For Patients & Caregivers
Broccoli sprouts contain compounds that have anticancer effects. Further studies are warranted.
Broccoli sprouts are young broccoli plants. They contain compounds with strong chemopreventive effects. Small studies in humans suggest that broccoli sprouts can help to eliminate environmental toxins, protect against bacterial infections and against oxidative damage. More research is needed to confirm these effects.
- Cancer Prevention
Studies done in the lab and in animals have shown that broccoli sprouts contains sulforaphane, which has strong anticancer properties. In a study conducted in humans, broccoli sprouts were found to play a role in eliminating cancer-causing chemicals. Large scale studies are needed to confirm such effects.
- Bacterial Infections
Small studies in humans suggest that broccoli sprouts may help reduce inflammation of the stomach caused by the bacterium Helicobacter pylori.
For Healthcare Professionals
Broccoli sprouts are young broccoli plants that are rich in glucoraphanin, a precursor of sulforaphane. Sulforaphane has been shown in vitro studies to have anticancer effects against prostate (1), breast (2) (3), and urinary cancers (4). It may also protect the skin from ultraviolet radiation (5).
Consumption of broccoli sprouts was found to help reduce Helicobacter pylori induced gastritis (6) (7), protect against oxidative stress-induced upper airway disease (8) and against oxidative DNA damage (9). Glucoraphanin extracted from broccoli sprouts may play a role in the excretion of environmental toxicants (10). A small Phase I study in healthy volunteers found broccoli sprout extract to be safe and well tolerated (11). Further research is warranted.
No adverse effects have been reported with consumption of broccoli sprouts.
Sulforaphane, the isothiocyanate present in broccoli sprouts, blocks the initiation stage in carcinogenesis by inhibiting enzymes that convert procarcinogens to carcinogens, and by inducing phase 2 enzymes that detoxify carcinogens facilitating their excretion from the body. Induction of phase 2 enzymes is done via anti-oxidant response element (ARE)-driven gene expression whose targets include NAD(P)H:quinone reductase (NQO1), heme oxygenase 1 (HO1) and gamma-glutamylcysteine synthetase (ã-GCS), a rate-limiting enzyme in glutathione (GSH) synthesis. These genes are regulated by nuclear factor E2-factor related factor (Nrf2) (13). Sulforaphane also suppresses cancer development through various molecular targets. It induces G2/M cell cycle arrest suppressing proliferation via cyclin-dependent kinases (CDKs) and triggers dose-dependent apoptosis via death-receptor caspase cascades or the mitochondrial caspase cascades. Also, sulforaphane inhibits histone deacetylase (HDAC) by its metabolites in vitro (13).