The Rationale of Anti-Aging Cosmetic Ingredients

tomography (epidermis and dermis thickness), fringe projection (wrinkles), colorimetry (skin color, pigmentation evenness), devices for measuring visco-elastic properties, surface texture, and hydration (SkinChipTM), have been published.^10-12

First line of defense against UV induced skin damage is daily application of photo-stable sunscreens with high UVA protection index. Even short term exposures over long periods of time can add to cumulative damage to the dermal and epidermal structures and functions. The harmful effects of skin exposure to sun (and simulated solar UVA’s) including sub-erythemal doses and the efficient prevention of damage afforded by broad spectrum sunscreens have been thoroughly documented albeit mainly on subjects with light skins of phototypes I-III, ie, the most concerned people. Interestingly, a recent study on an ethnically diverse subject cohort treated for 8 weeks with either a SPF 30/UVA PF 20 or SPF 60/UVA PF 20 product showed a significant decrease in lightening of pre-existing face and hand pigmentary abnormalities and the overall lightening of facial skin in subjects with skin of color.¹³ No difference was found between the two sunscreens, suggesting the relevance of high UVA protection to prevent hyperpigmentation disorders of sun exposed skin areas, a sign of perceived age in dark-skinned subjects. Prevention of skin aging can also be obtained by using highly photo-protective products that combine effective UVB and UVA sunscreens, in all skin color phenotypes. The efficiency of combinations of antioxidants (Vit C, Vit E) in alleviating the signs of skin aging has also been extensively studied.

Topical antioxidants are among the most adequate complementary products to sunscreens as they protect cells from oxidative stress and UVA-induced ROS that are highly involved in skin photo-aging process. Hydrophilic vitamin C (Vit C) and lipophilic vitamin E (Vit E) are the gold standards for this purpose. Topically applied Vit C enhances the mRNA levels of collagen I and III and epidermal turnover, which improves skin surface condition.¹⁴ Combining vitamins C and E provides an interactive, synergistic pair of antioxidants in tissues, Vit C regenerating and Vit E involved in neutralization of ROS.¹⁴ Stabilized by the plant antioxidant ferulic acid, the combination turned out to ef ciently supplement the protection against UV-induced cell damage.¹⁵ Many reported studies show that extrinsic aging is at least partially reversible and may be retarded or corrected by some cosmetic ingredients. One of the most investigated ingredient has been vitamin A (Retinol), and its derivatives, where a number of clinical trials have proven its benefits. Collagen synthesis becomes stimulated, together with an enhanced regulation of epidermal cell proliferation and differentiation. Among others, two 6-month clinical studies on a retinol lotion vs vehicle¹⁶ and on a retinol-sunscreen combination¹⁷ in elderly and 45-60-year-old cohorts led to a significant reduction of wrinkles, as compared to their respective vehicles. Another successful anti-aging agent is dehydrojasmonic acid, a derivative of a plant stress hormone that possesses various activities. It favors a gentle desquamation of the upper layers of the stratum corneum (SC) thus restoring a “younger” rate of epidermal renewal. It also induces a significant deposit of brillin-rich micro brils in the papillary dermis of photo-aged volunteers¹⁸ and reverses steroid-induced atrophy.¹⁹ Twice daily application for 3 months resulted in significant improvement of crow’s feet wrinkles, skin texture, and reduction in facial skin pores. Other restoring approaches are illustrated by the results of studies on a new C-xylopyranoside derivative and fragmented hyaluronic acid that respectively show improved morphogenesis of the whole dermal epidermal junction and clues to the remodeling of the dermal architecture network.

The daily use of mild exfoliating agents such as alpha hydroxy-acids (AHA’s) has been widely recommended to help remove the outermost layers of SC and improve epidermal renewal. In this respect, a close member of this family (β-hydroxyacids), n-capryloyl salicylic acid (LHA), has been demonstrated to have unique properties. Being lipophilic, with slow penetration into the SC layers, LHA acts on loose interfaces, closely mimicking the normal physiological process of desquamation through a controlled thinning of SC leading to epidermal cell renewal similar to that of younger skin. It thus reduces age-related changes including hyper pigmentation, fine lines, and wrinkles.²⁰ An interesting boosting approach is by modulating the glucos-aminoglycan (GAG) and proteoglycan (PEG) content of the skin. GAG and PEG are major players in inter-cellular communications, cell migration, and tissue modeling. Significant changes in GAG’s and PEG’s have been identi ed in aged skin. Hyaluronic acid (HA) is a unique non-sulfated GAG the role of which appears essential in re-epithelialization process, control of proliferation, and migration of keratinocytes from the epidermal basal layer. The high molecular weight (MW) of HA (around 106 Da) makes it a surface protective lm that cannot penetrate when applied as a lotion onto skin but maintains hydration by trapping water. A fragmented HA, with low MW fragments, that can penetrate and contribute to remodel the architecture of the collagen network has been tested successfully in reconstructed skin models.²¹ Skin aging entails dramatic changes in the extracellular matrix (ECM), particularly in the superficial dermis and dermal epidermal junction (DEJ), the outline of which loses papillary structure and anchor fibers, thus attening with age. These alterations gather pace with exposure to extrinsic factors. A C-xylopyranoside derivative (C-xyloside) was shown to stimulate the expression and deposit of GAG and key ECM proteins in the super cial dermis, thereby improving the morphogenesis of the whole functional DEJ.^22-25 The clinical efficacy of C-xyloside combined with blueberry extract was shown on diabetic subjects older than 50 yrs where