Camellia sinensis, an evergreen tree belonging to the Theaceae family and used by human beings for approximately 4,000 years, is the source of the beverage tea, which is popular throughout the world, especially in Asia.1 Of the four main true teas (that is, derived from the tea plant C. sinensis), green and white are unfermented, black tea is fermented, and oolong tea is semifermented.2,3
Polyphenols, many of which act as strong antioxidants, are a diverse family of thousands of chemical substances found in plants. Theaflavins are black tea polyphenols with well-documented tumor-suppressing activity.4 In fact, they are thought to be the primary constituents of black tea responsible for conferring chemoprotection against cancer.5 Black tea, through oral administration and topical application, has been shown in the laboratory setting to protect skin from UV-induced erythema, premature aging, and cancer.6
Halder et al. have found that theaflavins and thearubigins, another key class of black tea polyphenols, can suppress A431 (human epidermoid carcinoma) and A375 (human malignant melanoma) cell proliferation without adversely impacting normal human epidermal keratinocytes. The researchers concluded that theaflavins and thearubigins appear to impart chemopreventive activity via cell cycle arrest and promotion of apoptosis in human skin cancer cells through a mitochondrial death cascade.7
In a 2005 English-language literature review, Thornfeldt cited green and black tea, as well as pomegranate, as the only ingredients supported by clinical trial evidence for effectiveness in treating extrinsic aging.2
Oral administration findings in animals and humans
More than 2 decades ago, Wang et al. found that the effects of orally administered black tea were comparable to those of green tea in suppressing UVB-induced skin carcinogenesis in 7,12-dimethylbenz[a]anthracene (DMBA)-initiated SKH-1 mice.8
In 1997, Lu et al. found that orally administered black tea inhibited the proliferation of skin tumors and enhanced apoptosis in nonmalignant and malignant skin tumors in female CD-1 mice with tumors initiated by the application of DMBA and promoted with 12-O-tetradecanoylphorbol-13-acetate (TPA).9 Record et al. reported in 1998 that black tea may confer greater protection than green tea against simulated solar irradiation.10
Hakim and Harris conducted a population-based case-control study in 2001 to assess the effects of the consumption of citrus peel and black tea on squamous cell skin cancer. They found that participants who reported intake of hot black tea and citrus peel had a significant reduction in the risk of squamous cell carcinoma. Further, they concluded that hot black tea and citrus peel displayed independent potential protection against SCC.11
Two years earlier, Zhao et al. used cultured keratinocytes and mouse and human skin to evaluate the effect of both orally and topically administered standardized black tea extract and its two major polyphenolic subfractions against UVB-induced photodamage. Topical pretreatment with the extract on SKH-1 hairless mice significantly lowered the incidence and severity of erythema and diminished skinfold thickness, compared with UVB-exposed nontreated mice. The black tea extract was similarly effective in human subjects. UVB-induced inflammation in murine as well as human skin also was reduced when the standardized extract was administered 5 minutes after UVB exposure. The investigators suggested that their findings indicated that black tea extracts have the capacity to mitigate UVB-generated erythema in human and murine skin.12
In 2011, George et al. assessed the chemopreventive effects of topical resveratrol and oral black tea polyphenols in blocking skin carcinogenesis in a two-stage mouse model initiated and promoted by DMBA and TPA, respectively. The combined treatment was found to reduce tumor incidence by approximately 89% (resveratrol alone, approximately 67%; black tea polyphenols alone, approximately 75%). Tumor volume and number also were significantly diminished by the synergistic combination, which, histologically, was noted for suppressing cellular proliferation and inducing apoptosis. The investigators concluded that oral black tea polyphenols combined with topical resveratrol exert greater chemopreventive activity than either compound alone and warrant study in trials for treating skin and other cancers.13
Animal studies on topical application
In 1997, Katiyar et al. investigated the anti-inflammatory effects of topically applied black tea polyphenols, primarily theaflavin gallates and (-)-epigallocatechin-3-gallate (EGCG), against TPA-induced inflammatory responses in murine skin. Significant inhibition against TPA-promoted induction of epidermal edema, hyperplasia, leukocyte infiltration, and proinflammatory cytokine expression was rendered by the preapplication of black tea polyphenols prior to TPA exposure. The investigators concluded that black tea polyphenols may be effective against human cutaneous inflammatory responses.14
Just over a decade later, Patel et al. investigated the in vivo antitumor-promoting effects of the most plentiful polymeric black tea polyphenols (thearubigins) in mice exposed to tumor-initiating DMBA and tumor-promoting TPA over a 40-week period. Pretreatment with topical thearubigins resulted in antipromoting effects in terms of latency, multiplicity, and incidence of skin papillomas. The black tea polyphenols also were found to reduce TPA-induced cell proliferation and epidermal cell apoptosis. The researchers attributed the protective effects of these compounds to their inhibitory impact on TPA-induced cellular proliferation.15
In 2011, Choi and Kim assessed the whitening effect of black tea water extract topically applied twice daily (6 days a week for 4 weeks) to UVB-induced hyperpigmented spots on the backs of brown guinea pigs. Treatment was divided into control (UVB and saline), vehicle control (UVB, propylene glycol, ethanol, and water), positive control (UVB and 2% hydroquinone), and two experimental groups (UVB and 1% black tea; UVB and 2% black tea). The investigators observed that the hyperpigmented spots treated with hydroquinone and black tea were clearly lighter than those treated by the control or vehicle-control groups. Histologic examination revealed that melanin pigmentation, melanocyte proliferation, and melanin production were significantly diminished in the groups treated with hydroquinone and both concentrations of black tea. The authors concluded that black tea suppresses melanocyte proliferation and melanosome synthesis in vivo, thus displaying the capacity to whiten skin in brown guinea pigs.16
In 2013, Yeh et al. found in nude mouse skin in vitro that niosomes appear to be feasible as a delivery vehicle for the dermal administration of black tea extracts as a sunscreen agent.17
Topical studies in humans
Building on findings 3 years earlier18, Türkoglu et al., in 2010, assessed the photoprotective effects of dermal gels produced from green and black tea aqueous extracts tested in vivo in the forearms of six volunteers exposed to artificial UV light (200-400 nm). In addition to the green tea and black tea gels, a 0.3% caffeine gel, a carbomer gel base, and a control were tested. The investigators reported no eruptions of UV-induced erythema in any of the black and green tea gel sites, but erythema was present to varying degrees at the areas treated with caffeine gel, carbomer gel, and control. The investigators concluded that the black and green tea extracts exhibited potent UV absorbance and that the formulated gels were effective in protecting the skin against UV-induced erythema. Further, the investigators suggested that these agents have the potential to protect against other harm caused by UV radiation, including photoaging.19
Conclusion
Though not as widely investigated as green tea, the therapeutic potential of black tea is of great interest. Although an abundance of laboratory evidence has emerged, clinical evidence is sparse. Nevertheless, laboratory data suggest the potential uses of black tea in the dermatologic realm and justify more human trials.
References
1. Cancer Lett. 1997 Mar 19;114(1-2):315-7.
2. Dermatol. Surg. 2005;31(7 Pt 2):873-80.
3. Oxid Med Cell Longev. 2012:2012:560682.
4. J Environ Pathol Toxicol Oncol. 2010;29(1):55-68.
5. Mol Carcinog. 2000 Jul;28(3):148-55.
6. Am J Clin Dermatol. 2010;11(4):247-67.
7. Carcinogenesis. 2008 Jan;29(1):129-38.
8. Cancer Res. 1994 Jul 1;54(13):3428-35.
9. Carcinogenesis. 1997 Nov;18(11):2163-9.
10. Mutat Res. 1998 Nov 9;422(1):191-9.
12. Photochem Photobiol. 1999 Oct;70(4):637-44.
13. PLoS One. 2011;6(8):e23395.
14. Carcinogenesis. 1997 Oct;18(10):1911-6.
15. Cell Prolif. 2008 Jun;41(3):532-53.
16. Toxicol Res. 2011 Sep;27(3):153-60.
17. Int J Dermatol. 2013 Feb;52(2):239-45.
18. Int J Cosmet Sci. 2007 Dec;29(6):437-42.
19. Drug Discov Ther. 2010 Oct;4(5):362-7.
Dr. Baumann is chief executive officer of the Baumann Cosmetic & Research Institute in the Design District in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann wrote the textbook “Cosmetic Dermatology: Principles and Practice” (New York: McGraw-Hill, 2002) and a book for consumers, “The Skin Type Solution” (New York: Bantam Dell, 2006). She has contributed to the Cosmeceutical Critique column in Dermatology News since January 2001. Her latest book, “Cosmeceuticals and Cosmetic Ingredients,” was published in November 2014. Dr. Baumann has received funding for clinical grants from Allergan, Aveeno, Avon Products, Evolus, Galderma, GlaxoSmithKline, Kythera Biopharmaceuticals, Mary Kay, Medicis Pharmaceuticals, Neutrogena, Philosophy, Topix Pharmaceuticals, and Unilever.
