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
Dr. Leslie S. Baumann
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
Phyzome/Wikimedia Commons/CC BY-SA 3.0
The tea plant, Camellia sinensis, is the source of black tea and the other three main true teas.
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