There are two failures of physiology in the human lens that cause it to be destined for cataracts over time. Don’t get me wrong: the human lens is such a marvel of precision engineering that we can’t get even close to matching its capabilities when it is healthy. One of the features of biological tissue, however, is an ability to perform miracles compared to technological invention, but at the cost of durability. We have intra-ocular lenses (IOLs) that last, unchanged, for a lifetime. They can’t perform anything like the flexible, smooth autofocus of a healthy lens. Perfect and complicated proteins in a matrix of other large complicated molecules are necessary for clear, dynamic autofocus.
It is those crystalline proteins of the lens that suffer the fate of the exquisitely fine-tuned biology. To steal from Edna St. Vincent Millay, their candle burns at both ends, it will not last the night.
The way those flexible and crystal-clear proteins work is limited over time for two reasons:
• First, the lens keeps making more layers of protein, and the ones in the center get more and more compact and dense over time. That hardening causes the loss of autofocus for near vision we see throughout the decade of our 40s.
• Second, proteins only do what they’re supposed to if they stay shaped in the correct way. When the crystalline proteins of the lens start to get squished into each other like a fraternity in a phone booth, they get twisted and turned into the wrong shapes. These proteins are supposed to be clear. When they aren’t shaped the right way or spaced apart the right distance, they turn cloudy. You can watch the same thing happen with proteins changing shape—denaturing is the scientific word—when you throw an egg on the skillet. The “white of an egg” starts off as the clear of an egg until the heat from a frying pan denatures the protein in it and turns it white.
Inside our lens, the proteins are doing the same thing.
Due to some favorable conditions (chief among them I’ve got to hand the award to the condition of not being in a frying pan) it usually takes half a century instead of half a minute to see visible changes. But the process of proteins changing from crystal clear to crystal cloudy is otherwise pretty similar.
The layered and sectoral arrangement of proteins in our lens causes the cloudy crystals to form in specific formations. Sometimes they look like radially-arranged spokes like a circle of icicles. Sometimes it just looks like someone threw a tiny snowball into the back of the lens and splattered a central area with white powder. These patterns, and several others, all have specific names when we see them in a lens. And all of them are names for different kinds of cataracts.
As light travels through our lens with a final destination aimed at the retina, these spokes and patches of white, cloudy crystals wreak havoc. If you’ve ever seen sunlight hit a windshield with salt on it, you’ll have an idea for how much light can scatter on little opaque crystals. When you drive at night, you’ve got a big pupil to let lots of light in, and headlights shining your way to scatter light into an astonishing array of glare and starburst. Driving at night gives the worst cataract symptoms because the whitened crystals in your lens can scatter those point sources of light best under those conditions.
That Edna St. Vincent Millay poem finishes after the candle burning at both ends and not lasting the night with, “but ah, my foes, and oh, my friends—it gives a lovely light!” I assume she probably wasn’t talking about cataracts, but the coincidence does seem amazing, right? Maybe she would have used different words than “lovely light” to describe glare and halos from night driving, but she was a wonderful poet, so who knows? What’s that? Oh, everyone knows she wasn’t talking about cataracts? Well, that’s disappointing. We ophthalmologists have so few great poets. Nonetheless, all the other facts in this article remain true.