Is myopia a failure of homeostasis?

This review examines the hypothesis that human myopia is primarily a failure of homeostasis (i.e. regulated growth) and also considers the implications this has for research into refractive errors. There is ample evidence for homeostatic mechanisms in early life. During the first few years of life the eye grows toward emmetropia, a process called emmetropization. The key statistical features of this process are a shift of the mean population refraction toward emmetropia and a reduction in variability. Refractive errors result when either this process fails (primary homeostatic failure) or when an eye that becomes emmetropic fails to remain so during subsequent years (secondary homeostatic failure). A failure of homeostasis should increase variability as well as causing a possible shift in mean refraction. Increased variability is indeed seen in both animal models of myopia such as form deprivation and in human populations from the age of 5 or 6 onwards. Considering ametropia as a homeostatic failure also fits with the growing body of evidence that a wide range of factors and events can influence eye growth and refraction from gestation, through infancy, childhood and into adulthood. It is very important to recognize that the refraction of an eye is not a simple trait like eye colour but the consequence of the complex process of eye growth throughout life. To understand how an eye ends up with a specific refraction it is essential to understand all the factors that may promote the attainment and maintenance of emmetropia. Equally important are the factors that may either disrupt early emmetropization or lead to a loss of emmetropia during later development. Therefore, perhaps the most important single implication of a homeostatic view of myopia is that this condition is likely to have a very wide range of causes. This may allow us to identify subgroups of myopia for which specific environmental influences, genes or treatments can be found, effects that might be lost if all myopes are considered to be equivalent.

► In early life the eye grows toward emmetropia, a process called emmetropization. ► Emmetropization produces a shift of the mean population refraction and reduces variability. ► Animal models of myopia produce a shift in the mean refraction and an increase in variability. ► From the age of six onwards human refraction shows a pattern of increasing variability. ► The increased variability associated with ametropia points to a failure in homeostasis.