Since the growing popularity of repeated low-level red light (RLRL) in the past decade for myopia control, many researchers have been trying to understand the mechanism behind this treatment. RLRL therapy results do not match with classical emmetropization theory in that red light, which is a long wavelength, would focus behind the retina and therefore induce axial elongation.
One explanation for this was introduced by Gawne et al., who proposed a theory that under red light irradiation, the long-wavelength opsin was over-activated and the short-wavelength opsin was underactivated. This signaled the eye to develop in the direction of hyperopia to compensate for the imbalance of short- versus long-wavelength activation.4
Furthermore, studies have shown that red light may provide a protective effect on the retinal tissue. It was found in one study that red-light enhanced mitochondrial function and increased the survival rate of cells.5 In support of this finding, red light therapy has been shown in both animal and clinical studies to reduce oxidative stress and inflammation which may be involved in regulatory pathways of myopia.6,7
Many studies examining red light therapy for myopia control have found an increased choroidal thickness (discussed later). The choroid has been found to play a crucial role in relaying signals from the retina to the sclera. Many scientists believe that alteration of the synthesis of scleral extracellular matrix results in changes to ocular size and therefore axial length.8,
