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January 09, 2025

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Some megatrends in health care are occurring that deserve our attention.

We already know that as much as one-third of the U.S. population will be diabetic by 2050 unless something changes. Perhaps equally concerning is the growing prevalence of myopia. Ten years ago, one-fourth of the world’s population was nearsighted. By 2030, that will increase to 50% (Holden and colleagues).

Who cares? Can’t we just prescribe glasses, use contact lenses or do LASIK surgery? Yes, we can correct myopia, but only if the eye isn’t already on its way to blindness by some of the very bad actors that accompany it.

First of all, open-angle glaucoma is 50% more common among patients with moderate to high myopia (defined as 6 D or greater) (Marcus and colleagues). Retinal detachment occurs three times more commonly among patients with just 2 D of myopia, nine times higher with high myopia and 22 times higher in patients with 8 D or more of myopia (Holden and colleagues).

Finally, myopic macular degeneration (MMD) may be the most concerning risk of epidemic nearsightedness. This degeneration of the central retina often causes legal blindness in young, healthy people, much as age-related macular degeneration is the leading cause of blindness in people older than 65 years. MMD is up to 22 times more common in patients with high myopia, occurring in as many as two-thirds of these patients. That risk drops to 8% among moderate myopes and 0.1% to 7% in low myopes (Vongphanit and colleagues).

But the very best way to treat these complications of nearsightedness is never to have nearsightedness in the first place, or at least to minimize it. Indeed, in kids, we can see myopia coming and do something about it. Throughout young life, the eye grows in axial length as the body grows — a natural process. When the eye grows to about 23 mm or 24 mm, myopia starts, and when longer than 26 mm, the most risks increase dramatically (Holden and colleagues).

Certainly, genetics play a role in causing myopia; children of one myopic parent have two to three times the risk compared with parents with normal vision, with five to six times the risk with two myopic parents (Marcus and colleagues). Genetics are not to blame for the global increasing trend, though, as our genetics are not changing rapidly. There’s clear evidence that less time spent outdoors, lower light intensity and the increase in near activity (yes, screens) are driving myopia development (Flitcroft).

How do we stop myopia from progressing in young patients? It’s clear that prescribing typical glasses and contact lenses is ineffective. In the U.S., there are three soft contact lenses approved to actually stop the progression of myopia. They work in a manner that is not completely understood by defocusing the peripheral vision. These lenses are made by CooperVision, Bausch + Lomb and Johnson & Johnson.

Orthokeratology is the process of wearing rigid contact lenses during sleep but not during the day. This temporarily alters the corneal shape the following day. Like the soft contact lenses worn during the day, these seem to help slow the progression of myopia. Finally, low-dose atropine drops have minimal effect on pupil size but seem to limit the muscular action in the eye that derives growth of axial length.

At this time, no formulations of atropine drops are FDA approved for myopia control. Many compounding pharmacies make these for patients, and three companies are pursuing approval in the U.S. and abroad. As doctors, it’s our duty to do everything we can to notify the parents about the importance of screening their young children and taking active steps to control myopia progression.

When you consider that each diopter of myopia progression increases the risk for MMD by 67% (Bullimore and colleagues), we can’t afford to let children become more nearsighted any more than we can look the other way when our patients with diabetes go running to the candy store.

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References:

• Biswas S, et al. J Physiol Anthropol. 2024;doi:10.1186/s40101-024-00354-7.
• Bullimore MA, et al. Optom Vis Sci. 2019;doi:10.1097/OPX.0000000000001367.
• Flitcroft DI. Prog Retin Eye Res. 2012;doi:10.1016/j.preteyeres.2012.06.004.
• Holden BA, et al. Ophthalmology. 2016;doi:10.1016/j.ophtha.2016.01.006.
• Marcus MW, et al. Ophthalmology. 2011;doi:10.1016/j.ophtha.2011.03.012.
• Mutti DO, et al. Invest Ophthalmol Vis Sci. 2002;43(12):3633-3640.
• Vongphanit J, et al. Ophthalmology. 2002;doi:10.1016/s0161-6420(01)01024-7.

For more information:

John A. Hovanesian, MD, FACS, an ophthalmologist specializing in cataract, refractive and corneal surgery at Harvard Eye Associates in Laguna Hills, California, can be reached at drhovanesian@harvardeye.com.

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** Disclosures: ** Hovanesian reports no relevant financial disclosures.

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