Photobiomodulation for Dry AMD: Is There Benefit Beyond Visual Acuity?

Photobiomodulation has changed the conversation around dry age-related macular degeneration. With Valeda, the FDA-authorized light therapy for dry AMD, much of that conversation has understandably focused on the improvement in visual acuity demonstrated in the clinical trials.

Improved acuity is a good outcome. But for me, the more important question is whether photobiomodulation is doing anything to alter the course of dry AMD.

What Are We Trying to Accomplish with AMD?

Historically, our goals in dry AMD have centered on slowing progression and preserving useful vision.

That is how we think about AREDS and AREDS2 supplementation. We do not recommend AREDS2 because we expect patients to gain a line on the eye chart. We recommend it because, in the appropriate patient, it can reduce the risk of progression to advanced AMD.

Photobiomodulation gives us the possibility of improving vision while also affecting disease progression. Both outcomes matter.

If I have a patient with intermediate AMD who is 20/20 today, I want to know whether treatment may help that patient remain 20/20 and lower the likelihood of developing geographic atrophy or neovascular AMD several years from now.

That led me to look beyond visual acuity and ask three practical questions:

• Can photobiomodulation reduce drusen?
• Can it reduce progression to geographic atrophy?
• Is there evidence that it may reduce conversion to neovascular AMD?

The available data make me more comfortable discussing PBM as a disease-management option with appropriate patients.

Can PBM Reduce Drusen?

A useful study for answering this question was published by Iovino and colleagues in the British Journal of Ophthalmology in 2026.

This prospective, multicenter, double-masked, sham-controlled randomized trial included 138 eyes from 78 patients with early or intermediate dry AMD. The primary endpoint was mean drusen volume at 12 months.

Drusen volume decreased by 0.03 mm³ in the PBM group and increased by 0.02 mm³ in the sham group. The between-group difference was statistically significant, with a p-value of less than .001.

For clinicians, this provides fairly strong evidence that PBM can produce a measurable anatomical effect.

Patients are not particularly concerned with drusen volume in cubic millimeters. They want to know whether they will continue to see well.

Still, if we are asking whether PBM is affecting the underlying disease process, a reduction in drusen is relevant.

The finding is also consistent with earlier work. LIGHTSITE I reported a substantial reduction in central drusen volume, while sham-treated eyes gained drusen.

When similar anatomical changes appear across separate studies, the finding becomes harder to dismiss as noise.

What About Conversion to Wet AMD?

The Iovino trial also reported four conversions to macular neovascularization in the sham group and none in the PBM group. The difference reached statistical significance at p=.044.

I would interpret that finding cautiously.

The result is based on only four conversion events. With such small numbers, one or two different outcomes could materially change the statistical result.

So I would not tell a patient that PBM has been proven to prevent wet AMD.

What we can say is that, in this randomized trial, four sham-treated eyes converted to macular neovascularization while no PBM-treated eyes did. That is a clinically interesting signal, but it needs confirmation in larger datasets.

What About Geographic Atrophy?

The geographic atrophy data give us another piece of the story. Iovino did not demonstrate a reduction in geographic atrophy, but LIGHTSITE III did. At 24 months, new geographic atrophy occurred in 6.8 percent of PBM-treated eyes compared with 24 percent of sham-treated eyes.

Putting the Evidence Together

Now I can start putting the evidence together. We have multiple studies showing drusen reduction. We have a randomized trial with fewer conversions to macular neovascularization in the PBM group. We have another trial demonstrating a lower incidence of new geographic atrophy.

I don’t need one study to demonstrate all three outcomes before I can use this information clinically. That’s not how I make most clinical decisions.

I look at the available evidence, consider whether there is a reasonable pattern across that evidence and then determine how it applies to the patient sitting in front of me.

For me, there is enough here to reasonably expect a benefit.

There are also functional outcomes worth considering. LIGHTSITE I reported improvements in contrast sensitivity, and other studies have examined low luminance visual acuity and microperimetry. PBM4AMD is particularly interesting because investigators evaluated several of these outcomes together, including drusen volume, contrast sensitivity, low luminance visual acuity, and scotopic microperimetry.

Early after treatment, drusen volume decreased, contrast sensitivity improved, and low luminance visual acuity improved. By week 24, however, the drusen volume improvement was no longer statistically significant. Contrast sensitivity had returned to baseline, and the improvement in low luminance visual acuity had declined. Scotopic microperimetry actually worsened during follow-up.

I don’t look at those findings and conclude that PBM doesn’t work. I think they tell us something much more practical. We probably need to keep treating.

How Long Does the Benefit Last?

LIGHTSITE I used treatment series separated by approximately six months. Patients improved after treatment, but some of that benefit appeared to decline before the next series.

PBM4AMD showed a similar pattern. A single treatment series produced measurable changes, but several of those improvements had diminished by approximately six months.

LIGHTSITE III used a shorter retreatment interval.

Patients received nine treatment sessions, generally three times per week over three to five weeks, and repeated the series every four months. With that schedule, benefits were sustained over 24 months.

That does not tell us that four months is the only effective interval. It tells us that the four-month schedule has evidence supporting sustained benefit, while studies using longer intervals suggest that some effects may begin to fade.

For a chronic disease, that is not particularly surprising.

We already manage glaucoma, diabetic eye disease, and many other chronic conditions with ongoing treatment rather than expecting one course of therapy to provide indefinite benefit.

PBM may need to be viewed in a similar way: as ongoing management of dry AMD rather than a treatment series we complete once and walk away from.

Can We Reduce the Treatment Burden?

That brings me to what I think is the more interesting unanswered question. How much treatment do we actually need?

The LIGHTSITE III protocol requires nine treatment sessions repeated every four months. In practical terms, that is approximately 27 treatment visits per year.

If we are going to treat patients for years, that’s a significant commitment, so naturally I wanted to know whether we could do less.

Could we provide six treatments instead of nine? 

Could we treat twice per week rather than three times per week? 

Could we repeat the treatment every five months rather than every four months? 

I went looking for that evidence, and I couldn’t find it.

We have evidence that treatment every four months works. We have evidence suggesting that waiting approximately six months allows some of the effect to disappear. What we don’t have is a good prospective study testing the space between those two schedules.

We also don’t have a dose de-escalation study comparing nine treatments with six treatments or another abbreviated treatment series. Earlier TORPA work actually used more treatment, with approximately 18 sessions delivered three times per week over six weeks. That obviously doesn’t help us much if we are trying to make treatment easier for our patients.

ALIGHT went in a different direction and evaluated an overnight 505 nanometer light mask. Patients used the device for eight hours nightly for 12 months, and the study did not demonstrate a benefit on progression. There are also smaller studies using wearable devices and other PBM protocols. Those are interesting, particularly because effective home treatment could dramatically change the treatment burden, but we don’t have enough evidence to replace the protocol that has demonstrated sustained benefit.

Right now, the lowest treatment burden with good evidence of sustained benefit is nine treatment sessions repeated every four months. That doesn’t mean nine treatments every four months is the biological minimum required to produce an effect. It means that’s the lowest burden protocol where we currently have good evidence showing sustained benefit.

I suspect we will eventually learn that we can do less. Maybe some patients will need treatment every four months while others can go five months. Maybe we can reduce the number of treatments in a series based on the patient’s response. Maybe imaging or functional testing will eventually help us determine when an individual patient needs retreatment. Those are the studies I would really like to see next. 

At this stage, another trial showing a few additional letters of improvement is less clinically useful to me than a trial showing whether we can treat six times instead of nine, or every five months instead of every four.

That would immediately change how we manage these patients.

What Do We Tell Our Patients?

The patient conversation should include both the potential benefit and the treatment burden. We have evidence that PBM can reduce drusen volume. We also have evidence suggesting a possible reduction in geographic atrophy and conversion to neovascular AMD.

The strongest long-term protocol we have currently requires nine treatments, generally given three times per week, with the series repeated approximately every four months.

Some patients will find that reasonable. Others will not.

A patient who watched a parent lose central vision from AMD may view 27 treatment visits per year very differently from someone who has never seen what advanced AMD can do.

Our job is to explain what the evidence shows, where the uncertainties remain, and what the treatment requires.

The patient can then decide whether the potential benefit justifies the treatment burden.

The Bottom Line

I think this brings us back to how we have always approached dry AMD. Our goal is to reduce the likelihood of progression and preserve useful vision for as long as possible. The fact that Valeda may also improve visual acuity is a bonus, but it doesn’t need to be the sole measure of whether treatment is successful.

If I can shrink drusen and reduce the patient’s likelihood of progressing to geographic atrophy or wet AMD, I have accomplished something meaningful for that patient. The question I am left with isn’t whether PBM provides a benefit. I think we have enough evidence to reasonably expect that it does.

The question is how much treatment we need to maintain that benefit. Right now, our best evidence supports nine treatments repeated every four months, and we don’t have the data to tell us how much we can reduce that treatment burden.

Until we do, the patient conversation can remain fairly simple:

1. Here is what the evidence suggests.
2. Here is what treatment requires.
3. Is that tradeoff worthwhile for you?

That’s the conversation I think we should be having about photobiomodulation for dry AMD.

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