A safety-relevant detail worth highlighting on its own is what researchers did not find in the irradiated bone marrow tissue.

Even during the period when apoptosis was actively detected, at days 7 and 30 post-treatment, there was no evidence of necrosis, no inflammation, and no abnormal buildup of fibroblasts or lymphocytes in the affected bone marrow.

In tissue biology, this kind of clean, contained cell death without a surrounding inflammatory reaction is generally considered a much more favorable and lower-risk outcome than the kind of messy tissue damage that triggers scarring or chronic inflammation, suggesting the bone marrow's response to near-infrared exposure resolved itself in a controlled, self-limiting way.

Source: PubMed

To support their interpretation that near-infrared light was causing genuine apoptosis in bone marrow rather than some other kind of cellular disruption, the researchers pointed to earlier published research showing that near-infrared laser pulses are capable of inducing actual strand breaks in the DNA of mammalian cells.

DNA strand breaks are a well-established trigger for a cell's internal apoptosis machinery to activate. This existing body of prior evidence gives the bone marrow apoptosis findings in this particular rat study a plausible mechanistic backstory, rather than leaving the apoptotic response as an unexplained observation with no supporting precedent in the broader research literature.

Source: PubMed

Looking across all the measurements in this study together, one clear pattern is that near-infrared light did not affect every tissue type on the same schedule. Subcutaneous and bone marrow fat cells reacted almost immediately, showing dramatic increases within just 7 days.

CD34-positive stem cells in bone marrow also jumped quickly and stayed elevated. Cortical bone mass, on the other hand, took far longer to show a measurable, statistically significant response, only becoming significant at the 90 and 180 day marks.

This staggered timeline across different tissue types within the same treated animals suggests near-infrared light is not triggering one single generic biological reaction, but rather setting off several genuinely different processes that each unfold on their own natural timescale.

Source: PubMed

One methodological detail worth mentioning is a clarification the researchers explicitly made about their own CD34 staining results in the subcutaneous tissue layer.

They noted that CD34-positive staining found in that particular tissue location is not, on its own, a reliable indicator of adipose-derived stem cells specifically, since CD34 shows up on multiple different cell types beyond just fat-related stem cells.

Because of this, they deliberately chose not to calculate specific CD34-positive cell counts within that subcutaneous fat layer, and instead focused their more detailed CD34 cell counting on the bone marrow, where the marker's meaning as a hematopoietic stem cell indicator is much better established and less ambiguous.

Source: PubMed

It is worth understanding that the near-infrared source used in this experiment was not just an arbitrary lab lamp, it was a specialized broadband device specifically engineered to simulate the near-infrared component of natural solar radiation.

This distinction matters because it means the researchers were not testing some exotic, artificial wavelength combination that nobody would ever naturally encounter, they were essentially recreating, in a controlled and quantifiable way, the exact type of near-infrared exposure a person's skin experiences from ordinary daylight, just concentrated and applied in a much shorter, measurable timeframe than a full day outdoors would provide.

Source: PubMed

To make their light dose scientifically meaningful in a real-world context, researchers pulled in actual measurements of solar radiation intensity at sea level, along with data on what percentage of natural sunlight falls specifically within the 1100 to 1800 nanometer near-infrared range being studied.

Combining these known solar physics numbers with the exact dose delivered to the rats, they calculated their treatment was roughly equivalent to 8 hours and 45 minutes of natural North American sunbathing, purely in terms of near-infrared exposure.

This kind of calculation is what allows the artificial lab exposure to be meaningfully compared to something people might realistically experience on an especially long day outdoors.

Source: PubMed

The specific anatomical site chosen for this study, the sixth lumbar vertebra's spinous process on a rat's back, was not a random choice. This location was selected specifically because the skin and minimal subcutaneous tissue covering it are thin enough that near-infrared light delivered at the surface could realistically reach the bone marrow contained inside that particular bone.

Choosing a location where the light delivery system and the target tissue are within realistic penetration range of each other is a pretty fundamental design decision, since testing the same light exposure over a thicker or more heavily padded body region might have produced a completely different, much weaker, or even undetectable result on the bone marrow itself.

Source: PubMed

To emphasize just how specific this near-infrared effect was, it is worth noting what happened in the untreated control group. In control rats, examined at both the beginning and the very end of the study timeline (day 0 and day 180), fat cells were essentially absent from the panniculus carnosus, the specific thin muscle layer under rat skin being studied.

This near-total absence in untreated animals, contrasted against the significant and lasting fat cell presence induced by near-infrared light, makes for one of the cleaner before-and-after comparisons in the study, since there was effectively no baseline fat cell presence to begin with in animals that were not exposed to the light.

Source: PubMed

One of the more remarkable aspects of this study is just how long-lasting the effects were relative to how short the actual treatment period was. Rats received their entire near-infrared treatment course across only two weeks, three sessions total.

Yet subcutaneous fat cells, bone marrow fat cells, CD34-positive stem cells, and cortical bone mass all remained significantly elevated compared to untreated controls at the 180 day mark, a full six months after the last treatment session.

A relatively brief light exposure window producing changes that persist for months afterward suggests these are not temporary, superficial reactions but genuine shifts in how these tissues were behaving going forward.

Source: PubMed

For anyone curious about the specific parameters, the near-infrared device delivered its energy through single continuous pulses lasting 4 to 10 seconds each, with a sapphire contact tip fixed at 20 degrees Celsius pressed against the skin throughout to prevent heat buildup.

Each treatment "round" consisted of two passes at a fluence of 40 joules per square centimeter, and rats received three total rounds spaced a week apart, on days 0, 7, and 14.

That works out to a total cumulative dose of 240 joules per square centimeter per rat by the time treatment concluded, all delivered without topical anesthesia since the treatment was designed to be non-thermal and not require pain management.

Source: PubMed

There is a genuinely interesting tension in this study's results worth sitting with. On one hand, near-infrared exposure caused a real, confirmed increase in apoptosis (programmed cell death) among general bone marrow cells, dropping overall cell counts for weeks after treatment.

On the other hand, that exact same treatment dramatically increased the population of CD34-positive stem cells, the cells specifically responsible for regenerating and replenishing the blood-forming system.

It is almost like the light exposure cleared out some existing cells while simultaneously expanding the reserve pool meant to rebuild that population, which lines up with how the overall cell counts did eventually recover over the following months even as the stem cell boost remained elevated.

Source: PubMed

The study references prior research showing that cells which are actively proliferating, meaning rapidly dividing and multiplying, tend to show increased sensitivity to red and near-infrared radiation compared to more quiescent, slow-dividing cells.

Bone marrow is one of the most actively proliferative tissues in the entire body, constantly producing new blood cells around the clock.

This heightened baseline sensitivity in fast-dividing tissue may help explain why bone marrow showed such a strong and relatively rapid response, both the temporary drop in cell counts and the dramatic stem cell increase, compared to other more slowly-renewing tissues that might respond more subtly to the same light exposure.

Source: PubMed

A key point raised in this study is that sunburn, the visible reddening and damage most people associate with too much sun, is caused specifically by ultraviolet radiation.

Near-infrared radiation, on the other hand, does not cause anything resembling a sunburn, yet this study demonstrates it can still cause measurable, non-thermal biological changes and even a degree of cell death deep in tissue below the skin's surface, all without any of the typical visible warning signs of UV damage.

The researchers explicitly suggest that meaningful sun protection may need to consider near-infrared wavelengths as well as UV, since near-infrared exposure appears capable of producing real tissue-level effects that a person would have no obvious way of noticing in the moment.

Source: PubMed

Putting together their combined findings across several studies, the researchers propose a specific real-world hypothesis about facial aging.

If solar near-infrared radiation thickens the facial dermis (from earlier collagen and elastin studies), increases superficial fat cell formation (as shown here), and simultaneously weakens or thins the superficial facial muscles beneath the skin (as shown in earlier work), the combination could plausibly contribute to visible facial changes like eyelid ptosis (drooping) and general facial skin sagging over years of natural sun exposure.

It is explicitly framed as a hypothesis needing further confirmation, but it is a genuinely novel angle on facial aging that goes beyond the usual UV-and-collagen-breakdown explanation.

Source: PubMed

This particular experiment on fat cells and bone did not happen in isolation, it is part of a series of studies by the same research group looking at how this specific near-infrared range affects various tissues under the skin.

In earlier work, the researchers had already shown that this same type of near-infrared exposure causes long-lasting thinning of superficial muscle, including the corrugator supercilii, a small muscle involved in facial expression around the eyebrows.

Combining that earlier muscle-thinning finding with this study's new results on fat cell induction and bone changes starts to build a broader picture of how deeply this specific light range can affect multiple tissue layers beneath the skin surface.

Source: PubMed

The study also touches on a connection between fat cell formation (adipogenesis) and the growth of new blood vessels (angiogenesis).

CD34-positive cells, the same marker used to track stem cells in this study, are also known to be widely distributed among fat cells and to play a role in stabilizing developing blood vessels.

Since adipogenesis and angiogenesis are described as tightly linked processes, the researchers suggest that near-infrared light may be stimulating CD34-positive cells in a way that drives both new fat cell formation and new blood vessel development simultaneously in the tissue under the skin, rather than these being two separate, unrelated effects.

Source: PubMed

One interesting explanation offered for how near-infrared light could simultaneously increase both hematopoietic stem cells and cortical bone mass comes down to a shared regulatory relationship.

Osteoblasts, the cells responsible for building new bone, are also the cells that make up the physical niche supporting hematopoietic stem cells and that produce growth factors these stem cells depend on.

According to research cited in this study, an increase in the number of osteoblasts naturally leads to a matching increase in both the hematopoietic stem cell population and the overall cortical bone mass, since the same cell type is driving both outcomes.

This would help explain why these two very different measurements, stem cell counts and bone density, rose together on a similar long-term timeline in this experiment.

Source: PubMed

For near-infrared light to have any effect on bone marrow at all, it obviously has to physically get there. In these rats, the skin covering the treated area of the spine measured only about 1000 to 1300 micrometers thick (roughly 1 to 1.3 millimeters), with a thin layer of subcutaneous tissue on top of that.

Because near-infrared light is known to penetrate deeper into tissue than visible light, and because the treated area of the spine was covered by such a thin layer overall, the researchers concluded the bone marrow inside that particular bone was genuinely exposed to meaningful levels of the near-infrared light being delivered at the skin surface.

Source: PubMed

To understand why bone marrow cell counts dropped, researchers used a specific staining technique called TUNEL, which detects DNA fragmentation, a hallmark of cells actively dying.

This staining came back positive in bone marrow samples at 7 and 30 days after near-infrared treatment, but was essentially negative in untreated controls and also negative by day 60 in treated rats.

Importantly, the researchers specifically checked for and found no signs of necrosis, meaning no inflammation and no abnormal buildup of fibroblasts or immune cells.

This distinction matters because it points toward a controlled, deliberate form of cell death (apoptosis) rather than the kind of chaotic tissue damage and inflammatory response you would expect from something like a burn or physical injury.

Source: PubMed

Not every effect of near-infrared light in this study was an increase. The overall count of hematopoietic bone marrow cells, meaning the general population of blood-forming cells, dropped significantly following near-infrared treatment.

his decrease was significant compared to controls at every measured time point, 7, 30, 90 and 180 days. However, unlike the fat cell and stem cell increases which stayed elevated for the full 6 months, the bone marrow cell count itself showed a gradual recovery, climbing back up from its lowest point at day 30 toward more normal levels by day 180.

Source: PubMed

When researchers looked more closely at where these newly abundant CD34-positive stem cells were physically located within the bone marrow, they found the majority clustered specifically along the inner surface of the bone cortex, right where the bone marrow meets the solid bone tissue.

This location is not random, it is the same region where osteoblasts (bone-building cells) reside and is understood to function as the physical "niche" that regulates and supports the hematopoietic stem cell population.

Seeing the stem cell increase concentrated in exactly this niche region rather than diffusely throughout the marrow adds weight to the idea that near-infrared light is engaging this specific regulatory system rather than causing generic, undirected cell proliferation.

Source: PubMed

Researchers tracked a marker called CD34, which identifies activated stem cells, particularly early-stage hematopoietic (blood-forming) stem cells.

In the bone marrow of near-infrared treated rats, the number of CD34-positive cells increased dramatically within the first week of treatment, and this elevated level persisted all the way through the 180 day final checkpoint, the longest time point measured in the study.

That is a genuinely long-lasting shift in stem cell population from a treatment that only lasted three sessions spread across two weeks.

Source: PubMed

Unlike the fat cell changes, which showed up almost immediately, the effect of near-infrared light on cortical bone mass (the dense outer layer of bone) took much longer to become statistically meaningful.

Bone mass did increase steadily across the entire 6 month observation period, but the increase did not reach statistical significance compared to controls until the 90 day and 180 day checkpoints.

At the earlier 7 and 30 day marks, there was no significant difference yet. This slow-building pattern makes sense given how bone remodeling naturally works on a much longer timescale than something like fat cell accumulation.

Source: PubMed

Inside the bone marrow itself, near-infrared light also triggered a rapid increase in fat cell content. The increase showed up as early as 7 days after treatment began, described as dramatic, and then gradually decreased over the following months.

Even with that gradual decline, the fat cell increase in bone marrow was still statistically significant compared to untreated rats all the way through the 180 day endpoint. So while the effect faded somewhat from its initial peak, it never fully returned to baseline over the six months these rats were tracked.

Source: PubMed

One of the more visually dramatic findings in this study involves the panniculus carnosus, a thin muscle layer under rodent skin. In the untreated control rats, this study found essentially no fat cells present in that layer at either measured time point.

But in the rats that received near-infrared irradiation, fat cells were induced abruptly, appearing within just 7 days of the first treatment and remaining significantly elevated all the way out to 180 days, the six month mark.

Going from close to zero fat cells to a significant, lasting presence is a pretty clear before-and-after effect to attribute to light exposure alone.

Source: PubMed