Modern myopia treatments, such as optical and pharmaceutical interventions, have slowed the condition via structural remodelling of the axial-growth process, which may modify the consequences of axial elongation by slowing progression.1 That said, the effect of these treatments can plateau.2 However, recent research reveals that restoring the dopamine-melatonin axis could enhance the effect of these treatments.3-8 This article will define the dopamine-melatonin axis, what disrupts it, and how it can be restored.
The Dopamine-Melatonin Axis
The dopamine-melatonin axis operates via neurochemical modulation, shaping the temporal and neurochemical environment that drives axial growth. Specifically, this axis links daytime outdoor light with retinal dopamine, and nighttime darkness and sleep with melatonin.4,7
Retinal dopamine acts as a “stop signal” to axial elongation, helping to maintain emmetropization.3,4 According to the literature, light stimulates retinal dopamine release, whereas darkness and sleep regulate melatonin. Disruption here (eg, poor sleep or low light) creates the initial “growth” signal. This signal eventually reaches the scleral fibroblasts, activating dopamine receptors to inhibit extracellular matrix degradation (stopping the scleral thinning process), rather than strictly inhibiting collagen “growth.”
Melatonin secretion helps to align ocular tissues with circadian growth rhythms and guides scleral remodelling.7,8 Scleral remodelling can help prevent myopia development.2,5 There may be a dual-protective mechanism: In the daytime, dopamine acts as the inhibitor of elongation in response to bright light, whereas at night, melatonin appears to be protective as well, because lower output and delayed timing are associated with myopia.
What Disrupts It
Excessive evening screen exposure introduces blue light, which suppresses melatonin, delays sleep, and desynchronizes circadian rhythms, amplifying susceptibility to myopia onset.7-10 Over time, this process can accelerate the condition’s progression in children who have irregular sleep schedules and prolonged digital exposure.11-12
How It Can Be Restored
Optometrists can prescribe the following behaviors in patients to restore the dopamine-melatonin axis and, thus, complement optical and pharmaceutical interventions:
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Ceasing screen use 60 to 90 minutes before sleep to prevent melatonin suppression and cognitive arousal.
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Optimizing sleep darkness using blackout curtains or eye masks to ensure total darkness, which supports robust melatonin secretion.
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Maintaining consistent wake/sleep times on weekends to avoid “social jetlag,” which is linked to increased myopia risk.
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Taking outdoor recess or breaks to spike daytime dopamine levels, acting as the counterbalance to nighttime rest.
These behaviors are all low-cost, high-impact targets for intervention. Additionally, they are not just “good habits,” they are biological levers that modulate the growth environment of the eye.
A Treatment Evolution?
Restoring the dopamine-melatonin axis may represent an evolution in myopia care from reacting to progression to shaping the biological environment that drives it. OM
References
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Hussain A, Gopalakrishnan A, Scott H, et al. Associations between systemic melatonin and human myopia: a systematic review. Ophthalmic Physiol Opt. 2023;43(6):1478-1490. doi:10.1111/opo.13214
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He M, Xiang F, Zeng Y, et al. Effect of time spent outdoors at school on the development of myopia among children in China: a randomized clinical trial. JAMA. 2015;314(11):1142-1148. doi:10.1001/jama.2015.10803
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Xu S, Zong Z, Zhu Y, et al. Association between sleep-wake schedules and myopia among Chinese school-aged children and adolescents: a cross-sectional study. BMC Public Health. 2023;23(1):135:1-8.
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Liu S, Zhou X, Zhao J. How sleep disturbance promotes myopia: a perspective on potential biological mechanisms. Exp Eye Res. 2025;261:110645. doi:10.1016/j.exer.2025.110645


