National Academies Press: OpenBook

Myopia: Prevalence and Progression (1989)

Chapter: Appendix D: The Etiology of Myopia

« Previous: Appendix C: Review of the Progression Literature
Suggested Citation:"Appendix D: The Etiology of Myopia." National Research Council. 1989. Myopia: Prevalence and Progression. Washington, DC: The National Academies Press. doi: 10.17226/1420.
Page 89
Suggested Citation:"Appendix D: The Etiology of Myopia." National Research Council. 1989. Myopia: Prevalence and Progression. Washington, DC: The National Academies Press. doi: 10.17226/1420.
Page 90
Suggested Citation:"Appendix D: The Etiology of Myopia." National Research Council. 1989. Myopia: Prevalence and Progression. Washington, DC: The National Academies Press. doi: 10.17226/1420.
Page 91
Suggested Citation:"Appendix D: The Etiology of Myopia." National Research Council. 1989. Myopia: Prevalence and Progression. Washington, DC: The National Academies Press. doi: 10.17226/1420.
Page 92

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Appendix D The Etiology of Myopia Although our review was not directed toward studies specifically addressing etiology or the evaluation of etiological theories, it ~ difficult to avoid their consideration: not only are such theories proposed by many of the authors whose articles were reviewed, but they also provide a structure within which to organize the many observations encountered. Moreover, etiological theories have important implications both for future research and for clinical management. Thus, while a rigorous review of etiological theories is beyond the scope of this report, we mention the more prominent theories and how they refer to observed prevalence patterns. The use of myopia prevalence data to address etiology has two serious limitations. First, etiology is concerned with the development of a condition and is most directly addressed by incidence rates in longitudinal studies. Prevalence, which measures the proportion of people who are myopic at a given time, is affected not only by the incidence (development) of myopia experienced by a population, but also by persistence of the condition and longevity of individual with myopia. Furthermore, when there is an observed relationship of myopia prevalence with other subject characteristics (risk factors), it is not always possible to determine which preceded the other. Thus, prevalence data must be interpreted with special caution. Second, since an individual's refraction results from the combination of several ocular components, an understanding of the variation and coordination of these components ~ essential to an understanding of myopia etiology. Articles concerning both incidence and ocular components are mentioned in relation to etiological theories but neither has been systematically reviewed for this appendix. TYPES O1? MYOPIA It is a widespread view that myopia is not a single condition but several different etiological and possibly physiological entities. There is, however, no clear agreement about what distinctions should be made and how the different types of myopias would best be defined and recognized. Many of the distinctions in effect separate the more severe from the less severe myopias. This distinction may be made in terms of refractive error (severe versus mild myopia) or the presence of axial elongation outside the range found in emmetropes ("axial" versus "correlational myopias). An early argument that the severe myopias represent a separate entity from the milder myopias was based on the observation of the skewed shape of the refraction curve. It had been observed that the refraction 89

go curve becomes essentially symmetrical when the more severe myopes, or individuals with other pathological ocular changes, are removed from the population suggesting that these individuals represent a separate population. This argument is supported by the observation that severe myopia has different patterns of Retribution than mild and moderate myopia. Severe myopia is more likely to be asac~ciated with ~ ~rarint.v Of nt.h`?r nr~hl~mo Allah ac' ~e ~· ~, e ~ ~ ~ ^ ¢ ^ ~ ~, ~ _ ~ prematurity, ~ntect~ous disease, etc., and seems likely to appear at a much earlier age than the milder forms. Goldechmidt (1968) noted that, unlike myopia in general, severe myopia appears to be equally prevalent in all occupational categories and appears to have decreased in prevalence from the 1880e to the 1960e in Denmark. Goldschmidt suggested a negative error of 6 to 9 D. as the limits of the range of severe myopia. Sorsby et al. (1957) proposed that failure in the correlation of the optical components resulting in correlational myopia should be considered an aberration of emmetropia. They further porposed that, although the view that myopia is due to an abnormally long eyeball is valid, this validity is limited to refractive errors outside the range of those caused by faulty correlation of normal optical components. More modern statistical analyses suggest axial length is equally well correlated at all refractive errors (Gernet, 1964~. In summary, despite differences in views as to what particular distinction should be made, there appears to be general agreement that very severe myopia represents a separate entity from low and moderate myopia. Goldschmidt (1968) also suggested that a Extinction should be made between myopia developing during school ye are and stabilizing in the third decade and myopia that is seen in specific occupations, appears to develop at a later age, and does not stabilize but rather continues to progress with continued work in that occupation (i.e. childhood- versus adult-onset myopia). GENETIC COMPON1:NT OF ETIOLOGY The few genetic studies that were included in the articles summarized suggest a genetic component to the etiology of myopia, although no specific mode of inheritance was specified. Goldschmidt (1968), after reviewing the literature and presenting his own data, concluded that mild myopia is probably polygenic, while the severe myopias represent a heterogeneous group, some types of which may follow a monogenic mode of inheritance. The report of an association of myopia with consanguinity also suggests a genetic role in the etiology of myopia. The observation of racial differences in myopia prevalence may be due to genetic differences but may also be due to cultural differences. A continued high rate of myopia upon migration, ~ with the Asian groups in Hawaii, supports a genetic role, although cultural differences in ethnically defined subpopulations are certainly possible. However, it is ~difflcult to explain observed trends in myopia, such as those believed to have occurred among the Eskimos and American Indians bv Dc~tl~l~tin~ mirier a~net.i~ ,~l~an-~o Ever c,''^L a short period of time. it. . . . . . . - ~ ~-O ~---~- ~o-~^--~ ~- ~ ~-COMA ~ he Important point, however, is that genetic and environmental etiologies are not mutually exclusive- a point that does not appear to have been appreciated by many early authors, who refute one by providing evidence supporting the other. Whereas understanding the genetic role in the etiology of myopia is of interest, it may be of more practical importance to pursue an understanding of the environmental causes of myopia and their relative importance in various populations and to identify possible means of intervention.

91 ENVIllONMl:NTAI THEORI1:S O1? MYOPIA ETIOLOGY Near Work The near-work theory postulates that myopia is caused by certain near visual activities, including reading. Evidence consistent with this hypothesis includes high rates in cultural groups with high literacy; an association of myopia with educational level, amount of time spent reading, and near work; and reports linking increased myopia with the introduction of schools into a population. Those disagreeing with the near-work hypothesis suggest that myopes tend to read more than nonmyopes because of their myopia, giving rise to the observed association (see, for example, Ashton, 1985~. Studies claiming to refute this explanation show that myopic children tended to be readers before their myopia developed, presumably establishing the directionality of the association. There is an unstated assumption in this argument, however, which is that future myopes are refractively the same as future nonmyopes. This assumption is contradicted by longitudinal studies. For example, Hirsch (1964b) followed 383 children and observed that refraction at age 14 was in part predicted by refraction at age 6. Sato (1957) proposes that the mechanism by which near work causes myopia is through accommodation i.e., the contraction of the ciliary muscle during reading leading to an organic chance in and increased refractive power of, the crystalline lens. Such a mechanism ~ ~ , , ~ . ~ ~ 1 ~ ~ ~ ~ _ ~ 1 ~ 1 - ~ _ AL _ L Lt _ ~ ~ ~ L _. _ has been used by some authors to account tor reports suggesting tnat one use of negative lenses for the correction of myopia leads to progression (Angle and Wissmann, 1980b; Sato, 1957) and the use of reading lenses leads to regression (Rasmussen, 1954~. A related theory of myopia etiology was proposed by Young (1967), who, citing stud- ies on primates, suggested that myopia may result from near environmental conditions. According to these studies, animals raised in laboratories developed more myopia than ani- mals raised in open field situations. Young also proposed accommodation as the mechanism through which these changes occur, citing studies in which accommodation was immobilized and increases in myopia did not occur. Increase in myopia among submariners, if confirmed, would also be consistent with what might be termed a "close environments theory. Psychological Stress Van Alphen (1961, 1967) theorized that emmetropization proceeds through a feedback process involving the effect of parasympathetic activity on ciliary muscle tonus, which in turn limits the stretch of the sclera by counteracting the effect on the sclera of the intraocular pressure. Specifically, normal emmetropization of the initially hyperopic eye proceeds by a release of parasympathetic tone by higher centers, leading to a decrease in tone in the ciliary muscles, allowing the eye to expand until the emmetropic state is reached and then maintaining it through feedback between the macula and ciliary muscles. The association of myopia with schoolwork, he suggested, is due not to accommodation but to psychological and stress factors interfering with the normal emmetropization mechanism. Van Alphen cited studies showing personality and psychological differences between myopes and nonmyopes to support this hypothesis. Nutrition In his study in Tanganyika, McLaren (1960) found that the Mvumi schoolchildren, who had experienced a period of famine, had a similar mean refraction to the Mwanza children, who had not, but they differed from them in showing a greater scatter, more

92 high ametropias, and more astigmatism and anisometropia. Baldwin (1981) cites studies associated with general malnutrition but notes that no studies to date have shown any relationship between myopia and any specific vitamin deficiency. Dietary changes have also been suggested as one possible explanation for the increase in myopia observed among Eskimos and American Indians. Other Causes The above discussion touches on some of the hypotheses regarding the etiology of the preponderance of myopia as suggested by the prevalence studies that have been reviewed. There are, of course, many special etiologic forms of myopia. Fairly common among these are the myopias seen associated with diabetes ant! with prematurity. Myopia associated with malnutrition in the sense of deficiency should probably be considered in this category, an well as the myopias associated with specific genetic diseases and with other eye problems leading to a reduction in visual acuity. In populations with a high prevalence of myopia, these special etiologies probably account for a small proportion of myopes, for example, among diabetics and among premature infants, less than one-third of the observer! myopia was attributable to diabetes or prematurity (FIedelius, 1980, 1983~. Other special etiologies may have a stronger association but are even more rare in the general population. It is not clear what the contribution of these special types ~ in populations with low myopia prevalence when all factors may be very different.

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This book considers the issues surrounding the occurrence, progression, and predictability of myopia (near-sightedness), with special emphasis on the 16- to 26-year-old population. Myopia reviews only the most pertinent published research in this area, analyzing the findings and drawing conclusions from these studies. The observations and recommendations will undoubtedly be of considerable interest to vision scientists and clinicians alike.

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