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Myopia Regulation: Myth or Megatrend?
This US clinical paper provides a review of the causes of short-sightedness and assesses how a range of different treatment approaches have performed in achieving both correction and control of this major problem which is estimated to have a cost to the US economy of almost $5bn per annum. Referencing existing research, the paper considers in turn the impact of treating short-sightedness with conventional contact lenses, under-correcting, drug therapy and vision training and concludes that while varying levels of success in correcting short-sight are evident, none of these treatments show any material ability to prevent the short-sight deteriorating over time. However, when Overnight Vision Correction (OVC) is also considered, the evidence of the LORIC, CRAYON and SMART studies all indicate that wearing overnight ortho-k corrective contact lenses can slow down or halt the further development of short-sight.
EXTRACT: In 1990, the financial cost of myopia in the United States was estimated at $4.8 billion.1 And, in addition to this societal burden, myopia carries an increased risk of associated pathology, including cataract, retinal degeneration, retinal holes and choroidal neovascularization.2 Although it is just the seventh most frequent cause of legal blindness in the U.S., myopia has a significant public health impact because resultant vision loss tends to extend over a longer period of life.3 Patients with myopic retinopathy are legally blind for an average of 17 lifetime years, vs. five lifetime years of blindness due to diabetes or age-related maculopathy.4
Efforts to better understand myopic genesis are escalating. By isolating the stimulus and response factors behind myopia, researchers are beginning to understand how to regulate myopic progression. Given the significant worldwide prevalence of myopia, interest in regulating myopic development runs high.5-7
What Causes Myopia to Develop?
The question of nature vs. nurture persists. Most researchers agree that environmental and genetic factors contribute to myopia, yet the specific factors involved, as well as their relative contributions, remain elusive.8 Environment and genetics may interact together to determine myopia.
One recent review of familial studies indicates a definite genetic basis for high myopia, and a strong genetic basis for low myopia.9 Also, twin studies provide compelling evidence that myopia is inherited.10
Meanwhile, the concept of environmental influence on myopia was bolstered by a 2008 study that found higher levels of outdoor activity are associated with a reduced prevalence of childhood myopia-even after adjusting for near work, parental myopia and ethnicity.11 Perhaps outdoor light releases a retinal neurotransmitter that inhibits eye growth.
A leading model for myopic progression incorporates important roles by optical stimuli, neurotransmitters, and choroidal and scleral growth factors. Data show that hyperopic defocus in the retinal periphery, even in the absence of visual signals from the fovea, can stimulate myopic progression.12
Hyperopic peripheral defocus is also implicated as a stimulus for myopic progression, according to research in which central refraction was compared to peripheral refraction.13 This study found that hyperopic peripheral defocus is present in eyes of myopic children. In his discussion of aberrations and myopia, William N. Charman, Ph.D., concluded, "There is stronger evidence in favour of differences in patterns of peripheral refraction in both potential and existing myopes, with myopes tending to show relative hyperopia in the periphery. These differences appear to be related to a more prolate eyeball shape."14
By Jerome A. Legerton, O.D., M.S., M.B.A., and Brian Chou, O.D.
