March 16, 2007
Eye Light Needs Double From Age 30 to 50

Jane Brody of the New York Times outlines some of the dismal details of eye aging.

How well do you see at night? If you're over 50, probably not as well as you think, no matter how many carrots you eat. The typical 50-year-old driver needs twice as much light to see as well after dark as a 30-year-old.

That is both inconvenient and dangerous. Some people are content to grow old and even try to justify the changes which happen to our bodies as the various pieces break down. But the changes to our bodies due to aging all seem like losses to me and with no compensating upside.

The tiny muscles in your irises become less able to adjust pupil sizes and so your pupils can't dilate as far and as quickly to let in more or less light as needed. As far as I'm concerned this is yet another argument for treating the development of rejuvenation therapies as an urgent matter deserving a massive research push.

In dim light or darkness, eyes adapt by widening the pupils to let in as much light as possible. The iris (the colored part of the eye surrounding the pupil) contains tiny muscles that control the size of the pupil. As you get older, these muscles (like most in the body) weaken and do not respond as well to the need to let in more light. The result is a small pupil when you try to see in poor light. It's as if your eyes were still young but you were wearing sunglasses at night.

Does the world seem darker as you get older? It literally is as far as the retinas of your eyes are concerned.

According to one account I found you start out with about 120 million rods for black/white seeing. You also start with about 6 to 7 million cones of 3 types for color sensitivity. The rods age more rapidly and hence the black/white night-time vision deteriorates so much.

There is also evidence that as we age we lose more rods than cones. In the young eye, rods outnumber cones by nine to one in the part of the retina called the macula. But an autopsy study of older adults found that while the cones remained intact, almost a third of the rods in the macula had been lost.

Plus, pigment production for rods slows as you age. Also, your lenses become more cloudy as UV light causes cross linkages to form in the lenses.

The diminished number of rods may be a factor, but in addition, the light-sensitive pigment in the rods regenerates more slowly in older eyes.

Another common change in older eyes is a gradual clouding of the lens - the formation of cataracts - which makes the lens less transparent and reduces the amount of light reaching the retina.

Some labs are working on designs of artificial replacement lenses. Also, other labs are working on ways to grow natural replacement lenses using cells and tissue engineering. One way or another we'll some day be able to replace aged lenses with lenses as young as those of a baby.

But we need much more in order to do eye rejuvenation. First off, we need cell therapies created from stem cells to send in youthful replacement muscle cells in the iris and around the eyeball. Plus, gene therapies might reinvigorate some of the aged eye muscle cells so as to avoid need for their replacement.

Aging muscles in the rest of the body also suffer from deaths of nerves that connect to them. This probably happens with eyeball muscles as well. So we might need cell therapies that grow new neurons to hook up to rejunvenated eyeball muscles.

We also need replacement cells for making rod pigments. Plus, we need cell therapies to replace lost rods and cones. Replacement rods and cones will need new nerve connections to them. Rejuvenation therapies that repair existing rods and cones would reduce the need for replacement neural connections by avoiding the loss of target rods and cones which the original eye neurons formed connections to.

We'll also need replacement cells for eye blood vessels so that the eye cells get plenty of nutrients. Creation of replacement vascular cells might also reduce the incidence of Age-related macular degeneration (AMD) diseases of the eye which involve aged arteries in the eye. On AMD Lou Pagnucco points me to a study which finds a role for excessive zinc deposits in the eye as contributors to AMD. We might also need therapies that remove built up zinc deposits.

Further on down the road we'll eventually witness the development of tissue engineering technologies so advanced that they can grow whole organ replacement parts. Replacement eyeballs will then provide much more thorough and comprehensive solutions to the problems of aging eyes. Though even if such eyeballs could be grown today we'd face the extremely difficult problem of how to hook up a replacement eyeball to all the nerves that stretch into eyes. Repairing our existing eyes might remain preferable many years due to the difficulty in connecting up new replacement eyes.

Share |      Randall Parker, 2007 March 16 11:54 PM  Aging Studies

K said at March 17, 2007 11:28 AM:

I have long been disgusted about how makers of equipment, and nearly all electronics, seem determined to use small white letters on flat black finishes. It makes it extremely difficult for the elderly. And the rare offering that isn't black will have dull aluminum with tiny black letters. Any other color/design combination costs more if you can find a suitable product at all. Products from Northern Europe seem to avoid this black hole (from which no information escapes) but are very expensive.

The obvious answer is that black/tiny white is a low cost finish. And if everyone does it then the consumer has no choice.

Doug said at March 19, 2007 10:09 PM:

Maybe we'll learn to grow new eyes in situ--you know, pluck out the old ones and wait for the new ones to grow in. I'm half joking, but only half joking.

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