Category Archives: Noticias

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Managing Nausea with Cannabis

Category : Noticias

A patient’s perspective

Laura was a physician who spent much of her clinical time treating substance abuse disorders, and she had no recent experience with cannabis herself. Her aversion to using cannabis when she was going through chemotherapy for breast cancer did not surprise me. Nausea, and the anxiety that preceded its inevitable occurrence, were disabling. I trained with Laura in family medicine, and I had appreciated the beneficial effects of cannabis used by my cancer patients, but it was hard getting Laura to accept my advice.

Finally, I introduced her to a calibrated vaporizer – a method of administration that could provide quick relief, but was different than the ‘smoke a joint out behind the barn’ approach she had imagined. She started with a CBD-rich herb that had a ratio of 2:1 CBD:THC, hoping that the resulting intoxication would be mild enough to tolerate.

I received a call from Laura three days after her latest chemo, and quickly answered it to see if her trial of cannabis had been helpful to her. At first I was concerned because she was crying into the phone, but when I could understand her words I was thrilled. She reported, “It worked faster, better, and more completely than any of the prescriptions my oncologist gave me.”

If even reading about nausea and vomiting will make you queasy, you may want to jump to the end of this article and skip the potentially nauseating details. Nausea is like that – easy to feel if you are so inclined.

Nausea and vomiting are each distinctive, different problems – clearly related, but quite different when it comes to cause and treatment. Those who suffer know that nausea is worse to live with than vomiting because it is a continuous sensation, and is harder to control.

What is nausea?

Nausea and vomiting are protective defense mechanisms in the human body, and short-term episodes can be therapeutic, though miserable. But what if nausea is not short-term? What if it is an unavoidable side effect, or chronic, with no relief in sight?

If there is no clear trigger for nausea, a patient should work with their doctor to discover the underlying problem.  This is true especially if the nausea does not resolve within a day or two because that may be a sign of more serious problems.

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Growing Pains: Can Sustainable Farmers Survive Legalization?

Category : Noticias

Securing local and state licenses to cultivate cannabis is costly

The California counties of Humboldt, Mendocino and Trinity, which comprise the Emerald Triangle, emerged as the epicenter of domestic cannabis cultivation in the late 1970s and early ‘80s. After the Golden State legalized medical marijuana in 1996, the nascent cannabis industry spread throughout much of Northern California’s remote regions and into the Central Valley. But today anxiety is high in weed country, which desperately needs the industry to survive.

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Thank you Dennis Peron

Category : Noticias

Dennis Peron

To accommodate a deluge of new members, Dennis Peron moved the San Francisco Cannabis Buyers Club in 1995 to a converted five-story warehouse at 1444 Market Street, a busy locale near the San Francisco Civic Center.

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Green Rush Blues: California Cannabis After Legalization

Category : Noticias

The huge underground cannabis economy was woven into the commercial fabric of California long before the 2016 passage of Proposition 64, which legalized marijuana for adult use. Transforming a shadowy, multibillion-dollar industry into a heavily taxed and regulated structure presents unique and enormous challenges. Who will gain and who will lose under the new regime? Will the expected financial dividend from legalization be broadly distributed throughout the Golden State?

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Cannabinoid-Pharmaceutical Interactions: What You Need to Know

Category : Noticias

Cannabis samples being prepared at Sonoma Lab Works for analysis

Interactions between medications are very common, especially in elderly populations that medicate for pain, diabetes and high cholesterol. The geriatric population is also the fastest-growing group of medical cannabis users. Cannabis has demonstrated efficacy in treating pain, and some phytocannabinoids have been suggested for various metabolic conditions.

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Treasure Hunt

Category : Noticias

Nine ways that scientists are targeting the endocannabinoid system with synthetic drugs and isolates
By Martin A. Lee On December 13, 2017

In recent years, cannabis has been at the center of one of the most important developments in modern science, which has significantly advanced our understanding of health and disease.

Research on marijuana’s effects led directly to the discovery of a major biochemical signaling system in the human body – the endocannabinoid system – which plays a pivotal role in regulating a wide range of physiological processes that affect our mood, our blood pressure, our bone density, our metabolism, our intestinal fortitude, our energy level, how we experience pain, stress, hunger, and much more.

“By using a plant that has been around for thousands of years, we discovered a new physiological system of immense importance,” says Israeli scientist Raphael Mechoulam. “We wouldn’t have been able to get there if we had not looked at the plant.”

Described by Mechoulam as “a medicinal treasure trove,” cannabis contains more than 100 unique biologically active compounds known as “cannabinoids,” including tetrahydrocannabinol (THC) and cannabidiol (CBD). THC causes the high that cannabis is famous for, CBD does not; both have important therapeutic attributes.

In addition to phytocannabinoids produced by the plant, there are endogenous cannabinoids – marijuana-like molecules – that occur naturally in the human brain and body. And there are also synthetic cannabinoids created by pharmaceutical researchers, who are developing new medicines that target the endocannabinoid system for therapeutic benefit.

Some of these novel synthetic compounds activate the same cannabinoid receptors – CB1 and CB2 – in the brain and body that respond pharmacologically to THC and other cannabis components.1

Medical scientists are also experimenting with synthetic drugs designed to improve “endocannabinoid tone” without binding directly to cannabinoid receptors.

Here are nine strategies that scientists are currently pursuing in an effort to harness the healing potential of the endocannabinoid system:



1. Single-molecule plant cannabinoids

Dronabinol, marketed in pill form as Marinol, is a single-molecule THC extract combined with sesame oil. It got fast-tracked for approval by the Food and Drug Administration in 1985 in response to rising patient demand for medical marijuana.

Other THC preparations are also on the FDA’s radar, including Syndros, a liquid THC drug produced by Insys. But patented single-molecule THC is a poor substitute for whole plant cannabis.

Even though it is highly psychoactive and potentially dysphoric, pharmaceutical THC is legally accessible in all 50 states as a prescription medication.

Cannabidiol, unlike pure THC, is not yet legal in all 50 states. But CBD will soon become a legal pharmaceutical, as the FDA is poised to approve Epidiolex, a botanically derived anti-seizure medication produced by GW Pharmaceuticals. Epidiolex is pure CBD with a dash of cannabidivarin (CBDV), a “minor” cannabinoid that also has potent anti-epileptic properties.

Along with the imminent advent of pharmaceutical CBD, several R&D firms have begun to harvest single-molecule cannabinoids, such as CBDV, from a yeast substrate. As this biotechnology improves, drug developers and pharmacists will have access to numerous single-molecule cannabis compounds.


Image Credit: Bryan Satalino

2. Synthetic cannabinoid analogs

Scientists have created synthetic analogs of plant cannabinoids for research purposes and for commercial sale and distribution. Nabilone, a synthetic THC analog, was developed by Eli Lilly and Co. as a treatment for chemotherapy-induced nausea and vomiting.

Marketed under the trade name Cesamet, this synthetic cannabinoid is used as an adjunct therapy for chronic pain management in Canada and other countries. Clinical trials of Nabilone have indicated some effectiveness for fibromyalgia, Parkinson’s, PTSD-related nightmares, irritable bowel disease, and multiple sclerosis.

Researchers are using various synthetic analogs to investigate the biochemical pathways and molecular mechanisms of the endocannabinoid system. Some of these compounds (such as WIN55,212-2 and CP55,940) bind to both cannabinoid receptors – CB1 and CB2 – much like THC. Other experimental drugs target only one type of cannabinoid receptor and not the other. 2

A cannabinoid agonist binds to a cell receptor and causes it to initiate a signaling cascade that modulates various physiological processes and protects neurons against toxic insults. A cannabinoid antagonist binds to a cell receptor and prevents it from signaling.


Image Credit: Bryan Satalino

3. Synthetic cannabinoid antagonists

Cannabinoid CB1 receptors, which mediate the psychoactive effects of THC, are concentrated in the brain and central nervous system. When THC binds to CB1, it can make a person feel stoned – and hungry. The “munchies,” scientists confirmed, are linked to stimulation of CB1 receptors in areas of the brain that regulate hunger and satiety. If activated, CB1 receptors induce appetite; if blocked, they reduce it.

SR141716,” a synthetic CB1 antagonist developed by the French pharmaceutical giant Sanofi-Aventis, was initially utilized as a research tool: By blocking CB1 and monitoring which functions were altered, scientists advanced their understanding of the endocannabinoid system.

Sanofi strategists believed they had invented the perfect diet pill, and they promoted SR141716 as an appetite suppressant in Europe. But the diet drug, sold as “Rimonabant,” proved to be too blunt an instrument. Before long, the synthetic CB1 antagonist was pulled from circulation because of dangerous side effects – high blood pressure, nausea, vomiting, anxiety, mood swings, depression, headaches, seizures, sleep disorders, and a heightened risk of suicide.

If nothing else, the CB1 antagonist debacle provided vivid evidence that a well-functioning endocannabinoid system is essential for good health.3


4. Peripherally restricted CB1 agonists

Cannabinoid CB1 receptors, the most prevalent protein receptors in the human brain, influence many neurological functions, including marijuana’s mood-altering effects. CB1 receptors are also expressed in the enteric nervous system (the gut), the liver, kidneys, heart and other peripheral organs.

Stimulating CB1 receptors can deliver significant therapeutic benefits, but THC’s psychoactivity limits its medical utility, according to Big Pharma catechism, which defines the CB1-mediated marijuana “high” as an adverse side effect that drug designers should avoid if they hope to win regulatory approval of their patented synthetic novelties.

So pharmaceutical researchers have created peripherally-restricted CB1 agonists (such as AZ11713908) that only activate CB1 receptors outside the central nervous system, but don’t cross the blood-brain barrier.

A peripherally restricted CB1 agonist won’t cause side effects such as disconcerting dysphoria or useless euphoria. But such a compound has never been approved for therapeutic use by the FDA.


Researchers studying impact on CB2 receptors in animals

5. Selective CB2 agonists

Scientists have been hot on the trail of another type of synthetic cannabinoid – a “selective CB2 agonist” – that will bypass the brain while acting on the peripheral nervous system, where CB2 receptors are concentrated. CB2 receptors regulate immune function, pain perception, and inflammation.

Tinkering with synthetic compounds (such as HU 308 and JWH 133) that selectively stimulate CB2 receptors raises the prospect of healing without the high because CB2 receptors are localized primarily outside the brain and thus do not induce psychoactivity.

Cannabinoid researchers have their eyes on the ultimate prize, the pharmaceutical Holy Grail – a non-addictive painkiller bereft of adverse side effects. Animal experiments focusing on the CB2 receptor initially showed promise.

Thus far, however, drug companies have not been able to synthesize clinically effective CB2-selective compounds, though not for lack of trying. “If drug discovery is a sea, then CB2 is a rock that is surrounded by shipwrecked-projects,” remarked Italian scientist Giovanni Appendino.



6. Water-soluble cannabinoids

In their natural form, plant cannabinoids and endocannabinoids are oily, hydrophobic substances that don’t dissolve in water. But these lipid molecules can be structurally altered so that they become water soluble without diminishing their therapeutic attributes.

Scientists have developed several ways of synthesizing water-compatible derivatives of THC and other cannabinoids that are more bioavailable and thus potentially more potent than their oily, naturally-occurring counterparts.

The first water-soluble version of THC was created in 1972. Subsequent research found that water-friendly cannabinoid derivatives can lower intraocular pressure in rabbits. A water-soluble cannabinoid ester, “O-1057,” exhibited stronger analgesic properties than THC in preclinical experimentation.

Internet retailers are claiming to sell water-soluble CBD formulated as a nanoemulsion. Pure CBD delivered via nanotechnology is supposed to provide exceptionally high bioavailability and remedial effect compared to a hydrophobic CBD oil extract.

But a CBD isolate typically requires a much higher dose for therapeutic efficacy than a whole plant CBD-rich concentrate – and this factor may cancel out the alleged advantages of nanoemulsified single-molecule CBD.


ZCZ011 {Image source Wikipedia}

7. Allosteric cannabinoid receptor modulators

Because direct, full-on stimulation of cannabinoid receptors in the brain may trigger undesirable psychoactive effects, scientists have developed synthetic compounds that change the shape of the CB1 receptor and influence how it signals without causing a THC-like high. These compounds, known as allosteric modulators, can either amplify or decrease a receptor’s ability to transmit a signal.

A “positive allosteric modulator” increases the potency and/or efficacy of CB1 receptor activation by anandamide and 2AG (the two main endogenous cannabinoids), thereby boosting the protective effects of the endocannabinoid system.

Scientists at the University of Aberdeen in Scotland have synthesized a positive allosteric modulator of CB1 to treat pain and neurological disorders. When researchers at Virginia Commonwealth University tested this experimental drug (“ZCZ011”) on mice, it reduced inflammatory pain by magnifying the CB1 receptor’s response to anandamide.

But allosteric effects are rarely consistent across species, which significantly impedes drug development in this area.4



The brain on cannabis

8. Inhibitors of endocannabinoid metabolizing enzymes

Medical scientists are experimenting with synthetic designer drugs to enhance endocannabinoid tone without binding directly (or allosterically) to cannabinoid receptors.

Pharmacological augmentation of endocannabinoid signaling can be achieved by inhibiting fatty acid amide hydrolase (FAAH) and/or monoglycerol lipase (MAGL), the catabolic enzymes that break down the brain’s own marijuana-like molecules, anandamide and 2AG, respectively.

Simply put, less FAAH and MAGL means more anandamide and 2AG, resulting in greater cannabinoid receptor activity throughout the body. Drugs that suppress endocannabinoid-metabolizing enzymes indirectly boost cannabinoid receptor signaling, causing a natural high without the vivid psychoactive effects associated with synthetic and plant-based CB1 agonists.

Preclinical research suggests that indirect modulation of endocannabinoid signaling could become a treatment option for various inflammatory conditions and stress-related disorders. FAAH and MAGL inhibition have been shown to ease pain, anxiety, colitis, hypertension, opiate withdrawal, diarrhea and arthritis in animal models.

While drug developers investigate synthetic FAAH-inhibitors (such as URB597) and MAGL-inhibitors (such as JZL 184), one need look no further than the kitchen spice rack for phytonutrients that regulate endocannabinoid tone by inhibiting the same catabolic enzymes. Nutmeg, one of many culinary spices that interact with the endocannabinoid system, inhibits the breakdown of both anandamide and 2AG, the brain’s own marijuana.


AM404 {Image source Wikipedia}

9. Endocannabinoid reuptake inhibitors

Another way to augment endocannabinoid tone entails delaying the reuptake of anandamide and 2AG. Scientists have synthesized reuptake inhibitors (such as AM404) that target transport molecules known as fatty acid binding proteins. These membrane-penetrating fatty acid binding proteins facilitate the intracellular transport and reuptake of endogenous cannabinoids.

By blocking access to these critical transport molecules, synthetic reuptake inhibitors increase endocannabinoid levels in the brain’s synapses. This results in heightened cannabinoid receptor signaling and endocannabinoid-induced protective effects.

THC and CBD also inhibit endocannabinoid reuptake. Enhancing endocannabinoid tone via reuptake inhibition may be a key mechanism whereby plant cannabinoids confer protective effects against seizures and neurodegeneration, as well as many other health benefits.

Fool’s gold?

Despite repeated setbacks, the possibility of healing without the high persists as an idée fixe among cannabinoid scientists and pharmaceutical researchers.

The lack of success with selective CB2 agonists, peripherally restricted CB1 agonists, allosteric modulators, CB1 antagonists and other non-euphoric cannabinoids underscores the challenges and limitations of synthetic, monomolecular medicine that targets a single protein receptor while forsaking whole plant synergies.

Synthetic CBD analogs are also in development. By tweaking the mother molecule and removing, adding or editing a molecular side chain, pharmaceutical researchers hope to create a marketable compound that is more potent and more effective than botanical CBD.

But a CBD isolate is not inherently superior to a whole plant CBD-rich extract. Preclinical studies that compare the efficacy of single-molecule CBD and full spectrum CBD-rich oil concentrates indicate that CBD solo is effective only at precise, high doses – whereas whole plant CBD-rich extracts have a much wider and safer therapeutic window and are effective at significantly lower doses. Problematic drug interactions are also much likelier with high dose single-molecule CBD.

Regulatory policy should not privilege single-molecule meds over full spectrum cannabis remedies. Patients are best served by having access to a wide range of cannabinoid-based therapeutic options, including artisanal whole plant preparations and synthetic isolates, if and when they become available.

Martin A. Lee is the director of Project CBD and the author of Smoke Signals: A Social History of Marijuana – Medical, Recreational and Scientific.


  1. Only four cannabis compounds bind directly to either one or both cannabinoid receptors. THC activates CB1 and CB2. Cannabinol (CBN), a THC breakdown component, activates the CB1 receptor, though with less potency than THC. Tetrahydracannabivarin (THCV), the propyl variant of THC, binds to both cannabinoid receptors, activating CB2 while blocking CB1. And beta caryophyllene, an aromatic terpene found in many cannabis strains, green leafy vegetables, and common kitchen spices, activates CB2. Other cannabinoids, including CBD, interact with the endocannabinoid system indirectly without binding like lock and key to a cannabinoid receptor.
  2. Developed as a research tool to study that endocannabinoid system, JWH-018 is a synthetic cannabinoid compound that activates the CB1 receptor but not CB2. After the formula for this potent CB1 agonist was published in the scientific literature, JWH-018 surfaced as a street drug known as “Spice” or “K2.” Media accounts typically mischaracterize Spice as “synthetic marijuana.”
  3. U.S. government scientists have not given up entirely on Rimonabant. The fact that this compound blocks the euphoric effects of cannabis is a big plus to the National Institute on Drug Abuse, which has sponsored research on utilizing CB1 blockers to treat various addictions, including “cannabis dependence.”
  4. Canadian scientists have identified CBD as a “negative allosteric modulator” of the CB1 receptor based on in vitro research. This means that CBD, when administered in combination with THC, will alter the shape of the CB1 receptor in a way that weakens its binding affinity for THC. As a negative allosteric modulator of CB1, CBD lowers the ceiling on THC’s psychoactivity, which might be why people don’t feel as high when using CBD-rich cannabis as compared to a THC-infused product.


• Han S, Thatte J, Buzard DJ, Jones RM. Therapeutic utility of cannabinoid receptor type 2 (CB(2)) selective agonists. J Med Chem. 2013 Nov 14;56(21):8224-56. PubMed PMID: 23865723.
• Ignatowska-Jankowska BM, Baillie GL, Kinsey S, Crowe M, Ghosh S, et al. A Cannabinoid CB1 Receptor-Positive Allosteric Modulator Reduces Neuropathic Pain in the Mouse with No Psychoactive Effects. Neuropsychopharmacology. 2015 Dec;40(13):2948-59. PubMed PMID: 26052038; PubMed Central PMCID: PMC4864630.
• Mitjavila J, Yin D, Kulkarni PM, Zanato C, Thakur GA, et al. Enantiomer-specific positive allosteric modulation of CB1 signaling in autaptic hippocampal neurons. Pharmacol Res. 2017 Nov 20;PubMed PMID: 29158048.
O’Hearn S, Diaz P, Wan BA, DeAngelis C, Lao N, et al. Modulating the endocannabinoid pathway as treatment for peripheral neuropathic pain: a selected review of preclinical studies. Ann Palliat Med. 2017 Aug 31;PubMed PMID: 29156899.
• Pertwee RG, Gibson TM, Stevenson LA, Ross RA, Banner WK, et al. O-1057, a potent water-soluble cannabinoid receptor agonist with antinociceptive properties. Br J Pharmacol. 2000 Apr;129(8):1577-84. PubMed PMID: 10780961; PubMed Central PMCID: PMC1572002.
• Schindler CW, Scherma M, Redhi GH, Vadivel SK, Makriyannis A, et al. Self-administration of the anandamide transport inhibitor AM404 by squirrel monkeys. Psychopharmacology (Berl). 2016 May;233(10):1867-77. PubMed PMID: 26803499; NIHMSID: NIHMS754451; PubMed Central PMCID: PMC4846479.
• Wasilewski A, Misicka A, Sacharczuk M, Fichna J. Modulation of the endocannabinoid system by the fatty acid amide hydrolase, monoacylglycerol and diacylglycerol lipase inhibitors as an attractive target for secretory diarrhoea therapy. J Physiol Pharmacol. 2017 Aug;68(4):591-596. PubMed PMID: 29151076.
• Yu XH, Cao CQ, Martino G, Puma C, Morinville A, et al. A peripherally restricted cannabinoid receptor agonist produces robust anti-nociceptive effects in rodent models of inflammatory and neuropathic pain. Pain. 2010 Nov;151(2):337-44. PubMed PMID: 20696525.

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The Origins of Reefer Madness [Book Excerpt]

Category : Noticias

On August 11, 1930, Harry Jacob Anslinger became the director of the newly formed Federal Bureau of Narcotics (FBN) in Washington, D.C. The Voldemort of vipers, he would run the FBN with an iron fist through six presidential administrations spanning more than three decades.
By Martin A. Lee On October 15, 2017

The War on Cannabis "Reefer Madness"

Excerpted from Smoke Signals: A Social History of Marijuana—Medical, Recreational and Scientific. Reprinted at FAIR online.

Yellow Journalism and the Anti-Cannabis Crusade

On August 11, 1930, Harry Jacob Anslinger became the director of the newly formed Federal Bureau of Narcotics (FBN) in Washington, D.C. He would run the FBN with an iron fist through six presidential administrations spanning more than three decades.

An imposing, husky, bull-necked figure nearly six feet tall, he looked like a tough law-and-order drug buster. With a large square head, huge ears, a cleft chin, and glowering eyes, Anslinger took great pride in his role as the archnemesis of marijuana smokers. He was the godfather of America’s war on drugs, and his influence on public policy would be felt long after death stiffened his fingers in 1975.

When Anslinger grabbed the reins at the FBN, marijuana had already been banned in 24 U.S. states, but there still was no coordinated federal attempt to outlaw the plant. During its first few years, the FBN issued annual reports that minimized the marijuana problem, which Anslinger believed was best dealt with by state and local officials.

The stuff grows “like dandelions,” he complained. Trying to stamp out a plant that flourished everywhere in the world except Antarctica and the Arctic Circle seemed like a dubious proposition. Anslinger had only 300 G-men on his roster, hardly enough to tackle heroin and cocaine, let alone a common weed.

Anslinger didn’t pay much attention to cannabis until 1934, when the FBN was floundering. Tax revenues plummeted during the Great Depression, the bureau’s budget got slashed, and Harry’s entire department was on the chopping block. Then he saw the light and realized that marijuana just might be the perfect hook to hang his hat on. A savvy operator and an extremely ambitious man, he set out to convince Congress and the American public that a terrible new drug menace was threatening the country, one that required immediate action by a well-funded Federal Bureau of Narcotics.

Determined to criminalize the herb and build his bureaucratic fiefdom, America’s top narc promoted all the hoary myths about marijuana-induced mayhem and sexual depravity—stories of pot-crazed axe murderers, playground pushers, sordid drug dens and buxom reefer babes whose lives were ruined by the drug.

“If the hideous monster Frankenstein came face-to-face with the hideous monster Marihuana, he would drop dead of fright,” declared the FBN chief (Washington Herald, 4/1⅔7). Anslinger pulled no punches as he orchestrated a nationwide campaign against marijuana, “the most violence-causing drug in the history of mankind.”

In the world according to Anslinger, cannabis was a deadly, addictive drug that enslaved its users and turned them into deranged criminal freaks. He fed titillating tidbits to reporters, who wrote articles that the FBN chief would then cite in making the case that society was in imminent danger of moral collapse because of marijuana.

Anslinger whipped up enthusiasm for the cause in speeches to temperance organizations, religious groups and civic clubs around the country. His anti-cannabis confabulations were given credence by hellfire-and-brimstone preachers who castigated hemp smokers as fallen sinners. A plant that provided the paper on which Gutenberg first printed the Bible was denounced as “the Devil’s weed.”

Perhaps it was the constant pressure from waging war against a figment of his imagination, or maybe his job was simply too demanding, but on April 1, 1935, an angst-ridden Anslinger checked into the U.S. Marine hospital in Norfolk, Virginia. The FBN chief complained of exhaustion and insomnia—he woke up too early and couldn’t get back to sleep, a condition, ironically, which was treatable with cannabis.

While Anslinger convalesced, others picked up the slack. The FBN chief had a strong ally in the press baron William Randolph Hearst, a megalomaniac obsessed with marijuana, whose newspaper chain stretched across the nation. With an instinc-tual grasp of mass psychology, Hearst used his media empire to influence public policy (as when he pushed the U.S. government into war with Spain in 1898). His contempt for facts, his penchant for fabricated stories and doctored photos, and the hysterical tone of his newspapers gave rise to the pejorative expression “yellow journalism.”

Hearst launched a smear campaign against Mexican migrants and their herb of choice. “Murder Weed Found Up and Down Coast—Deadly Marihuana Dope Plant Ready for Harvest That Means Enslavement of California Children,” the Los Angeles Examiner (1⅕/33) screeched in 1933.

By stigmatizing marijuana and the “foreigners” who smoked it, Hearst succeeded in exacerbating anti-Mexican sentiment during the Great Depression, when many Anglos felt they were competing with brown-skinned migrants for scarce jobs. More than 2 million Mexicans, who had been welcomed while the U.S. economy boomed in the 1920s, were deported when it faltered in the 1930s—a policy of ethnic cleansing vociferously championed by the Hearst conglomerate.

Hearst also cheered the rise of fascist forces in Europe. “Mussolini Leads Way in Crushing Dope Evil” was the headline of a Hearst press screed (3/9/28) that combined two of the owner’s pet passions—his support for fascism and the war on narcotics. Hearst Sunday papers published columns by German Nazi leaders, who conveyed Hitler’s point of view to 30 million readers without space for rebuttal.

During the Third Reich, the verminization of religious and ethnic minorities went hand in hand with Rauschgiftbekämpfung, the “combating of drugs” to promote racial hygiene. Nazi racialist policies and the demonization of marijuana by Anslinger and Hearst were parallel historical phenomena—both exploited fear and hatred of the Other.

The FBN commissioner understood that the likelihood of prohibitory legislation increased if the substance in question was associated with ethnic minorities. Thus Anslinger disclosed in 1936 that 50 percent of violent crimes committed in districts occupied by “Mexicans, Greeks, Turks, Filipinos, Spaniards, Latin Americans and Negroes may be traced to the use of marihuana.” The headlines and the plotlines were antidrug and anticrime, but the subtext was always about race.

Anslinger brandished the non-English term like a truncheon to emphasize the weed’s connection to alien elements that crept over the Mexican border into the United States. Popularized during the Depression, the new name marihuana was, in effect, the evil twin of cannabis, a word familiar to Americans as a medicinal ingredient.

Anslinger eschewed references to benign-sounding cannabis and hemp, while calling for a federal ban on marihuana. Very few Americans knew that marijuana, the weed that some blacks and Chicanos were smoking, was merely a weaker version of the concentrated cannabis medicines that everyone had been taking since childhood.

To gain public support for his crusade, Anslinger depicted marijuana as a sinister substance that made Mexican and African-American men lust after white women. One of the worst things about marijuana, according to the FBN chief, was that it promoted sexual contact across color lines. “Marijuana causes white women to seek sexual relations with Negroes,” Anslinger frothed. He rang alarm bells in segregated America, warning that blacks and whites were dancing cheek-to-cheek in tea houses and nightclubs, where pot-maddened jazz bands performed what the Hearst papers called “voodoo-satanic music.”

In addition to hexing blacks and Mexicans, Anslinger’s antimarijuana diatribes served as a not-so-subtle reminder to white women, who had only recently won the right to vote, that they still needed strong men to protect them from the “degenerate races.” He never tired of telling new versions of the same morality tale, which featured a vulnerable young white woman whose tragic downfall is triggered by smoking marijuana with dark-skinned rogues.

During the run-up to federal legislation that banned cannabis, Anslinger pounded home the message: White women are in mortal peril because of marijuana—and so are American children. That was the upshot of a July 1937 American Magazine article by Anslinger, entitled “Assassin of Youth,” which led with the usual purple prose:

“How many murders, suicides, robberies, criminal assaults, holdups, burglaries and deeds of maniacal insanity it causes each year, especially among the young, can only be conjectured,” the FBN chief warned.

With Anslinger pitching script ideas, cannabis was demonized in several low-budget exploitation flicks, some of which were financed by major distilling companies that stood to lose sizable sums if marijuana were a legal competitor.

The film Marijuana! (1935) featured the lurid tagline “Weird orgies! Wild parties! Unleashed passions!” But when it came to ridiculous anti-marijuana propaganda, nothing could top Hot Fingers Pirelli, the bug-eyed piano player who pounds out jazz tunes in Tell Your Children (1936), better known by its later title Reefer Madness.

A perverted pot addict, Pirelli sneaks into a closet and fires up the Devil’s doob, prompting frightful facial twitches as he morphs into an insane killer. Drug-policy critic Jacob Sullum (Saying Yes) calls it “voodoo pharmacology”—the idea that certain substances are molecularly program-med to compel weird, immoral behavior.

Although it bombed at the box office, Reefer Madness was destined to become a cult humor classic among American college students in later years. A vivid example of the national frenzy that set the stage for federal pot prohibition, this film epitomized the synchronicity among Washington, Hollywood and mainstream media in the war against cannabis.

In April 1937, Rep. Robert L. Doughton of North Carolina introduced House Bill 6385, which sought to prohibit the use of marijuana by imposing an exorbitant tax on the drug. When he testified before the House Ways and Means Committee, Harry Anslinger trotted out examples from the “Gore File,” his infamous scrapbook full of Hearst press editorials, racial slurs and anecdotal accounts of horrific murders falsely attributed to marijuana smokers. Bereft of actual scientific data to back up his reefer madness claims, the FBN director presented no evidence of a statistical correlation between marijuana use and criminal behavior.

Members of Congress held only two one-hour hearings to consider the Marihuana Tax Act. The final witness and lone voice of dissent was Dr. William Woodward, the legislative counsel for the American Medical Association, who challenged Anslinger’s claim that cannabis was a dangerous drug with no therapeutic value. AMA doctors, Woodward asserted, were wholly unaware that the “killer weed from Mexico” was actually cannabis. He accurately predicted that federal legislation banning marijuana would strangle any medical use of the plant.

Just four years after relegalizing the consumption of liquor, Congress overwhelmingly passed the Marihuana Tax Act by a voice vote without a recorded tally. Signed by President Franklin D. Roosevelt without fanfare, the law went into effect on October 1, 1937. It was a day of infamy for pot smokers everywhere. Yellow journalism, racial bias and political opportunism had triumphed over medical science and common sense.

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Bugs, Mold and Excrement

Category : Noticias

Welcome to the Brave New World of California Cannabis
By Adrian Devitt-Lee On November 26, 2017

Project CBD critiques the new regulations for America’s largest marijuana market

On November 16, 2017, California officials released a new set of regulations for cannabis manufacturing, testing, and growing. In many respects, these updates are a significant improvement to the initial draft regulations, however, some major problems remain. 

Two important issues pertain to regulations on mold and foreign filth, which are absurdly loose. And unlike the initial proposal, no statement as to the rationale behind the new regulations has been released.

Safety requirements

Allowable limits for contaminants including pesticides, solvents, and microbes are described in sections 5718-5723 of the new regulations. These regulations have fixed a major issue in the initial draft where two different units were confused – parts per million by weight (µg/g) and parts per million by volume. Now solvent and pesticide limits are given in µg/g.

Other significant changes:

  • Solvent limits are largely improved. Certain class 2 solvents have been banned, as Project CBD had previously suggested.
  • Pesticide limits have swung from being very strict to being overly lax. The environmental concerns related to pesticide overuse appear more problematic than the health effects for consumers.
  • Many pesticide safety limits are still based on regulations for tobacco, which is entirely inappropriate.
  • Required tests for microbial contamination are minimal.
  • Limits on mold – one of the most common contaminants of cannabis – are nearly nonexistent. A product is deemed to pass regulations if less than 1/4th of it is covered in mold.

Solvents – §5718

Solvents are broken into two categories for the purpose of regulations. Category 1 solvents are banned and are not permissible at any detectable levels in cannabis products. Category 2 solvents are allowed up to set action limits that depend on the solvent in question and whether the product is inhaled or not. Action limits for non-inhaled products were appropriate in the initial draft proposal and have not changed.

The initial proposed regulations allowed for the use of highly dangerous solvents, including benzene, which Project CBD suggested be banned from use in cannabis manufacturing. We also suggested that regulators consider banning “class 2” solvents such as chloroform, since they are unnecessary for producing most kinds of cannabis extracts.The new regulations now ban the use of benzene and some class 2 solvents like chloroform, but allow other class 2 solvents, including hexane. (Hexane is rarely used to extract oil from cannabis, but is sometimes used to clean the oil of pesticides or other adulterants.) Although Project CBD hopes that cannabis manufacturers avoid using hexane to extract or clean oil, we believe these regulations are appropriate.

Each permissible solvent has a maximum allowable concentration in inhaled cannabis products (e.g. vape cartridges). In the initial draft proposal, these limits were based on safety data from California’s Occupational Health and Safety Administration (OSHA), although the limits were improperly calculated due to confusion with units. (“Parts per million” can have multiple meanings, as mentioned above. See the previous Project CBD statement for more detail.) The new limits are particularly stringent for some class 2 solvents and are overly lenient for ethanol residues.2   On the whole, the new limits are sensible.


Pesticides – §5719

Similar to solvents, pesticides are broken into banned pesticides, which are not allowed at any detectable concentration, and allowed pesticides. The action limits for permitted pesticides depend on whether the product is inhaled or not.

The regulations were released with only 5 days for public comments – including the weekend – and were not accompanied by any statement of reasons explaining how new safety limits were determined. As such, Project CBD’s comments on the new pesticide regulations point out potential problems without necessarily suggesting how these issues could be fixed or their extent.

In the new regulations, the list of banned pesticides has shrunk dramatically, from 42 to 21. One of these now-allowed pesticides is a neonicotinoid (acetamiprid) and four others have “high acute toxicity” to humans, according to the initial statement of reasons (bifenthrin, cyfluthrin, naled, and abamectin). Most of the rest of the now-allowed pesticides were banned in the original proposal due to environmental concerns, including myclobutanil (often sold Eagle-20).

The initial set of draft regulations on pesticides were very strict in some regards. The limit of detection (LOD) – which is the lowest concentration of a compound that can be detected reliably – was arbitrarily set at 0.01 – 0.02 µg/g. This is lower than the actual LOD of pesticides in cannabis for most labs. This has changed – now labs will determine their LODs scientifically and list these LODs on lab reports.3 This is an important fix.

To reiterate: because no statement of reasons has been released, we do not know the rationale behind the limits for pesticides on non-inhaled products. But we can say with some certainty that it is not based on the relative safety of these pesticides.

Safe limits for pesticide ingestion are given as the acceptable daily intake (ADI) or acute reference dose (ARfD), and are reported by the World Health Organization. The ADI indicates a level of pesticide ingestion that is considered safe for chronic daily use, which makes sense for food or medicine. Converting the ADI into a limit for a pesticide in cannabis products depends on the amount of product that is consumed. If the limits were based on safe ingestion limits, the ratio of the ADI to the action limit would be constant. In the current proposal, this ratio varies from 2.5 to 750, a 300-fold difference. Pesticides like trifloxystrobin, bifenazate, and permethrin have very high action limits compared to their toxicity when ingested.

It appears that the limits were not based on environmental concerns either: Of the seven least regulated pesticides (i.e. those with the highest allowable limits), five were originally banned due to potential ground water contamination.

For inhaled products, the limits still appear to be based on tobacco, as described in the initial statement of reasons. This may be because very little is known about the effects of heating or burning pesticides (an information vacuum attributable to lobbying from the tobacco industry). Some pesticides will, in fact, become safer when burned, while many others will break down to much more toxic compounds.

The EPA has previously stated that it need not study the health effects of burning pesticides at concentrations below 0.1 µg/g in cigarettes because those individuals are already smoking tobacco. After all, nicotine is the insecticide upon which neonicotinoids are based.

It may be true that inhaling less than 0.1 µg/g of most pesticides is safe. But regulations need to be based on scientific data. If safety data on burning and inhaling pesticides is not available, then the law should include provisions to be updated as new data emerges.

The outcomes of the tobacco industry’s war against science should never be used as the basis of safety regulations for another industry. Tobacco is the leading cause of preventable deaths in the United States, killing roughly half a million people every year. This is precisely because the tobacco industry lobbied to ensure that scientific data on health and safety was not used to inform laws or regulations. That should not be the starting point for any aspect of the emerging cannabis industry.


A sample could pass with one rodent hair

Foreign material – §5722

The foreign material testing, described in §5722, is beyond the pale. §5722(e) states that:

A sample shall be deemed to have passed the foreign material testing if the presence of foreign material does not exceed:
(1) 1/4 of the total sample area covered by sand, soil, cinders, or dirt;
(2) 1/4 of the total sample area covered by mold;
(3) 1 insect fragment, 1 rodent hair, or 1 count mammalian excreta per 3.0 grams; or
(4) 1/4 of the total sample area covered by an
imbedded foreign material.

A small piece of chocolate weighs about 3.5 grams. Under the new regulations, a 16-piece chocolate bar would be considered acceptable if four pieces were covered in dirt, four more were covered in mold, and each of the 16 pieces had an insect part or rat poop on it.


Labs are not required to test for mold

Microbes – §5720


There is an unprecedented change in regulations on microbial contamination. Cannabis is not required to be free of mold nor are labs required to test for mold. The only limit on mold is given in (2) of the foreign filth section quoted above, which states that up to 1/4th of a product can be covered in mold.

Under the new proposal, products only need to be screened for three microbes: pathogenic E. coli, salmonella, and in the case of inhaled products, aspergillus. Since no statement of reasons were released with the regulations, it is not clear why California is so loose with microbes. Giving regulators the benefit of the doubt, it may be that they are trying not to restrict the use of beneficial microbes, an organic growing practice that uses non-harmful microbes as an alternative to pesticides. But mold is one of the most common contaminants on cannabis. It is absolutely essential to test for mold on cannabis, particularly when grown indoors.


Testing will be phased in over the course of a year

Phase in of safety testing – §5715

The regulations have been released with just over a month before they will be implemented. To ease the burden on labs, testing will be phased in over the course of a year. This gives labs time to develop and validate methods for each kind of product and each kind of test.

On January 1, 2018, all legal products must be tested for cannabinoids, allowed solvents, banned pesticides, microbes, and product homogeneity.4  On July 1, 2018, three additional tests will be required: banned solvents, allowed pesticides, and foreign material. On January 1, 2019, heavy metals, mycotoxins, and possibly terpenes will also be tested before sales.

Project CBD hopes that terpene testing will become more commonplace, as this will help to illuminate the therapeutic properties of these important plant components.

Other regulations

There are many important aspects of the new regulations that address issues beyond consumer safety. Here are some key points:

  • There is effectively no longer a limit on the size of grows. Each license allows a group or individual to grow up to one acre of cannabis, but there is no limit on the number of licenses a group can get. Project CBD shares the concerns of farmers who are worried that this will allow large-scale agriculture to push out smaller, more sustainable gardens. Privileging wealthy out-of-state investors and big players at the expense of family farmers is bad policy with unhealthy long-term implications for California’s economy and environment.
  • Law enforcement are allowed to copy the materials, records, and books of any employee of any licensed cannabis business. See §5800(a)(4).
  • Recreational products can’t be given away for free. Medical patients can be given free products through a compassionate care program, but this program must be run by a local jurisdiction, not a cannabis business. Moreover, only licensed retailers (e.g. a legal dispensary), not product manufacturers, can provide free products to patients. See §5411.
  • Medical patients under the age of 18 cannot be served at a dispensary. Their caregiver must buy product for them. See §5400(b).
  • Edibles are required to contain no more than 10 mg THC per serving and 100 mg THC per package. Other products must contain less than 1000 mg or 2000 mg THC per package, depending if the product is recreational or medical. See §40306.
  • Edibles cannot contain any other addictive substances, including caffeine, alcohol, and nicotine. Exceptions are made for cannabis chocolate, tea, and coffee. See §40300(b).
  • Labs are required to be certified by one of two groups (the International Standard Oganization or International Electrotechnical Commission). This will help ensure the accuracy and consistency of lab tests, which has been problematic in the past.
  • It is now much easier to get a license to do ethanol extraction, since it is considered a “nonvolatile solvent.” See the definition of “nonvolatile solvent” in §40100.

Adrian Devitt-Lee, a Project CBD contributing writer, is a research associate at CannaCraft, Inc., a Northern California-based medical marijuana company.

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

1 Solvents are classified into one of three groups by the FDA. Class 1 solvents like benzene are either very toxic or environmental hazards and should be avoided in manufacturing if at all possible. Class 3 solvents like ethanol and butane are fairly safe at low concentrations. Class 2 solvents like chloroform and dichloromethane are less dangerous than class 1 solvents, but should be avoided if the use of a class 3 solvent is possible.
2 This is not to say that the allowable limits are wrong. But compared to safety data from OSHA, limits are disproportionately lax for ethanol and strict for class 2 solvents.
3 A second number to be listed on lab reports is the limit of quantification (LOQ), which is at least as large as the LOD. The LOQ is the limit at which the concentration of a chemical can be accurately discerned. The range between the LOD and the LOQ is the range of concentrations where a test can show that a chemical is present, but cannot determine its exact concentration.
4 Products with multiple servings (e.g. a chocolate bar) will be tested every 6 months to ensure that every piece has roughly the same amount of cannabinoids in it. Specifically, the relative standard deviation must be less than 10% of the mean amount of each cannabinoid.

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Epilepsy, Endocannabinoids and Phytocannabinoids

Category : Noticias

Cannabidiol and several other cannabis components can help patients with seizure disorders, and sometimes it’s best to combine CBD with conventional anti-epileptic meds.
By Stacey Kerr, M.D. On November 25, 2017


• More than 5 million Americans suffer from epilepsy.
CBD is helping many patients, including children with seizure disorders.
THCA, the unheated form of THC, and linalool, an aromatic terpene present in many varieties of cannabis, are potent anticonvulsant compounds.
• Oftentimes, patients must experiment with different cannabis products to find the best remedy for their condition.

“David,” a 10 year old boy, had his first seizure at 2 months of age. The convulsions were photosensitive generalized tonic-clonic seizures that occurred 1-4 times each day. These events were occurring daily, even though he was being treated with two anti-seizure medications – lamotrigine (Lamictal) and valproic acid. But they had already tried carbamazepine, phenobarbital, zonisamide and levetiracetam (Keppra) without success.

On the recommendation of his physician, THCA was added to his medication at 0.05mg/kg/day and his parents immediately noticed a reduction in seizure frequency. They then increased the THCA dosage to 2.2mg/kg/day, and even though there was no benefit noted to this increased dosage, the parents continued at this higher amount. After three months of THCA treatment, his parents reported to his physician a 40% reduction in seizure activity, shorter seizures, and the ability to discontinue the anti-seizure medication Diastat, which they had been using for seizure rescue.  Hoping for even more control, they began a formula that contained THC at a THCA:THC ratio of 4:1. This caused transient side effects of somnolence but did nothing to improve the frequency of seizures.

Even if it did not completely resolve his seizure disorder, the phytocannabinoid THCA was able to make a significant difference in David’s quality of life. He is not alone. Cannabis holds hope for many, like David, who suffer from seizure disorders.

Epilepsy is a complex medical, economic, and social issue that affects at least 5.1 million of the US population by 2013 population reports. In Hawaii, there are an estimated 15,000 patients with seizure disorders. The total indirect and direct cost of epilepsy in the United States is estimated to be $15.5 billion yearly. 1, 2 For the individuals and families of those patients with seizure disorders, life can be limited and extremely complicated depending on the type and frequency of seizures and on the effects of anti-seizure medications, both therapeutic and undesirable.

Seizures occur when a part of the brain becomes overly excited or when nerves in the brain begin to fire in an abnormal way. An abrupt imbalance between the triggers of excitatory signals and inhibitory signals causes the excitatory forces to take over. This excitation then spreads to surrounding cells which all start firing in the same abnormal way. Increased excitation of nerve cells, or decreased inhibition of nerve cells due to a variety of potential insults can lead to a seizure. Balance, or homeostasis, is disrupted.

Most epileptics have no known cause for their seizures. The minority have numerous identified causes that include trauma, infections, inborn metabolic errors, drugs (or withdrawal from drugs), and inherited conditions.

Conventional treatment

There are no treatments for the underlying causes of seizures, and no treatments to reliably prevent the development of seizures after head traumas. There are only medications to limit the seizure intensity or frequency, and these medications are not always effective. In fact, a third of epileptic patients fail to become seizure free even after trying and tolerating two or more appropriately prescribed anti-epileptic drugs (AEDs).3

More than 20 new seizure medications have been developed over the past few decades, but the percentage of patients with uncontrolled seizures has not changed as much as we would hope or expect. Patients who are resistant to AEDs have a higher risk of complications and sudden death due to epilepsy.  The need for multiple AEDs also increases the occurrence of significant side effects. The need for better, safer, and more effective treatment is clear.

Safety profile

Cannabis is a safe medication with no incidence of fatalities due to the lack of cannabinoid receptors in the brainstem. The most common side effects reported among patients using cannabis for seizure control are fatigue, decreased appetite, and somnolence, all of which resolve when cannabis is discontinued. AEDs can have significant side effects, and contrary to cannabis some of these can be fatal.

It is important to note that there are some drug-drug interactions when using cannabis with AEDs because cannabinoids are primarily metabolized by the Cytochrome P-450 system in the liver. Competition for these enzymes can affect the serum levels of AEDs, so patients using cannabis in addition to prescribed AEDs should be monitored, and dosage adjustments may be needed.


The endocannabinoid system in epilepsy

The job of the endocannabinoid system is to maintain homeostasis, so it is no surprise that cannabis has been used to help control seizures for centuries. Well-designed studies on rats have shown that the endocannabinoid system is a significant part of the brain’s response to seizure disorders.

We know that cannabinoid receptors are particularly dense in the central nervous system, and while we do not yet completely understand all the mechanisms that explain the anti-seizure effects of cannabis, we do have theories.

There are cannabinoid receptors in the hippocampus, that part of the brain that handles emotions and memory encoding. Abnormal changes in cells in the hippocampus are a cause of medial temporal lobe epilepsy, which is one of the most common forms. In this type of epilepsy, hippocampal cells create an excitatory feedback loop that causes seizures. Animal and human studies show that cannabinoids seem to be protective of the normal hippocampal cells, and may make the abnormal cells less active.4

In acutely seizing animals, the endocannabinoid 2-AG was significantly increased compared to controls. By testing the levels of both anandamide and 2-AG we have seen that both are synthesized on demand when seizures occur, thus activating the CB1 receptors. It also appears that there is a significant increase in CB1 receptor expression in epileptic animals, a receptor increase that is prolonged and probably permanent.

In studies done on rats with refractory seizures, it was noted that THC completely terminated those seizures without causing sedation, while maximal levels of phenobarbital or phenytoin were unable to do the same. This indicates that phytocannabinoids may offer advantages in treating refractory seizures compared to currently prescribed anti-convulsants.5

In more recent years research on animal models and human clinical observations have rekindled interest in using cannabis to control epilepsy. Cannabinoids decrease glutamate synthesis throughout the central nervous system, which in turn decreases inflammation and seizure activity.6 Regardless of the mechanism, human clinical observations are promising for the use of cannabis as an anti-epileptic medication, either alone or as adjunctive therapy.

Specific cannabinoids as medicine

The evidence continues to indicate that whole-plant usage is more effective than any single isolated constituent, perhaps due to the entourage effect. Cannabis contains many cannabinoids, THC and CBD being only two of over 80 possibles. In addition, the plant contains terpenes which are medically active chemicals that give the plant its fragrance. Combining these constituents can decrease side effects from any single cannabinoid and together, and may be more effective in controlling seizures. 7 We do not yet know what the best combination is for any specific type of seizure but the evidence is strong enough to encourage more research efforts for answers.

CBD: Is CBD the primary cannabinoid that treats seizure disorders? It seems so if you consider the recent reports of use in severely affected children. CBD is certainly a major player, but not the only one. CBD has been clinically proven as an anticonvulsant for many and at worst, for a minority of patients with epilepsy, it gave no benefit. Its anti-convulsive effects are probably due to a combination of beneficial activities. CBD blocks NMDA receptors (similar to the AED Felbamate) and enhances GABA receptors (similar to phenobarbital and Depakote). It stabilizes ion channels (similar to Dilantin and Keppra), acts as an anti-inflammatory, and also as a neuroprotectant.8

THC: In some study models, THC reduced seizure frequency and intensity, but in others there was no effect. Some patients treated with THC had increased seizure activity.6

THCA: THCA, the acidic raw form of THC is non-psychoactive and also appears to have anti-seizure qualities.9

CBDV: Cannabidivarin or CBDV, is a non-intoxicating cannabinoid that also has significant anti-convulsant properties which were even more effective when combined with CBD.6,10

Alpha-linalool: The terpene alpha-linalool has been shown to have anti-seizure activity in pre-clinical models, especially when combined with cannabinoids.7,9


Cannabis has a biphasic dose-response, meaning that more is not always better or more effective. This is more prevalent in THC than in CBD but patients and clinicians are cautioned to avoid the assumption that if a dose is not working, it should be increased. It very well may need to be decreased, especially if THC is part of the preparation.

Dosing for adults has been noted at amounts as small as .02 mg cannabinoids/kg/day, but the clinical trials done on Epidiolex (a purified CBD product made by GW Pharmaceuticals) tested a range of 2-50mg/kg/day. While dosing cannabis for seizures is still an evolving science, an experienced physician treating children for intractable seizures shares the following guidelines. First, an EEG is recorded prior to starting CBD oil and then repeated at 1-3 months if the child is showing improvement. Oral or sublingual dosing of a quality-controlled, lab-analyzed CBD oil with a ratio of at least 10:1 CBD:THC is started at 1mg/kg/day divided into every 8 hour doses. These doses are increased every 1-2 weeks depending on the child’s results. She notes that the therapeutic range for many patients appears to be between 4-9 mg/kg/day. As the seizures decrease in frequency, it is possible that the AEDs can be slowly weaned.10

The latest publication on the use of cannabis for the treatment of epilepsy comes from three physicians with experience in the states of Maine, Washington, and California. Of their 272 combined patients, fourteen percent found cannabis to be ineffective at reducing seizures, fifteen percent experienced a 1-25% reduction in seizures, twenty-eight percent experienced a 76-99% reduction, and ten percent had a complete clinical response.

CBD made the difference

When Sam was 4, he had his first myoclonic seizure, and those progressed to myoclonic absence seizures. Sam did not fall to the floor and twitch. Instead, sometimes 100 times a day, he lost consciousness for 20-30 seconds at a time. He stopped, stared vacantly, his head bobbed rhythmically and then it would all be over. He didn’t even notice these seizures, only that when he would come to, everything around him had shifted slightly. But it kept him from a normal life: having full conversations, from learning in school, and from participating in sports.

Sam had tried almost two-dozen treatments including intravenous immunoglobulin and a ketogenic diet. Few of these were effective, and those that were either had worrisome side effects (hand tremors, hives, zombie consciousness, etc.) or they quit working after a short while. By the time he was 11, he was on massive doses of corticosteroids – the only thing they’d found that made any difference – but the side effects were devastating. He’d been hospitalized twice and seen six neurologists in three states.

Then, as a last resort, his parents decided to try CBD. The effects were profound, but the road was “not a straight line,” to quote his father. CBD had immediately helped – dropping the seizure rate from 68 on a Thursday to 6 on the following Monday. A few years after starting the CBD, Sam was down to between 0 and 5 seizures a day on 1000mg of CBD and taking no other seizure medications. Then, he had his first-ever generalized tonic-clonic seizure. Three weeks later he had another, so Depakote was added to his regimen. The Depakote worked.

Sam is now 15 years old and has had 15 months without a seizure. To his parents, this is a relief and a miracle. He is taking 875mg of Depakote a day, and 250mg of CBD twice a day. Now active in sports, fly fishing and rock climbing, Sam gets to be a normal boy.

Clearly, there is promise in the use of cannabis to manage epilepsy and still much to learn.

Stacey Kerr MD is a teacher, physician, and author living and working in Northern California. Dr. Kerr was in private practice until she decided to write and educate full-time. After several years working with the Society of Cannabis Clinicians, and co-developing the first comprehensive online course in cannabinoid medicine, she is now serving as the Medical Director for Hawaiian Ethos, an evidence-based cannabis company on the Big Island of Hawaii.

This article was reprinted by Project CBD with permission. It may not be reproduced in any form without approval from the source.

1.     (

2.     (

3.     Kwan P. Brodie MJ. Early identification of refractory epilepsy. N Engl J Med 2000;342(5):314-9

4.     Gloss, Vickrey. Cannabinoids for Epilepsy. The Cochrane Library, 2012

5.     Wallace M.J. et al. The Endogenous Cannabinoid System Regulates Seizure Frequency and Duration in a Model of Temporal Lobe Epilepsy, Journal of Pharmacology and Experimental Therapeutics, Vol. 307:129–137, 2003

6.     Devinsky et al. Cannabidiol: Pharmacology and potential therapeutic role in epilepsy and other neuropsychiatric disorders. Epilepsia, 55(6):791–802, 2014

7.     Rosenberg EC, Tsien RW, Whalley BJ, Devinsky O. Cannabinoids and epilepsy. Neurotherapeutics. 2015;12:747–768

8.     Jones NA, et al. 2010. Cannabidiol displays anti-epileptiform and anti-seizure properties in vitro and in vivo. Journal of Pharmacology and Experimental Therapeutics 332(2):569-577

9.     Sulak D, et al. The current status of artisanal cannabis for the treatment of epilepsy in the United States, Epilepsy Behav (2017),

10.  Hill et al, Cannabidivarin is Anticonvulsant in Mouse and Rat, Br J Pharmacol. 2012 Dec;167(8):1629-42. doi: 10.1111/j.1476-5381.2012.02207.x.

11.  Elisabetsky E, Brum LS, Souza DO. Anticonvulsant properties of linalool in glutamate related seizure models. Phytomedicine 1999;6(2):107-13

12.  Bonnie Goldstein MD.

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