Thanks to Two Leaves and a Bud for sending us tea samples! I just sipped on my cup of Alpine Berry tea and it was delicious. This tea is described as an “herbal potpourri of hibiscus, apple peel, rose hips, blackberry leaves and orange peel.” The slight tartness of the citrus flavors balanced the sweetness of the berries to make it quite pleasant to sip on. While I like my sweeter teas piping hot, this would probably make a nice iced tea as well.

Two Leaves and a Bud offer both loose leaf tea and tea in nice sachets that allow the tea to move around and brew up a delicious cup. Yum!

• 2oz Rum
• 2oz Tequila
• 2oz Vodka
• 2oz Gin
• 2oz Bourbon Whiskey
• 2oz Triple Sec
• 2oz Sweet and Sour Mix
• Coca-Cola to taste

Fill a pitcher with ice. Add all of the ingredients except the coca-cola. Stir or shake, then add coca-cola to taste and stir again. Serve over ice and enjoy!

Bar not fully stocked? Here’s a simpler version of the Texas Tea recipe:

• 2 oz Bourbon
• 1 oz triple sec
• 2 oz Sweet and Sour Mix
• Coca-Cola to taste

It’s really the bourbon that makes it “Texas Tea”!

Researchers in the United States say that a compound found in green tea kills off cancer cells in one form of leukaemia.

A team led by Neil Kay at the Mayo Clinic used laboratory cell cultures to show that the compound, known as epigallocatechin-3-gallate (EGCG), helped to kill leukaemia cells.

Writing in the journal Blood, the researchers reported that patients with B-cell chronic lymphocytic leukaemia (CLL), common among people in their mid-to-late sixties, showed a reduction in cancer cells after being given the compound.

The EGCG from green tea interrupted survival signals, prompting leukaemia cells to die in eight of 10 patient samples tested.

The team said they would continue to look for therapeutic agents that were non toxic to the patient but kill cancer cells.

Kay said the EGCG finding was “an excellent start”. 

He said researchers now had a lot to work with in finding earlier, less toxic therapies for CLL patients, who are normally only given chemotherapy if the disease progresses.

CLL progresses at a different pace, and towards a different outcome, depending on the individual.

For some patients, it is a question of managing the disease over many years, and for others it may be fatal within just a few months, in spite of treatment.

Physicians have tended to adopt a “wait-and-see” attitude with CLL in its early stages, in the hope of sparing elderly patients the exposure to toxic chemotherapy.

The problem is now focused around how to identify which patients have the more aggressive form of the disease at a relatively early stage.

Non-toxic therapies like EGCG could be offered as an early-stage therapy before patients consider whether or not to have chemotherapy, researchers said.

Epidemiological studies since the 1970s have shown lower incidence of solid tumour cancers in parts of the world where green tea is consumed.

In mice, green tea has been shown to protect against solid tumour formation, while EGCG has also been shown to kill solid tumour cells in the laboratory.

The researchers speculate that EGCG kills leukaemia cells by inhibiting their ability to communicate with each other, and to receive blood flow.

We've got the freshest recipes at Hottest Tea !

Mmmm, a refreshing and bubbly afternoon beverage as the weather heats up…

• 1 cup water
• 2-inch knob frest gingerroot, sliced (1/4 cups)
• 6 green tea bags or 6 tsp loose green tea
• 1 cup sugar
• 3 cups club soda
• lime wedges

Bring water and gingerroot to a boil. Remove from heat and let cool for one minute; add tea. Steep for 5 minutes. Remove and discard tea and gingerroot. Whisk sugar into tea until completely dissolved. Pour tea over ice into large pitcher. Stir in club soda.

Pour into glasses and garnish with lime.

Moms will enjoy some beautiful, healthy tea, teapots, teacups, and tea accessories. Here are a few of our favorite Mothers Day Tea Gifts, with free shipping for orders over $50:

Mother’s Day Teapots and other lovely gifts

For the bargain shopper, this $9 teapot is a steal – pair it with a tin of tea and you’ve got a great gift for under $20!

Tea Starter Set includes a dishwasher and microwave safe tea maker and four different loose leaf teas in reusable tins.

Membership to a Tea of the Month Club, Mom will receive new teas each month to sample for just $20 per month.

May 2009 Journal Club Article: Green Tea Prevents Skin Cancer by Two Mechanisms

Inhibition of UVB-Induced Skin Tumor Development by Drinking Green Tea Polyphenols Is Mediated Through DNA Repair and Subsequent Inhibition of Inflammation
Syed M Meeran, Suhail Akhtar and Santosh K Katiyar
Journal of Investigative Dermatology (2009) 129: 1258-1270; doi:10.1038/jid.2008.354

Green Tea Prevents Skin Cancer by Two Mechanisms
Navid Bouzari 1, Yvonne Romagosa 1 and Robert S. Kirsner 1
Journal of Investigative Dermatology (2009) 129, 1054. doi:10.1038/jid.2009.64

Skin cancer accounts for more new cases of cancer than all other cancers combined. Exposure to UV radiation is the most important risk factor for development of skin cancer (LeBlanc et al., 2008). Primary prevention has reduced the incidence of skin cancer in the geographic regions at highest risk, such as Australia (Geller et al., 2009), but researchers are actively seeking ways to augment prevention through chemoprevention. Candidate agents include commonly used medications and foods such as nonsteroidal anti-inflammatory agents, lipid-lowering agents, angiotensin-converting enzyme and receptor blockers, and green tea (Christian et al., 2008). Polyphenols from green tea (GTPs) have been shown to reduce UV-induced skin cancer in animal models (Mantena et al., 2005). The mechanisms by which this is achieved remain unclear, but it is thought that the ability of GTPs to reduce the inflammation associated with UV exposure may be an important factor in this process.

To study the mechanisms by which GTPs affect inflammation and DNA repair and by which GTPs may prevent skin cancers induced by chronic UV exposure, Meeran and co-workers (2009) fed GTPs through drinking water to IL-12 (an important mediator of inflammation) knockout (KO) and wild-type mice. Compared with control mice, chronically UV-exposed and GTP-fed mice exhibited a delay in tumor onset, as well as smaller and fewer tumors. The benefit of GTPs was observed in IL-12 KO mice, but it was markedly less dramatic.

Mediators of inflammation, such as prostaglandin E2 and cyclooxygenase-2 (Katiyar and Meeran, 2007), as well as markers of cell proliferation, such as proliferating cell nuclear antigen and cyclin D1, were also affected by GTP administration; these effects were weaker in IL-12 KO mice. Repletion of IL-12 in KO mice and anti-IL-12 administration in wild-type mice confirmed the role of IL-12. Because GTP benefits appeared to be only partly mediated through IL-12, DNA repair of cyclopyridine dimers was studied after acute UV exposure. GTP-fed mice showed greater DNA repair than control mice, suggesting a dual mechanism by which GTP might reduce skin cancer development in animal models.

Through the following questions, we examine this paper in greater detail.

QUESTIONS
1. What are the mechanisms by which UV induces skin cancer?
2. What is the rationale for studying green tea to prevent skin cancer?
3. What were the hypotheses in this study, and how were they tested?
4. What were the findings of this study?
5. What were the limitations of this study?
6. How might the article affect your recommendations to patients?

ANSWERS
1. The human skin is a highly dynamic and protective organ. It is exposed daily to UVR from sun and occupational light sources, and sometimes to phototherapy systems. UVR is part of the spectrum of electromagnetic radiation, and it is divided into three regions: UVC, 200–290 nm; UVB, 290–320 nm; and UVA, 320–400 nm. UVC radiation is completely absorbed by the Earth’s atmosphere and is therefore irrelevant to solar-induced cutaneous carcinogenesis. UVB radiation is only partly absorbed by the atmospheric ozone layer, and UVA radiation is not absorbed at all (de Laat et al., 1996). When the photons that make up UVR enter the skin, they may be absorbed by any one of several biomolecules, leading to excited energy states. Following this, the excited molecule can re-emit some of the energy (as fluorescence), lose energy as heat, or undergo photochemical reactions that form new molecules (photoproducts).

In the skin, the main absorbing biomolecules are melanin, DNA, amino acids, carotene, and urocanic acids (Anderson and Parrish, 1981). Among these, DNA is most critical. UVR, especially that in the UVB range, leads to the formation of cyclobutane–pyrimidine dimer and pyrimidine pyridone photoproducts in DNA. Other effects of UVR on DNA are the induction of cytosin photohydrates, purine photoproducts, and single-strand breaks. Erroneous repair of these products may lead to mutations, most commonly substitutions of T for C or TT for CC. If these mutations affect the function of specific oncogenes, tumor-suppressive genes, or important housekeeping genes such that cell growth and site or residence are no longer regulated, transformation is a recognized consequence (Hussein, 2005; de Laat et al., 1996). This is referred to as mutagenesis.

In addition to direct mutagenesis, UVR can indirectly affect the frequency of mutations, usually by altering the cell cycle to allow less time for DNA repair prior to subsequent rounds of replication. In this process, alterations in tumor suppressor genes (TSGs), oncogenes, and mismatch repair proteins occurs. The tumor-suppressor genes, such as p53, p16, and PTCH, ordinarily regulate normal cellular growth and differentiation. Every living cell has two copies of these TSGs; if one is lost or damaged, the other copy can maintain normal cell function. The proto-oncogenes involved in photocarcinogenesis are bcl-2, ras, and c-fos. UVR can activate these proto-oncogenes, transforming them into oncogenes.

2. Green tea is one of the most commonly consumed beverages, accounting for almost 20% of tea consumption worldwide. It is manufactured from the fresh leaves of the plant Camellia sinensis by drying and steaming them at high temperatures. Its polyphenols have antioxidant and anti-inflammatory properties, and they have been shown to have a protective role against a variety of cancers, including skin cancer in laboratory animals. Green tea polyphenols (GTPs) have protective effects against the UV-induced sunburn response, UV-induced immunosuppression, and photoaging of skin.

Several basic and epidemiologic studies have suggested that green tea prevents cancer in many organ systems, including skin (Katiyar and Mukhtar, 1996). Wang et al. (1991) were among the first to suggest that green tea might have protective effects against UV-induced skin cancers. They showed that administration of green tea to SKH-1 hairless mice led to a dose-dependent prolongation in the mean time of tumor development when the mice were exposed to UVR. Although the mechanism of photoprotection by green tea is not known, there is a growing body of evidence concerning its protective effects at the cellular, molecular, and biochemical levels (Figure 1).

Figure 1. Protective effects of green tea at the cellular, molecular, and biochemical levels.

At the cellular level, GTPs have been shown to induce apoptosis in premalignant and squamous cell carcinoma keratinocytes but have anti-apoptotic effects in normal keratinocytes. GTPs deter the movement of macrophages and neutrophils to UV-irradiated skin and, as a result, decrease the reactive oxygen radicals. On the other hand, GTPs have been shown to increase the number of Langerhans cells. These important antigen-presenting cells are thought to have a protective role in the pathogenesis of UV-induced skin cancers. Additionally, GTPs have been shown to reduce the number of sunburn cells, increase the level of IL-12, decrease IL-10, inhibit tumor angiogenesis, decrease oxidative stress, increase DNA-repair ability, and increase apoptosis of photodamaged cells (Yusuf et al., 2007). Because GTPs have been shown to reverse the immunosuppressive effects of UV radiation, there has been considerable interest in defining the effects of green tea on UV-induced modifications in cytokine production.

At the molecular level, there is considerable evidence to indicate that GTPs protect against UV-induced oxidative injury in the skin. They not only decrease the production of free oxygen radicals but also protect against depletion of glutathione, glutathione peroxidase, and catalase, which have antioxidant activity. Several studies have demonstrated that GTPs can directly prevent UV-induced DNA damage. It is thought that this protective effect is at least partly due to GTP-induced p53 increase. Other mechanisms include inhibition of NF-κB and suppression of angiogenic factors such as vascular endothelial growth factor and matrix metalloproteinases. Because GTPs have been shown to reverse the immunosuppressive effects of UV radiation, there has been considerable interest in defining the effects of green tea on UV-induced modifications in cytokine production.

3. Based on the facts that GTPs increase IL-12 and that IL-12 plays a role in the removal or repair of UVB-induced DNA damage, Meeran et al. (2009) hypothesized that treating mice with GTPs would enhance IL-12 production and decrease UVB-induced DNA damage, resulting in reduced inflammation and tumorigenesis. If this theory is correct, GTPs should not be able to show the above effects in IL-12-deficient mice. With this in mind, the authors conducted two experiments, one using wild-type (C3H/HeN) mice and the other using IL-12-KO mice on a C3H/HeN background. Each experiment included three groups of mice: mice that were not UVB exposed (control), mice that were exposed to a photocarcinogenesis protocol, and mice that were exposed to a photocarcinogenesis protocol and provided drinking water containing GTPs. The photocarcinogenesis protocol consisted of exposure to longer-term UV light, predominantly in the UVB range. Following the prescribed protocols, the authors recorded the number of tumors, their size, and the time elapsed for tumor development. They subsequently examined the level of cytokines (TNF-α, IL-1β, and IL-6) using ELISA, COX-2 expression using western blot, and level of PGE2 using enzyme immunoassay. Then they looked at the differences in the above factors between the two sets of mice (wild-type vs. IL-12-KO), as well as the differences among the groups in each set (control vs. UVB-treated vs. GTP- and UVB-treated). Markers of keratinocyte proliferation were also examined (PCNA and cyclin D1). Additionally, using a different protocol consisting of acute UV exposure, the authors examined the skin as well as tumor cells for formation of cyclobutane pyrimidine dimers (CPDs) using immunohistochemical and southwestern dot-blot analysis.

4. The investigators demonstrated that UVB induces skin cancers in wild-type mice. In this group, treatment with GTPs not only decreased tumor incidence but also increased the latency period of the tumors by 2 weeks. IL-12-KO mice were more susceptible to UVB-induced carcinogenesis compared with their wild-type counterparts. Moreover, GTPs did not protect against UVB-induced tumorigenesis in these mice. Hence, the authors concluded that prevention of photocarcinogenesis by oral GTPs is IL-12 dependent. In the same manner, Meeran et al. observed more inflammation in IL-12-KO mice compared with wild-type mice and a reduced effect of GTPs in decreasing the inflammatory mediators (COX-2 and PGE2) in these mice compared with the wild type following UVB radiation.

When the investigators evaluated two of the markers of keratinocyte proliferation, PCNA and cyclin D1, the results were similar to the findings observed for inflammatory mediators. That is, greater keratinocyte proliferation was seen in IL-12-KO than in wild-type mice. In addition, a significant decrease in these proliferation markers was observed in wild-type mice treated with GTPs; this was not observed in GTP-treated IL-12-KO mice. The investigators found the inhibitory effect of GTPs on UVB-induced proinflammatory cytokines (TNF-α, IL-1β, and IL-6) to be higher in wild-type but not in IL-12-KO mice.

Subsequently, these researchers undertook additional experiments to determine whether the inhibitory effect of GTPs on UVB-induced inflammation and tumorigenesis was attributable to a GTP-mediated enhancement of the repair or removal of UVB-induced DNA damage. They evaluated the CPDs and inflammatory mediators (COX-2 and PGE2) at several time points (30 minutes, and 24, 48, and 72 hours) after acute UV exposure and found that GTPs significantly decreased the above factors at 48 and 72 hours in wild-type mice, but not in their IL-12-KO counterparts. Injection of recombinant IL-12 in UVB-irradiated IL-12-KO mice led to exhibition of GTP-mediated anti-tumorigenesis and anti-inflammatory activity. Conversely, injection of anti-IL-12 antibodies in UVB-irradiated wild-type mice resulted in a failure in the repair or removal of CPD and in high levels of COX-2 and PGE2.

5. While the study of Meeran et al. provides valuable data on the mechanism by which GTPs exert their antitumorigenesis and anti-inflammatory activities, the study was limited in several respects. The investigators accurately showed that the chemical composition of GTPs added to the drinking water was consistent over the 3 days. But they did not measure the level of GTPs in the serum or tissue of the study animals, so we cannot exclude the possibility that the lack of GTP-mediated antitumorigenesis effects in IL-12-KO mice is attributable to a lack of GI or tissue absorption of the GTPs in this model. Furthermore, the amount of fluid (GTP-containing water and regular water) consumed by the mice was not measured (or at least not reported). One could argue that mice did (or did not) like the taste of the GTP-containing water and hence drank more (or less) fluid.

Another possible explanation for the lack of GTP-mediated antitumorigenesis effects in IL-12-KO mice might be the high incidence of the tumors in this model (80% of the irradiated mice developed skin cancer), which statistically decreases the power of GTPs in the prevention of cancer. Simply, one could argue that GTPs are effective in both wild-type and IL-12-KO mice but they lose their significance in the IL-12-KO mouse because there are more cancers in this model. In this study, the GTPs were started 2 weeks prior to the initiation of UVB irradiation and continued throughout the study. In humans, the likely scenario is that UVB exposure occurs months to years before the consumption of green tea begins. It would be interesting to examine whether GTPs could exert their effects if started after UVB irradiation. It would also be interesting to study what would happen if the GTPs were discontinued.

6. The mechanistic study by Meeran et al. (2009) supports the potential nutritional value of green tea in skin photoprotection. The authors show that GTPs are effective via oral administration in drinking water. Hence, GTPs, in combination with sunscreens, may provide an effective strategy for reducing the risk of skin cancers. In addition, the data presented in this study indicate that UVB-induced DNA damage and inflammatory responses are causally related to an increased risk of photocarcinogenesis. The ability of IL-12 to repair UV-induced DNA damage and decrease subsequent inflammation makes it a potential “cytokine sunscreen” with the ability to protect against both skin cancer and sunburn. In summary, the outcome of this study suggests that endogenous enhancement of IL-12-mediated DNA repair by GTPs may be considered an effective strategy for the prevention of inflammation-associated skin diseases, including skin cancers. Nonetheless, clinical trials are needed to validate the usefulness of GTPs, either alone or in combination with existing modes of skin cancer prevention.

REFERENCES
Anderson RR, Parrish JA (1981) The optics of human skin. J Invest Dermatol 77:13–9

Christian JB, Lapane KL, Hume AL, Eaton CB, Weinstock MA, VATTC Trial (2008) Association of ACE inhibitors and angiotensin receptor blockers with keratinocyte cancer prevention in the randomized VATTC trial. J Natl Cancer Inst 100:1223–32

de Laat A, van Tilburg M, van der Leun JC, van Vloten WA, de Gruijl FR (1996) Cell cycle kinetics following UVA irradiation in comparison to UVB and UVC irradiation. Photochem Photobiol 63:492–7

Geller AC, Elwood M, Swetter SM, Brooks DR, Aitken J, Youl PH et al. (2009) Factors related to the presentation of thin and thick nodular melanoma from a population-based cancer registry in Queensland, Australia. Cancer 115:1318–1327

Hussein MR (2005) Ultraviolet radiation and skin cancer: molecular mechanisms. J Cutan Pathol 32:191–205

Katiyar SK, Meeran SM (2007) Obesity increases the risk of UV radiation induced oxidative stress and activation of MAPK and NF-kB signaling. Free Rad Biol Med 42:299–310

Katiyar SK, Mukhtar H (1996) Tea in chemoprevention of cancer: epidemiologic and experimental studies. Int J Oncol 8:221–38

LeBlanc WG, Vidal L, Kirsner RS, Lee DJ, Caban-Martinez AJ, McCollister KE et al. (2008) Reported skin cancer screening of US adult workers. J Am Acad Dermatol 59:55–63

Mantena SK, Meeran SM, Elmets CA, Katiyar SK (2005) Orally administered green tea polyphenols prevent ultraviolet radiation-induced skin cancer in mice through activation of cytotoxic T cells and inhibition of angiogenesis in tumors. J Nutr 135:2871–7

Meeran SM, Akhtar S, Katiyar SK (2009) Inhibition of UVB-induced skin tumor development by drinking green tea polyphenols is mediated through DNA repair and subsequent inhibition of inflammation. J Invest Dermatol 129:1258–70

Wang Z, Agarwal R, Bickers D, Mukhtar H (1991) Protection against ultraviolet B radiation-induced photocarcinogenesis in hairless mice by green tea polyphenols. Carcinogenesis 12:1527–30

Yusuf N, Irby C, Katiyar SK, Elmets CA (2007) Photoprotective effects of green tea polyphenols. Photodermatol Photoimmunol Photomed 23:48–56

1 Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, Florida, USA

To this add:
* 2 eggs
* 10 tablespoons of olive oil
* 2/3 cup buttermilk.

Directions
In a 400 degree oven toast oats for 8-10 minutes. Mix dry ingredients thoroughly. To the dry ingredients add the eggs, oil and buttermilk. Stir just till ingredients are moistened. Let stand for five minutes.

Pat the dough into two six inch rounds, cut each round into six wedges. Brush the top with a little olive oil. Bake for 16-18 minutes in the 400 degree oven.

Makes 12 good sized scones

* 4 tsp. black tea
* 1 peice of dried ginger
* 3 crushed cardamon pods
* 3 whole cloves
* 1 cinnamon stick
* milk and sugar to taste

Brew tea and spices for 30-45 seconds, then remove from heat and let steep for another 1-2 minutes. Strain out the tea and spices. Add a touch of milk and sugar and enjoy.

Steep tea, ginger, and cranberries in hot water for 15 minutes. Strain and add nutmeg and cranberry juice – serve warm. (This tea recipe would make a tasty “hot toddy” with a splash of rum!)

Bring milk almost to a boil in a saucepan – add tea bag and steep for about 5 minutes. Remove and stir in brown sugar – enjoy!