What are the benefits and risks of low level light therapy (photobiomodulation) for treating dry age-related macular degeneration (a degenerative eye condition)?

Why is this question important?
Age-related macular degeneration (AMD) is a common condition of the eyes. It usually develops in people aged over 50, and leads to progressive loss of central vision. People with AMD may find it difficult to read or recognise faces, and they can become partially sighted.

AMD progresses in stages. To begin with, yellow spots (drusen) develop under the retina (the back of the eye). These are not visible to the naked eye, but can be seen by health professionals during examinations of the eyes. As AMD progresses, cells located in the macula (the central area of the retina) that are needed for vision die. If blood vessels in the eye go on to leak, the condition is classed as ‘wet’ AMD. If there is no leakage, the condition is known as ‘dry’ AMD.

There is no cure for dry AMD. However, it may be possible to use low level light therapy (photobiomodulation) to stop vision from worsening. To find out how effective photobiomodulation is for treating dry AMD and whether it is associated with unwanted effects, we reviewed the evidence from research studies.

How did we identify and evaluate the evidence?
First, we searched for randomised controlled studies (clinical studies where people are randomly put into one of two or more treatment groups), because these studies provide the most robust evidence about the effects of a treatment. We then compared the results, and summarised the evidence from the studies. Finally, we rated our confidence in the evidence, based on factors such as study methods and sizes, and the consistency of findings across studies.

What did we find?
We found two studies that involved a total of 90 people with dry AMD. Both studies received public funding.

In one study, with 60 people, set in the UK, 30 people wore a light-emitting eye mask for eight hours every night for one year. Their results were compared to those of 30 people who received no treatment.

In the other study, with 30 people, set in Canada, people received either:

→ low level light therapy for five minutes per eye, three times a week for three weeks, which was repeated after a six-month break; or

→ a sham treatment, three times a week for three weeks, which was repeated after a six-month break.

Five of the investigators of this study had links to the manufacturer of the light therapy device used (three of these were employed by the manufacturer).

We have little to very little confidence in the evidence we found, because it is based on only two small studies. The way these studies were conducted is likely to have introduced errors in their results.

The evidence suggests that:

→ photobiomodulation may make little or no difference to changes in clarity of vision one year after starting treatment compared to no treatment or a sham treatment;

→ photobiomodulation may make little or no difference to disease progression of AMD after one year;

→ photobiomodulation may improve a person’s ability to distinguish an object against its background;

→ photobiomodulation may make little or no difference to clarity of vision as reported by patients.

We have too little confidence in the evidence to be able to determine whether, after one year of treatment, photobiomodulation affects:

→ progression to wet AMD.

Since neither study reported information about some outcomes, we cannot determine from the evidence whether, after one year of treatment, photobiomodulation affects:

→ near vision;

→ vision in low light; or

→ reading speed.

What does this mean?
Compared to no treatment or a sham treatment, photobiomodulation may make little or no difference to clarity of vision or disease progression in people with dry AMD one year after starting treatment.

We do not know if photobiomodulation affects other aspects such as progression to wet AMD or changes in near vision. This is because too few, or no, robust studies have investigated this.

How up-to-date is this review?
The evidence in this Cochrane Review is current to May 2020.

Authors' conclusions: 

Currently there remains uncertainty whether PBM treatment is beneficial in slowing progression of non-exudative macular degeneration. There is a need for further well-designed controlled trials assessing dosimetry, powered for both effectiveness and safety outcomes. Consideration should be given to the adoption of agreed clinical outcome measures and patient-based outcome measures for AMD.

Read the full abstract...

Age-related macular degeneration (AMD) is one of the leading causes of blindness in high-income countries. The majority of cases of AMD are of the non-exudative type. Experts have proposed photobiomodulation (PBM) therapy as a non-invasive procedure to restore mitochondrial function, upregulate cytoprotective factors and prevent apoptotic cell death in retinal tissue affected by AMD.


To assess the effectiveness and safety of PBM compared to standard care, no treatment or sham treatment for people with non-exudative AMD.

Search strategy: 

We searched CENTRAL (which contains the Cochrane Eyes and Vision Trials Register) (Issue 5, 2020), Ovid MEDLINE, Embase, ISRCTN, ClinicalTrials.gov and the WHO ICTRP to 11 May 2020 with no language restrictions.

Selection criteria: 

The review included randomised controlled trials (RCTs) on participants receiving any type of PBM therapy for non-exudative AMD compared to standard care, sham treatment or no treatment.

Data collection and analysis: 

We used standard methodological procedures expected by Cochrane. We considered the following outcome measures at 12 months: best-corrected visual acuity (BCVA) ; contrast sensitivity; near vision; low luminance density score; reading speed; vision-related quality of life score; and adverse events such as progression of AMD and conversion to exudative AMD. We graded the certainty of the evidence using GRADE.

Main results: 

We included two published RCTs from single centres in the UK and Canada, which recruited 60 participants (60 eyes) and 30 participants (46 eyes) respectively. Participants in these trials were people with non-exudative AMD with Age-Related Eye Disease Study (AREDS) categories 2 to 4. One study compared single wavelength PBM with no treatment. This study was at risk of performance bias because the study was not masked, and there was attrition bias. One study compared multi-wavelength PBM with sham treatment and conflicts of interest were reported by study investigators. We also identified three eligible ongoing RCTs from searching the clinical trials database.

When comparing PBM with sham treatment or no treatment for non-exudative AMD, there was no evidence of any meaningful clinical difference in BCVA at 12 months (mean difference (MD) 0.02 logMAR, 95% confidence interval (CI) -0.02 to 0.05; 2 RCTs, 90 eyes; low-certainty evidence). One study comparing multi-wavelength PBM with sham treatment showed an improvement in contrast sensitivity at Level E (18 cycles/degree) at 12 months (MD 0.29 LogCS, 95% CI 0.23 to 0.35; 1 RCT, 46 eyes; low-certainty evidence). Visual function and health-related quality of life scores were comparable between single wavelength PBM and no treatment groups at 12 months (VFQ-48 score MD 0.43, 95% CI -0.17 to 1.03; P = 0.16; 1 RCT, 47 eyes; low-certainty evidence).

When comparing PBM with sham treatment or no treatment for non-exudative AMD, there was no evidence of any meaningful clinical difference in conversion to exudative AMD (risk ratio (RR) 0.97, 95% CI 0.17 to 5.44; 2 RCTs, 96 eyes; very low-certainty evidence) at 12 months. There was inconclusive evidence that single wavelength PBM prevents the progression of AMD (RR 0.79, 95% CI 0.41 to 1.53; P = 0.48; 1 RCT, 50 eyes; low-certainty evidence). Disease progression was defined as the development of advanced AMD or significant increase in drusen volume.

No included study reported near vision, low luminance vision or reading speed outcomes.