Petri dishes show tea flavonoids damaging tumor cells and blocking cell division, yet population data show no guaranteed cancer protection for regular tea drinkers. The gap starts with dose. Cell culture studies often expose cells to flavonoid levels far above what blood plasma reaches after a cup of tea under normal absorption conditions.
In the body, enzymes in the liver drive biotransformation and change the chemical structure of flavonoids, altering their bioavailability and binding to DNA repair or apoptosis pathways. In contrast, in vitro experiments bypass digestion, first‑pass metabolism, and renal clearance, so compounds stay stable and potent. Real tissues also contain extracellular matrix barriers and variable blood flow, which limit how much of these molecules actually reach a premalignant lesion.
Cancer risk itself is shaped by multistep carcinogenesis, involving genomic instability, oxidative stress, and baseline mutation rates rather than a single pathway. That means the marginal effect of one dietary factor is small compared with tobacco exposure, ultraviolet radiation, infections, and overall energy balance. Large cohort studies and randomized trials show at best modest associations, often confounded by lifestyle clustering, so the mechanistic promise seen in glassware rarely converts into a deterministic shield against cancer.
