A 400-Year-Old Shark May Be Teaching Us Something About Eye Aging

The Greenland shark is one of the strangest animals on the planet. It lives in near-freezing water a mile below the surface of the North Atlantic. It moves slowly, grows slowly, and does almost everything slowly. The oldest known individual was estimated at around 400 years old, which makes it the longest-lived vertebrate ever documented.

So here is the obvious question. What happens to an eye that has to work for four centuries?

A team of vision scientists at the University of California, Irvine decided to find out. Their paper, published in Nature Communications in late 2025, is the first detailed look at how a Greenland shark retina stays functional across that kind of timescale. And the answers turn out to be relevant for anyone thinking about human eye aging.

What Did the Researchers Actually Do?

The team obtained retinal tissue from Greenland sharks and used a combination of modern genomics and functional assays to map what is going on inside those cells. They looked at gene expression, DNA damage repair machinery, and the molecular pathways that tend to break down in aging retinas.

For context, a human retina is already one of the most metabolically demanding tissues in the body. Photoreceptor cells are so hard working that they essentially rebuild a chunk of themselves every day. That pace creates a constant flood of oxidative damage, and over decades, the cleanup systems start to fall behind. That is part of why age-related eye disease is so common in people over 60.

Now imagine what it would take to keep that system running for four centuries. That was the question the researchers wanted to answer.

What Did They Find?

Two findings stand out.

First, Greenland sharks have unusually strong DNA repair activity in their retinal cells. The genes involved in fixing oxidative damage to DNA appear to be constantly expressed at high levels, rather than being turned on only in response to stress. In other words, their retinas are always cleaning up the mess, not waiting for it to pile up.

Second, the sharks show preserved mitochondrial function across their very long lifespan. The researchers found that their retinal mitochondria (the tiny energy factories inside every cell) maintain output and integrity at a level you would not expect in such an old tissue. In most aging mammals, mitochondrial decline is one of the earliest and most predictable problems in the retina.

Both of these findings point to the same two themes that show up over and over again in human retinal aging research: energy metabolism and damage control.

Are We Talking About Humans or Sharks?

Okay, reality check. You are not a Greenland shark. Your retina is not going to pick up shark biology by reading a blog post. The value of research like this is not that it tells you how to copy an animal. It is that it tells you which biological systems actually matter for keeping a retina healthy over the long run.

When a completely different species, evolving in isolation for millions of years, lands on the same answer that mammalian aging research keeps landing on, that is a strong signal. It says: this pathway is not an accident. It is fundamental to how long a retina can function.

And the pathway is clear. Cells that preserve their energy production and aggressively repair damage hold up longer.

How Does This Connect to Human Eye Aging?

In humans, the decline in retinal function with age tracks almost exactly with the loss of mitochondrial energy production and the accumulation of unrepaired cellular damage. This is why researchers studying conditions like age-related macular degeneration, glaucoma, and diabetic retinopathy keep coming back to the same biology. Mitochondria. Oxidative stress. NAD+ levels. DNA damage response.

This is the same story we followed in our post on the first human trial of epigenetic reprogramming in the eye. Different species, different technology, same underlying question. How do you keep an aging cell doing its job?

The Greenland shark paper adds another data point to a growing consensus: retinal longevity is a function of cellular resilience, not luck.

What About NAD+ and the Shark?

This is where the connection to human supplement science gets interesting. NAD+ is a molecule your cells use to produce energy and run DNA repair enzymes. It declines with age in almost every tissue studied, including the retina. A lot of the pathways the Greenland shark appears to have hardwired into its biology (strong DNA repair, preserved mitochondrial output) are the same pathways that depend on NAD+ in humans.

The researchers did not make claims about NAD+ in the shark study specifically. But the mechanisms they highlighted are the downstream systems that require NAD+ to operate. That alignment between a 400-year-old shark and the molecule driving a lot of current eye-longevity research is notable.

What Does This Mean for You?

Nothing in this paper says anything about a supplement. It is a study of a shark. But the framework it reinforces is the one that has been taking shape across eye research for the last decade:

The retina is an energy problem before it is anything else. Supporting mitochondrial function and the systems that protect DNA from oxidative damage is where the long-term wins tend to come from.

That is not a new idea, and it is not unique to any one product. It is the direction eye longevity research is already pointed.

Sight Guard was formulated around that same idea. If you are curious how we translate this kind of research into a daily routine, you can read more about our science and how we built the formula.

The Bigger Picture

The reason a story like this matters is not the novelty of a long-lived shark. It is the convergence. When studies of laboratory mice, human clinical trials, and a 400-year-old fish all point at the same biological pathways, that is as close to a consensus as biology gets.

Your retina is not going to last 400 years. But the mechanisms that help a shark's retina last that long are the same ones that help a human retina hold up across the 80 or 90 years we actually get. And those are the mechanisms worth paying attention to now, not after something goes wrong.

If you want to go deeper on the product side, here is how Sight Guard is put together and what it is for.

References

1.     Skowronska-Krawczyk D, et al. Visual system and retinal biology of the Greenland shark Somniosus microcephalus. Nature Communications. 2025. PMID: 41491153.

2.     Nielsen J, et al. Eye lens radiocarbon reveals centuries of longevity in the Greenland shark (Somniosus microcephalus). Science. 2016;353(6300):702-704.

3.     Jarrett SG, Boulton ME. Consequences of oxidative stress in age-related macular degeneration. Molecular Aspects of Medicine. 2012;33(4):399-417.

4.     Kauppinen A, et al. Inflammation and its role in age-related macular degeneration. Cellular and Molecular Life Sciences. 2016;73(9):1765-1786.

5.     Williams PA, et al. Vitamin B3 modulates mitochondrial vulnerability and prevents glaucoma in aged mice. Science. 2017;355(6326):756-760.