Recently New York governor Cuomo called for the use of medical marijuana in his state for the treatment of cancer, glaucoma and other chronic diseases:
Always on the top of lists of qualifying conditions, marijuana has long been known to lower the intra ocular pressure (IOP) that leads to the destruction of the optic nerve and blindness:
Despite this evidence, the Institute of Medicine (IOM) strongly recommends against using marijuana for the following reasons:
1) it is only effective for 3-4 hours after inhalation dosing
2) so many other safe and effective topicals are available
3) the hypotensive effects would be counter to nourishing the optic nerve and
4) smoking so much is bad for the lungs.
However there are cannabinoid CB1 receptors all over the eye, in particular in the trabecular mesh (TM). So the current research is aimed at developing targeted cannabinoid analogs that influence the chemistry in the TM, enabling better aqueous flow through the eye, but without the aforementioned drawbacks:
Additionally this article explores the cannabinoid/bimatoprost synergy. Presumably this would lead to a greater hypotensive effect with lower doses of both agents.
‘The role of endocannabinoid system in glaucoma may thus be of importance, not only because of the direct positive effects on outflow of the endocannabinoid molecules, but also for the provision of substrates for prostamide production, in addition to a potential neuroprotective contribution to the optic nerve.70 The reduced endocannabinoid levels demonstrated in outflow pathways in human glaucomatous eyes59 may exert a marked effect on outflow, both directly through reduced cannabinoid-induced outflow and indirectly, via reduced prostamide production. Irrespective of the final mediator (endocannabinoid or prostamide), there is a potential to investigate the inhibition of endogenous cannabinoid metabolism as a potential antiglaucoma therapy. ( or add some mj – my comment). Anandamide and 2-AG are broken down by the FAAH enzyme. Inhibitors of FAAH or FAAH gene knockouts increase tissue endocannabinoid concentrations,39 including in the trabecular meshwork of the eye.57 Studies will firstly need to directly measure the formation of prostamides to verify their place in the control of intraocular pressure and altered expression in the setting of glaucoma.’
Clin Ophthalmol. 2009; 3: 663–670.
Published online 2009 December 29.
Role of prostaglandins and specific place in therapy of bimatoprost in the treatment of elevated intraocular pressure and ocular hypertension: A closer look at the agonist properties of bimatoprost and the prostamides
Scott D Smid
Given the latest research, it is possible to address the negative claims of the IOM:
1) synergies with current treatment could limit dosing (see above)
2) current agents are not always well tolerated especially in otherwise healthy patients and the search for new treatment continues: http://www.hindawi.com/isrn/ophthalmology/2013/261386/
3) cannabinoids are neuroprotective: http://www.sciencedirect.com/science/article/pii/S0028390813001640
4) lung damage not a given: http://www.medicalnewstoday.com/articles/240146.php and see 1) above.