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Antioxidant-mitoprotective supplement may reverse mitochondrial dysfunction


In a small study, a combination over-the-counter supplement with antioxidant and mitoprotective properties significantly reversed mitochondrial dysfunction.

By Vanessa Caceres;Reviewed by Robert Ritch, MD

A supplement with antioxidant and mitoprotective properties has shown to reverse mitochondrial dysfunction and may be neuroprotective for glaucoma, according to a recent study.

Robert Ritch, MD, the Steven and Shelley Einhorn Distinguished Chair, professor of ophthalmology, New York Eye and Ear Infirmary of Mount Sinai, New York, outlined the results of the study that focused on whether a combination of over-the-counter supplements with antioxidant and mitoprotective properties could reverse mitochondrial dysfunction by reducing mitochondrial flavoprotein fluorescence compared with placebo.

A total of 14 patients (n = 28 eyes) were divided into either a placebo group or a group that received a combination of curcumin, Ginkgo biloba extract, citicoline, coenzyme-Q10 (ubiquinol, Cognizin), N-acetyl-cysteine, alpha-lipoic acid, grapeseed extract, and green tea extract. All of the aforementioned are part of a supplement called Glauco-Health (Guardion Health Sciences).

Dr. Ritch and co-investigators from Ramathibodi Hospital, Mahidol University, Bangkok, Thailand; and Columbia University, New York, conducted the study as part of an Investigational New Drug application from the FDA.



Basis of study

Visual fields, optical coherence tomography (OCT), and retinal metabolic analysis were performed at baseline and at 1 and 3 months after randomization. Researchers monitored for changes in visual fields, OCT, and retinal metabolic analysis over time. The initial demographic characteristics of the two groups were similar.

There were no significant differences in visual field or OCT indices in either group (all P > 5%). However, there was a significant decrease in optic nerve-adjusted mitochondrial flavoprotein fluorescence and average curve width from baseline to 1 month in those treated with Glauco-Health (β = –39, P = 0.003; β = –0.25, P = 0.01, respectively) but not in patients who were treated with placebo (P = 0.47 and 0.23).

“Mitochondrial dysfunction and death are increasingly implicated in retinal ganglion cell death in glaucoma and neuronal death in other neurodegenerative disorders,” Dr. Ritch explained. “Mitochondria become dysfunctional and die prior to neuronal cell death. Formulations with IOP-dependent neuroprotective effects could be additive in slowing progression rates by reversing mitochondrial dysfunction.”

Research such as that from this study could shift the treatment paradigm to stabilize mitochondria at an earlier disease stage, and prevent or retard neuronal cell death.

The findings “serve as a proof-of-concept for future trials testing the neuroprotective effect of supplement combinations in glaucoma,” according to the study.

Robert Ritch, MD

e. ritchmd@earthlink.net

This article is based on a poster presented by Dr. Ritch and colleagues at the 2018 American Glaucoma Society meeting.

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