Sulforaphane has been shown to be an effective antioxidant, antimicrobial, anticancer, anti-inflammatory, anti-aging, neuroprotective, and anti-diabetic (R). It also protects against cardiovascular and neurodegenerative diseases (R).
Sulforaphane appears to be most protective against colon and prostate cancer but has also been studied for its effects on many other cancers, such as breast, leukemia, pancreatic and melanoma (R).
Recent research shows that Sulforaphane can help control blood glucose levels in type 2 diabetic patients as effectively as the most commonly used prescription medicine Metformin (R).
Sulforaphane and Broccoli Sprouts
Unlike the glucoraphanin, sulforaphane degrades quickly (R).
The quantity of glucoraphanin varies greatly in different plants. In general, levels of glucoraphanin and sulforaphane are highest in broccoli sprouts (R), but 3 day-old sprouts can contain up to 100 times more glucoraphanin than in mature plants (R).
Sulforaphane activation of AMPK pathway is key to wide range of benefits
There are many hundreds of studies of Sulforaphane’s effect in fighting various disease and metabolic problems. Activation or Inhibition of several different genes are described in how it manages to impact such a wide range of health problems.
As with vitamin antioxidants the notion that supplements act as “antioxidants” in human cells is called into question . Emerging evidence suggests that the most effective supplement exert their intracellular effects not as direct “antioxidants” per se but as modulators of signaling pathways.
Compared with widely used phytochemical-based supplements like curcumin, silymarin, and resveratrol, sulforaphane more potently activates Nrf2 – which researchers call the “Master Regulator” of Cell Defense (R).
A list of genes and enzymes Sulforaphane influences is at the bottom of this page.
Perhaps even more meaningful is that like Metformin and Berberine (R), Sulforaphane strongly activates AMPK, which raises the intracellular NAD+ concentrations and activates SIRT1 which has been shown to have numerous disease fighting and anti-aging potential(R).
It’s possible many of the health benefits are at least partially related to this AMPK/NAD+/SIRT activity.
Sulforaphane helps prevent and can even kill cancer
3-5 servings per week of Cruciferous vegetables decrease the risk of cancer by 30-40% (R).
Even ONE serving of cruciferous vegetables per week significantly reduced the risk of pharynx, colorectal, esophageal, kidney and breast cancer (R).
In vitro, Sulforaphane has been demonstrated to kill breast cancer cells (R),oral squamous cell carcinoma cells (R), colorectal cancer cells (R), cervical, liver, prostate, and leukemia cancer cells (R, R), while having little to no effect on healthy cells (R)
Sulforaphane combats cancer by multiple mechanisms:
- Sulforaphane reduces inflammation by inhibiting the NF-κB pathway(R).
- Sulforaphane induces cancer cell death (R).
- SFN inhibits Phase I enzymes that enable cancer cell growth (R).
- SFN induces Phase II enzymes that clear DNA damaging chemicals (R).
- Sulforaphane thereby inhibits cancer cell proliferation (R)
In addition to the numerous cancer fighting mechanism of Sulforaphane, it is also very effective at enhancing commonly used anti-cancer drugs such as cisplatin, gemcitabine, doxorubicin, and 5-fluorouracil , allowing for smaller dosages and limiting toxicity to healthy cells (R).
Sulforaphane helps lower Cholesterol
Twelve healthy subjects that consumed 100 grams per day of broccoli sprouts lowered LDL cholesterol, increased HDL cholesterol, and improved maarkers for oxidative stress (R).
Sulforaphane May Help Parkinson’s, Alzheimers, Huntingtons
Sulforaphane activates a protein that slows huntingtins disease in mice (R).
Sulforaphane Prevents and Combats Heart & Cardiovascular Disease
Observational studies in humans has shown those who eat 3-5 servings of cruciferous vegetables a week have a significantly decreased risk of cardiovascular disease (R).
Rats that were given Sulforaphane after heart attack exhibited reduced heart damage (R).
Sulforaphane reduces formation of blood clots and platelet aggregation in humans (R).
Sulforaphane helps control Diabetes and fight Obesity
- vascular complications .
- diabetes-induced heart dysfunction
- heart damage in mice
- tissue damage
Mice fed a high fat diet to induce obesity that were subsequently treated with sulforaphane for 3 weeks had significantly less weight gain, and improved insulin resistance, glucose and cholesterol levels (R,R).
Sulforaphane is Antiviral
Sulforaphane Combats Bacterial and Fungal Infections
Human β-defensin-2 (HBD-2) is a key part of our defense against bacterial invasion. Sulforaphane increases HBD-2 in response to to 23 of 28 bacterial species (R).
Cystic fibrosis patients have increased levels of Mycobacterium abscessus. Treatment with Sulforphane of such macrophages significantly decreased bacterial burden (R).
Sulforaphane Combats Inflammation
Nuclear Factor Kappa-B (NF-kB) is a well known driver of inflammation. Sulforaphane greatly decreases NF-kB activity (R).
Sulforaphane May Combat Depression and Anxiety
Repeated SFN administration reverses depression– and anxiety-like behaviors in chronically stressed mice, likely by inhibiting the hypothalamic-pituitary-adrenal (HPA) axis and inflammatory responses to stress (R, R).
In another study, it was shown that Nrf2 deficiency in mice results in depressive-like behavior, while the induction of Nrf2 by sulforaphane has antidepressant-like effects (R).
Also, dietary intake of glucoraphanin during the juvenile and adolescent periods in mice prevents the onset of depression-like behaviors at adulthood (R).
Sulforaphane Protects the Brain and Restores Cognitive Function
Sulforaphane increases neuronal BDNF in mice, a factor that supports the survival of existing neurons and encourages the formation of new neurons and synapses (R).
Sulforaphane promotes microglia differentiation from pro-inflammatory M1 to anti-inflammatory M2 state. This reduces brain inflammation and restores spatial learning and coordination in rats (R).
Sulforaphane is beneficial in various pathological conditions:
- SFN improves cognitive performance and reduces working memory dysfunction in rats after traumatic brain injury (R).
- SFN attenuates cognitive deficits in mouse models of psychiatric disease. Also, the intake of glucoraphanin during the juvenile and adolescent periods prevents the onset of cognitive deficits at adulthood (R).
- SFN alleviates brain swelling in rats, by attenuating the blood-brain barrier disruption, decreasing the levels of pro-inflammatory cytokines, and inhibiting NF-κB (R). SFN also increases AQP4 (a water channel protein) levels, thereby reducing brain swelling (R).
- SFN prevents memory impairment and increases the survival of hippocampal neurons in diabetic rats (R).
Insufficient NRF2 activation in humans has been linked to neurodegenerative diseases such as Parkinson’s disease, Alzheimer’s disease and amyotrophic lateral sclerosis (R). SFN, as a potent Nrf2 activator, may help in the treatment of these diseases.
Sulforaphane Improves Symptoms of Autism
Sulforaphane activates several genes that lower inflammation and protect cells from oxidative stress and DNA damage, which are much higher in those with Autism (R).
In a clinical trial of 29 young men with moderate to severe autism (age 13-27), Sulforphane treatment over 13 weeks resulted in a 35% improvement in disruptive behavior(R).
Sulforaphane relieves Gastrointestinal inflammation, colitis, and ulcers
Sulforaphane May be Beneficial in Airway Inflammation and Asthma
Sulforaphane received airway inflammation and asthma symptoms in mice (R)
Broccoli sprout extract relieved airway inflammation in humans exposed to vehicle exhaust levels similar to those on a Los Angeles freeway (R).
Sulforaphane Can Be Beneficial in Arthritis
We previously pointed out that Sulforaphane strongly activates Nrf2, which relieves inflammation in many conditions. In additions, sulforaphane was found to inhibit metalloproteinases that cause osteoarthritis and cartilage destruction (R).
Sulforaphane also decreases inflammatory cytokines, reducing symptoms of arthritis in mice (R).
Sulforaphane Protects the Eyes
Negative Side Effects
Possible liver Toxicity at extreme dosages
There has been a single report of liver toxicity in one individual that consumed over 800 ml per day of broccoli juice for 4 weeks, but function returned to normal wishing 15 days or discontinuing the juice (R).
Note this individual was making juice from mature broccoli plants which have many different active substance and are not recommended for source of glucoraphanin/sulforaphane as the young sprouts have up to 100 times higher glucoraphanin levels.
Broccoli has the highest amounts of glucoraphanin of any vegetable, but it is also found in Brussel sprouts, Kale, Cabbage, Bok Choy, and several others (R).
Myrosinase also required
Remember, Sulforaphane is only formed when it comes in contact with the enzyme myrosinase, by chewing or chopping or other processing.
Myrosinase is a fragile enzyme that is quickly damaged by heating (boiling over 1 minute), or freezing (R).
Many Supplements do not provide active Myrosinase
Broccoli has long been known to provide many health benefits and as such, broccoli sprout supplements are not new to the market. Unfortunately, many of these were developed before researchers realized the Myrosinase + Glucoraphanain = Sulforaphanin equation required great care in processing to protect the Myrosinase.
Sulforaphane was found to be 7 times greater in fresh broccoli sprouts vs supplements with inactive myrosinase (R).
Glucoraphanin powder with inactive tyrosinase can be combined with a good source of tyrosinase such as broccoli sprouts or mustard seeds to greatly increase Sulforaphane absorption (R).
The myrosinase found in broccoli is quite fragile and inactivated by freezing or heat. A much more robust form of myrosinase is found in Mustard seeds. The addition of powdered mustard seed to heat processed broccoli dramatically increases sulforphane (R).
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Sulforaphane activates genes and enzymes that stimulate antioxidant production:
- inhibits Phase I enzymes CYP1A1, CYP1A2, CYP1B1, CYP2B2 and CYP3A4 (R, R).
- activates (R, R). SFN reacts with Keap1, thereby releasing Nrf2 from Keap1 binding (R).
- increases other Phase II enzymes: NQO1, GSTA1, and HO-1 (R, R, R, R).
- blocks SXR (R).
Sulforaphane inhibits inflammation:
- inhibits NfkB (R, R, R).
- inhibits TNF-α (R, R), NLRP3, IL-1β, IL-18 (R), IFN-gamma and IL6 (R, R, R).
- inhibits IL-17 (R, R).
- inhibits TGF-β/Smad (R).
- increases IL-10 (R, R, R), IL-4, Arg1, and YM-1 (R).
- inhibits NO, iNOS and COX-2 (R, R, R).
- silences Th17/Th1 (R, R).
- inhibits IL-23 and IL-12 (R).
- inhibits MMP-9 (R, R).
- inhibits LDH and PGE2 (R).
Sulforaphane changes gene expression:
- Sulforaphane inhibits DNMT1 and DNMT3A (R)
- SFN is one of the most potent (histone deacetylase) HDAC inhibitors found to date (R).
- SFN inhibits HDAC1, HDAC2, HDAC3, and HDAC4 (R, R).
- SFN decreases miR-21 and TERT (R).
Sulforaphane induces cell death (apoptosis) in cancer:
- SFN activates caspase-3, caspase-7, caspase-8, caspase-9 (R, R).
- SFN decreases anti-apoptotic Bcl-2 (R) and Bcl-XL (R).
- SFN increases pro-apoptotic Bax (R).
- SFN induces p21 (CDKN1A) (R) and p53 (R).
- SFN inactivates PARP (R).
- SFN decreases HIF1A (R).
- SFN decreases β-catenin (CTNNB1) (R).
More on Sulforaphane and Cancer
The mechanisms of SFN effects on cancer cells have been well studied. It suppresses the proliferation of cancer cells via diverse mechanisms including cell-cycle arrest, apoptosis induction, ROS production, and manipulation of some signaling pathways (166). SFN inhibits proliferation of PC-3 cells in culture in concentrationand time-dependent manner. Singh et al. (167) showed that oral administration of SFN led to >50% reduction in PC-3 xenograft tumor volume in SFN-treated mice in 10 days and more than 70% reduction in 20 days after starting treatment with no effect on body weight.
They also reported that SFN changes the Bax: Bcl-2 ratio, activates caspases 3, 8, and 9, and cleaves and inactivates PARP protein. The authors proposed that SFN induces apoptosis in PC-3 xenograft tumors in a p53-independent manner through cytoplasmic and mitochondrial pathways. Liquid chromatography–mass spectrometry (LC-MS) analyses performed by Rose et al. (17) showed the presence of 7-methylsulphinylheptyl isothiocyanates in watercress (Rorippa nasturtium aquaticum) extract and 4-methylsulfinylbutyl nitrile and 4-methylsulfinylheptyl isothiocyanates in the broccoli extract. Their investigations showed that these compounds contribute to the inhibitory effects of broccoli and watercress extracts on the invasion of MDA-MB-231 cancer cells through suppression of MMP-9 activity.
Treatment of HEK293 cells with different concentrations of SFN with and without TSA, as a HDAC1 inhibitor, leads to the increase in TOPflash reporter activity without affecting b-catenin protein levels. Further studies showed that this increase is due to the decrease in HDAC activity and consequently the increase in histone acetylation following SFN treatment (168).
It has been demonstrated that mamosphere formation in breast cancer cells is dependent on E-cadherin expression (168). It is showed that SFN could target breast cancer stem cells. The mammosphere formation test on two cancer cell lines, MCF7 and SUM195, indicated that SFN could reduce the proportion of cell with stem cell properties, and this was further supported by ALDEFLUOR assay. In vivo examination results of SFN effects on xenograft SUM159 cells in NOD/SCID mice were consistent with the in vitro results. More importantly, cells derived from SFN-treated primary tumors could not produce secondary tumors, while cells derived from the nontreated primary tumors rapidly produced the secondary tumors in the contralateral mammary fat pad of the same mice (168).
Aldehyde dehydrogenase activity is a stem cell marker for enriching tumorigenic stem/progenitor cells (169,170). Five mmol/L of SFN led to >80% reduction of ALDH-positive SUM159 cells in vitro, and daily treatment of xenograft of SUM159 tumors with 50 mg/kg of SFN for 2 weeks led to 50% reduction in tumor size through the reduction in ALDH-positive SUM159 cells by 50%, with no effect on body weight (171). ApcMin/C mice consumed SFN in their diet have fewer tumors with lower sizes in comparison with a control group, albeit, immunohistochemical (IHC) staining revealed that the b-catenin expression was not affected by SFN consumption (172).
Furthermore, the effect of SFN treatment on selfrenewal contributing to signaling pathway, Wnt pathway, was examined by analysis of b-catenin and some other downstream genes at mRNA and/or protein levels (171).
Treatment of T24 bladder cancer cells with SFN results in induction of miR-200c expression (173).
Previous studies demonstrated that miR-200c targets the E-cadherin repressors ZEB1 and ZEB2. Ectopic expression of miR-200c resulted in upregulation of E-cadherin in cancer cells (174). Therefore, treatment of T24 cells with SNF led to E-cadherin induction and EMT suppression (173). However, it seems that these results depend upon cell type and treatment conditions. Although clinical trials seem necessary, there is a large body of investigations about anticancer effects of SFN, and the explicit point is that SFN inclusion into the diet promises a safe and confident strategy.
Another active ingredient of broccoli and other cruciferous vegetables is Indole-3-carbinol (I3C) that has anticancer effects too. Meng et al. (175,176) reported despite a somehow prohibiting effect of I3C on cell attachment in vitro, and I3C could also suppress the invasion and motility of cells. The effect of I3C on cellular metastasis was also evaluated by injecting treated cells into the tail vein of mice and tracing surface metastasis in the lung of the sacrificed animal. Their results indicated that I3C treatment reduced the metastatic capability of the cells.