Display color gamut as a spectral risk factor for myopia: a unifying hypothesis linking chromatic emmetropization, cone circuitry dysfunction, and the spectral deficiency of digital screens.

Abstract

The global prevalence of myopia in children rose from 24% in 1990 to 36% in 2023, with projections exceeding 39% by 2050. While time spent outdoors is robustly protective against myopia, the specific spectral properties of light responsible for this protection remain insufficiently characterized. We propose that the spectral power distribution (SPD) of modern digital displays may represent a previously unrecognized environmental risk factor for myopia through the systematic elimination of two wavelength bands critical to emmetropization. All current display technologies emit no measurable light below approximately 420 nm, entirely excluding the violet band (360-400 nm) that activates OPN5/neuropsin (λmax ≈ 380 nm) in retinal ganglion cells. Additionally, the narrow-band RGB primary architecture of displays distorts the cyan-green region (490-560 nm), potentially perturbing the SWS/LWS opponent chromatic signal that the Gawne-Norton dual-detector model identifies as the primary longitudinal chromatic aberration (LCA)-based drive for emmetropization. These two mechanisms are consistent with the dose-response relationship between screen time and myopia risk documented in large-scale epidemiological studies. The hypothesis is grounded in five converging lines of evidence: (1) the OPN5/violet light pathway; (2) the LCA dual-detector emmetropization model; (3) genetic evidence from Blue Cone Monochromacy and Bornholm Eye Disease; (4) red-light therapy trials; and (5) subgroup analyses by display device type. We propose that display color gamut - and the spectral power distribution it determines - currently optimized exclusively for colorimetric fidelity, merits evaluation as a modifiable variable in the global myopia control agenda.