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You are here: Skin Protection >

Infrared light and skin aging: UV shielding is not enough

A person applying sunscreen before going outdoors, especially a strong, broad spectrum UVA+UVB blocking sunscreen, often feels good about herself. After all she has presumably done everything possible to protect her skin from premature aging due to sunlight. She will thus retain her youthful looks for as long as her genes and perhaps cosmetic surgery budget allow. All is right with the world...

Unfortunately, biology is messy and scientists keeps discovering nasty surprises. One such nasty surprise is that UV light apparently is not the only aspect of sun exposure contributing to skin aging. The other potentially significant contributor is infrared radiation type A aka IRA.

Solar radiation that reaches earth's surface contains three main spectral bands: ultraviolet radiation (UV, wavelength 290-400 nm), visible light (400-760 nm), and infrared radiation (IR, 760-4000 nm). Infrared radiation is subdivided into IRA (760-1440nm), IRB (1440-3000nm) and IRC (3000-1000 nm). While a photon of UV radiation carries far more energy than an infrared photon (enough to break chemical bonds), UV light accounts for only 7% of total sun energy (at earth's surface) while infrared accounts for over half, most of which being IRA. Furthermore, IRA also penetrates skin better than IRB, IRC, visible light and even UV, with about 50% of IRA reaching the dermis (a deeper layer of the skin where wrinkles form). All in all, even though IRA does not directly break chemical bonds like UV does, it delivers enough energy deep into the skin to contribute to skin aging over time.

So, what exactly does infrared, and IRA in particular, do to the skin? One notable effects is that IRA increases the production of matrix metalloproteinases, particularly MMP-1 (aka fibroblast collagenase) in dermal fibroblasts, the cells most critical to skin's vitality and youthful appearance. MMP-1 digests several types of collagen (I, II, III, VII and X). While appropriate level of MMP-1 activity is necessary (for skin maintenance as well as remodeling after injury) an abnormally high one, as in the case of infrared exposure, causes excessive collagen destruction. Furthermore, IRA appears to inhibit the expression of some collagen-encoding genes, which results in a decreased collagen synthesis. Taken together, these effects lead to weakening of the skin matrix, formation of wrinkles and thinning of the dermis – all hallmarks of skin aging. Other pro-aging effects of IRA include activation of inflammatory reactions; excessive cell division (and hence accelerated accumulation of senescent cells); and excessive growth of blood vessels (potentially leading to persistent skin redness). See this review article for more biological details.

At the microscopic level, most if not all cellular changes, including the aforementioned ones, involve breakdown of chemical bonds. So, how can infrared A cause such seemingly considerable damage if IRA photons do not possess enough energy to break chemical bonds? Apparently IRA can break chemical bonds indirectly – as opposed to UV that can do it in a single direct hit. The chain of events starts with IRA photons disrupting to the so-called electron transport chain (aka ETC). ETC is a critical part of the cellular energy production system residing in mitochondria. ETC helps convert the energy released during the breakdown of food molecules into the form usable by cells called ATP. This process has some side effects: just like a car engine releases unintended pollutants, mitochondrial ETC releases harmful by-products called free radicals. Free radicals are very reactive and can break almost any chemical bond they bump into. Under normal circumstances, mitochondria produce a relatively small amount of free radicals, most of which are quickly mopped up by the cell's free radical-scavenging systems. However, when something goes wrong (in particular, when ETC is disrupted), mitochondrial production of ATP drops while the production of free radicals dramatically increases, potentially causing widespread damage. A crude analogy would be a malfunctioning engine that is less efficient yet releases more pollutants.

Excess of free radicals is a well known contributor to skin matrix breakdown, inflammation, excessive cell proliferation and blood vessel growth. Hence it appears likely that pro-aging affects of IRA are partly or entirely due to its disruptive effect on mitochondrial ETC and the resulting “flood" of free radicals.

What can be done minimize pro-aging effects of IRA in ones skin? An obvious step is to reduce IRA exposure, most of which comes from the sun. Unfortunately, sunscreens do not protect against IRA. To avoid infrared exposure one needs to prevent sun from hitting the skin, either by staying out of direct sunlight or perhaps by wearing protective clothing. The potential of clothing to protect against IRA remains poorly researched but there is evidence that black cloth offers at least partial protection. The problem is that sun avoidance has its drawbacks. Sunlight is required for the synthesis of vitamin D and may have other health benefits. A more balanced approach could be to protect from direct sun the most critical and aging-prone areas of the skin, face and neck, (e.g. by wearing a wide brimmed hat) while allowing a modest controlled sun exposure of the limbs, for example.

Sun is not the only source in infrared exposure. Hot baths and shower are another. While IRA is not a predominant pathway of heat transfer during hot baths and showers it is likely that dialing down the water temperature from hot to warm will reduce both infrared and chlorine exposure of your skin.

Still, avoiding IRA exposure completely seems unrealistic. And even if it were possible, the complete avoidance might be to the detriment of one's lifestyle or even other aspects of one's health. So, can something be done to neutralize the negative effects of IRA upon exposure?

As mentioned above, research indicates that IRA does most of its damage by making mitochondria produce more free radicals. In that case, the so-called mitochondrial-targeted antioxidants could be a remady. These antioxidants not only neutralize free radicals but also selectively accumulate in the mitochondria, i.e. exactly where IRA-indicated free radicals are generated. Unfortunately, the field of mitochondrial antioxidants is relatively immature. Only a few have been fairly well studied and even fewer are commercially available. In particular, mitoQ and pyrroloquinoline quinone, are available in creams and as oral supplements. However, it remains to be researched whether these mitochondrial antioxidants actually work to fully or even partially neutralize IRA damage and, if they do, what would be their optimal strength/dosage and usage.


     
     


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