Yes, hyperbaric oxygen therapy can change your eyesight, and it happens more often than most clinics mention. The most common change is a temporary shift toward nearsightedness (myopia) that builds up over a course of treatment and usually fades within weeks to months after you finish. A rarer, more serious effect is the formation or speeding up of cataracts, which can be permanent.
This article walks through what the published research actually shows about HBOT and vision: how often these changes happen, why they happen, who is at higher risk, and how to tell the reversible blur from the permanent damage. The evidence here is decades old in some cases and surprisingly thin in others, so we grade it honestly rather than overselling either the risk or the reassurance.
The Short Version: Two Different Eye Effects
People lump "HBOT and vision" into one bucket, but there are really two separate things going on, and they have very different stakes.
The first is hyperoxic myopia, sometimes called a myopic refractive shift. Your vision gets blurrier at distance, as if your glasses prescription suddenly got stronger. This is common, predictable, and almost always reversible.
The second is nuclear cataract, a clouding of the central part of the eye's lens. This is rare, tied to very long courses of treatment, and usually permanent once it forms. It may eventually require lens-replacement surgery.
Both effects trace back to the same root cause: oxygen, at high pressure, is hard on the proteins in your eye's lens. The difference is dose. A normal 20-to-40-session course is enough to cause myopia in many people. Cataracts mostly show up in patients who go far beyond that, often 150 sessions or more.
| Effect | How common | Reversible? | When it shows up | Stakes |
|---|---|---|---|---|
| Hyperoxic myopia (nearsighted shift) | Very common with longer courses; reported as the single most common HBOT complication in one provider survey (24.4%) | Yes, usually within days to months after stopping | Builds gradually, often noticeable after 20-30 sessions | Low; annoying, temporary blur |
| Nuclear cataract (lens clouding) | Rare; mainly seen after very long courses (150+ sessions) | No, generally permanent | After prolonged, repeated treatment | High; may need cataract surgery |
What the Myopic Shift Actually Feels Like
If you wear glasses or contacts, the most common report is that the world gets a little fuzzier at distance over the course of treatment. Street signs, the TV across the room, faces down the hallway. Your reading vision may actually feel sharper for a while, because a myopic shift can make close-up work easier even as distance gets worse.
The change is measured in diopters, the same unit your eye doctor uses for your prescription. A shift of one or two diopters toward myopia over a treatment course is well documented. In some cases the change is larger.
Here's the reassuring part. In the classic studies, the shift is gradual, it tracks with how many sessions you've had, and it reverses after you finish. The Undersea and Hyperbaric Medical Society describes hyperoxic myopia as the textbook reversible ocular side effect of HBOT, and StatPearls' clinical reference notes that myopia changes are "usually reversible within days to months after therapy cessation."
So the practical takeaway: don't rush to buy new glasses in the middle of a treatment course. Your prescription is a moving target until a few months after your last session.
How long until it reverses?
Recovery timing depends on how much pressure-oxygen exposure you got and over how long. In a Navy case series of four divers exposed to high oxygen partial pressures, the myopic shift resolved spontaneously over the next two to three weeks with no lasting symptoms. Standard clinical HBOT courses, which spread exposure over more sessions, can take weeks to a few months to settle. Most eye doctors will tell you to wait at least one to three months after your final session before getting a new prescription.
One detail worth understanding: the more cumulative oxygen exposure you've had, the longer the wind-down tends to take. A diver who got a concentrated pulse over five days clears it fast. A patient who completed 40 medical sessions over eight weeks may need a couple of months for the lens to settle back. And the small subset of people who push into 100-plus sessions are also the group where the shift may not fully reverse, because at that point the line between reversible myopia and early permanent lens change starts to blur. That's not a reason to panic over a standard course; it's a reason to respect the dose.
A second practical note. Some patients notice their reading vision improves during treatment even as distance gets worse. If you've been relying on reading glasses, you might find you can suddenly read a menu without them mid-course. That's the myopic shift working in your favor at near distance, and it's temporary too. Don't throw out the reading glasses; you'll want them back within a few months.
Why Oxygen Blurs Your Vision: The Mechanism
The lens of your eye sits behind the iris and focuses light onto the retina. It's made mostly of tightly packed proteins called crystallins, arranged so precisely that the lens stays crystal clear. Anything that disturbs that arrangement scatters light and degrades vision.
High-pressure oxygen disturbs it in two ways.
First, the refractive (myopia) effect. Breathing 100% oxygen at pressure floods the lens with far more oxygen than it normally sees. This appears to change the shape and water content of the lens slightly, shifting its focusing power toward nearsightedness. Because the lens proteins themselves aren't permanently destroyed, the effect winds back down once oxygen levels return to normal. That's why myopia is reversible.
Second, the oxidative (cataract) effect. Oxygen at high pressure drives up production of reactive oxygen species, the unstable molecules that damage tissue. The eye has natural antioxidant defenses, like the enzyme superoxide dismutase, but repeated high-dose exposure can overwhelm them. The damage cross-links the lens crystallins into large, light-scattering clumps. StatPearls describes molecular oxygen inducing "cross-linking of lens nuclear crystallins into large disulfide-bonded aggregates capable of scattering light," and notes this may be the end-stage of the same myopic shift seen in most patients. In other words, the reversible blur and the permanent cataract may be two points on the same spectrum of oxidative stress, separated mostly by dose.
There's even animal evidence. In guinea pigs exposed to hyperbaric oxygen, the protein aggregates in the lens nucleus grew to nearly double the diameter of the control animals', mirroring what's seen in human nuclear cataracts.
Two more pieces of the mechanism are worth knowing, because they explain why the eye is unusually vulnerable. First, the lens has almost no blood supply. It can't flush out damage the way most tissues can, and its proteins are made early in life and never replaced. Damage to lens crystallins is essentially permanent damage to proteins you'll carry for decades. That's why oxidative stress that other tissues would shrug off can leave a lasting mark on the lens.
Second, the lens normally lives in a low-oxygen environment. The vitreous gel behind it acts like an oxygen sink, keeping the back of the lens shielded. As you age, that gel liquefies and the shield weakens, so an older lens already sees more oxygen at baseline. Stack high-pressure HBOT on top of an aging eye and you're delivering a large oxygen load to a structure that evolved to stay protected from it. This is the leading theory for why both age and HBOT independently drive nuclear cataract, and why combining them is the riskiest scenario.
Why myopia but not the cataract reverses
It comes down to whether the protein change is structural and permanent. The myopic shift seems to involve a temporary change in lens hydration and shape, not destruction. Once the oxygen flood stops, the lens rehydrates and the focusing power drifts back. The cataract, by contrast, involves crystallins that have been chemically cross-linked into stable, light-scattering aggregates. Those bonds don't simply undo themselves. The clouding stays. So you can think of myopia as the lens bending under load and springing back, and cataract as the lens taking a permanent set after too much load for too long.
The Hard Numbers: What the Studies Show
This is where honesty matters, because the strongest data here is genuinely old, and the modern data is patchy.
The foundational study is Palmquist 1984. Researchers examined 25 patients before, during, and after a course of 150 or more hyperbaric oxygen exposures. The findings were striking:
- All 25 patients shifted their refraction toward myopia during treatment.
- Of the 15 patients who started with clear lens nuclei, 7 developed a nuclear cataract with reduced visual acuity during treatment.
That's the study everyone cites for the cataract risk. But read the dose carefully: 150+ exposures. That is far beyond a normal clinical course. The seven cataracts appeared in people getting roughly three to five times the typical number of sessions.
The modern adverse-effect picture comes from a 2024 UHMS survey. Researchers surveyed Undersea and Hyperbaric Medical Society members, with 265 responses. Among listed adverse effects, myopia was the single most common complication reported, at 24.4%, ahead of ear barotrauma (14.9%) and confinement anxiety (11.5%). That tells you myopia isn't a rare curiosity; it's the most frequently flagged side effect by the people who run these chambers. The survey did not single out cataracts as a common reported complication, consistent with cataracts being a rarer, high-dose event.
A 2024 systematic review tried to pin down a safe limit and couldn't. A PRISMA-guideline review pulled in 22 articles (case reports, cohort studies, one randomized trial, and reviews) on hyperoxic refractive change in both HBOT patients and divers. The authors found the data "too heterogeneous to perform meaningful statistical analyses" and concluded they could not set a safety threshold to prevent myopia. So as of 2026, there is no agreed-upon number of sessions or pressure dose below which myopia is guaranteed not to happen.
| Study | Year | Population | Key finding | Evidence grade |
|---|---|---|---|---|
| Palmquist et al., Br J Ophthalmol | 1984 | 25 HBOT patients, 150+ exposures | 100% developed myopic shift; 7 of 15 with clear nuclei developed nuclear cataract | Small but landmark; old, no control group |
| Laspro et al., UHMS survey | 2024 | 265 UHMS member providers | Myopia most common reported adverse effect (24.4%) | Survey of provider recall, not direct patient data |
| Sokolowski et al., systematic review | 2024 | 22 articles (divers + HBOT) | Confirms myopic shift is real; data too heterogeneous to set a safety limit | Systematic but limited by weak underlying studies |
| Brügger et al., Navy diver case series | 2020 | 4 divers, high-PO2 exposure | Myopic shift after concentrated exposure; resolved in 2-3 weeks | Tiny case series, diver (not clinical HBOT) context |
The honest bottom line on grading: the myopia effect is well established but poorly quantified. The cataract effect is plausible and biologically supported, but the human evidence rests heavily on one small 1984 study of patients getting extreme session counts. Anyone telling you HBOT "definitely will" or "definitely won't" cause cataracts at normal doses is going beyond what the data supports.
Who Is at Higher Risk
Risk isn't evenly spread. A few factors push you up the curve.
Number of sessions. This is the big one. Myopia tracks with cumulative exposure, and cataracts show up almost exclusively after very long courses. A 20-session diabetic foot ulcer protocol is a different risk world than a 150-session off-label wellness regimen. If you're doing dozens of "maintenance" dives at a cash clinic, you're stacking the dose that drives both effects.
Higher pressure. Effects are tied to oxygen partial pressure, so 2.4 ATA medical protocols deliver more oxygen to the lens than 1.3 ATA "mild" setups. That said, myopia and even cataract have been reported across a range of pressures, so low pressure is not a free pass.
Age and existing lens changes. Older adults already have age-related lens stiffening and may have early cataracts. Adding oxidative stress to a lens that's already changing can tip a borderline cataract into a clinically meaningful one. The lens of an older eye also sees more oxygen as the vitreous gel breaks down with age, which StatPearls flags as a contributing factor.
Pre-existing nearsightedness. If you're already myopic, a further shift may push you past the point where your current glasses work, even if the absolute change is the same as someone with sharper vision.
Total course length and "maintenance" stacking. It's worth separating a single defined course from a habit. Someone who does one 40-session course for a wound and stops is in a very different position from someone who runs course after course for years as a wellness routine. The lens doesn't reset between courses the way your wallet does. Oxidative damage to crystallins is cumulative over a lifetime, which is exactly why StatPearls points to lifetime oxygen exposure as a primary contributor to nuclear cataract in general. Repeated long courses are the realistic way an otherwise low cataract risk creeps upward.
There's also a quieter risk factor: clinics that don't track your eyes at all. If nobody measured your refraction before you started, nobody can tell whether a change happened. Plenty of off-label wellness operations never mention vision in their consent process. That doesn't raise your biological risk, but it raises the odds that a real change goes unnoticed until it's harder to interpret.
How to Tell Reversible Blur From Real Damage
This is the practical question patients actually care about: how do I know if I should worry?
Reversible hyperoxic myopia looks like this: gradual onset over a treatment course, blur that's worse at distance than up close, no pain, no flashes or floaters, and a prescription that drifts back toward your baseline in the weeks and months after you stop. It's a nuisance, not an emergency.
Warning signs that deserve a prompt eye exam rather than a "wait and see":
- Vision that keeps getting worse months after you finished HBOT, instead of recovering.
- A persistent cloudy or "looking through a foggy window" quality, especially central, that doesn't reverse. That pattern fits cataract, not simple myopic shift.
- New flashes, floaters, a curtain over part of your vision, or sudden vision loss. None of these are typical HBOT myopia and all warrant urgent care.
- Eye pain or significant visual-field loss.
The single best protective move is simple: get a baseline eye exam before a long HBOT course, and a follow-up after. Documenting your refraction before you start lets your eye doctor tell a temporary shift from a true structural change later.
What should that baseline include? A measured refraction (your prescription in diopters), a visual acuity reading, and ideally a slit-lamp look at the lens to note any existing cataract. If you're heading into a long off-label course, ask whether the lens was graded for nuclear opacity. That single line in your chart is what makes a follow-up exam meaningful. Without a starting point, an eye doctor a year later is guessing whether your lens always looked that way.
A simple self-check helps you read your own symptoms. Reversible myopia tends to start gradually during the course, gets better once you stop, blurs distance more than near, and comes with no pain, flashes, or floaters. Cataract is the opposite pattern: often noticed later, stable or worsening rather than recovering, and hazier in quality, with glare, a "foggy window" look, and washed-out color. Pain, flashes, floaters, or a curtain over your vision don't fit either pattern and need urgent care regardless. If your honest answers line up with the cataract column of that comparison, that's your cue to book an eye exam rather than wait it out.
How This Compares to Other HBOT Side Effects
Vision changes are real, but they're not the side effect most likely to send you home early. For perspective on the broader risk picture, here's how the eye effects sit next to the other common ones.
Ear and sinus barotrauma from pressure changes is the most frequent acute complaint and the one most likely to interrupt a session, though it's manageable with equalization technique. Confinement anxiety is common too, especially in monoplace chambers. Oxygen toxicity seizures are rare but serious. Against that backdrop, myopia is unusual in that it's common but slow, painless, and reversible, while cataract is the rare effect with the most lasting consequences. For a fuller rundown, see our guides on HBOT side effects and risks and oxygen toxicity in HBOT.
What This Means for Your Decision
If a doctor has prescribed HBOT for an evidence-backed indication, the vision effects rarely change the calculus. For something like carbon monoxide poisoning, a diabetic foot ulcer, or radiation tissue injury, a temporary myopic shift over a 20-to-40 session course is a minor cost against a real medical benefit, and cataract risk at those session counts is low.
The math shifts when you're considering long, off-label, cash-pay courses for wellness, anti-aging, or unproven conditions. There, you're paying out of pocket to stack the exact exposure that drives both myopia and, at the far end, cataract, often for benefits the evidence doesn't strongly support. That trade-off deserves a harder look. Our breakdown of who is a good candidate for HBOT and the HBOT safety profile from published trials can help you weigh it.
Whatever you decide, the protective steps are cheap and effective: get a baseline eye exam, treat at the lowest pressure and session count that fits your medical need, report vision changes to both your hyperbaric and eye doctors, and don't update your glasses until your prescription has stabilized after treatment.
Frequently Asked Questions
Will HBOT permanently ruin my eyesight?
Almost certainly not from a normal treatment course. The common effect, a myopic (nearsighted) shift, is reversible and usually fades within days to months after you stop. Permanent damage in the form of nuclear cataract is rare and tied mainly to very long courses, on the order of 150 sessions or more in the landmark study. A standard 20-to-40 session medical course carries a low cataract risk.
How many HBOT sessions before my vision changes?
There's no exact threshold, and a 2024 systematic review specifically concluded the data is too heterogeneous to set one. In practice, the myopic shift often becomes noticeable somewhere around 20 to 30 sessions and builds with more exposure. Some people notice it sooner, some later, depending on pressure and individual sensitivity.
Is the cataract risk real or just one old study?
Both. The strongest human evidence is the 1984 Palmquist study, in which 7 of 15 patients with clear lenses developed nuclear cataract after 150+ exposures. It's small and old, but the biological mechanism, oxidative cross-linking of lens proteins, is well supported and reproduced in animal studies. The fair summary: real but rare, and driven by very high cumulative dose.
Should I get new glasses during HBOT treatment?
No. Your prescription is unstable during and shortly after a course because of the reversible myopic shift. New glasses bought mid-treatment will likely be the wrong strength once your vision settles. Most eye doctors advise waiting one to three months after your final session before updating your prescription.
Does lower-pressure "mild" HBOT avoid the vision risk?
It lowers it but doesn't eliminate it. The effects scale with oxygen partial pressure, so lower-pressure protocols deliver less oxygen to the lens. But hyperoxic myopia has been documented across a range of pressures, including relatively low exposures in divers, so even mild HBOT can cause a refractive shift with enough cumulative exposure.
This article is for general information only and is not medical advice. Talk to your doctor and an eye care professional before starting hyperbaric oxygen therapy, and report any vision changes promptly.
Sources
- Palmquist BM, Philipson B, Barr PO. Nuclear cataract and myopia during hyperbaric oxygen therapy. Br J Ophthalmol. 1984. PMID 6691953 (full text, PMC)
- Laspro M, et al. Hyperbaric Oxygen Therapy Regimens, Treated Conditions, and Adverse Effect Profile: a UHMS Survey Study. Undersea Hyperb Med. 2024. PMID 39821765
- Sokolowski SA, et al. Development of myopia in scuba diving and hyperbaric oxygen treatment: a case report and systematic review. Diving Hyperb Med. 2024. PMID 39675741
- Brügger JW, Rauscher GA, Florian JP. Hyperoxic myopia: a case series of four divers. Undersea Hyperb Med. 2020. PMID 32574443
- Bennett MH, Cooper JS. Hyperbaric Oxygen Therapy and Associated Cataracts. StatPearls. PMID 29261974
- Gengel KC, Hendriksen S, Cooper JS. Hyperbaric Related Myopia and Cataract Formation. StatPearls. PMID 28613605
- U.S. FDA. Follow Instructions for Safe Use of Hyperbaric Oxygen Therapy Devices: Letter to Health Care Providers
- PubMed: hyperbaric oxygen, myopia and cataract (literature search)