I was lucky enough to spend some time corresponding with and meeting Professor Glen Jeffery — a researcher who’s spent much of his career exploring the systemic effects that light has on the body. A super nice guy who was very generous with his time. Recently, Glen’s work has gone viral among those following red light therapy or longevity science more broadly, and for good reason.
We had a fascinating conversation towards the end of last year. And honestly, it’s hard not to speculate on the broader implications of what he’s uncovering. Because from what the early stages of this research suggest, light — specifically red light — could play a surprisingly influential role in how our bodies regulate blood glucose.
How Light Influences Glucose: Red vs Blue
In Glen’s recent human study, participants were exposed to different wavelengths of light — red at 670nm and blue at 480nm — for a short period before consuming a glucose-rich drink. Blood glucose levels were then monitored over the hours that followed.
Those exposed to red light saw peak blood glucose levels drop by around 27% compared to the control group, suggesting their bodies became more efficient at absorbing and using the sugar. Meanwhile, blue light had the opposite effect — glucose levels stayed elevated for longer, likely reflecting disrupted mitochondrial function.
So, what’s actually going on here? Glen proposed the following:
Mitochondria — the tiny powerhouses inside our cells — respond directly to light. Red and near-infrared wavelengths stimulate an enzyme called cytochrome c oxidase, also known as Complex IV in the electron transport chain. This is the final stage where ATP, the body’s core energy molecule, is produced — fuelling everything from muscle contractions to cellular repair.
In simple terms, red light helps mitochondria do their job more efficiently.
But — and this is a crucial point — better mitochondrial performance doesn’t just happen in a vacuum. These little engines still need fuel. Mitochondria require both oxygen and glucose to produce ATP. So when we enhance their function with red light, we also increase the demand for those resources.
By turning up mitochondrial activity, you’re effectively revving the engine — and that means pulling more oxygen and glucose out of the bloodstream to meet the increased energy demand.
It’s not unlike what athletes track with VO₂ max — the maximum amount of oxygen the body can utilise during exercise. A higher VO₂ max usually means more efficient mitochondria, greater oxygen extraction, and better endurance. What we’re seeing here is a similar mechanism — but triggered by light. Photobiomodulation boosts cellular efficiency, increases metabolic demand, and in doing so, drives more glucose consumption.
Fuelling the Engine
To support the findings from the human trial, a recent cell culture study led by Cecile Angrand and colleagues (published in Antioxidants, 2023) looked at how red and near-infrared light influenced cellular energy production — specifically ATP levels. But the researchers added an important and revealing addition: they tested the effect both with and without glucose present in the culture medium.
Red light only increased ATP production when glucose was available. Without glucose, the mitochondria didn’t respond. The light alone wasn’t enough.
This reinforces the idea that photobiomodulation enhances what’s already there — it doesn’t override basic biology. Mitochondria still need the natural raw materials — oxygen and glucose — to function effectively and generate energy. Red/NIR light appears to improve the efficiency and speed of this process.
It’s a subtle but important distinction: red light is a highly effective boost to metabolic function, but it plays a part in the broader system of mitochondrial health — a system that still depends on proper nutrition, good sleep, movement, and the right supplementation where appropriate.
Beyond the Target Area: Systemic Effects and Mitochondrial Signalling
While red light therapy has its most powerful effects at the site of application, emerging research suggests it may also trigger systemic responses that extend beyond the illuminated area.
Some studies have shown that even when light is applied to a specific region, cells elsewhere in the body may respond. This appears to be driven by mitochondrial signalling — a referral effect that is both delayed and diminished compared to the direct, local impact.
However, this becomes particularly interesting in the context of blood glucose regulation. If this referral effect leads to a sustained, system-wide increase in glucose uptake, it could mean that red light therapy continues to support metabolic function for several hours — or even days — after treatment.
What this could mean for Blood Glucose Disorders
The research shows early promise that red light therapy could be an effective, non-invasive tool for modulating blood glucose levels.
Given that mitochondrial dysfunction is central to many metabolic conditions, improving mitochondrial efficiency may help increase cellular demand, glucose uptake, and energy turnover — potentially shifting the system back toward balance.
The literature is still in its early stages, but the potential here is exciting. We’re only just beginning to understand how light can influence metabolism — and where this leads could be far more impactful than we ever expected.
References
Jeffery, G., et al. (2022). Systemic glucose levels are modulated by specific wavelengths in the solar light spectrum that shift mitochondrial metabolism. BMJ Open Diabetes Research & Care, 10(6).
Angrand, C., Pernet, D., et al. (2023). Glucose Improves the Efficacy of Photobiomodulation in Changing Intracellular ATP and ROS Levels. Antioxidants, 12(10), 1907.
Santos, N. R., et al. (2020). Can photobiomodulation therapy (PBMT) control blood glucose in diabetic patients? A systematic review. Photodiagnosis and Photodynamic Therapy, 32, 101889.
Zhou, Y., et al. (2022). Effects of photobiomodulation on mitochondrial function in diabetic adipose-derived stem cells. Biochimica et Biophysica Acta (BBA) - Bioenergetics, 1863(10), 148614.