The sun protection segment is one of the fastest growing personal care sectors; in the US, sales have increased by nearly 50% since 2005. Despite a sluggish and unsettled economic environment, consumers are willing to invest in sun protection because they are increasingly aware that UV exposure promotes skin aging and cancer.
Several manufacturers are cooperating with cancer organizations to promote sun protection and it now appears that educational sun campaigns are bearing fruit. Educated consumers are becoming more demanding; they expect products to provide excellent protection and be fun to use at no additional cost.
Moreover, chances for persistent and crisis-resistant growth have led to increased competition as more players are looking for a share of the segment.
SPF Is Not the Answer
Gone are the days when it was enough to create a safe product that meets simple SPF requirements. Modern sunscreen products must provide cosmetic properties, such as a pleasant texture and application format, to convince consumers to buy and use them regularly. Current strategies aim to maximize efficacy or optimize the delivery system of existing filters to increase formulation flexibility. The development of new and really innovative filters is hampered by substantial regulatory hurdles.1
In the EU, SPF claims are limited to a few numbers (e.g., 20, 25, 30, 50+), and UVA protection is judged on simple pass/fail criteria. The finalized FDA Sunscreen Monograph presumably will further restrict sun protection claims; the maximum SPF value on sunscreen labeling will probably be limited to 50+. It is therefore becoming increasingly difficult for manufacturers to differentiate their products based only on SPF and UVA claims.
Manufacturers responded to these issues with multidimensional products that stand out from the crowd and gain market share.2,3 The newest generation of products combines effective sun protection with skin care features, such as hydration, nourishment or radical scavenging. The crossover between sun protection and skin care benefits both groups of products; sunscreen products get a point of difference, and anti-aging creams get the extra benefit of sun protection.
New products not only add active cosmetic ingredients, they avoid certain ingredients (e.g., nanoparticles). Some claims, such as “nano-free,” must be used with great caution, as they could arouse ill-founded consumer concerns about safety (e.g., nano-sized TiO2). The reputation of our most-effective filters could be irrevocably damaged if consumers associate them with ingredients that make them uncomfortable. In stark contrast, cosmetic actives offer real added value.
Cosmetic Actives Add Benefits
UV filters are obviously the most important ingredients in sun protection products as they prevent the penetration of UV light into the skin. UV filters, thus, build the first line of defense by providing chemical and physical protection. Cosmetic actives provide a valuable second line of defense by providing biological protection. They reduce detrimental secondary skin damages or enhance the skin’s natural resistance to UV stress. Finally, cosmetic actives pave the way for new performance and marketing claims. This article presents three examples of active ideas.
Free RadicalAnd ROS Protection
Degenerative processes related to aging are primarily a consequence of oxidative stress associated with free radicals and reactive oxygen species (ROS). The skin is constantly exposed to harmful ROS from the environment or the body’s metabolism. ROS are highly reactive molecules that oxidize all sorts of cellular components, leading to DNA, lipid and protein damage and provoking a series of toxic effects. To defend itself against ROS damage, the skin’s antioxidant defense system normally uses antioxidant defense enzymes and nonenzymatic, small-molecule antioxidants.
After excessive UVA exposure, ROS can quickly overload the defense system. In particular, photo-unstable filters may behave as exogenous UVA sensitizers and contribute to overload since ROS-inducing intermediates are produced during the photolysis of photo-unstable filters. Moreover, the concomitant decrease of UV protection further favors ROS burst. The uncontrolled distribution of ROS accelerates skin aging and induces consequences ranging from the formation of erythemas, edemas, wrinkles, photoaging and ultimately skin cancer.4
UV filters never provide 100% protection. Incorporating cosmetic actives into sunscreens can help decrease the risk of skin cancer and early skin aging. This second line of defense neutralizes ROS that emerges despite the presence of UV filters. Plant extracts are especially effective in this demanding task.
Cosmetic Active 1 is a powerful combination (INCI: Water, melissa officinalis leaf extract, disodium rutinyl disulfate, hordeum distichon (barley) extract) of the natural radical scavenger rosmarinic acid from lemon balm and the flavonoid rutin, with the valuable trace elements (Mn, Zn, Se) from barley. The nonenzymatic antioxidants rosmarinic acid and rutin are extremely efficient radical scavengers and interrupt the destructive chain reactions. Radicals are stopped before they cause damage. Most antioxidant defense enzymes require co-factors, and Mn, Zn, and Se are essential for these ROS-eliminating enzymes. Mn and Zn are co-factors of superoxide dismutase and Se is a co-factor of glutathione peroxidase. Indeed, our first example features excellent protection against ROS (Figure 1).
UV-irradiation-induced cutaneous peroxides were more than 66% less than untreated control or placebo. The effectiveness for removing peroxides from skin exposed to UV irradiation was calculated as 261%. This means that levels of peroxides in the skin were reduced to levels even lower than those in unexposed skin. Thus, cosmetic actives help to reduce the risk of UVA-induced ROS damage.
Cell and DNA Protection
Genetic information is stored on DNA as a sequence of nucleotides: A (adenine), T (thymine), G (guanine) or C (cytosine). Like the letters in the words of a sentence, these DNA “letters” encode the information to make proteins. Changes in the nucleotide sequence or DNA mutations alter the information and lead to faulty proteins. Those faulty proteins can adversely affect cell functions or, even worse, induce skin cancer.
Mutations result from many factors, but an important source is exposure to both kinds of UV light. UVA wavelengths are thought to mutate DNA indirectly by causing the formation of ROS: ROS favors the modification of G to 8-oxo-G. During cell division, A instead of C is incorporated into the DNA helix, and a silent “point mutation,” which is invisible to the body’s repair systems, is established. UVB, in contrast, may interact directly with DNA to initiate another common form of DNA damage called thymine-thymine dimers. Cells have evolved efficient DNA repair systems. If cells fail to repair the DNA, they will not survive.
To prevent this damage, UV filters are increasingly being combined with innovative anti-aging ingredients, such as Example 2, to protect the skin’s DNA from light-induced damage and activate the cells’ repair mechanisms.
Cosmetic Active 2 (INCI: Helianthus annuus (sunflower) seed oil, ethyl ferulate, polyglyceryl-5 trioleate, rosmarinus officinalis (rosemary) leaf extract, water, disodium uridine phosphate) combines ethyl ferulate and carnosolic acid from rosemary to combat ROS and counteract indirect DNA damage and mutations. Uridine monophosphate (UMP) is a biochemical building block that cells use to make nucleotides. Thus, this formulation supports cellular DNA repair as it accelerates the supply of urgently required nucleotides (Figure 2, upper panel).
In fact, DNA damage (such as thymine-thymine dimers) was prevented when cells were treated with cosmetic active 2 before being exposed to UV irradiation (Figure 2; lower panel). Cells were exposed to a dose of 1500 mJ/cm2, which corresponds roughly to the UV stress of three hours of midday sun. We hypothesized that less DNA damage and faster DNA repair translates to less skin redness upon exposure to the sun. Indeed, cosmetic active 2 accelerated the regeneration of UV-stressed skin. After just one day, the regeneration process was twice as advanced as that in placebo-treated skin (Figure 3).
The same concept applies to protecting stem cells. Stem cells play a crucial role in skin rejuvenation,5 and protecting them from daily stresses (such as UV light) slows stem-cell aging and extends skin rejuvenation further into old age. Cosmetic active 2 protected epidermal stem and progenitor cells against sunlight. It maintained their ability to restore the proper three-dimensional structure to the epidermis after UV stress and thus protects the function of epidermal stem cells (not shown).
Carefully adding select compounds that protect cells and DNA to sun care products will help repair the consequences of an overdose of solar radiation and maintain the epidermal protective barrier in the long run.
Age Spot Protection
Sun and age induce the formation of the pigments melanin and lipofuscin. Keratinocytes in the epidermis retain and accumulate these pigments, and together with melanocytes, grow downward from the basal membrane into the dermis, where they form bud-shaped micro-invaginations.6 As a result, the desquamation process; i.e, the natural shedding of older skin cells, breaks down, and forms age spots containing melanin and lipofuscin. Lipofuscin is a heterogeneous structure of oxidized proteins and fat products. With aging, the proteasomal system, the cellular recycling factory, becomes less effective. Lipofuscin, as cellular waste, can be neither degraded nor removed. To minimize the formation of both pigments, thus, presents a promising approach to tackle the formation and treatment of age spots.
Cosmetic active 3 (INCI: Glycerin, water, olea europaea (olive) leaf extract, ascorbyl glucoside, zinc PCA) combines substances to combat melanin and lipofuscin formation. The polyphenol oleuropein from olive leaves reduces lipofuscin formation by re-activating the proteasomal recycling factory. Stabilized vitamin C inhibits tyrosinase, the key enzyme in melanogenesis, to block the mechanism behind melanin formation. Zinc PCA increases the concentration of vitamin C transporters and facilitates the uptake of vitamin C (Figure 4).
Cosmetic active 3 effectively reduced the size (not shown) of existing age spots and diminished their contours (Figure 4). By combating melanin and lipofuscin, the cosmetic active also prevents the emergence of aging in the future.
Preventing age spots involves using sunscreen and limiting sun exposure. Cosmetic actives interfere with melanin and lipofuscin synthesis and help to reverse the effects of sun damage by fading any brown skin blemish, whether it is a tan, freckle or age spot.
Gone are the days when sun protection merely meant preventing sunburn. The boundaries between sun protection and skin care are blurring as the perception of beauty and youth is more associated with sun protection. Preventing sunburn will remain the No. 1 priority, but anti-aging and skin care benefits will become increasingly important. Manufacturers must look beyond SPF and UVA to create multifunctional products that will attract consumers with improved convenience and skin feel.
Cosmetic actives will be increasingly important for enhancing the status of sun care products. As a biological second line of defense, they prevent, reduce or repair detrimental effects from UV overexposure, such as oxidative stress, DNA-damage, spot formation and erythema. Sun protection strategies that complement other attractive features, such as convenience and skin feel, provide opportunities for exciting new marketing concepts and claims that will help to differentiate these products from the rest of the field.
1. Hewitt J (2011) Bright ideas. SPC. pp. 85-92.
2. Di Martino N (2011) Added benefits. SPC. pp. 75-83.
3. Branna T (2011) Burnt Offerings. Happi. pp. 91-100.
4. Trouba KJ, Hamadeh HK, Amin RP, Germolec DR (2002) Oxidative stress and its role in skin disease. Antioxid Redox Signal 4: 665-673.
5. Blanpain C, Fuchs E (2009) Epidermal homeostasis: a balancing act of stem cells in the skin. Nat Rev Mol Cell Biol 10: 207-217.
6. Noblesse E, Nizard C, Cario-Andre M, Lepreux S, Pain C, et al. (2006) Skin ultrastructure in senile lentigo. Skin Pharmacol Physiol 19: 95-100.