Why Does Our Eyesight Deteriorate As We AGE?
Eye spy with my little eye a number of eye problems that can come up with age.
We tend to associate old age with failing eyesight. It’s not that easy to see as we get older, and that ain’t really helped with the aid of reading glasses or other gadgetry at hand.
There are so many eye-related issues that can plague us as we age, including (but not limited to) glaucoma, cataracts or age-related macular degeneration (AMD).
In this article, I will be focusing on the issue of AMD. According to the National Eye Institute (NEI),
Age-related macular degeneration (AMD) is an eye disease that can blur the sharp, central vision you need for activities like reading and driving. “Age-related” means that it often happens in older people. “Macular” means it affects a part of your eye called the macula.
AMD is a common condition — it’s a leading cause of vision loss for people age 50 and older. AMD doesn’t cause complete blindness, but losing your central vision can make it harder to see faces, drive, or do close-up work like cooking or fixing things around the house.
AMD happens very slowly in some people. Even if you have early AMD, you may not experience vision loss for a long time. For other people, AMD progresses faster and can lead to central vision loss in one eye or both eyes.
The problem with AMD is that it is common, and that it also is a leading cause of vision loss for people age 50 and older.
But what does AMD do to our eyesight?
AMD is, according to the definition from the NEI, a degeneration of the macula. According to the VMR Institute,
The macula is the central area of the retina and is of particular interest to retina specialists. Remember, that the retina is the light sensitive tissue which lines the inside of the eye. The macula is the functional center of the retina. It gives us the ability to see “20/20” and provides the best color vision.
Therefore, any degeneration of the macula would result in a reduced sensitivity of our eyes to light stimulation, which would then “make it harder to see faces, drive, or do close-up work like cooking or fixing things around the house”.
The problem that arises from AMD is the accumulation of drusen on the retinae in our eyes, which are described as “small yellow deposits of fatty proteins (lipids) that accumulate under the retina”. These drusen particles will end up blocking light waves from hitting our retinae, and therefore cause an impeded vision — we would not be able to see things as clearly as we ought to.
Unfortunately, drusen deposits are linked to metabolic and inflammatory issues
According to this article,
AMD is a vascular-metabolic-inflammatory disease, in which two sets of extracellular deposits, soft drusen/basal linear deposit (BLinD) and subretinal drusenoid deposit (SDD), confer risk for end-stages of atrophy and neovascularization.
This review focuses on soft drusen/BLinD, summarizing evidence that a major ultrastructural component is large apolipoprotein B,E-containing, cholesterol-rich lipoproteins secreted by the retinal pigment epithelium (RPE) that offload unneeded lipids of dietary and outer segment origin to create an atherosclerosis-like progression in the subRPE-basal lamina space.
Which does indicate that the fatty drusen deposits are linked to cholesterol issues.
Also, other studies have found that Advanced Glycation End-products (AGEs) are found in those drusen deposits:
Advanced glycation endproducts (AGE) accumulate with aging and are linked to several age-related diseases such as Alzheimer’s disease, osteoarthritis, atherosclerosis and AMD. AGE deposits are found in drusen and in Bruch’s membrane of the eye and several studies have suggested its role in promoting oxidative stress, apoptosis and lipofuscin accumulation.
I did previously describe elsewhere how AGEs were formed as a result of the excess sugar in blood (especially in the case of diabetics). These AGEs are a result of the sugars reacting with the other biomolecules in our body via a chemical reaction known as glycation.
These AGEs are also able to target other Receptors of AGEs (RAGEs) for the RAGEs to send out an enhanced pro-inflammatory signal.
The moral of the story here, therefore, is that diabetes does provide a greater risk factor for the development of AMD (not that diabetics don’t have a chance of developing diabetic retinopathy first).
And of course, this intensified pro-inflammatory signalling can also lead to other biochemical pathways going wrong now, no?
Protecting our eyesight is key
We don’t want to end up going blind unnecessarily. Not when AMD is something that we can actually prevent in the first place. But a lot of people don’t even know how AMD comes about, and end up paying for it with a reduced quality eyesight in their later years.
There are quite a few things for us to target here:
- Waste management, or how our body eliminates stuff that ought to be eliminated, because we don’t want to have any excess accumulated cholesterol deal damage to our eyes too (not that it won’t deal damage to us via gallstones or oxidative stress beforehand).
- Oxidative stress, because all the electrons being transferred back and forth, if not regulated appropriately, will only worsen in the presence of those AGEs and RAGEs. And as oxidative stress begets inflammation, one problem will just lead to another problem in a spiralling cascade of events.
- And of course, stop staring at the computer screen for so darned long. Take a break!
Otherwise, the risk of having an impaired eyesight leading into blindness is real. Especially if we don’t take care of it properly in our younger years!
Do feel free to refer to Nutrients That Support Healthy Eye Functions for Dr J’s recommendations on how to support healthy eyes!
Joel Yong, PhD, is a biochemical engineer/scientist, an educator and a writer. He has authored 5 ebooks (available on Amazon.com in Kindle format) and co-authored 6 journal articles in internationally peer-reviewed scientific journals. His main focus is on finding out the fundamentals of biochemical mechanisms in the body that the doctors don’t educate the lay people about, and will then proceed to deconstruct them for your understanding — as an educator should.
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