EGCG: History and Discovery

Tea has been drunk for at least two thousand years; the molecule that now carries most of green tea's scientific reputation has had a name for less than eighty. Epigallocatechin gallate — EGCG — is the most abundant of the catechins in the leaf of Camellia sinensis, and its history is not a story of ancient healers but of chemists: a nineteenth century that could only call tea's astringent fraction "tannin"; a woman at a Tokyo institute who crystallised the first tea catechins in 1929 and 1930; two British chemists who reported EGCG itself in 1948; a Japanese cancer laboratory that put it on the map in 1987; and, in our own century, the clinical trials, the regulator's ointment approval, and the liver-safety reckoning that together define how EGCG is understood today. Where the record is firm we give the date and the name; where an attribution is uncertain we say so.

Table of Contents

  1. A Leaf Before a Molecule: Tea's Long Prelude
  2. The Nineteenth Century: Theine and the "Tannin" of Tea
  3. Michiyo Tsujimura and the RIKEN Catechins (1924–1934)
  4. Naming EGCG: Bradfield and Penney (1947–1948)
  5. Chromatography and the Black-Tea Chapter: Roberts and the Theaflavins
  6. The Chemoprevention Era: Fujiki, Yoshizawa and the 1987 Experiment
  7. The Bioavailability Problem
  8. Into the Clinic: Prostate Trials, Safety Studies and a Botanical Drug
  9. The Liver Signal: Case Reports and the EFSA Opinion (2008–2018)
  10. The 2020s: Where the Evidence Stands
  11. EGCG Today
  12. Key Research Papers
  13. Connections
  14. Featured Videos

A Leaf Before a Molecule: Tea's Long Prelude

EGCG cannot be separated from the plant that makes it. Camellia sinensis, the tea plant, is an evergreen shrub whose wild home is usually placed where the highlands of south-west China, Tibet, northern Myanmar and north-east India meet. Every true tea — green, white, oolong and black — is made from its leaves; what differs is how far the leaf is allowed to oxidise after picking, and that single processing choice, as we will see, decides how much EGCG survives into the cup.

China's own account of tea's discovery is a legend, and should be told as one. The story credits the mythical emperor Shennong, the "Divine Farmer" of Chinese tradition, with discovering tea around 2737 BCE when leaves drifted into water he was boiling. No document from anywhere near that date exists; the tale is a way of saying that tea is older than memory. Physical evidence is much later but still ancient: tea residues identified in a Han-dynasty tomb near Xi'an, reported in 2016, show that tea was being drunk at the imperial court by the second century BCE.

The first true book about tea, Lu Yu's Cha Jing (The Classic of Tea), was written in the Tang dynasty between about 760 and 762 CE and set down how tea should be grown, prepared and appreciated. Tea reached Japan with Buddhist monks; the monk Eisai is credited with bringing tea seeds to Kyoto in 1191 and, in 1211, with writing Kissa Yōjōki, a treatise on staying healthy by drinking tea — the earliest Japanese claim for tea as a medicine. Europe met tea late. A Dutch East India Company ship carried the first green tea leaves to Amsterdam early in the seventeenth century, and in 1657 a London merchant, Thomas Garway, became the first to sell tea in the city; the diarist Samuel Pepys recorded his first cup in 1660.

Through all of that history tea's reputation rested on experience and belief; nobody could say what was in the leaf. That question belonged to the chemists of the nineteenth century.

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The Nineteenth Century: Theine and the "Tannin" of Tea

The first molecule anyone pulled out of tea was not a catechin. In 1819 the German chemist Friedlieb Ferdinand Runge isolated caffeine from coffee beans; in 1827 the French chemist Oudry isolated a stimulant from tea leaves and called it théine, and in 1838 Gerardus Mulder and Carl Jobst showed, independently, that theine and caffeine were one and the same substance. Tea's alkaloid, in other words, was understood by the 1830s.

Its polyphenols were not. Nineteenth-century chemists knew that tea was astringent — that it puckered the mouth and precipitated proteins the way oak bark and gall nuts did — and they filed that whole fraction under the word tannin, the name for any plant substance that could tan hide. "Tea tannin" was for decades a catch-all for a mixture nobody could resolve into its parts, and the name lingered in the literature long after it had stopped being accurate: as late as 1987 the paper that launched EGCG's cancer-research career still described it in its title as "the main constituent of ‘tannin’ in green tea."

The word that would eventually replace it, catechin, comes from an older product altogether: catechu, a tanning and dyeing extract boiled from the heartwood of the acacia tree Acacia catechu. A crystalline substance obtained from catechu was called catechin in the nineteenth century, and in the twentieth the name was extended to the whole family of related flavan-3-ol molecules — of which tea, it turned out, contained the richest and most varied set of all. Sorting that set into named compounds required a new kind of chemistry, and it was done first in Japan.

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Michiyo Tsujimura and the RIKEN Catechins (1924–1934)

Michiyo Tsujimura (1888–1969) is the central figure in the early chemistry of green tea, and her career was remarkable by any measure. Trained as a science teacher, she joined the Institute of Physical and Chemical Research in Tokyo — RIKEN — in October 1923 as a research student in the laboratory of Umetaro Suzuki, the agricultural chemist who in 1910 had extracted from rice bran the anti-beriberi factor later identified as thiamine (vitamin B1). Suzuki's laboratory was a nutrition laboratory, and tea entered it as a food to be analysed. In 1924 Tsujimura and her colleague Seitaro Miura reported that green tea contained vitamin C, a finding that reportedly helped Japanese green tea exports and that turned her attention to the leaf for the rest of her working life.

Then came the catechins. In 1929 Tsujimura isolated catechin from green tea — the first tea catechin obtained in pure form — and published the work in 1930 in the Bulletin of the Agricultural Chemical Society of Japan under the plain title "On Tea Catechin Isolated from Green Tea." In the same volume she reported crystallising a second fraction, "tea tannin," from the leaf. In 1934 she isolated a third compound, which she called "tea catechin II" or gallocatechin — a catechin carrying the extra hydroxyl group on its B-ring that distinguishes the "gallo" catechins, and therefore the first published step toward the structure of EGCG, which is gallocatechin's epimer joined to a gallic acid ester.

Her 1932 doctorate in agriculture from Tokyo Imperial University made her the first woman in Japan to hold that degree. She patented a method of extracting vitamin C crystals from plants in 1935, rose through RIKEN's ranks, and in 1949 became a professor at Ochanomizu University, where she was the first dean of its Faculty of Home Economics. It is often said that Tsujimura discovered EGCG. The papers themselves do not quite say that: what they document is catechin (1929), crystalline "tea tannin" (1930) and gallocatechin (1934). Some accounts attribute the isolation of epigallocatechin gallate to her group in the mid-1930s; we could not confirm that attribution against her published titles, and the modern review literature dates the first report of EGCG itself to 1948, described next. The honest summary is that Tsujimura opened the door: she proved that "tea tannin" was a family of crystallisable catechins, and she named the gallo-catechin branch of that family to which EGCG belongs.

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Naming EGCG: Bradfield and Penney (1947–1948)

The compound we now call EGCG was characterised in Britain in the years just after the Second World War. In 1947 A. E. Bradfield, Margaret Penney and W. B. Wright published "The catechins of green tea. Part I" in the Journal of the Chemical Society, and in 1948 Bradfield and Penney followed it with Part II. Reviews of tea chemistry credit the 1948 paper with the first report of (−)-epigallocatechin gallate as a distinct compound: the ester formed between epigallocatechin and gallic acid, and the most abundant single catechin in the green leaf. From this point the four major green-tea catechins — epicatechin (EC), epigallocatechin (EGC), epicatechin gallate (ECG) and epigallocatechin gallate (EGCG) — had names, and the old word "tannin" began its slow retirement.

The name is a description. "Gallo" marks the third hydroxyl group on the molecule's B-ring and "gallate" the gallic acid ester on its C-ring; the ester in particular is what makes EGCG a stronger radical scavenger and a more avid protein-binder than its ungallated relatives — and, as it turned out, what makes it so poorly absorbed. Two minor digallate catechins were added to the roster by Coxon and colleagues in 1972. By then the frontier of tea chemistry had moved from green tea to black.

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Chromatography and the Black-Tea Chapter: Roberts and the Theaflavins

Paper chromatography — separating a mixture by letting it creep up a strip of paper — transformed natural-product chemistry in the 1940s and 1950s, and tea was an early beneficiary. Between 1957 and 1959 the tea chemist E. A. H. Roberts and his co-workers published a numbered series, "The phenolic substances of manufactured tea," in the Journal of the Science of Food and Agriculture. Part I (1957, with Cartwright and Oldschool) fractionated the water-soluble substances of tea by paper chromatography; Part II (1958) showed that the characteristic orange-red pigments of black tea are not present in the fresh leaf but arise as enzymic oxidation products formed during "fermentation" — the misnamed step in black-tea manufacture in which the leaf's own polyphenol oxidase acts on its catechins; and Part VI (1959, with Myers) described the preparation of theaflavin and theaflavin gallate.

This is the black-tea chapter of EGCG's story. When the leaf is bruised and left to oxidise, EGCG and its relatives are condensed into theaflavins and the larger thearubigins: black tea is a tea in which most of the EGCG has been used up to make new molecules. Green tea, whose leaf is steamed or pan-fired within hours of picking to kill the enzyme, keeps its catechins largely intact. That is why, when medical interest in EGCG arrived a generation later, it arrived in Japan — the country that drank its tea green.

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The Chemoprevention Era: Fujiki, Yoshizawa and the 1987 Experiment

For thirty years after Bradfield and Penney, EGCG was a food-chemistry curiosity. What changed was the rise of cancer chemoprevention — the idea, taking shape in the 1970s and 1980s, that cancer might be delayed or prevented by ordinary dietary compounds acting on the long "promotion" phase between an initial mutation and a visible tumour. The standard laboratory model was the two-stage mouse-skin experiment: a single dose of a carcinogen (DMBA) to initiate, followed by repeated applications of a tumour promoter such as TPA, a phorbol ester, or the related compound teleocidin.

At the Saitama Cancer Center Research Institute, Hirota Fujiki's group began in 1983 to screen plant polyphenols — thirty of them, supplied by the natural-products chemist Takuo Okuda of Okayama University — for the ability to interfere with tumour promoters. Because green tea was the everyday drink of the laboratory's own country, its main catechin drew special attention. In 1987 Sachiko Yoshizawa, Fujiki and colleagues reported in Phytotherapy Research that topical EGCG inhibited tumour promotion by teleocidin in DMBA-initiated mouse skin: fewer mice developed tumours, and those that did developed fewer of them. The title still called EGCG "the main constituent of ‘tannin’ in green tea" — the last echo of the nineteenth century — but the content was new. It was the first published demonstration that EGCG could prevent, rather than merely fail to cause, an experimental cancer. Fujiki has recalled that the British magazine New Scientist picked the result up almost at once under the headline "Green tea cuts cancerous growths," and the public story of EGCG began there.

What followed was an avalanche: through the 1990s and 2000s laboratories on three continents reported that EGCG or green tea extract inhibited tumours in the skin, lung, oesophagus, stomach, colon, liver, prostate and breast of rodents, and proposed dozens of mechanisms. The most influential synthesis was the 2009 review by Chung S. Yang and colleagues in Nature Reviews Cancer, which set the animal and mechanistic evidence beside the human data and asked how much of it was relevant to people. Its answer set the tone for the next decade: the animal evidence was strong and consistent, the human evidence suggestive and inconsistent, and the gap between them had a chemical explanation.

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The Bioavailability Problem

The explanation was bioavailability — how much of a swallowed compound actually reaches the bloodstream and the tissues. In a Petri dish EGCG can be applied at whatever concentration an experimenter chooses; in a person it must survive the gut, cross its wall, escape the liver's first pass and avoid being immediately modified. The first careful human measurements were made at the Arizona Cancer Center by H.-H. Sherry Chow and colleagues. In a phase I study published in 2001, twenty healthy volunteers took single oral doses of 200 to 800 mg of EGCG, either as the pure compound or as a standardised, decaffeinated green-tea catechin mixture known in the trial literature as Polyphenon E; blood and urine were sampled for 24 hours. In 2002 Mei-Jie Lee, Yang and colleagues described what happens to the catechins after ingestion of green tea or pure EGCG — the appearance of methylated and ring-fission metabolites — and in 2003 Chow's group published the first multiple-dose study, giving 800 mg of EGCG a day, in one or two doses, for four weeks.

The picture that emerged, and that has held ever since, is sobering. Only a small fraction of oral EGCG appears in plasma, at concentrations well below those used in most cell-culture experiments; the compound is rapidly methylated, conjugated and broken down by gut bacteria; and much of the dose never leaves the intestine at all. Two practical findings shaped everything afterwards. First, taking EGCG on an empty stomach raises blood levels several-fold compared with taking it with food — which is why later supplement trials specified fasting dosing, and, as the safety chapter shows, why that same practice turned out to matter for the liver. Second, four weeks of 800 mg a day was tolerated in healthy volunteers, a figure that would be quoted and re-examined for the next fifteen years. Yang's group summarised the whole field in a 2011 review of the chemistry and biotransformation of tea constituents.

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Into the Clinic: Prostate Trials, Safety Studies and a Botanical Drug

With safety and pharmacokinetics established, the 2000s brought EGCG's first real clinical tests. The most striking was published in Cancer Research in 2006 by Saverio Bettuzzi and colleagues at the University of Parma. Sixty men with high-grade prostatic intraepithelial neoplasia — a precancerous change that, at the time, was thought to progress to prostate cancer in about 30% of men within a year — were randomised to 600 mg a day of green tea catechins (about half of it EGCG) or placebo for one year. One cancer was diagnosed among the thirty treated men, nine among the thirty on placebo. No serious side effects were recorded. It was small, it was a single centre, and it was described by its authors as a proof-of-principle study, but a 3% against 30% result in a randomised trial was enough to make green tea catechins a serious chemoprevention candidate.

The same years produced the formal toxicology that any serious candidate needs. In 2006 Richard Isbrucker and colleagues published a three-part series of safety studies on EGCG preparations in Food and Chemical Toxicology, covering genotoxicity, acute and short-term toxicity, and reproductive toxicity in animals. In 2008 a review by the United States Pharmacopeia's dietary-supplement safety committee analysed 216 case reports on green tea products, 34 of them concerning liver damage, and concluded that such products could be the subject of a quality monograph provided their labels carried a caution statement.

Then came something no other tea catechin can claim. On 31 October 2006 the U.S. Food and Drug Administration approved a 15% ointment of sinecatechins — a defined water extract of green tea leaf, more than half of it EGCG — for the treatment of external genital and perianal warts. It was the first prescription drug approved under the FDA's botanical-drug pathway, meaning the first time the agency had licensed a complex plant extract, rather than a single purified molecule, as a medicine. The pivotal evidence was published in 2008 by Silvio Tatti and colleagues in Obstetrics & Gynecology: in a randomised, double-blind trial of 502 patients, complete clearance of warts was achieved in 57% of those using the 15% or 10% ointment against 34% with vehicle. (The site names the regulator and the generic drug, and not the product's brand, by policy.) Whatever else is said about EGCG, a catechin-based extract has been a licensed medicine since 2006.

The prostate story, meanwhile, ended more quietly than it began. A larger, multicentre American trial led by Nagi Kumar at the Moffitt Cancer Center, published in 2015, randomised 97 men with high-grade PIN or atypical small acinar proliferation to a decaffeinated catechin mixture supplying 400 mg of EGCG a day or placebo for one year. On the primary endpoint there was no difference in prostate cancers diagnosed — five of 49 against nine of 48 — though a secondary composite endpoint and serum PSA both favoured treatment, and the catechins were well tolerated. It was the classic pattern of a dramatic small trial followed by a sober larger one, and it left green tea catechins where they remain in oncology: interesting, plausible, and unproven.

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The Liver Signal: Case Reports and the EFSA Opinion (2008–2018)

The most important development in EGCG's recent history was not a benefit but a harm. Through the 2000s, as concentrated green-tea extracts became a staple of weight-loss supplements, physicians began reporting cases of acute hepatitis in people taking them. In 2009 Gabriela Mazzanti and colleagues in Rome reviewed the literature and found 34 published cases of green-tea-associated liver injury between 1999 and October 2008, plus two new cases from the Italian surveillance system for natural health products; there had been one death, and in seven cases the injury returned when the product was taken again — the "positive rechallenge" that is the strongest evidence of causation in a case report. Their 2015 update added nineteen further cases, most of them in women, most of them hepatocellular, and noted that the most serious outcomes, including four transplants, involved multi-ingredient products in which green tea was only one of several suspects.

The injuries were rare against the scale of use and did not follow a clean dose-response curve, which is the pattern of an idiosyncratic reaction — one that depends on the individual as much as on the dose. But the reports clustered around concentrated extracts taken as a bolus, often while fasting and often for slimming, exactly the conditions the pharmacokinetic studies had shown to maximise EGCG in the blood. Regulators took notice. Triggered by concerns from Nordic countries after reported cases of liver damage, the European Food Safety Authority's expert panel published its Scientific Opinion on the safety of green tea catechins in April 2018. Its conclusions have framed the subject ever since. Catechins from traditional green tea infusions, and from instant and ready-to-drink teas of similar strength, were judged generally safe: the average adult drinker takes in 90 to 300 mg of EGCG a day from tea, and heavy drinkers up to about 866 mg, without any sign of liver damage beyond rare, unpredictable reactions. For food supplements, however, doses of EGCG at or above 800 mg a day were associated with a statistically significant rise in liver enzymes (serum transaminases) in supervised human studies, and the panel was unable to identify a dose below that at which it could declare supplements safe.

A systematic review published the same year, covering 159 human intervention studies, reached a compatible conclusion: liver adverse events occurred in a dose-dependent way with concentrated catechin preparations taken as a bolus but not with brewed tea, and it proposed an intake of 338 mg of EGCG a day as safe for solid supplements and up to 704 mg a day for tea-type beverages. The distinction between the beverage and the pill, first drawn by a pharmacokinetic curve in 2001, had become the organising principle of EGCG safety. Green tea as a drink remained, on the evidence, one of the safest habits in nutrition; green tea extract as a concentrated supplement acquired a genuine and now well-documented caution.

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The 2020s: Where the Evidence Stands

Four decades after the mouse-skin experiment, the honest state of the evidence can be stated briefly. A 2020 Cochrane systematic review of green tea for the prevention of cancer, drawing on randomised trials and observational studies, found the results inconsistent: some signals of benefit at particular cancer sites in trials and case-control studies, but with small study numbers, methodological limitations, disagreement with cohort studies, and most of the data coming from Asian populations who already drink a great deal of green tea. It also recorded "several side effects associated with high intakes," and concluded that well-conducted, adequately powered trials would be needed before any preventive claim could be made.

The same pattern — a strong mechanism, a large laboratory literature, and modest or mixed human results — runs through the other fields in which EGCG has been studied: weight and metabolism, cholesterol and blood pressure, the brain. The reasons are the ones this history has traced: poor absorption, short small trials, and effective intakes that approach the intakes at which the liver signal begins. The one indication with a regulator's approval behind it, topical sinecatechins for genital warts, is a case where absorption did not matter because the drug was applied to the skin.

The detailed clinical evidence, dose by dose and outcome by outcome, is taken up in the companion EGCG Benefits articles, and the liver question specifically in EGCG Safety and Liver Health.

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EGCG Today

EGCG's history is unusual among the compounds on this site because it is so nearly entirely modern. Tea is ancient; the catechins are a discovery of living memory, and the people who made it can be named: Tsujimura in 1929, Bradfield and Penney in 1948, Roberts in the late 1950s, Fujiki and Yoshizawa in 1987, Chow and Yang on absorption, Bettuzzi and Kumar in the clinic, a regulator's approval in 2006, and Mazzanti and the EFSA panel on the one real harm that concentrated extracts can do.

That is a complete arc, and it points to a plain conclusion. The cup of green tea that Eisai praised in 1211 and that Tsujimura analysed in the 1920s delivers EGCG in the amount, the company and the pattern — a few hundred milligrams a day, with food, spread across the day — that eighty years of chemistry and twenty years of safety data agree is beneficial or at worst harmless. The concentrated capsule is a different product with a different history: more EGCG, faster, on an empty stomach, and a documented risk to the liver at the top of its dose range. The molecule is the same; the lesson of its history is that the form matters. Anyone weighing a green tea extract should read the EGCG hub and the liver-injury page first, and anyone who simply likes green tea can go on drinking it with the whole weight of the evidence on their side.

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Key Research Papers

The list below runs in historical order, from Tsujimura's first isolation papers through the 1948 characterisation of EGCG, the 1987 chemoprevention report, the pharmacokinetic and clinical studies of the 2000s, the hepatotoxicity reviews and the 2018 EFSA opinion, to the 2020 Cochrane review. Historical texts named in the article (the Cha Jing, Kissa Yōjōki) are sources of history, not modern citations. Every identifier was checked against Crossref or PubMed before it was written here.

  1. Tsujimura M (1930). On Tea Catechin Isolated from Green Tea. Bulletin of the Agricultural Chemical Society of Japan. — doi:10.1080/03758397.1930.10856939
  2. Tsujimura M (1934). Isolation of a New Catechin, Tea Catechin II or Gallo-Catechin from Green Tea. Bulletin of the Agricultural Chemical Society of Japan. — doi:10.1080/03758397.1934.10857092
  3. Bradfield AE, Penney M (1948). The catechins of green tea. Part II. Journal of the Chemical Society (Resumed). — doi:10.1039/JR9480002249
  4. Yoshizawa S, Horiuchi T, Fujiki H, Yoshida T, et al. (1987). Antitumor promoting activity of (−)-epigallocatechin gallate, the main constituent of "Tannin" in green tea. Phytotherapy Research. — doi:10.1002/ptr.2650010110
  5. Chow HH, Cai Y, Hakim IA, Crowell JA, Shahi F, et al. (2003). Pharmacokinetics and safety of green tea polyphenols after multiple-dose administration of epigallocatechin gallate and polyphenon E in healthy individuals. Clinical Cancer Research. — PubMed PMID: 12960117
  6. Bettuzzi S, Brausi M, Rizzi F, Castagnetti G, Peracchia G, Corti A (2006). Chemoprevention of human prostate cancer by oral administration of green tea catechins in volunteers with high-grade prostate intraepithelial neoplasia: a preliminary report from a one-year proof-of-principle study. Cancer Research. — doi:10.1158/0008-5472.CAN-05-1145
  7. Tatti S, Swinehart JM, Thielert C, Tawfik H, Mescheder A, Beutner KR (2008). Sinecatechins, a defined green tea extract, in the treatment of external anogenital warts: a randomized controlled trial. Obstetrics and Gynecology. — PubMed PMID: 18515521
  8. Mazzanti G, Menniti-Ippolito F, Moro PA, Cassetti F, Raschetti R, Santuccio C, et al. (2009). Hepatotoxicity from green tea: a review of the literature and two unpublished cases. European Journal of Clinical Pharmacology. — doi:10.1007/s00228-008-0610-7
  9. Yang CS, Wang X, Lu G, Picinich SC (2009). Cancer prevention by tea: animal studies, molecular mechanisms and human relevance. Nature Reviews Cancer. — doi:10.1038/nrc2641
  10. Kumar NB, Pow-Sang J, Egan KM, Spiess PE, Dickinson S, et al. (2015). Randomized, Placebo-Controlled Trial of Green Tea Catechins for Prostate Cancer Prevention. Cancer Prevention Research. — doi:10.1158/1940-6207.CAPR-14-0324
  11. Mazzanti G, Di Sotto A, Vitalone A (2015). Hepatotoxicity of green tea: an update. Archives of Toxicology. — doi:10.1007/s00204-015-1521-x
  12. EFSA Panel on Food Additives and Nutrient Sources added to Food (ANS): Younes M, Aggett P, Aguilar F, Crebelli R, Dusemund B, et al. (2018). Scientific opinion on the safety of green tea catechins. EFSA Journal. — doi:10.2903/j.efsa.2018.5239
  13. Hu J, Webster D, Cao J, Shao A (2018). The safety of green tea and green tea extract consumption in adults – Results of a systematic review. Regulatory Toxicology and Pharmacology. — doi:10.1016/j.yrtph.2018.03.019
  14. Filippini T, Malavolti M, Borrelli F, Izzo AA, Fairweather-Tait SJ, et al. (2020). Green tea (Camellia sinensis) for the prevention of cancer. Cochrane Database of Systematic Reviews. — doi:10.1002/14651858.CD005004.pub3

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