Suddenly everything is black. Where a brightly lit living room with cheerful people could just be seen, you seem completely blind in the unlit cellar. Only after a few minutes do your eyes start to distinguish some colorless objects again. How come?
The retina in our eyes contains cone-shaped and rod-shaped cells. The rods are spread over the entire retina, while the cones are more in the center. With the cones we distinguish colors and we can see clearly. They are active in full light. Rod-shaped cells come into action in the semi-darkness, but do not distinguish between colors. That’s why everything seems gray at night.
Vitamine A
On average, it takes a few minutes for the rods to come into action in the dark. However, for some people this takes half an hour and sometimes their eyes don’t get used at all. This can have various causes; very occasionally it is due to a lack of vitamin A.
Vitamin A is in our food, for example in carrots, spinach, goat cheese, butter and liver. The rods in our retina contain pigment that absorbs the light, and without vitamin A that pigment is destroyed. In that case, eating extra vitamin A will help. In Western countries, however, a vitamin A deficiency is very uncommon. It is therefore unwise to just take vitamin A supplements, or eat your lens on liver sausage as a precaution: an overdose of vitamin A is toxic and can actually affect vision.
The elderly often suffer from cataracts (cloudy lens of the eye) or glaucoma, a damage to the optic nerve. “They don’t see very well anyway, but they suffer from it even more in the dark,” says ophthalmologist Noël Bauer of Maastricht UMC+. And then there are also people with night vision. In the dark, our pupils dilate to receive more light, but in people with this condition, this causes nearsightedness. ‘As a result, they can see the dashboard well in the car, but not the traffic signs.’
Egg white
This is all quite annoying, but also treatable. The situation is different with retinitis pigmentosa, a form of night blindness in which something is wrong with the rod-shaped cells. ‘The rods capture light particles with pigment molecules, which ultimately leads to signals going to the optic nerve’, says professor of ophthalmology Camiel Boon of Amsterdam AMC and LUMC. ‘But it is a complex chain reaction that requires many steps involving all kinds of proteins and enzymes. The visual cycle is only as strong as its weakest link.’
That weakest link is often a missing or non-functioning protein, and in the case of retinitis pigmentosa, the cause is always a genetic defect. This form of night blindness is therefore congenital. There are more than a hundred different genes that, when they don’t work or work poorly, make a mess of the aforementioned chain reaction in the rods. This happens to about one in three or four thousand Dutch people and there is nothing that can be done about it.
Gene therapy
In fact, it only gets worse because night blindness is a progressive condition. What starts with poor vision in the dark slowly changes into a tube vision, because the patient has fewer and fewer functioning rods. ‘So it may well be that people are constantly bumping into doors and posts, but still read fine print fine’, says Bauer. After all, the cones in the eye center still work. The effects of night blindness can only be reduced somewhat by wearing glasses with yellow lenses that enhance all the contrasts.
Still, there is hope for a cure, albeit in the longer term. Much research is being done worldwide into gene therapy to treat congenital eye disorders. This can be done, for example, by placing a working copy of the defective gene in the rods. Scientists are experimenting with neutralized viruses that carry such a working gene. After the light-sensitive cells have been ‘infected’ with the virus with an injection, the working genes take over the function of the damaged originals. Although such genetic patching methods are on the rise, it will take at least five to ten years before they are successfully applied.
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