Is nearsightedness written in your DNA, or do lifestyle choices like excessive reading and studying leave you destined for a lifetime of glasses? According to a recent study from Columbia University Medical, both may be at fault. Researchers found that although there is a gene associated with nearsightedness, it is five times more likely to be activated in those who spend a large amount of time during their childhood doing “near-work,” such as reading.

Nearsightedness, also known as myopia, is characterized by a difficulty in seeing far-away objects and is believed to affect around 30 percent of the U.S. population. In 2011, scientists identified a main gene associated with myopia but noted that not every individual who possessed the gene was automatically destined to have poor eyesight. Rather, factors such as heavy studying and more time spent in school seemed to be a better predictor of both prevalence and severity of myopia. Now, researchers have identified just how these environmental factors play a role in the development of this largely genetic condition.

After analyzing a database of about 14,000 people, the team concluded that those who possessed a variant of the gene APLP2 were around five times more likely to develop myopia in their teens if they had read for an hour or more each day in their childhood. Individuals who possessed this genetic variant and did not spend large amounts of their childhood reading had no additional risk of developing myopia.

According to the study’s lead investigator, Andrei Tkatchenko in a recent statement, “This is the first known evidence of gene-environment interaction in myopia."

Our eyes continue to grow and take shape throughout our childhood. According to the American Optometric Association, nearsightedness occurs if the eyeball becomes too long or the cornea is too curved. This causes light entering the eye to focus incorrectly and as a result, distant objects look blurred.The team believes APLP2 promotes the production of a protein in the eye that causes the eye to undergo excessive elongation. Reading may stimulate an increased production of APLP2, and then in turn further increase the elongation process. The Columbia team observed that mice with less APLP2 proteins in their eyes were less likely to develop myopia, even after being exposed to an environment that mimicked excessive reading.

Unfortunately, the findings will do little to help fix myopia in those who have already developed it, since the elongation cannot be undone once it occurs. However, the team does hope their research could one day play a role in preventing the development of the common impairment.

“By reducing the level of APLP2 in the eye, you can reduce susceptibility to environmentally induced myopia,” Tkatchenko said. This gives us an opportunity to develop a therapy to prevent myopia in everyone, regardless of the APLP2 variant they carry.”

Source: Tkatchenko AV, Tkatchenko TV, Guggenheim JA, et al. APLP2 Regulates Refractive Error and Myopia Development in Mice and Humans. PLOS Genetics. 2015.