Red Light Therapy Improves Mitochondrial Function | W2R

Image by Michael Bußmann from Pixabay

I wrote here on benefits of red light therapy. It’s been studied and shown to aid in numerous localized conditions, from musculoskeletal injury and repair to wound healing to hair regrowth. It seems hard to believe that something as ubiquitous and benign as light can do all that, though. How does it work?

The mechanism turns out to be very fundamental: red light therapy is a way to locally stimulate the mitochondria.

The Mitochondria: A Review

Mitochondria are the powerhouse of the cells, producing the vast majority of ATP, the body’s energy currency, from food and oxygen.

Your body runs on ATP, of course. If you don’t have enough of it, you can’t repair damaged tissue and heal.

But it’s not just low ATP production (or the lack thereof) that’s the problem. ATP gets made via an electron pump in the inner mitochondrial membrane, called the Electron Transport Chain (ETC). If any part of the five complexes that make up the ETC aren’t working properly, electrons can “leak out” as free radicals, creating local oxidative damage in the cell. This is one of the major theories of both aging and degenerative disease.

Even the most efficient mitochondria will still have some leakage of electrons out into the cytosol, and this is actually a good thing in small doses (it’s hormetic—more on this here). But if the mitochondria lack the building blocks they need to do their job properly, or if they are otherwise dysfunctional, this means both too much oxidative stress, and too little ATP.

If this happens to only an occasional mitochondrion here or there, the body sends the signal to it to self-destruct, in a process called mitophagy. This is exactly how things are supposed to work; the body breaks down the dysfunctional mitochondria, and replaces them with brand new ones that can do their job properly.

But if there’s a tipping point, where there are too many dysfunctional mitochondria, or the signals for mitophagy don’t get sent or received, tissue healing is dramatically impaired.

Mitochondrial Support for Function

Most mitochondrial support products include building blocks to help mitochondria do their job directly—cofactors for the various complexes in the electron transport chain for instance, especially CoQ10. Supports to shuttle fatty acids inside the mitochondria for breakdown, like carnitine. Electron donors, like Vitamins B2 and B3, especially in the form of NADH+ and niacinamide. Most of the time these products also include some antioxidants to help quench oxidative stress from inefficient mitochondria, especially glutathione and NAC.

All of these things are good, but they’re only game changers when the problem is the lack of those ingredients. When those aren’t the issue, and the problem is more dysfunction, due to age or toxicity, these approaches don’t move the needle very impressively.

Ways to Stimulate Mitophagy

Mitophagy is a major focus in the longevity world at the moment, and for good reason—but we don’t have that many known tools to trigger it. The main one is to incorporate fasting into your regular routine, intermittent or otherwise.

A few supplements can be useful to this end too. One that has been studied to directly stimulate production of new mitochondria is PQQ.

Another is methylene blue, though there are a couple more caveats to that one (more on that here).

Ways to Improve Existing Mitochondrial Function

Methylene blue also can help toxic or otherwise dysfunctional mitochondria to work more efficiently—it’s one of very few things I know of that has this potential.

Visible red light is another, stimulating up to 190% more ATP production about twenty minutes after red light therapy is completed (and in fact, methylene blue and red light therapy together have a synergistic effect). This study also points out that red light therapy is another way to optimize functionality in otherwise toxic cells.

This study postulates that visible red light gets absorbed by cytochrome c oxidase, the enzyme at the fourth complex inside the mitochondrial electron transport chain, and the last step before ATP production. This study agrees that the same enzyme is a photoreceptor, meaning that it can directly interact with the light. In the process, the efficiency of the fourth complex speeds up, leading to more ATP production, and less oxidative damage.

This study shows that exposing fruit flies to red light at 670 nm wavelength increased ATP production, decreased inflammation (inflammation tends to be secondary to oxidative stress), and significantly increased average lifespan. This study also shows that along with increasing activity of cytochrome c oxidase, red light therapy also stimulates superoxide dismutase, an enzyme that quenches free radicals produced by oxygen that doesn’t get consumed in the production of ATP.

The Upshot

I’m excited to find another minimally invasive approach to at least locally stimulating dysfunctional, toxic, or injured mitochondria to greater efficiency.