Myopia, or nearsightedness, is an epidemic, with up to 90% of the population in some urbanized countries affected. Efforts have increased to understand the regulatory mechanisms underlying myopic eye growth due to the potentially blinding complications and socio-economic health problems associated with myopia. The choroid, a dynamic vascular structure posterior to the retina, has been implicated in eye growth control. Our long term goal is to elucidate the role of the choroid in myopia progression and treatment. Our central hypothesis is that the choroid is locally regulated by optical factors and visual input to influence thickness, modulate the position of the retina, and compensate for defocus in children. Evidence from animal studies suggests that diurnal patterns of choroidal thickness, which can be influenced by light exposure, are altered in myopic eye growth. Animal studies have also shown that narrow band long wavelength light (i.e. ?red?) thickens the choroid and ultimately prevents myopic axial elongation. However, potential effects of narrow band light have not been tested in humans. In adults, recent studies have shown that imposed full field spectacle lens defocus modulates choroidal thickness in a bidirectional manner. The observed choroidal changes to myopic and hyperopic blur may contribute to treatment effects from currently used optical strategies to slow myopia progression in children. Here, we will examine the choroid in children to understand how circadian rhythm, light exposure, and defocus modulate choroidal thickness through the following specific aims: 1) we will investigate the influence of light exposure and refractive error on diurnal patterns of choroidal thickness and relationships with other known light-dependent ocular and systemic diurnal processes in non- myopic and myopic children, including intraocular pressure, heart rate, and systemic melatonin concentration, 2) we will determine the operational range, dose-response relationship, sensitive period, and time-of-day effects of the choroid to imposed full field myopic and hyperopic defocus, as well as changes in choroidal thickness induced by peripheral myopic defocus, using soft multifocal contact lenses similar to those currently utilized for myopia control, and 3) we will determine the capacity to which narrow band long wavelength light drives choroidal thickness changes in humans, as demonstrated in animal models, and determine whether changes are dependent on defocus mechanisms induced by longitudinal chromatic aberrations. These finding will be significant because the proposed studies will fill a critical void in our understanding of the role of visual input on choroidal modulation in children, shed light on mechanisms underlying optical treatment strategies for myopia control, and aid in the development of novel myopia treatment options. The research is innovative because findings will contribute to the development of targeted treatment options to prevent myopia and slow progression.
Myopia is an epidemic, with up to 90% of the population in some urbanized countries affected, bringing with it potentially blinding complications and significant socio-economic burden. Our proposed studies aim to understand the role of visual input and circadian rhythm on the choroid, a regulator of scleral growth, in children. Findings will contribute our understanding of mechanisms involved in myopia control and to the development of targeted treatment options to prevent myopia and slow progression in children.
