Infrared (IR) is the “heat” part of sunlight and it makes up a substantial share of the solar energy that reaches us at ground level. The portion most discussed for skin ageing is infrared-A (IR-A, ~760–1,400 nm) because it penetrates deeper than UV—reaching into the dermis where collagen and elastin live.
From an ageing standpoint, the key issue isn’t that IR behaves like UV (it doesn’t). The risk is that IR—especially IR-A—can drive oxidative stress and signalling that upregulates collagen-degrading enzymes (notably MMP-1) in skin cells and human skin models, which is one of the same downstream pathways implicated in photoageing and wrinkle formation.
There’s also a very practical, visible mechanism: IR is converted into heat in the skin, and under direct irradiation skin temperature can rise to around/above 40°C, which can amplify inflammatory stress and accelerate the “wear and tear” environment that undermines barrier function and collagen stability over time. In vivo work has also shown IR-A exposure can reduce cutaneous antioxidant content, which matters because lower antioxidant reserves mean less capacity to neutralise day-to-day oxidative stressors.
Where it gets nuanced (and where clients often get mixed messages) is that near-infrared and red light are also used therapeutically in controlled settings (photobiomodulation). Dose, intensity, and treatment parameters matter: at appropriate settings, red/NIR light can support recovery pathways and is used for certain skin goals, but that’s very different from chronic, uncontrolled heat/IR exposure from sun/heat sources. Even expert reviews emphasise the “friend or foe” reality and the importance of intensity and dosing.
In real-world clinic terms, the most important takeaway is strategic: IR/heat is a risk amplifier for clients who are already managing inflammation-prone concerns (melasma, persistent redness, post-inflammatory marks, reactive barrier, post-procedure skin). It doesn’t replace UV as the primary ageing driver—UV remains the heavyweight—but IR and heat can meaningfully compound inflammation and collagen stress, which can slow progress and shorten the “longevity” of results if we don’t manage exposure intelligently.
From a prevention and performance perspective, sunscreen is still your core control point because it blocks UV (the biggest driver), but classic SPF labelling doesn’t mean robust IR protection. This is why many dermatology discussions on IR-A emphasise an “all-in” protection strategy: UV protection + behavioural heat management + antioxidant support as a sensible layered approach, rather than chasing one magic product claim.
Operationally, this translates into a simple client message: protect against UV daily, avoid deliberate heat loading (midday direct sun, prolonged heat exposure, overly hot rooms/saunas immediately around procedures if prone to pigmentation/redness), prioritise shade and protective clothing when outdoors, and keep skin barrier calm and supported so it can tolerate corrective work. That’s the risk-managed pathway that keeps outcomes compounding rather than cycling.
