Associate Professor Ranjay Chakraborty explores the emerging role of light-based therapies in myopia management, examining how different wavelengths may influence eye growth and refractive development.

A substantial body of cross-sectional and longitudinal evidence indicates that increased time spent outdoors is associated with a reduced risk of myopia onset.1,2 While this protective effect is likely multifactorial, encompassing optical factors3 and neurochemical mechanisms such as dopamine signalling,4,5 differences in the spectral composition of outdoor versus indoor light have been proposed as an additional contributor to the regulation of ocular growth in children.6

Supporting this hypothesis, animal studies demonstrate that both wavelength and spectral composition of light can differentially influence ocular growth and the development of experimental myopia.6 Experimental models further suggest that emmetropisation, the coordinated process by which the eye regulates axial growth to achieve clear retinal focus, utilises chromatic cues arising from longitudinal chromatic aberration (LCA) to encode the sign of defocus.7 LCA is an inherent optical property whereby shorter wavelengths (blue light) are refracted more strongly than longer wavelengths (red light), resulting in shorter wavelengths focusing anterior to the retina and longer wavelengths posterior to it. Consequently, ocular refraction varies systematically with wavelength, with longer wavelengths producing relatively more hyperopic (less myopic) refractive states.8,9 More recently, Gawne and Norton proposed that emmetropisation may involve comparison of image contrast signals between short- and long-wavelength-sensitive cones, enabling compensatory adjustments in ocular growth toward emmetropia.10

However, the observation that emmetropisation persists under narrowband lighting conditions, where LCA-derived chromatic cues are absent, suggests that wavelength-specific defocus signals, in addition to LCA-based cues, may contribute to growth regulation.11-13 Consistent with this, species-dependent effects of spectral environment have been reported. Guinea pigs,14 fish, and chicks11 develop myopia when reared under middle- to long-wavelength (green or red) light and hyperopia under short-wavelength (violet or blue) light.16,17 In contrast, primate and mammalian models, such as rhesus monkeys18 and tree shrews19,20 exposed to long-wavelength light, exhibit reduced axial elongation, choroidal thickening, and less myopic refractive outcomes. Overall, these findings indicate that narrowband lighting influences ocular growth via spectrally sensitive visual signalling pathways. This article discusses new and emerging spectral-based approaches for myopia treatment.

VIOLET AND ULTRAVIOLET LIGHT

A small number of studies have examined the potential role of short wavelength violet light, as well as ultraviolet light, in childhood myopia.

Modern light sources, windows, and spectacle lenses typically reduce or filter out violet and ultraviolet light, and it has been proposed that reduced exposure to violet light in modern indoor and light filtered environments may contribute to myopia risk.21 This hypothesis informed a study in myopic children aged 6–12 years, who were asked to wear glasses that emitted violet light for three hours per day and were compared with a placebo group over six months.22 No significant differences were observed between the two groups overall. However, in a subgroup of children aged 8–10 years, axial elongation was significantly smaller, and the choroid was significantly thicker than in controls after six months.22

A study of violet-light-transmitting spectacles similarly found no overall significant difference in axial elongation compared with controls, although a benefit was reported in a subgroup of children with less than 180 minutes of near work per day who were wearing glasses for the first time.23

Retrospective studies also examined myopic children wearing either violet-light-blocking spectacles or contact lenses that blocked or transmitted violet light.21,24 Torii et al. reported reduced axial elongation over one year in children wearing violet-light-transmitting contact lenses.21 A separate retrospective analysis of children and young adults (aged 12–29 years) found greater refractive error change over five years in those wearing contact lenses that blocked ultraviolet transmission, compared with those wearing lenses that transmitted ultraviolet light.24 The effects of violet light on myopia appear to be associated with stimulation of a violet-light-sensitive neuropsin (OPN5) and its downstream signalling pathways.25

Overall, the protective effects of violet and ultraviolet light on myopia progression appear to be modest, highlighting the need for further well-controlled studies.

RED LIGHT AND REPEATED LOW-LEVEL RED-LIGHT THERAPY

Repeated low-level red-light (RLRL) therapy, which uses low-to-moderate-power semiconductor laser diodes and was originally adapted from amblyopia treatment, has emerged as a promising non-invasive approach for myopia control,26 supported by animal studies in rhesus monkeys and tree shrews.18,27

Standard protocols involve twice-daily three-minute exposures to ~650 nm light, with a recent meta-analysis reporting a mean reduction of 0.77D (95% CI: 0.64 to 0.90D) in myopia progression and −0.36 mm (95% CI: −0.41 to −0.31 mm) in axial elongation after 12 months compared with single-vision correction in Chinese children, while some studies also report axial length regression and delayed onset.28-31 Similar protective effects have been observed in a pilot study of multi-ethnic Australian school-aged children.32 RLRL induces sustained choroidal thickening of ~15 μm33 to up to 30 μm34-36 after 12 months.

The effects of RLRL are irradiance-dependent, with devices delivering irradiances of >0.6 mW providing greater protection against myopia progression.28 The underlying mechanisms likely involve photobiomodulation of metabolic processes in the posterior eye or improved choroidal perfusion rather than conventional spectral signalling.30,33,37 However, treatment intensities in some devices may approach or exceed safety thresholds,38 and reports of rebound39 alongside retinal structural and functional changes40,41 highlight potential risks. Notably, the ocular effects of RLRL contrast with the short-term axial elongation and choroidal thinning observed following short-term (60-minute) exposure to red LED light in young adult humans.42,43 Despite promising efficacy, limited long-term evidence44 and unresolved safety concerns necessitate cautious interpretation and further rigorous evaluation. Interestingly, other long-wavelength sources, such as amber light (excluding wavelengths <500 nm), have demonstrated similar hyperopia-inducing effects to red light in tree shrews,45 suggesting a possible alternative spectral approach that merits further investigation.

BLUE LIGHT

Short-term exposure to blue light (60 min) induces small but significant choroidal thickening and axial length reduction in young human subjects.42,43,46

These effects are hypothesised to reflect multiple pathways, including activation of short-wavelength-sensitive cones, intrinsically photosensitive retinal ganglion cells (ipRGCs), retinoic acid signalling, altered retinal dopamine release, and improved choroidal perfusion,2,47,48 although the precise mechanisms remain unclear. ipRGCs express melanopsin (OPN4), a blue-light-sensitive photopigment with peak sensitivity at ~479–480 nm that is highly conserved across species.49,50 Despite comprising only ~0.2–2.5% of retinal ganglion cells, they exhibit extensive dendritic coverage and project widely to brain regions, primarily regulating non-image-forming functions such as circadian photoentrainment and the pupillary light reflex, while also contributing to visual processing, including contrast and pattern detection.51,52

A recent trial targeting ipRGC activation via blue light exposure to the optic nerve head reports good safety and tolerability, with preliminary evidence of efficacy for myopia control.53 However, no human studies have yet examined the long-term effects of targeted or diffuse short-wavelength light exposure on myopia progression, which remains to be elucidated.

CYAN LIGHT

Recent experimental studies have shown that two hours of exposure to cyan light (507 nm) produces a significant transient reduction in axial length and choroidal thickening compared with broadband white light in both young adults and children,46 and may attenuate the myopigenic effects of hyperopic defocus on ocular biometry.54 Similar findings have been reported following 30-minute morning exposures over seven days, resulting in a small (5 μm) but statistically significant increase in macular choroidal thickness and an enhanced diurnal variation in choroidal thickness.55 Evidence from animal models is less consistent: cyan light appears protective against axial myopia in zebrafish but disrupts emmetropisation in tree shrews.2 Importantly, human studies to date have been short-term and have reported choroidal changes in the order of only a few microns.

Whether these changes predict long-term eye growth or meaningful myopia control remains uncertain,56 highlighting the need for further research to establish the utility and efficacy of cyan light as a myopia-control intervention.

CHROMATICALLY SIMULATED MYOPIC DEFOCUS

Myopic defocus can be digitally simulated on a screen by low pass filtering individual colour channels of an RGB (red, green, blue) display, termed chromatically simulated myopic defocus (CSMD).75,58 In a recent study, Barbara et al.57 selectively blurred either the red channel (‘blue in focus’) or the blue channel (‘red in focus’) according to the human LCA function, and assessed axial length responses.

Blue-in-focus stimuli (~450 nm) induced significant axial elongation, whereas red-in-focus stimuli (~630 nm) produced axial shortening after 45 minutes, with effects observed in emmetropic but not myopic eyes, suggesting reduced chromatic sensitivity in myopia.59 Early human data further indicate that repeated CSMD exposure (two hours/ day for 12 days) can induce incremental choroidal thickening in young adults.60

Consistent with this, animal studies in tree shrews show that selectively blurring the blue channel while maintaining sharp red and green channels slows axial elongation, supporting a role for chromatic defocus in eye growth regulation.2 However, evidence remains limited to short-term structural changes, and the extent to which CSMD can produce sustained, clinically meaningful myopia control, particularly in children, remains uncertain.

SUMMARY

A large body of evidence supports increased outdoor time as an effective strategy to reduce the risk of myopia onset in children, with part of this benefit likely related to the spectral characteristics of light exposure.

Experimental and clinical studies indicate that eye growth may be influenced by wavelength-dependent visual signals, mediated by chromatic cues such as LCA. While these biological mechanisms are plausible, translation into clinical interventions remains variable.

Approaches involving increased exposure to violet or ultraviolet light show modest and inconsistent benefits, with effects generally limited to specific subgroups and not yet sufficient for routine clinical adoption.

In contrast, RLRL therapy has shown clinically meaningful reductions in myopia progression and axial elongation in short- to medium-term studies, making it one of the most promising emerging interventions. However, its mechanism appears to involve photobiomodulation and choroidal perfusion changes rather than traditional spectral signalling mechanisms, and important safety concerns remain, including the potential for thermal and photochemical retinal effects, dose-related risks, and rebound following discontinuation.

Other long-wavelength approaches, such as amber light, demonstrate similar hyperopia-inducing effects in animal models but lack human clinical evidence.

Short-term studies of blue and cyan light in humans show small, transient reductions in axial length and increases in choroidal thickness, likely mediated by activation of short-wavelength-sensitive pathways including ipRGCs and associated neurobiological signalling. However, these effects are transient and of uncertain clinical relevance for sustained myopia control at this stage.

Emerging strategies, such as CSMD, provide proof-of-concept that chromatic manipulation can influence ocular biometry, but evidence remains limited to short-term experimental settings with unclear long-term efficacy. Overall, although spectral manipulation represents a biologically plausible and rapidly developing area in myopia research, most interventions remain experimental, with evidence largely derived from short-term or preclinical studies.

From a clinical perspective, increasing outdoor exposure remains a robust, evidence-based recommendation, while light-based therapies should be considered adjunctive or investigational. Where RLRL is used, it should be applied cautiously, with careful patient selection, adherence monitoring, and awareness of safety considerations. Importantly, there is a need for large-scale, long-term randomised controlled trials across diverse populations to establish efficacy, optimal dosing protocols, treatment duration, and safety profiles. Until such data are available, clinicians should integrate these emerging approaches within a broader, evidence-based myopia management framework that includes established interventions such as optical and pharmacological therapies, while maintaining a cautious and critical approach to new light-based treatments.

At present, no single wavelength has been definitively established as superior for myopia control in humans; even for RLRL, its effects do not appear to be mediated by conventional chromatic signalling alone. Further well-designed, long-term trials are essential to clarify efficacy, safety, and optimal clinical application of these approaches.

Associate Professor Ranjay Chakraborty BS Optom PhD, completed his optometry degree in India in 2006. After working as an optometrist for three years in India, he joined the PhD program in Vision Science at the Queensland University of Technology, Brisbane. His PhD was one of the first investigations to bridge the work on diurnal rhythms and refractive error development in animal models to human eyes, and was awarded an Outstanding Doctoral Thesis Award. He completed a postdoctoral fellowship at Emory University in Atlanta, in the United States, before joining Flinders University in 2017.

Dr Chakraborty’s areas of research interest are myopia and refractive error development, visual optics, and retinal imaging. He leads the Myopia and Visual Development Lab at Flinders University and his current work is investigating the role of spectral and temporal features of ambient lighting and circadian rhythms in the pathogenesis of myopia. He is currently serving as Deputy Director at the Flinders University Caring Futures Institute.

References available at mivision.com.au.