Is the Increase in Refractive Errors in Children Caused by Modern Light Sources?
The headline always has to be a little provocative, but it is possible that this is indeed the case. Quite recently, I pointed out the historical work of Dr. Bates, who considers the main cause of vision problems to be excessive tension in opposing eye muscles, which shape the eyeball, affect the axial length of the eye, and thus focus or defocus the image on the retina. This strain is caused by stress in the brain. If the brain cannot recognize what it is looking at, this causes stress and increases the tension in the muscles around the eye, including the tension in those muscles that are supposed to remain relaxed.
How does modern science view refractive errors? It seems that studies are already emerging that consider feedback systems, in which the eye is exposed to various influences and therefore has to constantly "fine-tune" itself. They call them the GO signal and the STOP signal. The GO signal lengthens the eyeball, while the STOP signal stops this lengthening. Nothing has yet been said about the work of the eye muscles controlled by the brain and stress, but even this is apparently a major breakthrough.
The latest studies then show that the retina is sensitive not only to the three familiar primary colors, red, green, and blue, but also to ultraviolet and violet components of the spectrum that we cannot see. This is a very interesting area of research. It is even becoming apparent that these ultraviolet components are apparently capable of switching off the eye's adaptive mechanisms in animals and humans, specifically stopping the eyeball from lengthening even when the eye is exposed to stress and cannot see well. This is a model of induced myopia that is used in mice and tree shrews.
The problem with the mouse model is that mice are nocturnal animals and, moreover, their visual sensitivity is shifted toward the ultraviolet spectrum. Therefore, the tree shrew model is now used more often; tree shrews are diurnal animals and are related to primates. They are therefore much closer to us.
There are two models of myopia. One uses a diffuser placed in front of the eye, and the other uses lenses with minus diopters. The diffuser model is applied after birth and prevents a focused image from being formed on the retina. It therefore corresponds exactly to Dr. Bates's model: if the image cannot be recognized, stress causes the axial length of the eye to increase; in modern terms, it is now said that the GO signal is activated and the eye lengthens by as much as -7 diopters. The second model uses lenses with minus diopters in front of the eye, so the eye develops to be longer in order to see correctly even under these conditions, when the focused image is located behind the retina. Both models therefore produce myopic adults within a few weeks.
New research, however, shows that the GO and STOP signals can be controlled by activating the OPN5 protein with light from the near-ultraviolet part of the UV-A spectrum.
If we translate this into Dr. Bates's terminology, the stress in the brain and the tension in the eye muscles can be controlled. How? With violet light, partly even outside the visible spectrum, approximately 350 to 470 nm. But this is precisely the range that modern light sources do not have. There are even theories that this range of light is harmful to us, which is why yellow-tinted glasses exist that cut out the violet part of the spectrum and supposedly "protect" us. We are therefore entering an area that has not been studied very thoroughly, and it may turn out that the old advice to limit exposure of the eyes to ultraviolet light will be replaced by its exact opposite: a recommendation for a minimum daily exposure to near-ultraviolet light.
The latest research indicates that wavelengths of light that we thought were not needed at all, or even that were harmful, have an irreplaceable function. Artificial light should therefore probably contain them, but there is apparently still a long way to go before that happens.
Let us look at the first image above at the latest study published this year. Here, the scientists clearly show us that the STOP signal is triggered by ultraviolet light at a very specific wavelength. When they apply this light, the eye does not lengthen even under a strong stimulus such as placing a -10 diopter lens in front of the eye. The eye remains the same throughout the entire experiment. If this light is absent, the eye lengthens. The experiment was conducted on tree shrews, and the effective wavelength was 421 to 441 nm; the human eye may require slightly different wavelengths of light.
Finding the correct wavelength was not entirely easy. The first studies found the correct mechanism in mice, and in mice the most effective wavelength was 380 nm. The problem is that a mouse's eye does not block this ultraviolet light, whereas both the human eye and the tree shrew's eye completely block it. The eye's lens simply does not allow it to reach the retina. A different wavelength, longer than approximately 410 nm, must be used. Then it starts to work. However, the OPN5 photoreceptor that transmits this signal has limited sensitivity toward longer wavelengths as well. It turns out that only light with a wavelength shorter than approximately 450 nm can work. Thus, the window for this signal is between 420 and 440 nm. And it really does work. It is indigo blue-violet light.
In another, older study, scientists examined this ultraviolet photoreceptor OPN5 itself in greater detail and found that it essentially functions as a day/night, light/dark switch, with two stable states. One is switched on by ultraviolet light at a wavelength of 380 nm, which produces some chemical product with the highest absorption capacity at a wavelength of 470 nm. This state can be switched back by light with a wavelength greater than 480 nm in the absence of the ultraviolet component. For this purpose, they used yellow-green light with a wavelength of 550 nm. If I understand this correctly, ultraviolet light in the morning and during the day switches the OPN5 photoreceptor into the daytime state, which captures the 470 nm wavelength, while the absence of ultraviolet light in the evening ensures that it is switched back to the nighttime mode by the remainder of the daylight. In daytime mode, the ability to adjust the shape of the eye and lengthen it is suppressed. This makes sense because light causes greater constriction of the iris and thus increases depth of field, thereby suppressing the possibility of adjusting the axial length of the eye.
But what do our modern artificial light sources with their limited spectrum do to us? Even during the day, they trigger the nighttime mode, in which the optimal axial length of the eye is sought, increasing brain stress and the tension in the eye muscles. The eye therefore continues to lengthen even under strong artificial light; depth of field is high, so the initial lengthening is not a problem, but at lower light intensity it begins to matter, the axial length of the eye becomes too big, and myopia develops. The correct artificial light source should always also contain a component of the near-ultraviolet spectrum that switches off the eye's corrective mechanism and prevents it from unintentionally lengthening. Correction of the axial length of the eye can then take place in dim light, with the iris/aperture fully open and at minimum depth of field.
This is the current state of knowledge. It also follows that if we use UV-filtering glasses outdoors that limit the 420 to 440 nm component, we are probably also promoting axial elongation of the eye and may cause or worsen myopia.
Artificial light sources interact with our vision in the same way as stress and tension caused by an object that is difficult to recognize. The extent to which these sources of unnatural light contribute to vision problems still needs to be investigated, but the effects of the mechanisms already known are alarming. This applies particularly to lighting in school classrooms and workplaces. We surely do not want to further damage our children's eyesight with poor lighting!
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References:
UV-Sensitive Photoreceptor Protein OPN5 in Humans and Mice
Violet light suppresses lens-induced myopia via neuropsin (OPN5) in mice
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