How to Prevent Cataracts: A Biochemically Precise, Evidence-Based Guide
Cataracts are Ubiquitous, But Not Inevitable
Cataracts are, by far, the number one cause of blindness globally.
According to the World Health Organization, around 94 million people are affected by cataracts, and in the USA, around 70% of people over age 75 have cataracts.
Getting cataracts is extremely likely. But this overwhelming likelihood does not mean that one must resign oneself to such inevitability. It is possible to delay (and sometimes prevent—over the course of a normal human lifespan) significant cataract development.
But doing so requires targeted effort (and I do mean real effort), far beyond the usual “wear sunglasses and hope for the best.”
Cataracts are a clouding of the eye’s natural lens to the aggregation of proteins and distortion of natural structures secondary to environmental damage that is—very importantly—not being sufficiently countered by the body’s intrinsic defense mechanisms.
This cataract development process occurs over the course of decades—it’s a slow, gradual, observable growth occurring through reasonably well-understood, modifiable biochemical mechanisms.
And such cataract development mechanisms absolutely do not have to march forward with the relentless momentum of a bulldozer. There are things that you can do to delay or even prevent the need for cataract surgery, again if enough targeted effort is made, and with enough consistency.
The goal of this article is to help you understand how the human lens works, why cataracts develop, and what to do to try to prevent the need for surgery.
How the Eye Lens Works, and Why It’s So Vulnerable
Anatomy of the Lens
The human lens—that miracle disc-shaped structure that sits behind your iris and transmits and focuses all the light that you need to see—is composed of:
Epithelial cells (little structures that make up the front surface of the lens),
Fibers (elongated cells that make up the meat of the lens),
and the Capsules, the basement membrane that encloses and maintains the overall lens structure.
But there are two essential points to remember about this structure:
Firstly, the lens is avascular. This means that the lens is not embedded with blood vessels. Nutrients aren’t circulated into the interior of the lens using blood vessels but rather by gap junctions—little spaces between cells allowing for the flow of liquid and nutrients—and internal currents.
Secondly, the lens fibers—again, those things that make up the meat of the lens—are packed with crystallins.
Crystallins comprise 90% of the proteins inside the lens. They include:
β and γ-crystallins, which make up the transparent structure of the lens, as well as
α-Crystallin, which is a “molecular chaperone” which is responsible for ensuring that the other crystallins do not inapropriately aggregate.
In order for the lens to stay transparent (and thus not become a cloudy cataract), it requires several things:
The lens fibers must stay arranged in an orderly manner,
The proteins must stay soluble and undamaged,
The lens must be able to safely and efficiently manage the flow and exchange of electrons,
The lens must be able to safely regulate water and ions (sodium, potassium, etc.).
One last essential feature of the lens is that its proteins are not recycled. This means—quite surprisingly—that most (not all) of your lens proteins are literally the same ones you were born with.
Why the Lens Is Prone to Damage
This leaves us with two key vulnerabilities:
Nutrient Access and Accumulated Damage
In other words, the lack of vascular circulation inside the lens means that nutrient transportation can more easily become a limiting factor for lens healing.
And the fact that your lens fibers are never changed means that whatever damage occurs accumulates.
What Causes Cataracts: An Insidious Cellular Breakdown
The Real Mechanisms Behind Cataract Formation
It’s no secret that exposure to UV radiation is a primary driver of cataract formation. But what’s important to us is how that UV radiation leads to cataracts, because understanding that step-by-step process reveals key points where we can step in and break the sequence.
Why Oxidative Stress Matters Most
What UV (ultraviolet) light does is generate reactive oxygen species. These are basically highly reactive (hence the name) molecular forms of oxygen like (O2-, H2O2, etc.).
Those reactive oxygen species then (1) get in touch with the lens proteins—the crystallins we just mentioned—and, by nature of their reactivity, damage them via protein damaging processes called oxidation, carbonylation, and amino acid crosslinking.
They (2) react with the membranes of the lens cells and damage the phospholipids (fatty cell-lining molecules) that protect these cells.
And they (3) damage something called the sodium-potassium ATPase—an important little machine on the cell surface that’s important for regulating how much fluid and electrolytes are let into and out of the cell.
So we’ve got damage to proteins, phospholipids, and sodium-potassium ATPases (effectively the meat, barriers, and fluid regulators of the cells) that collectively drive this initial stage of cataract formation.
Together, these damages change the very structure of the lens:
Proteins aggregate, and
The cells’ physical external structure is damaged as fluid transport and barrier protection become inhibited.
Together, these things scatter incoming light, causing lens opacification—cataract.
The Role of Alpha-Crystallin
But the lens does have a protective mechanism.
Remember α-Crystallin? That protein is responsible for binding to other proteins to prevent them from aggregating and opacifying.
But reactive oxygen species (generated by UV light—and other factors) also damages that protein, preventing it from doing its protection function.
The Central Role of Glutathione in Cataract Prevention (that doesn’t mean you should supplement it, though)
Amidst all of this, as in other organs of the human body, the body does have a means for preventing oxidative damage (i.e. the damage from those reactive oxygen species we mentioned).
That mechanism is endogenous antioxidant function.
The body has built-in antioxidants that essentially douse that oxidative fire, so to speak, so that damage does not progress.
The master antioxidant responsible for this is glutathione (the trendy supplement). Your body makes its own glutathione, by itself, and the lens itself (specifically the surface layer of the lens) also makes its own glutathione.
That glutathione is transported to the inner layers of the lens, where it quenches that growing oxidative stress (generated by UV light, etc.), limiting the progression of a cataract, and keeping the lens transparent and clear!
But the problem here is that this glutathione has to be transported into the inside of the cell. Again, it’s made at the surface layer and moved inside to treat the oxidation happening there.
And as people age, these transportation mechanisms begin to fail—specifically due to gap junction problems and ATP decline—leading to around a 70% reduction in glutathione within the very center of the lens! T
This leaves the lenses of older people much more vulnerable to oxidative stress—the damage of UV light and the like—and thus likely to lose lens transparency and develop cataracts.
(NOTE: Diabetes has a very specific means by which it accelerates cataract development, but ultimately it converges with the above at the point of glutathione, so I’ll circumvent that discussion for the time being.)
Can Cataracts Be Prevented? The Pathophysiology—and the Clinical Science—Yields a Resounding YES
This is not purely a theoretical discussion.
Risk Factors That Accelerate Cataracts
Plenty of studies have demonstrated—in the real world—that certain behaviors significantly increase the risk of developing cataracts.
Things like:
Smoking - Smokers have a two times higher risk of nuclear cataracts (center of the lens) and up to a three times higher risk for posterior subcapsular cataracts (another type of cataract).
UV exposure - Cumulative UVB exposure (the bad type UV light) increases cataract risk by 60% in high-exposure people.
Diabetes - Diabetes increases cataract risk by two to five times, depending on duration and how well it’s controlled.
Some Medications - Take statins, for example. Some studies show up to a 27% increased risk in people taking statins, though findings are mixed.
What the Research Shows
What does this tell us? That you should stop smoking, limit UVB light, fix your diabetes, and limit use of medications like statins to the bare minimum?
Probably.
But more importantly, it tells us that the oxidative mechanism for cataract development is highly consequential.
Because where all these bad things converge is oxidative stress—likely including statins, but I’ll concede that that’s controversial.
Why Prevention Needs to Start Early
Now it’s important to remember that cataract development is not instantaneous. Damage is cumulative, meaning it grows additively over a long period of time. Therefore, we absolutely can intervene well before a full cataract has developed.
But you need to start before symptoms appear—or, otherwise, as early as possible.
The Cataract Prevention Protocol: Nutrients That Help Limit Lens Opacification
If cataracts are primarily driven by oxidation—damage from reactive oxygen species (ROS)—then it logically follows that nutrients and compounds which support antioxidant function, especially within the lens itself, should slow or delay their formation.
That’s exactly what we see in the clinical and experimental literature.
There are a number of nutrients that have shown, both in animal studies and human epidemiology, a significant protective effect against cataract progression—largely by improving antioxidant status, preserving glutathione, and reducing the lens’s susceptibility to protein damage and aggregation.
Core Supplements That Support the Lens
Let’s start with the nutrients that have the strongest data behind them and that actually make sense mechanistically.
N-Acetylcysteine (NAC): Cysteine Donor That Generates Glutathione
NAC is a supplemental form of cysteine—the amino acid that is the rate-limiting step in glutathione synthesis. Without cysteine, your body cannot make sufficient glutathione, and your lens (especially the inner portion) becomes vastly more vulnerable to oxidation.
Animal studies have shown that when NAC is administered systemically (by mouth), it actually does ultimately get to the lens and increase glutathione there, slowing down lens opacification.
Even more interesting: there are human studies using NAC as an eye drop (at around 1–3% concentration) showing some degree of improvement in early-stage lens clarity—likely due to NAC’s ability to reduce crosslinking in oxidized proteins (that amino acid damage we talked about).
This does not mean you should rush to buy some NAC eye drops off Amazon. Most of these are either unregulated or flat-out illegal to market as over-the-counter drugs in the U.S. That kind of stuff would require working directly with someone savvy enough to generate this with a direct pharmacy partnership.
But oral NAC is legal, cheap, and reasonably safe when taken at doses up to 2000 mg per day. The problem, however, is that testing is the best thing to do, because too much NAC also has the potential to backfire.
Alpha Lipoic Acid (ALA): Mitochondrial Redox Protection
ALA is a mitochondrial cofactor that plays a central role in regenerating other antioxidants—particularly glutathione and vitamin C. It also helps reduce oxidized lipids in membranes, which, as I’ve talked about, are one of the early casualties in cataract formation.
In multiple rat and rabbit cataract models, ALA supplementation led to preservation of lens transparency and lower levels of protein carbonyls and lipid peroxides—i.e. protein and barrier damage.
Doses between 300–600 mg/day (oral) are commonly used in human antioxidant protocols. In cataract models, even low-dose ALA improved redox capacity in the lens epithelium, preserved GSH levels, and helped maintain fluid and ion gradients.
This is one of the few antioxidant supplements that is not only biologically plausible, but also shows actual structural protection in the lens.
Taurine: Osmolyte with Antioxidant Effects
Taurine plays a role in osmoregulation (maintaining proper water and ion balance within cells, like via the sodium-potassium ATPase I talked about), particularly in excitable or high-exposure tissues like the retina and lens.
In the context of cataracts, taurine has been shown to:
Reduce oxidative stress in the lens,
Prevent calcium overload and membrane breakdown,
Preserve mitochondrial function in lens epithelial cells.
Taurine is also depleted in diabetes, which may partially explain why diabetic lenses degenerate more rapidly.
A standard oral dose is 500–2000 mg/day, sometimes more and it is widely available, inexpensive, and safe for nearly all people—again with testing being the optimal thing to do, because it can worsen sulfur issues.
Vitamin C: Long-Term Antioxidant Protection
Vitamin C is one of the most abundant antioxidants in the aqueous humor—the fluid that nourishes the front of the eye and the surface of the lens. It directly neutralizes ROS and also helps regenerate oxidized glutathione.
The EPIC-Norfolk Eye Study showed that people consuming over 364 mg of vitamin C daily had a 33–57% lower risk of developing cataracts compared to those consuming less than 125 mg/day.
Don’t megadose (very high doses of vitamin C, like over 2,000 mg/day, may increase the risk of kidney stones in some people, or deplete certain minerals, etc.). But a range of 250-500 mg/day is effective and safe for most.
Importantly, this vitamin seems to work best when consumed consistently over long periods of time. Intermittent or "rescue" use has not shown much impact.
What About Riboflavin, Selenium, and Zinc?
There are other nutrients that might help. Riboflavin, selenium, zinc, sulforaphane, and several others are (highly) important. But these often require a much higher degree of personalization based on genetics, metabolic patterns, or pre-existing imbalances. They’re not bad—but they’re not universally useful either.
The four covered above—NAC, ALA, taurine, and vitamin C—are what I consider the core, foundational, broadly-applicable supplements for preserving lens function and resisting cataract formation.
But just remember that they won’t work in isolation, and they’re not a magic fix.
Lifestyle Measures that Reduce Cataract Risk
UV Light Exposure: Reduce Without Eliminating
Given that UV light (and specifically UVB light) is a primary driver of oxidative stress in the lens, it’s only natural that limiting UV exposure would be an essential element of this protocol.
Of course, you can’t limit UV exposure completely (nor do you want to, given vitamin D needs, circadian adaptation needs, etc.), but reducing it at particularly high intensity times of day and geographical locations would be of benefit.
Go for UV400 glasses, which ultimately reduce up to 50% of UVB exposure to the lens.
You also need to strictly control blood sugar. And frankly, if diabetes is an issue, that is absolute top priority to fix ASAP, because that is arguably the single strongest predictor of early cataract development.
Foods That Defend Your Lens
Quit smoking, and focus on a diet high in:
Eggs - which gives you taurine and carotenoids
Leafy greens - which give you lutein and glutathione generators
Berries - which give you polyphenols and exogenous antioxidants supporters.
Experimental and Advanced Cataract Prevention
Several measures are in very budding stages of development for cataract prevention and potentially early-stage reversal. Keep in mind that I consider these very much secondary to the nutrient and lifestyle measures I mentioned above, but they’re worth mentioning.
Carnosine Eye Drops (N-Acetylcarnosine)
Carnosine prevents glycation and crosslinking of crystallins—i.e. damage to lens protein, as we discussed. The most studied version, N-acetylcarnosine, has been trialed in Russia under the brand CAN-C.
A 6-month double-masked trial showed 41% of patients with early cataracts with improved lens clarity.
It’s thought that it works by reducing that main driver: oxidative damage and protein aggregation.
Lanosterol Eye Drops
Lanosterol is a natural molecule the body uses to make steroids, but it may also help reverse protein clumping in the lens.
In a 2015 Nature study, lanosterol eye drops improved lens clarity in rabbits and dogs by helping dissolve protein aggregates—that kind that drive cataract formation.
No human trials yet nor any FDA-approved version.
Nrf2 Activators: Sulforaphane and Astaxanthin
These compounds don’t act directly on the lens; rather, they turn on your body’s own antioxidant defense systems, especially, again, that glutathione production system.
Sulforaphane (from broccoli sprouts) at 20-40 mg/day increased lens antioxidant capacity in lab studies.
Astaxanthin supports mitochondrial health and helps protect the lens from UV damage.
These two are pretty safe to try, especially sulforaphane, which you can get a lot of from simply eating 1/2-1 cup of broccoli sprouts.
How to Build Your Cataract Prevention Protocol
In order:
Step 1: Eliminate Primary Risks
Look at risk factors. As above, you absolutely must quit smoking and address diabetes thoroughly (which, of course, absolutely can be cured in most cases). You can also consider: wearing UV400 glasses during high exposure times, but not always.
Step 2: Monitor Key Biomarkers
Monitor your homocysteine levels (and, importantly, other methylation biomarkers), glutathione levels, and B vitamin status overall.
Step 3: Build Your Supplement Stack
Based on a thorough assessment of your biomarkers and lab data, build a core supplement stack. This may be something like:
NAC: 600-1200 mg
ALA: 300-600 mg
Taurine: 1000 mg
Vitamin C: 500-1000 mg
etc.
But keep in mind, the above is absolutely not a prescription for you, nor is it guaranteed to help. It’s essential to figure out your own, idiosyncratic, unique bottlenecks.
Step 4: Address Your Diet
Take a thorough look at your diet. Increase consumption of nutrient-dense foods that directly support lens health and antioxidant defense:
Eggs, for taurine and carotenoids like lutein and zeaxanthin
Leafy greens (spinach, kale, arugula), for glutathione precursors and methylation support
Berries, for polyphenols that reduce oxidative stress
Cruciferous vegetables (broccoli, Brussels sprouts), for sulforaphane to activate glutathione production
Step 5: Address Underlying Dysfunctions
Very importantly, address upstream dysfunctions. If your body isn’t making enough glutathione or clearing oxidative stress efficiently, you may need to look deeper: into things like mitochondrial function, methylation, or sulfur metabolism. This is where personalization matters immensely.
Want help applying this to your own case?
You can schedule a free call with Dr. Malek to explore whether a deeper consultation is right for you.
Keep in mind that this is not official medical advice. No doctor-patient relationship is established through this article or through any other information provided on this website.
