Eyes on cannabis #1: the eye basics
Kia ora e hoa,
When you have colourful friends, an occupation like mine, combined with a late night dinner conversation, this question is inevitable: what are the effects of cannabis on the eyes?
Apart from red eyes and pupil dilation, the point of interest was about cannabis and glaucoma — or that is how I believe the conversation steered.
Glaucoma ranks highly as a cause of irreversible blindness (Thylefors & Negrej, 1994). According to Blind Low Vision New Zealand, glaucoma ranks as the second most cause of blindness in Kiwi's over the age of 65 (Blind Low Vision New Zealand, n.d.). Blindness can be debilitating for an individual (Vuletić et al., 2016). There is a significant loss of independence, where you lose the ability to drive, enjoy watching TV and even navigate around your own household.
Known for its psychoactive effects, cannabis is a plant that is cultivated, dealt, and consumed, sometimes illegally (Ashton, 2001). There is strong debate for cannabis's medical usage (hence my friends' curiosity), as well as its potential harm (Clark et al., 2011).
And thanks to their intrigue, over the last few weeks, I've been deeply researching this topic. Writing the blog post for this topic is proven to be monumental. To help stay on track, I've decided to release this in four weekly newsletters as I collaborate this post. This newsletter will be the first of the issue.
Before we can delve into the exciting question of cannabis and glaucoma, we first need to go through the interesting act of gaining foundational knowledge. We will look at the relevant eye functions. Next:
in the 2nd week, we will look into what glaucoma is
the 3rd week will look into some current glaucoma treatments, and
in the finale week, what we have finally been waiting for: cannabis and glaucoma.
Disclaimer — this is for educational purposes only. If you have any eye issues please consult your local eye care professional.
As a note, I've written this for the public as well as eye care professionals. So there will be over-laboured points and potentially confusing ideas. You might have noticed already but in parenthesis, I've included some sources. In the final blog post, I will include diagrams to aid in understanding of these topics. In advance, I'd like to thank you for having to deal with this, and I hope you enjoy and become more educated/refreshed (please share this newsletter if you do too!).
How do our eyes work?
Pathology is disease. Disease is where we lose normal function. Before we understand the pathology of glaucoma, we need to understand how the eye functions normally.
The human eye acts as a simple camera. Light from the outside world enters the eye first through the cornea, going through many structures like the lens, until it reaches the back of the eye, or retina.
The retina is responsible for detecting light. It does this thanks to very important cells called photoreceptors. When light hits a photoreceptor, this information is transferred to a variety of nerve cells ultimately ending up at the retinal ganglion cells (RGC).
The retinal ganglion cell contains a very long cable-like structure called axons. Axons from all the RGCs from all over the retina converge at the optic nerve. This then travels all the way to the brain so the information from the retina can be processed (Zhu et al., 2012).
All the eyes do is capture light, whereas the brain does the 'seeing'.
Simply put, glaucoma is where this cable becomes damaged. A damaged cable is no longer able to take information from the eye to the brain, resulting in blindness.
Now we understand how we see, for glaucoma, it is important to understand the role of aqueous humour (AH)
Unrelated to blood pressure, the eye has it's own pressure. This is regulated by the production and removal of AH.
Since parts of the eye lack blood supply, AH is necessary in providing nutrients to, as well as removing waste products from, these internal structures (To et al., 2002).
AH is made by the ciliary epithelium located at the ciliary body and back surface of the iris.
The ciliary epithelium (CE) consist of two layers of cells, pigmented and non-pigmented. The responsibility of these cells is to facilitate the movement of water and nutrients from the blood to the posterior chamber, making up AH.
The pigmented CE lines the side with the blood vessels and the non-pigmented CE lines the side of the posterior chamber (Macknight et al., 2000).
There are three mechanisms responsible for AH formation. They are:
Diffusion and ultrafiltration are passive, involving no energy. Diffusion involves the movement of solutes (dissolved molecules in a fluid, like water) from the blood in capillaries around the ciliary body into the posterior chamber of the eye (Goel et al., 2010).
Ultrafiltration involves the movement of water and small molecules and particles dissolved in water (limited by size and charge) thanks to an osmotic gradient (phenomena where water moves into an area of high solute concentration to low solute concentration) (Goel et al., 2010).
Finally, active secretion makes up the bulk of AH formation, about 80-90%. Energy is used to move charged particles or ions from the blood into the posterior chamber. There are two primary ion movements:
sodium (Na⁺) via Na⁺/K⁺-ATPase, and
bicarbonate (HCO⁻) by carbonic anhydrase (To et al., 2002),
Other ions and molecules that are transported include:
chlorine (Cl⁻), through various transporters, and
ascorbic acid (or vitamin C), using a sodium-dependant vitamin C transporter 2.
The movement of these ions results in movement of nutrients and water from the blood to the AH. Later, we will see why this is important because these transporters become targets for drugs in the treatment of glaucoma (Goel et al., 2010).
Humour taketh away
With the formation of AH comes its drainage and subsequent removal. As the AH passively moves from the posterior to the anterior chamber, it approaches two main exit ways:
In the conventional pathway, the AH exits the eye through the trabecular meshwork (TM) located at the angle where the back of the cornea and iris meet. Eventually, the AH will end up back into the body's blood supply through the Schelemm's canal, collector channels, then into the aqueous veins and episcleral veins.
The unconventional pathway involves AH exiting through the ciliary muscle and out their the sclera (Goel et al., 2010).
Glaucoma, coined the 'silent thief of sight', is one of the significant causes of vision loss in New Zealand. Interestingly, cannabis usage and treatment of glaucoma has become a hot topic — among my friends anyway.
Before we are led by our curiosity. We need to first understand how the eye works and it's relevant functions.
This includes how the eye sees, and how the eye creates and removes aqueous humour.
The next step is to look at what glaucoma is and how it effects sight. So, please stay tuned.
Did you find this interesting? If you did, please forward this on to family and friends so they can find it useful too.
Thanks for reading and all the best for the week ahead.
Ngā mihi nua,
Blind Low Vision New Zealand. (n.d.). Blindness and Low Vision in New Zealand – Latest statistics. Blind Low Vision NZ. Retrieved March 7, 2021, from https://blindlowvision.org.nz/information/statistics-and-research/
Clark, P. A., Capuzzi, K., & Fick, C. (2011). Medical marijuana: Medical necessity versus political agenda. Medical Science Monitor, 17(12), RA249–RA261. https://doi.org/10.12659/msm.882116
Goel, M., Picciani, R. G., Lee, R. K., & Bhattacharya, S. K. (2010). Aqueous Humor Dynamics: A Review. The Open Ophthalmology Journal, 4(1), 52–59. https://doi.org/10.2174/187436410100401005
Macknight, A. D., McLaughlin, C. W., Peart, D., Purves, R. D., Carre, D. A., & Civan, M. M. (2000). Formation Of The Aqueous Humor. Clinical and Experimental Pharmacology and Physiology, 27(1-2), 100–106. https://doi.org/10.1046/j.1440-1681.2000.03208.x
Thylefors, B., & Negrej, A.-D. (1994). The global impact of glaucoma. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2486713/pdf/bullwho00414-0005.pd
To, C., Kong, C., Chan, C., Shahidullah, M., & Do, C. (2002). The mechanism of aqueous humour formation. Clinical and Experimental Optometry, 85(6), 335–349. https://doi.org/10.1111/j.1444-0938.2002.tb02384.x
Vuletić, G., Šarlija, T., & Benjak, T. (2016). Quality of life in blind and partially sighted people. Journal of Applied Health Sciences, 2(2), 101–112. https://doi.org/10.24141/2/2/3
Zhu, J., Zhang, E., & Del Rio-Tsonis, K. (2012). Eye Anatomy. ELS. https://doi.org/10.1002/9780470015902.a0000108.pub2
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