Studies were included if they met the following criteria: 1) English-language publications; 2) Human studies 3) Conducted in the last 20 years 4) Focused on black tea (as a beverage or extract) and 5) Identified publications were meta-analyses, systematic reviews, umbrella reviews, reviews or randomised controlled trials (RCTs).

Studies were excluded if they: 1) Were not full text, 2) Not undertaken during the specified timeline, 3) Used multi-interventions, 4) Related to another tea form and 5) Were irrelevant per se.

Inflammation is a broad term that can encompass local, systemic, acute (short-term; typically 8 - 10 days) and chronic (long-term) inflammation [37]. Systemic inflammation can be low-grade i.e. subtle, ongoing immune activity or high-grade which can contribute to tissue degeneration and age-related diseases [38]. Systemic inflammation, as mentioned, often referred to as “metabolic inflammation” is characterised by elevated levels of acute-phase proteins such as C-reactive protein (CRP) and interleukin-6 (IL-6) and Tumour Necrosis Factor (TNF-α) [39]. This therefore formed the basis of the search terms.

PubMed, Science Direct and Semantic Scholar were searched. Specified search terms included: (“black tea” [Title/Abstract] OR “Camellia sinensis” [Title/Abstract] OR “tea flavonoids” [Title/Abstract] OR “tea flavan-3-ols” [Title/Abstract] OR “tea catechins” [Title/Abstract]) AND (“C-reactive protein” [Title/Abstract] OR “CRP” [Title/Abstract] OR “interleukin-6” [Title/Abstract] OR “IL-6” [Title/Abstract] OR “tumour necrosis factor alpha” [Title/Abstract] OR “TNF-alpha” [Title/Abstract] OR “TNF-α” [Title/Abstract] OR “TNF” [Title/Abstract] OR “inflammatory diseases” [Title/Abstract] OR “inflammation” [Title/Abstract] OR “chronic inflammation” [Title/Abstract] OR “immune response” [Title/Abstract] OR “autoimmune diseases” [Title/Abstract]).

The search was restricted to English-language, human studies published in the last 20 years (1^st September 2005 up until 19^th September 2025). The filter was restricted to review (R), systematic review (SR) and meta-analysis (MA) publications and randomised controlled trials (RCTs). Reference lists were also searched to identify any additional relevant articles. This review was conducted according to the guideline of the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) statement as shown in Figure 1 [40].

Figure 1. Algorithm flow diagram for included publications. Source: Flow of studies through different phases of the narrative review [40].

Authors assessed the titles and abstracts of all the identified studies and independently reviewed these to determine which should be included in the publication.

The PICO (Population, Intervention, Comparison, Outcome) approach was used and the following information extracted from each trial: author, year, country, design, study population, intervention and comparison, outcomes, main findings and strengths/limitations and potential sources of bias. A strengths and limitation column was added to the RCT data extraction table as a measure of determining study quality.

Eleven review/systematic review, umbrella review or meta-analysis publications were identified (Table 2). Four were undertaken in China [41]-[44], two in Italy [45][46], two in the USA [47][48] and one in Morocco [49], India [50] and Canada [51] respectively.

Table 2. Key Studies – Reviews & Meta-analysis publications.

Key: CRC, Colorectal Cancer; CRP, C-reactive protein; CVD, Cardiovascular Disease; ECGC; Epigallocatechin-3-gallate; IBD, Inflammatory Bowel Disease; IL-6, Interleukin-6; MA, meta-analysis; MetS, metabolic syndrome; NFκB, Nuclear Factor kapper-light-chain-enhancer of activated B cells; RCTs, randomised controlled trials; SR, Systematic Review; TNF-α, Tumour necrosis factor-alpha.

Publications focused on a range of inflammatory conditions including inflammatory bowel diseases [42][46], cardiovascular disease (CVD) and metabolic syndrome [44][48], cancer [46][47][49], markers of inflammation and immunity [45][50], rheumatoid arthritis [41], depression [43] and Parkinson’s Disease [51].

Focusing on inflammatory bowel disease Hung et al. (2002) identified that tea and its bioactive constituents (polyphenols, tea pigments, and polysaccharides) exhibit anti-inflammatory and antioxidant properties that may be relevant to inflammatory bowel disease management, particularly through modulation of oxidative stress and inflammatory signalling pathways [42]. Another earlier review [46] similarly concluded that black tea components, including theaflavin-3,3'-digallate, may attenuate intestinal inflammation by reducing oxidative stress and inflammatory activity, although the evidence was largely derived from in vitro and laboratory models, highlighting the need for human studies assessing clinical inflammatory markers.

An umbrella review [48] collating 23 systematic reviews on cardiovascular disease (CVD) concluded that consumption of approximately two cups of unsweetened tea per day may provide sufficient flavonoids to reduce CVD risk and progression. Proposed mechanisms included favourable effects on inflammatory markers such as TNF-α and IL-6, although the review emphasised the need for further intervention studies to confirm these pathways [48]. A systematic review and meta-analysis collating studies on tea consumption and metabolic syndrome found that black tea consumption had protective effects on systolic blood pressure in those with a body mass index of 28 or higher [44]. Mechanisms were unclear but it remains unclear whether these effects were mediated through changes in systemic inflammatory markers such as CRP or cytokines [44].

Three publications focused on breast cancer, colon cancer or cancer prevention [46][47][49]. A recent systematic review by Lamchabbek et al., (2025) reported an inverse association between black tea consumption and breast cancer risk and noted that a higher dietary inflammatory index was associated with increased risk. However, as most included studies were case-control in design, causal relationships and direct effects on inflammatory markers could not be established. Further clinical and mechanistic studies looking at breast cancer, black tea consumption and anti-inflammatory markers would be worthwhile. An earlier review [46] suggested that theaflavin-3,3'-digallate may reduce colorectal cancer cell proliferation, potentially via anti-inflammatory and antioxidant mechanisms. Greater human data assessing markers such as NF-κB, TNF-α, or IL-6 is now needed. Another review by de Mejia et al. (2009) proposed that theaflavins and catechins may contribute to cancer prevention by mitigating chronic inflammation, a recognised driver of carcinogenesis [47].

Regarding markers of inflammation and immunity Peluso et al. (2013) evaluated data from 25 human trials finding that tea extracts which provide flavonoids reduced TNF-α and IL-6 levels in fixed and random effect models [45]. Another comprehensive review [50] explained that tea infusions provide black tea polyphenols, caffeine, EGCG, theaflavin, theophylline, theobromine, which have anti-inflammatory properties alongside certain micronutrients such as selenium, iron, copper, manganese and zinc (accrued from the soil medium) which could enhance innate immune response.

In relation to rheumatoid arthritis, a systematic review and meta-analysis of 47 RCTs (tea polyphenols were included in 2 RCTs) found that dietary polyphenols could improve disease activity, possibly mediating rheumatoid arthritis by reducing C-reactive protein and/or oxidative stress levels [41]. A further comprehensive review [43] concluded that compounds present in tea such as black tea polyphenols, theaflavins, EGCG, teasaponin, L-theanine, and combinations of tea catechins and their metabolites appear to act as anti-inflammatory agents via down-regulation of NF-κB signalling which could collectively help to lower the risk of depression, as the neurobiology of depression has been linked to inflammation. Similarly, in relation to Parkinson’s disease another review concluded that EGCG found in tea appears to inhibit neuroinflammation, oxidative stress, neuronal cell death and have neuroprotective effects [51].

Overall, black tea appears to have a potentially beneficial role in a range of conditions with inflammatory origins. The range of bioactive constituents present in black tea have been attributed to some of these potential anti-inflammation effects, alongside the suppression of oxidation stress [46][50][51]. However, much of the existing evidence is indirect or derived from non-habitual intake studies, demonstrating the need for well-designed human studies focusing on regular black tea consumption and clinically relevant inflammatory outcomes.

Eleven RCT publications were identified, with study durations ranging from 9 days to 6 months (Table 3). Three were undertaken in the USA [52]-[54], two in Iran [55][56], two in Japan [57][58], one in Kuwait [59], one in Mauritius [60], one in Israel [61] and one in the UK [62].

Across the studies, black tea was typically consumed in amounts ranging from 3 - 6 cups per day (approximately 600 - 900 ml), with intakes of 3 - 4 cups being most common [53][56]-[61]. Widlansky at al. (2025) allocated adults to either 2 cups (450 ml) black tea or 900 ml (3 - 4 cups) of black tea daily. Arent et al. (2022) and Neyestani et al. (2010) used black tea extract with participants in the latter study drinking this in beverage form [52][56].

Some research focused on typically healthy adult baseline populations. Tomioka et al. (2023) [57] in a single-blind, randomized, placebo-controlled trial allocated 72 adults to drink 3 cups of black tea/day (76.2 mg of black tea polymerized polyphenols) for 12 weeks and observed that an increase in butyrate-producing bacteria in the gut (Prevotella) may partly contribute to the suppressive effect of black tea consumption on acute upper respiratory tract inflammation. Earlier research [58] conducted by the same research team also providing 3 cups of black tea daily over 12 weeks found that this lowered acute upper respiratory tract inflammation risk. Steptoe et al. (2007) allocated 75 healthy non-smoking men to black tea or a placebo over 6-weeks, finding that the tea group had lower plasma CRP levels, which potentially may help contribute to sustained cardiovascular health [62].

Table 3. Key Studies—randomised controlled trials.

Key: BTE, black tea extract; CRP, c-reactive protein; DB, double-blind; DOMS, delayed onset muscle soreness; hs-CRP, high-sensitivity c-reactive protein; IL-17, interleukin-17; MMP-3, Matrix Metalloproteinase-3; NFκB, Nuclear Factor kapper-light-chain-enhancer of activated B cells; NK, natural killer; PC, placebo-controlled; RCT, randomised controlled trial; SB, single-blind; SSC, Stachys schtschegleevii; TB, triple blind; T2DM, type 2 diabetes mellitus. Note: CD3⁺ CD4⁺ IFN-γ⁺ are Th1 cells, a subset of T-helper cells.

Five studies [54][56][59]-[61] recruited adults with either type 2 diabetes mellitus or cardiovascular risk factors as baseline. Mahmoud et al. (2016) [59] and Neyestani et al. (2010) [56] both recruited adults with T2DM at the study start. Mahmoud et al. (2016) allocated adults (n = 38) to consumed either 200 ml (1 cup) or 600 ml (3 cups) black tea over a 12-week period finding that tea drinkers had more T cells, IL-10 cells (an anti-inflammatory signal) and produced fewer IL-17 and IFN-γ cells which tend to drive inflammation [59]. Neyestani et al. (2010) allocated patients with T2DM to different levels of black tea intake finding that 2 cups of black tea (extract dissolved in water) showed a suppressing effect on serum malondialdehyde (a marker of oxidative stress) [56]. Serum C-reactive protein levels significantly decreased, and glutathione levels increased following the intake of 4 cups (600 ml) of black tea extract daily [56].

Mukamal et al. (2007) recruited allocated 28 adults (55 years+) with diabetes or two or more cardiovascular risk factors at baseline and allocated them to drink 3 glasses of black tea (extract, dissolved in water), or water daily for 6 months, but no differences in inflammatory markers were observed [61]. A large randomized controlled study [60] (n = 232) with Mauritian adults susceptible to ischemic heart diseases allocated to 9 g/day of black tea leaves (equivalent to three cups and 738 mg polyphenols) for 12 weeks observed reductions in CRP levels. Another trial consisting of 66 adults with coronary heart disease and providing 450 ml or 900 ml black tea daily over 4 weeks found that catechin levels did not correlate with CRP or plasma markers of oxidative stress indicating that it could be other polyphenolic and flavonoid components in tea that responsible for anti-inflammatory effects [54].

In relation to other health conditions Henning et al. (2015) allocated men (n = 93) diagnosed with prostate cancer to six cups of black tea daily, green tea or a water control finding that black tea did not affect NFkB—a key inflammatory marker [53]. Arent et al. (2010) [52] provided male collegiate students (n = 18) with black tea extract (1760 mg/day) or a placebo for 9 days finding that whilst IL-6 response was unaffected levels of oxidative stress were reduced and rates of exercise recovery improved. Another study [55] combining 2.4 g/d black tea with the medicinal plant Stachys schtschegleevii (a medicinal plant from the mint family (Lamiaceae)) significantly reduced high-sensitivity CRP and IL-1β levels, although black tea alone did not lead to significant reductions in these markers.

In summary, in healthy adults, regular black tea intake reduced markers of inflammation such as CRP and appeared to support immune regulation, possibly via gut microbiota changes [57][58][62]. In people with type 2 diabetes or cardiovascular risk, black tea at times improved inflammatory and oxidative stress markers (e.g., increased IL-10, reduced IL-17, CRP, and malondialdehyde), although not all trials showed reported benefits [56][59]-[61]. In contrast, in men with prostate cancer, black tea did not alter key inflammatory markers (NF-κB), potentially reflecting differences in underlying inflammatory pathways, disease-driven immune dysregulation, or limited study duration and statistical power. Among athletes, black tea extract reduced oxidative stress and improved recovery without altering IL-6 [52]. Overall, the evidence suggests that black tea may exert anti-inflammatory and antioxidant effects, particularly in metabolic risk populations, with variability likely driven by population-specific biology and study design factors.

Tea polyphenols are proposed to exert anti-inflammatory effects via several pathways including: 1) acting as antioxidants and inducing the endogenous antioxidant defence system, 2) regulating and inhibiting major inflammatory signalling pathways such as NF-κB, activator protein-1 and 3) reinforcing gut barrier integrity and improving microbiota balance, which may benefit inflammatory bowel conditions [63]. Regarding flavonoids the presence of a C2-C3 double bond (C-ring) and hydroxyl groups at the C3', C4', C5, and C7 positions of both rings A and B of a flavonoid skeleton are thought to underpin its potential anti-inflammatory effects [64]. Research shows that such flavonoids activate antioxidant pathways that can exert anti-inflammatory effects [65]. In black tea catechins when oxidised to theaflavins and thearubigins can also induce their anti-inflammatory effects by operating at the gut level with their fermentation improving the profile of gut microbiota [66].

In black tea, theaflavins represent one of the principle bioactive groups of compounds [67]. Experimental studies show that black tea polyphenol extracts, including theaflavins show anti-inflammatory effects in murine models of high-fat, high-sugar (obesogenic diets) [68]. Theaflavin-2 has been found to exhibit anti-inflammatory effects in two murine models of inflammation [69]. Matrix metalloproteinase (MMP) are a group of enzymes that break down extracellular matrix proteins and are upregulated during certain inflammatory diseases such as rheumatoid arthritis, osteoarthritis, inflammatory bowel disease and Alzheimer’s disease, with polyphenols thought to suppress MMP gene expression and enzyme activity inducing anti-inflammatory effects [70]. Theaflavin-3,3'-digallate, in particular, could help to protect cartilage and prevent osteoarthritis, by inhibiting proinflammatory factors, scavenging reactive oxygen species and suppressing pathways that delay inflammatory processes [71]. In dental models black tea theaflavin mixtures have been found to reduce the secretion of key inflammatory mediators, including IL-1β, IL-6, IL-8 and TNF-α secretion [72]. Inhibition of interleukin-8 expression has also been reported, further supporting an anti-inflammatory role for theaflavin [73].