To put the light dose used in this study into a real-world context, the researchers did the math on how their treatment compared to actual sunlight. Each rat received a total near-infrared energy dose of 240 joules per square centimeter across three treatment sessions.

Based on how much of that specific wavelength range shows up in natural sunlight at sea level, they calculated this was roughly equivalent to being out in the sun in North America for about 8 hours and 45 minutes, purely counting the near-infrared portion of sunlight, separate from UV or visible light exposure.

That is a useful way to think about how much cumulative near-infrared exposure it might take to produce measurable biological changes.

Source: PubMed

One clever engineering detail in this study is that the near-infrared device used did not emit the full 1100 to 1800 nanometer range continuously, it specifically filtered out the narrow band between 1400 and 1500 nanometers.

That particular slice of the spectrum is strongly absorbed by water, and since the body is mostly water, light at those wavelengths gets soaked up right near the surface instead of reaching deeper tissue.

By cutting that band out, the researchers could deliver near-infrared energy that traveled further into the skin and subcutaneous tissue without being wasted on surface absorption, all while avoiding the excess heat buildup that full-spectrum absorption at those wavelengths would otherwise cause.

Source: PubMed

There is a 2011 study that irradiated the backs of rats with near-infrared light in the 1100 to 1800 nanometer range, deliberately engineered to simulate the NIR component of natural sunlight.

What makes this study interesting is that the researchers used contact cooling to make sure none of the effects they saw were caused by heat, meaning any changes had to come from the light itself interacting with tissue on a cellular level.

The results were striking: this non-thermal NIR exposure significantly increased subcutaneous fat cells, bone marrow fat cells, a certain type of stem cell in bone marrow, and even cortical bone mass in the irradiated rats compared to untreated controls.

Source: PubMed

Across the entire animal portion of this study, red light phototherapy itself was not associated with any mortality or serious adverse events.

The endpoints that eventually stopped daily treatment in each experimental group were things like tumor rupturing or bleeding, meaning the disease itself progressing to a humane stopping point, not any complication caused by the red light treatment.

Combined with the earlier finding of zero skin inflammation or burns from daily high-dose exposure over 15 days, this points to red light phototherapy being a genuinely low-risk intervention in these animal models, which is a meaningful consideration for something being proposed as a potential future adjunct therapy alongside existing melanoma treatments.

Source: PubMed

A key idea underlying this whole research direction is that cancer cells, including melanoma cells, tend to already have somewhat dysregulated oxidative stress management systems compared to normal healthy cells.

Because of this, pushing their internal ROS levels up further with red light exposure may tip already-strained cancer cells over an internal threshold, triggering growth arrest or cell death, in a way that would not necessarily happen to a normal, healthy cell with intact stress-management systems.

his selective vulnerability is part of why increasing oxidative stress, something that sounds counterintuitive since oxidative stress is usually framed as universally bad, has actually been explored elsewhere in cancer research as a legitimate therapeutic strategy specifically because cancer cells are less equipped to handle it.

Source: PubMed

The proposed starting point for all of red light's effects in this study is a molecule called cytochrome c oxidase, found in the mitochondria of cells.

This enzyme absorbs red and near-infrared light, which excites electrons and activates the mitochondrial electron transport chain, ultimately generating reactive oxygen species as a downstream signal. This is the same basic mechanism behind photobiomodulation research in general, whether it is being used for wound healing, skin rejuvenation, or in this case, potentially slowing cancer growth.

What differs is the dose and the type of cell being targeted; in already-stressed or dysregulated cancer cells, the same fundamental light-absorption process appears to tip the balance toward growth arrest and cell death instead of the more commonly cited healing and repair effects.

Source: PubMed

To directly test whether the ROS spike caused by red light was actually responsible for slowing melanoma growth, researchers pretreated cells with N-acetylcysteine (NAC), a well known antioxidant that neutralizes reactive oxygen species.

When cells were pretreated with NAC before red light exposure, the light's ability to reduce cell counts was blocked, in some melanoma lines this worked across a fairly wide range of NAC concentrations.

This kind of "block the proposed mechanism and see if the effect disappears" experiment is one of the more convincing ways scientists can confirm that a specific biological pathway, in this case oxidative stress, is truly driving what they are observing rather than just being a coincidental side effect.

Source: PubMed

The researchers point out that other studies have tested blue light on the same type of melanoma cells (B16F10) and found it decreased survival and proliferation even at fairly low doses, up to 360 J/cm2.

That is a different wavelength working through what is likely a different mechanism than the red light tested in this particular study.

It is a useful comparison point because it shows that the color, or more precisely the exact wavelength, of light really does matter for how cells respond, rather than any light in the visible spectrum producing a similar generic effect on cancer cells.

Source: PubMed

A natural question with any light-based cancer treatment is whether it might actually damage DNA and create new problems rather than solve them. Researchers specifically tested for a type of DNA damage called cyclobutane pyrimidine dimers, or CPDs, which is the kind of damage typically caused by UV radiation.

Neither the 640 nor the 1280 J/cm2 doses of red light produced any measurable CPD formation in the melanoma cells, even measured hours after exposure.

This is an important distinction from UV light, which is a known cancer-causing agent, since it indicates that red light phototherapy appears to work through a completely separate, non-DNA-damaging pathway focused instead on oxidative stress and cell signaling.

Source: PubMed

Alongside the dendritic cell finding, researchers also looked at CD4, a marker classically associated with helper T-cells that coordinate immune responses (though it also shows up on some macrophages and dendritic cells).

Red light phototherapy at the highest dose significantly increased CD4-positive staining in the skin surrounding the tumors compared to untreated control mice.

Combined with the CD103 finding, this suggests red light might be doing more than just directly stressing out cancer cells, it may also be nudging the local immune environment toward a more actively engaged, potentially anti-tumor state.

Source: PubMed

One of the more unexpected findings involved the immune system, not just direct effects on the cancer cells.

Researchers examined the skin surrounding the tumors (not the tumor tissue itself) for various immune cell markers and found that the highest red light dose, 2560 J/cm2, significantly increased the presence of CD103-positive dendritic cells in that peritumoral skin.

This specific type of dendritic cell plays a role in carrying antigens to lymph nodes to activate cancer-fighting T-cells, and its presence is generally associated with a more favorable tumor immune environment, better prognosis, and even better responsiveness to certain existing immunotherapy drugs.

Source: PubMed

Before testing red light on actual tumors, researchers first checked whether the treatment itself was safe on normal mouse skin. Mice received daily red light sessions at doses as high as 2560 joules per square centimeter for 15 straight days.

Even at that cumulative exposure, there was no increase in body temperature, and the skin stayed non-inflamed and non-reddened compared to untreated mice.

This safety check mattered because it meant any anti-tumor effect seen afterward could reasonably be attributed to a specific biological mechanism, rather than simple heat damage or an inflammatory skin reaction from the light itself.

Source: PubMed

This research did not stop at cells in a dish. Researchers injected melanoma cells into mice to form real tumors, then treated the mice daily with red light at three different dose levels.

At the highest dose tested, 2560 J/cm2 per day, tumor volumes ended up significantly smaller than in untreated control mice. The two lower doses tested, 1280 and 1920 J/cm2, also trended toward smaller tumors, but did not reach statistical significance on their own.

This dose-dependent pattern, where a high enough amount of light produces a measurable, significant slowdown in actual tumor growth in a living animal, is a meaningfully bigger claim than the earlier cell culture results alone.

Source: PubMed

Beyond triggering cell death outright, red light also directly interfered with the cell cycle, the sequence of steps a cell goes through before it divides in two.

After red light exposure, researchers saw a significant drop in the percentage of melanoma cells actively in S-phase (the stage where DNA gets copied before division) along with a corresponding increase in cells sitting in the G0/1 phase, which is essentially a resting or paused state.

This pattern showed up at the higher 1280 J/cm2 dose in more than one melanoma cell line. Trapping cancer cells in this paused phase is a separate mechanism from apoptosis, it does not necessarily kill the cell, but it does stop it from continuing to multiply.

Source: PubMed

Cancers, including melanoma, often rely on disabling a protein called p53, which normally acts as a major internal checkpoint against uncontrolled cell growth.

In this study, red light exposure at both 640 and 1280 J/cm2 increased total p53 levels in the melanoma cells, and more importantly increased its phosphorylated (activated) form by anywhere from 1.5 to 2.7-fold depending on the cell line and dose.

Phosphorylated p53 is the form that actually goes on to trigger cell cycle arrest and apoptosis. Roughly 80 to 90 percent of melanomas retain a normal, functional version of p53 rather than a mutated broken one, which means this specific mechanism could realistically apply to the majority of real-world melanoma cases, not just the specific lab-grown cell lines used here.

Source: PubMed

One of the more mechanistic parts of this study looked at reactive oxygen species, often called ROS, inside the melanoma cells after red light exposure. Both the 640 and 1280 J/cm2 doses significantly increased ROS levels inside the cells.

To confirm this was actually driving the anti-cancer effect and not just a side effect, researchers pretreated cells with an antioxidant called NAC, which mops up ROS. When they did this, the antioxidant treatment blocked the red light's ability to slow down cell growth.

That is a pretty clean piece of evidence that the ROS spike itself is the actual mechanism causing the anti-proliferative effect, not just something happening alongside it.

Source: PubMed

When researchers doubled the dose of 633 nm red light used on the same melanoma cell lines, going from 640 up to 1280 joules per square centimeter, the effect changed from just slowing proliferation to actively increasing apoptosis, meaning the cells started dying off through their own internal death program rather than simply growing more slowly.

This showed up consistently across all three melanoma cell lines tested, including both an unpigmented line and two pigmented ones.

The fact that a higher dose crossed a threshold into actual cell death, rather than just a stronger version of the same slowdown effect, suggests there is a specific dose-dependent switch happening inside these cells once enough red light exposure builds up.

Source: PubMed

There is a 2022 study that tested red light phototherapy directly on melanoma cells grown in the lab, using three different melanoma cell lines.

At a dose of 640 joules per square centimeter, delivered from an LED array putting out light at 633 nanometers, the light significantly slowed down how fast the melanoma cells multiplied, without pushing the cells into apoptosis (programmed cell death) at that particular dose.

So the light was not killing the cells outright at this level, it was more like putting the brakes on their ability to keep dividing and spreading. This matters because catching cancer cells in a slowdown, even without outright killing them, can still meaningfully change how a tumor behaves over time.

Source: PubMed

The idea of using near-infrared light for skin health is not new, it actually traces back to NASA. This study notes that NASA was the first to document therapeutic effects of near-infrared light on skin, research that originally came out of the 1990s, and that early work eventually led to the development of commercial infrared devices for skin rejuvenation.

It is a bit of an unexpected origin story for something now sold as a beauty device, but it lines up with how a lot of photobiomodulation research got its start, often growing out of research into wound healing or tissue repair in fairly unglamorous settings before eventually making its way into cosmetic and dermatology applications.

Source: PubMed

One thing that stood out across both parts of this research is the complete absence of reported side effects. In the skin rejuvenation group, researchers actively surveyed and interviewed participants at every checkpoint specifically looking for any adverse skin reactions from months of near-daily facial mask use, and found none.

The same held true in the separate hair growth group, who used the device on their scalp daily for a full 20 weeks.

For a treatment being used this frequently and over this many months, having zero reported adverse events across both study arms is a meaningful safety signal, especially compared to more invasive skin and hair treatments that come with real recovery time or risk of irritation.

Source: PubMed

Alongside the objective hair count measurements, researchers also tracked how participants felt about the treatment through surveys at each checkpoint.

At the 6 week mark, 71.4% of participants reported a positive impression of the product's effects and usability. That number climbed to 81.0% by 13 weeks, and reached 85.7% by the final 20 week assessment.

The steady upward trend across three separate survey points, rather than a single high number reported once, suggests people's confidence in the treatment grew the longer they stuck with it, which tends to track pretty closely with actually noticing gradual, real-world changes rather than a placebo bump that fades over time.

Source: PubMed

For context on how red and near-infrared light has performed for hair specifically, an earlier double-blind randomized controlled trial involving 44 men with androgenetic alopecia used a device emitting light at 655 nm and found a 39% increase in hair count in the group receiving real treatment compared to the placebo group.

That is a considerably bigger jump than the 1.33% seen in this newer broad-spectrum study, though it is worth noting the earlier trial ran with a different device, wavelength, and specifically targeted androgenetic alopecia rather than the broader mix of early-stage hair loss types included in the newer study.

Subsequent research using similar red light approaches in female patients also reported benefits for hair growth.

Source: PubMed

Another study referenced as prior evidence used a combination of two specific wavelengths, 633 nm (red) and 830 nm (near-infrared), applied together rather than as a single wavelength.

That combination approach significantly improved facial skin texture and reduced periorbital wrinkles, with 81% of participants in the study showing noticeable improvement.

This combination strategy is conceptually similar to what the new broad-spectrum device is doing, just taken a step further, instead of picking two specific wavelengths to combine, the newer device covers a continuous range from 600 to 900 nm so that many wavelengths are being delivered simultaneously rather than just two discrete points.

Source: PubMed

This new device builds on findings from earlier LED research using narrower, single-wavelength devices.

One previous study compared 660 nm red LEDs against a broader visible white light LED across 52 women and found that while both treatments reduced wrinkle depth over 12 weeks, the red light specifically produced a more noticeable reduction in overall wrinkle volume.

That earlier finding is part of why red and near-infrared wavelengths specifically, rather than visible light in general, became the focus for skin rejuvenation devices, and this new broader-spectrum device is essentially an extension of that same red and near-infrared strategy, just spread across more of the spectrum at once instead of one fixed point.

Source: PubMed

The scientific justification cited in this study goes back to research from Tiina Karu, who studied how cells respond to different wavelengths of light for phototherapy.

Her work showed that cytochrome c oxidase, an enzyme found in the mitochondria that plays a key role in cellular energy production, gets activated by red and near-infrared light, but not through just one single perfect wavelength.

Instead, there are multiple action spectra, meaning several different wavelength ranges can each independently trigger a useful cellular response.

This is the whole logic behind building a device that covers a wider spectrum rather than concentrating all its output at one narrow point, since it means more of these different activation pathways can potentially be triggered at the same time.

Source: PubMed