Health & Beauty

The Science Behind Tea

There are two flavonoids found in tea that receive the most attention, one being catechins, which tend to be most abundant in green teas.
There are two flavonoids found in tea that receive the most attention, one being catechins, which tend to be most abundant in green teas.
There are two flavonoids found in tea that receive the most attention, one being theaflavins, which tend to be most abundant in black teas.
There are two flavonoids found in tea that receive the most attention, one being theaflavins, which tend to be most abundant in black teas.

As someone with an interest in both tea and biomedicine, I’ve been incredibly excited about the amount of new research coming out about the potential effects of tea on immune health. I’ve always been an advocate of making sure that people have access to accurate, well-researched, and easily digestible information.

However, the current coronavirus pandemic makes it equally important to be responsible about drawing conclusions from research that deals with health and medicine.

When reading this article, please keep in mind that this discussion is not in any way, shape, or form meant to be taken as medical advice. Rather, it is meant to be an overview of recent findings presented in accessible language, with special emphasis on what conclusions can and cannot be responsibly drawn from the available data.

Most of the research regarding the interaction between tea and immune health focuses on flavonoids, a specific class of secondary (i.e. not essential for the organism’s everyday survival) compounds produced by plants, that are part of a larger class of compounds called polyphenols. Flavonoids from a variety of plants, from tea and wine to legumes to various spices, have long been known to have medicinal properties. The flavonoids found in tea that receive the most attention are catechins, which tend to be most abundant in green teas, and theaflavins, which tend to be most abundant in black teas.1

Pathogenic viruses and bacteria often rely on a suite of various proteins in order to enter a host, infect cells, and replicate. Therefore, the antiviral or antibacterial properties of flavonoids often involve interference with proteins involved in one or more of these crucial functions. In a review of the available literature on antiviral properties of black and green tea, Mhatre et al. (2020) identified several possible mechanisms by which tea compounds may interact with SARS-COV-2, the virus causing Covid-19.2 The enzyme chymotrypsin-like protease (3CLpro) is vital for several functions during the maturation process of SARS-COV, a close “cousin” of SARS-COV-2.

This makes 3CLpro an ideal target for therapeutics. A recent study shows that both theaflavin and EGCG (a specific catechin) inhibit activity of this enzyme in a dose-dependent manner.3 Additional research suggests that tea polyphenols may also interfere with infection by acting on human proteins that the virus utilizes during the infection process. One well-studied target of SARS-COV-2 is the human ACE2 receptor, a small protein that is expressed on the surface of many cells in the body. A recent computational study suggests that theaflavin-3 is capable of binding to the ACE2 receptor, which may inhibit SARS-COV-2 from using that receptor to enter host cells.4

The effect of tea flavonoids, however, is not only limited to direct interference with the function of viral particles. A large portion of the available research focuses on how tea flavonoids may influence the body’s overall immune response to infection. Particularly severe cases of Covid-19 often involve a “cytokine storm,” in which an overzealous and uncontrolled immune response to a coronavirus infection leads to the destruction of organ tissue. Tea flavonoids, among other polyphenols, may be a source of potential therapeutic agents that modulate the body’s inflammatory response so as to avoid this kind of immune-mediated destruction.5, 6

A recent review by Chowdhury and Barooah on the immunomodulatory effects of tea identified several potential mechanisms by which tea flavonoids might alter immune responses,7 including downstream suppression of pro-inflammatory cytokines via certain signaling proteins8, 9 and interference with neutrophil-elastase, an enzyme secreted by immune cells that can destroy host tissue.10 Although it may seem counterintuitive to inhibit the body’s immune response to a coronavirus infection, the well known anti-inflammatory effects of tea flavonoids make them a potential candidate for mitigating the worst effects of an overzealous immune response.

While these studies are promising, it is also important to understand the conditions under which these effects were observed. The computational study by Zhang et al. (2020), for example, only tells us that theaflavin-3 has a chemical structure which is capable of binding to ACE2 receptors under simulated normal conditions. Several of the studies carried out in a lab often use concentrated forms of polyphenols (usually extracts from tea leaves) administered directly to cell cultures, which are composed of one type of cloned cell from the human body (i.e. liver cells or intestinal cells). Mhatre et al. (2020) notes that drinking tea may not result in the same effects observed in these studies, since the concentration of polyphenols may be drastically reduced during digestion or the polyphenols themselves might be oxidized well before reaching any target protein.

So what does all this information mean for tea enthusiasts? For the time being, we should be skeptical of any broad claims about tea and Covid-19. The research simply doesn’t support any conclusion that positions tea as more effective than any of the treatments currently being administered by medical professionals. But even with a healthy dose of critical skepticism, we can still come to some positive conclusions! For me, at least, this recent research is confirmation that tea is an incredibly interesting source of biomedical knowledge and developments. While you’re at home observing social distancing guidelines during this pandemic, take some time to appreciate the biochemical awesomeness of your cozy cup of tea.

1Flavonoids. Linus Pauling Institute. Published April 28, 2014.

2Mhatre S, Srivastava T, Naik S, Patravale V. Antiviral activity of green tea and black tea polyphenols in prophylaxis and treatment of COVID-19: A review [published online ahead of print, 2020 Jul 17]. Phytomedicine. 2020;153286. doi:10.1016/j.phymed.2020.153286

3Jang M, Park Y-I, Cha Y-E, et al. Tea Polyphenols EGCG and Theaflavin Inhibit the Activity of SARS-CoV-2 3CL-Protease In Vitro. Evidence-Based Complementary and Alternative Medicine. 2020;2020:1-7. doi:10.1155/2020/5630838

4Zhang J-J, Shen X, Yan Y-M, WANG Y, Cheng Y-X. Discovery of anti-SARS-CoV-2 agents from commercially available flavor via docking screening. Published online March 2, 2020. doi:10.31219/osf.io/vjch2

5Desjarlais M, Wirth M, Lahaie I, et al. Nutraceutical Targeting of Inflammation-Modulating microRNAs in Severe Forms of COVID-19: A Novel Approach to Prevent the Cytokine Storm. Frontiers in Pharmacology. 2020;11. doi:10.3389/fphar.2020.602999

6Russo M, Moccia S, Spagnuolo C, Tedesco I, Russo GL. Roles of flavonoids against coronavirus infection. Chem Biol Interact. 2020;328:109211. doi:10.1016/j.cbi.2020.109211

7Chowdhury P, Barooah AK. Tea Bioactive Modulate Innate Immunity: In Perception to COVID-19 Pandemic. Frontiers in Immunology. 2020;11. doi:10.3389/fimmu.2020.590716

8Byun EH, Omura T, Yamada K, Tachibana H. Green tea polyphenol epigallocatechin-3-gallate Inhibits TLR2 signaling induced by peptidoglycan through the polyphenol sensing molecule 67-kda laminin receptor. FEBS Lett (2011) 585:814–20. 10.1016/j.febslet.2011.02.010

9Byun EB, Choi HG, Sung NY, Byun EH. Green tea polyphenol epigallocatechin-3-gallate inhibits TLR4 signaling through the 67-kDa laminin receptor on lipopolysaccharide-stimulated dendritic cells. Biochem Biophys Res Commun (2012) 426:480–5. 10.1016/j.bbrc.2012.08.096

10Xiaokaiti Y, Wu H, Chen Y, Yang H, Duan J, Li X. EGCG reverses human neutrophil elastase-induced migration in A549 cells by directly binding to HNE and by regulating α1-AT. Sci Rep (2015) 5:11494. 10.1038/srep11494