Frequently Asked Questions/Myopia/Quotes

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Axial elongation

“The homeostatic control of eye growth functions to keep images sharply focused on the retina. Therefore, if the eye length increases more slowly than does the focal length, the focal plane will be behind the retina, creating hyperopic defocus on the retina. The same occurs if one puts a negative lens over the eye (Figure 2A). To regain sharp focus, the retina needs to be displaced backward to where the image is. This is done in two ways: the eye is lengthened by increasing the rate of growth or of remodeling of the sclera at the posterior pole of the eye Gentle and McBrien 1999 and Nickla et al. 1997, and the retina is pulled back within the eye by the thinning of the choroid, the vascular layer between the retina and sclera ( Figure 2B; Wallman et al. 1995 and Wildsoet and Wallman 1995); once distant images are again focused on the retina (emmetropia), both the rate of ocular elongation and the choroid thickness return to normal.

Ocular Compensation for Lens-Induced Defocus

(A) A positive lens (blue, convex) causes the image to form in front of the retina (myopic defocus), whereas a negative lens (red, concave) pushes the image plane behind the retina (hyperopic defocus). With no lens (black rays), the image of a distant object is focused on the retina.

(B) The eye compensates for positive lenses by slowing its rate of elongation and by thickening the choroid, pushing the retina forward toward the image plane. It compensates for negative lenses by increasing the rate of elongation and thinning the choroid, pulling the retina back toward the image plane. The emmetropic eye is intermediate in length and in choroid thickness.

https://www.sciencedirect.com/science/article/pii/S0896627304004933

Glasses progressing myopia via hyperopic defocus

“This study investigated whether adolescent guinea pigs can develop myopia induced by negative lenses, and whether they can recover from the induced myopia. Forty-nine pigmented guinea pigs (age of 3 weeks) were randomly assigned to 4 groups: 2-week defocus (n = 16), 4-week defocus (n = 9), 2-week control (n = 15) and 4-week control (n = 9). A −4.00 D lens was worn in the defocus groups and a plano lens worn in the control groups monocularly. Refractions in the defocused eyes developed towards myopia rapidly within 2 days of lens wear, followed by a slower development. The defocused eyes were at least 3.00 D more myopic with a greater increase in vitreous length by 0.08 mm compared to the fellow eyes at 14 days (p < 0.05). The estimated choroidal thickness of the defocused eyes decreased rapidly within 2 days of lens wear, followed by a slower decrease over the next 4 days. Relative myopia induced by 4 weeks of negative-lens treatment declined rapidly following lens removal.”

From http://journals.lww.com/optvissci/Abstract/1991/05000/Inducing_Myopia,_Hyperopia,_and_Astigmatism_in.7.aspx

“Spectacle Lens Compensation. The homeostatic control of eye growth functions to keep images sharply focused on the retina. Therefore, if the eye length increases more slowly than does the focal length, the focal plane will be behind the retina, creating hyperopic defocus on the retina. The same occurs if one puts a negative lens over the eye (Figure 2A). To regain sharp focus, the retina needs to be displaced backward to where the image is. This is done in two ways: the eye is lengthened by increasing the rate of growth or of remodeling of the sclera at the posterior pole of the eye Gentle and McBrien 1999 and Nickla et al. 1997, and the retina is pulled back within the eye by the thinning of the choroid, the vascular layer between the retina and sclera ( Figure 2B; Wallman et al. 1995 and Wildsoet and Wallman 1995); once distant images are again focused on the retina (emmetropia), both the rate of ocular elongation and the choroid thickness return to normal.” Ocular Compensation for Lens-Induced Defocus.jpg

From https://www.sciencedirect.com/science/article/pii/S0896627304004933

Pseudomyopia

“Until the past decade or two, the conventional wisdom had been that myopia was principally genetic in origin both because of the higher incidence of myopia among the children of myopic parents and the large differences in myopia prevalence among ethnic groups (Mutti et al., 2002). This view was weakened by the discovery of homeostatic control of refractive error in animals, including primates. This gave credibility to the epidemiological evidence accumulating over decades that visual factors might contribute to myopia in humans. The evidence is of three types. First, there are epidemiological studies in many countries showing an association between the educational level attained and the prevalence of myopia (e.g., Goldschmidt 1968 and Sperduto et al. 1983), ranging from 3% for unskilled laborers to 30% for those with university educations. Second, a high proportion of young adults who do intensive professional studies (medical, law, engineering, or pilot school) become myopic over the few years of study (e.g., Kinge et al. 2000 and Zadnik and Mutti 1987). Third, cultures in which people lead outdoor lives have little myopia (Morgan and Rose, 2004), but when compulsory education and the other attributes of modern Western culture were introduced to Inuit or American Indian villages, there was a 4-fold increase in the incidence of myopia within one generation (Bear, 1991), although it is difficult to dissociate the visual changes from dietary and other changes (Cordain et al., 2002). The thrust of these findings is that education is associated with an increased prevalence of myopia. The risk factor most discussed as the intervening variable is reading, because the nearness of the page presents the eye with hyperopic defocus. Although the accommodation system reduces this hyperopic defocus, it cannot eliminate it, because accommodation is under negative feedback control, with defocus being the error signal that drives the accommodation output. Therefore, it is plausible that continuous hyperopic defocus during reading drives the emmetropization mechanism to correct this apparent refractive error by making the eye myopic.”

Near-Work and Myopia

Frequency distribution of refractive errors in four populations of Israeli students. Boys in religious schools, who do much sustained near-work, have a much higher prevalence of myopia than do girls in religious schools or than either girls or boys in secular schools (replotted from Zylbermann et al., 1993.)

https://www.sciencedirect.com/science/article/pii/S0896627304004933#BIB235

Hereditary factors of myopia

“In populations with little genetic heterogeneity, such as Inuit populations, studies have revealed that within a generation, the incidence of myopia has risen dramatically in line with the onset of formal education and literacy.3 4 In addition to this evidence for an environmental contribution to the aetiology of myopia, there is also abundant evidence for a genetic influence. These contrasting lines of evidence have stimulated the long running “nature versus nurture” debate, although it is now clear that myopia results from the interaction of environmental and genetic factors.5However, the observed increases in myopia over a generation indicate that the modern myopic epidemic is being fuelled by environmental changes. Furthermore, environmental influences are more easily altered than our genetic make up. Understanding how the visual environment can influence eye growth should therefore be central to any attempts to alter the natural history of myopia.”

http://bjo.bmj.com/content/82/3/210.full%C2%A0

Infant myopia

“1. The manifest refractions of 72 children were tracked at regular intervals starting soon after birth and continuing for 9-16 y. Near-retinoscopy, a non-cycloplegic refraction technique, was used for children aged 0-3 y, and non-cycloplegic distance retinoscopy after 3 y. Almost 1400 refractions have been obtained from this group. 2. During the first 6 months the mean spherical equivalent of the group is negative by a small amount. By one year of age the children have an average of 0.5 D of hyperopia which they maintain until 8 y. After 11 y the mean spherical equivalent once again becomes negative, largely because some of the children are becoming myopic. 3. The dispersion of refractions is largest shortly after birth and smallest at 6 y, reflecting the process of emmetropization during the preschool years. 4. The spherical equivalent at 1 y is most predictive of later spherical equivalents. Correlations of spherical equivalent at 1 y with other ages range from 0.43 during the period of emmetropization to 0.76 at some later ages. 5. Children with a negative spherical equivalent in infancy in conjunction with either against-the-rule astigmatism or no astigmatism are more likely to be myopic at school age than children with infantile with-the-rule astigmatism. 6. There is an increased incidence of myopia in children with two (compared to zero or one) myopic parents.”

https://www.sciencedirect.com/science/article/pii/S0896627304004933

Form deprivation

“Form-Deprivation Myopia. If, instead of being defocused by lenses, the images on the retina are obscured by diffusers or lid suture, eyes elongate and form-deprivation myopia results in all species studied (for example, tree shrew, Sherman et al., 1977; marmoset, Troilo and Judge, 1993; chick, Wallman et al., 1978; rhesus macaque, Wiesel and Raviola, 1977; mice, Schaeffel et al., 2004). Because no images are brought into focus by the excessive ocular elongation, it continues as long as vision is obscured, resulting in eyes whose vitreous chambers are as much as 25% longer than normal (Wallman and Adams, 1987). This dramatic response, conserved widely across taxa, implies that image quality is normally involved in restraining eye growth. When the diffusers are removed, causing the visual system to experience myopic defocus, the choroid thickens, the rate of ocular elongation slows, and the refractions return to normal.”

https://www.sciencedirect.com/science/article/pii/S0896627304004933