Cancer

Cannabis & Cancer: A Parable

Cannabis & cancer
By on January 11, 2016

Adapted from the forthcoming book, The Thinking Patient’s Guide to Cannabis & Cancer (vol. I)  by Jonathan Treasure, which Project CBD highly recommends. A free download of the complete 2nd chapter (partially excerpted below) is available here.

The Mechanic and the Gardener

Seeing herbs as either poison or panacea is unhelpful, but so is vilifying either modern mainstream or traditional herbal medicine. A more useful way to illustrate the differences between the two would be by comparing the approaches of a gardener and a mechanic.

Mainstream medicine tends to see the body as a machine—albeit a complex one. A machine is understood in terms of basic principles of engineering design, where the assembly of component parts follow predictable rules of organization and behavior; a malfunction can usually be fixed by logical fault-finding (diagnosis) and mending or replacing the defective part—a mechanical approach.

For herbal medicine, the body is more like a garden—an ecosystem unto itself, a complex network of inter-relating and interdependent systems in which the whole is more than the sum of its parts. Malfunction can arise from stressors or perturbances which, if uncorrected, lead to imbalances that, over time, manifest as patterns of disease. Fixing problems therefore involves adjustments to the terrain or ground . . . much like the job of a gardener.

Put another way, when things go wrong, mainstream medicine tends to focus on the problem in terms of the pathology and the disease, whereas herbal medicine tends to look at the person who has the disease.

In terms of cancer, this is classically described as the polarity between tumor and host, the latter being the terrain or ground in which the tumor develops. Extending our horticultural theme, cancer could be likened to an invasive weed. Weeds thrive in disturbed and neglected ground, so amending the soil (checking its pH, mineral content and feeding it with appropriate micronutrients) can prevent invasive weeds from taking root. Similarly, creating an internal "anti-cancer" garden or terrain within the body is one of the more important ways in which herbs can be used to prevent cancer and inhibit its progression. And, as is the case with chemotherapy and other heroic cancer treatments, killing weeds with poisons and herbicides that cause collateral damage to the surroundings is not necessarily the best way to clear them from a garden—although at times it may be the only way.

In any event, there will always be gardeners who have a mechanical approach, and mechanics who can be as artistic as gardeners. In practice, especially with cancer where the situation is rarely simple, the smart patient will seek out gardeners who understand mechanics and mechanics who are gardeners.

CBD-Drug Interactions: Role of Cytochrome P450

cbd drug interactions
By on September 08, 2015

With cannabidiol (CBD) poised to become widely available in pharmaceutical, nutraceutical, and herbal preparations, medical scientists are taking a closer look at CBD-drug interactions.

Cannabidiol is a safe, non-intoxicating, and non-addictive cannabis compound with significant therapeutic attributes, but CBD-drug interactions may be problematic in some cases.

CBD and other plant cannabinoids can potentially interact with many pharmaceuticals by inhibiting the activity of cytochrome P450, a family of liver enzymes. This key enzyme group metabolizes most of the drugs we consume, including more than 60 percent of marketed meds.

At sufficient dosages, CBD will temporarily deactivate cytochrome P450 enzymes, thereby altering how we metabolize a wide range of compounds, including tetrahydrocannabinol (THC), which causes the high that cannabis is famous for.

Metabolizing THC

When THC or any other foreign compound enters the body, it is metabolized. This process is generally very complicated. Metabolizing something properly can involve multiple molecular pathways and various enzymes that enable the body to get rid of the compound (often done by adding something to the original compound). Or metabolism can entail breaking down a compound into a more basic molecule that the body then uses.

Products of a drug’s metabolism are called its metabolites. These metabolites can have very different properties than the initial drug. Ethanol, for example, owes some of its effects, including much of the hangover, to its two-step metabolism. The buildup of acetaldehyde in the liver—while ethanol is converted first to acetaldehyde and then to acetic acid—is a major reason for ethanol’s liver toxicity and the nausea and vomiting caused by excessive consumption.

THC metabolites contribute significantly to the effects of cannabis consumption. Eleven-hydroxy-THC (11-OH-THC), for example, is a THC metabolite that activates the CB1 cannabinoid receptor in the brain and induces a high more potently than THC itself. This means that the body’s metabolism of THC can make it more potent.

Cytochrome P450 enzymes contribute to the metabolism of drugs by oxidizing them, which generally means incorporating an oxygen atom into the drug’s molecular structure. Oxidation will usually make a compound more water soluble and therefore easier for the kidneys to filter out. Both steps in the metabolism of ethanol, mentioned above, and the conversion of THC into 11-OH-THC involve oxidation (though ethanol is not oxidized specifically by cytochrome P450).

Different routes of cannabinoid administration have different effects. Inhaled THC enters capillaries in the lungs, passes into general circulation through the pulmonary arteries, and quickly crosses the blood-brain barrier. When ingested orally, however, THC is absorbed in the small intestine and then carried to the liver, where it is metabolized by subclasses of cytochrome P450 (abbreviated CYP), specifically the CYP2C and CYP3A enzymes.

These liver enzymes also metabolize CBD, converting it into 7-OH-CBD and 6-OH-CBD. But there has been relatively little research into the properties of these CBD metabolites.

Metabolizing CBD

The way CBD interacts with cytochrome P450 is pivotal; in essence, they deactivate each other. Preclinical research shows that CBD is metabolized by cytochrome P450 enzymes while functioning as a “competitive inhibitor” of the same liver enzymes. By occupying the site of enzymatic activity, CBD displaces its chemical competitors and prevents cytochrome P450 from metabolizing other compounds.

The extent to which cannabidiol behaves as a competitive inhibitor of cytochrome P450 depends on how tightly CBD binds to the active site of the metabolic enzyme before and after oxidation. This can change greatly, depending on how—and how much—CBD is administered, the unique attributes of the individual taking this medication, and whether isolated CBD or a whole plant remedy is used.

If the dosage of cannabidiol is low enough, it will have no noticeable effect on CYP activity, but CBD may still exert other effects. There is no clearly established cut-off dose, below which CBD does not interact with other drugs. A 2013 report on a clinical trial using GW Pharmaceutical’s Sativex, a whole plant CBD-rich sublingual spray, found no interactions with CYP enzymes when approximately 40mg of CBD were administered. A subsequent clinical trial, however, found that 25mg of orally administered CBD significantly blocked the metabolism of an anti-epileptic drug.

How do CBD-generated changes in cytochrome P450 activity impact the metabolic breakdown of THC? Animal studies indicate that CBD pretreatment increases brain levels of THC. That’s because CBD, functioning as a competitive inhibitor of cytochrome P450, slows down the conversion of THC into its more potent metabolite, 11-OH-THC. Consequently, THC remains active for a longer duration, but the peak of the extended buzz is blunted somewhat under the influence of cannabidiol.

Other factors figure prominently in CBD’s ability to lessen or neutralize the THC high.

Grapefruit and Ganja

Lester Bornheim, a research pharmacologist at the University of California in San Francisco, was among the first scientists to study the metabolism of CBD. In 1987, he was awarded a NIDA grant to investigate the effects of phytocannabinoids on cytochrome P450 enzymes. THC and cannabinol (CBN) also inhibit CYP activity, but CBD, of all the plant cannabinoids studied, is the strongest cytochrome P450 deactivator.

“It’s a very unusual enzyme. Almost all other enzymes are designed to fit a single substrate and carry out a single chemical process resulting in a single product,” Bornheim noted, whereas numerous drugs are substrates for cytochrome P450, which seems to function like a generic breakdown mechanism for a wide range of exogenous and endogenous substances.

In 1999, Bornheim addressed the annual gathering of the International Cannabinoid Research Society (ICRS) and drew attention to the possibility that CBD could interfere with the metabolism of many medications. A year earlier, a team of Canadian scientists identified certain compounds in grapefruit that inhibit the expression of some cytochrome P450 enzymes—which is why physicians often warn patients not to eat grapefruit before taking their meds. CBD, it turns out, is a more potent inhibitor of cytochrome P450 enzymes than the grapefruit compound Bergapten (the strongest of several grapefruit components that inhibit CYPs).

What does this mean in practical terms for a medical marijuana patient on a CBD-rich treatment regimen who takes a prescription blood-thinner like warfarin, for example? CBD reduces the enzymatic degradation of warfarin, thereby increasing its duration of action and effect. A person taking a CBD-rich product should pay close attention to changes in blood levels of warfarin, and adjust dosage accordingly as instructed by their doctor.

Cancer and Epilepsy

In cancer treatment, the precise dosing of chemotherapy is extremely important; doctors often struggle to find the maximum dose that will not be catastrophically toxic. Many chemotherapy agents are oxidized by CYPs before their inactivation or excretion. This means that for patients using CBD, the same dose of chemotherapy may produce higher blood concentrations. If CBD inhibits the cytochrome-mediated metabolism of the chemotherapy and dosage adjustments aren’t made, the chemotherapy agent could accumulate within the body to highly toxic levels.

By and large, however, there have been few reported adverse cannabinoid-drug interactions among the many cancer patients who use cannabis to cope with the wrenching side effects of chemotherapy. It is possible that whole plant cannabis, with its rich compensatory synergies, interacts differently than the isolated CBD that is administered in most research settings. As well, the cytoprotective effects of the cannabinoids may mitigate some of the chemotherapeutic toxicity.

Some epileptic patients have encountered issues with how CBD interacts with their anti-seizure medication. A small clinical study at Massachusetts General Hospital involving children with refractory epilepsy found that CBD elevated the plasma levels and increased the long-term blood concentrations of clobazam, an anticonvulsant, and norclobazam, an active metabolite of this medication. A majority of these children needed to have their dose of clobazam reduced due to side effects. Given that both clobazam and CBD are metabolized by cytochrome P450 enzymes, a drug-drug interaction is not surprising. Published in May 2015, the study concluded that “CBD is a safe and effective treatment of refractory epilepsy in patients receiving [clobazam].” But the report also emphasized the importance of monitoring blood levels for clobazam and norclobazam in patients using both CBD and clobazam.

Dr. Bonni Goldstein has observed cases in which small doses of high-CBD/low-THC cannabis oil concentrate seemed to aggravate seizure disorders rather than quell them. How could this happen, given CBD’s renown anti-epileptic properties?

A 1992 review by Lester Bornheim and his colleagues indicated that CBD inhibits some cytochrome P450 enzymes at smaller doses than what is required for CBD to exert an anti-epileptic effect. This means that a certain dose of CBD could alter the processing of an anti-epileptic drug taken by the patient, but this amount of CBD might not be enough to provide any anti-epileptic relief itself. The advice some physicians offer in this situation may seem counterintuitive: Increase the dose of CBD—perhaps even add a little more THC (or THCA, the raw, unheated, non-psychoactive version of THC)and this may be more effective for seizure control.

Enigmatic Enzymes

But why would preventing the breakdown of an anti-epileptic drug reduce its effect? There are a number of possible answers, depending on the drug in question. The active component of the drug (the chemical that exerts an anti-epileptic effect) may be a breakdown product of the actual drug taken. So, by slowing the metabolism of the original drug, CBD would make that drug less active.

Other explanations are conceivable. For example, if the activity of certain CYPs is slowed, the drug may be broken down by another metabolic pathway, the products of which could then interfere with the drug’s activity. Or perhaps the inhibition of CYPs is not the predominant way that CBD interacts with certain anti-epileptic medications.

To complicate matters even further, a presentation by Dr. Kazuhito Watanabe at the 2015 International Cannabinoid Research Society meeting in Nova Scotia disclosed preliminary evidence that cannabidiol may “induce”—meaning amplify the activity ofsome cytochrome P450 enzymes. (Induction of a protein involves increasing the transcription of its corresponding mRNA, which leads to greater synthesis of the protein.) This suggests that CBD can either increase or decrease the breakdown of other drugs. Again, it depends on the drug in question and the dosages used.

Any pharmaceutical, nutraceutical or green rush scheme to exploit the therapeutic potential of CBD must reckon with the fact that cannabidiol can both inactivate and enhance various cytochrome P450 enzymes in the liver—and this can potentially impact a wide range of medications. Drug interactions are especially important to consider when using life-saving or sense-saving drugs, drugs with narrow therapeutic windows, or medications with major adverse side effects. In particular, those who utilize high doses of CBD concentrates and isolates should keep this in mind when mixing remedies.

Adrian Devitt-Lee is a senior at Tufts University, studying mathematics and chemistry.

Learn More:

AED Potential Interactions with CBD

Copyright, Project CBD. May not be reprinted without permission.


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Cannabis & Cancer

CBD, cannabis and cancer
By on February 15, 2015

Published in full in Freedom Leaf Magazine.

Synergy: The interaction of elements that when combined produce a total effect that is greater than the sum of the individual elements, contributions, etc.

Millions of Americans now have access to medical marijuana. When it comes to cancer treatment, the plant may have an amazing impact when used in concert with traditional therapies. Beyond helping with the nausea of chemotherapy, there is strong scientific evidence of a deeper benefit of using cannabis with conventional therapies. Cancer cells can become extremeley sensitive to THC and CBD after being exposed to radition or chemotherapy.

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Marijuana Smoking and Lung Cancer

Marijuana and lung cancer
By on February 07, 2014

Published in full on Alternet.

Media Ignored Expert’s Shocking Findings That Marijuana Helps Prevent Lung Cancer: Now It’s Med-School Material

You'd think it would have been very big news in the spring of 2005 when Donald Tashkin, a professor of pulmonology at UCLA's David Geffen School of Medicine, revealed at a conference that components of marijuana smoke, although they damage cells in respiratory tissue, somehow prevent them from becoming malignant. But headlines announcing "Pot Doesn't Cause Cancer" did not ensue. 

Tashkin will review his findings and discuss current research this Thursday in Santa Monica, California as part of a course for doctors accredited by the University of California San Francisco. (It is open to the public; pre-registration is $95.)  

Tashkin has special credibility. He was the lead investigator on studies dating back to the 1970s that identified the compounds in marijuana smoke that are toxic. It was Tashkin who published photomicrographs showing that marijuana smoke damages cells lining the upper airways. It was the Tashkin lab reporting that benzpyrene—a component of tobacco smoke that plays a role in most lung cancers—is especially prevalent in marijuana smoke. It was Tashkin's data documenting that marijuana smokers are more likely than non-smokers to cough, wheeze and produce sputum. 

The National Institute on Drug Abuse supported Tashkin's marijuana-related research over the decades and gave him a grant to conduct a large, population-based, case-controlled study that would prove definitively that heavy, long-term marijuana use increases the risk of lung and upper-airways cancers. What Tashkin and his colleagues found, however, disproved their hypothesis.

Tashkin's team interviewed 1,212 cancer patients from the Los Angeles County Cancer Surveillance program, matched for age, gender, and neighborhood with 1,040 cancer-free controls. Marijuana use was measured in "joint years" (number of years smoked times number of joints per day). It turned out that increased marijuana use did not result in higher rates of lung and pharyngeal cancer (whereas tobacco smokers were at greater risk the more they smoked). Tobacco smokers who also smoked marijuana were at slightly lower risk of getting lung cancer than tobacco-only smokers.

The Tashkin scoop was still there for the taking in April 2009 when Tashkin reviewed his findings at a conference at Asilomar organized by "Patients Out of Time." Investigators from New Zealand had recently gotten widespread media attention for a study contradicting Tashkin's results. "Heavy cannabis users may be at greater risk of chronic lung disease—including cancer—compared to tobacco smokers," is how BBC News summed up the New Zealanders' findings. The very small size of the study—79 smokers took part, 21 of whom smoked cannabis only—was not held against the authors. As conveyed in the corporate media, the New Zealand study represented the latest word on this important subject.

Tashkin criticized the New Zealanders' methodology in his talk at Asilomar: "There's some cognitive dissonance associated with the interpretation of their findings. I think this has to do with the belief model among the investigators and—I wish they were here to defend themselves—the integrity of the investigators... They actually published another paper in which they mimicked the design that we used for looking at lung function."

Tashkin, who is 70ish and wears wire-rimmed spectacles, spoke from the stage of an airy redwood chapel designed by Julia Morgan: "For tobacco they found what you'd expect: a higher risk for lung cancer and a clear dose-response relationship. A 24-fold increase in the people who smoked the most... What about marijuana? If they smoked a small or moderate amount there was no increased risk, in fact slightly less than one. But if they were in the upper third of the group, then their risk was six-fold... A rather surprising finding, and one has to be cautious about interpreting the results because of the very small number of cases (14) and controls (4)."

Tashkin said the New Zealanders employed "statistical sleight of hand." He deemed it "completely implausible that smokers of only 365 joints of marijuana have a risk for developing lung cancer similar to that of smokers of 7,000 tobacco cigarettes... Their small sample size led to vastly inflated estimates... They had said 'it's ideal to do the study in New Zealand because we have a much higher prevalence of marijuana smoking.' But 88 percent of their controls had never smoked marijuana, whereas 36% of our controls (in Los Angeles) had never smoked marijuana. Why did so few of the controls smoke marijuana? Something fishy about that!"

Those are strong words for a UCLA School of Medicine professor.

As to the highly promising implication of his own study—that something in marijuana stops damaged cells from becoming malignant—Tashkin noted that an anti-proliferative effect of THC has been observed in cell-culture systems and animal models of brain, breast, prostate, and lung cancer. THC has been shown to promote known apoptosis (damaged cells die instead of reproducing) and to counter angiogenesis (the process by which blood vessels are formed—a requirement of tumor growth). Other antioxidants in cannabis may also be involved in countering malignancy, Tashkin said.

Much of Tashkin's talk at Asilomar was devoted to chronic obstructive pulmonary disease, another condition prevalent among tobacco smokers. Chronic bronchitis and emphysema are two forms of COPD, which is the fourth leading cause of death in the United States. Air pollution and tobacco smoke are known culprits. Inhaled pathogens cause an inflammatory response, resulting in diminished lung function. COPD patients have increasing difficulty clearing the airways as they get older.

Tashkin and colleagues at UCLA conducted a major study in which they measured lung function of various cohorts over eight years and found that tobacco-only smokers had an accelerated rate of decline, but marijuana smokers—even if they smoked tobacco as well—experienced the same rate of decline as non-smokers. "The more tobacco smoked, the greater the rate of decline," said Tashkin. "In contrast, no matter how much marijuana was smoked, the rate of decline was similar to normal." Tashkin concluded that his and other studies "do not support the concept that regular smoking of marijuana leads to COPD."


Note: The half-day series of talks, dubbed "MMJ13001B" by UCSF, is newsworthy in itself, as medical schools typically do not include cannabis in the curriculum. ("MMJ13001A" will be offered in San Francisco Oct. 24.)

The media has never taken note of the reality that there is a spectrum of expertise among doctors who approve marijuana use by patients. They have portrayed "potdocs" as quick-buck artists practicing sub-standard medicine, ignoring the serious, research-minded clinicians who understand why compounds in the plant alleviate a wide range of symptoms.

UC San Diego psychiatrist Igor Grant, director of the Center for Medicinal Cannabis Research, recently published a paper in the Open Neurology Journal concluding "it is not accurate that cannabis has no medical value, or that information on safety is lacking, and calling for its rescheduling by the federal government.

The CME course was organized by the Canadian Consortium for the Investigation of the Cannabinoids with support from the Society of Cannabis Clinicians, a California-based group. It provides 2.75 AMA PRA Category 1 Credit(s)(tm).

CBD, THC, and Cancer

Cannabis, CBD and cancer
By on February 05, 2014

Originally published on the Daily Beast.

Marijuana Fights Cancer and Helps Manage Side Effects, Researchers Find

Mounting evidence shows ‘cannabinoids’ in marijuana slow cancer growth, inhibit formation of new blood cells that feed a tumor, and help manage pain, fatigue, nausea, and other side effects.

Cristina Sanchez, a young biologist at Complutense University in Madrid, was studying cell metabolism when she noticed something peculiar. She had been screening brain cancer cells because they grow faster than normal cell lines and thus are useful for research purposes. But the cancer cells died each time they were exposed to tetrahydrocannabinol (THC), the principal psychoactive ingredient of marijuana.

Instead of gaining insight into how cells function, Sanchez had stumbled upon the anti-cancer properties of THC. In 1998, she reported in a European biochemistry journal that THC “induces apoptosis [cell death] in C6 glioma cells,” an aggressive form of brain cancer. 

Subsequent peer-reviewed studies in several countries would show that THC and other marijuana-derived compounds, known as “cannabinoids,” are effective not only for cancer-symptom management (nausea, pain, loss of appetite, fatigue), they also confer a direct antitumoral effect. 

A team of Spanish scientists led by Manuel Guzman conducted the first clinical trial assessing the antitumoral action of THC on human beings. Guzman administered pure THC via a catheter into the tumors of nine hospitalized patients with glioblastoma, who had failed to respond to standard brain-cancer therapies. The results were published in 2006 in the British Journal of Pharmacology: THC treatment was associated with significantly reduced tumor cell proliferation in every test subject

Around the same time, Harvard University scientists reported that THC slows tumor growth in common lung cancer and “significantly reduces the ability of the cancer to spread.” What’s more, like a heat-seeking missile, THC selectively targets and destroys tumor cells while leaving healthy cells unscathed. Conventional chemotherapy drugs, by contrast, are highly toxic; they indiscriminately damage the brain and body. 

There is mounting evidence, according to a report in Mini-Reviews in Medicinal Chemistry, that cannabinoids “represent a new class of anticancer drugs that retard cancer growth, inhibit angiogenesis [the formation of new blood cells that feed a tumor] and the metastatic spreading of cancer cells.”

Dr. Sean McAllister, a scientist at the Pacific Medical Center in San Francisco, has been studying cannabinoid compounds for 10 years in a quest to develop new therapeutic interventions for various cancers. Backed by grants from the National Institute of Health (and with a license from the DEA), McAllister discovered that cannabidiol (CBD), a nonpsychoactive component of the marijuana plant, is a potent inhibitor of breast cancer cell proliferation, metastasis, and tumor growth. 

In 2007, McAllister published a detailed account of how cannabidiol kills breast cancer cells and destroys malignant tumors by switching off expression of the ID-1 gene, a protein that appears to play a major role as a cancer cell conductor.   

The ID-1 gene is active during human embryonic development, after which it turns off and stays off. But in breast cancer and several other types of metastatic cancer, the ID-1 gene becomes active again, causing malignant cells to invade and metastasize. “Dozens of aggressive cancers express this gene,” explains McAllister. He postulates that CBD, by virtue of its ability to silence ID-1 expression, could be a breakthrough anti-cancer medication. 

“Cannabidiol offers hope of a non-toxic therapy that could treat aggressive forms of cancer without any of the painful side effects of chemotherapy,” says McAllister, who is seeking support to conduct clinical trials with the marijuana compound on breast cancer patients.

McAllister’s lab also is analyzing how CBD works in combination with first-line chemotherapy agents. His research shows that cannabidiol, a potent antitumoral compound in its own right, acts synergistically with various anti-cancer pharmaceuticals, enhancing their impact while cutting the toxic dosage necessary for maximum effect.

Investigators at St. George’s University in London observed a similar pattern with THC, which magnified the effectiveness of conventional antileukemia therapies in preclinical studies. THC and cannabidiol both induce apoptosis in leukemic cell lines. 

At the annual summer conference of the International Cannabinoid Research Society, held this year in Freiburg, Germany, 300 scientists from around the world discussed their latest findings, which are pointing the way toward novel treatment strategies for cancer and other degenerative diseases. Italian investigators described CBD as “the most efficacious inducer of apoptosis” in prostate cancer. Ditto for cannabidiol and colon cancer, according to British researchers at Lancaster University. 

Within the medical science community, the discovery that cannabinoids have anti-tumoral properties is increasingly recognized as a seminal advancement in cancer therapeutics.

Copyright, Project CBD. May not be reprinted without permission.

5 Marijuana Compounds That Could Help Combat Cancer, Alzheimer's, Parkinson's (If Only They Were Legal)

Medical marijuana, cancer, Alzheimer's, Parkinson's
By on February 02, 2014

Published in full on Alternet.

They don’t even get you high, so why are these natural, non-toxic substances illegal? Because they’re derived from cannabis.

Imagine there existed a natural, non-toxic substance that halted diabetes, fought cancer, and reduced psychotic tendencies in patients with schizophrenia and other psychiatric disorders. You don’t have to imagine; such a substance is already here. It’s called cannabidiol (CBD). The only problem with it is that it’s illegal.

Cannabidiol is one of dozens of unique, organic compounds in the cannabis plant known as cannabinoids, many of which possess documented, and in some cases, prolific therapeutic properties. Other cannabinoids include cannabinol (CBN), cannabichromene (CBC), cannabigerol (CBG), and tetrahydrocannabivarin (THCV). Unlike delta-9-tetrahydrocannabinol (THC), the primary psychoactive cannabinoid in marijuana, consuming these plant compounds will not get you high. Nonetheless, under federal law,  every one of these cannabinoids is defined as schedule I illicit substances because they naturally occur in the marijuana plant.

That’s right. In the eyes of the US government, these non-psychotropic cannabinoids are as dangerous to consume as heroin and they possess absolutely no therapeutic utility. In the eyes of many scientists, however, these cannabinoids may offer a safe and effective way to combat some of the world’s most severe and hard-to-treat medical conditions. Here’s a closer look at some of these promising, yet illegal, plant compounds.

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