Ramón Gutiérrez
Professor of Ophthalmology at the University of Murcia
Myopia develops from a genetic load and environmental factors. Today we know that the most important of these are excessive work in near vision and spending a lot of time in poorly lit environments. These environmental factors, during childhood and adolescence, in children with certain genetic variants, will generate excessive eye growth, i.e. myopia.
This relationship between near work, genetic load and myopia is not new. We have old scientific studies, with questionable methodologies, but which concluded that children who work a lot at close range develop more myopia. In the 17th century the astophysicist Kepler already published it.
Ware in 1813 observed that only 12 out of 10,000 recruits from rural backgrounds with a low level of education were rejected from the army because they were short-sighted and that, in contrast, at Oxford University, 32 out of 127 students were short-sighted.
A classic in myopia forums is an Israeli paper showing that orthodox boys, who receive a very strict religious upbringing, develop much more myopia than other boys and girls.
An analysis that can be considered a precedent to the work we are now assessing analysed genetic and environmental risk together and showed that, in genetically predisposed children, accommodative effort generates more myopia than in children who are not genetically predisposed. In this and many other studies of the time, genetic predisposition was considered as a function of whether neither, one or both parents were myopic.
Can we now know which genetic variants, together with visual strain, cause myopia? That is the question that the work we are now assessing aims to answer. (We are conducting a thesis to obtain myopia SNPs from a saliva drop, in which we need pairs of siblings: one with myopia and one emmetropic).
In 2015, an analysis was published which shows that the time spent reading has little influence on the development of myopia in the general population. In contrast, when people with the RS 188 663 068 variant are analysed, there is a big difference between those who read very little, who hardly develop myopia, and those who spend a lot of time reading, who do develop much more myopia.
The work we are now analysing goes a step further, and tries to find other genetic mutations or SNPs [single nucleotide polymorphisms] involved in the fact that near vision work is a determining factor in the development of myopia in some people and not in others.
Of note from the results is that they find five variants involved in the interactions between gene load and education. Two of these variants are already known, and the biological mechanism through which they might influence eyeball growth has even been studied, and three others are contributions made in the present work.
Overall, this is a good paper published in a journal with a high impact index, which uses a huge sample and employs procedures that can be considered standard for this type of work. Unfortunately, in this UK database not all the subjects analysed had a refraction, and the variable of spectacle prescription between 5 and 25 years of age is introduced to consider who is myopic. This can be considered a weakness.
The importance of finding out which SNPs generate myopia in certain environments lies in the fact that it would later be possible to investigate how to carry out reading and with what aids so that it does not generate the effort, the environmental factor that triggers the growth of the eye.