A 2025 meta-analysis pooling 18 observational studies with 58,929 participants found that green tea consumption was associated with 37% lower odds of cognitive impairment (OR 0.63, 95% CI: 0.54–0.73). Protective associations held separately for dementia (OR 0.74, 95% CI: 0.56–0.99) and mild cognitive impairment (OR 0.64, 95% CI: 0.43–0.96), and were largest in adults aged 50–69. The association was significant in Asian populations but absent in European ones, and the authors note that large-scale longitudinal studies are still needed to establish dose-response and long-term effects. Mechanism remains preclinical: green tea polyphenols show neuroprotectant activity in cell cultures and animal models, such as preventing neurotoxin-induced cell injury.
A 2024 meta-analysis of 38 prospective cohort datasets covering 1,956,549 participants compared the highest with the lowest categories of tea consumption and found lower all-cause mortality (0.90, 95% CI: 0.86–0.95) and lower cardiovascular mortality (0.86, 95% CI: 0.79–0.94). Those pooled estimates are for tea of mostly unreported type rather than green tea specifically; the single included study that separated types reported that drinking green tea 3 or more times a week, versus fewer than 3, carried 21% lower all-cause and 22% lower cardiovascular mortality, with no significant association for black tea. For tea generally, the paper reports a non-linear dose-response: the greatest risk reductions appeared at 2.0 cups per day for all-cause mortality and 1.5 cups per day for cancer mortality, with no further reduction at higher intake; for cardiovascular mortality it reports a plateau at 1.5 to 3.0 cups per day followed by a sustained reduction at higher intake. The inverse association was stronger in Asia than in Europe, which the authors attribute to regional differences in which tea is drunk. Effects on cholesterol and blood pressure are far less settled, the cited literature review suggests green tea may lower blood pressure without quantifying it, and the lipid reductions it reports come from tea-fed rats rather than human trials.
EGCG and other green tea polyphenols are scavengers of reactive oxygen species. In vivo studies report that green tea catechins raise total plasma antioxidant activity, increase serum superoxide dismutase activity and aortic catalase expression, and lower malondialdehyde, a marker of oxidative stress. Catechins have also been reported to raise vitamin E concentration within low-density lipoprotein and thereby protect it against peroxidation, and green tea leaves inhibited tert-butyl hydroperoxide-induced lipid peroxidation. Human data are thinner: in 25 patients with gastrointestinal pathologies, tableted green tea was well tolerated and the lipid peroxidation index fell from 4.63 to 4.14.
The glucose evidence is dominated by animal models. Green tea polyphenols improved glucose tolerance in normal rats and cut elevated serum glucose by 29% to 44% in alloxan-diabetic rats, and EGCG inhibits intestinal glucose uptake via the SGLT1 transporter in vitro. Human evidence is limited to smaller studies, green tea promoted glucose metabolism in healthy volunteers on an oral glucose-tolerance test, and the review that collects this work concludes that human clinical evidence remains limited and that the safe range and magnitude of benefit are not yet defined. Effects on body weight are similarly modest: a crossover trial found a beverage containing green tea catechins, caffeine, and calcium raised 24-hour energy expenditure by 4.6%, though the contribution of the individual ingredients could not be separated, and a pilot trial in six overweight men given 300 mg EGCG per day for two days found increased fat oxidation but no significant change in resting energy expenditure.
The best evidence synthesis here is a 2020 Cochrane review of 142 studies, and its findings are inconsistent rather than confirmatory. Its nonexperimental evidence included more than 1.1 million participants across 46 cohort and 85 case-control studies, but the highest-versus-lowest estimate for overall cancer incidence came from three studies involving 52,479 participants (summary risk ratio 0.83, 95% CI: 0.65–1.07), while the cancer-mortality estimate came from eight studies involving 504,366 participants (0.99, 95% CI: 0.91–1.07); neither was statistically significant, and both were low-certainty. Eleven randomized trials allocating 1,795 participants to green tea extract or placebo were likewise inconclusive: prostate cancer incidence 0.50 (95% CI: 0.18–1.36), gynaecological cancer 1.50 (95% CI: 0.41–5.48), non-melanoma skin cancer 1.00 (95% CI: 0.06–15.92). For several sites, oesophageal, prostate, urinary tract, and leukaemia, cohort and case-control designs pointed in opposite directions. The reviewers concluded that the evidence for a beneficial effect on overall or site-specific cancer risk is limited, and noted that most included studies were conducted in Asian populations with high green tea intake, which limits generalisability elsewhere.
The cohort dose-response findings above concern tea generally, not a stable green-tea beverage dose. Catechin content varies with leaf variety, origin, growing conditions, and preparation, and brewing does not extract all catechins from the leaf, so a cup is not a fixed dose. Extracts are not interchangeable with the beverage: green tea extract intake in randomized trials produced gastrointestinal disorders and elevated liver enzymes, and more rarely insomnia, raised blood pressure, and skin reactions, and EGCG from extract is cytotoxic to liver cells at high exposure. Green tea infusions also reduce dietary iron bioavailability, which matters for anyone at risk of iron deficiency.