PEER-REVIEW | DERMATOLOGY | THE IMPORTANCE OF
Carl R. Thornfeldt explains how an effective barrier function improves the results of sunscreens and reduces the damage caused by environmental factors, such as ultraviolet light
ABSTRACT The most effective sunscreens are those that block ultraviolet radiation while simultaneously reducing chronic inflammation and improving the health of the stratum corneum permeability barrier. Skin problems can be linked to chronic inflammation, and compromised skin can be more vulnerable to damage, including skin cancer caused by UV radiation.
CARL R. THORNFELDT, MD, FAAD, Dermatologist, CEO and Founder of Episciences, Inc., Fruitland, ID
email:
drcarl@epionce.com P
KEYWORDS Barrier repair, chronic inflammation, smart photoprotection
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Sunscreens that optimize barrier function should contain anti-inflammatory, repair and photoprotective properties, all of which increase the effectiveness of the sunscreen against cancer-causing UV radiation. There are multiple botanical sources found to contain these types of ingredients to create an ideal environment in the skin for sunscreen to be most effective, while helping to
RACTICING DERMATOLOGY IN THE region of America with the highest incidence per capita of skin cancer, particularly melanoma, the author has a significant interest in reducing the incidence of cancer by improving
prevention as well as therapeutic modalities. These preventative technologies can also be expected to reduce the incidence of skin problems and diseases that share similar cutaneous anomalies to those that drive neoplasia. Understanding these anomalies that drive premalignant and malignant tumors can be expected to help optimize the function of sunscreen products. Solar radiation damage includes
WITH SUNSCREENS
SKIN BARRIER FUNCTION
reduce a variety of skin problems caused by chronic inflammation. Products with sunscreen ingredients significantly reduce photoaging and neoplasia; yet the skin cancer epidemic rages on. The incidence of 11 other common diseases activated by UVL continue to increase. This article presents key missing pieces and strategies to solve these epidemiologic puzzles.
Solar radiation
damage includes UVA-induced
epidermal cells induced by UVB.
UVA-induced immunosuppression that is coupled with dysplasia of epidermal cells induced by UVB. These activate an inflammatory cascade upregulating matrix metalloproteinases (MMPs) and gene transcription manipulation to produce the cancerous skin cells1
. The March 2015 |
prime-journal.com
UVL radiation damage is further enhanced by two cutaneous abnormalities that afflict most adults: a compromised stratum corneum permeability barrier (SCPB), and overt or occult chronic inflammation of the epidermis and dermis. Chronic inflammation becomes destructive when exaggerated MMP activity is coupled with reduced tissue inhibitor of MMPs (TIMPs), generating an imbalance of catabolism of cutaneous structural components2
. Several of the nine MMPs
immunosuppression that is coupled with dysplasia of
fracture collagen, elastin, and glycosaminoglycans and upregulate transcription factors that activate keratinocyte and melanocyte dysplasia. Approximately 70% of American adults that are Fitzpatrick skin types I–III have a significantly reduced SCPB as determined
by transepidermal water loss (TEWL)3 increased , measured by
evaporimeter. A persistent or recurrently damaged SCPB activates chronic inflammation and basal keratinocyte DNA synthesis to repair the injured skin4 This barrier compromise may be induced and/or
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