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Cannabis, Cannabinoids And Cancer – The Evidence So Far

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Cannabis, Cannabinoids and Cancer – The Evidence So Far

April 29, 2014 | by Anonymous


Photo credit: Gerhard Taatgen Jr.

Note: This article was written by Kat Arney and first appeared as a blog post on Cancer Research UK.

You can read the original article here and donate to Cancer Research UK here.

Few topics spark as much debate on this blog and on our Facebook page than cannabis.

So we thought we’d take a look at the common questions raised about the evidence and research into cannabis, cannabinoids (the active chemicals found in the plant and elsewhere) and cancer, and address some of the wider issues that crop up in this debate.

We’ve broken it down under a number of headings:

  • What are cannabinoids and how do they work?
  • Can cannabinoids treat cancer? (including lab research, clinical research and unanswered questions)
  • Can cannabis prevent or cause cancer?
  • What about controlling cancer symptoms such as pain or sickness?
  • Is Cancer Research UK investigating cannabinoids?
  • It’s natural so it must be better, right?
  • “Have you seen this video? This guy says cannabis cures cancer!”
  • “It’s all a big conspiracy – you don’t want people to be cured!”
  • “What’s the harm? There’s nothing to lose.”
  • “Big Pharma can’t patent it so they’re not interested.”
  • “Why don’t you campaign for cannabis to be legalised?”

This post is long, but can be summarised by saying that at the moment there isn’t enough reliable evidence to prove that cannabinoids – whether natural or synthetic – can effectively treat cancer in patients, although research is ongoing around the world.

Read on to get the full picture.


What are cannabinoids and how do they work?

Cannabinoids” is a blanket term covering a family of complex chemicals (both natural and man-made) that lock on to cannabinoid receptors – protein molecules on the surface of cells.

Humans have been using cannabis plants for medicinal and recreational purposes for thousands of years, but cannabinoids themselves were first purified from cannabis plants in the 1940s. The structure of the main active ingredient of cannabis plants – delta-9 tetrahydrocannabinol (THC) – was discovered in the 60s. It wasn’t until the late 1980s that researchers found the first cannabinoid receptor, followed shortly by the discovery that we create cannabinoid-like chemicals within our own bodies, known as endocannabinoids.


The CB1 and CB2 receptors.Image source

We have two different types of cannabinoid receptor, CB1 and CB2, which are found in different locations and do different things. CB1 is mostly found on cells in the nervous system, including certain areas of the brain and the ends of nerves throughout the body, while CB2 receptors are mostly found in cells from the immune system. Because of their location in the brain, it’s thought that CB1 receptors are responsible for the infamous ‘high’ (known as psychoactive effects) resulting from using cannabis.

Over the past couple of decades scientists have found that endocannabinoids and cannabinoid receptors are involved in a vast array of functions in our bodies, including helping to control brain and nerve activity (including memory and pain), energy metabolism, heart function, the immune system and even reproduction. Because of this molecular multitasking, they’re implicated in a huge range of illnesses, from cancer to neurodegenerative diseases.

Can cannabinoids treat cancer?

There is no doubt that cannabinoids – both natural and synthetic – are interesting biological molecules. Hundreds of scientists around the world are investigating their potential in cancer and other diseases – as well as the harms they can cause – brought together under the blanket organisation The International Cannabinoid Research Society.

Researchers first looked at the anticancer properties of cannabinoids back in the 1970s, andmany hundreds of scientific papers looking at cannabinoids and cancer have been published since then. This Wellcome Witness seminar is also fascinating reading for aficionados of the history of medical cannabis, including the scientific, political and legal twists. [updated KA 26/03/14]

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.

Let’s take a closer look at the evidence.

Lab research

Virtually all the scientific research investigating whether cannabinoids can treat cancer has been done using cancer cells grown in the lab or animal models. It’s important to be cautious when extrapolating these results up to real live patients, who tend to be a lot more complex than a Petri dish or a mouse.


Virtually all the research into cannabinoids and cancer so far has been done in the lab.

Through many detailed experiments, handily summarised in this recent article in the journal Nature Reviews Cancer, scientists have discovered that various cannabinoids (both natural and synthetic) have a wide range of effects in the lab, including:

  • Triggering cell death, through a mechanism called apoptosis
  • Stopping cells from dividing
  • Preventing new blood vessels from growing into tumours
  • 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

All these effects are thought to be caused by cannabinoids locking onto the CB1 and CB2 cannabinoid receptors. It also looks like cannabinoids can exert effects on cancer cells that don’t involve cannabinoid receptors, although it isn’t yet clear exactly what’s going on there.

So far, the best results in the lab or animal models have come from using a combination of highly purified THC and cannabidiol (CBD), a cannabinoid found in cannabis plants that counteracts the psychoactive effects of THC. But researchers have also found positive results using synthetic cannabinoids, such as a molecule called JWH-133.

It’s not all good news though, as there’s also evidence that cannabinoids may also have undesirable effects on cancer.

For example, some researchers have found that although high doses of THC can kill cancer cells, they also harm crucial blood vessel cells, although this may help their anti-cancer effect by preventing blood vessels growing into a tumour. And under some circumstances, cannabinoids can actually encourage cancer cells to grow, or have different effects depending on the dosage and levels of cannabinoid receptors present on the cancer cells[Edited for clarity and to add reference - KA 27/07/12]

Others have discovered that activating CB2 receptors may actually interfere with the ability of the immune system to recognise and destroy tumour cells, although some scientists have found that certain synthetic cannabinoids may enhance immune defences against cancer.

Furthermore, cancer cells can develop resistance to cannabinoids and start growing again, although this can be got round by blocking a certain molecular pathway in the cells known as ALK.

And yet more research suggests that combining cannabinoids with other chemotherapy drugs may be a much more effective approach. This idea is supported by lab experiments combining cannabinoids with other drugs including gemcitabine andtemozolomide.

Combining cannabinoids with other chemotherapy drugs may be a much more effective approach

Clinical research

But that’s the lab – what about clinical research involving people with cancer? Results have been published from only one clinical trial testing whether cannabinoids can treat cancer in patients, led by Dr Manuel Guzman and his team in Spain. Nine people with advanced, terminal glioblastoma multiforme – an aggressive brain tumour – were given highly purified THC through a tube directly into their brain.

Eight people’s cancers showed some kind of response to the treatment, and one didn’t respond at all. All the patients died within a year, as might be expected for people with cancer this advanced.

The results from this study show that THC given in this way is safe and doesn’t seem to cause significant side effects. But because this was an early stage trial, without a control group, it’s impossible to say whether THC helped to extend their lives. And while it’s certainly not a cure,  the trial results suggest that cannabinoids are worth pursuing in clinical trials.

There is also a published case report of a 14-year old girl from Canada who was treated with cannabis extracts (also referred to as “hemp oil”), but there is limited information that can be obtained from a single case treated with a varied mixture of cannabinoids. More published examples with detailed data are needed in order to draw a fuller picture of what’s going on.[updated 26/03/14, KA]

A handful of other clinical trials of cannabinoids are currently being set up. We are helping to support the only two UK trials of cannabinoids for treating cancer, through our Experimental Cancer Medicine Centre (ECMC) Network funded by Cancer Research UK and the devolved Departments of Health. One early-stage trial is testing a synthetic cannabinoid called dexanabinolin patients with advanced cancer, and the other is an early-stage trial testing a cannabis extract called Sativex for treating people with glioblastoma multiforme brain tumours. [Edited to add more information about the trials - KA 22/08/12, KA 24/03/14]

Unanswered questions

There are still a lot of unanswered questions around the potential for using cannabinoids to treat cancer.


An antique bottle of cannabis extract. Image source

The biggest issue is that there isn’t enough evidence to show that they can treat cancer in people, although research is still ongoing around the world.

And it’s not clear which type of cannabinoid – either natural or synthetic – might be most effective, what kind of doses might be needed, or which types of cancer might respond best to them. So far there have been intriguing results from lab experiments with prostate, breast, lung cancer, skin, bone and pancreatic cancers, glioma brain tumours and lymphoma. But the take-home message is that different cannabinoids seem to have different effects on various cancer types, so they are far from being a ‘universal’ treatment.

Most research has been focused on THC, which occurs naturally in cannabis plants, but researchers have found that different cannabinoids seem to work better or worse different types of cancer cells. Lab experiments have shown promising results with THC on brain tumour and prostate cancer cells, while CBD seems to work well on breast cancer cells.

Then there’s the problem of the psychoactive effects of THC, particularly at high doses, although this can be counteracted by giving it together with CBD. Because of this problem, synthetic cannabinoids that don’t have these effects might be more useful in the long term.

There are also big questions around the best way to actually get the drugs into tumours. Because of their chemical makeup, cannabinoids don’t dissolve easily in water and don’t travel very far in our tissues. This makes it hard to get them deep into a tumour, or even just deliver them into the bloodstream in consistently high enough doses to have an effect.

The clinical trial led by Dr Guzman in Spain involved directly injecting cannabinoids into patients’ brains through a small tube. This isn’t an ideal method as it’s very invasive and carries a risk of infection, so researchers are investigating other delivery methods such as tablets, oil injections, mouth sprays or even microspheres.

We also don’t know whether cannabinoids will help to boost or counteract the effects of chemotherapy, nor which combinations of drugs might be good to try. And there are currentlyno biological markers to help doctors identify who might benefit from cannabinoids and who might not – remember that one patient on the brain tumour trial failed to respond to THC at all.

None of these issues are deal-breakers, but these questions need answering if there’s any hope of using cannabinoids to effectively and safely treat cancer patients.

It’s worth remembering that there are hundreds of exciting potential cancer drugs being developed and tested in university, charity and industry labs all over the world – cannabinoids are merely a small part of a much larger picture.

There are hundreds of exciting potential cancer drugs being developed and tested in university, charity and industry labs all over the world – cannabinoids are merely a small part of a much larger picture

Most of these compounds will never make it into the clinic to treat patients for a huge range of reasons including toxicity, lack of effectiveness, unacceptable side effects, or difficulty of delivering the drug to tumours.

Without doing rigorous scientific research, we will never sift the ‘hits’ from the ‘misses’. If cannabinoids are ever to get into clinical use, they need to overcome these hurdles and prove they have benefits over existing cancer treatments.

Can cannabis prevent or cause cancer?

So that’s a brief look at cannabinoids to treat cancer. But can they stop the disease from developing? Or could they play a role in causing cancer?


There’s controversy around the health risks of cannabis.Image source

In experiments with mice, animals given very high doses of purified THC seemed to have a lower risk of developing cancer, and there has been some research suggesting that endocannabinoids (cannabinoids produced by the body) cansuppress tumour growth. But there’s no solid scientific evidence at the moment to show that cannabinoids or cannabis can cut the risk of cancer in people.

When it comes to finding out whether cannabis can causecancer, the evidence is a lot murkier. This is mainly because most people who use cannabis smoke it mixed with tobacco, a substance that definitely does cause cancer.

This complex issue recently hit the headlines when the British Lung Foundation released a study suggesting that the cancer risks of cannabis had been underestimated, although this has been questioned by some experts including Professor David Nutt.

What about controlling cancer symptoms such as pain or sickness?

Although there’s a lack of data showing that cannabinoids can effectively treat cancer, there is good evidence that these molecules may be beneficial in other ways.

As far back as the 1980s, cannabinoid-based drugs – including dronabinol (synthetic THC) andnabilone – were used to help reduce nausea and vomiting caused by chemotherapy. But there are now safer and more effective alternatives and cannabinoids tend to only be used where other approaches fail.

In some parts of the world – including the Netherlands – medical use of marijuana has been legalised for palliative use (relieving pain and symptoms), including cancer pain. For example, Dutch patients can obtain standardised, medicinal-grade cannabis from their doctor, and medicinal cannabis is available in many states in the US.

But one of the problems of using herbal cannabis is about dosage – smoking it or taking it in the form of tea often provides a variable dose, which may make it difficult for patients to monitor their intake. So researchers are turning to alternative dosing methods, such as mouth sprays, which deliver a reliable and regulated dose.

Large-scale clinical trials are currently running in the UK testing whether a mouth spray called Sativex (nabiximols) – a highly purified pharmaceutical-grade extract of cannabis containing THC and CDB – can help to control severe cancer pain that doesn’t respond to other drugs.

There may also be potential for the use of cannabinoids in combating the loss of appetite and wasting experienced by some people with cancer, although a clinical trial comparing appetite in groups of cancer patients given cannabis extract, THC and a placebo didn’t find a difference between the treatments.

Is Cancer Research UK investigating cannabinoids?

We want to see safe, reliable and effective treatments become available for patients as quickly as possible. We receive no government funding for our research, and it is all paid for by the generosity of the public.  This is obviously not a bottomless purse, and we do not have financial reserves to draw on.

Because of this limitation, we can only fund the very best research proposals that come to us that will bring benefits to people with cancer.  We’ve previously written in detail about how we fund research projects.

Cancer Research UK has funded research into cannabinoids, notably the work of Professor Chris Paraskeva in Bristol investigating the properties of cannabinoids as part of his research into the prevention and treatment of bowel cancer. He has published a number of papers detailing lab experiments looking at endocannabinoids as well as THC, and written an interesting reviewlooking at the potential of cannabinoids for treating bowel cancer.

Our funding committees have previously received other applications from researchers who want to investigate cannabinoids that have failed to reach our high standards for funding. If we receive future proposals that do meet these stringent requirements, then there is no reason why they would not be funded – assuming we have the money available to do so.

We support the only two UK clinical trials of cannabinoids for treating cancer through our national network of Experimental Cancer Medicine Centres, funded by Cancer Research UK and the devolved Departments of Health. One is an early-stage trial testing a synthetic cannabinoid called dexanabinol for people with advanced cancer, the other is an early-stage trial testing a drug calledSativex (an extract from cannabis plants) for people with glioblastoma multiforme brain tumours[Added 22/08/12 - KA, Updated KA 25/03/14]

“It’s natural so it must be better, right?”

There’s no doubt that the natural world is a treasure trove of biologically useful compounds. But whole plants or other organisms are a complex mix of hundreds of chemicals (not all of which may be beneficial) and contains low or variable levels of active ingredients. This makes it difficult to give accurate doses and runs the risk of toxic side effects.


Foxgloves – a source of medically useful chemicals.Image source

For example, foxgloves (Digitalis) are a useful source of chemicals called cardiac glycosides, first purified in 1785 – a date widely considered to be the beginning of modern drug-based medicine. These drugs are now used to treat many thousands of people around the world with heart failure and other cardiac problems. But the entire plant itself is highly toxic, and eating just a small amount can kill.

As another example, although the antibiotic penicillin was first discovered in a fungus, it doesn’t mean that someone should munch some mould when suffering an infection. In fact, the bug-beating powers of ‘natural’ penicillin are confined to a relatively small range of bacteria, and chemists have subsequently developed a wider range of life-saving antibiotics based on the drug’s structure.

Aspirin is another old drug, first discovered in the form of salicylic acid in white willow bark. But this naturally-occurring chemical causes severe stomach irritation, which led to the German company Bayer developing an alternative version – acetylsalicylic acid – which was kinder to the tummy. Aspirin is now arguably one of the most successful drugs of all time, and is still being investigated for its potential inpreventing or even treating cancer.

Numerous potent cancer drugs have also been developed in this way – purifying a natural compound then improving it and testing it to create a beneficial drug – including taxol (originally from yew leaves); vincristine and vinblastine (from rosy periwinkles); camptothecin (from the Chinese Xi Shu tree); colchicine (from crocuses); and etoposide (from the May Apple). And we recently wrote about a clinical trial being run by our scientists to test whether curcumin, a purified chemical from the curry spice turmeric, could help treat people with advanced bowel cancer.

But it bears repeating that the fact that these purified drugs in controlled, high doses can treat cancer doesn’t mean that the original plant (or a simple extract) will have the same effect.  So although cannabis contains certain cannabinoids, it doesn’t automatically follow that cannabis itself can treat cancer.

As we said above, there is no good evidence that natural cannabinoids, at the doses present in simple cannabis preparations, can treat cancer in patients. It’s also completely unknown whether there may be any other chemicals in ‘street’ cannabis extracts that could be harmful to patients or even encourage tumour growth.

“Have you seen this video? This guy says cannabis cures cancer!”

There is a strong and persistent presence on the internet arguing that cannabis can cure cancer. For example, there are numerous videos and unverified anecdotes claiming that people have been completely cured of cancer with cannabis, hemp/cannabis oil or other cannabis derivatives.


YouTube videos are not scientific evidence.

Despite what the supporters of these sources may claim, videos and stories are not scientific evidence for the effectiveness of any cancer treatment. Extraordinary claims require extraordinary evidence – YouTube videos are emphatically not scientific evidence, and we are not convinced by them.

Based on the arguments presented on these kinds of websites, it’s impossible to tell whether these patients have been ‘cured’ by cannabis or not. We know nothing about their medical diagnosis, stage of disease or outlook. We don’t know what other cancer treatments they had. We don’t know about the chemical composition of the treatment they got. And we only hear about the success stories – what about the people who have tried cannabis andnot been cured? People who make these bold claims for cannabis only pick their best cases, without presenting the full picture.

This highlights the importance of publishing data from scientifically rigorous lab research and clinical trials. Firstly because conducting proper clinical studies enables researchers to prove that a prospective cancer treatment is safe and effective. And secondly because publishing this data allows doctors around the world to judge for themselves and use it for the benefit of their patients.

This is the standard to which all cancer treatments are held, and it’s one that cannabinoids should be held to too. Internet anecdotes and videos prove nothing and benefit no-one – we need reliable, scientific research, which (as discussed above) is exactly what is going on.

“It’s all a big conspiracy – you don’t want people to be cured!”

As we’ve previously said, accusations that we are somehow part of a global conspiracy to suppress cancer cures are as absurd as they are offensive. Not only to the thousands of our scientists, doctors and nurses who are working as hard as they can to find more effective treatments for the complex set of challenging diseases we call cancer, but also the hundreds of thousands of people in the UK and beyond who support this life-saving work through generous donations of money, energy and time.


Our aim is to beat cancer through research

Our aim is to beat cancer, and we believe that the best way to do this through rigorous scientific research aimed at understanding cancer on a biological level and working out how to prevent, detect and treat it more effectively. This approach has helped to change the face of cancer prevention, diagnosis, treatment, leading to a doubling in survival rates over the past 40 years.

As a research-based organisation, we want to see reliable scientific evidence to support claims made about any cancer treatment, be it conventional or alternative.  The claims made for many alternative cancer therapies still require solid evidence to support them, and it often turns out that these ‘miracle cures’ simply don’t work when they’re put to the test.

This doesn’t mean there’s a conspiracy to suppress the “True Cure for Cancer” – it means that doctors and researchers want to see solid evidence that the claims made by people peddling these treatments are true.

This is vital because lives are at stake. Some people may think that a cancer patient has nothing to lose by trying an alternative treatment, but there are big risks.

“What’s the harm? There’s nothing to lose.”

If someone chooses to reject conventional cancer treatment in favour of unproven alternatives, including cannabis, they may miss out on treatment that could save or significantly lengthen their life. They may also miss out on effective symptom relief to control their pain and suffering, or the chance to spend precious time with their loved ones.

Furthermore, many of these unproven therapies come at a high price, and are not covered by the NHS or medical insurance. And, in the worst cases, an alternative therapy may even hasten death.

Although centuries of human experimentation tells us that naturally-occurring cannabinoids are broadly safe, they are not without risks. They can increase the heart rate, which may cause problems for patients with pre-existing or undiagnosed heart conditions. They can also interact with other drugs in the body, including antidepressants and antihistamines. And they may also affect how the body processes certain chemotherapy drugs, which could cause serious side effects.

There is also a reported case where a Dutch lung cancer patient took cannabis extract that had been bought from a street source. Within a matter of hours she was in hospital in a coma. This highlights the risks of taking ‘street’ cannabis extracts of unknown concentration and quality in an uncontrolled way, and accentuates the need for careful research into how best to use cannabinoids for treating patients.

It is a sad fact that although huge progress has been made over recent years, many thousands of people in the UK lose their lives to cancer every year – a situation that we urgently want to change through research. But when conventional treatment fails, there is little chance that turning to an unproven alternative touted on the internet will provide a cure.

When conventional treatment fails, there is little chance that turning to an unproven alternative touted on the internet will provide a cure

In this situation, we recommend that cancer patients talk to their doctor about clinical trials that they may be able to join, giving them access to new drugs and providing valuable data that will help other sufferers in future.

“Big Pharma can’t patent it so they’re not interested.”

Some people argue that the potential of cannabinoids is being ignored by pharmaceutical companies, because they can’t patent the chemicals occurring in cannabis plants. But pharma companies are not stupid, and they are quick to jump on promising avenues for effective therapies.

As we’ve shown, there are hundreds of researchers around the world investigating cannabinoids, in both private and public institutions. And there are many ways that these compounds can be patented – for example, by developing more effective synthetic compounds or better ways to deliver them.

On the flip side, other people argue that patients should be treated with ‘street’ or homegrown cannabis preparations, and that the research being done by companies and other organisations is solely to make money and prevent patients accessing “The Cure”. This is also a false and misleading argument, analogous to suggesting that patients in pain should buy heroin or grow opium poppies rather than being prescribed morphine by a doctor.

The best way to ensure that the benefits of cannabinoids – whether natural or synthetic – are brought to patients is through proper research using quality-controlled, safe, legal, pharmaceutical grade preparations containing known dosages of the drugs.

To do this requires time, effort and money, which may come from companies or independent organisations such as charities or governments. And, ultimately, this investment needs to be paid back by sales of a safe, effective new drug.

We are well aware of the issues around drug pricing and availability – for example, the recent situations with abiraterone and vemurafenib – and we are pushing for companies to make new treatments available at a fair price. We would also hope that if any cannabinoids are shown to be safe and effective enough to make it to the clinic, they would be available at a fair price for all patients that might benefit from them.

“Why don’t you campaign for cannabis to be legalised?”

As things currently stand, cannabis is classified as a class B drug in the UK, meaning that it is illegal to possess or supply it.

It is not for Cancer Research UK to comment on the legal status of cannabis, its use or abuse as a recreational drug, or its medical use in any other diseases. But we are supportive of properly conducted scientific research that could benefit cancer patients.

In summary

At the moment, there simply isn’t enough evidence to prove that cannabinoids – whether natural or synthetic – works to treat cancer in patients, although research is ongoing. And there’s certainly no evidence that ‘street’ cannabis can treat cancer.

As a research-based organisation, we continue to watch the progress of scientists around the world for advances that may benefit people with cancer. And although cannabinoid research is an interesting avenue, it’s certainly not the only one.

As a research-based organisation, we continue to watch the progress of scientists around the world for advances that may benefit people with cancer.


Reminder: This article was written by Kat Arney and first appeared as a blog post on Cancer Research UK.

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“It’s natural so it must be better, right?”

There’s no doubt that the natural world is a treasure trove of biologically useful compounds. But whole plants or other organisms are a complex mix of hundreds of chemicals (not all of which may be beneficial) and contains low or variable levels of active ingredients. This makes it difficult to give accurate doses and runs the risk of toxic side effects.




they spend 5 paragraphs dancing around the toxicity of marijuana. the bolded sentence implies a correlation of marijuana being toxic.


As a research-based organisation, we want to see reliable scientific evidence to support claims made about any cancer treatment, be it conventional or alternative.  The claims made for many alternative cancer therapies still require solid evidence to support them, and it often turns out that these ‘miracle cures’ simply don’t work when they’re put to the test.

This doesn’t mean there’s a conspiracy to suppress the “True Cure for Cancer” – it means that doctors and researchers want to see solid evidence that the claims made by people peddling these treatments are true.


oh, i thought they wanted reliable scientific evidence of marijuana toxicity? i guess not. instead they talk about foxglove and aspirin. isnt that strange?



There may also be potential for the use of cannabinoids in combating the loss of appetite and wasting experienced by some people with cancer, although a clinical trial comparing appetite in groups of cancer patients given cannabis extract, THC and a placebo didn’t find a difference between the treatments.



thats an interesting study. they tested cannabis extract vs synthetic thc vs placebo.

2.5mg 2x daily for 6 weeks.

what does 5mg of marijuana even look like ?


this is a cancer paper, why are they bringing up aids studies ?


why not bring up the cbd epilepsy study ?


the cbd study gave 200mg of cbd while the wasting study was only 1mg of cbd. maybe theres a theraputic dose huh? 1mg what a waste of time.


hemp in usa can be sold up to .3% thc. did they just feed hemp oil to the study participants?


the only positive research studies they link to on marijuana are for the cannabinoids themselves. then they turn that around and say the extracts of marijuana are useful but regular marijuana is not useful at all.


But it bears repeating that the fact that these purified drugs in controlled, high doses can treat cancer doesn’t mean that the original plant (or a simple extract) will have the same effect. So although cannabis contains certain cannabinoids, it doesn’t automatically follow that cannabis itself can treat cancer.


As we said above, there is no good evidence that natural cannabinoids, at the doses present in simple cannabis preparations, can treat cancer in patients. It’s also completely unknown whether there may be any other chemicals in ‘street’ cannabis extracts that could be harmful to patients or even encourage tumour growth.


its just like the Court of Appeals ruling. 'the extracts of marijuana are not marijuana'. what? that is a really dumb argument made by prohibitionists. its like saying extracting 99% alcohol from 70% alcohol isnt alcohol. its still alcohol. its still marijuana. just because you put it in a pill does not make it magically better.

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Antineoplastic activity of cannabinoids

A.E. Munson, L.S. Harris, M.A. Friedman, W.L. Dewey, and R.A. Carchman

Journal of the National Cancer Institute, Vol. 55, No. 3, September 1975

Supported by Public Health Service grant DA00490 from the National Institute on Drug Abuse, Health Services & Mental Health Administration; by a grant from the Alexander and Margaret Stewart Trust Fund; and by an institutional grant from the American Cancer Society.

Department of Pharmacology and the MCV/VCU Cancer Center, Medical College of Virginia, Virginia Commonwealth University. Richmond, Va. 23298


Lewis lung adenocarcinoma growth was retarded by the oral administration of delta-9-tetrahydrocannabinol, delta-8-tetrahydrocannabinol, and cannabinol (CBN), but not cannabidiol (CBD). Animals treated for 10 consecutive days with delta-9-THC, beginning the day after tumor implantation, demonstrated a dose-dependent action of retarded tumor growth. Mice treated for 20 consecutive days with delta-8-THC and CBN had reduced primary tumor size. CBD showed no inhibitory effect on tumor growth at 14, 21, or 28 days. Delta-9-THC, delta-8-THC, and CBN increased the mean survival time (36% at 100 mg/kg, 25% at 200 mg/kg, and 27% at 50 mg/kg;, respectively), whereas CBD did not. Delta-9-THC administered orally daily until death in doses of 50, 100, or 200 mg/kg did not increase the life-spans of (C57BL/6 X DBA/2) F (BDF) mice hosting the L1210 murine leukemia. However, delta-9-THC administered daily for 10 days significantly inhibited Friend leukemia virus-induced splenomegaly by 71% at 200 mg/kg as compared to 90.2% for actinomycin D. Experiments with bone marrow and isolated Lewis lung cells incubated in vitro with delta-8-THC and delta-9-THC showed a dose-dependent (10 -4 10 -7) inhibition (80-20%, respectively) of tritiated thymidine and 14C -uridine uptake into these cells. CBD was active only in high concentrations (10 -4)


Investigations into the physiologic processes affected by the psychoactive constitutuents of marihuana [delta-9-tetrahydrocannabinol (delta-9-THC) and delta-8-tetrahydrocannabinol (delta-8-THC)] purified from Cannabis sativa are extensive (1). However, only recently have attempts been made to elucidate the biochemical basis for their cytotoxic or cytostatic activity. Leuchtenberger et al. (2) demonstrated that human lung cultures exposed to marihuana smoke showed alterations in DNA synthesis, with the appearance of anaphase bridges. Zimmerman and McClean (3), studying macromolecular synthesis in Tetrahymena, indicated that very low concentrations of delta-9-THC inhibited RNA, DNA, and protein synthesis and produced cytolysis. Stenchever et al. (4) showed an increase in the number of damaged or broken chromosomes in chronic users of marihuana. Delta-9-THC administered iv inhibited bone marrow leukopoieses (5), and Kolodny et al. (6) reported that marihuana; may impair testosterone secretion and spermatogenesis.

Furthermore, Nahas et al. (7) showed that in chronic marihuana users there is a decreased lymphocyte reactivity to mitogens as measured by thymidine uptake. These and other (8) observations suggest that marihuana (delta-9-THC) interferes with vital cell biochemical processes, though no definite mechanism has yet been established. A preliminary report from this laboratory (9) indicated that the ability of delta-9-THC to interfere with normal cell functions might prove efficacious against neoplasms. This report represents an effort to test various cannabinoids in several in vivo and in vitro tumor systems to determine the kinds of tumors that are sensitive to these compounds and reveal their possible biochemical sites of action(s).

Materials and methods

The tumor systems used were the Lewis lung adenocarcinoma, leukemia L1210, and B-tropic Friend leukemia.

In vivo systems.

Lewis lung tumor: For the maintenance of the Lewis lung carcinoma, approximately 1-mm3 pieces of tumor were transplanted into C57BL/6 mice with a 15-gauge trocar. In experiments involving chemotherapy, 14- to 18-day-old tumors were excised, cleared of debris and necrotic tissue, and cut into small fragments (=1mm3). Tumor tissue was then placed in 0.25% trypsin in Dulbecco's medium with 100 U Penicillin/ml and 100 mcg streptomycin/ml. After 90 minutes' incubation at 22 Degrees C, trypsin action was stopped by the addition of complete medium containing heat-inactivated fetal calf serum (final concentration, 20%). Cells were washed two times in complete medium, enumerated in a Coulter counter (Model ZB1) or on a hemocytometer, and suspended in serum-free medium at a concentration of 5 X 10 6 cells / ml. Next 1 X 10 6 cells were injected into the right hind gluteur muscle, and drugs administered as described in "Results." Standard regimens provided for 10 consecutive daily doses beginning 24 hours after tumor inoculation. Body weights were recorded before tumor inoculation and weekly for 2 weeks. Tumor size was measured weekly for the duration of the experiment and converted to mg tumor weight, as described by Mayo (10).

Friend leukemia: B-tropic Friend leukemia virus (FLV) was maintained in BALB / c mice, and drug evaluation performed in the same animals. Pools of virus were prepared from the plasma of mice given FLV and stored at -70 Degrees C. In experiments with FLV, 0.2 ml of a 1/20 dilution of plasma (derived from FLV-infected mice) in medium was inoculated ip into BALB / c mice. Cannabinoids were administered orally daily for 10 consecutive days beginning 24 hours after virus inoculation. Twenty-four hours after the last drug administration, the mice were killed by cervical dislocation, and the spleens removed and weighed. Mice not given FLV were treated as described above, to evaluate possible drug-induced splenomegaly.

L1210 leukemia: The murine leukemia L1210 was maintained in DBA/2 mice by weekly transfers of 10 (to the fifth power) cells derived from the peritoneal cavity. In these experiments, 10 (fifth power) leukemia cells were inoculated ip into (C57BL/6 X DBA/2) F 1 (BDF 1) mice, and the mice were treated daily for 10 consecutive days beginning 24 hours after tumor cell inoculation. Mean survival time was used as an index of drug activity.

In vitro cell systems

Lewis lung tumor: We obtained isolated Lewis lung tumor cells by subjecting 1-mm (third power) sections of tumor to 0.25% trypsin at 22 degrees C and stirring for 60-90 minutes. After trypsinization, the cells were centrifuged (1,000 rpm for 10 min) and washed twice in Dulbecco's medium containing 20% heat-inactivated fetal calf serum. They were then reconstituted to 10 7 cells/ml of 200 mm glutamine, 5,000 U penicillin, and 5,000 mcg streptomycin. Tumor cells (3-6 ml) were dispensed into 25-ml Erlenmeyer flasks and preincubated with eithe the drug or the drug vehicle for 15 minutes in a Dubnoff metabolic shaker at 37 degrees C in an atmosphere of 5% CO2--95% )2. After preincubation, 10 ucl tritiated thymidine (3H-TDR) (10 uCi, 57 Ci/mmole; New England Nuclear Corp., Boston, Mas.) was added to each flask and incubated for various times, after which 1-ml aliquots were removed and placed in 10 X 75-mm test tubes containing 1 ml 10% trichloroacetic acid (TCA) at 4 degrees C. The TCA-precipated samples were then filtered on 0.45-u Millipore filters and washed twice with 5 ml of 10% TCA at 4 degrees C. The filters were transferred to liquid scintillation vials and counted in a toluene cocktail containing Liquifluor (New England Nuclear Corp.) (4 liters toluene to 160 ml Liquifluor). Samples were then counted in a liquid scintillator.

Bone marrow: Bone marrow cells were derived from the tibias and fibulas of BDF 1 mice. One ml Dulbecco's medium containing 1 U heparin/ml was forced through each bone by a 1-ml syringe with a 26-gauge needle. The cells were washed three times, nucleated cells were enumerated on a hemocytometer, and cell viability was ascertained by trypan blue exclusion. Cell number was adjusted to 10 (seventh) cells/ml with heparin-free Dulbecco's medium and incubated at 4 degrees C for 15 minutes. Bone marrow cells were then dispensed (3-5 ml) into a25-ml Erlenmeyer flasks containing the test drug or the drug vehicle. This preincubation period was followed by the addition of 10 ul 3H-TDR and the procedures done as outlined for the isolated Lewis lung cells.

L1210: L1210 cells were derived from DBA/2 mice as described above. They were obtained from DBA/2 mice and inoculated 7 days before the experiment by the peritoneal cavity being flushed with 10 ml Dulbecco's medium containing heparin (5 u/ml). The cells were washed three times in medium, and the final medium wash did not contain heparin. The cells were resuspended at 10 (seventh) cells/ml and treated as described above. Cells were routinely counted with a hemocytometer for the determination of cell viability with trypan blue; for Lewis lung tumor and L1210 cells, a Coulter apparatus (Mode ZB1) was also used. All other reagents were of the highest quality grade available. Actinomycin D, 5-fluorouracil (5-FU), and cytosine arabinoside (ara-C) were provided by the Drug Development Branch, National Cancer Institute (NCI).

Cannabinoids: The structures of the four compounds are shown in text-figure 1.


All occur naturally in marihuana and were chemically synthesized. These drugs were provided by the National Institute on Drug Abuse or the Sheehan Institute for Research, Cambridge, Massachusetts. In the preparation of the drugs, the cannabinoids were complexed to albumin or solubilized in Emulphor-alcohol. Both preparations produced similar antitumor activity. With albumin, the cannabinoids were prepared in the following manner: A stock solution of 150 mg cannabinoid per ml absolute ethanol was made. Six ml of this solution was placed in a 200-ml flask. The ethanol was evaporated off under a stream of nitrogen and 2,100 mg lyophilized bovine serum albumin (BSA) added. After the addition of 20 ml distilled water, the substances were stirred with a glass rod in a sonicator until a good suspension was achieved. Sufficient distilled water was the aldded to make the desired dilution. Concentrations were routinely checked with a gas chromatograph. When Emulphor-alcohol was used as the vehicle, the desired amount of cannabinoid was sonicated in a solution of equal volumes by absolute ethanol and Emulphor (El-620; GAF Corp., New York, N.Y.) and then diluted with 0.15 N NaCL for a final ratio of 1: 1: 4 (ethanol: Emulphor: NaCL).


Effects of Cannabinoids on Murine Tumors

Delta-9-THC, delta-8-THC, and cannabinol (CBN) all inhibited primary Lewis lung tumor growth, whereas cannabidiol (CBD) enhanced tumor growth.

Oral administration of 25, 50, or 100 mg delta-9-THC/kg inhibited primary tumor growth by 48, 72, and 75% respectively, when measured 12 days post tumor inoculation (table 1).


On day 19, mice given delta-9-THC had a 34% reduction in primary tumor size. On day 30, primary tumor size was 76% that of controls and only those given 100 mg delta-9-THC/kg had a significant increase in survival time (36%). Mice treated with a delta-9-THC showed a slight weight loss over the 2-week period (average loss, 0.3 g at 50 mg/kg and 0.1 g at 100 mg/kg). This can be compared to cyclo-ohosphamide, which caused weight loss approaching 20% (table 2).


Delta-8-THC activity was similar to that of delta-9-THC when administered orally daily until death (table 2). However, as with delta-9-THC, primary tumor growth approached control values after 3 weeks. When measured 12 days post tumor inoculation, all doses (50-400 mg/kg) of delta-8-THC inhibited primary tumor growth between 40 and 60%. Significant inhibition was also seen on day 21, which was comparable to cyclophosphamide-treated mice. Although this was not the optimum regime for cyclophosphamide, it was the positive control protocol provided by the NCI (11). All mice given delta-8-THC survived significantly longer than controls, except those treated with 100 mg/kg. Mice given 50, 200, and 400 mg/kg delta-8-THC had an increased life-span of 22.6, 24.6, and 27.2%, respectively, as compared to 33% for mice treated with 20 mg cyclophosphamide/kg. Pyran copolymer, an immunopotentiator (12) when administered at 50 mg/kg, also significantly increased the survival time of the animals (39.3%).

CBN, administered by gavage daily until death, demonstrated antitumor activity against the Lewis lung carcinoma when evaluated on day 14 post tumor inoculation (table 3).


Primary tumor growth was inhibited by 77%, at doses of 100 mg/kg on day 14 but only by 11% on day 24. At 50 mg/kg on day 14 but only by 11% on day 24. At 50 mg/kg, CBN inhibited primary tumor growth by only 32% when measured on day 14, and no inhibition was observed on day 24; however, these animals did survive 27% longer.

CBD, administered at 25 or 200 mg/kg daily until death, showed no tumor-inhibitory properties as measured by primary Lewis lung tumor size or survival time (table 4).


In this experiment, CBD-treated mice showed enhanced primary tumor growth. However, the control tumor growth rate in this experiment was decreased as compared to the previous studies.

Survival time of BDF 1 mice hosting L1210 leukemia was not prolonged by delta-9-THC treatment (table 5).


Mice treated with delta-9-THC at doses of 50, 100, and 200 mg/kg administered orally daily until death, survived 8.5, 7.8, and 8.6 days, respectively, as compared to 8.6 days for mice treated with the diluent. However, delta-9-THC inhigited FLV-induced splenomegaly by 71% at 200 mg/kg as compared to 90.2% for the positive control actinomycin D (0.25 mg/kg). Although there was a dose-related inhibition, only the high dose was statistically significant (table 6).


Effect of Cannabinoids on Isolated Cells In Vitro

Isolated cells incubated in vitro represent a simple, reliable, and, hopefully, predictive method for the monitoring of the effects of agents on several biochemical parameters at the same time. The incorporation of 3H-TDR into TCA-precipitable counts in isolated Lewis lung cells is shown in text-figure 2. Similar types of curves were seen for bone marrow and L1210 cells. In all instances, for 15-45 minutes there was a linear increase in 3H-TDR uptake into the TCA-precipitable fraction. Qualitatively, similar data (not shown) were seen after a pulse with 14C-uridine. Actinomycin D (1 mcg/ml) preferentially inhibited 14C-uridine incorporation after uridine uptake had decreased to less than 30% that of control (data not shown). This is indirect evidence that we were measuring RNA synthesis.

Experiments (data not shown) done with 5-FU (10 -4 M) indicated that, in isolated bone marrow cells, both thymidine uptake with time by delta-9-THC (10 -5 M) on Lewis lung cells is depicted in text-figure 2.


In this experiment, delta-9-THC caused a nonlinear uptake of 3H-TDR. At 30 minutes, uptake of 3H-TDR into the acid-precipitable fraction was about 50% that of control Longer incubations (i.e., 60 min) did not significantly change the uptake pattern for control and de;ta-9-THC treated tumor cells. The effect of several cannabinoids on the uptake of 3H-TDR into cells incubated in vitro indicated that delta-9-THC, delta-8-THC, and CBN produced a dose-dependent inhibition of radiolabel uptake in the three cell types (table 7). These results, presented as percent inhibition of radiolabel uptake as compared to control, represented an effect of cannabinoids on one aspect of macromolecular synthesis.

CBD was the least active of the cannabinoids, but showed its greatest activity in the L1210 leukemia cells. Other data (not shown) indicate that these compounds similarly effect the uptake of 14C-uridine into the acid-precipitable fraction. Ara-C markedly inhibited 3H-TDR uptake more dramatically than did the cannabinoids (table 7). Note that delta-9-THC exhibited inhibitory properties in the isolated Lewis lung tumor and L1210 cells at concentrations that did not interfere with thymidine uptake into bone marrow cells. At certain concentrations of CBD (2,5 X 10 -6 and 2.5 X 10 -7M), radiolabel uptake was consistently stimulated in bone marrow cells and in several experiments with the isolated Lewis lung cells.


We investigated four cannabinoids for antineoplastic activity against three animal tumor models in vivo and for cytotoxic or cystostatic activity in two tumor cell lines and bone marrow cells in vitro.

The cannabinoids (delta-9-THC, delta-8-THC, and CBN) active in vivo against the Lewis lung tumor cells are also active in the in vitro systems. The differential sensitivity of delta-9-THC against Lewis lung cells versus bone marrow cells is unique in that delta-8-THC and CBN are equally active in these systems. Johnson and Wiersma (5) reported that delta-9-THC administered iv caused a reduction in bone marrow metamyelocytes and an increase in lymphocytes. It is unclear from the data whether this is a depression of myelopoiesis or if it represents a lymphocyte infiltration into the bone marrow. The use of isolated bone marrow cells, which represent a nonneoplastic rapidly proliferating tissue, enables the rapid evaluation and assessment of drug sensititity and specificity, and thereby may predict toxicity related to bone marrow suppression.

CBD showed noninhibitory activity either against the Lewis lung cells in vivo or Lewis lung and bone marrow cells in vitro at 10 -5M an 10 -6M, respectively. Indeed, the tumor growth rate in mice treated with CBD was significantly increased over controls. This may, in part, be the consequence of the observation made in vitro (i.e., 10 -7M CBD stimulated thymidine uptake), which may be reflected by an increased rate of tumor growth. One problem related to the use of cannabinoids is the development of tolerance to many of its behavioral effects (13). It also appears that tolerance functions in the chemotherapy of neoplsms in that the growth of the Lewis lung tumor is initially markedly inhibited but, by 3 weeks, approaches that of vehicle-treated mice (tables 1, 3). This, in part, may reflect drug regimens, doses used, increased drug metabolism, or conversion to metabolites with antagonistic actions to delta-9-THC. It may also represent some tumor cell modifications rendering the cell insensitive to these drugs.

Of further interest was the lack of activity of delta-9-THC against the L1210 in vivo, whereas the invitro L1210 studies indicated that delta-9-THC could effectively inhibit thymidine uptake. The apparent reason for this discrepancy may be related to the high growth fraction and the short doubling time of this tumor. The in vitro data does not indicate that the cannabinids possess that degree of activity; e.g., ara-C, which "cures" L1210 mice, is several orders of magnitude more potent on a molar basis than delta-9-THC in vitro.

Inhibition of tumor growth and increased animal survival after treatment with delta-9-THC may, in part, be due to the ability of the drug to inhibit nucleic acid synthesis. Preliminary data with Lewis lung cells grown in tissue culture indicate that 10 -5M delta-9-THC inhibits by 50% the uptake of 3H-TDR into acid-precipitable counts over a 4-hour incubation period. Simultaneous determination of acid-soluble fractions did not show any inhibitory effects on radiolabeled uptake. Therefore, delta-9-THC may be acting at site(s) distal to the uptake of precursor. We are currently evaluating the acid-soluble pool to see if phosphorylation of precursor is involved in the action of delta-9-THC.

These results lend further support to increasing evidence that, in addition to the well-known behavioral effects of delta-9-THC, this agent modifies other cell responses that may have greater biologic significance in that they have antineoplastic activity. The high doses of delta-9-THC (i.e., 200 mg/kg) are not tolerable in humans. On a body-surface basis, this would be about 17 mg/m(2) for mice. Extrapolation to a 60-kg man would require 1,020 mg for comparable dosage. The highest doses administered to man have been 250-300 mg (14). Whether only cannabinoids active in the central nervous system (CNS) exhibit this antineoplastic property is not the question, since CBN, which lacks marihuana-like psychoactivity, is quite active in our systems (15).

With structure-activity investigations, more active agents may be designed and synthesized which are devoid of or have reduced CNS activity. That these compounds readily cross the blood-brain barrier and do not possess many of the toxic manifestations of presently used cytotoxic agents, makes them an appealing group of drugs to study.


1. Singer AJ: Marihuana: Chemistry, pharmacology and patterns of social use. Ann NY Acad Sci 191: 3-261, 1971

2. Leuchtenberger C, Leuchtenberger R, Schneider A: Effects of marijuana and tobacco smoke on human lung physiology. Nature 241: 137-139,1973

3. Zimmerman AM, McClean DK: Action of narcotic and hallucinogenic agents on the cell cycle. In Drugs and the Cell Cycle (Zimmerman AM, Padilla GM. Cameron IL, eds.). New York, Academic Press, 1973, pp.67-94

4. Stenchever MA, Kunysz TJ, Allen MA: Chromosome breakage in users of marihuana. Am J Obstet Gynecol 118: 105-113, 1974

5. JohnsonRT, Wiersema V: Repression of bone marrow leukopoieses by delta-9-THC . Res Commun Chem Pathol Pharmacol 7: 613-616, 1974

6. Kolodny RC, Masters WH, Kolodner RM, et al: Depression of plasma testosterone levels after chronic intensive marijuana use. N Engl J Med 290: 872-874, 1974

7. Nahas GG, Suchu-Foca N, Armand JP, et al: Inhibition of cellular immunity in marihuana smokers. Science 183: 419-420, 1974

8. Levy JA, Munson AE, Haris LS, et al: Effect of delta-8 and delta-9-tetrahydrocannabinol on the immunre response in mice. The Pharmacologist 16: 259, 1974

9. Harris LS, Munson AE, Friedman MA, et al: Retardation of tumor growth by delta-9-tetradydrocannabinol. The Pharmacologist 16: 259, 1974

10. Mayo JG: Biologic characterization of the subcutaneously implanted Lewis lung tumor. Cancer Chemother Rep 3: 325-330, 1972

11. Geran RI, Greenberg NH, MacDonald MM, et al: Protocols for screening chemical agents and natural products against animal tumors and other biological systems. Cancer Chemother Rep 3: 13, 1972

12 Munson AE, Regelson W, Lawrence W: The biphasic response of the reticuloendothelial system (RES) produced by pyran copolymer and its relationship to immunologic response. J Reticuloendothel Soc 7: 375-385, 1970

13. McMillan DE, Dewey WL, Turk RF, et al: Blood levels of 3H-delta-9-tetrahydrocannabinol and its metabolites in tolerant and non-tolerant pigeons. Biochem Pharmacol 22: 383-397, 1973

14. Jones RT: The 30-day trip-clinical studies of cannabis tolerance and dependence. Proceedings of the International Conference on the Pharmacology of Cannabis. Savanah, Georgia, 1974, p.29

15. Hollister LE: Structure-activity relationships in man of cannabis constituents and homologs and metabolites of delta-9-tetrahydrocannabinol. Pharmacology 11: 3-11, 1974



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i posted it only to show when they first learned of it's benefits relating to cancer treatment... the above video is much newer info ( in the video it refers to that test study and our government knowing long ago).. as well as a plethora of even newer stuff..

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