Marijuana and Mental Illness
The link between the use of marijuana and mental health problems is an issue that receives a great deal of media attention. Although severe illnesses such as schizophrenia have received a large deal of this attention, there is also debate about whether the use of marijuana can lead to more common psychiatric disorders such as depression and anxiety. Similarly, the link between marijuana and mental health problems has been used politically in order to substantiate the necessity for the continuance of marijuana prohibition. For instance, the Office of National Drug Control Policy (U.S.), Executive Office Of The President released a report in 2007 that outlined this:
“The research literature has long shown a link between marijuana use and illnesses such as depression, schizophrenia, and suicidal ideation. Beyond comorbidity, however, more recent research makes a stronger case that cannabis smoking itself is a causal agent in psychiatric symptoms, particularly schizophrenia. During the past five years a number of prominent studies have strengthened our understanding of that association and found that the age when marijuana is first smoked and the frequency of use are crucial risk factors in later development of mental health problems.”
The paper cited numerous research papers to support this position. There was, however, one glaring oversight and that was the paper failed to cite numerous papers that contradict their position.
So what’s the deal?
To date, while evidence suggests that early marijuana use may trigger schizophrenia in some vulnerable people, and it may also make relapses more likely in some people with existing schizophrenia, many of the studies about marijuana use seem to be inconclusive for a number of complex reasons.
In perhaps the most authoritative work to date, D Castle and R Murray (Marijuana and Madness, 2004), argue that most of the research linking cannabis to mental illness is old and has methodological flaws. And while it is plausible that excessive cannabis use in of itself can cause a clinical psychosis it would be rare, due to the large amounts needed. The authors further note that cannabis is neither sufficient nor necessary to cause schizophrenia and that it is merely a component, whose strength as a causal factor remains to be seen. I.e. Since some schizophrenics ‘self-medicate’ with cannabis, it can be difficult to determine the lines of causation.
There are several key arguments in medicine suggesting that it is biologically plausible that cannabis is involved in the occurrence of psychotic symptoms. Firstly, high concentrations of cannabinoid receptors (binding sites) in the brain are found in areas of the brain that are thought to be linked to schizophrenia, such as the hippocampus. Secondly, cannabis receptors appear to be important in modulating the activity of dopamine, which is thought to be involved in psychosis. Thirdly, the endogenous cannabinoid system may be abnormal in those living with schizophrenia, such that levels of endocannabinoids, like anandamide, are elevated in those with psychotic disorders, and this may be a response to psychosis. In contrast, a more recent study has found that frequent cannabis use may reduce this anandamide activity, providing a mechanism for the exacerbation of psychotic symptoms by cannabis. Finally, a gene for a cannabinoid receptor in the brain has been found to be associated with a specific type of schizophrenia, although not all studies have found an association, while yet other studies have comprehensively disproven links between cannabis use and schitzophrenia.
Studies that Link Cannabis to Mental Illness
One 16-year study found that individuals who were not depressed and then used cannabis were four times more likely to become depressed at follow-up. (Bovasso, 2001)
Another study investigated changes over a 14-year period and found that cannabis use was a predicator in later major depressive disorders. (Brook, 2002)
A study over a 21-year period found that cannabis use was associated with depression, suicidal thoughts and suicide attempts. (Fergusson, 2002)
A 15-year study conducted in Sweden argued the link between schizophrenia and heavy cannabis use. This was then reanalyzed and replicated in further studies (Andreasson, 1987 and Zammit, 2002)
A 21-year longitudinal study showed that cannabis use was associated to psychotic symptoms and suggested a causal relationship. (Fergusson, 2003)
A review of five studies found that using cannabis is one of several components that contribute to the onset of schizophrenia. (Smit, 2004)
Some studies have shown that cannabinoid receptors in the brain are related to the pathology of schizophrenia (Dean, 2001)
A study from New Zealand, conducted over a 30-year period with 259 test subjects, demonstrated that participants who smoked cannabis at a young age were 6 times more likely to suffer schizophrenia in later life, confirming/substantiating earlier Swedish assertations. (Ferguson, 2005)
A synopsis of the New Zealand study had this to say:
“Using cannabis in adolescence increases the likelihood of experiencing symptoms of schizophrenia in adulthood. Our findings agree with those of the Swedish study1 and add three new pieces of evidence. Firstly, cannabis use is associated with an increased risk of experiencing schizophrenia symptoms, even after psychotic symptoms preceding the onset of cannabis use are controlled for, indicating that cannabis use is not secondary to a pre-existing psychosis. Secondly, early cannabis use (by age 15) confers greater risk for schizophrenia outcomes than later cannabis use (by age 18). The youngest cannabis users may be most at risk because their cannabis use becomes longstanding.5 Thirdly, risk was specific to cannabis use, as opposed to use of other drugs, and early cannabis use did not predict later depression. Our findings now require replication in large population studies with detailed measures of cannabis use and schizophrenia.
Although most young people use cannabis in adolescence without harm, a vulnerable minority experience harmful outcomes. A tenth of the cannabis users by age 15 in our sample (3/29) developed a schizophreniform disorder by age 26 compared with 3% of the remaining cohort (22/730). Our findings suggest that cannabis use among psychologically vulnerable adolescents should be strongly discouraged by parents, teachers, and health practitioners. Policy makers and law makers should concentrate on delaying onset of cannabis use.”
The Christchurch Press reported on March 22, 2005, that “The lead researcher in the Christchurch study, Professor David Fergusson, said the role of cannabis in psychosis was not sufficient on its own to guide legislation. ‘The result suggests heavy use can result in adverse side-effects,’ he said. ‘That can occur with ( heavy use of ) any substance. It can occur with milk.’ Fergusson’s research, released this month, concluded that heavy cannabis smokers were 1.5 times more likely to suffer symptoms of psychosis than non-users. The study was the latest in several reports based on a cohort of about 1000 people born in Christchurch over a four-month period in 1977. An effective way to deal with cannabis use would be to incrementally reduce penalties and carefully evaluate its impact, Fergusson said. ‘Reduce the penalty, like a parking fine. You could then monitor (the impact) after five or six years. If it did not change, you might want to take another step.’ Source: Bleakley, Louise, “NZ Study Used in UK Drug Review,” The Press (Christchurch, New Zealand: March 22, 2005.
However, a 2009 study in the UK has cast doubt on the supposed link between cannabis use and schizophrenia.
This study led by Dr Martin Fisher of Keele University, examined the records of 600,000 patients aged between 16 and 44, but failed to find a similar link. The authors noting, “An important limitation of many studies is that they have failed to distinguish the direction of association between cannabis use and psychosis.”
They point out that “although using cannabis is associated with a greater risk of developing psychosis, there is also evidence of increased cannabis use following psychosis onset.”
Frisher and colleagues compared the trends of cannabis use with general practitioner records of schizophrenia and psychosis. They argue if cannabis use does cause schizophrenia, then an increase in cannabis should be followed by an increase in the incidence of schizophrenia. According to the study, cannabis use in the UK between 1972 and 2002 has increased four-fold in the general population, and 18 fold among under 18s.
Based on the literature supporting the link, the authors argue that this should be followed by an increase in schizophrenia incidence of 29 per cent between 1990 and 2010. But the researchers found no increase in the rates of schizophrenia and psychosis diagnosis during that period. In fact, some of the data suggested the incidence of these conditions had decreased.
A recently published study found that genetic predisposition moderated the effect of cannabis on psychosis. The gene of interest in this study coded for catechol-O-methyltransferase (COMT). The COMT gene product is involved in the metabolism of dopamine (the neurotransmitter thought to be involved in psychotic symptoms), and has been implicated in studies of the genetic basis of schizophrenia.
However, a 2009 study, the largest study of its kind so far, showed that recreational cannabis users do not release significant amounts of dopamine from an oral THC dose equivalent to a standard cannabis cigarette. This result challenges current models of dopamine release as the mechanism mediating cannabis as risk factor for schizophrenia.
The hypothesis behind the study was cannabis use in early adolescence may be a risk factor for development of schizophrenia. In animals, Delta9-tetrahydrocannabinol (THC) increases the rate of dopamine neuronal firing and release in the striatum. Thus cannabis use may increase dopamine release in the human striatum leading to vulnerability to psychosis. The findings, however, disproved this theory. 1
Understanding Cannaboids and Psychosis
THC and CBD
In simple terms THC and CBD are the two most important cannaboids where psychological and other cause and effect are concerned. That is, while cannabis contains various cannabinoids, THC and CBD have almost opposing actions: Δ9-tetrahydrocannabinol (Δ9-THC) is psychotomimetic (capable of producing symptoms similar to those of a psychosis), whereas cannabidiol (CBD) has antipsychotic effects.
Thus, as more is understood about cannaboids, we are beginning to understand that CBD plays a much more important role in the overall cannabis experience than was originally thought.
In research conducted by Sagnik Bhattacharyya et al (2010) it was shown that oral administration of Δ-9-THC was associated with the acute induction of both psychotic symptoms and anxiety, whereas following CBD there was no change in psychotic symptoms, and a trend for a reduction in subjective anxiety.
Similarly, in a study undertaken by Zerrin Atakan and Professor Philip McGuire they conclude:
“These studies show that THC and CBD have distinct effects on brain function in humans, and these may underlie their correspondingly different effects on cognition and psychiatric symptoms. Determining how the constituents of cannabis act on the brain is fundamental to understanding the role of cannabis use in the aetiology of psychiatric disorders.”
While Paolo Fusar-Poli et al (2010) demonstrated that from a neurological level CBD but not Δ9-THC disrupts forward connectivity between the prefrontal-subcortical effective connectivity. In this study, dynamic causal modelling and Bayesian model selection (probabilistic relationships between diseases and symptoms) were used to explore the effects of pure compounds of C. sativa [600 mg of cannabidiol (CBD) and 10 mg Δ9-tetrahydrocannabinol (Δ9-THC)] on prefrontal-subcortical effective connectivity in 15 healthy subjects who underwent a double-blind randomized, placebo-controlled fMRI paradigm while viewing faces which elicited different levels of anxiety. In the placebo condition, BMS identified a model with driving inputs entering via the anterior cingulate and forward intrinsic connectivity between the amygdala and the anterior cingulate. CBD but not Δ9-THC disrupted forward connectivity between these regions during the neural response to fearful faces. This was the first study to show that the disruption of prefrontal-subocrtical connectivity by CBD may represent neurophysiological correlates of its anxiolytic (preventing or reducing anxiety) properties. This was the first study to show that the disruption of prefrontal-subocrtical connectivity by CBD may represent neurophysiological correlates of its anxiolytic (preventing or reducing anxiety) properties.
Additionally research conducted by Morgan CJ et al (2010) the authors found that cannabis which is high in CBD does not cause the memory impairment which has commonly been asserted as a detrimental side effect of smoking cannabis.
Framing this in simple terms, the interesting thing is CBD is it almost the polar opposite of THC in its effects. If THC is linked to psychotic type episodes, CBD has anti psychotic properties. If THC is thought to cause panic attacks, CBD calms those impulses, if THC is linked to memory loss CBD isn’t.
Traditionally, potency has been framed in terms of either delta-9 THC content or total THC content, without regard to other psychoactive cannabinoids. The practicality of this is that talking of cannabis, simply in terms of “potency” is meaningless. We need a totally different and far more sophisticated way to monitor and describe it. The measure of “potency” via analysis of Δ9-THC as used by governments is flawed, which is no surprise really as it came from the law enforcement.
1. Stokes PR. Mehta MA. Curran HV. Breen G. Grasby PM (2009) Can recreational doses of THC produce significant dopamine release in the human striatum?
There are 3 main species of Cannabis plants. These are sativa, indica and ruderalis. Indica and sativa are the two main varieties used by cannabis cultivators. There are many strains that are crosses of these two varieties. Within each of these varieties and crosses there are a huge number of individual strains, each with a different cannabinoid profile and effect.
Pure sativa have a high THC to CBD ratio. Sativas are tall thin plants, with much narrower leaves than indicas. They grow very quickly and can reach heights of 20 feet in a single season. Sativas have less chlorophyll then Indicas and more accessory pigments (accessory pigments protect the plant from excessive sunlight). As sativa strains have less chlorophyll than Indica they take longer to grow, mature, and require more light. Once flowering has initiated, they can take anywhere from 12 to 16 weeks to fully mature. Yield is usually lower than indica, but is very potent. As, sativas grow taller and have a longer flowering period they are better suited for outdoors. Some of the more legendary potent sativas include Panama Red, Punta Roja, Santa Marta Gold, Columbian Gold, Acapulco Gold, Thai, and Burmese.
A Cannabis indica plant may have a CBD/THC ratio four to five times that of Cannabis sativa plant. The relatively large amount of CBD contained in Cannabis indica, means, compared to a sativa, the effects are modulated significantly. Indicas are short dense plants, with broad leaves, they mature early, have more chlorophyll and less accessory pigments (accessory pigments protect the plant from excessive sunlight). As indica strains have more chlorophyll than sativa they grow and mature faster and require less light. After flowering starts they will be mature in 6 to 8 weeks. The buds are thick and dense. Indica yield is typically higher than sativa, with a shorter growing season. Therefore, Indica varieties are more suited to indoor growing, because they don’t get as tall, finish earlier, yield more, and produce dense heavy buds which are visually more appealing. Legendary indica strains include Afghani and Hindu Kush.
The scientific community still hasn’t reached a consensus on the question of whether indica and sativa represent two distinct species (under the shared genus cannabis) or whether they represent subsets of the same species. This said, regardless of whether two different species evolved from the same genus or whether one species split along geographic lines, by the time mankind came around to getting high, the plant had divided into two easily distinguishable lines, with sativas growing wild in almost all equatorial regions of the globe (Mexico, Thailand, Colombia, Jamaica, etc) and indicas thriving in southern Asia and the Indian subcontinent (Afghanistan, Pakistan, India, Tibet, Nepal, etc.). In each case, the plants were eventually discovered, recognized, cultivated and bred for specific uses—sativas for straight smoking and indicas for making hashish and kif. These practices continued for thousands of years, without the two lines ever crossing paths, until the US led War on Drugs brought them together for the first time.
As the UNODC note in the 2006 World Drug Report:
“Experiments crossing sativa and indica strains led to the development of “skunk”, a hybrid said to be 75 per cent sativa and 25 per cent indica, which was among the first to capture the THC high of the sativas with the rapid growth cycle and yield of the indicas….
In just the last decade, sinsemilla cannabis has doubled in potency in a number of key markets, and a range of recent studies have highlighted the negative impact the drug has on mental health in particular.”
“The application of greenhouse technology
In addition to improved breeding and the rediscovery of sinsemilla, the movement towards indoor cultivation has also allowed the application of greenhouse technology to what had traditionally been a field crop.
Around 1985, some cannabis breeders from the United States fled for a country with more amenable drug policies – the Netherlands. At the time, indoor cultivation of cannabis was just starting to take off in the Netherlands, and the fusion of American breeding stock and Dutch agricultural practice sparked a revolution in cannabis breeding and production. Today, Dutch ‘seed banks’ sell the product of this breeding over the Internet, in competition with a growing number of rivals, notably those based in Canada.
One of these U.S. breeders was David Selezny, now traveling as David Watson, AKA “Sam the Skunkman”. Another important US entity that joined Watson/Selezny, at least in part, was Robert Connell Clarke – a renowned cannabis botany researcher and author.
Here’s where things get interesting!
According to Joe Pietri, author of King of Nepal The Ice Wars edition, Watson/Selezny had been busted for growing in Santa Cruz California in March of 1985 and resurfaced in Amsterdam. In his baggage was the research from the Sacred Seed Collective, a seed bank originally started in the 1940’s, and 250,000 cannabis seeds. Ed Rosenthal, who was the cultivation editor for High Times at that time, introduced Sam Selezny as David Watson to everyone who was anyone at the time on the Dutch scene. Shortly thereafter Watson/Selezny started Cultivators Choice, one of Amsterdam’s early seedbanks. Surviving members of the Sacred Seed Collective still question how Watson managed to pull this off? Pietri puts it more directly, “Was Watson/Selezny working undercover to bring Sacred Seed collective down?”
Either way, after Watson’s arrival in Amsterdam strange things began occurring – not the least of which was Neiderweit went from crap to chronic with the introduction of the Sacred Seed Collective’s genetics. THC levels vastly increased within a short timeframe after Watson/Selezny introduced Skunk #1 – a 75% sativa (Acapulco Gold + Columbian Gold) + 25% indica (Afghani) hybrid with the potency of sativa and the growing vigor and early finishing times of an indica.
So profound was Skunk #1’s effect on the market that today “Skunk” has become a generic term in the UK and Europe for describing super potent pot. Breeders today regard Skunk #1 as the benchmark of reliable performance and as a rock-solid genotype that has influenced a hundred modern hybrids. Growth and flowering are mostly-Indica in appearance (dark green, short and squat with dense heavy flower clusters), with Skunk #1 gaining a little more height than a pure Indica when blooming.
Keep in mind that these were also the years in which the indoor growing culture was on the rise. A super potent, mostly sativa strain with a high THC to low CBD ratio, which was perfect for indoor growing shouldn’t be underestimated. The perfect strain for indoor growing was now widely available to growers around the globe. Skunk was about to go meteoric! And frankly, its legacy would become insane (pardon the pun!).
The next interesting thing that occurred was Watson’s/Selezny’s influence in creating the Cannabis Cup.
In an article written by High Times editor Steven Hager in 2004, he recounts:
“I first visited the Netherlands in 1987 to write an article on the founder of Holland’s first cannabis seed company. Titled “The King of Cannabis,” the article described how an Australian named Nevil (Schoenmaker) established a mail order company in Holland. He lived in a mansion filled with grow rooms that I dubbed “Cannabis Castle.” While working on the article, I met the founders of Cultivators Choice, an almost defunct American cannabis-seed company. They told me about the spectacular California harvest festivals of the ‘70s. That’s where I got the idea of holding a cannabis harvest festival in Amsterdam.”
According to Pietri what actually happened was Hager had been appointed as editor of High Times in 1987. In the same year Hager went to Amsterdam to interview Neville Shoenmaker of the Seed Bank. While there he meets Watson/Selezny who relates stories to him about harvest festivals in Santa Cruz and suggests having a Cannabis Cup in Amsterdam as a yearly event. As Watson/Selezny expands on the concept Hager is taken in.” From this point on everything stated by either Watson/Selezny or his partner Robert Connell Clarke is taken as fact, Remember Rosenthal is cultivation editor, and Clarke used to write under R. Connoisseur at High Times as well.” Hager being wet behind the ears was enthralled.
Coincidently, Operation Green Merchant was conceived of in the same year. This allowed the DEA to infiltrate the ascending cannabis scene – both locally and abroad. Obviously, one of their key targets outside of the U.S. was Holland due to its liberal cannabis laws and its source as a port of origin for illegal shipments of seeds across U.S. boarders.
In 1988 the first Cannabis Cup was held and surprise, surprise, Watson/ Selezny takes first prize for Skunk #1. In the following year Neville Schoenmaker’s Early Pearl/Skunk #1 x Northern Lights #5/Haze from Seed Bank took first prize and the year after that Schoenmaker’s Northern Lights #5 took first prize.
The impact of the breeding, marketing and distribution efforts of Neville Schoenmaker on the cannabis world cannot be stressed enough; he wasn’t labeled the original ‘King of Cannabis’ without justification. During the 1980’s, Neville Shoenmaker, a dual Australian and Dutch citizen, allegedly traveled to the Netherlands to obtain treatment for a drug addiction, because at the time, the Dutch were renowned for their addiction treatment facilities. While there, he slowly started the first Dutch marijuana mail order seed bank, and over the course of time became very successful, ultimately becoming a legend in the marijuana breeding community for his efforts to introduce, market, breed and distribute some of the most high profile varieties of cannabis of our time. His home, dubbed the ‘Cannabis Castle’ was a breeder’s laboratory where Neville worked on lines of cannabis for years while filling mail order requests from cultivators all over the world.
Enter Green Merchant -the DEA’s ill-fated, albeit, comprehensive attempt to destroy pot magazines and hydroponics and indoor marijuana growing industries.
Hager later writes of Schoenmaker, “Unfortunately, a few weeks later the DEA launched an operation designed to shut down the Seed Bank and High Times.”
Peter Gorman, a former High Times journalist writes, “the main targets of ‘Operation Green Merchant’ according to his Justice Department sources were Neville of ‘The Seed Bank’, High Times magazine and Sensimilla Tips, a now defunct cannabis culture magazine due to ‘Operation Green Merchant.’
Steven Hager later wrote of Schoenmaker that, “The Dutch government refused to extradite Neville, who was forced into hiding to prevent a DEA kidnapping” and that he was “eventually nabbed while visiting his family in Australia…”
Schoenmaker, was arrested in Australia in July of 1990, several weeks after winning his second cannabis cup. Extradition proceedings were launched to transport Schoenmaker to Federal court in New Orleans, where he would face charges of violating the Controlled Substances Act. The 44-count indictment alleged that Schoenmaker, “in concert with at least five other persons,” knowingly distributed, through the US Postal Service, a total of 1,921 seeds to DEA agents and marijuana growers in the New Orleans area from 1985 to 1990. The indictment also alleged that Schoenmaker “did knowingly…manufacture (grow) more than 1,000 marijuana plants, a Schedule 1 drug controlled substance.”
Shoenmaker’s lawyer noted on his court records that the police had dossier on Schoenmaker as well as everyone who was anyone on the Dutch scene, and that they were compiled by an undercover operative working in the Dutch scene. That undercover, according to Joe Pietri, was David Watson/Sam Selezny.
Bummer for the US Feds, the Australians dropped the ball and Shoenmaker was never extradited from Australia to the U.S. He held both a Dutch and Australian passport and after making bail fled Australia on his Dutch passport, leaving authorities red-faced and angry. Shoenmaker than went into hiding, albeit allegedly operating behind the scenes as a partner and breeder for Sensi Seeds, a company responsible for many famous genetics and winner of numerous cannabis cup awards. He later publically surfaced in the early 21st century and now works with ShantiBaba (a fellow Australian compatriot who appeared on the Dutch scene in the early nineties) and Howard Marks – the legendary drug runner – at Mr Nice Seeds.
The next interesting thing then happens. Watson/Selezny creates HortaPharm B.V with Robert C Clarke in 1994 and in 1997 they are issued a cannabis research license ahead of legitimate Universities and PhD’s due to the strong endorsement by the DEA, instead of extraditing him back to Santa Cruz for a grow bust in 1985? To this day HortaPharm B.V is one of two companies allowed to import cannabis product into the US, and the only supplier licensed by the DEA to supply seeds of predictable quality for research.
I mean, it’s all starting to sound somewhat like a conspiracy theory right? Could this be? The DEA starting a seed company in Amsterdam, placing a deep undercover into the Dutch scene, creating a cannabis cup which would bring all the leading cannabis cultivators and breeders from around the world straight to them on a yearly basis. Take this one step further. Were the DEA directly responsible for changing the THC/CBD profile of cannabis on a global scale? Did law enforcement inadvertently increase the potency of marijuana or were they far more directly involved? Fact or fiction? Hypothesis or reason? Let’s look at the facts…
Oleh Janet Elizabeth Joy et al note in the book Marijuana and Medicine: Assessing the Science Base (page 214):
“Under DEA regulations, marijuana can be imported, provided that the researcher is registered with the DEA, has approval for marijuana research (21 CFR 1312.11, .12, and .13), and has a DEA-approved permit for importation (21 CFR 1312.11, .12, and .13) and that the exporter in the foreign country has appropriate authorization by the country of exportation. Importation would enable U.S. researchers to conduct research from grown by Hortapharm. However, no U.S. researcher has imported Hortapharm’s marijuana because Dutch authorities have refused to issue an export permit, despite the insurance of an import permit by the DEA (D.Pate, Hortapharm, personal communication, 1998).”
While, M. David Marks et al (2009) note:
“Seeds from the marijuana cultivar Skunk no. 1 were provided by HortaPharm BV (Amsterdam, The Netherlands) and imported under a US Drug Enforcement Administration (DEA) permit to a registered controlled substance research facility. “
Let’s face it, how did Watson/Selezny get DEA approval and endorsement when he should have been on the DEA’s most wanted list? One could argue, for instance, that his crimes committed in the U.S. in 1985 had outrun the statute of limitations. However, there are special circumstances where the statute of limitations will be extended by the court after petition by the US Attorney. One of these being that the offense took place in a foreign country, or evidence is located in foreign territory. Given Watson/Selezny was selling/posting seeds into the U.S. illegally for many years before receiving “official” DEA “endorsement” how was it that so many others in his trade were targeted and/or arrested while he seemed immune to prosecution? Other than this, the statute of limitations does not apply to those who flee to avoid prosecution and regardless of the offense/s, a person who is a fugitive from justice is not protected by any statute of limitations for that offense. Odd?!
Back to HortaPharm B.V.
Details have been disclosed of the collaboration between GW Pharmaceuticals – the British Company licensed by the Home Office to conduct research into the medicinal uses of cannabis – and Dutch medicinal cannabis plant breeding company HortaPharm B.V. Since 2001, the HortaPharm programme has continued at GW Pharmaceuticals in the UK.
Speaking at the International Cannabinoid Research Society (ICRS) conference in Montpellier, Dr Geoffrey W Guy, Chairman of GW Pharmaceuticals, said that HortaPharm will provide GW with exclusive access to its entire range of cannabis varieties for the development of medicines. The worldwide rights acquired by GW for an undisclosed sum cover varieties grown to date with certain exceptions and all varieties to be bred in future. Plant registrations arising from the Dutch breeding programme will be owned by GW. Under the agreement GW will be responsible for the development of specific drug delivery technologies to administer the pharmaceutical grade medicinal cannabis. This work will include a vaporiser for which HortaPharm has a patent pending. In addition GW will fund HortaPharm’s botanical research and HortaPharm scientists will assist in the UK Glasshouse propagation, cloning and cultivation programme.
An article published in the Independent on Sunday 27 September 1998 by Vannessa Thorpe reads:
“It looks like dope, but really it’s hope,” explains the proprietor, American entrepreneur David Watson. What he means is that many of these plants have been specifically bred not to produce an intoxicating resin or hashish. Indeed, HortaPharm hopes to thwart the aims of the average recreational user.
The team are already close to finding their own commercial Holy Grail – seeds that will produce a one-off, female, seedless crop of plants with no psychotropic effects (or THC highs, to the layman) for the consumer. Why, you might ask, would they want to do that?
The answer is that Mr Watson and his Amsterdam-based scientists are working to create a stable, plant-based medical product. They want to isolate the beneficial effects of cannabis’ various properties and then reproduce them, ad infinitum, from specialised parent plants.
HortaPharm is only interested in developing female plants that are sterile, but this is not just to protect their genetic copyright. “If a plant is not kept busy producing seeds, all its energy can go into resin production,” says Mr de Miejer.”
Hmmm? Sounds strangely like GMO seeds! It’s not a leap and a bound to consider that once Watson/DEA has this technology it could just as easily be applied to male plants, pollen spread world wide and viola – a monopoly and sterile seeds. Let’s face it, stranger things have happened (Paraquat anyone?).