Until last month, he was the top international anti-drug official in the U.S. Now he says it is likely that the federal government will have to reclassify marijuana as more states enact legalization.
“Let the experiment advance. Consider its positive and negative effects,” William Brownfield, who resigned only weeks ago as Assistant Secretary of State for International Narcotics and Law Enforcement Affairs, said in a new interview.
“Let’s see how many other states advance in this direction because we are a democracy and for the moment we do not have a consensus position. In California, the most populous state, they voted for legalization, but in Texas, the second most populous state, they have not even wanted to consider it. When the conclusions are drawn, it is likely that substances may be reclassified.”
That’s a remarkable statement coming from someone who was in charge of representing the U.S.’s position in the global drug war for more than six years, as Brownfield was until a few weeks ago.
But even as he acknowledges it may soon be time for the government to remove marijuana from Schedule I — the most restrictive category in federal law, which is supposed to be reserved for substances with a high potential abuse and no medical value — don’t mistake Brownfield for an anti-prohibition activist.
“I am not a fan of legalization,” he said in the new interview with Colombian newspaper El Tiempo.
Brownfield did acknowledge, however, that legalization is an “experiment that allows us to observe and learn.”
Even while citing traffic accidents and emergency room visits allegedly associated with cannabis, and arguing that local governments’ desire to generate revenue from legal marijuana sales “doesn’t seem like anything healthy,” he clarifies that he’s “not saying that [legalization] is a failure.”
“But,” he says, “I insist that we must be able to adjust policies to ensure that they do the least possible harm.”
Brownfield, who previously served as U.S. ambassador to Colombia, Venezuela and Chile during the Bush administration, made headlines in recent years by shepherding along a new U.S. posture on drugs under President Obama. While the country historically pressured other nations into maintaining a prohibition approach, that became more difficult once U.S. states started legalizing marijuana.
“How could I, a representative of the government of the United States of America, be intolerant of a government that permits any experimentation with legalization of marijuana if two of the 50 states of the United States of America have chosen to walk down that road?” Brownfield asked in 2014, when Colorado and Washington were the only states to have ended prohibition. That number has since quadrupled.
Also in the new interview, Brownfield sharply criticized comments his former boss, President Trump, made about Colombia’s role in the war on drugs.
Trump threatened to “decertify” the country as a partner in drug policy last month, a move that could have harsh consequences for fiscal aid and trade between the two nations.
To decertify Colombia would have been “a fundamental error, counterproductive, false, and very stupid,” Brownfield said, adding that it would be “nonsense, an insult, an insult to the hundreds of Colombians who have given their lives” in the drug war.
All Brownfield quotes in this story were automatically translated by Google and then cleaned up with the help of a few fluent Spanish speakers.
Published 3 weeks ago on October 24, 2017 By Tom Angell
Photo courtesy of M a n u e l
Sourced from: marijuanamoment.net
The Liquor Control Board of Ontario (LCBO) has created a website to keep the public updated on their process of preparing for the sale of legal cannabis by July 2018.
The website, lcbocannabisupdates.com, provides introductory information to the general public to help understand the steps the LCBO is taking to find the 40 initial cannabis store locations that the province has said they intend to have in place for legalization. The province intends to have 80 stores by 2019 and ‘up to’ 150 stores by 2020.
Although still short on specifics, the website contains a FAQ section that says the government plans to train all employees selling cannabis in the LCBO to know about the products and related safety information relating to them.
It also states that the Government of Ontario will be choosing locations for their first 40 stores with the goal of reducing the amount of illegal stores, “including dispensaries,” that are currently operating in Ontario.
Municipalities identified for a location will have an opportunity to have input in the process.
The age limit for consumption and possession in the province will be 19 and all cannabis sales will be through employees, not direct-to-customers sales, via traditional vending machines, for example.
Sourced from: Lift News – https://news.lift.co/lcbo-unveils-retail-cannabis-website/
So far, all the states that have legalized marijuana have done so through grassroots petitions and ballot initiatives meant to bypass risk-averse lawmakers in state houses.
California, Nevada, Maine, Massachusetts, Alaska, Oregon, and the District of Columbia have all followed Colorado and Washington either to legalize the sale and use of recreational marijuana or, at a minimum, to decriminalize possession and consumption of small amounts of the drug.
But 2018 may be a tipping point — the moment when the momentum of pot makes it impossible for state lawmakers to avoid. State legislatures are poised to begin passing marijuana reform laws next year. The taboos against smoking dope may go up in a cloud of narcotic smoke.
Lawmakers must still juggle serious public safety issues, even as they eye what they hope will be new revenue streams from pot that they don’t want flowing to neighboring states.
Vermont, Rhode Island, and New Jersey all devoted serious debate to this in 2017, and their state legislatures could send legislation to their governors next year to sign into law.
Vermont is the only state legislature to pass a legalization measure, although Democratic Gov. Phil Scott vetoed it.
With recreational use and sales opening within months in Canada and Massachusetts, neighboring states feel compelled to study and implement new public safety measures. Beyond that, however, lawmakers in these states are also emboldened by polls showing public support for recreational use.
Tom Gorman, director of the Rocky Mountain High Intensity Drug Trafficking Agency, believes 2018 could be a tipping point.
“What I was hoping was the rest of the states would say, ‘OK, we’ve got Washington, and we’ve got Colorado, let’s wait and see what happens so we can make an informed decision one way or the other,” said Gorman, whose Denver-based organization supports federal and local anti-drug policing. “Either it wasn’t as bad as the anti-marijuana folks said it was, or, ‘My God, this is disastrous, we don’t want this for our state.’”
But Gorman’s longtime adversary in the recreational legalization battle, Brian Vincente, an attorney who has been a leader in Colorado’s decades-long fight over legalization, thinks otherwise. “I think we’ve probably cleared the tipping point,” he told the Washington Examiner. “I think when California and Massachusetts came on board and legalized — I mean, California’s such a massively recognized global economy and Massachusetts, this puritanical, historic state — I think those two for me signaled that it’s the beginning of the end for prohibition.”
What develops next in pot policy is likely to be shaped by data from the early legalizers, Colorado and Washington, by how it is interpreted, by how legislatures respond to legalization as opposed to citizen ballot initiatives, and by whether the federal government will step in.
If Vermont, Rhode Island, and New Jersey make moves, and even if only one or two other voter-based initiatives passed, fewer states would remain that didn’t share border with a state with legal marijuana. Some people thought Colorado and Washington were “experiments” and would remain highly quarantined, but it was an illusion.
Getting a clear “before and after” picture of the effects of legalized marijuana isn’t easy. Some experts have suggested that a comprehensive picture could take 20 years or more to become clear because data can be affected by so many other sociological factors.
“What I hear from Colorado is that, they say, you need to wait a couple years. Because the data sets right now are very immature and we don’t really know as much as we’d like to know,” said Vermont State Rep. Scott Beck, a Republican.
Beck’s concerns about “immature” data are well-founded. For example, one of the first comprehensive studies on the effects of legalization was published by the Colorado Department of Public Safety in March, 2016. It began with a strong caution:
“It is too early to draw any conclusions about the potential effects of marijuana legalization or commercialization on public safety, public health, or youth outcomes, and this may always be difficult due to the lack of historical data. Furthermore, the information presented here should be interpreted with caution. The decreasing social stigma regarding marijuana use could lead individuals to be more likely to report use on surveys and to health workers in emergency department and poison control centers, making marijuana use appear to increase when perhaps is has not.
“Finally, law enforcement officials and prosecuting attorneys continue to struggle with enforcement of the complex and sometimes conflicting marijuana laws that remain. Thus, the lack of pre-commercialization data, the decreasing social stigma, and challenges to law enforcement combine to make it difficult to translate these early findings into definitive statements of outcomes.”
Just four months before pot sales began in Colorado, Dr. Larry Wolk became the executive director and chief medical officer for the Colorado Department of Public Health and Environment. Wolk says he’s often in contact with officials from other states and other countries, and says the number one piece of advice he gives them is usually the same, and it is about data.
“Conceptually, stop thinking about this as a ‘starting from zero’ — you know, if it’s not legalized — to some dramatic number as a result of legalization,” Wolk said. “So recognizing, what’s the base use of marijuana amongst adults and kids.
In Colorado, public safety concerns have broken along two lines: Concerns about the effects on those underage, whether it’s direct use by teens or children being born with THC detectable in their systems, and concerns about public safety on the roads, mainly because of people driving while stoned.
Perhaps nothing has confounded policymakers more than the inability to measure impairment due to marijuana use quickly in the same way a breathalyzer gauges a driver’s blood alcohol level, which is a reliable measurement of impairment. Not only does the absence of a similar testing tool make roadside analysis difficult for law enforcement, it also makes studying the issue murky as well.
Complicating those factors is the notion, which many experts say is incorrect, that marijuana “impairment” on driving can be measured like alcohol.
“Peak impairment does not occur when THC concentration in the blood is at or near peak levels,” a 2017 report by the National Highway Traffic Safety Administration noted. THC is the active compound in marijuana responsible for its psychoactive effects. “Peak THC level can occur when low impairment is measured, and high impairment can be measured when THC level is low.”
A January release by the Colorado Department of Transportation noted that traffic fatalities were up 24 percent since 2014, the first year that recreational pot was legal. But the word “marijuana” never appeared in that release, and officials never singled out any overriding factors for blame. The same release noted that those figures came during a population boom and also said, “The rise in fatalities is part of a national trend. Fatalities are up nationally by about 8 percent.”
Beck says legislators in that state have struggled with what to do about drugged driving, absent any test similar to a breathalyzer.
“Now we’re basically talking about having officers doing ‘driving under the influence’ tests roadside, which is kind of a throwback to the ’70s and ’80s, ‘walk the line, touch your nose,’” Beck said.
“It’s subjective. How’s it going to fare in a court of law? How does an officer determine whether it’s alcohol, or THC, or some other substance? We have trained many people in the state to be drug recognition experts. But I don’t think we have enough of them that people are confident that we can identify all these people.”
Especially concerning to Beck is that Vermont will have to deal with an increase in drugged drivers whether or not the state decriminalizes marijuana because tit has drivers on its roads from Massachusetts and Canada, where dope will be legal.
Effects on underage people
Supporters of legalization in Colorado have promoted a pair of studies they say show no increase in teen usage.
The state’s “Healthy Kids Colorado” survey polls 17,000 youth. From 2013 to 2015, the percentage of youth who said they had used marijuana once in the last month inched up from 20 percent to 21 percent, and that 21 percent is comparable to the national average.
Even though there was an uptick from 20 to 21 percent over two years, scientists have said this isn’t “statistically significant.”
“There’s some corridor of variability or error when you do any kind of study,” Wolk explained, “and so the reason why we say not to make much of the small increase that occurred the one year which then actually was followed by a small decrease is that, that’s within the corridor of variability that … researchers say is what’s attributed to chance.”
The other study on teen use of marijuana showed a similarly small increase, but relied on a much smaller sample.
Opponents of legalization, meanwhile, highlight statistics from a Pueblo-based hospital showing about a third of all babies tested have shown a presence of THC in their systems.
Tom Tancredo served as a congressman from Colorado for five terms, and ran for president in 2008 on a hardline immigration stance. But he lent his name and voice to pro-legalization radio ads in the run-up to the 2012 vote. He says he’s lost friends over this and says he would also support legalization again. Nevertheless, he acknowledges that lawmakers must consider secondary effects. Babies born with THC in their systems are a prime example, he says.
“I think that that should be dealt with legally,” he told the Washington Examiner. “Because I believe that’s child endangerment. And I think people should go to jail for that. Again, I don’t care what you do to yourself, as an adult, but I certainly care what you do to those who are not.”
Wolk says there is no data that proves that a mother passing THC to her baby is doing more harm, or as much harm, a mother using alcohol or tobacco during pregnancy. The studies are lacking in part because the federal government’s labeling marijuana as a “Schedule 1” drug has prevented many labs from getting the strict permissions needed to do marijuana testing.
“We know enough to say there’s not a lot in the way of short-term or acute harm if a baby is born to a THC-positive mom, but there’s likely the potential that it does affect or impact the developing brain,” Wolk said.
“So, obviously, our policy statement based on all available research we have says that pregnant mothers and breast-feeding mothers should not be using marijuana, period.”
Taxation and competition
Some state lawmakers in Vermont and Rhode Island who support either decriminalization or retail legalization often suggest that part of the “inevitability” they feel about the issue is something akin to the “domino theory” from the Cold War era. Once a single region “falls,” then so do neighboring regions. It sets off a chain reaction that can’t be stopped.
There’s also a “funding paradox” for states looking at decriminalization as opposed to full-on commercial sales and legalization. If a state decriminalizes pot rather than legalizes it and collects revenue from taxing it, it feels it’s missing out on money for road safety and education and prevention programs for youth.
“In general, our state has no taxing capacity left to run our programs, to educate our children,” said Republican Vermont State Rep. Heidi Scheuermann. “Even [former] Gov. [Peter] Shumlin said that a number of years ago, and that’s still a fact.
“So, if we’re going to create new needs, as a result of — whether it’s decrim or legalization of marijuana, we’re going to have to find some revenue somewhere to do that.
“I don’t know if it has to be done all at once, though,” she added, noting that she’s depending on a study commissioned by the governor to draw conclusions and find solutions.
Other lawmakers appear to be succumbing to the fear of missing out.
“When Massachusetts goes to a tax-and-regulate structure next year, anybody who’s interested in accessing marijuana can easily go to Massachusetts,” said Rhode Island State Sen. Joshua Miller, referring not only to the way Colorado taxes pot sales, but also oversees virtually every detail regarding cultivation and distribution, which includes tracking every plant grown with its own barcode. “Then it becomes more of, the revenue is either going to be Massachusetts’ revenue or Rhode Island’s revenue. And those that think it’s a good idea or a bad idea have a different reality to also consider.”
Miller, a Democrat, compared the potential for new tax revenues through a tax-and-regulate structure to the expansion of state lotteries in the ’80s, or casino gambling in the ’90s. When neighboring states adopt the new revenue, other states find it hard to resist.
Competitive pressures come back to Colorado. Its pot revenues, such as they are, could deflate as soon as other states legalize. So a state can be left with the costs of marijuana legalization, but see its revenue hopes dashed.
“There’s three times as many people in Los Angeles as there are in the state of Colorado. Now that California has legalized marijuana, I do think they’re going to be taking the helm in a lot of ways,” Vicente said.
Those who have opposed all movements toward new leniency with marijuana say the taxation lure will remain a Faustian bargain.
“There has been some extra [tax] money, no doubt about it,” Gorman said. “Where we missed the boat is, what is it costing us, what are the societal costs? And if you look at alcohol and tobacco, and you say ‘highly taxed products,’ the taxes only cover about 10 to 12 percent of societal costs, that’s probably not a good investment. And we don’t know that yet with marijuana. But we will down the road. And if we use illegal drugs as an example, we’d have to say the odds are it’s not going to be a good investment for us.”
The federal void
All of this state action comes in a broad federal void. Despite Attorney General Jeff Sessions’ dislike of liberalizing of marijuana laws, little action has come from the Department of Justice to roll back activities by states.
Sessions sent a letter to Colorado’s Democratic Gov. John Hickenlooper in August asking him how the state was responding to a report of increases in traffic deaths, youth consumption, and emergency room visits.
The response came not only from the Colorado governor, but the state’s Republican Attorney General Cynthia Coffman (popular in her party for joining a lawsuit against the EPA’s Clean Power Plan). She and Hickenlooper vigorously defended the state’s marijuana laws, telling Sessions, “When abuses and unintended consequences materialize, the state has acted quickly to address any resulting harms.”
Don Murphy, director of conservative outreach for the Marijuana Policy Project, a lobbying organization dedicated to ending marijuana prohibition, says the quick adoption of recreational marijuana by other states is pushing the federal government into a corner.
“The states don’t care anymore what the federal government says or doesn’t say. And so, they’re just moving along doing their own thing,” Murphy said.
Elected officials at the federal level seem uninterested in diving into the issue. The Washington Examiner reached out to representatives on Capitol Hill from Rhode Island, Vermont, and Michigan (where a ballot issue could appear in 2018), and none would comment.
Still, the nation will get a clear preview of just how far legal pot may go, and how willing states are to continue to challenge federal laws, when voters cast ballots in New Jersey this November. Voters there will choose a successor to long-time marijuana foe Gov. Chris Christie. The candidates there have drawn a clear distinction between themselves. The Democratic candidate is ready to work on loosening the state’s marijuana laws, and the Republican candidate is firmly opposed.
The legislative hurdle appears to be the most comprehensive test for supporters of legalization. If elected representatives and senators in any of these states can find compromise on a bill, and if a governor of a state feels he or she can sign such a bill into law, then supporters of legalization believe the fight against marijuana prohibition will effectively be over.
“We’re at the precipice of actually legalizing it, I believe,” said New Jersey State Sen. Nicholas Scutari, a leading advocate for adopting a retail structure based on Colorado’s. “So, we might as well be at the head of the pack instead of at the rear, like we have been on so many other issues.”
By GFarma News – October 23, 2017
The budding marijuana industry is spurring new research around cannabis that will have long-term effects on a variety of fields, from farming to new medicine, as companies look for solid scientific data on the substance.
With the looming legalization of recreational pot next summer, and the expansion of licensed medical marijuana producers, scientists at the University of Guelph say more organizations are turning to researchers for help growing better plants.
The Ontario university has a long horticultural research history and some of its staff and students are already deep into the study of medicinal marijuana.
20,000 ideas and counting: B.C. offers feedback on legal cannabis
Toronto cannabis lounges to ask for the right to exist legally
Ontario unveils pot plan, including online ordering, 150 stand-alone stores
On Friday, a team of two environmental science professors and a graduate student published a research paper — one they called the first of its kind and the first of many to come — about optimizing the growth of medicinal cannabis indoors.
The study looked at the rate of organic fertilizer in soilless products holding cannabis before it flowered and the optimization of tetrahydrocannabinol — the primary psychoactive part of cannabis — and cannabidiol, which has been touted as a potential treatment for certain forms of epilepsy.
“There is hardly any scientific information on how to produce these plants and now there is so much interest in this area,” said Youbin Zheng, who led the study funded by a licensed medical marijuana producer as well the federal government.
Words such as “OG kush” and “grizzly” — types of marijuana strains — have now appeared in a scientific journal, this time in HortScience, and there’s more to come.
Zheng and fellow professor Mike Dixon have a series of studies in the pipeline that examine the effects of irrigation, lighting, fertilization and soilless technology on cannabis growth as they try to bring scientific rigour to marijuana research.
Building on anecdotal evidence
Dixon is blunt when reflecting on the current cannabis research landscape.
“Much of the work now is largely based on anecdotal bulls–t from people who think they have it all figured out and did all their research in their basements,” he said.
The idea now, he notes, is to take the medicinal marijuana world from the backwoods to pharmaceutical-grade production.
Liberals’ pot bill tweaked to add timeline for edibles
Cannabis black market will thrive without an inclusive legal industry, MPs hear
Dixon has been part of pioneering research into the growth of plants in space and is using that knowledge and technology to help grow better medicinal marijuana. He plans to leverage the windfall of research money coming in from cannabis companies for his work.
“I’m shamelessly taking advantage of the cannabis industry sector’s investment,” he said.
“The bottom line is we’re developing technologies that will allow Canadians to exploit production systems in harsh environments.”
Marijuana production companies — there are more than 60 approved by Health Canada now — need a “huge number of trained scientists,” Zheng noted.
Then there are the potential medical applications associated with marijuana — there are more than 150 compounds found in cannabis that need to be explored, Dixon said.
Another big area is vertical farming — where crops are grown in stacks in vast warehouses with artificial lighting, either in solution or with soilless products — that can allow cold-climate countries to grow food year round, Dixon said.
The results of research on marijuana — driven by interest from the cannabis industry — could be applied to other areas, he explained.
“The funding isn’t coming from food, which has the lowest possible margin as a commodity, but pharmaceuticals,” Dixon said.
“But we can use this research to develop life-support technology, as in food, which can become an economic engine for a country like Canada that will carry us for the next 300 years.”
The dean of the Ontario Agricultural College, at the University of Guelph said the cannabis industry is also expected to help draw new students to the school’s programs.
“One of our greatest challenges is recruiting people into our programs because people typically don’t understand the fact that agriculture and food are high-tech, high-growth sectors and demand an awful lot of people for really interesting careers,” said Rene Van Acker.
“The cannabis industry is doing us a favour by drawing a lot of attention to the sector and drawing attention to the fact it is a high-skill, high-tech area.”
© The Canadian Press, 2017
The Canadian Press
Onerous regulations appear to be negatively impacting the cannabis business growth in Canada.
Specifically, current organizational structures may be too strict to allow production to meet demand for cannabis oils and extracts. While the number of applications for cannabis licensing continues to climb, many entrepreneurs are skipping the step of extraction, presumably in a move to limit potential liabilities by keeping initial operations to the basics of production and distribution.
Tyler Nvquvest of Business Vancouver cited a recent Health Canada report which shows a growth in the cannabis oil sector of more than 871% between April 2016 and March 2017, and pointed out the overall lack of cannabis oil production licenses – only 18 of the 51 licenses granted by Canadian authorities include a plan to produce and sell oil:
“The regulatory system is not structured to solely license companies exclusively focused on oil extraction, said Rosy Mondin, executive director at the Cannabis Trade Alliance of Canada. Oil extraction carries extra restrictions and regulations governing dosage and application.
“‘The way the system is set up is that it is a complete seed-to-sale license,’ said Mondin. ‘If you want to process oils, you are forced to cultivate [marijuana].’
“…’When you look at consumption trends in the U.S. and use [them] as predicators to Canada, the prediction is that consumption of extracted oil and oil-based products is going to increase 198,000% over the next five years,’ Mondin said.”
While Canada is currently losing out on the cannabis oil market due to regulatory hurdles, that will likely change in the near future. Over regulation and supply chain bottlenecks have temporarily plagued other marijuana markets, but the cannabis community is creative and persistent and elected officials like tax dollars. We can expect advocates and politicians to work out some common sense solutions, especially as legalization becomes more mainstream in Canada.
Keep up with the latest in Canada’s cannabis business development! Join the International Cannabis Business Conference in Kauai, Hawaii on December 1-3, 2017, and Vancouver, British Columbia in June 24 and 25, 2018.
Author: AMBER IRIS LANGSTON- Date: OCTOBER 3, 2017
Indica vs Sativa: What are the Differences?
If you’re looking for a quick answer, cannabis Indica is more of a sedating high, while cannabis sativa is more uplifting/energizing.
Or, so we’re told.
But then you have experts like, Jeffrey Raber P.h.d, that claim the difference between indica and sativa is simply morphology, and that there is no difference in the highs.
Well, which one is it?
Do the fancy names and classifications matter?
Let’s take a look at indica vs sativa vs hybrid to find out.
What Is Indica?
Indica plants are use to growing in much harsher environments than their sativa counterparts.
Having to adapt to the cold and turbulent conditions of the kush mountain regions, indica evolved to be dense, short and stubby.
They also evolved to produce thick THC resin to help protect itself from its environment.
Indicas also naturally have high levels of CBD, making them a favorite of many looking for a pain-killing cannabis strain.
What Is Sativa?
The scraggly cousin of indica, sativa, is different from indica, not only in appearance but also in the effects it has on your body, its THC to CBD ratios, cannabinoids and terpenes.
Sativa is often paired with coffee thanks to its naturally uplifting properties.
The plants grow to be tall and lean with leaves that have a thinner face, very much unlike the typical indica marijuana leaf you see plastered all over bongs and grinders at festivals.
The Difference Between Indica and Sativa
There are two camps when it comes to the differences between indica and sativa: those who boldly claim that all indica and sativa give you a certain high and those starting to test and see if it boils down to more than just the different species of the same genus.
After all, some sativa cannabis can give you the “indica” high, and the same goes vice versa.
But we’ll dive more into this research in just a bit.
For now, let’s take a look at the differences that we know.
First named in 1785 by, Jean-Baptiste Lamarck, Indica was named after where the plants were collected—India.
I briefly mentioned earlier that indica evolved in the kush mountains.
More specifically, it grew wild in the areas between 30° and 50° latitudes.
This climate is susceptible to intense, cold winter and warm summers.
Sativa was named earlier than indica, 1753, and was first thought to be the only species of cannabis.
It originates from areas that are between 0° and 30° latitudes.
Namely, equatorial regions of Mexico, Colombia, Thailand and Southeast Asia.
Being subject to the harsh heat of these areas, sativa evolved to be long and lanky to conserve water.
Thankfully, you don’t have to do chemical composition tests to tell the species apart.
You can easily tell the difference between indica and sativa by their leaf shape.
Indica leaves are broad and thicker.
More akin to the prototypical marijuana leaf you see everywhere.
Sativa leaves, on the other hand, are skinny and scraggly like the rest of the plant.
You won’t have any luck using this method to identify a hybrid, though.
They can have a mix of the two or one or the other.
Sativa vs Indica High
The biggest reason we want to compare the two most important cannabis genus is to help get the kind of high or symptom relief we are looking for.
And, while the debate is still ongoing about whether it’s the species of the plant or the terpenes/cannabinoid make up of a plant that determines this, we can still look at the ways we commonly categorize the two different plants.
Cannabis indica will generally give you a more relaxed, body high.
The calm, sedating effects are ideal for when you’re looking to chill out after a long day, binge-watch Netflix or sleep.
It’s also known to enhance sensations such as sound, taste and touch.
Sativas tend to be more of a cerebral, energized high that can lead to an increase in creativity and a more psychedelic high.
This high is perfect for anyone looking to smoke early in the day without feeling like a zombie the rest of the day.
It’s also a great high for reading, writing and making art.
Just wanted to drop another disclaimer here before we look at the symptoms a particular genus can help with.
The result will vary from strain to strain, and this should just be used as a general guideline to help you in the right direction.
As a muscle relaxer
Headaches and migraines
As an energy boost
Mood disorders such as depression
Mild aches and pains
Which one has more THC?
Now, thanks to the advancement in breeding were able to achieve cannabis plants with up to 51% THC.
But what about when we just look at pure strains?
Well, one study has, and they found that, on average, indica strains tend to be significantly higher in not only THC but CBD as well.
The big flaw with this study is that it only looked at six different strains.
Leafy.com has over 720 indica strains and 1177 sativa strains as of 2017, and the number is only going to keep on growing.
We need a bigger picture and thanks to data that’s being collected by cannabis testing labs I’m sure we’ll get it.
The Differences in Growing
Where you are really able to tell the difference between indica and sativa is when you are growing them side by side.
Never will you be able to see such definitive differences.
Indica vs Sativa Buds
Indica buds are dense, and they also tend to condense themselves in clusters around the nodes.
The buds internodal gaps are almost non-existent.
Indica buds are known for being the buds with the strongest odor too.
With sativa buds, It’s pretty common to have a reddish hue when grown in warm environments and purple when grown in colder climates.
They also are far more spread out on the branches.
You can expect them to weigh less than indica after drying because they are less dense buds.
Indica strains are the best cannabis strains to grow indoors.
Commonly growing to be 3 to 6 feet tall they make the perfect plant for closets or grow tents that have a defined ceiling.
You can grow Sativa indoors, but be prepared to fight it and do some extensive plant training.
Believe it or not, sativa cannabis can grow up to 20 feet tall.
Many breeders like to mix indica into sativa strains to try and tame this height.
Flowering Time & Yield Size
Indica cannabis has a much faster flowering time than sativa coming in at between 8 to 9 weeks.
This is even faster than autoflowering plants that are usually around ten weeks.
It’s not just the fast flowering time that makes indica a favorite of many growers.
They also boast larger yields.
Sativa plants will usually flower between 12 to 14 weeks making them the longest flowering species of all.
The fact that most sativa plants take longer to grow and yields less has made breeders insert some of those traits into indica strains to get a better-growing plant while maintaining a sativa high.
And that brings us to our next topic—hybrids.
What is a Hybrid Strain?
Hybrid strains aren’t new to the cannabis scene.
As master breeders began the search for the perfect cannabis, they started to selectively pick traits from various indica and sativa strains creating hybrids of the two.
Hybrids can fall into any of three categories:
Hybrids can be the best of both worlds.
Let’s look at one of the most popular hybrid strains of all time—Blue Dream.
Blue Dream is a sativa-dominant strain forged from mixing Blueberry indica with sativa Haze.
This combination gives you a relaxed body while also giving you a light head high—creating a perfect, calm euphoria.
A hybrid strain like this can provide quick symptom relief all while avoiding the sedative side effects.
Popular Hybrid Strains
Hybrids are a lot of smokers favorite because you can blend the many effects from different cannabinoid profiles.
Here are some of the most popular hybrid strains:
Although there’s a lot of strains with no rhyme or reason to their names, a lot of indica strains take up the moniker, Kush, after the Kush Mountains from which they were born.
Here are a few of the popular Indica strains:
Sativa strains are all over the place with their names.
The only real common thread you’ll see is that a lot are named haze (I’m not sure why, if you do let me know!).
Here are a few of the most popular sativa strains:
Alaskan Thunder Fuck
What are Ruderalis?
Wait, there is a third species of cannabis?
Ruderalis is never talked about thanks to its low THC levels.
But, it’s thanks to them and breeding that we’ve made huge strides in growing cannabis.
First identified in 1924, cannabis ruderalis was discovered in southern Siberia by the botanist, Janiszewski.
While studying cannabis, he happened across these plants that showed a more weedy growth compared to other strains.
This new species was smaller than the others—hardly ever growing taller than two feet.
And it reached flowering much quicker than either indica or sativa—only 5-7 weeks after seed.
Sativa and indica lean on a photoperiod to determine when it starts flowering, while ruderalis depends solely on the maturity of the plant.
This means while you can keep an indica or sativa plant in vegetative stage indefinitely by keeping your grow lights on long cycles, ruderalis will ignore the light cycle completely and start flowering.
Master growers have taken advantage of this to create autoflowering seeds that dramatically reduce the time it takes to harvest a particular strain.
More weed in less time is never a bad thing.
It’s not just the flowering time breeders use ruderalis for.
They are hardy and shorter than the other species, so they are often used to help curb the crazy heights of sativa.
But, that’s not all ruderalis is good for.
While they may be low in THC, they make up for it in CBD.
Some medical cannabis users grow ruderalis for the CBD, and some breeders use this genetic trait to create CBD heavy strains.
When it comes to indica vs sativa a lot is still unknown.
We need more studies done on the different effects of the two, so we can provide a better experience for recreational users and better medical care for medical users.
Hopefully, with states legalizing marijuana, we will start to see real progress made that will tell us if it’s the strains or the cannabinoids and terpenes that we need to focus our attention on to make the best cannabis we can.
Did I miss any differences between indica and sativa?
Can you tell the difference in highs?
If so, let me know in the comments below!
Sourced from www.thcoverdose.com
Yes, You Need a Prescription for Medical Marijuana At Work and This Controversial Logging Case Proves Why
Although there is little case law on medical cannabis use in the Canadian workplace, there are a few cases that can guide both employees and employers on this topic.
Last week, we looked at the case of a man who was fired for using marijuana to relieve back pain and migraine headaches. Today we will examine the case of French vs. Selkin Logging.
In 2014, John French was an equipment operator for Selkin Logging in northern British Columbia and used cannabis to treat pain from cancer. He had spoken with his doctor about cannabis as a treatment but did not have a valid medical cannabis prescription. French was caught smoking cannabis at work and Selkin Logging enacted their zero tolerance drug policy requiring he stop consuming cannabis in the workplace. French was subsequently terminated for breach of this policy.
The British Columbia Human Rights Tribunal found that Selkin Logging was enacting the drug policy on the appropriate grounds – that an impaired equipment operator in the logging sector could be a serious safety risk. However, the Tribunal cautioned against zero tolerance drug policies saying “strict application of the zero tolerance rule, without consideration of accommodation, may offend the Code in circumstances where the individual may be legitimately using marijuana for medical purposes.”
Although the Tribunal found that the drug policy was enacted in good faith, they also stated that French’s termination was discriminatory because he was fired for using cannabis to alleviate the pain of a disability.
In the end, the termination was upheld because French did not hold a valid medical cannabis prescription.
What went wrong?
In the absence of a medical marijuana prescription, French was using cannabis illegally. He had talked with his doctor about using it to treat the symptoms of his cancer, but the doctor had not prescribed it or condoned its use at work. Human Rights legislation does not extend to requiring an employer to accommodate illegal drug use.
Employers that have a zero tolerance drug policy that does not address accommodation for medical cannabis may breach human rights legislation. Employees must have a valid cannabis prescription to be protected by Human Rights legislation. Employers are not required to accommodate illegal cannabis use.
This article was originally published on Civilized. View it here. January 20, 2016
Medicinal cannabis: Rational guidelines for dosing
Gregory T Carter 1*, Patrick Weydt 2, Muraco Kyashna-Tocha 3 & Donald I Abrams 4
1 Department of Rehabilitation Medicine
2 Departments of Neurology and Laboratory Medicine
University of Washington School of Medicine Seattle WA 98531 USA
Email: [email protected]
3 The Cyber Anthropology Institute Seattle WA 98145 USA
4 San Francisco General Hospital Division of Hematology/Oncology
Department of Medicine University of California San Francisco CA 94110 USA
*To whom correspondence should be addressed
IDrugs 2004 7(5):464-470
The Thomson Corporation ISSN 1369-7056
The medicinal value of cannabis (marijuana) is well documented in the medical literature. Cannabinoids, the active ingredients in cannabis, have many distinct pharmacological properties. These include analgesic, anti-emetic, anti-oxidative, neuroprotective and anti-inflammatory activity, as well as modulation of glial cells and tumor growth regulation. Concurrent with all these advances in the understanding of the physiological and pharmacological mechanisms of cannabis, there is a strong need for developing rational guidelines for dosing. This paper will review the known chemistry and pharmacology of cannabis and, on that basis, discuss rational guidelines for dosing.
Keywords Cannabinoids, cannabis, dosing, marijuana, pharmacology
Introduction and brief historical background
Possibly the first references to the medicinal use of cannabis are found in the Chinese pharmacopoeia of Emperor Shen-Nung, written in 2737 BC. This document recommended cannabis for analgesia, rheumatism, beriberi, malaria, gout and poor memory . Eastern Indian documents in the Atharvaveda, dating to about 2000 BC, also refer to the medicinal use of cannabis . Archeological evidence has been found in Israel indicating that cannabis was used therapeutically during childbirth as an analgesic . This use of cannabis continued in the West until the mid-1880s and continues today in parts of Asia. In ancient Greece and Rome, both the Herbal of Dioscorides and the writings of Galen refer to the use of medicinal cannabis .
The medicinal use of cannabis in western medicine occurred much later. There is mention of it in a treatise by Culpepperwritten in medieval times. British East India Company surgeon William O’Shaughnessy introduced cannabis for medicinal purposes into the United Kingdom following observations he made while working in India in the 1840s. He used it in a tincture for a wide range of uses, including analgesia , and Queen Victoria used cannabis for relief of
dysmenorrhea in the same era [6•]. In 1937, against the advice of the majority of the medical community and much of the American Medical Society, the federal government criminalized non-medical cannabis. Cannabis was removed from the United States Pharmacopoeia in 1942 but, up until that time, had still been prescribed by physicians .
The physiological mechanisms and therapeutic value of cannabinoids continue to be well documented in the medical literature[6•, 7, 11,12••,13,14,15••,16• ,17••,18••,19-21,22••, 23,24••,25-27,28•,29,30,31••,32-36]. However, there has been little written on appropriate dosing regimens for the medicinal use of cannabis. With current and emerging laws allowing physicians in many areas of the world to recommend the use of cannabis to treat symptoms of certain diseases and medical conditions, there is a need for medical literature describing rational dosing guidelines. This paper will review the known chemistry and pharmacology of cannabis and then, on that basis, discuss rational guidelines for dosing.
Chemistry and pharmacology of cannabis
Cannabis is a complex plant, with several existing phenotypes, each containing over 400 chemicals [14,15••]; approximately 60 are chemically unique and classified as plant cannabinoids [11,15••]. Naturally occurring cannabinoids are also produced in the human body . The cannabinoids are 21-carbon terpenes, biosynthesized predominantly via a recently discovered deoxyxylulose phosphate pathway [16••], and are lipophilic. Δ9-tetrahydro-cannabinol (THC) and Δ8-THC appear to produce the majority of the psychoactive effects of cannabis. Δ9-THC, the active ingredient in dronabinol (Marinol), is the most abundant cannabinoid in the plant and this has led researchers to hypothesize that it is the main source of the effects of the drug . Dronabinol is available by prescription as a schedule III drug.
Other major plant cannabinoids include cannabidiol and cannabinol, both of which may modify the pharmacology of THC and have distinct effects of their own. Cannabidiol is the second most prevalent active ingredient in cannabis and may produce most of its effects at moderate, mid-range doses. Cannabidiol converts to THC as the plant matures and over time this THC degrades to cannabinol. Up to 40% of the cannabis resin in some strains is cannabidiol [6•,26]. The amount varies according to plant; some varieties of Cannabis sativa have been found to contain no cannabidiol [6•]. As cannabidiol may help reduce anxiety symptoms, cannabis strains without cannabidiol may produce morepanic or anxiogenic side effects. Cannabidiol may exaggerate some of the effects of THC (including increasing THC-induced euphoria), while attenuating others, and competitively slows THC metabolism in the liver.
Consequently, a dose of THC combined with cannabidiol will create more psychoactive metabolites than the same dose of THC alone [27,31••]. In mice, pre-treatment with cannabidiol increased brain levels of THC by 3-fold and there is strong evidence that cannabinoids can increase the brain concentration and pharmacological actions of other drugs [10,11]. Some researchers have proposed that many of the negative side effects of dronabinol, including sedation and altered mental activity, could be reduced by combining it with cannabidiol or possibly other non-psychoactive cannabinoids .
Much less is known about cannabinol, although it appears to have pharmacological properties that are quite different from cannabidiol. Cannabinol has significant anticonvulsant, sedative and other pharmacological activities that are likely to interact with the effects of THC . Cannabinol may induce sleep and may provide some protection against seizures for epileptics [14,28•,32].
Two physiologically occurring lipids, anandamide (AEA) and 2-arachidonylglycerol (2-AG), have been identified as endogenous cannabinoids (endocannabinoids), although there are likely to be more . The physiological roles of these endocannabinoids have been only partially clarified but availableevidence suggests that they function as diffusible and short-lived intercellular messengers that modulate synaptic transmission. Recent studies have provided strong experimental evidence that endocannabinoids mediate signals retrogradely fromdepolarized post-synaptic neurons to presynaptic terminals to suppress subsequent neurotransmitter release, driving the synapse into an altered state [29,31••]. Signaling by the endocannabinoid system appears to represent a mechanism by which neurons can communicate backwards across synapses to modulate their inputs.
There are two known cannabinoid receptor subtypes. Subtype 1 (CB1) is expressed primarily in the brain whereas subtype 2 (CB2) is expressed primarily in the immune system[29,31••]. Cannabinoid receptors constitute a major family of G protein-coupled, seven-helix transmembrane nucleotides, are similar to the receptors of other neurotransmitters such as dopamine, serotonin and norepinephrine, and are the most abundant G protein-coupled receptor in the brain [8,10,11]. Activation of protein kinases may be responsible for some of the cellular responses elicited by the CB1receptor .
Because of this biochemical complexity, characterizing the clinical pharmacology of cannabis is challenging. Further complicating the evaluation of cannabis is the variable potency of the plant material used in research studies. The concentration of THC and other cannabinoids in cannabis varies greatly depending on growing conditions, plant genetics and processing after harvest [6•,7,8]. The highest concentrations of bioactive compounds are found in the resin exuded by the flowering female plants [6•,7,8]. Leaf mixtures of cannabis have concentrations of THC ranging from 0.3 to 4% by weight [6•,7,8]. However, cannabis today is typically distributed as flowers and can contain 8 to ≥ 25% of THC. Thus, 1 g of cannabis flowers would typically contain 80 to 250 mg of THC [6•].
The clinical pharmacology of cannabis containing high concentrations of THC may differ from plant material containing small amounts of THC and higher amounts of the other cannabinoids. Moreover, the bioavailability and pharmacokinetics of inhaled cannabis are substantially different than when cannabis is ingested [6•].
Although it is a potent drug that may produce psychoactive effects, THC (and the other cannabinoids) has relatively low toxicity, and lethal doses in humans have not been described [25,26]. The theoretical LD50 value is estimated to be 1 to 20,000 or 1 to 40,000, using a single
cannabis cigarette as a unit of dose. Conversely stated, a human would have to consume 20,000- to 40,000-fold the amount of cannabis contained in one cigarette, in a short period of time, to achieve lethality. Using this as a basis, it has been estimated that 628 kg of cannabis would have to be smoked in 15 min to induce a lethal effect .
Central effects of cannabinoids include disruption of psychomotor behavior, short-term memory impairment, intoxication, stimulation of appetite, antinociceptive actions (particularly against pain of neuropathic origin) and anti-emetic effects. Although there are signs of mild cognitive impairment in chronic cannabis users there is little evidencethat such impairments are irreversible, or that they are accompanied by drug-induced neuropathology. A proportion of regular users of cannabis will develop some tolerance . A study by Hart and co-workers demonstrated that acute cannabis smoking produced minimal effects on complex cognitive task performance in experienced cannabis users, while still subjectively providing a euphoric ‘high’ [38••]. The potential medical applications of both natural and synthetic cannabinoids are currently being tested in a number of clinical trials.
Delivery system and pharmacokinetics
The route of administration is an important determinant of the pharmacokinetics of the cannabinoids in cannabis, particularly absorption and metabolism [39-42]. Typically, cannabis is smoked as a cigarette with a mass of between 0.5 and 1.0 g. After combustion and inhalation, peak venous blood levels of 75 to 150 ng of THC per ml of plasma have been measured when smoking is finished [39,43,44]. The main advantage of smoking is rapid onset of effect and ease of dose titration. When cannabis is smoked, cannabinoids in the form of an aerosol in the inhaled smoke are absorbed and delivered to the brain rapidly, as would be expected of a highly lipid-soluble drug [41,45].
Individual smoking behavior during an experiment is difficult for a researcher to control, and smoking behavior is not easily standardized, although some research protocols for standardization of smoking have been developed . An experienced cannabis smoker can titrate and regulate dose to obtain the desired acute effects and to minimize undesired effects [46,47]. Each inhalation delivers a discrete dose of cannabinoids to the body. Inhalation volume changes with phase of smoking, tending to be highest at the beginning and lowest at the end of smoking a cigarette. Some studies found frequent users to have higher inhalation volumes than less frequent cannabis users. Heavy users could absorb as much as 27% of available THC, which maybe twice as much as an infrequent user may absorb . During smoking, as the cigarette length shortens, the concentration of THC in the remaining cannabis increases. Thus, each successive inhalation contains an increasing concentration of THC . However, up to 40% of the available THC may be completely combusted in the process of smoking and may not be biologically available. Assays of cannabinoids in blood or urine after smoking can partially quantify dose actually absorbed, but the analytic procedures are methodologically demanding [47,48].
After smoking, venous blood levels of THC fall precipitously within minutes, and an hour later they are 5 to 10% of the peak level [40,41,43,44]. Plasma clearance of THC is ≥ 950 ml/min,
which is relatively high and is essentially the rate of hepatic blood flow. However, the rapid disappearance of THC from blood is largely due to redistribution to other tissues in the body rather than cannabinoid metabolism [40,41]. Metabolism in most tissues is relatively slow. Slow release of cannabinoids from tissues and subsequent metabolism results in a long elimination half-life. The terminal half-life of THC is estimated to range from 20 h to as long as 10 to 13 days, although reported estimates vary considerably and are likely to reflect the sensitivity of the measurement assay.
Smoking anything, including cannabis, is not beneficial for the lungs and airway system [49,50]. A healthier option may be vaporization; because cannabinoids are volatile, they will
vaporize at a temperature much lower than actual combustion . Heated air can be drawn through cannabis, the active compounds will vaporize, and these can then be inhaled. Vaporization delivers the substance in a rapid manner that, like smoking, can be easily titrated to the desired effect . Theoretically, this removes most of the health hazards of smoking, although this has not yet been studied. Furthermore, there may be differing vaporization points for the individual cannabinoids. Vaporized cannabis may have differing concentrations and ratios of cannabinoids compared to smoked cannabis, although this also needs further study.
Cannabis can also be ingested orally or through a feeding tube. Orally ingested THC or cannabis has quite different pharmacokinetics than when it is inhaled. The onset of action is delayed and titration of dosing is more difficult [52-54,55•]. Maximum THC and other cannabinoid blood levels are only reached 1 to 6 h after an oral dose, with a half-life of 20 to 30 h [52-54,55•]. This is also reflected in the pharmacokinetics of dronabinol capsules, which contain only synthetic THC and none of the other cannabinoids .When orally ingested, THC is degraded in the liver to the byproduct 11-hydroxy-THC, which also has potent psychoactive effects. This metabolite occurs at a much lower concentration when cannabis is inhaled. Thus, when THC (dronabinol or cannabis) is ingested orally, more sedation occurs because of the presence of the 11-hydroxy-THCpsychoactive metabolite .
Metabolism, bioavailability and drug interactions
Some inactive carboxy metabolites have terminal half-lives of 50 h to ≥ 6 days and thus serve as markers of priorcannabis use in urine tests [55•,56]. Most of the absorbed THC dose is eliminated in feces, and 33% is eliminated in urine. THC enters enterohepatic circulation and undergoes hydroxylation and oxidation to 11-nor-9-carboxy-Δ 9-THC (9-COOH-9-THC). The glucuronide is excreted as the major urine metabolite along with 18 non-conjugated metabolites. Frequent and infrequent cannabis users are similar in the way that they metabolize THC . THC bioavailability from smoked cannabis varies greatly among individuals and also depends on the composition of the specific cannabis preparation. Bioavailability can range from 1 to 27%, with variable bioavailability resulting from significant loss of THC in side stream smoke, as well as variation in individual smoking behaviors. This includes incomplete absorption from inhaled smoke, metabolism in lung, and cannabinoid pyrolysis (ie, destruction by combustion).
Cannabinoids appear to partially inhibit the metabolism of drugs metabolized by the hepatic cytochrome P450 enzyme system [57,58,59••,60]. Thus, the absorption or clearance of other drugs taken with cannabis may be slowed or hastened depending on timing and sequence of drug ingestion and past exposure. THC is highly bound to plasma proteins (97 to 99%) and is likely to interact with other highly bound drugs because of competition for binding sites on plasma proteins [61,62].
The Food and Drug Administration (FDA) first licensed and approved dronabinol in 1986 for the treatment of nauseaand vomiting associated with chemotherapy. The indication was expanded in 1992 to the treatment of anorexia associated with weight loss in patients with AIDS wasting syndrome. In a randomized, double-blind, placebo-controlled, 6-week study involving 139 patients, dronabinol provided a statistically significant improvement in appetite and non-statistically significant trends toward improved body weight and mood, and decreases in nausea [63•]. In 1999, the United States Drug Enforcement Administration, in cooperation with the FDA, reclassified the scheduling status of dronabinol from a Schedule II (CII) to a Schedule III (CIII) controlled substance (for definitions of schedules, refer to https://www.dea.gov/pubs/csa/812.htm).
In 454 patients with cancer who received a total of 750 courses of treatment for various malignancies, dronabinol capsules provided complete or partial success in easing nausea and vomiting in 68% of patients given < 7 mg/m 2/day of dronabinol and 64% of patients given > 7 mg/m2/day of dronabinol [64••]. According to the manufacturer, Unimed Pharmaceuticals Inc, the prescribed dose of dronabinol for appetite stimulation is 2.5 mg twice-daily, to be taken before lunch and dinner. For nausea, vomiting and pain the dosing is 5 mg/m2. If the 5-mg dose is ineffective, incremental increases of 2.5 mg, up to a maximum of 15 mg, is recommended. The same dose can be taken every 2 to 4 h for a maximum of four to six doses a day. Regardless of the clinical setting in which it is prescribed, the maximum total recommended dose of dronabinol is 15 mg/m2 four- to six-times-daily or 100 to 120 mg/day .
There are a limited number of well-performed clinical trials from which to draw succinct dosing regimens. Clinical trials have typically used cannabis cigarettes supplied by the NIDA (National Institute on Drug Abuse) containing 3.5 to 4.0% of THC by weight [59••,66,67]. Recently, Abrams and co-workers conducted an open-label study in patients with confirmed HIV neuropathy with persistent neuropathic pain . All patients had prior experience of smoking marijuana but had ceased for 30 days prior to admission. After a 2-day lead-in period, patients smoked one cigarette containing 3.56% of THC three-times-daily for 7 days. A heat-capsaicin-induced experimental pain model was used to clarify the effects of THC. Marijuana smoking led to a reduction in pain score to 20/100, with ten of 16 patients experiencing a 30% reduction in average daily pain. An excellent correlation was noted in the response to the heat-capsaicin model, as 14 of 16 patients experienced a 30% reduction in the area of secondary hyperalgesia after smoking .
Wade and co-workers compared plant-derived cannabis extracts to standard treatments for neurogenic symptoms unresponsive to standard treatment in a double-blind, randomized, placebo-controlled, cross-over trial with 2-week treatment periods . The enrolled patients (n = 24) had multiple sclerosis (n = 18), spinal cord injury (n = 4), brachial plexus injury (n = 1) and limb amputation due to neurofibromatosis (n = 1). Whole-plant extracts of either THC only, cannabidiol only, a mixed cannabinoid extract of both THC and cannabidiol in a 1:1 ratio, or a matched placebo were self-administered by sublingual spray at doses determined by titration against symptom relief or unwanted effects within the range of 2.5 to 120 mg/24 h. The results demonstrated that pain relief associated with both THC and cannabidiol was significantly superior to placebo. The mixed cannabinoid extract, compared to placebo, was significantly superior in providing pain relief and improving bladder control, muscle spasms and spasticity. Side effects were rare. Three patients had transient hypotension and intoxication with rapid initial dosing of the THC extract.
Deriving dosing recommendations and guidelines
Cannabis has many variables that do not fit well with the typical medical model for drug prescribing. If the plant is used, the variations are extreme. Plants vary immensely by phenotypes, and even the time of harvest affects which cannabinoids are present and in what percentages. An individual may be much more sensitive than another, heavy smokers may experience different chemical effects than light smokers and ingestion may alter bioavailability. The bulk of the research into cannabis has primarily examined THC, the other cannabinoids have been studied to a lesser degree, while little research has been performed on combinations of cannabinoids, although this is beginning to change. These combinations are important to medicinal users of cannabis as a number of positive synergistic effects could be involved [70-72]. All of these points make it imperative that the dosing is highly individualized, so a patient-determined, self-titrated dosing model is recommended. This self-titration model is acceptable given the variables discussed above, as well as the low toxicity of cannabis. This construct
is not unique to cannabis. There are other drugs that have relatively low toxicity and high dosing limits (gabapentin being one notable example), and are titrated to effect.
To facilitate an understanding of the determination of these guidelines, an estimate of the actual amount of THC obtained by a patient when smoking different strengths of cannabis must be derived. As noted earlier, with smoking as the delivery, 40% of the active ingredients are lost in side stream or combustion, and a maximum of 27% of the remaining active ingredients can actually be absorbed by the patient. Given this, the maximum THC absorbed by a patient using 1 g of cannabis containing 10% of THC would
be 16.3 mg.
The only form of cannabinoid that is available by a formal,dose-specific prescription is dronabinol. There are too many variables in the published clinical trials and case series with raw cannabis to use those studies as a basis for deriving doses. Therefore, we will use the dronabinol prescription guidelines as published by the manufacturer and accepted by the FDA as the basis for formulating our dosing recommendations for natural cannabis. It is critical to note that dronabinol is an oral preparation and contains only THC. Most medicinal cannabis
patients use smoking as the route of delivery. As we have previously noted there are significant differences in pharmacokinetics between oral consumption and smoking. Furthermore, there are varying physiological effects when the other cannabinoid forms are present, as is the case with natural cannabis plant material. It is also not clear how the original dosing construct for
dronabinol was arrived at, although we assume it was derived from clinical testing for therapeutic benefit versus side effects. Despite these inherent limitations, these calculations do provide approximate dose equivalents by weight and are useful as long as one recognizes these.
Applying the known pharmacokinetics of cannabis, as described above, to a conservative dronabinol dosing model of 2.5 to 60 mg/day, we calculated the doses for cannabis containing particular percentages of THC (Table 1). These derived figures lie closely within the range of reported amounts. In informal surveys from patients in Washington and California (USA), the average reported consumption of cannabis by medicinal users typically ranges between 10 to 20 g of raw cannabis per week, or 1.42 to 2.86 g/day of cannabis. The average strength of medical cannabis used by the patients who reported these doses was 15% THC. Thus, these patients were actually absorbing between 34 and 68 mg/day of THC from the raw cannabis. The mean strength of medical cannabis in this study was 19% THC, which corresponds to 44 to 88 mg/day of THC actually being consumed by the patient . These figures are all within a similar range.
Table 1. Amount of cannabis calculated to contain equivalent amounts of THC to dronabinol (2.5 to 60 mg).
Amount of cannabis (g) required to obtain: % of THC in cannabis
2.5 mg of THC
10 mg of THC
30 mg of THC
60 mg of THC
Our recommended doses are further reinforced by two studies that utilized smoked cannabis in a well-documented dosing regime. Chang and co-workers studied the effects of smoked cannabis dosed at 10 mg/m2five-times-daily, which is equivalent to 87.5 mg/day of THC for an average-sized person. This would be the equivalent of 3.6 g of cannabis containing 15% of THC . Vinciguerra and co-workers studied smoked cannabis dosed at 5 mg/m2 four-times-daily, or 35 mg/day of THC for an average person. This is the equivalent of 1.4 g of cannabis containing 15% of THC . For the purposes of these calculations, we assumed an average-sized person to be 1.70 m in height with a mass of 63.6 kg and a body surface area of 1.75 m2.
These doses all fall within the medical cannabis guidelines allowed in the Canadian medical system. The Canadian medical allowance for cannabis is 1 to 12 g/day, with an average of > 5 g/day. These doses are also highly similar to the dosing range reported in a recent survey of patients who use cannabis to control symptoms of amyotrophic lateral sclerosis . Thus, despite all of the noted variables, there is remarkable consistency among our derived doses and the reported doses from a number of different sources notedhere.
A final comment should be made regarding physiological tolerance to cannabinoids. Tolerance plays a significant role in cannabis use since tolerance may develop to any of the various cannabinoids . With regard to treating chronic, intractable pain, physicians will often prescribe increasingly larger doses of long-acting opioids as patients develop tolerance. These patients are also generally prescribed fast onset, short-acting opioids for ‘breakthrough pain’. This is accepted practice, despite the fact that opioids, even in an opioid-dependent patient, have the capacity to suppress breathing to the extent of inducing respiratory arrest. Long-term cannabis users can develop tolerance but, as previously discussed, there is essentially no risk for overdose. Thus, it is conceivable that a long-term cannabis user may require significantly larger amounts of cannabis to achieve a therapeutic effect. In addition, those who ingest cannabis may also require significantly higher amounts. Until more refined and purified cannabinoid preparations are available it will not be possible to derive a more specific or exact dosing schedule.
We have outlined reasonable guidelines for dosing of medical cannabis, based on the known pharmacology. Our dosing model is primarily derived from dronabinol (THC), since that is the only clearly defined, FDA-approved dosing paradigm currently available. However, our derived dosing schedule did match reasonably well with the amounts of natural cannabis reported by medical users. In using our dosing guidelines clinicians must be aware that THC is not the only clinically useful and pharmacologically activecannabinoid. The effects of THC are clearly modulated by other cannabinoids, which may have unique effects of their own. The clinician must also be aware of patient tolerance, and differing routes of intake and delivery systems, which can affect pharmacokinetics and bioavailability. Recognizing this, we recommend that our guidelines are used as aconstruct to allow the physician and patient to develop an individual, self-titration dosing paradigm. Given the current state of the known, published pharmacology of cannabis, this is the best dosing model that can be derived.
This work is supported by Research and Training Center Grant HB133B980008 from the National Institute on Disability and Rehabilitation Research, Washington, DC, USA. The authors would like to acknowledge Dale Gieringer, Martin Martinez and Ethan Russo for their help in preparing this manuscript.
••of outstanding interest •of special interest
1. Li HL: An archaeological and historical account of cannabis in China. Econ Bot (1974) 28:437-448.
2. Indian Hemp Drugs Commission: Report of the Indian Hemp Drugs Commission, 1893-94. Government Central Printing House, Simla, India (1894).
3. Zias J, Stark H, Sellgman J, Levy R, Werker L, Breuer A, Mechoulam R: Early medical use of cannabis. Nature (1993) 363(6426):215.
4. Dioscorides P: The Greek Herbal of Dioscorides. Translated by Goodyear J, Gunther RWT. Hafner Publishing, London, UK (1968).
5. O’Shaughnessy WB: On the preparations of the Indian hemp, or gunjah (Cannabis indica): Their effects on the animal system in health, and their utility in the treatment of tetanus and other convulsive diseases. Trans Med Phys Soc Bengal (1838-1840).
6. Martinez M: A brief history of marijuana. In: The New Prescription:Marijuana as Medicine. Podrebarac F (Ed), Quick American Archives, Oakland, CA, USA (2000):1-18. • This well-
referenced book provides a balanced view of historical, medical and legal issues regarding medical marijuana.
7. Fankhauser M: History of cannabis in Western medicine. In: Cannabis and cannabinoids: Pharmacology, toxicology and therapeutic potential. Grotenhermen F, Russo R (Eds), The Haworth Integrative Healing Press, Oxford, UK (2002):37-49.
8. Carter GT, Weydt P: Cannabis: Old medicine with new promise for neurological disorders. Curr Opin Invest Drugs (2002) 3(3):437-440. Medicinal cannabis: Rational guidelines for dosing Carter et al 469
9. Campbell VA: Tetrahydrocannabinol-induced apoptosis of cultured cortical neurones is associated with cytochrome c release and caspase-3 activation. Neuropharmacology (2001) 40(5):702-709.
10. Valjent E, Pages C, Rogard M, Besson MJ, Maldonado R, Caboche J: Δ9 tetrahydrocannabinol-induced MAPK/ERK and Elk-1 activation in vivo depends on dopaminergic transmission. Eur J Neurosci(2001) 14(2):342-352.
11. Friedman H, Klein TW, Newton C, Daaka Y: Marijuana, receptors and immunomodulation. Adv Exp Med Biol (1995) 373:103-113.
12. Chen Y, Buck J: Cannabinoids protect cells from oxidative cell death: A receptor-independent mechanism. J Pharmacol Exp Ther(2000) 293(3):807-812. •• This study, along with references [15••], [16••], [17••], [18••], [22••] and [24••], confirms the neuroprotective effects of cannabinoids.
13. Guzman M, Sanchez C, Galve-Roperh I: Control of the cell survival/death decision by cannabinoids. J Mol Med (2001) 78(11):613-625.
14. Akinshola BE, Chakrabarti A, Onaivi ES: In-vitro and in-vivo action of cannabinoids. Neurochem Res (1999) 24(10):1233-1240.
15. Hampson AJ, Grimaldi M, Axelrod J, Wink D: Cannabidiol and (-)Δ9-tetrahydrocannabinol are neuroprotective antioxidants. Proc Natl Acad Sci USA (1998) 95(14):8268-8273. •• This study, along with references [12••], [16••], [17••], [18••], [22••] and [24••], confirms the neuroprotective effects of cannabinoids.
16. Hampson AJ, Grimaldi M, Lolic M, Wink D, Rosenthal R, Axelrod J: Neuroprotective antioxidants from marijuana. Ann NY Acad Sci(2000) 899:274-282. •• This study, along with references [12••], [15••], [17••], [18••], [22••] and [24••], confirms the neuroprotective effects of cannabinoids.
17. Nagayama T, Sinor AD, Simon RP, Chen J, Graham SH, Jin K, Greenberg DA: Cannabinoids and neuroprotection in global and focal cerebral ischemia and in neuronal cultures. J Neurosci (1999) 19(8):2987-2995.•• This study, along with references [12••], [15••], [16••], [18••], [22••] and [24••], confirms the neuroprotective effects of cannabinoids.
18. Eshhar N, Striem S, Biegon A: HU-211, a non-psychotropic cannabinoid, rescues cortical neurones from excitatory amino acid toxicity in culture. Neuroreport (1993) 5(3):237-240. •• This study, along with references [12••], [15••], [16••], [17••], [22••] and [24••], confirms the neuroprotective effects of cannabinoids.
19. Hollister LE: Marijuana and immunity. J Psychoact Drugs (1988) 20(1):3-8.
20. Carter GT, Rosen BS: Marijuana in the management of amyotrophic lateral sclerosis. Am J Hospice Palliative Care (2001) 18(4):264-270.
21. Hansen HH, Schmid PC, Bittigau P, Lastres-Becker I, Berrendero F, Manzanares J,Ikonomidou C, Schmid HH, Fernandez-Ruiz JJ, Hansen HS: Anandamide, but not 2-arachidonoylglycerol, accumulates during in vivo neurodegeneration.J Neurochem(2001) 78(6):1415-1427.
22. Panikashvili D, Simeonidou C, Ben-Shabat S, Hanus L, Breuer A, Mechoulam R, Shohami E: An endogenous cannabinoid (2-AG) is neuroprotective after brain injury. Nature (2001) 413(6855):527-531. •• This study, along with references [12••], [15••], [16••], [17••], [18••] and [24••], confirms the neuroprotective effects of cannabinoids.
23. Ferraro L, Tomasini MC, Cassano T, Bebe BW, Siniscalchi A, O’Connor WT, Magee P, Tanganelli S, Cuomo V, Antonelli T: Cannabinoid receptor agonist WIN 55,212-2 inhibits rat cortical dialysate γ-aminobutyric acid levels. J Neurosci Res (2001) 66(2):298-302.
24. Sinor AD, Irvin SM, Greenberg DA: Endocannabinoids protect cerebral cortical neurons from in vitro ischemia in rats. Neurosci Lett (2000) 278(3):157-160. •• This study, along with references [12••], [15••], [16••], [17••], [18••] and [22••], confirms the neuroprotective effects of cannabinoids.
25. Young F: In the Matter of Marijuana Rescheduling Petition. US Department of Justice, DEA (1988):Docket No 86-22.
26. Gurley RJ, Aranow R, Katz M: Medicinal marijuana: A comprehensive review. J Psychoact Drugs (1998) 30(2):137-147.
27. Robson P: Therapeutic aspects of cannabis and cannabinoids. Br J Psychiatry (2001) 178:107-115.
28. Rice AS: Cannabinoids and pain. Curr Opin Invest Drugs (2001) 2(3):399-414. • An excellent review article summarizing the analgesic effects of cannabinoids.
29. Di Marzo, Bisogno T, De Petrocellis L: Endocannabinoids: New targets for drug development. Curr Pharm Des(2000) 6(13):1361-1380.
30. Tramer MR, Carroll D, Campbell FA, Reynolds DJ, Moore RA, McQuay HJ: Cannabinoids for control of chemotherapy induced nausea and vomiting: Quantitative systematic review. Br Med J (2001) 323(7303):16-21.
31. Pertwee RG: Cannabinoid receptor ligands: Clinical and neuropharmacological considerations, relevant to future drug discovery and development. Expert Opin Investig Drugs(2000) 9(7):1553-1571. •• An excellent review article outlining the future directions for drug development in cannabinoid-based medicines.
32. Renn E, Mandel S, Mandel E: The medicinal uses of marijuana. Pharm Ther (2000) 25(10):536-524.
33. Hubbard JR, Franco SE, Onaivi ES: Marijuana: Medical implications. Am Fam Phys (1999) 60(9):2583-2588.
34. Voth EA, Schwartz RH: Medicinal applications of Δ9-tetrahydrocannabinol and marijuana. Ann Intern Med (1997) 126(10):791-798.
35. Baker D, Pryce G, Croxford JL, Brown P, Pertwee RG, Huffman JW, Layward L: Cannabinoids control spasticity and tremor in a multiple sclerosis model. Nature (2000) 404(6773):84-87.
36. Consroe P, Musty R, Rein J, Tillery W, Pertwee R: The perceived effects of smoked cannabis on patients with multiple sclerosis. Eur Neurol (1997) 38(1):44-48.
37. Abrams DI: Medical marijuana: Tribulations and trials. J Psychoact Drugs (1998) 30(2):163-169.
38. Hart CL, van Gorp W, Haney M, Foltin RW, Fischman MW: Effects of acute smoked marijuana on complex cognitive performance. Neuropsychopharmacology (2001) 25(5):757-765. •• This study confirms the minimal side effects of cannabis use on cognitive performance, particularly in chronic users.
39. Adams IB, Martin BR: Cannabis: Pharmacology and toxicology in animals and humans. Addiction (1996) 91(11):1585-1614.
40. Pertwee RG: Sites and mechanisms of action. In: Cannabis and Cannabinoids: Pharmacology, Toxicology and Therapeutic Potential. Grotenhermen F, Russo R (Eds), The Haworth Integrative Healing Press, Oxford, UK (2002):73-81.
41. Agurell S, Halldin M, Lindgren JE, Ohlsson A, Widman M, Gillespie H, Hollister L: Pharmacokinetics and metabolism of Δ1-tetrahydrocannabinol and other cannabinoids with emphasis on man. Pharmacol Rev (1986) 38(1):21-43.
42. Barnett G, Licko V, Thompson T: Behavioral pharmacokinetics of marijuana. Psychopharmacology (Berl) (1985) 85(1):51-56.
43. Huestis MA, Henningfield JE, Cone EJ: Blood cannabinoids. 1. Absorption of THC and formation of 11-OH-THC and THC-COOH during and after smoking marijuana. J Anal Toxicol (1992) 16(5):276-282.
44. Huestis MA, Sampson AH, Holicky BJ, Henningfield JE, Cone EJ: Characterization of the absorption phase of marijuana smoking. Clin Pharmacol Ther (1992) 52(1):31-41.
45. Matthias P, Tashkin DP, Marques-Magallanes JA, Wilkins JN, Simmons MS: Effects of varying marijuana potency on deposition of tar and Δ9-THC in the lung during smoking. Pharmacol Biochem Behav(1997) 58(4):1145-1150.
46. Heishman SJ, Stitzer ML, Yingling JE: Effects of tetrahydrocannabinol content on marijuana smoking behavior, subjective reports, and performance. Pharmacol Biochem Behav(1989) 34(1):173-179. 470 IDrugs 2004 Vol 7 No 5
47. Herning RI, Hooker WD, Jones RT: Tetrahydrocannabinol content and differences in marijuana smoking behavior.Psychopharmacology (1986) 90(2):160-162.
48. Johansson E, Halldin MM, Agurell S, Hollister LE, Gillespie HK: Terminal elimination plasma half-life of Δ1-tetrahydrocannabinol (Δ1-THC) in heavy users of marijuana. Eur J Clin Pharmacol (1989) 37(3):273-277.
49. Polen MR, Sidney S, Tekawa IS, Sadler M, Friedman GD: Health care use by frequent marijuana smokers who do not smoke tobacco. West J Med (1993) 158(6):596-601.
50. Benowitz NL, Jones RT: Cardiovascular and metabolic considerations in prolonged cannabinoid administration in man. J Clin Pharmacol (1981) 21(Suppl 8-9):214S-223S.
51. Gieringer D: Cannabis vaporization: A promising strategy for smoke harm reduction. J Cannabis Ther (2001) 1(4):153-170.
52. Jones RT, Benowitz NL, Herning RI: Clinical relevance of cannabis tolerance and dependence. J Clin Pharmacol (1981) 21(Suppl 8-9):143S-152S.
53. Kelly P, Jones RT: Metabolism of tetrahydrocannabinol in frequent and infrequent marijuana users. J Anal Toxicol (1992) 16(4):228-235.
54. Grotenhermen F: Effects of cannabis and cannabinoids. In: Cannabis and Cannabinoids: Pharmacology, Toxicology and Therapeutic Potential. Grotenhermen F, Russo R (Eds), The Haworth Integrative Healing Press, Oxford, UK (2002):55-72.
55. Mechoulam R, Devane WA, Breuer A, Zahalka J: A random walk through a cannabis field. Pharmacol Biochem Behav (1991) 40(3):461-464. • This paper delineates many of the complexities of the cannabis plant, including variations in species subtypes.
56. Hollister LE: Interactions of cannabis with other drugs in man. In: Strategies for Research on the Interactions of Drugs of Abuse. National Institute on Drug Abuse Research Monograph 68. Braude MC, Ginzburg HM (Eds), DHHS Publication No (ADM)86-1453. Superintendent of Documents, US Government Printing Office, Washington, DC, USA (1986):110-116.
57. Fellermeier M, Eisenreich W, Bacher A, Zenk MH: Biosynthesis of cannabinoids. Incorporation experiments with 13 C-labeledglucoses. Eur J Biochem (2001) 268(6):1596-1604.
58. Rueda D, Galve-Roperh I, Haro A, Guzman M: The CB1 cannabinoid receptor is coupled to the activation of c-Jun N-terminal kinase. Mol Pharmacol (2000) 58(4):814-820.
59. Kosel BW, Aweeka FT, Benowitz NL, Shade SB, Hilton JF, Lizak PS, Abrams DI: The effects of cannabinoids on the pharmacokinetics of indinavir and nelfinavir. AIDS (2002) 16(4):543-550. •• This paper describes the hepatic metabolism of cannabinoids through the cytochrome P450 system.
60. Benowitz NL, Jones RT: Effect of Δ 9-tetrahydrocannabinol on drug distribution and metabolism: Antipyrine, pentobarbital and ethanol. Clin Pharmacol Ther (1977) 22(3):259-268.
61. Gustafson RA, Levine B, Stout PR, Klette KL, George MP, Moolchan ET, Huestis MA: Urinary cannabinoid detection times after controlled oral administration of Δ9-tetrahydrocannabinol to humans. Clin Chem (2003) 49(7):1114-1124.
62. Benowitz NL, Nguyen T, Jones RT, Herning RI, Bachman J: Metabolic and psychophysiologic studies of cannabidiol-hexobarbital interaction. Clin Pharmacol Ther (1980) 28(1):115-120.
63. Nelson K, Walsh D, Deeter P, Sheehan F: A phase II study of Δ9-tetrahydrocannabinol for appetite stimulation in cancer-associated anorexia. J Palliat Care (1994) 10(1):14-18. • This is an important clinical trial defining the benefit of cannabis in appetite stimulation.
64. Abrams DI, Hilton JF, Leiser RJ, Shade SB, Elbeik TA, Aweeka FT, Benowitz NL, Bredt BM, Kosel B, Aberg JA, Deeks SG et al: Short-term effects of cannabinoids in patients with HIV-1 infection: A randomized, placebo-controlled clinical trial. Ann Intern Med (2003) 139(4):258-266. •• This is a major clinical trial examining the effects of cannabinoids in the HIV-infected population.
65. Unimed Pharmaceuticals Inc: Marinol Capsules product information package insert. (2001).
66. Kelly TH, Foltin RW, Emurian CS, Fischman MW: Effects of Δ9-THC on marijuana smoking, dose choice, and verbal report of drug liking. J Exp Anal Behav (1994) 61(2):203-211.
67. Ware MA, Doyle CR, Woods R, Lynch ME, Clark AJ: Cannabis use for chronic non-cancer pain: Results of a prospective survey. Pain(2003) 102(1-2):211-216.
68. Jay C, Shade S, Vizoso H, Reda H, Petersen K, Rowbotham M, Abrams D: The effect of smoked marijuana on chronic neuropathic and experimentally induced pain in HIV neuropathy: Results of an open-label pilot study. Int Conf Retroviruses Opportunistic Infect(2004):Abs 496.
69. Wade DT, Robson P, House H, Makela P, Aram J: A preliminary controlled study to determine whether whole-plant cannabis extracts can improve intractable neurogenic symptoms. Clin Rehabil (2003) 17(1):21-29.
70. Carlini EA, Karniol IG, Renault PF, Schuster CR: Effects of marijuana in laboratory animals and man. Br J Pharmacol (1974) 50(2):299-309.
71. Fairbairn JW, Pickens JT: Activity of cannabis in relation to its Δ9-trans-tetrahydro-cannabinol content. Br J Pharmacol (1981) 72(3):401-409.
72. Gieringer D: Medical Cannabis Potency Testing Project. Bull Multidisciplinary Assoc Psychedelic Studies (1999) 9(3):20-22.
73. Chang AE, Shiling DJ, Stillman RC, Goldberg NH, Seipp CA, Barofsky I, Simon RM, Rosenberg SA: Δ9-tetrahydrocannabinol as an antiemetic in cancer patients receiving high-dose methotrexate. A prospective, randomised evaluation. Ann Intern Med (1979) 91(6):819-824.
74. Vinciguerra V, Moore T, Brennan E: Inhalation marijuana as an antiemetic for cancer chemotherapy. New York State J Med (1988) 88(10):525-527.
75. Amtmann D, Weydt P, Johnson K, Jensen MP, Carter GT: Survey of cannabis use in patients with amyotrophic lateral sclerosis. Am J Hosp Palliat Care (2004) 21(2):95-104.
76. Wilkinson JD, Whalley BJ, Baker D, Pryce G, Constanti A, Gibbons S, Williamson EM: Medicinal cannabis: Is Δ9-tetrahydrocannabinol necessary for all its effects. J Pharm Pharmacol (2003) 55(12):1687-1694.
MariCann expansion establishes Norfolk as primary site today, in future
Photo by Jeff Tribe
MariCann Inc. looks forward to ‘growing green with green’ in its state-of-the-art $8-million 180,000-square-foot expansion.
“This is the field of dreams,” said VP of Operations Richard Kropman, indicating a large, fenced rectangle dotted with heavy machinery.
On a drizzly January morning, the target area on the MariCann property southeast of Glen Meyer was a muddy expanse. But for what Director of Media and Investor Relations Shawn Alexander describes as a startup company in a startup industry, ambitious dreams are well on their way to reality.
“We refer to it as scaling up,” understated Alexander of a 700-per-cent expansion from the current 30,000 square-foot self-contained indoor grow, production and distribution facility.
“In eight months, you’re going to see roughly 180,000 square feet of buildings standing where that second dirt pile is,” added Kropman, pointing.
MariCann Inc. is a licenced producer under Health Canada Access to Cannabis for Medical Purposes Regulations (ACMPR), one of 23 in Ontario and 38 nationwide. Created in 2013 by a founder who believes in the therapeutic practicality and effectiveness of cannabis, the company says its expertise includes a track record of creating shareholder wealth combined with experience in the pharmaceutical sector. Although currently a private company, plans are for its listing as a public entity on the Toronto Stock Exchange.
The emergence of cannabis from black market to highly-regulated and quality-assured white market medical product with multi-billion-dollar potential is driving what MariCann CEO Ben Ward (who holds an MBA with a dual concentration in operations and finance from Bradford University School of Management in England) calls only the ‘first big new phase’ on the 97.5-acre property. There are 90 acres of buildable space in total says Ward, cradling the long-term goal of creating the largest operation in the world.
“Right in Norfolk County. Norfolk County offers all the opportunity and infrastructure to allow us to do that.”
MariCann’s roots were planted via a September, 2013 handshake deal with the former owner of a MMAR (earlier Medical Marijuana Access Regulations for smaller ‘cottage industry’ operations where patients grew their own cannabis or had it grown for them) site.
The existing MMAR facility assisted in the transition to contemporary ACMPR licensing on a property with ample access to water, electrical grid and natural gas. Combined with required facilities, Health Canada regulations create a significant financial barrier to entry into the medical marijuana business, Kropman indicating a generally accepted ballpark of $9-million, and MariCann’s own $8-million startup total.
“It’s not throwing seeds in the ground and watching money come in, it’s not easy,” says VP Information Technology and Security Stephen Lem, who has 30 years of experience including working with Fortune 500 companies DuPont, Amgen and Actavis. “It requires a lot of discipline and a lot of planning.”
MariCann began operations with roughly a dozen employees, received its licence to sell in December, 2014 and sold its first product on the 20th of that month. The operation currently employs 60 in a self-contained production, processing and distribution facility which doubled sales in its second year. Expansion was always part of long-term planning and the current phase began November 22, 2016.
“We’re moving to 205,000 square feet in total,” said general contractor Jeff Ayotte, noting the new facility will have a 30,000 square-foot nursery, equal in size to the current total. First production is scheduled for the end of March, 2018.
Employment is anticipated to rise from current levels to between 80 and 100 upon project completion says Kropman. Due to its higher-tech automated nature, a majority of the new hires will be in quality control and supervisory roles.
“It will be more operations.”
It was Ayotte who mentioned the phrase ‘growing green with green’ for a project which includes lowering carbon footprint as a design element. The possibility of installing solar panels on the production facility’s roof has been investigated says Ayotte, along with various options for the site’s operational natural gas well, including gas-fired co-gen electricity production under island (off the grid) or parallel (selling back to the grid) models.
“Energy conservation on this project is huge.”
MariCann’s No. 1 priority is producing top-quality cannabis under practices which not only meet, but exceed the high bar of standards set by Health Canada. But environmentally-responsible operations also lower significant input costs for its controlled-environment (greenhouse) agriculture base, display a leading-edge approach for Health Canada, and offer ‘green’ branding advantages for clients.
“It’s a comfort level with our customers as well,” said Ayotte.
The first expansion project’s size is only part of a story that includes evolving technology in creating consistent production of a consumable food-grade item destined for pharmacy-level processing inside a controlled but fluctuating growing environment. Ayotte touched on some of the more technical aspects of a facility that to sum up succinctly, will not rely as heavily on equipment or practices converted from other uses, but more so feature dedicated state-of-the-art cannabis-producing technology.
“It kind of puts Norfolk County on the map and sets standards for production facilities.”
The process has been assisted says Ayotte, not only by the county’s support, but its natural and human advantages.
“We have a large talent pool to draw from and support us in this expansion.”
The site is currently MariCann’s lone production facility and will remain the company’s key production facility moving forward, says Kropman.
“This is an exciting phase of the industry,” he concluded. “MariCann is looking forward to expanding in Norfolk County and being part of a long-term win-win situation.”
A study conducted at Columbia University’s Mailman School of Public Health found that there were fewer drivers killed in car crashes who tested positive for opioids in states with medical marijuana laws than before the laws went into effect.
The study is one of the first to assess the link between state medical marijuana laws and opioid use at the individual level. Findings are published in the American Journal of Public Health.
Researchers analyzed 1999-2013 Fatality Analysis Reporting System data from 18 U.S. states that tested for alcohol and other drugs in at least 80 percent of drivers who died within one hour of crashing.
They looked at opioid positivity among drivers ages 21 to 40 who crashed their cars in states with an operational medical marijuana law compared with drivers crashing in states before those laws went into effect.
There was an overall reduction in opioid positivity for most states after implementation of an operational medical marijuana law.
“We would expect the adverse consequences of opioid use to decrease over time in states where medical marijuana use is legal, as individuals substitute marijuana for opioids in the treatment of severe or chronic pain,” explained June H. Kim, MPhil, the lead author.
Among the 68,394 deceased drivers, approximately 42 percent were fatally injured in states that had an operational medical marijuana laws, 25 percent died in states before an operational law went into effect, and 33 percent died in states that had never passed a medical marijuana law.
In 1996, California was the first state to pass a voter-initiated medical marijuana law.
Since then, 22 additional states and the District of Columbia have enacted their own medical marijuana laws either by voter initiatives or through state legislation.
“The trend may have been particularly strong among the age group surveyed because minimum age requirements restrict access to medical marijuana to patients age 21 and older, and most medical marijuana patients are younger than 45,” noted Kim.
According to the authors, they would expect to see similar reductions in opioid use among older cohorts if medical marijuana is increasingly embraced by older generations.
“This study is about the possible substitution relationship between marijuana and opioids.
The toxicological testing data for fatally injured drivers lend some suggestive evidence that supports the substitution hypothesis in young adults, but not in older adults,”said Guohua Li, MD, DrPH, the senior author.
“As states with these laws move toward legalizing marijuana more broadly for recreational purposes, future studies are needed to assess the impact these laws may have on opioid use,” noted Kim.