Reclassifying Myopia From Refractive Error to Chronic Disease

The child is eight years old. Her subjective refraction sits at -0.50DS, her axial length is running well ahead of the growth curves, and neither parent wears spectacles.

I explain to the parents that this is the opening phase of a progressive biological condition. I begin walking them through our modern myopia control options: atropine, orthokeratology, myopia control in either daily disposable contact lenses or spectacles.

I discuss behavioural habits, including the importance of adequate outdoor time, keeping the language simple enough that the parents stay with me through the whole explanation.

But the numbers are sprinting before me. Each additional dioptre of myopia carries a 67% increase in the lifetime risk of myopic maculopathy.¹ I visualise what her posterior pole might look like when she is 30, 50, and 60 years old.

The parents listen intently. They look down at the mild prescription, look back up at me and tell me, completely reasonably, that it simply “doesn’t seem that bad”. They say they will take the information home and think about it.

I know what happens next. The moment they leave, my clinical advice competes with everything else they will hear. Friends, grandparents, or the family GP will say “it’s just a pair of glasses”. In that context, my voice can sound like overreaction.

This conversation plays out every day in consulting rooms across Australia.

The landscape of myopia management has been transformed over the past decade. What was research-grade theory now sits routinely in clinical practice. The evidence for intervention is substantial. The treatments are effective. What is missing is a public health message.

That communication gap will not close on its own. Industry has done its part with innovations that make modern management possible. But this is not a commercial question. It is a professional obligation, led by the practitioners who deal with the long-term complications of high myopia in their chairs every week.

Every primary care practitioner should view a surging axial length or an early-onset myopic refraction in a young child as a clinical red flag, the same way we respond to an intraocular pressure (IOP) above 22 mmHg.

Why the Biology Matters

Myopia is not just optics. It is a structural disease process. Excessive axial elongation is a progressive change in the posterior segment, consistent with early pathological progression.

The sequence is documented in current research.² The choroid thins first. The sclera then undergoes matrix remodelling, thinning behind it. The eventual consequences are increased risk of pathologies we manage in our older patients: myopic maculopathy, retinal detachment, cataracts, and glaucoma.

The relationship is steep. A 2025 cohort of 282,810 patients confirmed that retinal disease risk climbs exponentially with each dioptre of myopia.3 Blinding complications arrive earlier.

Refractive state is the downstream consequence of those underlying changes, not their cause. By the time we measure the dioptric shift, the biology has already moved.

What we currently label the ‘pre-myope’ is the clearest demonstration that our traditional system has reached its limit. Picture a six-year-old with 6/6 uncorrected acuity, a subjective refraction of +0.50DS, but a heavy family history of high myopia. Through a predominantly refraction-based model of care, she appears healthy. Her parents are reassured, and she is asked to return in 12 months.

The structural biomarkers consistent with early elongation are never measured. Current practice does not require them. She is invisible to us, not because the trajectory is hidden, but because we have not been asked to look for it. Delaying onset by even one year may yield greater lifetime benefit than years of subsequent progression control.⁴ This is the highest-leverage window we have, and the framework that defines myopia by refraction is structurally blind to it.

Measurement has changed what we can know. Optical biometry, axial length percentile tracking, and, increasingly, choroidal thickness assessment have made paediatric risk prediction more accessible than it once was. The clinical evidence has caught up.

The classification has not.

Every primary care practitioner should view a surging axial length or an early-onset myopic refraction in a young child as a clinical red flag, the same way we respond to an intraocular pressure (IOP) above 22 mmHg.

A Framework That No Longer Fits

Our administrative and clinical frameworks in Australia still position myopia as a refractive error. The label is technically accurate at an optical level, but the wrong description of what is happening in that child’s globe.

Our clinical literature recognises disease at the worst-case end. We use terms like pathologic myopia, degenerative myopia, or high myopia with macular complications. By the time an adult patient arrives in an ophthalmologist’s chair, the chorioretinal atrophy, posterior staphyloma, and choroidal neovascularisation (CNV) are established.

Progressive axial elongation in childhood has no equivalent disease terminology. We call it myopia, the same word we used before we understood what was happening underneath.

This mismatch shapes every encounter around the child. General practitioners, paediatricians, school nurses, and even eye care practitioners operate from the same refractive model. The parent arrives in our chair with a settled belief that the issue is not urgent. Nothing in the chain has told them otherwise.

Ophthalmology has long managed the end-stage consequences of myopia. The challenge now is aligning earlier optometric and primary care action with that end-stage burden.

The Global Case for Classification

Over the past decade, significant efforts have laid the foundation for treating myopia as a health priority and for classifying it as a disease: The World Health Organization (WHO) / Brien Holden Sydney meeting in 2015.⁵ The International Myopia Institute’s classification standards in 2019.⁶ The American Academy of Ophthalmology’s cross-disciplinary task force the same year, with the Academies of Optometry, Family Physicians, and Pediatrics as founding partners.⁷ Successive International Agency for the Prevention of Blindness (IAPB) summits have convened international stakeholders.⁸

The first explicit call for disease classification came from the US National Academies of Sciences, Engineering, and Medicine (NASEM). In September 2024, NASEM published its report. Recommendation 8-5 reads in plain English:

“Myopia should be classified as a disease and therefore a medical diagnosis.”⁹

This was reinforced in early 2025 by the Singapore International Myopia Summit statement.10 Forty global experts agreed on three priorities: redefining myopia as a progressive disease with clinical stages, preventing progression to high myopia, and preventing and treating pathologic myopia.

The scientific argument has been building for a decade. The administrative reality has not.

Most children with progressing myopia will live full visual lives with appropriate management. But there is no safe threshold of myopia.

Addressing the Pushback

Is it overreach to equate risk with disease? Critics argue that just as ocular hypertension (OHT) is not glaucoma, a risk factor should not be classified as a disease. The starting point is fair. How we treat OHT supports the disease framing, even if the terminology is a separate question. OHT is classified as a risk factor because the optic nerve is intact when IOP is elevated. Excessive axial elongation is different. The structural change is happening as we measure it. The dioptric shift is the lagging indicator, not the disease itself. What OHT shows is that risk-based action is established within our discipline. We risk-stratify, monitor, and treat high-risk OHT patients prophylactically.¹¹ We do not dismiss OHT because some patients never progress. The progressing myope warrants the same proactive posture. Monitoring a refractive error means watching the prescription. Monitoring a chronic disease means tracking the trajectory.

The prediction horizon is too long. Connecting an eight-year-old’s current biometry to retinal pathology at 60 is the kind of timeframe paediatric medicine routinely accepts. Paediatric hypertension, type 1 diabetes, and childhood obesity all rely on probabilistic claims about outcomes far into adulthood. A documented trajectory of biological risk is a legitimate basis for disease status, especially when childhood is the only time we can intervene.

The risk of over-medicalisation. There is an understandable fear of turning a manageable optical condition into a lifelong medical label. Most children with progressing myopia will live full visual lives with appropriate management. But there is no safe threshold of myopia.¹² Even moderate levels increase lifetime risk of vision-threatening complications. Refusing to classify is also a choice; the one that produced the prevalence curve we now see. A framework recognising that one in two children worldwide will be myopic by 2050 is not over-medicalisation.¹³ It is overdue recognition.

The pattern is familiar from other chronic conditions. Hypertension was once understood as an elevated measurement, not a disease. That reframe took decades and the policy and clinical consequences followed.14 Myopia sits at a similar inflection point.

What Reclassification Changes

Disease classification is the frame around the chair conversation, not equivalent to it. The clinician still calibrates language to the parent in front of them. What changes is the world it enters when it leaves the chair.

Beyond our consulting room doors, general practitioners and paediatricians gain a standardised framework that places progressive myopia alongside other paediatric conditions they screen for, like asthma. We are not asking them to install biometers. We are asking them to recognise excessive axial elongation as a true disease process, and to support its investigation and management. Referral pathways become coordinated rather than accidental.

Disease classification makes the costs visible. Myopia currently carries a low disability weight in global burden calculations, which means it is systematically undercounted in the systems that allocate health resources.¹⁰ Right now, no one tracks the lifetime cost of what myopia produces. The complications get counted. The disease that caused them does not. When a 30-year-old loses central vision to myopic CNV, that cost sits in a hospital surgical budget, never linked back to a childhood myopia spend line 20 years earlier. Reclassification links those costs. Cost-benefit studies and public health priority setting follow.

Myopia currently carries a low disability weight in global burden calculations, which means it is systematically undercounted in the systems that allocate health resources.

Where We Start

There is a broader language change to make. The word ‘myopia’ is burdened by its refractive history, constantly dragging instinct back toward optical correction with a piece of glass.

‘Pre-myopia’ is the clearest example. It is a hedge term that admits the structural disease process is active in a child whose refraction does not yet read as myopic. However, it fails to communicate that danger to parents because it reassures them the structural changes have not begun. Our task is to upgrade what the word ‘myopia’ means to the public and the broader healthcare community.

We do not need to wait for institutional updates or government policy. The clinical action begins with how we describe what we see. The framing is the intervention.

When I was seeing patients, I changed how I described what I saw. I talked about the eye, not the refraction. The biometry, the elongation, the trajectory, the years we could still influence. Many minds changed. Many stayed the same. And where they changed, they changed because I had the time, the equipment, and the deep reading to bring them with me. That effort builds the demand and the data the system responds to.

We need more than individual passion to drive change beyond our consulting rooms. We must carry this framing into how we educate our peers, new and old, how we write about eye care for our communities, how we describe what we do to GPs and paediatricians. Position statements from peak professional bodies will follow once the profession itself speaks with one voice. By unifying our clinical language, across optometry and ophthalmology, we build the change from the chair up.

The clinical method is risk stratification – family history, age of onset, ethnicity, progression rate, outdoor time, biomarkers where available. The disease label is what makes this method fundable, teachable, and systemic.

It is time to call myopia what it is: a chronic, progressive disease.

The eight-year-old we met at the start is still in the chair. Her axial length is still running ahead of the curve. Her refraction is still mild. I tell the parents she is at the early phase of a disease we now know how to slow. I pace them through the same options I would today. They listen. They want to take the information home. They want to think about it. But when they get home, the GP says the same thing. The grandparents have read about it. The ‘thinking about it’ is now stepping through, not stepping around. Reclassification simply puts the chair conversation inside a system that needs to hear it.

John Nguyen BOptom is an optometrist and founder of Zoom Optics in Sydney. He works at the intersection of clinical care and health innovation, with collaborative models that improve early detection of preventable eye diseases and reduce avoidable vision loss. He is committed to developing practical, community-based approaches that expand access to timely eye care.

References

1. Bullimore MA, Brennan NA. Myopia control: why each diopter matters. Optom Vis Sci. 2019;96(6):463-465. doi: 10.1097/OPX.0000000000001367.
2. Ostrin LA, Harb E, Wildsoet CF, et al. IMI – The dynamic choroid: new insights, challenges, and potential significance for human myopia. Invest Ophthalmol Vis Sci. 2023;64(6):4. doi: 10.1167/iovs.64.6.4.
3. Arnal L, Mesfin Y, Ludwig CA, et al. Beyond refractive error: myopia’s exponential burden on retinal health with each diopter. Int J Retina Vitreous. 2025;11:64. doi: 10.1186/s40942-025-00745-7.
4. Tahhan N, Bullimore MA, Flitcroft I et al. IMI – 2025 Digest. Invest Ophthalmol Vis Sci. 2025;66(12):27. doi: 10.1167/iovs.66.12.27.
5. World Health Organization. The impact of myopia and high myopia: report of the Joint World Health Organization-Brien Holden Vision Institute Global Scientific Meeting on Myopia, University of New South Wales, Sydney, Australia, 16–18 March 2015. Geneva: World Health Organization; 2017. ISBN 978-92-4-151119-3. Available at: myopiainstitute.org/wp-content/uploads/2020/10/Myopia_report_020517.pdf [accessed June 2026].
6. Flitcroft DI, He M, Yannuzzi L, et al. IMI – Defining and classifying myopia: A proposed set of standards for clinical and epidemiologic studies. Invest Ophthalmol Vis Sci. 2019;60(3):M20-M30. doi: 10.1167/iovs.18-25957.
7. Modjtahedi BS, Abbott RL, Tan D, et al; for the Task Force on Myopia. Reducing the global burden of myopia by delaying the onset of myopia and reducing myopic progression in children: the Academy’s Task Force on Myopia. Ophthalmology. 2021;128(6):816-826. doi: 10.1016/j.ophtha.2020.10.040.
8. Pan W, Morgan I, Weizhong L, et al. The need to address the myopia pandemic: summary report of the global myopia public health summit 2024. Glob Health Res Policy. 2025;10(1):45. doi: 10.1186/s41256-025-00445-7.
9. National Academies of Sciences, Engineering, and Medicine. Myopia: Causes, prevention, and treatment of an increasingly common disease. Washington, DC: The National Academies Press; 2024. doi: 10.17226/27734.
10. Eppenberger LS, Davis A, Qu J; International Myopia Summit Workgroup; Ang M; Key strategies to reduce the global burden of myopia: consensus from the International Myopia Summit. Br J Ophthalmol. 2025;109(5):bjo-2024-326643. doi: 10.1136/bjo-2024-326643.
11. Kass MA, Heuer DK, Gordon MO, et al; Ocular Hypertension Treatment Study Group. Assessment of cumulative incidence and severity of primary open-angle glaucoma among participants in the Ocular Hypertension Treatment Study after 20 years of follow-up. JAMA Ophthalmol. 2021;139(5):558-566. doi: 10.1001/jamaophthalmol.2021.0341.
12. Flitcroft DI. The complex interactions of retinal, optical and environmental factors in myopia aetiology. Prog Retin Eye Res. 2012;31(6):622-660. doi: 10.1016/j.preteyeres.2012.06.004.
13. Holden BA, Fricke TR, Resnikoff S, et al. Global prevalence of myopia and high myopia and temporal trends from 2000 through 2050. Ophthalmology. 2016;123(5):1036-1042. doi: 10.1016/j.ophtha.2016.01.006.
14. Kotchen TA. Historical trends and milestones in hypertension research: a model of the process of translational research. Hypertension. 2011;58(4):522-538. doi: 10.1161/HYPERTENSIONAHA.111.177766.