Red light therapy

Glen Jeffery, email interviewed by Peter Makai

Recently, several companies have started to offer red light glasses, which supposedly reduces vision loss in ageing eyes, through influencing mitochondria. Since ADOA is a mitochondrial disease, we were naturally curious if it can be safe and possibly beneficial for ADOA patients. ADOA is caused by a damaged gene (OPA1) causing several problems in the mitochondria within the so-called retinal ganglion cells, the cells which transmit information between the eyes and the brain. Mitochondria are primarily responsible for energy production by making a substance called ATP. ATP is produced within the mitochondrial membrane, where the OPA1 gene is necessary for several functions. If there is insufficient ATP, the mitochondria is damaged. When damaged, mitochondria release a substance signaling cell death, and vision loss.

To give us some insights into how this device works, we have contacted Professor Glen Jeffery from the University College London, who has spent several decades on researching the mechanism in the eyes in relation to red light. He was kind enough to share his thoughts with us.

1. Can you please describe in layman’s terms how the approach works?

When mitochondria are challenged by age or disease they have reduced membrane potential – they have a charge, like a battery and this declines. When this happens they produce less ATP, which is needed for cell function. When it declines significantly it can result in channels opening in the mitochondrial membrane causing cell death. The pumps that make ATP spin within a relatively sticky layer of water molecules. Most experts think that the absorbance of long wavelengths by the water molecules reduces the stickiness and the spinning pump picks up more speed that can be sustained. This in turn increases ATP production. Although scientists are not entirely sure, this is currently the most likely mechanism, in part because the wavelengths that improve mitochondrial function overlap with those absorbed by water. So when exposed to red light, ATP is increased, the mitochondria keeps functioning, and does not trigger cell death.

2. A question on the safety of the new red light glasses. Usually, there are extensive studies available on the safety of such new therapies, but at this point, I’m not aware of such studies (the company claims that it was approved by the ethics committees of Moorfield’s and UCL, and is not marketed as a therapy, only as an anti-aging device). Are there any biological mechanisms which point to this not being safe, in adults and/or in children?

Safety of devices depends on energy and wavelength. Generally longer wavelength devices are much safer at the same energy than short wavelength devices. I have no commercial relationship with the two companies (Eye-Power and Eyecharger), but I have tested their prototypes because I thought it was important that there was something out there that I knew was safe. Both products work with energies and wavelength for which I have obtained ethical permission from Moorfields Eye Hospital and also University College London. This confirmed that they are well within the safe range. However, they do not have a clinical seal of approval on them. Obtaining this can be a long process. I have told both companies that we would strongly disapprove of any attempt to claim that their devices were officially clinically approved and I stand by this.

Having said this, in the 8 or so years I have been working in this area I have yet to come across any down side to the use of long wavelength light when energies have been appropriate. Researchers in this field have talked a lot to one another and this issue has been raised many times. No one has identified a problem. We know that there are situations in which it simply does not work e.g. when given at the wrong time of day or when exposures are too long (>1h)

 3. Can red light therapy restore lost vision by making the remaining retinal ganglion cells (RGCs) “work harder”, or does red light therapy potentially stop the gradual decline in vision typical for ADOA?

When it comes specifically to ADOA there are a lot of unknowns, but we can make educated assumptions. Based on mouse models (mice with modified OPA1 genes), there are possible benefits, but this has not been confirmed in human ADOA patients.

A conservative view would be that it may reduce the progression of the disease. We know it slows cell death and I have seen this in many situations. Can it restore something? Well not if the cell has died, but if the cell is dormant prior to cell death then perhaps yes. It certainly restores human cone function that mediates colour vision. These cells do not die with age but they do become partially dysfunctional.

4. As far as I’m aware, your research was focused on photoreceptor cells, which are not in the disease pathway of ADOA. Do you think red light therapy can have benefits for older ADOA patients (whose eyesight declines not only because of the decreasing number of RGCs, but also because the photoreceptor cells work less), even if nothing changes within the RGCs themselves?

So can it help ADOA? My response is that this is possible and with the correct devices there is no harm. So the worst case is that you waste 3 mins of your time once or twice a week exposing your eyes. The more hopeful scenario is that the pace of the disease slows down when measured over a long enough time period. Photoreceptor function will improve in the aged, although not everyone detects it in everyday life. I have certainly seen some interesting

​As a final note from the Cure ADOA Foundation: we strive to keep you informed of research developments, we do not recommend specific treatments at this time. The only treatments for which safety has been confirmed are those that your doctor (eventually) prescribes. Anything else is at your own risk.