FAQs: Do cannabis Strains Differ?
By Dr. Ethan Russo
Cannabis consumers have always maintained that different types (strains, or chemical varieties, chemovars) produce distinct effects, whether this be with respect to their psychoactivity or to their therapeutic attributes. Strains are often designated as sativa, indica, or a hybrid. These labels are quite misleading as applied in the marketplace, however. In contrast, the scientific community has generally focused on tetrahydrocannabinol (THC) as the primary or only important variable. It is clear that until very recently, selective breeding in cannabis for the recreational and medicinal markets have produced THC-predominant cannabis to the exclusion of other cannabinoids. Some researchers have stressed the importance of additional components, especially terpenoids, the aromatic components of cannabis that like cannabinoids are produced in glandular trichomes, as important modulators of cannabis effects (McPartland & Russo, 2001, Russo 2011).
What are other cannabinoids in cannabis?
The most common phytocannabinoid besides THC is cannabidiol (CBD). It was previously common in cannabis landraces from Afghanistan and Morocco, for example, but has largely disappeared from recreational cannabis. It is also present in hemp fibre and seed strains, but usually in low titre. In the medicinal arena, CBD has received increasing attention due to its many medicinal attributes, including its pain-relieving and anti-inflammatory benefits without intoxication or sedation. It also reduces side effects of THC when administered concomitantly, specifically, anxiety and tachycardia. Taken together, the two components may demonstrate synergy in many applications.
Another cannabis component of interest is tetrahydrocannabivarin (THCV), traditionally found in small amounts in Southern African cannabis chemovars (chemical varieties). It is currently under investigation as a treatment for metabolic syndrome, often seen as a prelude to the development of Type II diabetes.
Other phytocannabinoids under investigation include cannabigerol (CBG) for prostate cancer, cannabidivarin (CBDV) for epilepsy, and several others.
What about terpenoids?
Abundant evidence supports that these low concentration components contribute to the phytocannabinoids in whole cannabis preparations by adding their own therapeutic benefits or allaying side effects of THC. Worthy of particular mention are limonene, with known anti-depressant effects, pinene, which attenuates short-term memory deficits engendered by THC, myrcene, which is sedating, and beta-caryophyllene, which stimulates the non-psychoactive CB2 receptor, and produces anti-inflammatory and analgesic effects. Further research will address the relative importance of these agents in various cannabis preparations.
About the author:
Dr. Ethan Russo is a board-certified neurologist, who serves as Senior Medical Advisor to GW Pharmaceuticals. He is a past chairman of the International Association for Cannabinoid Medicines, and is the current president of the International Cannabinoid Research Society.
Additional Reading:
Fischedick, J. T., Hazekamp, A., Erkelens, T., Choi, Y. H. & Verpoorte, R. (2010). Metabolic fingerprinting of Cannabis sativa L., cannabinoids and terpenoids for chemotaxonomic and drug standardization purposes. Phytochemistry, 71, 2058-73.
Izzo, A. A., Borrelli, F., Capasso, R., Di Marzo, V. & Mechoulam, R. (2009). Non-psychotropic plant cannabinoids: new therapeutic opportunities from an ancient herb. Trends Pharmacol Sci, 30, 515-27.
Russo, E. B. (2007). History of cannabis and its preparations in saga, science and sobriquet. Chemistry & Biodiversity, 4, 2624-2648.
FAQs: What is the best and healthiest way to produce cannabis oil?
by Dr Arno Hazekamp
What is Cannabis oil?
Concentrated cannabis extracts, also known as Cannabis oils because of their sticky and viscous appearance, are increasingly mentioned by self-medicating patients as a cure for cancer. In general, preparation methods for Cannabis oil are relatively simple and do not require particular instruments. The purpose of the extraction, often followed by a solvent evaporation step, is to make cannabinoids and other beneficial components such as terpenes available in a highly concentrated form. Cannabis oil is usually taken orally, by ingesting a small number of drops several times a day.
How is Cannabis oil prepared?
Various methods have been described for the preparation of Cannabis oil. The most popular method, as described by former (skin)cancer patient Rick Simpson from Canada, suggests the use of naphtha or petroleum ether as a solvent for the extraction. Following the success of Simpson oil, a number of related recipes have sprung up, emphasizing small but significant changes to the original recipe. Examples include focusing on safer solvents such as ethanol, or preventing exposure to organic solvents altogether, by using olive oil.
What is naphtha or petroleum-ether?
In general, petroleum-ether and naphtha refer to very similar products, even though different names may be used around the world; e.g. in some countries naphtha is equivalent to diesel or kerosene fuel. Both solvents are a mixture of petroleum hydrocarbons (PHCs), often available in a wide range of qualities. All the solvent components should be considered harmful and flammable, and some of them, such as hexane and benzene, may be neurotoxic. Both naphtha and petroleum-ether are considered potential cancer hazards according to their manufacturers. Moreover, products sold as naphtha may contain added impurities (e.g. Coleman® fuel) which may have harmful properties of their own.
Are residual solvents a health risk?
Although Cannabis oils are usually concentrated by evaporating the solvents that were used for extraction, this does not completely eliminate residual solvents. As a result of sample viscosity, the more concentrated an extract becomes, the more difficult it will be to remove the residual solvent from it. In such a case, applying more heat will increase solvent evaporation, but simultaneously more beneficial components (such as cannabinoids or terpenes) may be lost as well. The use of non-toxic solvents should therefore always be advised, so that potential residues are not harmful to health.
What is the best and healthiest way to prepare Cannabis oil?
Recently, an analytical study was performed to compare several generally used preparation methods on the basis of cannabinoids, terpenes, and residual solvent components. Solvents tested included ethanol, naphtha, petroleum-ether, and olive oil. Based on this study, the following recommendations can be made:
As extraction solvents, ethanol and olive oil were shown to perform the best, extracting the full range of terpenes and cannabinoids present in cannabis plant material very efficiently. Additionally these solvents are safe for consumption.
Unfortunately, pure ethanol also extracts large amounts of chlorophyll from cannabis material, which will give the final extract a distinct green, and often unpleasant, taste. Removing chlorophyll by filtering the ethanol extract over activated charcoal was found to be effective, but it also removed a large proportion of cannabinoids and terpenes, and is therefore not advised. Additionally, in many countries consumption-grade ethanol is an expensive solvent, as a result of added tax on alcohol products.
Of the solvents tested, this leaves olive oil as the most optimal choice for preparation of cannabis oil for self-medication. Olive oil is cheap, not flammable or toxic, and the oil needs to be heated up only to 100°C (by placing a glass jar containing the product in boiling water for 1-2 hours) so no overheating of the oil can occur. After cooling down and filtering the oil it is immediately ready for consumption. As a trade-off, however, olive oil extract cannot be concentrated by evaporation, which means patients will need to consume a larger volume of it in order to get the same therapeutic results.
Preheating of cannabis to ‘activate’ (decarboxylate) the cannabinoids may result in loss of terpenes as a result of evaporation. If the full range of terpenes is desired in the final Cannabis oil, dried buds and leaves can be used directly for extraction, without preheating.
About the author
Dr Arno Hazekamp is a phytochemical researcher at the Department of Plant Metabolomics of Leiden University, The Netherlands. He also coordinates the R&D program at Bedrocan BV.
FAQs: Do cannabinoids cure cancer?
by Dr Manuel Guzmán
Cannabinoids, the active components of cannabis and their derivatives, exert palliative effects in cancer patients by preventing nausea, vomiting and pain and by stimulating appetite. In addition, these compounds inhibit the growth of tumour cells in laboratory animals -mice and rats. However, at the moment there is not solid evidence to prove that cannabinoids –whether natural or synthetic- can effectively treat cancer in patients, although research is ongoing around the world.
Comprehensive FAQ sections -including scientific references- on cannabinoids and cancer can be found at the Cancer Research UK website and the National Cancer Institute of the US website. Here that information is summarized and discussed.
What is cancer?
Cancer is a broad term used for diseases in which abnormal cells divide without control and are usually able to invade other tissues, causing metastases and high rates of mortality and morbidity. Cancer is not just one disease but many diseases: more than 100 different cancers are well-typified from a histopatological point of view by the WHO and, most likely, there are hundreds if not thousands types of cancers according to molecular and genetic profiling.
Most cancers are named for the organ or type of cell in which they start. In addition, cancer types are usually grouped into the following broader categories:
- Carcinoma: cancer that begins in the skin or in tissues that line or cover internal organs.
- Sarcoma: cancer that begins in bone, cartilage, fat, muscle, blood vessels, or other connective or supportive tissue.
- Leukaemia: cancer that starts in blood-forming tissues such as the bone marrow and causes large numbers of abnormal blood cells to be produced and enter the blood.
- Lymphoma and myeloma: cancers that begin in the cells of the immune system.
- Central nervous system cancers: cancers that begin in the tissues of the brain and spinal cord.
Conclusion: Cancer is a very serious and heterogeneous disease, so fighting it therapeutically remains an extremely difficult challenge. Cannabinoids might therefore exert beneficial effects in some cancers but not in others.
Do cannabinoids inhibit cancer growth? (Laboratory research)
Virtually all the research into cannabinoids and cancer cells has been conducted so far using cancer cells grown in the lab or in animal models. Many scientific studies have reported that various cannabinoids (both natural and synthetic) exert a wide range of growth-inhibiting effects on cancer cells, including:
- Triggering cell death, through a mechanism called apoptosis.
- Stopping cells from dividing.
- Preventing new blood vessels from growing into tumours –a process termed angiogenesis.
- Reducing the chances of cancer cells to metastasize 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.
Conclusion: Cannabinoids are efficacious drugs to treat at least some types of cancers in laboratory animals –mice and rats.
Do cannabinoids inhibit cancer growth? (Anecdotal evidence in humans)
As mentioned above, basically all the research investigating whether cannabinoids can treat cancer has been done in the lab. It is therefore important to be very cautious when extrapolating these results up to real live patients, who are a lot more complex than a Petri dish or a mouse. Anecdotal reports on cannabis use have been historically helpful to provide hints on the biological processes controlled by the endocannabinoid system and on the potential therapeutic benefits of cannabinoids. In the precise case of cancer there is a notable presence of videos and reports on the internet arguing that cannabis can cure cancer. These anecdotal claims may be completely or partially true in some cases, but overall remain –at least to date- weak and obscure. For example:
- We do not know whether the (supposed) effect of cannabis was due to a placebo effect.
- We do not know whether the tumour has (supposedly) stopped growing by natural/endogenous reasons -some tumours regress spontaneously/owing to the body’s anti-tumour defences.
- We do not know how many patients have taken cannabis and have not obtained any therapeutic benefit, that is, what is the (supposed) efficacy of the cannabis-based therapy.
- As most likely patients have gone through standard therapy prior to or concomitantly with cannabis use, we do not know whether the (supposed) effect of cannabis was in fact due -at least in part- to the standard therapy -perhaps enhanced by cannabis, but we have no proof.
- We do not know what are the parameters of tumour progression that have been monitored and for how long the patient has been monitored -many potentially beneficial effects of antineoplastic drugs (or of cannabis in this case) are just short-term actions, but what about long-term progression-free survival and overall survival?
- Cancer is a very heterogeneous disease, and so far none has put together a sufficient number of patients for a particular type of cancer to support that cannabinoids are efficacious drugs in that precise cancer.
Conclusion: Although it is possible –and of course desirable- that cannabis preparations have exerted some antineoplastic activity in some particular cancer patients, the current anecdotal evidence reported on this issue is pretty poor, and, unfortunately, remains far from supporting that cannabinoids are efficacious anticancer drugs for large patient populations.
Do cannabinoids inhibit cancer growth? (Clinical research)
Results have been published from only one Phase I clinical trial testing whether cannabinoids can treat cancer in patients. Nine people with advanced, recurrent glioblastoma multiforme –an aggressive brain tumour– that had previously failed standard therapy were given highly purified THC through a catheter directly into their brain. Under these conditions cannabinoid delivery was safe and could be achieved without significant unwanted effects. In addition, although no statistically-significant conclusions can be extracted from such a small cohort of patients and without a control group, the results obtained suggested that some patients responded -at least partially- to THC treatment in terms of decreased tumour growth rate, as evaluated by imaging and biomarker analyses. These findings were encouraging and substantially reinforced the interest on the potential use of cannabinoids in cancer therapies. However, they also highlighted the need for further research aimed at optimizing the use of cannabinoids in terms of patient selection, combination with other anticancer agents and use of other routes of administration.
Conclusion: There are still many unanswered questions around the potential for using cannabinoids as anticancer drugs, and it is necessary and desirable that exhaustive clinical studies are conducted to determine how cannabinoids can be used, other than for their palliative effects, to treat cancer patients.
About the author
Dr Manuel Guzman is professor at the Department of Biochemistry and Molecular Biology at Complutense University in Madrid, Spain. He coordinates the Cannabinoid Signaling Group.
FAQs: Does cannabis use increase the risk for schizophrenia?
by Franjo Grotenhermen
The use of cannabis may be a risk factor for the development of schizophrenia, a type of psychosis. It is currently assumed that cannabis doubles the risk (or increases the risk by 2) if heavily used in adolescence. There are other factors that increase schizophrenia risk. For example having grown up in a big city also increases the risk by about 2 compared to having grown up in the countryside. This small increase in risk means that 1 to 2 out of 100 heavy cannabis users and 1 to 2 out of 100 city dwellers will develop schizophrenia during their lifetime, compared to 0.5 to 1 out of 100 people without any risk factor.
What is psychosis?
Psychosis is a serious medical condition of unknown origin. It refers to an abnormal condition of the mind, and is a generic psychiatric term for a mental state often described as involving a "loss of contact with reality". The term “psychosis” is most often used as an “umbrella term” instead as a distinct diagnosis. People suffering from psychosis are described as psychotic. Psychosis is given to the more severe forms of psychiatric disorder, during which hallucinations and delusions and impaired insight may occur. Although there are drugs available that can ameliorate some of the symptoms, the disorder can not be cured. Schizophrenia is a special form of a psychotic disorder.
What is schizophrenia?
Schizophrenia is a mental disorder characterized by a breakdown of thought processes and by poor emotional responsiveness. It most commonly manifests itself as auditory hallucinations, paranoid beliefs, or disorganized speech and thinking. Hallucinations are perceptions in a conscious and awake state in the absence of external stimuli, which have qualities of real perception. For example, schizophrenics may hear voices in the absence of any voices. Beliefs, which are called delusions, are associated with strong conviction despite evidence to the contrary. For example, somebody may believe that he is an important historical personality such as Jesus or Napoleon. Often deficits of normal emotional responses are associated such as flat or blunted affect and emotion, poverty of speech, inability to experience pleasure, and lack of motivation. Depending on the clinical symptomatology schizophrenia can be classified in different subtypes.
How prevalent is schizophrenia?
About 15 to 20 new cases per 100.000 inhabitants of Western countries develop schizophrenia every year. The onset of symptoms typically occurs in young adulthood between the age of 18 and 35, and about 0.5 to 1.0 per cent of all citizens of Europe and North America develop schizophrenia during their lifetime. Delusions, thought disorders (e.g. thought broadcasting), and acoustic hallucinations are preliminary employed in diagnosis. These symptoms are often highly dramatic and dangerous, but these so-called “positive symptoms” normally improve over the years. On the other hand, the “negative symptoms” such as depression, inability to make social contacts, impoverishment of feelings often remain, resulting in psychosocial problems and unemployment.
What causes schizophrenia?
Both genes and the environment play a role in the development of schizophrenia. Certain variants of genes are associated with a higher risk of schizophrenia. This may explain, why schizophrenia is observed more often in some families compared to others. However, these genetic variants do not cause the disease, but play a role in the disposition to the disease. Somebody, who has a first-degree relative (parents, brother, sister) with schizophrenia, has a risk of 6.5 per cent to also develop the disease during lifetime. This means that of 100 first-degree relatives of people with schizophrenia 6 to 7 also develop the disease.
Environmental risk factors that have been established are pregnancy complications including stress, infections and malnutrition of the mother, birth complications, growing up in a large city, low but normal IQ (intelligence quotient), and drug consumption including cannabis use. Other factors, which may play an important role, are social isolation, family dysfunction and other heavily distressing factors. People with schizophrenia in the northern hemisphere are more likely to have been born in winter or spring compared to summer and autumn.
How to prevent schizophrenia?
Since risk factors are only associated with a relatively low increase of risk, they cannot be used for early detection and prevention of schizophrenia (Klosterkötter 2008). On the other hand, it is desirable to detect schizophrenia at an early stage, since early detection and early treatment is associated with a more favourable course of the disease, less depression and less suicide. Thus, prevention efforts and programs are concentrated on the detection of risk symptoms during the so-called prodromal state (early warning signs) and on making a correct diagnosis after outbreak of the disease as early as possible.
In about three quarters of all cases the outbreak of schizophrenia is preceded by a prodromal state for an average of five years. During this period the person may have thought disturbances, unusual experiences of perception, paranoid ideas, decreased ability to discriminate between ideas and perception, fantasy and true memories, and similar symptoms several times a week. There is a high risk for people experiencing prodromal symptoms to develop psychotic symptoms and psychotic episodes finally leading to schizophrenia.
What is the role of cannabis in the development of schizophrenia?
In a review of seven longitudinal studies on the association between cannabis use and schizophrenia researchers found that individuals who had ever used cannabis had an increased risk of psychosis or psychotic symptoms of 41 per cent compared to individuals who had never used cannabis. In longitudinal studies a large number of people are followed for several years, ideally from birth to adulthood, to identify for example causes of diseases or protective factors against diseases. Frequent cannabis users had twice the risk of non-users (odds ratio: 2.09) (Moore et al. 2007). Researchers noted that the uncertainty about whether cannabis causes psychosis is unlikely to be resolved by further longitudinal studies. It is most likely that cannabis use precipitates schizophrenia in individuals who are vulnerable because of a personal or family history of schizophrenia (Degenhardt and Hall 2006).
It is difficult to prove that cannabis is indeed a causal factor in the development of schizophrenia, since the association may be non-causal, at least in part. For example, some people with schizophrenia may self-medicate with cannabis to treat some of their symptoms, especially negative symptoms. However, there is increasing evidence from long-term epidemiological studies that cannabis plays a causal role.
What is the role of cannabinoids in the treatment of schizophrenia?
There are two published case series, which demonstrate that cannabis or THC may be of therapeutic value in some cases of schizophrenia, who do not respond to conventional medication (Schwarcz et al. 2009, Schwarcz et al. 2010). The authors of these reports assume that with regard to brain physiology the cause of schizophrenia in these patients may differ from other patients with schizophrenia, who respond to conventional anti-psychotic medication, that these patients may suffer from low endocannabinoid brain function.
There is clinical evidence that the natural plant cannabinoid cannabidiol (CBD) at a daily dose of 800 mg may be as effective as conventional medication in the treatment of schizophrenia (Leweke et al. 2012). CBD is known to decrease or abolish the psychological effects of THC. The treatment with CBD is associated with an increase in anandamide blood levels, and this increase is thought to be responsible for symptom improvement.
About the author
Dr Franjo Grotenhermen is chairman of the German Association for Cannabis as Medicine (ACM) and executive director of the International Association for Cannabinoid Medicines (IACM). He is working for the nova-Institut in Huerth/Rhineland, Germany.
FAQs: Does cannabis cause anxiety or does it reduce anxiety or may both occur?
US Institute of Medicine
Although euphoria is the more common reaction to smoking marijuana, adverse mood reactions can occur. Such reactions occur most frequently in inexperienced users after large doses of smoked or oral marijuana. They usually disappear within hours and respond well to reassurance and a supportive environment. Anxiety and paranoia are the most common acute adverse reactions, others include panic, depression, dysphoria, depersonalization, delusions, illusions, and hallucinations.
Source: Joy JE, Watson SJ, Benson JA, eds. Marijuana and medicine: Assessing the science base. Institute of Medicine. Washington DC: National Academy Press, 1999.
US Institute of Medicine
The 'high' associated with marijuana is not generally claimed to be integral to its therapeutic value. But mood enhancement, anxiety reduction, and mild sedation can be desirable qualities in medications particularly for patients suffering pain and anxiety. Thus, although the psychological effects of marijuana are merely side effects in the treatment of some symptoms, they might contribute directly to relief of other symptoms.
Source: Joy JE, Watson SJ, Benson JA, eds. Marijuana and medicine: Assessing the science base. Institute of Medicine. Washington DC: National Academy Press, 1999.
Giovanni Marciano and colleagues
Here we show that the endogenous cannabinoid system has a central function in extinction of aversive memories. (…) Mice were trained to associate a tone with an electric footshock (conditioning). After conditioning, animals shivered when they heard the tone. This response served as an indicator of aversive memory, and is gradually extinguished on repeated tone presentations. (...) Mice without cannabinoid-1 receptors showed strongly impaired short-term and long-term extinction of the aversive memory (...).
Overall our findings suggest that the endogenous cannabinoid system could represent a therapeutic target for the treatment of diseases associated with inappropriate retention of aversive memories or inadequate response to aversive situations, such as posttraumatic stress disorders, phobia, and certain forms of chronic pain.
Modified according to: Marsicano G, et al. The endogenous cannabinoid system controls extinction of aversive memories. Nature 2002;418(6897):530-534.
Pankaj Sah
Marciano and colleagues propose a new role for this endocannabinoid system - extinguishing fear-related memories in mice. The finding might have implications for treating anxiety disorders in humans.
It has been argued that the neuronal circuitry underlying fear conditioning has similarities to that responsible for fear-related clinical conditions, such as post-traumatic stress disorder. Behavioural therapies for these conditions - including systematic desensitization and imagery therapies - share features with extinction. The finding that the endocannabinoids contribute to extinction raises the possibility that drugs that target these molecules and their receptors could be useful new treatments for anxiety disorders. Finally there is much anecdotal evidence of patients using cannabis heavily in the early stages of psychiatric illness. This has often been thought to contribute to acute illness. But it seems possible that it may instead be a form of self-medication for the sometimes extreme anxiety that these people experience.
Source: Sah P. Neurobiology: Never fear, cannabinoids are here. Nature 2002;418(6897):488-9.
Franjo Grotenhermen
I would like to present a case of successful cannabis use in panic attacks. A Swiss who was suffering from panic attacks recently reported me, that cannabis use was very helpful for him between the attacks. He had not used cannabis during the attack since it would be too late then.
The attacks had started about nine months ago without recognizable cause and occured nearly daily. He also suffered from nausea, loss of appetite and dizziness. He had been prescribed strong medical drugs from his doctor, which he would not like to take permanently. Five months ago he started to use cannabis, which he takes about three times a week now. The panic attacks declined in frequency and intensity. Dizziness and nausea have disappeared completely and he regained appetite. The panic attacks nearly disappeared as well.
Source: Grotenhermen F. Kann Cannabis bei einer aufkommenden Panikattacke sinnvoll eingesetzt werden? [Can cannabis be used in an arising panic attack?] Hanf-Magazin, September 2002.
http://www.cannabis-med.org/index.php?tpl=faq&red=faqlist&id=278&lng=en
For more information, consult Dr. David Frederick Hepburn online material:
Cannabis Hemp Conference and Expo: http://www.cannabishempconference.com/dr-dave-hepburn-md/
Market Wired, Award Winning Columnist Dr. David Frederick Hepburn Embarks on Speaking Tour: http://www.marketwired.com/press-release/award-winning-columnist-dr-dave-hepburn-embarks-on-speaking-tour-2166319.htm
CBC News, Q&A with Dr. David Frederick Hepburn, B.C. doctor going on medical marijuana speaking tour: http://www.cbc.ca/news/canada/british-columbia/q-a-with-dr-dave-hepburn-b-c-doctor-going-on-medical-marijuana-speaking-tour-1.3213458
Patients out of time: http://patientsoutoftime.org/doctors/david-hepburn-md/
Leafly contributors: https://www.leafly.com/news/author/dr-dave-hepburn
Keynote Speakers Canada: http://keynotespeakerscanada.ca/speaker/dave-hepburn-md
National Speakers Bureau: https://www.nsb.com/speakers/dave-hepburn/
Cannabis Culture, Q&A with Dr. David Frederick Hepburn, B.C. Doctor Going on Medical Marijuana Speaking Tour: http://www.cannabisculture.com/content/2015/09/04/qa-with-dr-dave-hepburn-b-c-doctor-going-on-medical-marijuana-speaking-tour
The globe and mail, On a mission to change how family doctors view medical marijuana: https://www.theglobeandmail.com/news/british-columbia/on-a-mission-to-change-how-family-doctors-view-medical-marijuana/article25791287/
Cannabis Digest, Teaching Cannabis Medicine in Canada: Interviews with Dr. David Frederick Hepburn and Dr. Robert Sealy: https://cannabisdigest.ca/teaching-cannabis-medicine-canada-interviews-dr-david-hepburn-dr-robert-sealy/
https://phil420.com/tag/dr-dave-hepburn/
https://www.pinterest.com.mx/pin/853643304340545028/
Leafly, Cannabis Shows Great Promise in Treating Cancer—Let’s Not Wreck It With Hyperbole: https://www.leafly.com/news/health/cannabis-shows-great-promise-treating-cancer-lets-not-wreck-hyperbole
By Dr. Ethan Russo
Cannabis consumers have always maintained that different types (strains, or chemical varieties, chemovars) produce distinct effects, whether this be with respect to their psychoactivity or to their therapeutic attributes. Strains are often designated as sativa, indica, or a hybrid. These labels are quite misleading as applied in the marketplace, however. In contrast, the scientific community has generally focused on tetrahydrocannabinol (THC) as the primary or only important variable. It is clear that until very recently, selective breeding in cannabis for the recreational and medicinal markets have produced THC-predominant cannabis to the exclusion of other cannabinoids. Some researchers have stressed the importance of additional components, especially terpenoids, the aromatic components of cannabis that like cannabinoids are produced in glandular trichomes, as important modulators of cannabis effects (McPartland & Russo, 2001, Russo 2011).
What are other cannabinoids in cannabis?
The most common phytocannabinoid besides THC is cannabidiol (CBD). It was previously common in cannabis landraces from Afghanistan and Morocco, for example, but has largely disappeared from recreational cannabis. It is also present in hemp fibre and seed strains, but usually in low titre. In the medicinal arena, CBD has received increasing attention due to its many medicinal attributes, including its pain-relieving and anti-inflammatory benefits without intoxication or sedation. It also reduces side effects of THC when administered concomitantly, specifically, anxiety and tachycardia. Taken together, the two components may demonstrate synergy in many applications.
Another cannabis component of interest is tetrahydrocannabivarin (THCV), traditionally found in small amounts in Southern African cannabis chemovars (chemical varieties). It is currently under investigation as a treatment for metabolic syndrome, often seen as a prelude to the development of Type II diabetes.
Other phytocannabinoids under investigation include cannabigerol (CBG) for prostate cancer, cannabidivarin (CBDV) for epilepsy, and several others.
What about terpenoids?
Abundant evidence supports that these low concentration components contribute to the phytocannabinoids in whole cannabis preparations by adding their own therapeutic benefits or allaying side effects of THC. Worthy of particular mention are limonene, with known anti-depressant effects, pinene, which attenuates short-term memory deficits engendered by THC, myrcene, which is sedating, and beta-caryophyllene, which stimulates the non-psychoactive CB2 receptor, and produces anti-inflammatory and analgesic effects. Further research will address the relative importance of these agents in various cannabis preparations.
About the author:
Dr. Ethan Russo is a board-certified neurologist, who serves as Senior Medical Advisor to GW Pharmaceuticals. He is a past chairman of the International Association for Cannabinoid Medicines, and is the current president of the International Cannabinoid Research Society.
Additional Reading:
Fischedick, J. T., Hazekamp, A., Erkelens, T., Choi, Y. H. & Verpoorte, R. (2010). Metabolic fingerprinting of Cannabis sativa L., cannabinoids and terpenoids for chemotaxonomic and drug standardization purposes. Phytochemistry, 71, 2058-73.
Izzo, A. A., Borrelli, F., Capasso, R., Di Marzo, V. & Mechoulam, R. (2009). Non-psychotropic plant cannabinoids: new therapeutic opportunities from an ancient herb. Trends Pharmacol Sci, 30, 515-27.
Russo, E. B. (2007). History of cannabis and its preparations in saga, science and sobriquet. Chemistry & Biodiversity, 4, 2624-2648.
FAQs: What is the best and healthiest way to produce cannabis oil?
by Dr Arno Hazekamp
What is Cannabis oil?
Concentrated cannabis extracts, also known as Cannabis oils because of their sticky and viscous appearance, are increasingly mentioned by self-medicating patients as a cure for cancer. In general, preparation methods for Cannabis oil are relatively simple and do not require particular instruments. The purpose of the extraction, often followed by a solvent evaporation step, is to make cannabinoids and other beneficial components such as terpenes available in a highly concentrated form. Cannabis oil is usually taken orally, by ingesting a small number of drops several times a day.
How is Cannabis oil prepared?
Various methods have been described for the preparation of Cannabis oil. The most popular method, as described by former (skin)cancer patient Rick Simpson from Canada, suggests the use of naphtha or petroleum ether as a solvent for the extraction. Following the success of Simpson oil, a number of related recipes have sprung up, emphasizing small but significant changes to the original recipe. Examples include focusing on safer solvents such as ethanol, or preventing exposure to organic solvents altogether, by using olive oil.
What is naphtha or petroleum-ether?
In general, petroleum-ether and naphtha refer to very similar products, even though different names may be used around the world; e.g. in some countries naphtha is equivalent to diesel or kerosene fuel. Both solvents are a mixture of petroleum hydrocarbons (PHCs), often available in a wide range of qualities. All the solvent components should be considered harmful and flammable, and some of them, such as hexane and benzene, may be neurotoxic. Both naphtha and petroleum-ether are considered potential cancer hazards according to their manufacturers. Moreover, products sold as naphtha may contain added impurities (e.g. Coleman® fuel) which may have harmful properties of their own.
Are residual solvents a health risk?
Although Cannabis oils are usually concentrated by evaporating the solvents that were used for extraction, this does not completely eliminate residual solvents. As a result of sample viscosity, the more concentrated an extract becomes, the more difficult it will be to remove the residual solvent from it. In such a case, applying more heat will increase solvent evaporation, but simultaneously more beneficial components (such as cannabinoids or terpenes) may be lost as well. The use of non-toxic solvents should therefore always be advised, so that potential residues are not harmful to health.
What is the best and healthiest way to prepare Cannabis oil?
Recently, an analytical study was performed to compare several generally used preparation methods on the basis of cannabinoids, terpenes, and residual solvent components. Solvents tested included ethanol, naphtha, petroleum-ether, and olive oil. Based on this study, the following recommendations can be made:
As extraction solvents, ethanol and olive oil were shown to perform the best, extracting the full range of terpenes and cannabinoids present in cannabis plant material very efficiently. Additionally these solvents are safe for consumption.
Unfortunately, pure ethanol also extracts large amounts of chlorophyll from cannabis material, which will give the final extract a distinct green, and often unpleasant, taste. Removing chlorophyll by filtering the ethanol extract over activated charcoal was found to be effective, but it also removed a large proportion of cannabinoids and terpenes, and is therefore not advised. Additionally, in many countries consumption-grade ethanol is an expensive solvent, as a result of added tax on alcohol products.
Of the solvents tested, this leaves olive oil as the most optimal choice for preparation of cannabis oil for self-medication. Olive oil is cheap, not flammable or toxic, and the oil needs to be heated up only to 100°C (by placing a glass jar containing the product in boiling water for 1-2 hours) so no overheating of the oil can occur. After cooling down and filtering the oil it is immediately ready for consumption. As a trade-off, however, olive oil extract cannot be concentrated by evaporation, which means patients will need to consume a larger volume of it in order to get the same therapeutic results.
Preheating of cannabis to ‘activate’ (decarboxylate) the cannabinoids may result in loss of terpenes as a result of evaporation. If the full range of terpenes is desired in the final Cannabis oil, dried buds and leaves can be used directly for extraction, without preheating.
About the author
Dr Arno Hazekamp is a phytochemical researcher at the Department of Plant Metabolomics of Leiden University, The Netherlands. He also coordinates the R&D program at Bedrocan BV.
FAQs: Do cannabinoids cure cancer?
by Dr Manuel Guzmán
Cannabinoids, the active components of cannabis and their derivatives, exert palliative effects in cancer patients by preventing nausea, vomiting and pain and by stimulating appetite. In addition, these compounds inhibit the growth of tumour cells in laboratory animals -mice and rats. However, at the moment there is not solid evidence to prove that cannabinoids –whether natural or synthetic- can effectively treat cancer in patients, although research is ongoing around the world.
Comprehensive FAQ sections -including scientific references- on cannabinoids and cancer can be found at the Cancer Research UK website and the National Cancer Institute of the US website. Here that information is summarized and discussed.
What is cancer?
Cancer is a broad term used for diseases in which abnormal cells divide without control and are usually able to invade other tissues, causing metastases and high rates of mortality and morbidity. Cancer is not just one disease but many diseases: more than 100 different cancers are well-typified from a histopatological point of view by the WHO and, most likely, there are hundreds if not thousands types of cancers according to molecular and genetic profiling.
Most cancers are named for the organ or type of cell in which they start. In addition, cancer types are usually grouped into the following broader categories:
- Carcinoma: cancer that begins in the skin or in tissues that line or cover internal organs.
- Sarcoma: cancer that begins in bone, cartilage, fat, muscle, blood vessels, or other connective or supportive tissue.
- Leukaemia: cancer that starts in blood-forming tissues such as the bone marrow and causes large numbers of abnormal blood cells to be produced and enter the blood.
- Lymphoma and myeloma: cancers that begin in the cells of the immune system.
- Central nervous system cancers: cancers that begin in the tissues of the brain and spinal cord.
Conclusion: Cancer is a very serious and heterogeneous disease, so fighting it therapeutically remains an extremely difficult challenge. Cannabinoids might therefore exert beneficial effects in some cancers but not in others.
Do cannabinoids inhibit cancer growth? (Laboratory research)
Virtually all the research into cannabinoids and cancer cells has been conducted so far using cancer cells grown in the lab or in animal models. Many scientific studies have reported that various cannabinoids (both natural and synthetic) exert a wide range of growth-inhibiting effects on cancer cells, including:
- Triggering cell death, through a mechanism called apoptosis.
- Stopping cells from dividing.
- Preventing new blood vessels from growing into tumours –a process termed angiogenesis.
- Reducing the chances of cancer cells to metastasize 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.
Conclusion: Cannabinoids are efficacious drugs to treat at least some types of cancers in laboratory animals –mice and rats.
Do cannabinoids inhibit cancer growth? (Anecdotal evidence in humans)
As mentioned above, basically all the research investigating whether cannabinoids can treat cancer has been done in the lab. It is therefore important to be very cautious when extrapolating these results up to real live patients, who are a lot more complex than a Petri dish or a mouse. Anecdotal reports on cannabis use have been historically helpful to provide hints on the biological processes controlled by the endocannabinoid system and on the potential therapeutic benefits of cannabinoids. In the precise case of cancer there is a notable presence of videos and reports on the internet arguing that cannabis can cure cancer. These anecdotal claims may be completely or partially true in some cases, but overall remain –at least to date- weak and obscure. For example:
- We do not know whether the (supposed) effect of cannabis was due to a placebo effect.
- We do not know whether the tumour has (supposedly) stopped growing by natural/endogenous reasons -some tumours regress spontaneously/owing to the body’s anti-tumour defences.
- We do not know how many patients have taken cannabis and have not obtained any therapeutic benefit, that is, what is the (supposed) efficacy of the cannabis-based therapy.
- As most likely patients have gone through standard therapy prior to or concomitantly with cannabis use, we do not know whether the (supposed) effect of cannabis was in fact due -at least in part- to the standard therapy -perhaps enhanced by cannabis, but we have no proof.
- We do not know what are the parameters of tumour progression that have been monitored and for how long the patient has been monitored -many potentially beneficial effects of antineoplastic drugs (or of cannabis in this case) are just short-term actions, but what about long-term progression-free survival and overall survival?
- Cancer is a very heterogeneous disease, and so far none has put together a sufficient number of patients for a particular type of cancer to support that cannabinoids are efficacious drugs in that precise cancer.
Conclusion: Although it is possible –and of course desirable- that cannabis preparations have exerted some antineoplastic activity in some particular cancer patients, the current anecdotal evidence reported on this issue is pretty poor, and, unfortunately, remains far from supporting that cannabinoids are efficacious anticancer drugs for large patient populations.
Do cannabinoids inhibit cancer growth? (Clinical research)
Results have been published from only one Phase I clinical trial testing whether cannabinoids can treat cancer in patients. Nine people with advanced, recurrent glioblastoma multiforme –an aggressive brain tumour– that had previously failed standard therapy were given highly purified THC through a catheter directly into their brain. Under these conditions cannabinoid delivery was safe and could be achieved without significant unwanted effects. In addition, although no statistically-significant conclusions can be extracted from such a small cohort of patients and without a control group, the results obtained suggested that some patients responded -at least partially- to THC treatment in terms of decreased tumour growth rate, as evaluated by imaging and biomarker analyses. These findings were encouraging and substantially reinforced the interest on the potential use of cannabinoids in cancer therapies. However, they also highlighted the need for further research aimed at optimizing the use of cannabinoids in terms of patient selection, combination with other anticancer agents and use of other routes of administration.
Conclusion: There are still many unanswered questions around the potential for using cannabinoids as anticancer drugs, and it is necessary and desirable that exhaustive clinical studies are conducted to determine how cannabinoids can be used, other than for their palliative effects, to treat cancer patients.
About the author
Dr Manuel Guzman is professor at the Department of Biochemistry and Molecular Biology at Complutense University in Madrid, Spain. He coordinates the Cannabinoid Signaling Group.
FAQs: Does cannabis use increase the risk for schizophrenia?
by Franjo Grotenhermen
The use of cannabis may be a risk factor for the development of schizophrenia, a type of psychosis. It is currently assumed that cannabis doubles the risk (or increases the risk by 2) if heavily used in adolescence. There are other factors that increase schizophrenia risk. For example having grown up in a big city also increases the risk by about 2 compared to having grown up in the countryside. This small increase in risk means that 1 to 2 out of 100 heavy cannabis users and 1 to 2 out of 100 city dwellers will develop schizophrenia during their lifetime, compared to 0.5 to 1 out of 100 people without any risk factor.
What is psychosis?
Psychosis is a serious medical condition of unknown origin. It refers to an abnormal condition of the mind, and is a generic psychiatric term for a mental state often described as involving a "loss of contact with reality". The term “psychosis” is most often used as an “umbrella term” instead as a distinct diagnosis. People suffering from psychosis are described as psychotic. Psychosis is given to the more severe forms of psychiatric disorder, during which hallucinations and delusions and impaired insight may occur. Although there are drugs available that can ameliorate some of the symptoms, the disorder can not be cured. Schizophrenia is a special form of a psychotic disorder.
What is schizophrenia?
Schizophrenia is a mental disorder characterized by a breakdown of thought processes and by poor emotional responsiveness. It most commonly manifests itself as auditory hallucinations, paranoid beliefs, or disorganized speech and thinking. Hallucinations are perceptions in a conscious and awake state in the absence of external stimuli, which have qualities of real perception. For example, schizophrenics may hear voices in the absence of any voices. Beliefs, which are called delusions, are associated with strong conviction despite evidence to the contrary. For example, somebody may believe that he is an important historical personality such as Jesus or Napoleon. Often deficits of normal emotional responses are associated such as flat or blunted affect and emotion, poverty of speech, inability to experience pleasure, and lack of motivation. Depending on the clinical symptomatology schizophrenia can be classified in different subtypes.
How prevalent is schizophrenia?
About 15 to 20 new cases per 100.000 inhabitants of Western countries develop schizophrenia every year. The onset of symptoms typically occurs in young adulthood between the age of 18 and 35, and about 0.5 to 1.0 per cent of all citizens of Europe and North America develop schizophrenia during their lifetime. Delusions, thought disorders (e.g. thought broadcasting), and acoustic hallucinations are preliminary employed in diagnosis. These symptoms are often highly dramatic and dangerous, but these so-called “positive symptoms” normally improve over the years. On the other hand, the “negative symptoms” such as depression, inability to make social contacts, impoverishment of feelings often remain, resulting in psychosocial problems and unemployment.
What causes schizophrenia?
Both genes and the environment play a role in the development of schizophrenia. Certain variants of genes are associated with a higher risk of schizophrenia. This may explain, why schizophrenia is observed more often in some families compared to others. However, these genetic variants do not cause the disease, but play a role in the disposition to the disease. Somebody, who has a first-degree relative (parents, brother, sister) with schizophrenia, has a risk of 6.5 per cent to also develop the disease during lifetime. This means that of 100 first-degree relatives of people with schizophrenia 6 to 7 also develop the disease.
Environmental risk factors that have been established are pregnancy complications including stress, infections and malnutrition of the mother, birth complications, growing up in a large city, low but normal IQ (intelligence quotient), and drug consumption including cannabis use. Other factors, which may play an important role, are social isolation, family dysfunction and other heavily distressing factors. People with schizophrenia in the northern hemisphere are more likely to have been born in winter or spring compared to summer and autumn.
How to prevent schizophrenia?
Since risk factors are only associated with a relatively low increase of risk, they cannot be used for early detection and prevention of schizophrenia (Klosterkötter 2008). On the other hand, it is desirable to detect schizophrenia at an early stage, since early detection and early treatment is associated with a more favourable course of the disease, less depression and less suicide. Thus, prevention efforts and programs are concentrated on the detection of risk symptoms during the so-called prodromal state (early warning signs) and on making a correct diagnosis after outbreak of the disease as early as possible.
In about three quarters of all cases the outbreak of schizophrenia is preceded by a prodromal state for an average of five years. During this period the person may have thought disturbances, unusual experiences of perception, paranoid ideas, decreased ability to discriminate between ideas and perception, fantasy and true memories, and similar symptoms several times a week. There is a high risk for people experiencing prodromal symptoms to develop psychotic symptoms and psychotic episodes finally leading to schizophrenia.
What is the role of cannabis in the development of schizophrenia?
In a review of seven longitudinal studies on the association between cannabis use and schizophrenia researchers found that individuals who had ever used cannabis had an increased risk of psychosis or psychotic symptoms of 41 per cent compared to individuals who had never used cannabis. In longitudinal studies a large number of people are followed for several years, ideally from birth to adulthood, to identify for example causes of diseases or protective factors against diseases. Frequent cannabis users had twice the risk of non-users (odds ratio: 2.09) (Moore et al. 2007). Researchers noted that the uncertainty about whether cannabis causes psychosis is unlikely to be resolved by further longitudinal studies. It is most likely that cannabis use precipitates schizophrenia in individuals who are vulnerable because of a personal or family history of schizophrenia (Degenhardt and Hall 2006).
It is difficult to prove that cannabis is indeed a causal factor in the development of schizophrenia, since the association may be non-causal, at least in part. For example, some people with schizophrenia may self-medicate with cannabis to treat some of their symptoms, especially negative symptoms. However, there is increasing evidence from long-term epidemiological studies that cannabis plays a causal role.
What is the role of cannabinoids in the treatment of schizophrenia?
There are two published case series, which demonstrate that cannabis or THC may be of therapeutic value in some cases of schizophrenia, who do not respond to conventional medication (Schwarcz et al. 2009, Schwarcz et al. 2010). The authors of these reports assume that with regard to brain physiology the cause of schizophrenia in these patients may differ from other patients with schizophrenia, who respond to conventional anti-psychotic medication, that these patients may suffer from low endocannabinoid brain function.
There is clinical evidence that the natural plant cannabinoid cannabidiol (CBD) at a daily dose of 800 mg may be as effective as conventional medication in the treatment of schizophrenia (Leweke et al. 2012). CBD is known to decrease or abolish the psychological effects of THC. The treatment with CBD is associated with an increase in anandamide blood levels, and this increase is thought to be responsible for symptom improvement.
About the author
Dr Franjo Grotenhermen is chairman of the German Association for Cannabis as Medicine (ACM) and executive director of the International Association for Cannabinoid Medicines (IACM). He is working for the nova-Institut in Huerth/Rhineland, Germany.
FAQs: Does cannabis cause anxiety or does it reduce anxiety or may both occur?
US Institute of Medicine
Although euphoria is the more common reaction to smoking marijuana, adverse mood reactions can occur. Such reactions occur most frequently in inexperienced users after large doses of smoked or oral marijuana. They usually disappear within hours and respond well to reassurance and a supportive environment. Anxiety and paranoia are the most common acute adverse reactions, others include panic, depression, dysphoria, depersonalization, delusions, illusions, and hallucinations.
Source: Joy JE, Watson SJ, Benson JA, eds. Marijuana and medicine: Assessing the science base. Institute of Medicine. Washington DC: National Academy Press, 1999.
US Institute of Medicine
The 'high' associated with marijuana is not generally claimed to be integral to its therapeutic value. But mood enhancement, anxiety reduction, and mild sedation can be desirable qualities in medications particularly for patients suffering pain and anxiety. Thus, although the psychological effects of marijuana are merely side effects in the treatment of some symptoms, they might contribute directly to relief of other symptoms.
Source: Joy JE, Watson SJ, Benson JA, eds. Marijuana and medicine: Assessing the science base. Institute of Medicine. Washington DC: National Academy Press, 1999.
Giovanni Marciano and colleagues
Here we show that the endogenous cannabinoid system has a central function in extinction of aversive memories. (…) Mice were trained to associate a tone with an electric footshock (conditioning). After conditioning, animals shivered when they heard the tone. This response served as an indicator of aversive memory, and is gradually extinguished on repeated tone presentations. (...) Mice without cannabinoid-1 receptors showed strongly impaired short-term and long-term extinction of the aversive memory (...).
Overall our findings suggest that the endogenous cannabinoid system could represent a therapeutic target for the treatment of diseases associated with inappropriate retention of aversive memories or inadequate response to aversive situations, such as posttraumatic stress disorders, phobia, and certain forms of chronic pain.
Modified according to: Marsicano G, et al. The endogenous cannabinoid system controls extinction of aversive memories. Nature 2002;418(6897):530-534.
Pankaj Sah
Marciano and colleagues propose a new role for this endocannabinoid system - extinguishing fear-related memories in mice. The finding might have implications for treating anxiety disorders in humans.
We can form memories in several different ways, one of which is Pavlovian conditioning - the classic example being that of Pavlov's dogs, which learned to expect food whenever they heard a ringing tone. We all form these types of associations; for instance, we may associate a particular piece of music with our first love affair. But the connection need not always be pleasant. Imagine you are having a quiet walk in a park when you are threatened by an armed person. During the attack you are terrified; your heart races and your palms are sweaty. You run and escape. Later, you may find that entering the same park brings back in detail the memory of attack, right down to the sweaty palms.(...)
Source: Sah P. Neurobiology: Never fear, cannabinoids are here. Nature 2002;418(6897):488-9.
Franjo Grotenhermen
I would like to present a case of successful cannabis use in panic attacks. A Swiss who was suffering from panic attacks recently reported me, that cannabis use was very helpful for him between the attacks. He had not used cannabis during the attack since it would be too late then.
The attacks had started about nine months ago without recognizable cause and occured nearly daily. He also suffered from nausea, loss of appetite and dizziness. He had been prescribed strong medical drugs from his doctor, which he would not like to take permanently. Five months ago he started to use cannabis, which he takes about three times a week now. The panic attacks declined in frequency and intensity. Dizziness and nausea have disappeared completely and he regained appetite. The panic attacks nearly disappeared as well.
Source: Grotenhermen F. Kann Cannabis bei einer aufkommenden Panikattacke sinnvoll eingesetzt werden? [Can cannabis be used in an arising panic attack?] Hanf-Magazin, September 2002.
http://www.cannabis-med.org/index.php?tpl=faq&red=faqlist&id=278&lng=en
For more information, consult Dr. David Frederick Hepburn online material:
Cannabis Hemp Conference and Expo: http://www.cannabishempconference.com/dr-dave-hepburn-md/
Market Wired, Award Winning Columnist Dr. David Frederick Hepburn Embarks on Speaking Tour: http://www.marketwired.com/press-release/award-winning-columnist-dr-dave-hepburn-embarks-on-speaking-tour-2166319.htm
CBC News, Q&A with Dr. David Frederick Hepburn, B.C. doctor going on medical marijuana speaking tour: http://www.cbc.ca/news/canada/british-columbia/q-a-with-dr-dave-hepburn-b-c-doctor-going-on-medical-marijuana-speaking-tour-1.3213458
Patients out of time: http://patientsoutoftime.org/doctors/david-hepburn-md/
Leafly contributors: https://www.leafly.com/news/author/dr-dave-hepburn
Keynote Speakers Canada: http://keynotespeakerscanada.ca/speaker/dave-hepburn-md
National Speakers Bureau: https://www.nsb.com/speakers/dave-hepburn/
Cannabis Culture, Q&A with Dr. David Frederick Hepburn, B.C. Doctor Going on Medical Marijuana Speaking Tour: http://www.cannabisculture.com/content/2015/09/04/qa-with-dr-dave-hepburn-b-c-doctor-going-on-medical-marijuana-speaking-tour
The globe and mail, On a mission to change how family doctors view medical marijuana: https://www.theglobeandmail.com/news/british-columbia/on-a-mission-to-change-how-family-doctors-view-medical-marijuana/article25791287/
Cannabis Digest, Teaching Cannabis Medicine in Canada: Interviews with Dr. David Frederick Hepburn and Dr. Robert Sealy: https://cannabisdigest.ca/teaching-cannabis-medicine-canada-interviews-dr-david-hepburn-dr-robert-sealy/
https://phil420.com/tag/dr-dave-hepburn/
https://www.pinterest.com.mx/pin/853643304340545028/
Leafly, Cannabis Shows Great Promise in Treating Cancer—Let’s Not Wreck It With Hyperbole: https://www.leafly.com/news/health/cannabis-shows-great-promise-treating-cancer-lets-not-wreck-hyperbole
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