Skin is the body’s second-largest organ in terms of surface area. It protects the body against external factors that may affect health. Time and environment are the primary factors that affect the skin. The spectrum of skin disorders, from wrinkling and dryness to an array of nonmelanoma skin cancers, affect most of us (Nichols & Katiyar, 2010). About 90% of the nonmelanoma skin cancers are associated with exposure to excessive solar radiation, particularly ultraviolet B (UVB).
Skin is comprised of several layers (epidermis and dermis) and cell types. The outermost layer is the stratum corneum, composed of unique cells that continually proliferate and differentiate and which ultimately transform to corneocytes. These cells, with their lipid regions of cholesterol, saturated fat, and ceramides, present an altered composition and organization during disease states (Bouwstra & Ponec, 2006). Within the dermis (deep) skin tissue, collagens, elastic fibers, and unique proteoglycans and oligosaccharides provide structure and function. These layers provide a barrier to prevent water and heat loss and entry of pathogens while performing continuous repair or remodeling to maintain skin integrity (Naylor et al., 2011).
Throughout the aging process, there is a progressive shortening of telomere length, increased cellular senescence, mitochondrial damage, and production of reactive oxygen species. This process contributes to stages that ultimately lead to the inability of skin cells to proliferate and to remodel the extracellular matrix. On the other hand, continuous exposure to UV radiation directly initiates DNA damage and alters some UV-sensitive amino acids, which, like intrinsic aging, leads to protein damage and the inability to adequately rebuild or replenish the skin matrix.
Unlike topical agents with declared SPF values, which indicate the products help protect the user’s skin from UVB solar radiation, various vitamins and polyphenols appear to function at the dermis level by reducing the penetration of UVB as well as components of ultraviolet C (UVC) and ultraviolet A (UVA) wavelengths (Nichols & Katiyar, 2010). Vitamin A, applied in many forms of retinoids, may be effective at regulating epithelial cell growth and differentiation, thus potentially reducing signs of photoaging (Babamiri et al., 2010). Skin cells, particularly keratinocytes in the epidermis, produce vitamin D from 7-dehydrocholesterol and have vitamin D receptors. This function of vitamin D along with calcium in skin affects cellular proliferation and differentiation as well as innate immunity and suppression of tumorgenesis following UVB exposure (Bikle, 2011; Hart et al., 2011).
Polyphenols may provide photoprotective effects by reducing inflammation, DNA damage, and dysregulation of cellular signaling pathways post UVB exposure (Afaq & Katiyar, 2011). While the topical application of polyphenols seems promising, this route of administration requires a cream-based, organic solvent-based or lipid-soluble matrix, which may increase polyphenol delivery into the skin. Despite our scientific sophistication, the complexity and variability of transdermal pharmacokinetics continues to make many clinicians justifiably uneasy.
Everyone will agree that “moderation” is a safe and even requisite convention. The same may be said of adequate hydration and protein calorie nutrition adjusted to health status and specific needs. There are other less obvious variables. Silica is a trace mineral that is a component of the body’s connective tissues and their healing following injury. Yet, there is evidence that silica can stimulate collagen and fibronectin formation, which can contribute to silica-induced fibrosis (Li et al, 2012). Zinc is an important component of healthy skin, as suggested by cell culture studies that indicate topical applications can reduce the risk of photo induced melanoma (Sweigert et al., 2012). Mouse skin studies show DHA, an omega-3 fatty acid, can directly benefit dry, inflamed skin (Rahman et al., 2011). Selenium (Se) is a mineral with antioxidant properties, though one of several enzymes and complexes affect cellular apoptosis, thereby reducing the risk of melanoma development and or progression (Chung et al., 2011). Yet an earlier review suggests that Se supplementation may actually increase the risk for the development of nonmelanoma skin cancer (Duffield-Lillico et al., 2003). Vitamin E is another nutrient that, in some cases, functions as an antioxidant that may reduce the impact of solar exposure on the skin (Pedrelli et al., 2011). When combined with vitamin A, vitamin E appears especially effective at reducing the development of certain skin lesions (Gaspar and Campos, 2007).
The future of stabilizing and improving skin health is not simple or obvious. Yet it is incumbent upon the scientific community to aggressively address intrinsic and extrinsic processes that affect the skin.
Peter Pressman, M.D.,
CDR, Medical Corps, U.S. Navy,
Director Expeditionary Medicine,
Task Force for Business & Stability Operations
Roger Clemens, Dr.P.H.,
Chief Scientific Officer,
Horn Company, La Mirada, Calif.