Cannabis la pharmacopeia (Part 1)

Cannabis, something for everyone

There are some things in this world which, when you learn about them, you learn about much more than you bargained for. Some ‘things’ connect to so many subjects from different magisteria that anyone can find something that interests them. Cannabis might be the prime example of that. It was for me, serendipitously turning me (back?) into a scientist at the ripe old age of 20.

Plainly stated, there is no aspect of this plant that is not interesting. Historically, it was used as fenders for the first car (Ford model T).

Ship ropes were made from it and drafts of the American Constitution were written on its paper. Spiritually, Rastafarians and countless religions have adopted it for its psychotropic effects thought to connect them with deities. Artistically, it’s been the muse of many a painter, poet, author and sculptor, like the French poet Charles Baudelaire’s ode to ‘hashish’ (cannabis oil) called “The poem of hashish” [x].

Legally, it was the pillar upon which the abysmal War on Drugs was rationalized and saying that this changed the course of human history might be an understatement. Its only aspect that’s not particularly interesting might be its nutritional profile. As a food, its seeds are not something humans need or will find much benefit from, but as far as plant seeds go it has a respectable amino acid profile [1, 2].

And medicinally? This is what I want to focus on in this series on cannabis, or marijuana, terms which I’ll use interchangeably. In this part 1 I will first explain the chemical reaction happening outside of your body enabling the psychotropic effects happening to you when taking in. Then I will address one of the many persistent myths about cannabis, that smoking it is as bad for your lungs as is smoking cigarettes – if not worse!

What’s a pharmacopeia?

A pharmacopeia is “a book, especially an official publication, containing a list of medicinal drugs with their effects and directions for their use”. I learned what it was because I frequently found scientists and clinicians referring to cannabis to a pharmacopeia, unto itself. This is to emphasize its very large number of actual and potential medical uses. The first references to cannabis were found in China around 12,000 years ago (10,000 BC).

1839 was the first time a ‘modern’ reference to its medicinal properties was recorded and it was done by an Irishman called Sir William O’Shaughnessy, a “physician famous for his wide-ranging scientific work in pharmacology, chemistry, and inventions related to telegraphy and its use in India” [3].

As you can see from the above picture, the medical record was about an infant suffering terrible convulsions. After only 20 days being given ‘heroic doses’ of cannabis tinctures, that is cannabis oil dissolved in a little alcohol, was she able to enjoy “robust health” and “her natural plump and happy appearance”. Convulsions are common symptoms of some types of epilepsy and today cannabis drugs are being developed by some Big Pharma players. You can learn more about this in this video lecture I attended in London with Andrew Scarborough

If you’re skeptical that this plant can be a medicine and an extremely safe and efficacious one at that, please take a quick look at how quickly this severely sick child stops convulsing after being given drops of cannabis extract (CBD specifically).


THCa and THC?

Cannabis has male and female plants that are pollinated by the wind rather than relying heavily on bees for example. The female cannabis plant makes flowers, affectionately known as buds. It distinguishes itself amongst plants for its approximately 483 compounds, a litany of molecules capable of interacting with our biology and that of many other life forms.

The most abundant molecules in cannabis are cannabinoids and 63 have been identified so far, of which THCa (delta 9-tetrahydrocannabinolic acid) is the most abundant making up 17.3% of a bud’s weight. THCa sounds a lot like THC, the (in)famous compound in cannabis that gets people high, but THCa isn’t psychoactive. So where’s the THC?


If you cut a bud of cannabis off its branch and let it dry for a few weeks in a dark and dry space with a little air circulating, THCa slowly turns to THC via the process of decarboxylation.

This conversion happens way faster as the temperature increases, such as when using a lighter to combust (‘burn’) the bud and inhaling its smoke. In doing so your lungs quickly diffuse molecules (like THC) into your bloodstream thanks to the design of the lung and its large surface which allows it to capture many molecules.

Once circulating in blood, THC gets distributed to organs with receptors it can stick to, such as cannabinoid 1 receptor (CB1). This receptor is particularly abundant in your brain and is basically where THC must end up to get you high.

That high may only take 20 seconds to a minute to come on. A ‘quick high’ is mistakenly thought to always be a poor way of administering drugs but this method provides quick subjective feedback allowing you to more accurately titrate (dispense) a dose of cannabis you’re comfortable with.

Other methods of delivery, for example cannabis edibles (aka space cakes) are much slower to give this feedback. First time users are thus cautioned to avoid edibles for fear of ‘overdosing’ and will be better off with a joint or vaporizer.

The obvious question to ask about smoking cannabis is

since smoking cigarettes is bad for you and especially your lungs, won’t smoking cannabis also be bad?

Enter JAMA: The Journal of the American Medical Association

Let’s first look at a 2012 study published in JAMA by Pletcher et al. called Association Between Marijuana Exposure and Pulmonary Function Over 20 Years. It’s a longitudinal study, the kind that draws associations from “repeated observations of the same variables (e.g., people) over long periods of time, often many decades”.

Epidemiological studies are notoriously low-quality and should thus be used sparingly, but this one meets enough of the Bradford Hill criteria [x], criteria which in fact surfaced from the famous studies linking cigarette smoking to lung cancer.

They took data from a larger study called CARDIA, the Coronary Artery Risk Development in Young Adults study, enrolling 5,115 men and women from 4 US cities over 20-years from 1985 to 2006 aged 18 to 30. 31% of participants dropped out of the study and those that remained averaged 3.9 visits over 20-years, providing 19,705 total measures.

Maybe counterintuitively, “leaving [the] study was more common in tobacco smokers but not associated with marijuana use”. Aren’t pot smokers supposed to be lazy and unreliable?

What did they measure and how?

Pletcher et al. decided to look at Forced Expiratory Volume (FEV) and Forced Vital Capacity (FVC) to assess basic lung function. FEV is the volume of air in milliliters (mL) exhaled. In the first second of expiration it’s termed FEV1 (FEV2 for the second, and so on). FVC is the sum total volume of air from a complete exhale (FEV1 + FEV2 + FEV3 … = FVC). Participants had their baseline FEV1 and FVC taken year 0, then year 2, 5, 10 and 20 with a device called a spirometer

Lung function was then correlated with questionnaires probing into exposure to cigarette and marijuana smoke. The cumulative lifetime exposure to cigarettes, in terms of pack-years, was calculated by assuming

1-pack year = 7,300 cigarettes

(1 year x 365 days per year) x (1 pack per day x 20 cigarettes per pack)

Interestingly, although this kind of self-reported data is notoriously unreliable its quality was assessed by comparison with serum cotinine, the metabolite of nicotine that serves to quantify tobacco exposure. It was found to be “low in these young adults; however, within certain race/education groups, self-report may underestimate smoking prevalence by up to 4%” [x]. I’ll take that. Then, the measure for cannabis exposure consisted of intensity of use within the last 30-days plus joint-years, assuming the following for the latter

1 joint-year = 365 joints or filled pipe bowls smoked

(1 year x 365 days per year) x (1 joint per day)

Before we see how cigarette and marijuana exposure is correlated or not with FEV1 and FVC, let’s look at how these measures change with age. Very little in fact! Turns out age is a poor predictor of lung function.


Lifetime cigarette (tobacco) exposure was given in 5 time categories, 0, 1-5, 6-10, 11-20 and >20  pack-years, whilst marijuana exposure was only given in 4 time categories, 0, 1-5, 6-10 and >10 joint-years. Let’s just compare the highest life-time exposures in both groups. As regards Forced Expiratory Volume and Forced Vital Capacity, to no one’s surprise smoking cigarettes for >20 year (1 pack a day for 20 years) compared with people who never reported smoking either substance, was bad. Smoking this much was associated with a 63 mL lower FEV1. This result is given with a  p-value of < 0.001 and a 95% confidence interval (CI) of −89 to −36mL. To clarify, a 95% CI indicates the range within which we are ‘highly confident’ the relevant values lie. What about FVC values after 20 years? Cigarette smokers had 69 mL less air (95% CI, -97 to -41; p < 0.001). Cigarette smoking and lung function(s) follows a positive linear association, meaning the more you smoke the worse off you are but your first and last cigarette add to your risk equally. See the table below.

So what about marijuana smokers? >10 years of lifetime marijuana smoking (1 joint a day for 10 years) was associated with a slighylu higher FEV1 and FVC. They found 36 mL more air for FEV1 (CI -6.5 to 79; p = 0.049) and 59 mL more air for FVC (CI 12 to 107; p = 0.01). I’ll quote the authors so that it sinks in…

“exposure to marijuana (both current and lifetime) was associated with higher FVC and lifetime exposure with higher FEV1

Unlike cigarette smoking, the association for marijuana was non-linear, meaning that your first and last joint do not add to or decrease your risk equally. In this study, they found that “at higher exposure levels, we found a leveling off or even a reversal in this association, especially for FEV1”. At much more common levels of exposure they “found no evidence that increasing exposure to marijuana adversely affects pulmonary function”.

Should you smoke cannabis for improving lung function?

No. This is not strong evidence for marijuana smoking improving lung function. What it is, is showing that smoking marijuana is not equivalent to smoking cigarettes. Marijuana smoke appears pretty neutral in terms of affecting lung function. People predominantly smoke it, whether for medicinal and/or recreational reasons, so it’s great to know you can do so without fear of damaging your lungs.

What’s next?

There are so many myths surrounding cannabis due its legal status (amongst other things) that I will certainly address many of them. However, although debunking nonsense can be fun and is certainly useful, it’s less fun that telling you about our very own endocannabinoids system (ECS). So that’s what I’ll do in part 2.



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