Williams · Frontiers in nutrition 2021 · narrative review · n=?

Indoles Derived From Glucobrassicin: Cancer Chemoprevention by Indole-3-Carbinol and 3,3'-Diindolylmethane.

Cited 94 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

Narrative review of mechanistic, preclinical, and preliminary clinical studies without systematic review methodology.

PubMed 34660663 · doi:10.3389/fnut.2021.734334 · record verified 2026-08-30

What was done

This narrative review summarizes preclinical and clinical literature on the metabolism, pharmacokinetics, and cancer chemopreventive mechanisms of glucobrassicin-derived indoles, specifically indole-3-carbinol (I3C) and its in vivo derivative 3,3'-diindolylmethane (DIM). It evaluates mechanism of action (including aryl hydrocarbon receptor modulation and cytochrome P450-dependent estrogen metabolism), compares whole-food cruciferous vegetable intake with purified supplementation, and discusses combinatorial potential with sulforaphane.

What was found

The abstract reports no numerical effect sizes or trial statistics. It notes dose-dependent cancer prevention by I3C in rainbow trout exposed to multiple carcinogens (aflatoxin B1, polycyclic aromatic hydrocarbons, nitrosamines, and N-methyl-N'-nitro-nitrosoguanidine) and inhibition of transplacental carcinogenesis in pregnant mice. Human studies have primarily investigated breast and prostate cancer targets, identifying robust in vivo DIM mono- and di-hydroxylation and conjugation. The review notes that achieving circulating DIM concentrations comparable to clinical supplement doses requires consuming kilogram quantities of Brussels sprouts daily, while tested supplement regimens showed few to no adverse effects.

Why it matters

The paper outlines the pharmacological gap between dietary intake and therapeutic dosing of cruciferous indoles, indicating that chemopreventive DIM exposure typically demands targeted supplementation rather than standard dietary consumption.

Limits

The abstract provides no quantitative clinical outcome data, participant counts, or systematic appraisal of trial quality. Much of the presented evidence relies on non-mammalian and rodent carcinogenesis models, and definitive clinical efficacy endpoints for human cancer prevention are not quantified.

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