Sulforaphane: benefits, dosage, contraindications

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Glucosinolates, found in all cruciferous vegetables, are converted into isothiocyanates when they come into contact with a specific enzyme: the myrosinase. This process, called hydrolysis, is triggered when the plant is disrupted: chewing, cutting, or digestion. Glucoraphanin is a glucosinolate precursor to sulforaphane, a compound directly active in the body. Sulforaphane is therefore a sulfur-containing isothiocyanate produced by the reaction of glucoraphanin with the enzyme myrosinase. Sulforaphane is present in particularly high amounts in broccoli sprouts, and other cruciferous vegetables such as cabbage, cauliflower, kale, radish, as well as mustard, horseradish, arugula, and many others. However, cooking vegetables destroys the naturally occurring myrosinase enzyme, which can reduce the bioavailability of sulforaphane in these foods. Discovered in the 1990s, sulforaphane quickly attracted scientific interest for its many health-promoting properties. Studies have linked it to antioxidant, anti-inflammatory, and anticancer effects, as well as potential benefits in the prevention of cardiovascular, metabolic, and neurodegenerative diseases. Its mechanism of action is mainly based on the activation of the Nrf2 pathway, a key regulator of the body's antioxidant defenses. Through this pathway, sulforaphane increases the production of enzymes involved in phase II detoxification, which neutralize toxic substances and protect cells from oxidative and inflammatory damage. This mechanism makes it a promising candidate for preventing and treating various chronic pathologies. Studies have shown that sulforaphane, thanks to its action on the Nrf2 pathway, inhibits the proliferation of tumor cells. Clinically, it is valued for its role in cancer prevention, notably prostate cancer.

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Phytochemicals


Indications

Scoring methodology

EFSA approval.

Several randomized, double-blind, controlled clinical trials (> 2), including a significant number of patients (>100), with consistently positive conclusions for the indication.
Several randomized, double-blind, controlled clinical trials (> 2), including a significant number of patients (>100), with positive conclusions for the indication.
One or more randomized studies, or several cohorts or epidemiological studies, with positive conclusions for the indication.
Clinical studies exist but are uncontrolled, with conclusions that may be positive or conflicting.
No clinical studies to date that can demonstrate the indication.


Prostate cancer
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The PSA (Prostate-Specific Antigen) is a protein produced by prostate cells. Its measurement in the blood is commonly used as a biomarker to assess prostate health. An abnormal elevation of PSA levels can indicate inflammation, benign prostatic hyperplasia, or, in some cases, prostate cancer. A study found that supplementation with 20 mg of sulforaphane (Prostaphane) three times daily for six months slowed the increase in PSA levels, extending the PSA doubling time by 86% compared with placebo. Another study, using a sulforaphane-rich extract derived from broccoli sprouts (35.2 mg per day for 20 weeks), also increased this doubling time by 57% in patients with recurrent prostate cancer. A recent ESCAPE study found that weekly consumption of soup enriched with glucoraphanin (a precursor of sulforaphane) for 12 months in men on active surveillance significantly reduced gene expression changes associated with oncogenic pathways, potentially lowering the risk of cancer progression. These promising results suggest a beneficial role for sulforaphane in the clinical management of prostate cancer.

Posologie

posologieOral administration

posologie35 - 60 mg

formulationstandardized extract


Synergies


Cognitive decline
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Clinical research has evaluated the effect of sulforaphane on cognitive decline. A randomized study in older adults examined the impact of taking glucoraphanin, a precursor of sulforaphane, at 30 mg per day for 12 weeks. The results showed modest improvements in working memory and processing speed compared with placebo. Another randomized double-blind study assessed the impact of sulforaphane on cognitive decline in adults with cognitive deficits related to frontal brain injuries. The trial included 90 participants aged 18 to 65, divided into two groups, receiving either sulforaphane (Avmacol) or a placebo for 12 weeks, with dosing adjusted by weight. The results showed that the group treated with sulforaphane exhibited modest but significant improvements in cognitive functions, notably working memory and processing speed, compared with the placebo group. These benefits were attributed to the action of sulforaphane on brain-protective mechanisms, such as the reduction of oxidative stress and inflammation. The study also explored brain and blood biomarkers, including glutathione (GSH), a key antioxidant, and brain-derived neurotrophic factor (BDNF), essential for synaptic plasticity. An increase in these markers was observed in the sulforaphane group, indicating a potential improvement in cognitive functions. Further studies are needed to confirm these findings.

Posologie

posologieOrally

posologie30 mg

formulationstandardized extract


Autism
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The effects of sulforaphane on autism are variable across studies. In children aged 4 to 12 years, 10-20 mg of sulforaphane per day, combined with risperidone for 10 weeks, reduced irritability by 14% and hyperactivity by 12%, with no impact on social interactions or communication. A study of young males (13-27 years) showed that a weight-based treatment (8.8 to 26.6 mg per day) for 18 weeks improved behavioral scores by 33% and social scores by 17%, these effects disappearing after discontinuation. A larger clinical trial conducted on 108 participants in China showed that a 12-week sulforaphane treatment allowed one third of participants to reduce their symptom scores by 30% or more, according to clinician assessments. Effects were more pronounced in children over 10 years old, and sulforaphane was found to be safe and well tolerated, including among the youngest participants.

Posologie

posologieOral administration

posologie8 - 30 mg

formulationstandardized extract


Properties


Anticancer

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Sulforaphane acts on several key mechanisms to slow the development of tumors. First, sulforaphane stimulates phase II detoxification enzymes, such as glutathione S-transferase, which neutralize carcinogens. At the same time, it inhibits phase I enzymes, such as cytochrome P450, responsible for activating carcinogenic substances. These combined effects reduce cells' exposure to carcinogens. Second, sulforaphane acts directly on tumor cells by blocking their growth cycle, inhibiting angiogenesis (formation of new blood vessels that feed the tumor), and limiting metastasis. It also induces the death of cancer cells while sparing healthy cells. Finally, its antioxidant and anti-inflammatory action protects cells against oxidative damage and chronic inflammation, two processes involved in cancer initiation and progression. Research also shows that sulforaphane can enhance the effectiveness of chemotherapies, such as cisplatin or doxorubicin, while reducing their side effects. These multiple actions make sulforaphane a promising ally in cancer prevention and as a complementary treatment.

Usages associés

Prostate cancer

Antioxidant

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Sulforaphane is known for its powerful antioxidant properties. It acts primarily by activating the Nrf2 pathway, a key regulator of cellular defenses against oxidative stress. Once activated, Nrf2 stimulates the production of protective enzymes such as heme oxygenase (HO-1), glutathione peroxidase (GPX), and quinone reductase (NQO1). These enzymes neutralize free radicals, reducing oxidative damage at the cellular level. This antioxidant action of sulforaphane is particularly beneficial for preventing conditions associated with oxidative stress, such as cardiovascular diseases, neurodegenerative disorders, and cancer. For example, in animal models, sulforaphane has shown the ability to restore glutathione levels, a major antioxidant, and to protect cells against oxidative damage caused by toxic or inflammatory agents. Additionally, sulforaphane acts on mitochondrial metabolism, the main source of free radicals in cells. It protects mitochondria from lipid peroxidation and preserves their function, which is essential for cellular health.


Neurological

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Sulforaphane shows promise in preventing and treating neurodegenerative diseases due to its antioxidant and anti-inflammatory properties. By activating the Nrf2 pathway, it stimulates the production of protective enzymes that reduce the accumulation of toxic proteins associated with conditions such as Alzheimer's and Parkinson's disease. In the Alzheimer's disease, studies show that sulforaphane prevents the formation of amyloid plaques and phosphorylated tau, protects neurons, and improves cognition. When administered to affected mice, it restores antioxidant levels and reduces inflammatory markers, with an optimal effect if treatment begins early and degeneration is minimal. For Parkinson's disease, sulforaphane protects dopaminergic neurons by reducing oxidative stress and apoptosis, while improving motor function and coordination. In multiple sclerosis, it reduces neuronal demyelination by decreasing pro-inflammatory cytokines and strengthening the blood-brain barrier. Furthermore, preliminary research has explored its potential in the treatment of autism in children and young adults. Results indicate a modest improvement in social skills and behaviors, correlated with changes in urinary markers associated with oxidative stress, inflammation, and amino acid metabolism and the gut microbiota. Finally, sulforaphane is also being studied for its potential impact on depression. It appears to modulate the hypothalamic-pituitary-adrenal (HPA) axis, a pathway involved in the stress response, while providing antioxidant and anti-inflammatory protection. These effects could improve depressive symptoms, particularly in patients with imbalances in oxidative stress or inflammation. Thus, sulforaphane emerges as a promising candidate in the management of neurological disorders, both for conditions associated with neurodevelopment and for stress-related psychiatric disorders. Its neuroprotective potential could complement conventional treatments.

Usages associés

Cognitive decline, Autism

Cardiovascular

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Sulforaphane has shown protective effects on the cardiovascular system. By activating the Nrf2 signaling pathway, it stimulates the production of antioxidant enzymes that reduce oxidative stress and inflammation in cardiac and renal tissues. These actions could help lower the risk of diseases such as hypertension and atherosclerosis. Additionally, studies in animal models suggest that sulforaphane improves cardiac function by modulating the expression of genes involved in the regulation of intracellular calcium, a key element of myocardial contraction and relaxation.


Safe dosage

Adult: 10 mg - 60 mg (standardized extract)

Primarily administered as extracts of broccoli sprouts containing glucoraphanin, the precursor of sulforaphane. - Prostaphane: 10-60 mg per day for 6 months. - BroccoMax: 180 mg of glucoraphanin per day for 8 weeks. - Aqueous extracts: Up to 35.2 mg of sulforaphane per day for 20 weeks.

Child: 8 mg - 26 mg

Sulforaphane administered as extracts of broccoli containing glucoraphanin. Studied dosages: Vary by weight — for example, 8.8 to 26.6 mg/day based on body mass in clinical studies.


Interactions

Médicaments

CYTOCHROME P450 1A2: moderate interaction

Sulforaphane may alter the levels and clinical effects of CYP1A2 substrates. It inhibits CYP1A2 enzymatic activity according to in vitro studies, while its precursor, glucoraphanin, may increase the expression of this enzyme, affecting the metabolism of drugs dependent on CYP1A2. Examples: Caffeine, theophylline, clozapine, olanzapine.

Cytochrome P450 3A4: moderate interaction

Sulforaphane may increase the levels and effects of CYP3A4 substrates. Animal and in vitro studies suggest that it inhibits CYP3A4 activity and reduces its expression, which could intensify the effects of drugs metabolized by this enzyme. Examples: Simvastatin, cyclosporine, midazolam, ethinylestradiol.


Precautions

Pregnant women: avoid

May be consumed in amounts found in foods. No reliable data on medicinal doses.

Breastfeeding women: avoid

May be consumed in amounts found in foods. No reliable data on medicinal doses.