- Previous studies on the protective benefits of metformin in AMD have produced mixed results.
- In this study, patients prescribed metformin had a similar risk of AMD development and progression compared with those not prescribed metformin.
- Due to its retrospective nature, the study does not directly address causality between metformin and the development or progression of AMD.
Older adults prescribed metformin had a similar risk of developing age-related macular degeneration (AMD) and having AMD progression compared with those not prescribed metformin, a retrospective study suggested.
In a cohort of patients with no AMD, those prescribed metformin had a generally similar risk of developing any AMD versus those without a prescription (risk ratio [RR] 0.90, 95% CI 0.86-0.94), with the risk remaining similar at 5 years (RR 0.94, 95% CI 0.90-0.99) and 10 years (RR 0.91, 95% CI 0.87-0.94), reported Katherine E. Talcott, MD, of the Cole Eye Institute at the Cleveland Clinic, and colleagues in JAMA Ophthalmology.
In addition, in a cohort of patients with mild or moderate nonexudative AMD, those prescribed metformin had a comparable risk of AMD progression compared with those not prescribed metformin:
- Geographic atrophy: RR 0.87 (95% CI 0.76-1.01)
- Neovascular AMD: RR 1.03 (95% CI 0.91-1.17)
The risks were also similar at 5 and 10 years.
However, Talcott and team didn't close the door on a possible benefit from the diabetes drug. "Further studies and prospective analyses are necessary to better evaluate whether dosage and longevity of metformin use may influence AMD development or progression," they wrote.
According to co-author Darren A. Jindal, PhD, of Case Western Reserve University School of Medicine in Cleveland, there's been interest in metformin's possible preventive powers in AMD "because studies have shown that the drug regulates fat breakdown, reduces inflammation, and inhibits aberrant and weak blood vessel growth in the setting of stress. These secondary functions of metformin are considered part of AMD pathogenesis."
Studies have produced mixed results on whether the drug is protective, Jindal told MedPage Today, suggesting the need for more research. Even in the age of GLP-1 agonists, exploring the possible impact of metformin is still important "despite changing trends in metformin prescription, discontinuation, and adherence," he said.
Jindal cautioned that the study is retrospective and "does not directly address causality between metformin and the development or progression of AMD."
In an accompanying commentary, Su-Hsun Liu, MD, MPH, PhD, of Sue Anschutz-Rodgers Eye Center in Aurora, Colorado, and colleagues cautioned that "until high-quality causal evidence is available, the totality of the currently available evidence does not support the consideration of clinicians to prescribe metformin for the sole purpose of preventing AMD or slowing its progression."
They noted that metformin "can cause gastrointestinal side effects, vitamin B12 deficiency with long-term use, and, in rare cases, lactic acidosis, particularly in individuals with kidney impairment."
For the study, Talcott and colleagues analyzed data from 70 institutions via the TriNetX database from January 2013 to June 2025. They used propensity score matching to control for confounders, such as age, sex, race, hypertension, diabetes, and other systemic conditions.
After matching, the cohort with no AMD included 379,450 patients divided evenly into those exposed and not exposed to metformin. Mean age was 76, 54% were women, and about 60% were white. Of these patients, 80% had diabetes.
The cohort with mild or moderate AMD included 18,488 patients divided evenly into those exposed and not exposed. Mean age was 80.5, 57% were women, and 78-80% were white; 85% had diabetes.
In regard to limitations, the authors noted that they "did not exclude additional diabetic medication use in the exposed group or include this in the propensity match, and it is possible that use of these medications abrogated a theorized AMD risk reduction by metformin."
Disclosures
The study was funded by the NIH, Research to Prevent Blindness, the Cleveland Eye Bank Foundation Grant, and the Clinical and Translational Science Collaborative of Northern Ohio.
Talcott reported receiving consulting fees from Alimera, Apellis, Bausch and Lomb, EyePoint, and Genentech; serving on the speaker's bureaus for Genentech and Iveric Bio; and receiving research fees from Regeneron, Regenxbio, and Zeiss.
Jindal had no disclosures.
Co-authors reported relationships with Impact Education-Regeneron, Elsevier, Iveric Bio, Samsara, AbbVie/Allergan, Alcon, Apellis, Regeneron, Astellas, Roche/Genentech, Ocular Therapeutix, EyePoint, Boehringer Ingelheim, 4D Molecular, Zeiss, AGTC, DRCR Retina Network, NGM Bio, Regenxbio, Bausch and Lomb, and Janssen.
Liu and a co-author reported receiving grant support from the National Eye Institute.
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