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Since 2018, a dozen of studies on the deleterious impact of blue light on skin have been published. They demonstrate that chronically exposing the skin to the light emitted by our mobile phones, desktops or tablet screens leads to premature skin aging and disruption of the biological functions of skin cells. For example, in 2018, a study demonstrated that fibroblasts exposed to the light generated by electronic devices for 1 hour at a distance of 1 cm generated reactive oxygen species (ROS)^[1], whose link with aging is now well-known^[2]. A consequence of aging is the appearance of pigmented spots on the skin: blue-light exposure increases melanin production by melanocytes^[3], and hyperpigmentation induced by blue-violet light is more pronounced and lasts longer than the one induced by UVBs^[4].

Recent discoveries rewarded by the Nobel Prize of Medicine in 2017 highlight the fact that blue-light disturbs the circadian rhythm of the cells and some important biological functions are linked to the day and night rhythm^[5]. Among these, studies demonstrated that aquaporin-3, a protein responsible for water circulation in the cells with a major role in skin hydration, exhibits a 24-hour rhythm linked with the expression of circadian genes^[6]. Consequently, dysregulation of the circadian rhythm is a cause of skin dehydration. Also, circadian genes mediate expression of MMP-1^[7], an enzyme that degrades collagen type I, another cause for premature skin aging.

Based on these understandings, B-Circadin™, a natural active ingredient inspired from Lespedeza capitata plant’s biorhythm, specifically targets the skin cells’ circadian rhythm disrupted by blue light. Its ability to restore a normal expression of the circadian genes Per-2, Cry-1 and Bmal-1 was demonstrated in-vitro on innovative tailor-made desynchronized skin explant model exposed to blue light. As a consequence, B-Circadin is able to restore essential biological functions such as aquaporin-3, thus reinforcing skin hydration levels. By acting on MMP-1, it also prevents collagen degradation. In addition, B-Circadin is able to block the oxidative stress directly induced by blue light radiating from digital screens.

A clinical evaluation was conducted to evaluate the impact of B-Circadin on volunteers showing signs of fatigue due to a dysregulated circadian rhythm caused by night shift work. B-Circadin showed outstanding performance on the volunteers: they saw their complexion visibly upgraded by over 17% compared to the placebo after only 1 week and by 35% after 4 weeks.

A second clinical study done was performed and included volunteers who had sedentary lifestyles, worked full time, and experienced tiredness during the week which caused dark circles around the eyes. They were asked to apply daily half face a formula containing B-Circadin and half face a placebo formula and to watch electronic tablets screens for two hours every evening for four days. Eye contour was noticeably improved, and puffiness decreased by 18% thanks to B-Circadin, after only four days of treatment.

All these tests demonstrate the ability of B-Circadin to resynchronize the skin and therefore protect it from direct and indirect causes of damages generated by our modern lifestyle and the increasing exposure to blue light from screens.

^{[1] Electronic device generated light increases reactive oxygen species in human fibroblasts. J. Lasers Surg Med. (2018)
[2] Oxidation events and skin aging. Ageing Res Rev. (2015)
[3] Melanocytes sense blue light and regulate pigmentation through opsin-3. J Invest Dermatol. (2018)
[4] Differences in visible light-induced pigmentation according to wavelengths: a clinical and histological study in comparison with UVB exposure. Pigment Cell Melanoma Res. (2014)
[5] Blue light disrupts the circadian rhythm and create damage in skin cells. Int J Cosmet Sci (2019)
[6] 24-hour rhythm of aquaporin-3 function in the epidermis is regulated by molecular clocks. J Invest Dermatol.(2014)
[7] PER, a Circadian Clock Component, Mediates the Suppression of MMP-1 Expression in HaCaT Keratinocytes by cAMP. Molecules (2018)}