Magnesium Citrate Improves Vision in Normotensive Glaucoma

Study offers promise for a condition not effectively treated by conventional medication

By Michael T. Murray, ND

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Aydin B, Onol M, Hondur A, et al. The effect of oral magnesium therapy on visual field and ocular blood flow in normotensive glaucoma. Eur J Ophthalmol. 2010;20(1):131-135.


Controlled clinical trial to evaluate the effect of oral magnesium therapy on ocular blood flow and visual field perimetry indices in patients with normotensive glaucoma (NTG). Blood magnesium level measurement, visual field analysis, and color Doppler imaging of the orbital vessels were done before treatment and at 1 month.


Fifteen patients with NTG (study group) received 300 mg oral magnesium citrate for 1 month, while 15 patients with NTG (control group) received no treatment.

Key Findings

In the study group, visual field measurements improved significantly: Mean deviation improved from -3.7+/-1.9 (mean +/- standard deviation) at baseline to -2.5+/-1.8 at 1 month (P<0.05) and pattern standard deviation improved from 3.6+/-2.3 at baseline to 2.8+/-2.6 at 1 month (P<0.05). Color Doppler imaging indices did not change after magnesium therapy. Other mechanisms than increased ocular blood flow may be responsible for the improvement in the visual field with oral magnesium therapy.

Practice Implications

Glaucoma reflects damage to the optic nerve. Glaucoma can result in the gradual loss of peripheral vision resulting in tunnel vision and ultimately blindness. Usually, the damage to the optic nerve is caused by increased pressure within the eye, which results from greater production than outflow of the fluid of the eye (the aqueous humor). The normal intraocular pressure (IOP) is about 10 to 21 mm Hg. In chronic glaucoma, the intraocular pressure is usually mildly to moderately elevated (22 to 40 mm Hg). In acute glaucoma, the intraocular pressure is greater than 40 mm Hg.

In some cases glaucoma develops in people with normal IOP. Referred to as low-tension glaucoma or normotensive glaucoma, this form accounts for approximately 25 to 30 percent of all glaucoma cases in the United States.

Low-tension glaucoma or normotensive glaucoma accounts for approximately 25 to 30 percent of all glaucoma cases.

Since elevated IOP is not a factor in NTG, other factors are responsible for the optic nerve damage. Suggested causes include:

  • Reduced blood flow
  • Early nerve cell death
  • Nerve irritation
  • Excess glutamate production
  • Autoimmune disease

The condition is more common in women than in men and affects adults averaging 60 years old. A common risk factor for NGT is low blood pressure.

This study showing benefits in visual field improvements after oral magnesium supplementation is highly significant, as NTG is not effectively treated by conventional medications. It is also extremely thought-provoking, as a mechanism of action must be identified.

Since the benefits of magnesium therapy are not due to changes in blood flow, it is possible that the benefit is related to reducing increased glutamate concentrations in the extracellular spaces around the optic nerve. Glutamate is a major excitatory neurotransmitter and an important neurotoxin that promotes neuronal cell death. It is definitely implicated in NTG. Since magnesium has been shown to stimulate the blockade of neural receptors that result in a decrease in glutamate release during ischemia,1 this mechanism could also explain its benefits in NTG.

About the Author

Michael T. Murray, ND, is President and CEO of Dr. Murray Natural Living and is Chief Science Officer for Enzymedica. Dr. Murray is a graduate, faculty member, and serves on the Board of Regents of Bastyr University, where he received his doctorate in Naturopathic Medicine. He is co-author of A Textbook of Natural Medicine and the Encyclopedia of Natural Medicine. He has also written over 30 other books including his latest book, The Magic of Food. For more information please visit


1. Kang SW, Choi SK, Park E, et al. Neuroprotective effects of magnesium-sulfate on ischemic injury mediated by modulating the release of glutamate and reduced of hyperreperfusion. Brain Res. 2011;1371:121-128.