Glaucoma is a group of diseases that can damage the eye’s optic nerve. It is a leading cause of blindness in the United States. It usually happens when the fluid pressure inside the eyes slowly rises, damaging the optic nerve. The increased pressure, called intraocular pressure, can damage the optic nerve, which transmits images to the brain.
Recent years have brought a wealth of new scientific understanding regarding how medical marijuana or cannabis can be beneficial for treating Glaucoma.
A comprehensive eye exam can tell if you have glaucoma. People at risk should get eye exams at least every two years.
- African Americans over age 40
- People over age 60, especially Mexican Americans
- People with a family history of glaucoma
There is no cure, but glaucoma can usually be controlled. Early treatment can help protect your eyes against vision loss. Treatments usually include prescription eyedrops and/or surgery.
Glaucoma / Eye Problems Information & Juicing Recipes for Glaucoma
Glaucoma refers to a group of eye conditions that lead to damage to the optic nerve. This nerve carries visual information from the eye to the brain.
In most cases, damage to the optic nerve is due to increased pressure in the eye, also known as intraocular pressure (IOP).
Beta-Carro (Serves 1)
- 3 – Carrots
- 3 – Fresh apricots, pitted
- 3 – Peaches, pitted
Blueberry (Serves 1)
- 1 cup – Blueberries
- 1 – 2 inch slice of watermelon
- 1/4 cup – Whole cranberries
Neuroprotective effect of (-)Delta9-tetrahydrocannabinol and cannabidiol in N-methyl-D-aspartate-induced retinal neurotoxicity: involvement of peroxynitrite.
- Department of Pharmacology and Toxicology, Medical College of Georgia, 1120 15th Street, Augusta, GA 30912, USA.
In glaucoma, the increased release of glutamate is the major cause of retinal ganglion cell death. Cannabinoids have been demonstrated to protect neuron cultures from glutamate-induced death. In this study, we test the hypothesis that glutamate causes apoptosis of retinal neurons via the excessive formation of peroxynitrite, and that the neuroprotective effect of the psychotropic Delta9-tetrahydroxycannabinol (THC) or nonpsychotropic cannabidiol (CBD) is via the attenuation of this formation. Excitotoxicity of the retina was induced by intravitreal injection of N-methyl-D-aspartate (NMDA) in rats, which also received 4-hydroxy-2,2,6,6-tetramethylpiperidine-n-oxyl (TEMPOL,a superoxide dismutase-mimetic), N-omega-nitro-L-arginine methyl ester (L-NAME, a nitric oxide synthase inhibitor), THC, or CBD. Retinal neuron loss was determined by TDT-mediated dUTP nick-end labeling assay, inner retinal thickness, and quantification of the mRNAs of ganglion cell markers. NMDA induced a dose- and time-dependent accumulation of nitrite/nitrate, lipid peroxidation, and nitrotyrosine (foot print of peroxynitrite), and a dose-dependent apoptosis and loss of inner retinal neurons. Treatment with L-NAME or TEMPOL protected retinal neurons and confirmed the involvement of peroxynitrite in retinal neurotoxicity. The neuroprotection by THC and CBD was because of attenuation of peroxynitrite. The effect of THC was in part mediated by the cannabinoid receptor CB1. These results suggest the potential use of CBD as a novel topical therapy for the treatment of glaucoma.
Effect of sublingual application of cannabinoids on intraocular pressure: a pilot study.
- Department of Ophthalmology, Aberdeen Royal Infirmary, Institute of Medical Sciences, University of Aberdeen, UK.
The purpose of this study was to assess the effect on intraocular pressure (IOP) and the safety and tolerability of oromucosal administration of a low dose of delta-9-tetrahydrocannabinol (Delta-9-THC) and cannabidiol (CBD).
PATIENTS AND METHODS:
A randomized, double-masked, placebo-controlled, 4 way crossover study was conducted at a single center, using cannabis-based medicinal extract of Delta-9-THC and CBD. Six patients with ocular hypertension or early primary open angle glaucoma received a single sublingual dose at 8 AM of 5 mg Delta-9-THC, 20 mg CBD, 40 mg CBD, or placebo. Main outcome measure was IOP. Secondary outcomes included visual acuity, vital signs, and psychotropic effects.
Two hours after sublingual administration of 5 mg Delta-9-THC, the IOP was significantly lower than after placebo (23.5 mm Hg vs. 27.3 mm Hg, P=0.026). The IOP returned to baseline level after the 4-hour IOP measurement. CBD administration did not reduce the IOP at any time. However, the higher dose of CBD (40 mg) produced a transient elevation of IOP at 4 hours after administration, from 23.2 to 25.9 mm Hg (P=0.028). Vital signs and visual acuity were not significantly changed. One patient experienced a transient and mild paniclike reaction after Delta-9-THC administration.
A single 5 mg sublingual dose of Delta-9-THC reduced the IOP temporarily and was well tolerated by most patients. Sublingual administration of 20 mg CBD did not reduce IOP, whereas 40 mg CBD produced a transient increase IOP rise.
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