Ingredients1,2-Di-galloyl-4,6-hexahydroxydiphenoyl-Ī²-D-glucose ā abbreviated throughout the scientific literature as GHG ā is a monomeric hydrolyzable tannin of the ellagitannin subclass. Its full systematic name is 1,2-di-O-galloyl-4,6-O-(S)-hexahydroxydiphenoyl-Ī²-D-glucopyranose, reflecting the precise stereo- and regiochemistry of the molecule. The compound is sometimes written as 1,2-di-O-galloyl-(4,6-(S)-hexahydroxydiphenoyl)-Ī²-D-glucopyranose in the analytical literature.
Ellagitannins as a class are a diverse group of hydrolyzable tannins, a type of polyphenol formed primarily from the oxidative linkage of galloyl groups in 1,2,3,4,6-pentagalloyl glucose. They are hexahydroxydiphenoic (HHDP) acid esters having a complex chemical structure with a D-glucose carbohydrate moiety. GHG exemplifies this structural type: its glucose core carries two free galloyl ester groups at the 1- and 2-positions, while the 4- and 6-positions are bridged by a single (S)-hexahydroxydiphenoyl (HHDP) unit forming a characteristic macrocyclic biaryl linkage. Within the systematic classification of ellagitannins, 1,2-di-O-galloyl-4,6-HHDP-Ī²-glucose is designated compound 14, belonging to the nine digalloyl-HHDP-glucoside constitutional isomers.
Ellagitannins are characterized by the presence of biarylic dehydrodigalloyl units, i.e., hexahydroxydiphenoyl (HHDP) groups, which are frequently linked to glucose. The biosynthetic origin of GHG, like all ellagitannins, begins with pentagalloylglucose: gallic acid, mediated by uridine diphosphate glucose (UDP-glucose) galloyltransferase, is directly esterified with UDP-glucose to form Ī²-glucogallin. The successive transgalloylation of Ī²-glucogallin leads ultimately to Ī²-1,2,3,4,6-pentagalloyl-D-glucose (Ī²-PGG), which is the basic structure from which ellagitannins are derived. Oxidative coupling of adjacent galloyl groups on the glucose core then generates the HHDP unit that defines the ellagitannin scaffold.
The compound bears the CAS registry designation for its glucopyranose form and carries a molecular weight consistent with two galloyl residues plus one HHDP unit esterified to glucose. Its hydrophobicity characteristics have been catalogued alongside other monomeric hydrolyzable tannins, classified among the ā“C1 glucose core ellagitannins.
Purple tea is a variety of Camellia sinensis developed by the Tea Research Foundation of Kenya (TRFK) and is currently cultivated in Kenya. In addition to the usual polyphenolic compounds found in green tea, such as epigallocatechin gallate (EGCG) and epicatechin gallate (ECG), purple tea is unique in that it also contains anthocyanidins (malvidin, pelargonidin and cyanidin 3-O-galactoside) and 1,2-di-O-galloyl-4,6-O-(S)-hexahydroxydiphenoyl-Ī²-D-glucose (GHG), a hydrolysable tannin. Purple tea is the only cultivar that contains the hydrolysable tannin 1,2-di-O-galloyl-4,6-O-(S)-hexahydroxydiphenoyl-Ī²-D-glucose (GHG).
The Kenyan purple tea cultivar (TRFK306) was developed from standard Camellia sinensis var. assamica by the Kenyan Tea Research Institute over the past 25 years by a process of extensive breeding and selection. Purple tea was developed through selective breeding of wild purple-leafed tea bushes found in the Assam region of India. The Tea Research Foundation of Kenya spent 25 years perfecting this variety to create a tea that is rich in antioxidants and low in caffeine.
Kenyan purple tea, scientifically known as Camellia sinensis var. assamica, traces its roots to Kenya's expansive tea estates, predominantly located in regions such as Nandi Hills, Kericho, and Thika. The tea plants thrive at elevations ranging from 4,000 to 7,000 feet, where the combination of altitude, soil composition, and climatic conditions imparts unique characteristics to the tea leaves.
GHG content varies among tea accessions. UPLC-qTOF-MS/MS analysis has identified GHG (1,2-di-O-galloyl-(4,6-(S)-hexahydroxydiphenoyl)-Ī²-D-glucopyranose) among specialized metabolites of ancient tea plants from Yunnan, China. Significant differences existed between the metabolic profiles of ancient tea plants, among which GHG was highly accumulated in some of them, with peak contents of 228.28 mg/g ā 2.61Ć higher than previously reported.
GHG is not confined solely to purple tea. The polyphenolic composition of Camellia irrawadiensis, which is a closely related species of Camellia sinensis (cultivated tea), was investigated. The most predominant polyphenol, a kind of ellagitannin, was isolated from leaves of C. irrawadiensis. Its structure was established as 1,2-di-O-galloyl-4,6-O-(S)-hexahydroxydiphenoyl-beta-D-glucose (GHG) on the basis of spectral and chemical evidence. 1,2-Di-O-galloyl-4,6-O-(S)-hexahydroxydiphenoyl-beta-D-glucopyranose (GHG) has also been isolated as a major compound from Camellia taliensis.
GHG as an isolated, characterized compound is a product of modern phytochemical research and does not have a documented history of traditional use under its chemical name. Its historical context is properly situated within the broader tradition of tea use.
The leaves of Camellia sinensis (the tea plant) have been utilized over countless years as a popular beverage with potential health benefits. Tea (Camellia sinensis) has been consumed for centuries as traditional medicine for various diseases, including diabetes.
Purple tea itself, as a named cultivar, is a recent development. Purple tea, a cultivar developed in Kenya during the 1980s, is used in various traditional ways around its regions of origin. In the late 20th century, Kenyan tea researchers began exploring the potential opportunities for this purple-colored tea leaf.
GHG has also been identified in Camellia irrawadiensis, a species found in Myanmar, and in ancient tea trees in Yunnan Province, China ā regions with multi-century traditions of tea consumption in which GHG-containing material would have been present as an uncharacterized constituent of the broader polyphenolic profile. Tea, derived from Camellia sinensis, is a globally cherished beverage due to its rich secondary metabolites. These compounds both affect taste quality and have medicinal applications, including chemoprevention of cancers, chronic inflammation, heart and liver diseases, and diabetes. However, it must be noted that no traditional medical system specifically identified or utilized GHG by name or as a purified fraction; its isolation and pharmacological characterization are entirely products of late-20th and 21st-century analytical science.
Purple tea (Camellia sinensis var. assamica) leaves can be prepared using several methods, with the most common being the standard hot brewing technique using water at 85ā90Ā°C for 2ā3 minutes with 2ā3 g leaves per 240 ml water. Purple tea is usually prepared in a similar way to green tea, with minimal oxidation performed to protect the anthocyanins, but sometimes it may be partially oxidized.
GHG is the dominant and diagnostically distinctive polyphenol of purple tea, but it occurs alongside a rich ensemble of other bioactive molecules. In addition to the usual polyphenolic compounds found in green tea, such as epigallocatechin gallate (EGCG) and epicatechin gallate (ECG), purple tea contains anthocyanidins (malvidin, pelargonidin, and cyanidin 3-O-galactoside) alongside GHG. The phytochemical profile of purple tea varies according to growing conditions, processing methods, and tea leaf age. Purple tea is known for having higher total polyphenol content and antioxidant activity than green or black tea.
Targeted UPLC-MS/MS analysis has been employed to quantify the ellagitannins corilagin, strictinin, and tellimagrandin I in commercial teas. These co-occurring ellagitannins complement GHG in the overall bioactive profile. Corilagin, strictinin, and tellimagrandin I (ellagitannins) have been identified as potent inhibitors of Ī±-amylase and Ī±-glucosidase, with Ki values significantly lower (p < 0.05) than acarbose.
GHG as an ellagitannin is a hydrolyzable tannin. As hydrolyzable tannins, ellagitannins undergo hydrolysis producing HHDP, which is then spontaneously converted into ellagic acid. The ellagitannin class including 1,2-digalloyl-4,6-hexahydroxydiphenoyl-Ī²-D-glucopyranose, pedunculagin, and geraniin can generate a common compound of ellagic acid via hydrolysis, deprotonation, and oxidative transformation under basic pH conditions.
The most extensively studied mechanism of GHG is inhibition of pancreatic lipase, the principal enzyme mediating dietary fat digestion and absorption in the small intestine. Preliminary studies reveal that GHG can effectively modulate key metabolic pathways by inhibiting pancreatic lipase activity. Purple tea is known for its potential to prevent obesity, specifically through GHG's potent inhibitory effects on pancreatic lipase, which is vital in fat digestion and absorption. Purple tea GHG was found to be a better inhibitor of lipase than EGCG, which is a famous green tea catechin. In preclinical work, a standardized purple tea extract (Porelisā¢, 3ā5% GHG) markedly inhibited in vitro pancreatic lipase activity with an ICā ā of 223.3 Āµg/ml.
GHG suppresses the maturation of fat cells at the transcriptional level. Research has shown that GHG from purple tea inhibits adipogenesis ā the production of new fat cells. GHG can downregulate PPARĪ³ and C/EBPĪ±, thereby inhibiting preadipocyte maturation into mature adipocytes, hence controlling excessive body fat production.
A 12-week high-fat-diet mouse study showed that Porelis treatment (the GHG-standardized extract) markedly reduced body weight, fat pad weights, hepatic lipid accumulation, and oxidative stress. The adipogenic markers C/EBPĪ±, PPARĪ³, and SREBP1 were significantly down-regulated in Porelis-treated mice compared to the high-fat-diet model group (P < 0.0001).
In the same murine study, Porelis treatment reduced serum leptin levels (P < 0.0001) while increasing adiponectin (P < 0.01) in high-fat-diet mice. Circulating trimethylamine N-oxide (TMAO) and insulin levels were also significantly reduced in the Porelis groups compared to the high-fat-diet-alone group.
In LPS-stimulated RAW 264.7 macrophages, the GHG-containing Porelis extract significantly inhibited the generation of NO, IL-6, and TNF-Ī± (p < 0.0001). Adipocyte differentiation, fat accumulation, and protein expression of PPARĪ³ and C/EBPĪ± were also significantly inhibited in a dose-dependent manner (p < 0.0001).
Both purple tea extract (PTE, 10 Āµg/mL) and isolated GHG (10 Āµg/mL) enhanced protein expression of CPT1A (carnitine palmitoyltransferase 1A) in HepG2 hepatoma cells. CPT1A is the rate-limiting enzyme in mitochondrial fatty acid Ī²-oxidation. Its upregulation represents a plausible mechanism for increased fat burning at the hepatic level.
The bioactive compound GHG is unique to purple tea and has been found to have potent Ī±-amylase inhibitory activity, suggesting potential anti-diabetic effects. Commercial purple teas with ellagitannins were proposed to be more potent inhibitors against Ī±-glucosidases than green teas and acarbose. Together, Ī±-glucosidase and Ī±-amylase inhibition delay the post-prandial breakdown of dietary carbohydrates, blunting the glucose spike after meals.
Research has indicated improvements in insulin sensitivity and reduction of inflammatory markers associated with obesity from the synergistic effects of anthocyanins, catechins, and other polyphenols found alongside GHG in purple tea. Specifically, the GHG-containing extract significantly inhibited the generation of NO, IL-6, and TNF-Ī± in LPS-stimulated macrophages (p < 0.0001).
GHG is reported to increase lipolysis ā the breaking down of stored fats. Additional metabolic benefits reported in the literature include increased energy expenditure, improved insulin sensitivity, and enhanced glucose metabolism regulation.
Like all ellagitannins, GHG is not absorbed intact from the gastrointestinal tract. Ellagitannins are hydrolyzed in the acidic environment of gastric acids, resulting in the formation of HHDP acid, which then spontaneously lactonizes to ellagic acid. No presence of ellagitannins in blood and urine has been observed, indicating that they are metabolized by the digestive system. The resulting ellagic acid is subsequently acted upon by colonic microbiota to produce urolithins. The consequence of ellagitannin hydrolysis in the gastrointestinal tract is a prolonged release of ellagic acid and its gradual degradation to urolithins, followed by absorption into the bloodstream. The most common metabolite detected in human urine following the ingestion of raw materials containing ellagitannins is 3,8-dihydroxy-6H-dibenzo[b,d]pyran-6-one, known as urolithin B. This is mainly present in the glucuronic acid-conjugated form and, in smaller amounts, as the corresponding aglycone.
Urolithin A and urolithin B derived from ellagitannin metabolism have been found to increase cellular glucose uptake and decrease cellular lipid accumulation in in vitro models. This suggests that at least part of GHG's biological activity may be mediated through its gut-derived metabolites rather than the parent molecule.
This is the most extensively investigated application of GHG and the area with the strongest convergence of preclinical and human data, though the overall evidence base remains limited in scale and requires replication.
Human evidence: A study reported that 4-week daily consumption of a purple tea drink in humans improved obesity parameters compared to baseline, including body weight (79.9 Ā± 3.1 kg vs. 80.8 Ā± 3.2 kg, p < 0.05), body mass index (BMI) (26.8 Ā± 0.6 vs. 27.0 Ā± 0.6, p < 0.05), and body fat mass (21.0 Ā± 1.4 kg vs. 21.8 Ā± 1.5 kg, p < 0.01). This study by Shimoda and colleagues described human ingestion of purple tea (two times per day from a 1.5-gram portion of tea leaves brewed in 100ā200 mL of water) for four weeks.
Clinical investigations demonstrated significant reductions in BMI, waist circumference, and body weight among individuals consuming purple tea extracts with high GHG levels. However, a 2024 systematic review noted that more comprehensive research is needed to fully elucidate the optimal dosage and long-term effects.
Preclinical (animal) evidence: In olive oil-loaded mice, purple tea extract (100 mg/kg) and caffeine (25 mg/kg) suppressed fat absorption. In a 12-week murine study, male C57BL/6 mice fed a high-fat diet (60% kcal from fat) received Porelis (a standardized purple tea extract with 3ā5% GHG) at doses of 25, 50, and 100 mg/kg body weight per oral. Porelis treatment markedly reduced body weight, fat pad weights, hepatic lipid accumulation, and oxidative stress in the high-fat-diet mice.
Evidence strength: Preliminary to modest. The human study by Shimoda et al. was small and not published with full randomization details typical of high-quality RCTs. The 2024 PMC review noted that 59 studies were ultimately included across the literature, but explicitly concluded that comprehensive RCT evidence for GHG specifically remains lacking.
The main hypothesis tested in dedicated studies is that purple teas and ellagitannins will have antidiabetic activity through the inhibition of Ī±-amylase and Ī±-glucosidase. Commercial purple teas containing ellagitannins were identified as potent Ī±-glucosidase inhibitors with ICā ā values significantly lower (p < 0.05) than green teas in in vitro enzyme assays. Ī±-Glucosidase was inhibited by anthocyanin-rich fractions from purple tea, thus delaying carbohydrate absorption within the small intestine and thereby improving glycemic control in experimental settings.
Additional metabolic benefits reported in the literature include improved insulin sensitivity and enhanced glucose metabolism regulation. In the high-fat-diet mouse model, Porelis treatment also significantly reduced circulating insulin levels (P < 0.001).
Evidence strength: Primarily in vitro and animal data. Direct human clinical evidence for GHG's antidiabetic activity is not yet established in dedicated trials; the evidence extrapolated from enzyme inhibition assays and animal studies is preliminary.
Purple tea exhibits a unique composition of chemical constituents that may exert favorable outcomes related to recovery from muscle damage, improvements in blood flow, perfusion, and recovery. A randomized, placebo-controlled, double-blind, crossover study enrolled 30 healthy men (33.5 Ā± 11.4 years, 178.4 Ā± 7.6 cm, 92.5 Ā± 13.3 kg) who completed an 8-day supplementation regimen consisting of either a maltodextrin placebo or 100 mg of purple tea extract (PurpleForceā¢, Oryza Oil & Fat, Ltd.), interspersed with a 2-week washout period. After five and eight days of supplementation, changes in muscle oxygenation, body composition, reactive hyperemia, visual analog responses, exercise performance, and muscle damage markers were assessed.
Limited human research, however, has been completed examining the ability of purple tea to impact health, performance, and recovery. Given the lack of research on purple tea and exercise, conclusions may be drawn from other tea types based on purple tea's distinctive composition. Antioxidants and anti-inflammatory components of purple teas may assist in recovery from training.
Evidence strength: Sparse. A single small RCT has investigated exercise-related outcomes, and results from this specific study have not been fully reported in accessible peer-reviewed detail at the time of writing. The evidence base for exercise applications is weak and largely inferential.
In a prophylactic in vitro model, purple shoot green tea inhibited inflammatory responses by attenuating expressions of IL-6 and TNF-Ī± in a dose-dependent manner. The prophylactic model demonstrated that the green tea extract from purple shoot tea exerts robust effects on modulating LPS-induced cytokine expressions of MCP-1, IL-6, and TNF-Ī± through scavenging free radicals and nitric oxide.
Ellagitannins are known to possess many beneficial and health-promoting properties, including antioxidant and antimicrobial effects, arising from the activity of both native compounds and the products of their degradation or metabolism. Purple tea possesses tremendous antioxidant and anti-inflammatory potential. It is well-established that chronic inflammation and oxidative stress contribute much to the onset and progression of diabetes.
Evidence strength: The antioxidant and anti-inflammatory data for GHG are primarily in vitro (cell culture) and animal model data. Clinical data establishing these effects in humans at specific GHG doses are not yet available.
GHG is not commercially available as a purified isolated compound for human use. It is encountered in the following forms, with dosages as reported in the cited studies:
No established human clinical dose has been validated in large controlled trials. While more comprehensive research is needed to fully elucidate the optimal dosage and long-term effects, current evidence suggests that GHG from purple tea could be a valuable natural intervention. No regulatory authority has formally established a recommended daily intake or an upper tolerable limit for GHG.
GHG, as a monomeric ellagitannin, is not absorbed intact. Ellagitannins are hydrolyzed in the acidic environment of gastric acids and no presence of ellagitannins in blood and urine has been observed, indicating that they are metabolized by the digestive system. The main circulating and urinary metabolites are therefore ellagic acid and urolithins. Urolithins are metabolites produced in the gut following consumption of ellagitannins and ellagic acid rich foods such as pomegranates, nuts, and certain berries. Urolithin A (UA) is one of the predominant isoforms of urolithins in humans and has demonstrated compelling biological activities. Investigation into genotoxicity, toxicokinetics, and repeated dose safety of Urolithin A in rats found that a battery of genotoxicity assays demonstrated that UA is not genotoxic.
Ellagitannins form complexes with proteins and polysaccharides, and this forms part of the defense system used by plants for protection against animal and bacterial attacks. This protein-binding property is relevant to considerations about potential interactions with dietary protein absorption and with pharmaceutical proteins or enzymes when GHG-containing preparations are consumed in high amounts. However, the low doses present in typical tea consumption are not established to be clinically problematic in healthy individuals.
Individual variability in gut microbiome composition affects the conversion of ellagic acid to bioactive urolithins. A study conducted on a group of volunteers supplemented with pomegranate juice over five consecutive days found that in some subjects low urolithin concentrations were observed as early as the first day, with maximum concentrations reached between days 3 and 4, followed by a slight decline. This means the downstream bioavailability and biological activity of GHG-derived metabolites are expected to differ substantially between individuals depending on their specific gut microbial ecology.
Monomeric ellagitannins including digalloyl-4,6-HHDP-glucose exhibited relatively high stability at pH 8 at ambient temperature, with a degradation rate constant of less than 0.1 in those conditions. However, under strongly alkaline conditions, GHG and related ellagitannins are progressively hydrolyzed to ellagic acid. This has implications for formulation: aqueous extracts stored at neutral to mildly alkaline pH should be expected to retain GHG longer than those at strongly basic conditions.
GHG-containing purple tea preparations also contain caffeine, although at lower levels than black tea. Even though purple tea has lower caffeine content compared to black tea, it still has some caffeine like other teas. Individuals sensitive to xanthines should account for this when consuming whole-plant preparations.
Well-controlled research using purple tea is limited. No long-term (beyond 12 weeks in animals; beyond 4 weeks in humans) safety or toxicity data for GHG or GHG-standardized extracts in humans have been published in the peer-reviewed literature to date. The absence of data should not be interpreted as established safety at high or long-term doses.
The 2024 PMC systematic review, the most comprehensive assessment published on GHG to date, identified 246 articles in its initial database search, with 173 articles retained after removing duplicates and studies published before 1999. Finally, 59 studies were included in the systematic review ā reflecting a still-small total evidence base. The review's conclusion that more comprehensive research is needed to fully elucidate the optimal dosage and long-term effects accurately characterizes the current state of knowledge.
The key limitations of the existing GHG literature are:
Health conditions that 1,2-di-galloyl-4,6hexahydroxydiphenoyl-D-glucose may help support.
Body systems that 1,2-di-galloyl-4,6hexahydroxydiphenoyl-D-glucose may help support.
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