cannabinoids seem to be among the least toxic of pretty much anything we call a drug”

          This statement is so qualified (- may? among the least? pretty much?) that it’s entirely meaningless.”

          As I mentioned before, I am merely a fairly-well informed layman, not an expert, hence the language I used. I suppose I could have made a much more definitive (and testable) statement like “CBD is significantly less toxic than most (or even all) of the drugs that Dr. Gorski feels are superior cancer treatment prospects” and left the onus on you anti-cannabis folks to disprove it…

          Perhaps it would be better to pose the question this way:

          May an expert please contrast the relative toxicity and tolerability of CBD with that of other, supposedly more promising, new cancer drugs?

          1. weing says:

            “CBD is significantly less toxic than most (or even all) of the drugs that Dr. Gorski feels are superior cancer treatment prospects” and left the onus on you anti-cannabis folks to disprove it…”

            No. The onus is on you to prove your claim. I am not pro or anti. You prove the claim, with good studies and research, you got me about toxicity. Now what about efficacy?

            1. Beavis says:

              I can certainly search for studies on the safety and tolerability of CBD and other cannabinoids. Although I’m not really sure what exactly I’m looking for, and it would probably be much easier for a researcher rather than a layman….

              http://www.ncbi.nlm.nih.gov/pubmed/21144973
              http://www.ncbi.nlm.nih.gov/pubmed/18801821
              http://www.ncbi.nlm.nih.gov/pubmed/23141881
              http://www.ncbi.nlm.nih.gov/pubmed/19896326

              This one sounds like it involved pretty substantial dosages (1280 mg/day of CBD): http://www.ncbi.nlm.nih.gov/pubmed/16401651

              1. MadisonMD says:

                OK, Beavis. Lets do the math.
                This study measures pharmacokinetics of CBD and finds peak serum concentration of 0.3-2.6 ng/ml (= 1- 8 nM) with half-life of 1 hour; this was with administration of oral 5.4 mg.

                If these PKs scale linearly with dose and t1/2 remains at 60 minutes–the most reasonable initial assumptions– and if the IC50 is 10uM to have a modest effect on cancer cell lines (as per Dr. Gorski’s essay above), you would need to take the following dose to slow down the growth of cancer by 50%:

                7 to 54 grams at time zero (highly variable per individual), followed by 3.5 to 27 grams every hour.

                Do you think this molecule is so magical that it could be nontoxic at these blistering doses? (Sure you do! But then you are a layman who apparently thinks cannabis is magic.)

              2. KayMarie says:

                And they have found with the legal edibles that there are doses that tend to make people decide it is time to go to the ER. So the you can’t possibly ever overdose on marijuana seems to be usually if you only smoke it you’ll get high enough to stop smoking before you get to a point you feel you are so sick you’ll call 911.

                Some of it is the delay in when the effects hit. So like with pills often people go nothing happened in the same amount of time as a toke so they decide to take more when they are still way too early to be seeing effects. Some may be how the can concentrate it in an oil vs what you can do with something that you can still smoke.

                Now it may vary with if you are concentrating mostly to get people high vs some of the other compounds, but that they have to regulate the doses in Colorado to keep people out of the ER tends to, IMO, say there is some upper limit to how much you can put in a person.

                Just because it isn’t common for people to take enough of something to have a negative effect doesn’t mean no negative effects exists. I’ve never managed to drink enough water to get the side effects of drinking too much water, but I do believe the data that says there is a toxic dose of water like there is a toxic dose of every other compound on the planet.

              3. Andrey Pavlov says:

                Those are excellent explanations Madison and Kay.

                I’ll be curious to see Mr. Beavis’ riposte.

              4. Windriven says:

                @MadisonMD

                I think this sums up the problem for some of our less rigorous commenters: math is haaaaard.

              5. Windriven says:

                My apologies in advance to anyone who thinks I was targeting females in the above linked video. It was only when reviewing it to test that the link worked that I realized -doh – that all contestants were women. Trust me, I am aware that many males have similar attitudes.

              6. n brownlee says:

                @Windrive
                It’s – ah, parody, right? TELL ME I’M RIGHT.

              7. Windriven says:

                It is a parody, Nancy. Kinda hard to tell though, isn’t it?

              8. Beavis says:

                MadisonMD, First of all, I would like to thank you very much for helping to further this discussion with some actual numbers and actual facts instead of the mere supposition, denial, condescension and insults supplied by some other responders.

                Now, I need some help here from you experts to help me understand this. The study you linked to involved taking pills of concentrated extracts. My first question would be: is 100% of the CBD taken in such a form absorbed into the bloodstream? If the answer to that is no, then might lower doses be required if different forms of administration were used (like for instance oromucosal spray such as Sativex, or direct injection/IV)?

                I did find something about CBD absorption efficiency for different administration methods, but this was in dogs (I’m not saying a similar study doesn’t exist for humans, just that this is what I found). I wonder if such differences might occur in humans as well…

                http://www.ncbi.nlm.nih.gov/pubmed/2900742

                I also wonder whether, in the study you linked, the presence of THC affects the absorption of CBD? Might more CBD be absorbed if THC were absent?

              9. MadisonMD says:

                Hi, Beavis. I get a bet snarky myself sometimes (the magic comment was amusing to me)… thanks for letting that pass.

                The study you link shows that there is a first-pass effect in dogs resulting in low systemic absorption of the oral route*…. That is likely true in humans too (although not necessarily to the same degree) explaining in part why oral CBD is relatively non-toxic (and doesn’t have much of a chance at being effective for cancer). You could likely achieve higher concentrations by the intravenous route. But here we are getting to a situation where you know much less about toxicity.

                We should know more about pharmacokinetics and absorption of CBD as it continues to be developed by GW in proper phase I/II for Dravet syndrome… though this is the oral route. They are doing phase I dose escalations so we will learn about toxicities with higher oral dosing by formal studies. Incidentally, we already know about toxicities of pharmacologic THC by the way.

                Regarding oromucosal sprays, this phase I trial suggests you are not going to achieve high concentrations either:

                The mean Cmax values (<12 ng/mL) recorded in this study were well below those reported in patients who smoked/inhaled cannabis, which is reassuring since elevated Cmax values are linked to significant psychoactivity.

                Note how the authors think that is a good thing… and it is if there is less toxicity and efficacy is still there. But we are still 3 orders away from the magnitude required to even slow down a cancer cell by half.

                So we are left with only with IV as viable route of administration. Yet, with short halflife, we would have to do something like this man and pump in continuous CBD at high levels even to hope to come close. That’s quite inconvenient, and at such levels there is no assurance that CBD or any other chemical would remain non-toxic. Moreover, there are many relatively non-toxic compounds due to poor absorption, first-pass effect, or other reasons. That alone does not validate any chemical as a good drug. To be a useful drug, you need efficacy and low toxicity at the same pharmacologically achievable (and maintainable) range of concentrations.

                Keep in mind that in oncology today, there is significant interest in matching a specific drug to a specific genetic abnormality within cancer. When you do that, you sometimes get rather satisfying results like this, this, and this. These type of results are much more satisfying to researchers, physicians, and most especially, to people with cancer. They come about by understanding and matching drugs that act by particular mechanisms to a particular genetic abnormality in cancer.

                So I’m much less excited about the idea of empirically testing CBD (or any other chemical) in all cancers 1970′s-style. Today, it is much better to identify compounds (from cannabis, or anywhere else–I don’t care) that can be used specifically for a matched type of cancer where I could predict it would work. In other words, I’d be much more excited about CBD or any other compound if matched to a particular disease.

                ———————-
                *The first pass-effect occurs with the oral route because your intestines have a separate circulatory system known as the portal system which effectively ensures everything absorbed passes through the liver immediately to be detoxified, if need be. This can be useful with prodrugs such as capecitabine or cyclophosphamide where the liver creates the active metabolite; it is less useful for other things like CBD for which it will be difficult to achieve good levels by the oral route.

              10. Beavis says:

                KayMarie,

                I’m sorry but your comment appears to be nothing more than a distraction from this discussion. People are not going to the ER due to overdosing on cannabinoids. What is causing people to go to the ER is inexperienced people (probably most of them first time users) who take several (often 8 or more!) adult doses of edibles that were likely intentionally made with high THC and subsequently “freak out”. The ER visits are caused by uneducated, inexperienced users suddenly taking a massive amount of THC.

                How exactly does this relate to the discussion of using non-psychoactive cannabinoids in controlled doses for medical purposes?

                It is also important to note that these people did not NEED to go to the ER. Their life and their health was not in danger. They may THINK they are going to die (hence the ER visit), but they won’t. Nor will they suffer any sort of measurable harm. What treatment is needed or given in the ER to these patients other than giving them time for the THC to clear their system?

                Can you produce some examples where someone had to go to the ER due to taking too much CBD (or other non-psychoactive cannabinoid(s))? Even a single case?

              11. n brownlee says:

                @Beavis

                “I saw the best minds of my generation destroyed by madness, starving hysterical naked,dragging themselves through the negro streets at dawn…”

                I’ve seen angelheaded hipsters smoke hash until their eyes rolled back in their heads, they puked themselves senseless, crapped their pants and then passed out for days. We called it “hashish sickness” and in 1967, it was not even rare.

                There may be cannabinoids that have some anticarcinogenic effects, but believe me, Sunny Jim, there are some cannabinoids that will set you free semi-permanently- and there are enough of us old rockers around to say so.

              12. KayMarie says:

                Most of the arguements is nothing in marijuana can be toxic at any dose so if you have to eat several grams of it to get enough of the one compound you want there can be no bad effects from any of it.

                FWIW most people I know of doing medical marijuana are doing whole plants or edibles not purified compounds so even if aimed at lower THC they are still going to get some as the plant is not a pure compound. How much of the mixture do you need to get the high dose of the one compound you want?

                http://www.sciencedirect.com/science/article/pii/0041008X81901228 is CBD in monkeys. So doesn’t sound incapable of any bad effect at all to me, but your mileage may vary. Not sure how the concentrations compare to the IC50s of the compounds. Usually you can get away with higher doses in monkeys than you would ever give a human, especially if you are trying to find an LD50. Usually the side effects seen in an LD50 can happen at lower doses.

                I dunno freaking out that severely doesn’t sound harmless to me, depends on whether or not someone (especially someone ill enough to be taking something for cancer) handles the stress.

              13. Beavis says:

                @MadisonMD:

                KayMarie was kind enough to post this:

                “http://www.sciencedirect.com/science/article/pii/0041008X81901228 is CBD in monkeys. So doesn’t sound incapable of any bad effect at all to me, but your mileage may vary. Not sure how the concentrations compare to the IC50s of the compounds. Usually you can get away with higher doses in monkeys than you would ever give a human, especially if you are trying to find an LD50. Usually the side effects seen in an LD50 can happen at lower doses.”

                I wonder if the concentrations found in this study to be somewhat tolerable (at least to monkeys) :

                “Ninetyday oral treatment with CBD (30–300 mg/kg) had little effect but liver and kidney weights rose 13–56% above controls without morphologic changes.”

                are high enough to achieve the IC50 values found in the previously discussed cancer studies?

                If they are on the same order of magnitude, is there any way to translate this dose from monkeys to humans? I wonder, if humans ARE able to reasonably tolerate such a dose, would that change researchers’ opinion of the viability of cannabinoids in cancer treatment at all?

            2. Beavis says:

              @weing:

              ““CBD is significantly less toxic than most (or even all) of the drugs that Dr. Gorski feels are superior cancer treatment prospects” and left the onus on you anti-cannabis folks to disprove it…”

              No. The onus is on you to prove your claim. I am not pro or anti. You prove the claim, with good studies and research, you got me about toxicity. Now what about efficacy?”

              Okay, I’m sorry. My bad. I made a mistake. That was definitely not the right approach. As a layman, I know MUCH less about this than you experts do. I SHOULD have instead worded the question like this:

              Are any of the drugs that Dr. Gorski feels are superior to cannabinoids as potential cancer treatments known to be equally or less toxic, or even presumably on the same order of magnitude of toxicity or tolerability in humans?

              I honestly do not know the answer to this, and would like to learn.

              1. Andrey Pavlov says:

                Are any of the drugs that Dr. Gorski feels are superior to cannabinoids as potential cancer treatments known to be equally or less toxic, or even presumably on the same order of magnitude of toxicity or tolerability in humans?

                Firstly I don’t know that this is an answerable question. There is no one such monolithic thing as “toxicity.” You can’t just assign a quantitative number to a chemical and say it is “more” or “less” toxic than something else. Yes, obviously there are extremes that are easy to distinguish. But in something that is physiologically tolerable and with specific effects, then it becomes more about what the side effects are, how common they are, and how extreme they can get. And from there people will be different and respond differently – hence why a number of people can’t tolerate specific therapies and must be switched over to others (though in cancer there are fewer options to switch than most other types of therapies).

                Next, it is a pointless question. Cannabinoids have shown very mediocre (at best) performance against cancer and only in cell culture. So whether there is another existing chemotherapeutic that is more or less toxic is entirely irrelevant.

                For proper research first there needs to be shown good efficacy at a good IC50. From there needs to be some good animal models (particularly ones that don’t show worrying effects like increases in liver weight). Next is Phase I trials to see what dosages are tolerable in human beings, and then onward to Phase II and III (if everything up to each point preceding it is favorable).

                You are asking to compare Phase IV stuff to pre-clinical stuff. That is basically comparing apples and oranges.

        2. Beavis says:

          @n brownlee ‘” Cannabinoids seem to be among the least toxic of pretty much anything we call a drug”

          This statement is so qualified (- may? among the least? pretty much?) that it’s entirely meaningless.’

          Okay, n brownlee. I will bite. I’m no expert, but no doubt you are… How many drugs can you name that are less toxic than cannabinoids?

          1. n brownlee says:

            See Andrey’s answer re: toxicity immediately above. I couldn’t say it that well if I worked at it for a month.

            1. Andrey Pavlov says:

              Danke n brownlee.

              I get the feeling Beavis is genuinely trying. Hence why I have bothered resuming writing more extensive (and at least slightly less snarky) comments. He know he is out of his depth, he just doesn’t realize just quite how far out of it he is. If he does, perhaps he’ll adopt the requisite humility to actually learn a thing or two.

      2. Andrey Pavlov says:

        his is why I asked if someone knowledgeable on the subject could respond.

        And yet when they do, you don’t listen and keep arguing. MadisonMD is an oncologist and researcher as is Dr. Gorski.

        Are the levels of CBD in the cancer studies that Dr. Gorksi mentioned achievable in humans without toxic and other serious negative side effects? (I’m guessing the answer to this question is “yes”, however as I said before, I’m just a fairly well informed layman, not an expert)

        We don’t know, but actual experts like us here would guess the answer is no.

        1. Beavis says:

          “This is why I asked if someone knowledgeable on the subject could respond.

          And yet when they do, you don’t listen and keep arguing. MadisonMD is an oncologist and researcher as is Dr. Gorski”

          I would like to sincerely apologize for this. I honestly did not know this, and please keep in mind that it is really difficult to determine such based purely on someone’s forum nickname. I was really asking more for an expert on cannabinoids than a cancer research expert.

          1. Andrey Pavlov says:

            I would like to sincerely apologize for this. I honestly did not know this, and please keep in mind that it is really difficult to determine such based purely on someone’s forum nickname. I was really asking more for an expert on cannabinoids than a cancer research expert.

            Well, obviously with MadisonMD that is indeed excusable. But Gorski has his profile right here on SBM. And you can even look him up on wikipedia. He is a surgical oncologist with a PhD and has a cancer research lab at the Barbara Ann Karmanos cancer center in Detroit.

            And as I said in a different comment, you don’t need to be an expert in a particular molecule to be an expert enough to comment on how it does, could, or may apply to cancer. You need a cancer and medicine expert and that is what you’ve got.

      3. MadisonMD says:

        I say:

        There is nothing magical about compounds from cannabinoids versus compounds from other sources

        Beavis says:

        Actually, there is.

        hehehehe Tell it to you-know-who, Beavis.

  38. Andrey Pavlov says:

    Interesting that Beavis has no response to my dissection of his comments about the NHTSA study and MadisonMD’s simple question about doctors toking up before going into work.

    Well, what say you Beavis? Are you really a genuinely interested layman who came here to learn or was I right in the first place that you are merely someone who has already decided the answer to your questions and are merely here trying to show us how wrong we are about the state of evidence and research on cannabis?

    1. Windriven says:

      “Interesting that Beavis has no response to my dissection of his comments about the NHTSA study and MadisonMD’s simple question about doctors toking up before going into work.”

      Perhaps not so much interesting as predictable. Confronted by reality there really isn’t all that much to say.

      1. Andrey Pavlov says:

        Oh, I know that Windriven. It was indeed a bit tongue in cheek.

        But he isn’t a true troll and he isn’t nearly as blinkered as many of the others here who fancy themselves iconoclasts. I still think there is some hope for him. And I’d like to give him the opportunity to prove it.

        1. Beavis says:

          YIkes! Relax, people. I’ve gotten myself into more discussions than I have time to keep up with at the moment. I’m only one person and there are quite a few of you. Reading studies is quite time consuming as well. I intend to respond to all, in time.

          I swear it seems like some of you sit here for hours every day hitting the refresh button so you can be the first to pounce on any poor layman who dares question any of the regulars or even ask (what you might think are) stupid questions. Science is all about asking questions, even dumb ones.

          Since many are chomping at the bit, I wonder if a few of you cancer research experts might read through the government’s patent and see if anything in there might add to any of the ongoing discussions concerning cannabiniods and cancer. There is a lot of discussion about THC and CBD, tolerability and toxicity, antioxidant effects, treatment action, etc. I mean, for example, maybe some biologic process involved in say, stroke damage or treatment action that they discuss might also be highly relevant to some specific cancer. Maybe a few things will jump out at you…

          United States Patent 6,630,507
          “Cannabinoids as antioxidants and neuroprotectants”
          http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.htm&r=1&f=G&l=50&s1=6630507.PN.&OS=PN/6630507&RS=PN/6630507

          1. MadisonMD says:

            @Beavis: It’s because you came here with silly claims and–at least at first–refused to listen to rational critiques. But to give you some credit, you actually seemed to come around and acknowledge some of these claims a bit… but not enough to admit you were wrong on some key points.

            But now you ignore all that and change the topic–now you are just asking questions about a patent you found (one of many on cannabis and cannaboids, why this one?)– I’m not too interested because, this being SBM,, patents fail to provide good evidence of efficacy or safety…

            1. Windriven says:

              Bevis came and remains a proseletyzer, not an investigator. Cannabis is grail kept from the needful people by an evil government and its medical-industrial complex lackeys. Having been repeatedly dope-slapped with reality, he is simply changing his angle of attack.

              It takes a peculiar arrogance to waddle into a community of scientists armed with little more than the hard certainty of the zealot and proceed to tell everyone what’s what.

          2. KayMarie says:

            I stopped as soon as I got to antioxidant in the title.

            Antioxidants are one of those supposed miracles that have never in all the history of studying them panned out. Even though many many supplement manufacturers consider their new and improved antioxidant the one that will be the one that cures all, once the sales from the last one drops off. What have the run out of fruits no one in America heard of and now we need to move on to pot?

            Diets that are high in antioxidants may be protective, but there is no evidence bumping up artificially one or more antioxidants cures anything. If anything artificially increasing one or two antioxidants tends to increase the risk for cancer at least in high risk individuals.

            Why the diet works may be more what the entire diet looks like (what you don’t eat when you eat 5 or more servings of fruits and veggies) rather than what one component or one class of components you get more than the average amount of.

            Every antioxidant is also an oxidant. The redux equation goes both ways and it depends on the conditions. The amounts we get in some diets already eaten by some human beings seem to be about the right amount. There is no evidence adding more and more and more and more of any particular one does anything beneficial.

            Sounds like they are just trying to hitch the something in pot must absolutely be a cure all wagon to the antioxidants are the king of cure all carriage.

            You want antioxidants proven to do something, eat at least 5 servings of fruits and veggies every day. Eat a variety of them, preferably get at least a couple of different colors of them (so not all green or all yellow) regularly so you get a wide variety of antioxidants and other potential antimutagens from your diet. Including cabbage family veggies as part of the mix at least a few times a week seems reasonable as well.

            Even more important if the only evidence of the antioxidant or other protective stuff they provide is in cell culture. Like I said this may be one of the few times where the gestalt is way more important than any one thing getting used to make up for not following Mom’s advice to eat your veggies, or improve on that advice.

          3. Andrey Pavlov says:

            @ beavis:

            No mate, we just happen to be pretty good at what we do. Which is why, for example, it took me only about 5 minutes to find the relevant parts of the NHTSA report to demonstrate that you clearly hadn’t actually read the report. Which is actually what I’d expect – it is rather long after all. The thing is though that you come here bandying around these “facts” of yours and including in your opening volley the rather sarcastic comment about vodka being 8 times more potent than beer ermagerd!! This ain’t our first time at the rodeo and we can get a pretty good sense of a person’s thought process pretty quickly. And I’d say we rather nailed it with you, precisely as MadisonMD said.

            You’ll also note that I did give you some credit where you deserved it. We here – myself included – don’t just bash for the sake of bashing. I’ll acknowledge when an interlocutor deserves kudos but I also don’t hold back when a bad idea needs a good bash. Also, unlike you, I can (and do) admit when I am wrong. As Windriven pointed out, you still have not responded to the rather important and serious critiques of your evidence and thoughts on the matter but managed to squeeze out this rather inane question about a patent.

            But I’ll give you the benefit of the doubt and distill down the two points for you to address.

            Firstly, I demonstrated how your read of the NHTSA study was false and your rhetoric involved evasive language and moving goalposts. Do you admit your error and thus change your opinion on the matter, or do you have a rebuttal?

            Secondly, and I think even more incisive, is MadisonMD’s question. Please do answer:

            So, Beavis, I’m wondering if you would be OK with your physician practicing medicine– actually admitting you to the hospital or operating on you– after a joint or two?

            Yes or no? And why do you give the answer you choose?

            1. Andrey Pavlov says:

              Hmm… and a flounce off from Beavis?

              I’m not terribly surprised, but I did hold out some hope. Prove me wrong Beavis!

            2. Beavis says:

              ” your opening volley the rather sarcastic comment about vodka being 8 times more potent than beer ”

              That comment was intentionally dripping with sarcasm, in order to point out the absurdity and false double standard (which seems VERY common when discussing cannabis for some reason) presented in the post I was replying to. Logically, if your drug of choice is 2x, 3x or even 8x more potent than what you normally use or formerly used, then you would merely consume 1/2, 1/3 or 1/8 as much respectively to achieve the same effect. Higher potency is not, in itself, a problem or something to be feared, particularly when discussing something that is pretty easy to self-titrate.

          4. Beavis says:

            I realize that most (if not ALL) of you are indeed cancer research experts. I also realize that most of you are NOT cannabinoid experts and many don’t know all that much about cannabinoids and the many ways they actually affect the human body, which is why I mentioned this patent and posted what I did. I thought that perhaps by reading the entire patent that one or more of you cancer research experts might POSSIBLY learn at least SOMETHING more about cannabinoids than you currently know and it might POSSIBLY add something useful to one or more of the current discussions, or even possibly spur new discussions, including adding ACTUAL NUMBERS OR DATA in some of the cases where some of you merely ASSUMED things about cannabinoids. If your minds are indeed closed (e.g. those who refuse to even read it) and you are definitely not interested in learning more about how cannabinoids affect the human body and how that could POSSIBLY relate to cancer research, then I would probably ask why you are posting in a topic that deals with “cannabinoids and cancer” in the first place… (I’m mainly addressing people here who refuse to even READ the patent OR learn more about cannabinoids than they currently know).

            1. Andrey Pavlov says:

              @beavis:

              Stop deflecting with bull$hit. Patents tell us nothing we don’t know already because patents aren’t scientific information. Period. If there is scientific information in there, then we want the original source documentation of it, not second hand from a patent. Provide the links to that data and perhaps you’ll get some more interest in evaluating that.

              And yes, we are experts in medical sciences. One does not need to be an expert in a specific class of molecules to be able to field the first and most fundamental questions about them. Meaning that learning something new and nuanced about cannabinoids is not going to magically make the objections we have made so far go away. Those objections are based upon what we already do know about cannabinoids and are a point of impasse. Like the serum concentrations necessary to elicit effects in cell cultures. There is nothing any of us could possibly learn about cannabinoids that will change the fact that the levels are orders of magnitude higher than those necessary to induce psychotropic effects.

              At least you finally answered MadisonMD’s question. But you completely and utterly missed the point.

              You don’t want your doctor to smoke weed before coming on shift to take care of you? Why not Beavis? Is it, oh I dunno, just maybe because you recognize that marijuana intoxication impairs judgment? You then even manage to go on and say that you would be even more stringent for surgeons! Could that be because it also affect motor skills?

              Gee Beavis, what two things are pretty important for driving a car? Could it be judgment and motor skills? So magically marijuana smoking will somehow not have a net negative effect on a cognitive and motor skill task like driving, but it will on doctoring? Do you not see the logical conundrum you are in here?

              Next you go on to monkey studies and toxicity. You ask a question:

              I wonder, if humans ARE able to reasonably tolerate such a dose, would that change researchers’ opinion of the viability of cannabinoids in cancer treatment at all?

              The answer is yes, that would change our opinions… slightly. The reason only slightly is twofold. Firstly, we recognize that some subtle and rare effects will inevitably be missed until Phase IV of drug testing. Having something that requires such high concentrations is raising the risk for such effects. Given the rather lackluster performance of cannabinoids on cancer that wouldn’t be justifiable risk. So we would need that and data showing us much better performance of cannabinoids on cancer.

              But also, because of this:

              had little effect but liver and kidney weights rose 13–56% above controls without morphologic changes.”

              That is very concerning. Raising organ weights, with or without morphological change, on the short timescale of an experiment like this is very concerning for what the longer term effects would be. That point would need to be well addressed before any thoughts of human toxicity are broached.

  39. Beavis says:

    “Provide the links to that data and perhaps you’ll get some more interest in evaluating that. ”

    Fair enough. If you tell me what data in there interests you then I can try to find links to that data (I’m pretty good at internet searching). As a layman, however, I have no idea what data might be interesting to a cancer researcher.

    “There is nothing any of us could possibly learn about cannabinoids that will change the fact that the levels are orders of magnitude higher than those necessary to induce psychotropic effects. ”

    I believe this is the second time you’ve said something along these lines. What do the levels “necessary to induce psychotropic effects” have to do with medical use? Psychotropic effects are merely a SIDE EFFECT of a significant amount of THC in absence of sufficient CBD quantities.

    “You don’t want your doctor to smoke weed before coming on shift to take care of you? Why not Beavis? Is it, oh I dunno, just maybe because you recognize that marijuana intoxication impairs judgment? You then even manage to go on and say that you would be even more stringent for surgeons! Could that be because it also affect motor skills?”

    I, unlike you, realize that drug use does not occur in a vacuum. Since we are talking (in this hypothetical situation) about irresponsible people who are willing or likely to drive and/or work while knowingly intoxicated, it stands to reason that if you somehow prevent them from doing those things under the influence of cannabis that they would likely substitute another, potentially MORE dangerous, drug in its place. No?

    Driving and surgery are not the same thing. I can easily imagine circumstances where the TINIEST of mistakes by a surgeon could easily be expected to kill the patient. As for driving, I am also aware that just about everyone makes an almost constant stream of small mistakes (such as checking out that hot girl on the corner, changing the radio station, looking at gas prices or a billboard, etc.) while driving that although they may raise accident risk, the VAST majority of the time they do not result in any problems. Driving has a FAR larger margin of error than does surgery, or doctoring in general.

    Also, consider that THC (or any other drug we might discuss) may cause impairments that while not affecting driving, could profoundly affect surgery, such as hand steadiness (quoted from the NHTSA study):

    “Neither hand steadiness nor body sway were related to
    performance in the standard driving test or the car following test”

    “The last study, for example, showed a highly significant effect of THC on hand unsteadiness but not on driving in urban traffic. ”

    So, while one’s hands being a bit unsteady may not adversely affect driving, no doubt you will agree that it can certainly PROFOUNDLY affect surgery.

    “The answer is yes, that would change our opinions… slightly.”

    How much would it change your opinions if, say, humans were capable of reasonably tolerating 10x the dose needed to reach the IC50 concentrations?

    ” had little effect but liver and kidney weights rose 13–56% above controls without morphologic changes.”

    That is very concerning.”

    Okay. Fair enough. However, my (and KayMarie’s) question about whether those levels are sufficient to reach the IC50 values in the studies has not yet been answered. If those dosages are HIGHER than the levels that would be required for treatment, then consider that perhaps a lower dosage would have showed considerably less or even no such side effects.

    1. Andrey Pavlov says:

      Oh Beavis.

      Fair enough. If you tell me what data in there interests you then I can try to find links to that data

      I’m afraid that’s not the way in which we operate in scientific circles. Find the parts that you find compelling, find the actual data relevant to it, and we go from there. That and the fact that we here are rather busy and don’t have the time or desire to try and prove your points for you. If you have a case, make it. If you don’t admit it and move on. It isn’t the duty of others to try and foster your pet ideas, particularly when we don’t think they are particularly promising.

      What do the levels “necessary to induce psychotropic effects” have to do with medical use? Psychotropic effects are merely a SIDE EFFECT of a significant amount of THC in absence of sufficient CBD quantities.

      Well Beavis, I already explained myself. I’ll explain again.

      What is the difference between an effect and a side effect? Nothing. They are all effects. We call something a “side effect” when it has an effect we don’t desire. Some drugs have side effects in one clinical context and effects in a different one.

      For example, viagra. The “effect” is an erection, correct? Well, I also happen to use viagra in my patients with pulmonary hypertension as a life saving drug. So when a person takes viagra for erectile dysfunction the effect is an erection and the side effect is decrease pulmonary artery pressures. When I give to a patient with pulmonary hypertension then the effect is decreased pulmonary artery pressures and the side effect is an erection. To account for this we administer the drug differently in the two contexts so that it only reaches the lung in the latter (via a catheter infusing it into the vena cava at a low but steady dose).

      So the point is that you cannot say that the psychotropic effects are “just a side effect” as if that doesn’t matter to the question at hand. There is no pharmacological difference between “effect” and “side effect.”

      So, what this means relevant to cannabis is that if there is any effect at tiny serum concentrations then it stands to reason that there are likely to be other effects that become more pronounced (or even changed) when you massively increase the amount in the serum.

      And yes, THC has more psychotropic effects, but CBD is not entirely devoid of them. And they do not exactly counterbalance each other. The point stands in general though – we see some sort of effect at tiny doses. Cranking the dose to 11 can only serve to magnify existing effects and produce ones we don’t yet see.

      So let me recap – drugs have what is called a http://en.wikipedia.org/wiki/Therapeutic_index“>therapeutic index which is the range between minimum dose for an effect and minimum dose for toxicity. Most drugs we use have a decent sized index, but it is pretty much never on the scale of multiple orders of magnitude. So if the minimum effect is tiny and the effect in cell culture is multiple orders of magnitude higher it is much more likely that this dose will be beyond the therapeutic index.

      Since we are talking (in this hypothetical situation) about irresponsible people who are willing or likely to drive and/or work while knowingly intoxicated, it stands to reason that if you somehow prevent them from doing those things under the influence of cannabis that they would likely substitute another, potentially MORE dangerous, drug in its place. No?

      So let me get this straight… your argument is that if we prevent people from smoking weed before they drive they will do worse drugs before driving? No. That is, quite honestly, rather silly thinking and not supported by any evidence.

      Plus, that still doesn’t actually address the question nor does it justify your position on driving while under the influence of marijuana. Your claim is that smoking weed does not increase your risk of traffic accidents. Your response here in no way refutes that. At best you are trying to say we should choose the lesser of evils, and that marijuana is the lesser evil. We here actually agree. But the argument we have been having is that you are trying to assert it is not evil at all.

      Driving and surgery are not the same thing. I can easily imagine circumstances where the TINIEST of mistakes by a surgeon could easily be expected to kill the patient.

      Funny that, I can easily imagine myriad circumstances where the TINIEST mistake by a driver can kill him, his passengers, and many other people.

      As for driving, I am also aware that just about everyone makes an almost constant stream of small mistakes (such as checking out that hot girl on the corner, changing the radio station, looking at gas prices or a billboard, etc.) while driving that although they may raise accident risk, the VAST majority of the time they do not result in any problems. Driving has a FAR larger margin of error than does surgery, or doctoring in general.

      And you, yet again, dodge the entire point. Yes, we can agree that driving has a larger margin for error than doctoring. But the point of MadisonMD’s question is to illustrate that you actually are admitting that marijuana makes the risk higher, contra to your claim. If you wish to now try and claim that the risk imparted by weed smoking is smaller than the margin of error allowable in driving, then that is different to what your argument has been. But more importantly it is not at all supported by the evidence. Otherwise there wouldn’t be much evidence at all that it increases risk and, even though data is conflicting, it is undeniable that there still exists plenty of data to support the increased risk. Additionally, it would necessarily mean that the risk is dose dependent. Which is something we’ve already agreed upon – take a tiny toke and it probably doesn’t increase risk enough to matter. Get baked and it does. Which is now where your sarcastic vodka vs beer comment comes into play: it is easier to get higher than you intended if the amount you need to smoke is significantly less because the ganj is more potent.

      In any event, you’ve illustrated that you do actually accept precisely what I have been saying – that the prior likelihood of marijuana intoxication leading to increased risk is undeniably there. Next take a bunch of conflicted data with at least a preponderance of it showing said increase risk and combine that with a dose response and you’ve arrived at our conclusion: smoking weed increases risk of traffic accidents.

      How much would it change your opinions if, say, humans were capable of reasonably tolerating 10x the dose needed to reach the IC50 concentrations

      Well then obviously the issue would have been addressed. But the data demonstrating that doesn’t exist and the prior probability is on the rather low end, as I described above.

      In other words, yes if everything about the issue were different then yes, we’d have different opinions. The problem is that you have those opinions without the different data.

      If those dosages are HIGHER than the levels that would be required for treatment, then consider that perhaps a lower dosage would have showed considerably less or even no such side effects.

      Sure. And if your grandmother had balls she’d be your grandfather.

      This is science based medicine, Beavis. Not “speculate about what may or may not be and argue as if it is because that’s what I’d like it to be.”

      Logically, if your drug of choice is 2x, 3x or even 8x more potent than what you normally use or formerly used, then you would merely consume 1/2, 1/3 or 1/8 as much respectively to achieve the same effect

      Certainly there would be that trend. But in actuality, it simply doesn’t work out that way. And if you actually knew stoner culture and weed smoking habits you should know this. People don’t buy a nug of Trainwreck so that they can take a micro-hit to get the same high as Sour Diesel. Additionally the paraphernalia for smoking tends to fit certain volumes of weed rather than titrating to effect. You don’t pack 1/8 a bowl because your stuff is 8 times stronger.

      So while I agree with you that in general the concerns about stronger weed are indeed vastly overblown, the fact that it is stronger will and does lead to “THC creep” if you will. It is simply easier to get more THC in your body. And since we’ve established that there is a dose response curve in terms of risk, that absolutely plays into the question of driving under the influence of weed. Not a huge effect, mind you, I agree partly with you here. But your sarcastic volley belied the fact that you haven’t really given the matter much deep and nuanced thought. You’ve merely come to a rather superficial and pedestrian conclusion and decided to run with it because it sounds good.

      And you still haven’t addressed my demonstration that your reading of the NHTSA paper was wrong.

    2. MadisonMD says:

      If you tell me what data in there interests you then I can try to find links to that data

      OK, sure.

      The first hoop*: Show a study wherein a cannaboid (or any other chemical) is given to some animal (usually a mouse) with a tumor (human xenograft in immunodeficient animal, or better yet an actual mouse cancer induced in a transgenic animal) and, as a result, the tumor definitively shrinks without actually killing the animal.

      Second hoop: Cancers are extremely diverse genetically and phenotypically, so identify which particular type or genetic subtype of cancer is likely to respond to the cannaboid (or any other chemical). For bonus points, describe why it works in this type– as knowledge of the mechanism can anticipate how cancer might evade the drug and let us assess if the drug is working in humans in the way that is necessary to elicit the intended effect.

      Have at it. I’d suggest Google Scholar or pubmed search engines, not just google.

      *Keep in mind there are other hoops as many many many chemicals that shrink tumors in mice have failed execrably in humans. But, this would be a start.

      1. Windriven says:

        Ahhh the arrogance of ignorance; no grasp of the fiendish complexity of doing battle with the Emperor of All Maladies. Isn’t it just a matter of embracing the weed? I mean there’s no cancer in Jamaica, right mon?

      2. KayMarie says:

        An example of a second hoop article.

        http://www.ncbi.nlm.nih.gov/pubmed/24369462. So this biological mechanism is about tumors that tend to grow more in the presence of sex hormones. Not all tumors grow more in the presence of sex hormones, some do. The question then is does it actually change the trajectory of the tumor (after all tumors have lots of receptors for lots of things). Also would this mechanism do more than blocking sex hormones to limit the growth while you are usually doing other things to kill it off. So this may not be a does it all by itself type of treatment mechanism.

        This is a free PMC article which means you can read the whole thing for free.

        You will notice in the conclusions they say

        Therefore, for this vital reason, and although it is early days, the endocannabinoid system has become an attractive novel target for pharmacological intervention in the fight against many hormone-related cancers.

        Which indicates this is about looking at what kinds of things might we want to maybe start looking at to see if we maybe should do hoop 1 type of study, but we may not even be quite at that point yet, and certainly is not proof that it cures all cancers in all humans or really addresses much about can you even get enough in to do something.

        And like we’ve said there is some pre-clinical evidence that there is some cancers it might have some potential for, but no more than hundreds if not thousands of other compounds both found in nature or completely invented by man. But certainly doesn’t back up the assertions of the websites that make marijuana something completely unlike all other plants or extracts of it are unlike every other chemical that has ever gone through some pre-clinical evaluations. (that is it cures all in doses that are normal for humans to get to through recreational use).

        1. KayMarie says:

          One note about receptors and things that may from nature attach to them.

          Sometimes a sythentic but altered from nature compound will do better than a whole plant extract or even a specific compound extracted from the plant. We can often do things that either makes it stay on the receptor longer or block it (or activate it) more effectively than the original compounds of interest.

          Based on some of the other data presented I wouldn’t be surprised that should this ever get into the testing it in humans stage it isn’t which strain from the medical marijuana shop but some synthetic derivative of a compound. Not because big pharma haz the ebils, but because more often than not this is how it works. We found something in nature but can tweak it to do something more effectively at lower doses and/or avoids side effects.

        2. MadisonMD says:

          Thanks for the review article cite. A few points:

          (1) The authors only say that CB1/CB2 receptors are present in a high fraction of tumors in breast, prostate, and endometrial cancers. This doesn’t necessarily mean these receptors are absent in other types.

          (2) Finding expression of CB1/CB2 receptors is not strong evidence that targeting these receptors is effective. Such strong evidence would require (a) evidence of anticancer effects specific to expression. i.e. cells that do express CB1/CB2 should respond at much lower questions than those lacking these receptors; (b) evidence that downregulation of CB1/CB2 protein would also have anticancer effects.

          (3) Within breast cancer, they find CB1/CB2 receptors on hormone-receptor negative cell types (MDA-MB-231, MDA-MD-468, and SkBr3), and correlates more highly with HER2– which seems to blow up the hypothesis that the effects are specific to hormone sensitive cancers.

          (4) The ligands for CB1/CB2 in cannabis mainly include THC and the drug targets that mediate its psychoactivity. Therefore, if this is used for this purpose, the side effects of getting high are unavoidable and limit the dose that is tolerable.

          (5) Finally, THC is FDA approved and has been used for decades in cancer patients. (OK, not used much any more because it is not very effective). I’d like to see some case reports or series of marked cancer improvements on THC that could not be attributed to other reasons. If truly effective, that should have happened by accident more than a few times with an FDA approved drug for nausea in cancer for a drug approved over 30 years ago.

  40. Andrey Pavlov says:

    @beavis:

    Did you flounce off mate?

  41. Britney says:

    My battle with Breast cancer started 2 years ago, after so many Chemo, Radiation and other natural therapy treatment that i took just to cure my Breast cancer, it all did not work for my condition. I have been treating this disease for the past 2 years, but today i am here telling the world about my final victory over Breast cancer with the help of cannabis oil medication. This is a breakthrough in my family with so much Joy in our life today, i do really appreciate all the help and contribution from every member of my family for all they did for me. And if you have any kind of cancer diseases, there is no need to waste money on Chemo or Radiation, go get cannabis oil from UK cancer research centre( ukcancerresearchcentre@gmail.com ),this is a medication that totally kill cancer cells.

    Britney Alja

    1. Windriven says:

      Glad to learn you are in remission, but I would not be in a hurry to credit the oil. In any event, anecdotes, even pleasant ones, carry no weight here.

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