Glaucoma is a multifactorial optic neuropathy in which intraocular pressure is the principal modifiable risk factor but not the whole of the disease. Three recurring observations in the epidemiology and pharmacology of open-angle glaucoma, each of which has several possible explanations, together motivate a mechanistic question: open-angle glaucoma incidence rises steeply across the presbyopic decades, glaucoma risk is increased in myopia, and the intraocular pressure of some normal-tension eyes falls in response to muscarinic agonists. This review develops, and then critically grades, the hypothesis that these observations are connected by the mechanical role that accommodation may play in the regulation of aqueous dynamics. The proposal, termed accommodative aqueous regulation (AAR), is that the cyclic ciliary-muscle engagement delivered to the anterior segment during ordinary accommodation contributes to the regulation of aqueous humour, principally by conditioning conventional (trabecular) outflow, the accommodative outflow mechanism (AOM), and that its progressive loss at presbyopia is one contributory, refractive-state-dependent factor in the outflow deterioration that predisposes susceptible eyes to glaucoma. The claim is deliberately limited. The mechanism is offered as a threshold-lowering modifier acting in susceptible eyes within a multifactorial disease, not as a necessary or sufficient cause, and the mapping of refractive state onto glaucoma subtype, associating emmetropia with high-tension open-angle disease, hyperopia with angle-closure, and high myopia with the normal-tension phenotype, is presented as a probabilistic tendency rather than a rule that any individual eye must obey. Established physiology is separated from hypothesis at every step. The mechanical coupling of the ciliary muscle to a mechanosensitive outflow apparatus is supported; the central claim, that ordinary accommodative cycling conditions outflow across a lifetime and that its loss contributes to glaucoma, remains untested and is graded as such. We conclude by specifying the experiments that would confirm or refute it.

Myopia has emerged as a major global public health challenge, with the prevalence of myopia among children increasing exponentially over the past two decades. Emerging evidence, however, indicates that delaying the onset of myopia through early intervention during the premyopic stage may be more impactful than attempting to control myopic progression after onset. Central to this prevention strategy is the concept of the hyperopic reserve, the physiological hyperopia present in early childhood that functions as a protective buffer against the development of myopia. This narrative review examines the definition and clinical significance of hyperopic reserve in identifying children at risk for myopia (premyopia), as well as evidence-based intervention strategies aimed at preserving this reserve. The recommended safety threshold for hyperopic reserve is +1.00 D before age 12 years. Recommended strategies include behavioral interventions, such as increasing outdoor time and implementing regular breaks during near work. Long-term monitoring and regular follow-up are crucial for identifying high-risk groups associated with factors such as insufficient outdoor time, prolonged near work (including screen time and cram school attendance), parental myopia, younger age with lower baseline hyperopia reserve, rapid myopia shift >0.5 D/year, and rapid axial length elongation >0.2 mm/year. Pharmacological or optical therapies may be considered for high-risk children. By understanding and maintaining hyperopic reserve during the critical premyopic stage, eye care practitioners can shift the clinical paradigm from myopia control to myopia prevention, thereby potentially reducing both the incidence and severity of myopia in future generations.