Sulforaphane

Mechanism: sulforaphane modifies cysteine residues on KEAP1 (Nrf2 inhibitor), releasing Nrf2 which translocates to the nucleus and activates ARE elements on DNA, inducing glutathione peroxidase, superoxide dismutase, catalase, heme oxygenase-1, NQO1, and phase II enzymes.

Clinical evidence:

Cancer: Fahey's team at Johns Hopkins has demonstrated faster elimination of carcinogens (aflatoxins, benzene) in trials in China. In localised prostate cancer, improvements in tumour markers with chronic supplementation. Autism: randomised trial by Singh et al. (2014, PNAS) showed significant improvements in behavioural symptoms in adolescents/young adults with autism after 18 weeks (effect reversible upon discontinuation). Cardiovascular: improvement of endothelial markers and reduction of blood pressure. Cognition: preliminary studies suggest benefit in mild cognitive impairment. Inflammation: reduction of systemic inflammatory markers in obesity and diabetes.

Bioavailability problem: sulforaphane is formed when glucoraphanin (stable storage form) is hydrolysed by the enzyme myrosinase. Cooking destroys myrosinase. Practical strategies:

1. Broccoli sprouts consumed raw (highest concentration + active myrosinase). 2. Lightly steamed broccoli (3 min, preserves partial myrosinase). 3. Powdered mustard added to cooked broccoli: provides exogenous myrosinase that reactivates glucoraphanin. 4. Supplements: standardised to glucoraphanin content + stabilised myrosinase (best commercial option: Avmacol, Prostaphane).

Dose: 30-90 μmol/day sulforaphane (equivalent to 100-300 g fresh sprouts, or 1-3 standardised capsules). No significant side effects at nutritional-supplementary doses.