About 87,000 new cases of melanoma of the skin are predicted to be diagnosed in the US in 2017. Nearly 10,000 Americans will die from metastatic melanoma.3
And according to the latest report by the Environmental Working Group,4 almost 75% of sunscreens contain “worrisome ingredients” and offer inferior sun protection. For example, about 70% still contain a compound that, when applied to the skin and exposed to sunlight, generates reactive oxygen species4-6 — meaning increased sunscreen use may be a factor in increased skin cancer rates! Few people realize that the highest-SPF products are often the riskiest.7
Game-changing sunscreen formulas have been developed that block the full spectrum of harmful ultraviolet radiation and provide plant extracts that inhibit and even reverse solar-induced skin damage.
Over the past 40 years, deadly skin melanoma cases have skyrocketed more than four-fold for young men — and more than eight-fold for young women!8 Non-melanoma cases of skin cancer affect over 3 million people.3 Meanwhile continuing ozone layer depletion continues to increase skin cancer risk globally.2
The Escalating Skin Cancer EpidemicThis daily risk goes beyond cancer.
Sun-induced aging of the skin (photoaging) is clinically characterized by deep wrinkles, mottled pigmentation, rough skin, skin-tone loss, dryness, spider veins, leathery appearance, loss of elasticity, and precancerous lesions.9,10 Photoaging occurs most frequently on sun-exposed areas such as the face, neck, upper chest, hands, and forearms.10
Only about 14% of men and 30% of women regularly wear sunscreen on their face and other exposed skin.11 Many people half-heartedly limit their sun exposure. But effective protection is needed every day, as solar rays damage skin far more than anyone realizes!
Even those who wear sunscreen daily generally apply it incorrectly and fail to reapply it regularly as required. Many consumers apply only 25% to 50% of the recommended amount.12 And it’s still important to avoid unnecessary sun exposure even after proper sunscreen application.13,14
Consumers are often fooled by a high and very misleading sun protection factor, or SPF. All SPF means is that these creams block the UVB rays that affect the superficial epidermis skin layer.7,15 Sure, this helps prevent sunburn — but does nothing to block the UVA radiation that makes up 95% of ultraviolet radiation and causes vastly greater damage.4,15 UVA penetrates more deeply — accelerating skinaging, suppressing immunity, and fostering skin cancer.16-18
Equally misleading are the labels on so-called “broad-spectrum” sunscreens that claim to block carcinogenic UVA radiation in addition to sunburn-causing UVB. The Environmental Working Group determined that only half of all sunscreens would offer enough UVA protection to be sold in Europe (which has much higher standards).19
Most frightening, the public is led to believe that higher SPF ratings are superior, but they give people a false sense of security. A 100 SPF blocks barely 1% more UV rays than a 50 SPF —although the higher rating encourages longer exposure.7
But any sunscreen will provide some cancer defense, right? Wrong. A 2016 review of sunscreen products found that almost three-fourths of the examined sunscreens contain “worrisome ingredients” that may increase cancer risk, thus defeating the purpose of using them. For example, 70% of the sunscreens evaluated in this report still contain a compound (oxybenzone) that, when applied to the skin and exposed to sunlight, generates reactive oxygen species (ROS).4-6
Armed with a unique new sunscreen option, individuals now have the ability to ensure they don’t become a part of these statistics.
Blocking the Multiple Mechanisms of Ultraviolet RadiationAn effective sun-protection formulation needs to work on different levels because skin damage itself occurs via multiple mechanisms.
UV rays generate free radicals and other substances that damage DNA.20
And ultraviolet light decreases Langerhans cells, specialized immune cells found abundantly in the skin that protect against invading pathogens and participate in the immune response against skin cancer.20-22
UV-ray photons oxidize proteins, correlating with accelerated aging.23-25 This activates matrix metalloproteinase (MMP) enzymes that break down elastin and collagen, proteins responsible for firm and supple skin.23
Solar radiation-induced oxidative stress also triggers the release of proinflammatory cytokines and growth factors, further damaging elastin and collagen and breaking down the skin’s structural integrity.26
Unique Formulation Safely Blocks Skin CancerScience-based topical formulas are now available that safely block solar radiation — while adding a second line of defense against the destructive mechanisms of any UV light reaching the skin.
One of these new sunscreens can be found in a light lotion that readily absorbs into the skin without a white, greasy mess. Health-conscious individuals should apply this formula daily, even on cloudy days, and reapply every two hours if they are remaining outdoors.
This new sunscreen lotion contains ingredients that safely block UV radiation and may reverse its DNA damaging and photoaging effects. Unlike many commercial products, the ingredients in this new lotion formulation rate scores of between 1 and 3 on the hazard scale of the independent Environmental Working Group — a scale that rates “high hazard” chemicals as being between 7 and 10.
The new lotion formulation includes zinc oxide, which blocks both UVA2 and UVA1 rays. Although some products exclusively rely on zinc oxide to fight UVB, it provides incomplete UVB protection. Therefore, this new lotion also contains titanium dioxide, which more effectively reflects and blocks UVB and further blocks UVA2.27
Convenient Spray Bottle OptionFor convenient whole body application, a new sunscreen spray has been developed that provides similar benefits to the new lotion. Zinc oxide and titanium dioxide cannot be used in this formula because they will clog a spray bottle.
To accommodate a spray mist, scientists combined the following UV-blocking agents: avobenzone to absorb UVA1 rays;27 octocrylene to filter out UVA2 and UVB;27,28 and octisalate and homosalate to fully enhance UVB radiation defense.27
Most spray-on sun products are slow-drying, but this formulation contains just enough alcohol, allowing for instant drying and encouraging convenient reapplications throughout the day.
A review panel assessing this (FDA-approved29) alcohol found no evidence of phototoxicity on the human skin, even at higher concentrations.30
This sunscreen innovation includes a botanical second line of defense against skin cancer and photoaging.
Let’s review its UV-protective mechanisms:
Inhibiting UV’s Skin-Damaging Mechanisms at the Cellular LevelFormulators included an exciting skin-protective discovery — oat beta-glucans — found in cell walls of whole oat (Avena sativa) kernels and clinically demonstrated to provide strong skin-regenerative effects.
Also included are extracts of green tea, licorice, milk thistle, and rosemary, collectively shown to deliver potent antioxidant, anti-inflammatory, anti-cancer, and DNA-protective effects that inhibit and repair UV radiation’s skin-destructive effects.
This lineup was specifically indicated by studies that concluded: “These botanicals may favorably supplement sunscreen protection and may provide additional anti-photocarcinogenic protection, including the protection against other skin disorders caused by solar UV radiation.”31
Oat Beta-GlucansPublished in Phytotherapy Research in 2014, a review concluded that beta-glucans strengthen the 24
skin’s ability to inhibit environmentally triggered aging and wrinkling.
Green Tea ExtractGreen tea-treated skin has shown less depletion of epidermal Langerhans cells, and photoprotective 25, 32-34
effects against UVA. Adding green tea extract to sunscreens may help thwart skin cancer at multiple stages in its development.
Beyond cancer, studies show that green tea and green tea extract prevent photoaging when used orally or topically.35-39 Significantly, a lab study demonstrated that topically applied green tea polyphenols and EGCG have clearly greater photoprotective efficacy than when taken orally.25
In 2017, a review of previous studies concluded that green tea polyphenols “protect against UV irradiation-stimulated skin photoaging” and inhibit its hyperpigmentation, wrinkling, and immunosuppression.40
Licorice Root ExtractA double-blind study concluded that licorice extract is potentially effective for treating atopic dermatitis — a chronic, inflammatory skin disease. 41 So it came as no surprise when two years later, other researchers found that the licorice constituent glycyrrhizin “might offer protection from the damage induced in humans by UVB radiation.”42
Milk Thistle ExtractStudies document that milk thistle compounds — silibinin and silymarin — deliver potent antioxidant, anti-inflammatory, and immune-enhancing properties. 43-48 Significant decreases in skin cancer number and size were shown for topical application of both silymarin and silibinin.47,48
Specifically investigating UV radiation, scientists found that silibinin blocks DNA skin damage and impedes cancer cell growth in mice.48 It may do this in part by enhancing the activity of the p53 gene, which protects against cancer.43 Compellingly, researchers found that silibinin helps repair DNA damage caused by previous exposure to UVB radiation.49
Similarly, silymarin exceptionally protected against skin tumor promotion.47 One investigation concluded that silymarin “may favorably supplement sunscreen protection and provide additional anti-photocarcinogenic protection.”43
Rosemary ExtractCritically, rosemary enhances the body’s ability to eliminate potential carcinogens.50 It slows or stops 51-53 Two rosemary compounds — carnosic and ursolic acids — particularly benefit the skin.54-56
DNA damage and tumor-cell proliferation, induces tumor-cell apoptosis, and markedly suppresses genes that enable tissue invasion and metastatic spread.
Ursolic acid inhibits reactive oxygen species in skin cells and prevents the skin-aging effects of UVA rays.57 Remarkably, ursolic acid also powerfully blocks the growth of cancerous melanoma cells.56
- Available at: http://www.cdc.gov/cancer/skin/statistics/index.htm. Accessed February 14, 2017.
- Available at: http://www.who.int/uv/faq/skincancer/en/index1.html. Accessed February 15, 2017.
- Available at: https://www.cancer.org/content/dam/cancer-org/research/cancer-facts-and-statistics/annual-cancer-facts-and-figures/2017/cancer-facts-and-figures-2017.pdf. Accessed February 14, 2017.
- Available at: http://www.ewg.org/sunscreen/report/executive-summary/. Accessed February 15, 2017.
- Schallreuter KU, Wood JM, Farwell DW, et al. Oxybenzone oxidation following solar irradiation of skin: photoprotection versus antioxidant inactivation. J Invest Dermatol. 1996;106(3):583-6.
- Hanson KM, Gratton E, Bardeen CJ. Sunscreen enhancement of UV-induced reactive oxygen species in the skin. Free Radic Biol Med. 2006;41(8):1205-12.
- Available at: http://www.ewg.org/sunscreen/report/whats-wrong-with-high-spf/. Accessed February 15, 2017.
- Reed KB, Brewer JD, Lohse CM, et al. Increasing incidence of melanoma among young adults: an epidemiological study in Olmsted County, Minnesota. Mayo Clin Proc. 2012;87(4):328-34.
- Yaar M, Eller MS, Gilchrest BA. Fifty years of skin aging. J Investig Dermatol Symp Proc. 2002;7(1):51-8.
- Helfrich YR, Sachs DL, Voorhees JJ. Overview of skin aging and photoaging. Dermatol Nurs. 2008;20(3):177-83; quiz 84.
- Available at: https://www.aad.org/media/news-releases/study-most-americans-don-t-use-sunscreen. Accessed February 17, 2017.
- Available at: https://www.aad.org/media/stats/prevention-and-care/sunscreen-faqs. Accessed February 20, 2017.
- Wang SQ, Dusza SW. Assessment of sunscreen knowledge: a pilot survey. Br J Dermatol. 2009;161 Suppl 3:28-32.
- Available at: https://www.ncbi.nlm.nih.gov/books/NBK247163/. Accessed February 20, 2017.
- Pandel R, Poljšak B, Godic A, Dahmane R. Skin photoaging and the role of antioxidants in its prevention. ISRN Dermatol. 2013 Sep 12;2013:930164.
- Available at: http://www.who.int/uv/faq/uvhealtfac/en/. Accessed February 20, 2017.
- Available at: http://www.skincancer.org/prevention/uva-and-uvb. Accessed February 20, 2017.
- Schwarz T. Ultraviolet radiation--immune response. J Dtsch Dermatol Ges. 2005;3 Suppl 2:S11-8.
- Available at: http://www.ewg.org/release/Sunscreens-Get-Flunking-Grade-for-UVA-Protection. Accessed February 15, 2017.
- Lee CH, Wu SB, Hong CH, et al. Molecular Mechanisms of UV-Induced Apoptosis and Its Effects on Skin Residential Cells: The Implication in UV-Based Phototherapy. Int J Mol Sci. 2013;14(3):6414-35.
- Kolgen W, Both H, van Weelden H, et al. Epidermal Langerhans cell depletion after artificial ultraviolet B irradiation of human skin in vivo: apoptosis versus migration. J Invest Dermatol. 2002;118(5):812-7.
- Nakano T, Oka K, Sugita T, et al. Antitumor activity of Langerhans cells in radiation therapy for cervical cancer and its modulation with SPG administration. In Vivo. 1993;7(3):257-63.
- Fisher GJ, Datta SC, Talwar HS, et al. Molecular basis of sun-induced premature skin ageing and retinoid antagonism. Nature. 1996 Jan 25;379(6563):335-9.
- Du B, Bian Z, Xu B. Skin health promotion effects of natural beta-glucan derived from cereals and microorganisms: a review. Phytother Res. 2014;28(2):159-66.
- Vayalil PK, Elmets CA, Katiyar SK. Treatment of green tea polyphenols in hydrophilic cream prevents UVB-induced oxidation of lipids and proteins, depletion of antioxidant enzymes and phosphorylation of MAPK proteins in SKH-1 hairless mouse skin. Carcinogenesis. 2003;24(5):927-36.
- Chen L, Hu JY, Wang SQ. The role of antioxidants in photoprotection: a critical review. J Am Acad Dermatol. 2012;67(5):1013-24.
- Available at: http://www.skinacea.com/sunscreen/uv-filters-chart.html#.Voj3MO9Iiob. Accessed February 21, 2017.
- Available at: http://www.smartskincare.com/skinprotection/sunblocks/sunblock_octocylene.html. Accessed February 21, 2017.
- Available at: https://www.fda.gov/Cosmetics/Labeling/Claims/ucm2005201.htm. Accessed February 21, 2017.
- Cosmetic Ingredient Review Expert Panel. Final report of the safety assessment of Alcohol Denat., including SD Alcohol 3-A, SD Alcohol 30, SD Alcohol 39, SD Alcohol 39-B, SD Alcohol 39-C, SD Alcohol 40, SD Alcohol 40-B, and SD Alcohol 40-C, and the denaturants, Quassin, Brucine Sulfate/Brucine, and Denatonium Benzoate. Int J Toxicol. 2008;27 Suppl 1:1-43.
- Baliga MS, Katiyar SK. Chemoprevention of photocarcinogenesis by selected dietary botanicals. Photochem Photobiol Sci. 2006 Feb;5(2):243-53.
- Chung JH, Han JH, Hwang EJ, et al. Dual mechanisms of green tea extract (EGCG)-induced cell survival in human epidermal keratinocytes. Faseb J. 2003;17(13):1913-5.
- Katiyar SK. Skin photoprotection by green tea: antioxidant and immunomodulatory effects. Curr Drug Targets Immune Endocr Metabol Disord. 2003;3(3):234-42.
- Chiu A, Kimball AB. Topical vitamins, minerals and botanical ingredients as modulators of environmental and chronological skin damage. Br J Dermatol. 2003;149(4):681-91.
- Katiyar S, Elmets CA, Katiyar SK. Green tea and skin cancer: photoimmunology, angiogenesis and DNA repair. J Nutr Biochem. 2007;18(5):287-96.
- Elmets CA, Singh D, Tubesing K, et al. Cutaneous photoprotection from ultraviolet injury by green tea polyphenols. J Am Acad Dermatol. 2001;44(3):425-32.
- Rees JR, Stukel TA, Perry AE, et al. Tea consumption and basal cell and squamous cell skin cancer: results of a case-control study. J Am Acad Dermatol. 2007;56(5):781-5.
- Chiu AE, Chan JL, Kern DG, et al. Double-blinded, placebo controlled trial of green tea extracts in the clinical and histologic appearance of photoaging skin. Dermatol Surg. 2005;31(7 Pt 2):855-60; discussion 60.
- Song XZ, Xia JP, Bi ZG. Effects of (-)-epigallocatechin-3-gallate on expression of matrix metalloproteinase-1 and tissue inhibitor of metalloproteinase-1 in fibroblasts irradiated with ultraviolet A. Chin Med J (Engl). 2004;117(12):1838-41.
- Roh E, Kim JE, Kwon JY, et al. Molecular mechanisms of green tea polyphenols with protective effects against skin photoaging. Crit Rev Food Sci Nutr. 2017;57(8):1631-7.
- Saeedi M, Morteza-Semnani K, Ghoreishi MR. The treatment of atopic dermatitis with licorice gel. J Dermatolog Treat. 2003;14(3):153-7.
- Rossi T, Benassi L, Magnoni C, et al. Effects of glycyrrhizin on UVB-irradiated melanoma cells. In Vivo. 2005;19(1):319-22.
- Katiyar SK. Silymarin and skin cancer prevention: anti-inflammatory, antioxidant and immunomodulatory effects (Review). Int J Oncol. 2005;26(1):169-76.
- Gazak R, Walterova D, Kren V. Silybin and silymarin—new and emerging applications in medicine. Curr Med Chem. 2007;14(3):315-38.
- Svobodova A, Zdarilova A, Maliskova J, et al. Attenuation of UVA induced damage to human keratinocytes by silymarin. J Dermatol Sci. 2007;46(1):21-30.
- Wright TI, Spencer JM, Flowers FP. Chemoprevention of nonmelanoma skin cancer. J Am Acad Dermatol. 2006;54(6):933-46; quiz 47-50.
- Lahiri-Chatterjee M, Katiyar SK, Mohan RR, et al. A flavonoid antioxidant, silymarin, affords exceptionally high protection against tumor promotion in the SENCAR mouse skin tumorigenesis model. Cancer Res. 1999;59(3):622-32.
- Mallikarjuna G, Dhanalakshmi S, Singh RP, et al. Silibinin protects against photocarcinogenesis via modulation of cell cycle regulators, mitogen-activated protein kinases, and Akt signaling. Cancer Res. 2004;64(17):6349-56.
- Singh RP, Agarwal R. Mechanisms and preclinical efficacy of silibinin in preventing skin cancer. Eur J Cancer. 2005 Sep;41(13):1969-79.
- Tsai CW, Lin CY, Wang YJ. Carnosic acid induces the NAD(P)H: quinone oxidoreductase 1 expression in rat clone 9 cells through the p38/nuclear factor erythroid-2 related factor 2 pathway. J Nutr. 2011;141(12):2119-25.
- Slamenova D, Kuboskova K, Horvathova E, et al. Rosemary-stimulated reduction of DNA strand breaks and FPG-sensitive sites in mammalian cells treated with H2O2 or visible light-excited Methylene Blue. Cancer Lett. 2002;177(2):145-53.
- Kar S, Palit S, Ball WB, et al. Carnosic acid modulates Akt/IKK/NF-kappaB signaling by PP2A and induces intrinsic and extrinsic pathway mediated apoptosis in human prostate carcinoma PC-3 cells. Apoptosis. 2012;17(7):735-47.
- Yesil-Celiktas O, Sevimli C, Bedir E, et al. Inhibitory effects of rosemary extracts, carnosic acid and rosmarinic acid on the growth of various human cancer cell lines. Plant Foods Hum Nutr. 2010;65(2):158-63.
- Huang MT, Ho CT, Wang ZY, et al. Inhibition of skin tumorigenesis by rosemary and its constituents carnosol and ursolic acid. Cancer Res. 1994;54(3):701-8.
- Offord EA, Gautier JC, Avanti O, et al. Photoprotective potential of lycopene, beta-carotene, vitamin E, vitamin C and carnosic acid in UVA-irradiated human skin fibroblasts. Free Radic Biol Med. 2002;32(12):1293-303.
- Harmand PO, Duval R, Delage C, et al. Ursolic acid induces apoptosis through mitochondrial intrinsic pathway and caspase-3 activation in M4Beu melanoma cells. Int J Cancer. 2005;114(1):1-11.
- Soo Lee Y, Jin DQ, Beak SM, et al. Inhibition of ultraviolet-A-modulated signaling pathways by asiatic acid and ursolic acid in HaCaT human keratinocytes. Eur J Pharmacol. 2003;476(3):173-8.
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