A considerable variation in biometric changes is observed between onset groups. For example, early-onset myopes tended to have a faster and longer lasting refractive error progression compared to later-onset myopes,
13 leading to higher amounts of myopia by the end of the study. This also was seen in the acceleration of the myopia development, which was larger for early-onset individuals,
13 and may result from more intense environmental stimuli (e.g., lack of outdoor time or more near work). The main determining factor of this development was axial growth, which seemed remarkably parallel between onset groups (
Fig. 1b). When changes in growth speed were considered, a subtler picture appeared where axial growth underwent a modest acceleration at onset, followed by a gradual deceleration in the years thereafter. This axial growth acceleration was concurrent with greater lens power loss before onset. This pattern was not found in persistent emmetropes, where lenticular changes remained modest at all times. This pattern is of paramount importance for homeostasis to succeed, while a breakdown in this balanced growth can lead to myopia.
1 Given that corneal power stabilizes early in life, at approximately age 2 to 3 years,
14 refractive homeostasis is mostly determined by the gradual changes in crystalline lens power and axial length. Based on animal studies, these lenticular changes are mostly passive in nature,
15 resulting from uncontrolled internal changes that gradually alter the lens thickness, curvature, and gradient index.
12,16,17 To explain lens thinning and associated power loss in ocular growth in humans, a theory implicating lens stretch by zonular traction has been proposed.
6,18 Axial length, on the other hand, undergoes a combination of somatic and regulated growth, and, therefore, can compensate for variations in lens power loss,
2 leading, for example, to longer emmetropic eyes with lower lens power.
16