The claims in this study are in line with other studies that indicate that infrared light in certain doses upregulates different MMP’s. I could have cited another study, but they are not difficult to find.
Indeed: the shorter wavelengths IR-A will have different effects. But studies suggest that exposure to not only IR-B, but also IR-A induces expression of different MMP’s. It seems your suggestion is that if one exposes him-/herself solely to specific wavelengths of IR-A, this induction of MMP-expression all of a sudden would not be present?
It is known hat UV-radiation and visible light (VL) upregulate different MMP’s. Studies have also shown that heat shock can induce the expression of MMP’s. IR light of course generates and conducts heat; the amount of which will vary depending on many factors, such as wavelength, and the effects will obviously also depend on power density and distance of the source, etc. Still, with all this knowledge we do have, personally I don’t understand how one would all of a sudden conclude that a LED-panel that irradiates a lot of (specific wavelengths of) IR-A light would not provoke any such response. Do you feel we can conclude this because the studies with these panels are still lacking?
Joovv claims their newest panels have a power density of >100mw/cm2. (Of course if you keep more distance from the panel you’d expose yourself to less radiation - which is why I’m stating that may be a good idea. But imho: you’d rather buy a panel with a lower power density in the first place for a fraction of the price).
The leds of Joovv’s panels are within the lower end of the IR-A spectrum, as are the leds of most commercially sold panels. But if one were to follow Joovv’s recommendations you’d get a lot higher amount of IR-A than you’d get if you go outdoors on a sunny day, even around the equator. Indeed, as mentioned: the studies with these panels are lacking and I doubt we will see any independent research anytime soon. Research with regard to the effects of IR-A is also conflicting. But given the information we do have and the information that is lacking, I personally think caution is warranted until we hopefully know more.
“Skin exposure to infrared (IR) radiation should be limited in terms of irradiance, exposure time and frequency in order to avoid acute or chronic damage. Recommendations aimed at protecting humans from the risks of skin exposure to IR (e.g. ICNIRP, ACGIH) are only defined in terms of acute effects (e.g. heat pain and cardiovascular collapse), whereas the actual exposure conditions (e.g. spectral distribution, exposure geometry, frequency and number of exposures, thermal exchange with the environment, metabolic energy production and regulatory responses) are not taken into consideration. Since the IR component of solar radiation reaching the Earth’s surface is mainly IR-A, and considering the increased use of devices emitting artificially generated IR-A radiation, this radiation band is of special interest. A number of in vitro and/or in vivo investigations assessing cellular or tissue damage caused by IR-A radiation have been undertaken. While such studies are necessary for the development of safety recommendations, the results of measurements undertaken to examine the interaction between skin and IR radiation emitted from different sources presented in this study, together with the detailed examination of the literature reveals a wide spectrum of contradictory findings, which in some instances may be related to methodological shortcomings or fundamental errors in the application of physical and photobiological laws, thus highlighting the need for physically and photobiologically appropriate experiments.”
https://www.researchgate.net/publication/43246206_Effects_of_Infrared-A_Irradiation_on_Skin_Discrepancies_in_Published_Data_Highlight_the_Need_for_an_Exact_Consideration_of_Physical_and_Photobiological_Laws_and_Appropriate_Experimental_Settings
“For many years skin aging has primarily been attributed to the effects of ultraviolet (UV) radiation. More recently it has become evident that other parts of solar radiation, especially infrared A (IR-A) 760-1440 nm and infrared B (IR-B) 1440-3000 nm, induce significant free radicals in the dermis and up-regulate matrix metalloproteinases (MMPs) that degrade collagen fibers. This suggests that IR radiation may be damaging to the skin barrier and compromise its function. The purpose of this study was to investigate the effects of IR radiation on skin physiology, specifically, evaluating changes in skin barrier function, inflammatory response, and levels of extracellular matrix proteins. Human reconstructed MatTek skin models were exposed to physiologically relevant doses of IR radiation, after which changes in barrier function were assessed by measuring transepithelial electrical resistance (TEER), transepidermal water loss (TEWL), and penetration of a fluorescein fluorescent marker through skin models; inflammatory response and ECM proteins were measured using ELISA assays for IL-1α, MMP-9, and procollagen production. Results showed that exposure of skin models to physiological doses of IR resulted in (1) reduced barrier properties of skin, as shown by significant reductions in TEER (p<0.01) and increases in TEWL (p<0.01) and fluorescein penetration (p<0.01) at higher IR doses, (2) significant reduction in procollagen production (p<0.01) and increases in MMP-9 production, and (3) increases in skin inflammatory response, indicated by significantly greater IL-1α levels (p<0.05). In addition to elucidating the harmful effects of IR irradiation on skin barrier function, the techniques presented here provide useful methods that can be extended beyond the scope of this study to evaluate ways of protecting skin from the damage caused by exposure to IR.”
https://www.jidonline.org/article/S0022-202X(16)30655-8/fulltext
“Sunlight damages human skin, resulting in a wrinkled appearance. Since natural sunlight is polychromatic, its ultimate effects on the human skin are the result of not only the action of each wavelength separately, but also interactions among the many wavelengths, including UV, visible light, and infrared (IR). In direct sunlight, the temperature of human skin rises to about 40°C following the conversion of absorbed IR into heat. So far, our knowledge of the effects of IR radiation or heat on skin aging is limited. Recent work demonstrates that IR and heat exposure each induces cutaneous angiogenesis and inflammatory cellular infiltration, disrupts the dermal extracellular matrix by inducing matrix metalloproteinases, and alters dermal structural proteins, thereby adding to premature skin aging. This review provides a summary of current research on the effects of IR radiation and heat on aging in human skin in vivo .”
" Although many studies have been performed to elucidate the molecular consequences of ultraviolet irradiation, little is known about the effect of infrared radiation on skin aging. In addition to photons, heat is likely to be generated as a consequence of infrared irradiation, and heat shock is widely considered to be an environmental stress. Here we investigated the effect of heat shock on the expressions of matrix metalloproteinase (MMP)-1, MMP-2, and MMP-3 in cultured human skin fibroblasts. Heat shock induced the expression of MMP-1 and MMP-3, but not MMP-2, at the mRNA and protein levels in a temperature-dependent manner, and caused the rapid activation of three distinct mitogen-activated protein kinases (MAPK), extracelluar signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 MAPK. The heat shock-induced MMP-1 and MMP-3 expression was suppressed by the inhibition of ERK and JNK but not by p38 MAPK inhibition. Furthermore, heat shock increased the synthesis and release of interleukin-6 (IL-6) into culture media. The specific inhibition of IL-6 using a monoclonal antibody against IL-6 greatly reduced the expression of MMP-1 and MMP-3 induced by heat shock. Taken together, our results suggest that ERK and JNK play an important role in the induction of MMP-1 and MMP-3 by heat shock and that the heat shock-induced expression of MMP-1 and MMP-3 is mediated via an IL-6-dependent autocrine mechanism."
