Humans rely on their eyes to give them clues about their environment. A complex network of ocular and cerebral neurons work in concert to provide us with four basic pieces of information: where we are, where an object is, what an object is, and how to get it.1 This is as true today as it was 10,000 years ago. However, the environment in which we operate today is radically different. The fact that you’re reading these words on a computer, tablet, phone, etc. illustrates that fact.

As hunter gatherers, our survival was dependent on identifying resources and threats, usually at a distance, in an outdoor setting. Native populations around the world that most closely mimic our ancestral groups (traditional diet and work) maintain a rate of nearsightedness (myopia) of less than 5%.2 However, the visual skills and ocular anatomical variations best suited for meeting the vision demands of the ancestral world are completely different from those many of us face today. Nearly every single person in the developed world spends some amount of their time extracting information from written words on either paper or an electronic device. And often, this takes place indoors under artificial lighting. We have gone from a species which habitual views distant objects in a relatively uncrowded visual space filled with natural light to one that spends the majority of its time viewing objects within hand's reach while being surrounded walls and artificial light sources. Not surprisingly, the rate of nearsightedness has skyrocketed in the last century and is projected to reach 50% worldwide by the year 2050.3

The huge increase in such a short period of time suggests that genetics are not the primary driver of the phenomenon. Certain genetic makeups may predispose an individual to become nearsighted in a specific environment but it is not guaranteed. Myopia is not a destiny, it is an adaptation. So, what kind of environment is responsible for the huge increase in myopia across the globe? The answer, not surprisingly, is multifactorial. Near work, lighting, diet, crowded visual spaces, and sleep/wake cycles likely all play a role influencing development of nearsightedness. While we don’t know the exact biochemical cascades that cause myopia, we do know the end result: eye elongation. The longer the eye grows, the longer the axial length, the higher the degree of myopia.

Today, our goal as vision care providers is to slow down, stop or better yet, prevent excessive eye growth. Our primary target is children. Unfortunately, it’s likely too late for you and I. Myopia typically begins to develop around the age of 7 to 13 and stabilizes before the age of 25 (though cases of adult onset and progression of myopia are becoming more frequent).4 But, there is plenty we can do for our children.

  1. Remove excess refined carbohydrates and sugars from the diet. There is evidence that insulin and IGF may play a role in eye growth. A diet that maintains proper insulin sensitivity reduces the risk of myopia development among many other health benefits.5,6
  2. Take breaks from near work in outdoor environments. Viewing a near target (phone, book, etc.) causes a significant increase in axial length as a result of vascular changes within the eye. These changes can persist for up to 10 minutes after the cessation of the task.7 It is important for children to take breaks of at least 10 to 15 minutes every hour and view distant targets in an uncrowded (open space) outdoor environment to ensure their axial lengths returns to baseline.
  3. Spend at least an hour outside every day. Light from sun is significantly more intense than indoor lighting, no matter how bright the lights inside may seem. The spectrum of light provided by the sun is also more complete. Both intensity and spectral properties have been shown to alter dopamine levels within the eye and reduce the rate of eye growth.8,9 Additionally, keep light exposure consistent with natural daylight hours. Too much light after the sun goes down can affect dopamine levels as well.

There are also optical and pharmaceutical interventions we can provide if lifestyle modifications are not enough but should remain second line treatment. Putting our children (and ourselves) in environments that mimic the visual space of our past, providing food that mimic meals of our past, and using the sun as the guide to when lights should be on and off is first step halting the rapidly increasing myopia epidemic.


  1. Shayler G. The Use of Models to Help Our Understanding of Vision. Optometry and Visual Performance 2015;3:138–50.
  2. Garner L, Owens H, Kinnear R, Frith M. Prevalence of Myopia in Sherpa and Tibetan Children in Nepal. Optom Vis Sci 1999;76:282–5.
  3. Holden BA, Fricke TR, Wilson DA, Jong M, Naidoo KS, Sankaridurg P, Wong TY, Naduvilath TJ, Resnikoff S. Global Prevalence of Myopia and High Myopia and Temporal Trends from 2000 through 2050. Ophthalmology 2016;123:1036–42.
  4. Zadnik K, Sinnott LT, Cotter SA, Jones-Jordan LA, Kleinstein RN, Manny RE, Twelker JD, Mutti DO, Collaborative Longitudinal Evaluation of Ethnicity and Refractive Error (CLEERE) Study Group. Prediction of Juvenile-Onset Myopia. JAMA Ophthalmol 2015;133:683–9.
  5. Cordain L, Eaton SB, Brand Miller J, Lindeberg S, Jensen C. An evolutionary analysis of the aetiology and pathogenesis of juvenile-onset myopia. Acta Ophthalmol Scand 2002;80:125–35.
  6. Galvis V, López-Jaramillo P, Tello A, Castellanos-Castellanos YA, Camacho PA, Cohen DD, Gómez-Arbeláez D, Merayo-Lloves J. Is myopia another clinical manifestation of insulin resistance? Med Hypotheses 2016;90:32–40.
  7. Woodman EC, Read SA, Collins MJ. Axial length and choroidal thickness changes accompanying prolonged accommodation in myopes and emmetropes. Vision Res 2012;72:34–41.
  8. Read SA, Collins MJ, Vincent SJ. Light Exposure and Eye Growth in Childhood.
  9. Feldkaemper M, Schaeffel F. An updated view on the role of dopamine in myopia. Exp Eye Res 2013;114:106–19.