Myopia prevalence has risen sharply across all demographics. In the United States, recent estimates show that roughly 40 to 45% of the population is myopic, nearly double the prevalence reported a few decades ago.1 Additionally, in parts of East and Southeast Asia, prevalence among young adults exceeds 80 to 90%, suggesting profound environmental and educational influences.2
By 2050, projections estimate that 50% of the world’s population will be myopic, with nearly 1 billion individuals expected to develop high myopia (≥ –5.00D).3 Importantly, the age of onset has continued to drop, and earlier onset correlates strongly with a higher lifetime risk of reaching high myopia.4
Even small increases in axial length matter. Each 1mm increase is associated with exponential increases in the risk of retinal detachment, myopic maculopathy, and open-angle glaucoma.5 Consequently, understanding the mechanisms that drive axial elongation is crucial for clinical decision-making.
Drivers of myopia onset and progression
Myopia progression is multifactorial, with overlapping influences that vary widely between patients. Genetic predisposition, visual environment, accommodative behavior, and retinal signaling each contribute differently to axial elongation. The effects of each often compound one another rather than acting alone.
This complexity explains why children with similar refractive errors may follow very different trajectories, reinforcing the need for individualized monitoring and early, tailored intervention.
Genetic predisposition
Children with one myopic parent have a two- to threefold increased risk of developing myopia, while in children with two myopic parents, the risk increases five to sixfold.6 However, genetics alone cannot account for the rapid rise in global prevalence, suggesting a strong environmental impact.
Near work and visual behavior
Intensive near work driven by academic load, reading habits, and prolonged device use is consistently associated with higher myopia prevalence. Furthermore, visual behaviors such as sustained accommodation, short working distances, and infrequent breaks can generate hyperopic retinal defocus during near tasks, stimulating axial elongation.
Notably, the odds of developing myopia increase by roughly 2% for every additional diopter-hour of near work performed per week, underscoring a clear dose–response relationship.7
Outdoor time
Multiple cohort studies demonstrate that daily outdoor time has a protective effect on myopia onset but a modest effect on myopia progression.8.9,10 Bright light stimulates dopamine release in the retina, inhibiting axial elongation. Less outdoor time correlates with reduced dopamine signaling and greater risk of progression.
Consequently, the current recommendation for outdoor time is at least 2 hours per day. These factors interact with biological pathways that regulate ocular growth, shaping the trajectory for each patient.
To learn more about identifying and treating patients at high risk of myopia progression, check out Understanding Myopia Risk Factors!
Biological mechanisms: How and why myopia develops and worsens
Multiple biological and optical mechanisms contribute to myopia progression, each offering insight into how the eye interprets visual signals and regulates growth.
Peripheral hyperopic defocus
One of the strongest and most consistent findings is that peripheral retinal hyperopic defocus is a potent signal for axial elongation. When central vision is corrected but peripheral light focuses behind the retina, the eye responds by lengthening to bring the peripheral image forward.11,12
This mechanism underlies many modern optical interventions, including:
- Dual-focus and multifocal soft lenses
- Orthokeratology
- Myopia control spectacles
Accommodative lag
Accommodative lag during sustained near work leads to central hyperopic blur, generating a growth signal similar to peripheral defocus. Some studies have shown that children with significant lag exhibit faster myopia progression.13,14
Despite these findings, the recent International Myopia Institute (IMI) report on Accommodation and Binocular Vision in Myopia Development and Progression concluded that “current evidence does not point toward a role for accommodation or binocular vision in myopia development and progression.”15
While these findings suggest that accommodative behavior may influence progression in some children, the overall body of research is too variable and inconclusive to confirm a definitive link.
Choroidal thickness changes
The choroid is now recognized as a key biomarker of both short-term and long-term ocular growth, reflecting highly dynamic structural and vascular responses to visual input.
Choroidal thinning correlates with axial elongation, while choroidal thickening, driven in part by increased choroidal blood flow and vascular engorgement, is consistently observed when the eye is exposed to myopic defocus, such as during orthokeratology or multifocal lens wear.
These rapid, perfusion-linked thickness changes can be noted before measurable shifts in axial length, offering clinicians a real-time indicator of treatment effect and early responsiveness.16
Figure 1: Comparison of choroidal thickness based on degree of myopia; the top image is of a normal patient and the bottom image is of a patient with high myopia.
Figure 1:Choroidal thickness in normal vs high myopic eye©Courtesy of Habibah Setyawati Muhiddin et al. Image cropped and used under CC BY 4.0.
For a deep dive into how choroidal thickness impacts myopia, read The Role of Choroidal Thickness in Myopia Development and Progression!
Scleral remodeling
Scleral remodeling is a fundamental mechanism behind axial elongation. Hyperopic defocus initiates retinal and choroidal signaling that alters the scleral extracellular matrix, reducing collagen content, increasing MMP activity, and lowering biomechanical stiffness.
These changes make the sclera more extensible and the eye more prone to elongation, particularly in childhood when the tissue is highly plastic.17 This pathway underscores why earlier intervention can more effectively modify growth.
Biological mechanisms of progression: Clinical relevance
Together, these mechanisms paint a consistent picture: myopia progression arises from retinal signaling pathways responding to hyperopic blur (central, peripheral, or both), with the choroid acting as a dynamic intermediary and early biomarker of these signals, ultimately triggering biochemical remodeling of the sclera and continued axial elongation.
From a clinical standpoint:
- Peripheral retinal defocus is not a theoretical concept. It directly informs the optics of almost every control strategy we prescribe.
- Although accommodation and binocular vision findings can guide clinical management, current evidence does not support these factors as primary drivers of myopia development or progression.
- The choroid is considered a functional marker of treatment direction, not just an anatomic structure.
- Axial length is the most sensitive measure of disease activity, providing insights that refraction alone cannot capture.18
Clinical insights into why early myopia treatment matters
- Earlier onset drives higher final myopia. Children who become myopic at a younger age progress faster and for a longer period of time.4
- The eye is most modifiable early. Younger scleral tissue responds more strongly to optical and pharmacologic treatments.
- Progression accumulates silently. Axial elongation rarely slows without active intervention.
- Retinal risk rises with every diopter. Even low myopia increases lifelong risk of maculopathy and other pathologies.19
Collectively, these realities create a clear clinical mandate: intervene early, monitor axial length closely, and adjust treatment proactively.
Overview of available myopia control options
A comprehensive treatment offering may include:
- Orthokeratology: Reshapes the cornea overnight to create peripheral myopic defocus during waking hours.
- Dual-focus / Multifocal soft lenses: Provide clear central vision while simultaneously delivering peripheral myopic defocus.
- Myopia-control spectacles: Employ structured optical designs intended to modify peripheral focus.
- Low-dose atropine: Dose-dependent slowing of axial elongation through biochemical modulation of ocular growth.
- Lifestyle measures: Increased outdoor time and healthier near-work behavior support overall risk reduction.
Key takeaways for clinicians
- Myopia is a chronic, progressive disease driven primarily by axial elongation not simply refractive error.
- Several well-established visual and structural signals, ranging from optical defocus to choroidal responses, play central roles in regulating axial elongation.
- Age of onset is one of the strongest predictors of lifetime severity. Early intervention is essential.
- Axial length measurement and choroidal imaging provide critical insight into disease activity and treatment response.
- Multiple evidence-based treatment modalities exist; therapy should be individualized based on age, progression rate, and risk profile.
- Ongoing monitoring and willingness to escalate treatment improve long-term outcomes.
