Sorting Out The Medical Cannabis Mess

6th July 2017: Community pharmacist and academic Neil Johnson discusses some ideas

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By design, or by accident, the legal introduction of medical cannabis to the Australian market ought to have been a very simple and straightforward process had any of the legislators undertaken their own investigations or excused themselves from any conflict of interest issues, arising through the legalisation of this substance.

Confusion has proliferated with each attempt to make medical cannabis more accessible to patients who could benefit, but it is currently more out of reach than it has ever been.

The starting point in reversing the mess needs to be in basic education and the correct naming of the bioactive substances found in the various strains of cannabis, in varying concentrations.

The cannabis plant contains dozens of active compounds called cannabinoids, which are found within the flower, leaf, and stem.

Researchers have identified over 80 unique cannabinoids within the plant, plus a range of other useful phytochemicals that act as anti-oxidants or enhance the therapeutic effect of the various cannabinoids.

What follows is a very brief description of nine of the most common cannabinoids and their abbreviated titles:

Tetrahydrocannabinolic Acid (THCA)

THCA is the main constituent in raw cannabis. THCA converts to Δ9-THC when burned, vaporized, or heated at a certain temperature.  THCA, CBDA, CBGA, and other acidic cannabinoids hold the most COX-1 and COX-2 inhibition, contributing to cannabis’ anti-inflammatory effects. This cannabinoid also acts as an antiproliferative and antispasmodic.

Tetrahydrocannabinol (THC)

The most abundant cannabinoid present in marijuana, THC is responsible for cannabis’ most well-known psychoactive effects. THC acts as a partial agonist at the CB1 and CB2 receptors. The compound is a mild analgesic, or painkiller, and cellular research has shown that it has antioxidant activity.

Cannabidiolic Acid (CBDA)

CBDA, similar to THCA, is the main constituent in cannabis with elevated CBD levels.  CBDA selectively inhibits the COX-2 enzyme, contributing to cannabis’ anti-inflammatory effects.

Cannabidiol (CBD)

CBD has tremendous medical potential. This is particularly true when the correct ratio of CBD to THC is applied to treat a particular condition. CBD acts as an antagonist at both the CB1 and CB2 receptors, yet it has a low binding affinity for both. This suggests that CBD’s mechanism of action is mediated by other receptors in the brain and body.

Cannabinol (CBN)

CBN is a mildly psychoactive cannabinoid that is produced from the degradation of THC. There is usually very little to no CBN in a fresh plant. CBN acts as a weak agonist at both the CB1 and CB2 receptors, with greater affinity for CB2 receptors than CB1. The degradation of THC into CBN is often described as creating a sedative effect, known as a “couch lock.”

Cannabigerol (CBG)

A non-psychoactive cannabinoid, CBG’s antibacterial effects can alter the overall effects of cannabis. CBG is known to kill or slow bacterial growth, reduce inflammation, (particularly in its acidic CBGA form,) inhibit cell growth in tumor/cancer cells, and promote bone growth. It acts as a low-affinity antagonist at the CB1 receptor. CBG pharmacological activity at the CB2 receptor is currently unknown.

Cannabichromene (CBC)

CBC is most frequently found in tropical cannabis varieties. CBC is known to relieve pain, reduce inflammation, inhibit cell growth in tumor/cancer cells, and promote bone growth. The effects of CBC appear to be mediated through non-cannabinoid receptor interactions.

Tetrahydrocannabivarin (THCV)

THCV is a minor cannabinoid found in only some strains of cannabis. The only structural difference between THCV and THC is the presence of a propyl (3 carbon) group, rather than a pentyl (5 carbon) group, on the molecule. Though this variation may seem subtle, it causes THCV to produce very different effects than THC. These effects include a reduction in panic attacks, suppression of appetite, and the promotion of bone growth. THCV acts as an antagonist at the CB1 receptor and a partial agonist at the CB2 receptor.

Cannabidivarin (CBDV)

Like THCV, CBDV differs from CBD only by the substitution of a pentyl (5 carbon) for a propyl (3 carbon) sidechain. Although research on CBDV is still in its initial stages, recent studies have shown promise for its use in the management of epilepsy. This is due to its action at TRPV1 receptors and modulation of gene expression.

Cannabinoids, like CBD, are fat-soluble compounds. It’s why their effects are prolonged, and taper off slowly. Your body stores cannabinoids in fat, and gradually releases them at sub-therapeutic levels. This is also why many cannabis users can fail drug tests days or weeks after ingesting cannabis. The tests do not measure concentrations in blood, only presence. Thus, they could be legally challenged. Women can be more sensitive to cannabinoids than men, as women have a greater proportion of body fat than men.

As you can see there is already a system for identifying the cannabinoid components of medical marijuana by generic name and each has a generic abbreviation derived from the generic name. By identifying what components you are talking about avoids the process that enables one commentator to label the entire collective components with a negative comment that might only pertain to a single cannabinoid.

There are three facts that ought to be known by regulators that do not seem to be talked about:

1. Cannabinoids are of low toxicity and no death has ever been recorded.
There is no known fatal overdose level for cannabis found among the decades of research on the topic, and no known deaths associated with cannabis use.

Here is the exact wording from US Patent #6,630,507 held by The US Department of Health and Human Services:

No signs of toxicity or serious side effects have been observed following chronic administration of cannabidiol to healthy volunteers (Cunha et al., Pharmacology 21:175-185, 1980), even in large acute doses of 700 mg/day (Consroe et al., Pharmacol. Biochem. Behav. 40:701-708, 1991).’

2. Cold extractions from the cannabis plant have no psychoactive effects whatsoever. It is only when heat is introduced (through smoking or extraction involving heat) that the naturally occurring THCa converts to psychoactive THC.

3. While the potential exists for cannabinoids to interact with some prescription drugs, the incidence and intensity is on the lower end of the scale.

Medical cannabis is currently scheduled as a narcotic in the Australian Poisons Drug Schedules as a Schedule 8 substance for medical use. It remains illegal for recreational use.

And this brings me to the issue surrounding the confused access to medical cannabis that involves the registration of medical prescribers. Currently, the AMA have been recommending that doctors not become involved with the prescribing of medical cannabis. Only a handful of doctors have become registered to prescribe and they are mostly concentrated in NSW and treating epilepsy in children.

Medical cannabis should never have been regulated under Schedule 8 because of its low toxicity and side effect profiles. Indeed there are a number of synthetic drugs that are sold over the counter (even in supermarkets) that have a more toxic profile and interactivity with other drugs than can be demonstrated with medical cannabis.

A more sensible regulation would have been to have all cannabinoids listed as Schedule 3 of the Poison’s Act (supervised sale by a pharmacist), including THC in concentrations under 5 percent. Higher THC concentrations to be relegated to Schedule 4 (doctor’s prescription) without any further registration or restriction.

This sensible infrastructure already exists. The regulators, through ignorance or other pressures, have ‘stuffed up’ what could have been a very orderly process.

Pharmacists, by the very calling, are experts in pharmacology and have the mechanism to oversee a patient’s profile to ensure compatibility with their other prescribed drugs when medical cannabis is used. Recording, using software designed for the sale of codeine products, is already developed to link pharmacist supply from any location. This process enables a strong supervision and quick identification of any abuses. It can also link into clinical trials and research programs.

More importantly, pharmacists are capable of improving health literacy levels for patients that could eventually see medical cannabis becoming a component of ‘self care’ that enables patients to take responsibility for their own care and in the process, reduces the national cost of all health care.

And this brings me to my final point in this deliberately confused issue and that is the point that medical cannabis has the potential to assist in the treatment (even cure) of many disease states that have given concern to government as they endeavour to provide quality subsidised care funding through the Pharmaceutical Benefits Scheme (PBS).

Medical cannabis could cut costs, in a major way because our bodies have an already existing endocannabinoid system that actually manufactures its own cannabinoids as part of the body’s repair and homeostatic systems. By supplementing cannabinoids, major illnesses have been discovered to be better managed – and the evidence is beginning to flow, in support of the many people who have experimented anecdotally and found benefit.

The potential for taxpayer-benefit cost reductions in PBS prescription requirements requiring less doctor visits would not have escaped the major drug companies. Herein lies a single major reason for the muddied confusion in trying to make medical cannabis out of reach for patients as well as burdening it with as much regulation as possible to make it uneconomical.

The drug company lobby is the largest political lobby in Australia and other western economies, and their political donations along with various doctor payments are unfortunately doing their job very effectively. Even to the extent that the limited formal access that patients (150 of them) only involves imported synthetic cannabinoids or extracts from genetically modified plants, both proven to be inferior to the locally produced (but illegal) versions, mostly provided cheaply or even compassionately (free).

Would it not have made better sense to provisionally licence all these illegal growers/manufacturers and encourage them (even through grants) to create a viable, legal and valuable Australian market, create extra local jobs, but above all have market control in Australian hands?

The politicians driving the market towards global growers and manufacturers are selling out their country, and their patient constituents, with personal acceptance of their “thirty pieces of silver”.
This practice has become too much embedded in all areas of Australian politics (the recent news of Chinese government lobbyists infecting the political landscape is just another extension of the problems discussed above), and it will eventually lead to social disruption and violence unless the “good guys” stand up and be counted to eventually root it out.

Neil first qualified at Sydney University and obtained post graduate qualifications in Management consultancy and clinical nutrition.

He was the first management consultant to specialise in the profession of pharmacy, commencing practice in 1972 and accredited to international level in 1992. He has owned (in partnership or as a sole trader) six community pharmacies over his career and from 1995 – 2005 worked in Lismore Base Hospital initially as a clinical pharmacist and eventually as chief pharmacist.

In later life Neil became the academic pharmacist for the Northern Rivers University Department of Rural Health for a period of three years and from 2000 to the present founded and runs the online e-zine ‘Information to Pharmacists’ directed at a pharmacy leadership audience.

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