Sulforaphane was identified at Johns Hopkins University in 1992. In the three decades since, it has accumulated one of the largest research portfolios of any phytonutrient. It has demonstrated anticancer effects in breast, prostate, colorectal, lung, bladder, and pancreatic cancer cell models. It has shown chemopreventive effects in animal carcinogenesis models. And it has been tested in human clinical trials for carcinogen detoxification, prostate cancer, and autism spectrum disorder.
The Nrf2 Mechanism
Sulforaphane is an indirect antioxidant. It does not directly neutralise free radicals. Instead, it activates the Nrf2 transcription factor, which migrates to the nucleus and switches on the expression of dozens of antioxidant and detoxification enzyme genes simultaneously. These include glutathione S-transferases, quinone reductase, thioredoxin reductase, and haem oxygenase-1. The resulting upregulation of antioxidant capacity persists for 24 to 72 hours after a single exposure to sulforaphane, unlike direct antioxidants whose effect is consumed immediately.
How to Maximise Sulforaphane from Food
Sulforaphane is not present in broccoli. Its precursor glucoraphanin is present in the broccoli cell, and the enzyme myrosinase is present in separate cells. When the vegetable is chopped or chewed, these cells are disrupted and the enzyme converts glucoraphanin to sulforaphane. Boiling broccoli before this conversion has had time to occur kills the myrosinase and prevents sulforaphane formation. The optimal method is to chop broccoli, wait 40 minutes, then cook gently. Broccoli sprouts contain 20 to 50 times more glucoraphanin than mature broccoli and are the most potent food source.