Why should you eat your greens? Sulforaphane, an active compound in broccoli and other Brassica vegetables, may help prevent prostate cancer from recurring. Researchers are also investigating possible benefits to cholesterol, diabetes, skin damage, autism, and much more. Learn the latest science here.
For more about sulforaphane and its food sources, check out this post.
Sulforaphane supplements have not been approved by the FDA for medical use and generally lack solid clinical research. Regulations set manufacturing standards for them but don’t guarantee that they’re safe or effective. Speak with your doctor before supplementing.
The benefits discussed in this section have been investigated in human trials, but these are not considered sufficiently large and powerful to determine whether sulforaphane is actually effective for the purpose. That is to say: sulforaphane may do these things, but more research is required.
Doctors almost universally recommend eating vegetables (broccoli, kale, brussels sprouts, etc.) that contain sulforaphane, though not necessarily because they contain sulforaphane. Eating a lot of brassica vegetables is likely to be a safer and more reliable way to achieve many of the health benefits attributed to sulforaphane.
In 12 healthy subjects, eating fresh broccoli sprouts (100 g/day) for 1 week decreased total and LDL cholesterol, and increased HDL cholesterol. Broccoli sprouts also improved oxidative stress markers .
Broccoli sprouts improve many parameters of diabetes. In type 2 diabetics, eating broccoli sprouts increased blood antioxidant capacity and HDL cholesterol, and decreased oxidative stress, triglycerides, insulin, insulin resistance, and CRP [5, 6, 7].
- Tissue damage
- Vascular complications
- Diabetes-induced heart dysfunction
- Thickening of the heart muscle
- Heart damage in mice
However, in rats, while SFN had positive effects on diabetes, markers of liver function and cholesterol declined after treatment .
Additional research is required on the role of sulforaphane in particular, but sulforaphane-rich greens like broccoli can and should be part of a healthy diet.
UV radiation induces direct DNA damage and inflammation, and suppresses the immune response. Sulforaphane-rich extracts of 3-day-old broccoli sprouts increased protected against UV radiation-induced inflammation and edema in mice and reduced susceptibility to erythema (skin redness) in humans .
UVA irradiation plays a role in the premature aging of the skin by triggering oxidative stress, and inducing collagen degradation, a hallmark of photoaged skin. Pretreatment of mouse skin with sulforaphane protected against UVA-mediated collagen depletion .
Sulforaphane improved skin blistering in epidermolysis bullosa simplex .
Epidermolysis bullosa simplex (EBS) is a rare inherited condition in which the skin loses its integrity after mechanical trauma.
In a small clinical trial of 44 young men with autism, sulforaphane improved behavioral symptoms .
Sulforaphane may activate certain genes that protect cells against oxidative stress, inflammation, and DNA-damage, all of which are associated with autism spectrum disorder .
These effects were temporary; values went back to their original levels 2 months after treatment was discontinued .
In another study, broccoli sprout extract did not inhibit H. pylori colonization, but nevertheless protected the stomach lining from damage .
In H. pylori-infected type 2 diabetic patients, broccoli sprout powder, in addition to standard triple therapy, considerably improved H. pylori eradication. It also improved markers of heart health in these subjects .
H. pylori increases oxidative stress, thereby causing damage to the stomach lining, slowing down damage repair, and eventually inducing gastric cancer. Sulforaphane activates Nrf2-dependent antioxidant enzyme activities, thereby protecting stomach cells from oxidative injury .
Improved stomach lining health also makes it more difficult for H. pylori to colonize the stomach, which explains the reduced rate of colonization found in some human studies .
Broccoli sprouts activated detoxification and glutathione production, increasing GST while decreasing AST and ALT in rat livers .
Sulforaphane also inhibited alcohol-induced fatty liver in mice .
Sulforaphane has had beneficial effects in animals with asthma and airway inflammation, but studies in humans are less conclusive .
Broccoli sprout extract suppressed airway inflammation in humans exposed to diesel exhaust particles (equivalent to daily PM exposure levels on a Los Angeles freeway) .
Sulforaphane also improved airway and lung constrictions caused by methacholine in 60% of moderate asthmatics. However, in 20% of the asthmatics, sulforaphane worsened the constrictions .
Patients with chronic obstructive pulmonary disease (COPD) have innate immune dysfunction in the lung, resulting in frequent bacterial infections. Sulforaphane restored bacteria recognition and phagocytosis in lung macrophages from COPD patients .
Sulforaphane enhanced bacterial clearance by lung macrophages and reduced inflammation in mice exposed to cigarette smoke for 6 months .
No clinical evidence supports the use of sulforaphane for any of the conditions listed in this section. Below is a summary of the existing animal and cell-based research, which should guide further investigational efforts. However, the studies listed below should not be interpreted as supportive of any health benefit.
As we said earlier, doctors do recommend eating sulforaphane-rich vegetables like broccoli, kale, and brussels sprouts.
Sulforaphane has demonstrated antiviral activity when infected cells are exposed directly; however, there is currently not enough evidence to support its use in an animal or human with a viral infection.
In people with the flu, eating broccoli sprouts reduced influenza viral load .
Eating broccoli sprouts also seemed to enhance the antiviral response of immune cells in humans .
Researchers are currently using cell studies to try to flesh out the mechanism by which sulforaphane might boost the immune system and fight viral infection.
- SFN exhibited significant antiviral activity against influenza (the flu), HIV, Epstein-Barr virus, and the hepatitis C virus [38, 38].
- SFN blocked HIV infection in macrophages. Macrophages play a critical role in HIV infection, forming long-lived viral reservoirs and distributing the virus in the body .
- On the other hand, SFN may exacerbate infections by viruses that hijack Nrf2, such as the Marburg virus, the Kaposi’s sarcoma-associated herpesvirus (KSHV), and Dengue virus .
In one study, 23 out of 28 tested bacterial and fungal species were inhibited by sulforaphane when directly exposed in a dish .
Mycobacterium abscessus is frequently found in patients with cystic fibrosis and in immunosuppressed patients. Pretreatment of macrophages with sulforaphane significantly decreased bacterial burden, but this has not been repeated in animals or humans .
Human β-defensin-2 (HBD-2) plays an important role against bacterial invasion. Sulforaphane may be able to increase antimicrobial peptides such as HBD-2 .
Sulforaphane is an indirect antioxidant. It boosts the antioxidant capacity of cells by at least 2 mechanisms :
- Inducing phase 2 detoxification enzymes – Sulforaphane is the most potent inducer of phase 2 enzymes identified to date. It acts by activating Nrf2 and ARE, and increasing glutathione S-transferase activity [43, 2, 44, 45]
- Increasing cellular glutathione levels
Sulforaphane may help the body detoxify airborne pollutants, pesticides, and heavy metals by activating detoxification systems, mainly the phase II enzymes. These potential benefits have only been studied in animals or cell so far; these studies may or may not translate to human trials.
In a farming community exposed to airborne pollutants with a high risk of hepatocellular carcinoma, eating broccoli sprouts enhanced the detoxification of airborne pollutants and reduced the risk of cancer .
Sulforaphane induced phase II enzymes in the upper airway of human subjects .
In mice, sulforaphane reduced the pro-inflammatory and pro-allergic effects typically caused by exposure to diesel exhaust particle .
Aflatoxin binds DNA and causes liver cancer. Sulforaphane reduced the binding of aflatoxin to DNA in rats .
Sulforaphane inhibited the mutagenicity caused by heterocyclic amines (cooked food mutagens) .
Sulforaphane lessened liver damage caused by cadmium selenide in mice .
Exposure to arsenic increases the risk of lung disease. Sulforaphane blocked DNA damage and mild lung damage caused by 2-week exposure of mice to arsenic-containing dust .
A diet rich in Brassica vegetables is believed to decrease the incidence of cardiovascular disease. The role of sulforaphane in this benefit is unclear .
Sulforaphane also reduced heart damage after infarct in rats .
SFN further possesses antithrombotic activities. SFN inhibited human platelet aggregation and reduced blood clot formation .
SFN reduced the mortality of acute lung thromboembolism in mice .
Finally, sulforaphane is beneficial in stroke. In rodents, SFN decreased brain infarct (damaged tissue from a stroke) volume, and maintained the blood-brain barrier (BBB) integrity and neurological function after stroke [61, 62].
A vegetable-rich diet is one of the first recommendations for weight management. Vegetables are low in calories and high in nutrients, and they are considered essential to a healthy lifestyle. However, the role of sulforaphane specifically is unclear.
In mice with Western diet-induced obesity, 3 weeks of sulforaphane supplementation reduced weight gain, leptin and insulin levels, and improved insulin resistance, glucose tolerance, and cholesterol .
Similarly, in another study, sulforaphane inhibited high-fat-diet-induced obesity and fat accumulation in mice. It also reduced total cholesterol, leptin, and liver triglyceride levels .
There is some evidence that sulforaphane benefits immunity, but human studies are lacking.
Indeed, in another study, treatment with SFN decreased inflammation in mice with colitis .
Sulforaphane decreases autoimmune inflammation .
SFN can be beneficial against T-cell driven autoimmune disorders, such as multiple sclerosis-like diseases in animals, but studies in humans are still lagging.
NRF2-deficient mice have exacerbated pathology in this model .
Sulforaphane activated the Nrf2/ARE pathway, which helps combat the disease .
A sulforaphane-rich diet improved osteoarthritis in mice. Sulforaphane inhibited key metalloproteinases implicated in osteoarthritis, independently of Nrf2, and blocked inflammation through NF-κB to protect against cartilage destruction .
Some of the SFN effects may be mediated by Nrf2 because enhanced oxidative stress and cartilage damage were observed in Nrf2-deficient mice with arthritis .
SFN reduced the severity of arthritis in mice by decreasing pro-inflammatory cytokines .
Several inflammatory autoimmune diseases, such as rheumatoid arthritis and osteoarthritis, trigger the transformation of monocytes into proinflammatory macrophages (M1 type). In a cell study, sulforaphane blocked the inflammatory responses specific to M1 macrophages (Th1) and shifted macrophage production to M2 macrophages, which tend to decrease inflammation and encourage tissue repair .
Repeated SFN administration reversed depression- and anxiety-like behaviors in chronically stressed mice, likely by inhibiting the hypothalamic-pituitary-adrenal (HPA) axis and inflammatory responses to stress [75, 76].
In another study, Nrf2 deficiency in mice resulted in depressive-like behavior, while the induction of Nrf2 by sulforaphane had antidepressant-like effects .
Also, dietary intake of glucoraphanin during the juvenile and adolescent periods in mice prevented the onset of depression-like behaviors at adulthood .
Sulforaphane promoted microglia differentiation from pro-inflammatory M1 to anti-inflammatory M2 state. This reduced brain inflammation and restored spatial learning and coordination in rats .
In animals, sulforaphane has been found to benefit the brain in a number of ways. It:
- Improved cognitive performance and reduced working memory dysfunction in rats after traumatic brain injury 
- Weakened cognitive deficits in mouse models of psychiatric disease. Also, the intake of glucoraphanin during the juvenile and adolescent periods prevented the onset of cognitive deficits at adulthood 
- Alleviated brain swelling in rats, by attenuating the blood-brain barrier disruption, decreasing the levels of pro-inflammatory cytokines, and inhibiting NF-κB; it also increased AQP4 (a water channel protein) levels, thereby reducing brain swelling [85, 86]
- Prevented memory impairment and increased the survival of hippocampal neurons in diabetic rats 
SFN exerted protective effects against brain damage induced by acute CO poisoning in rats .
In a cell study, sulforaphane also protected human neurons against prion-mediated neurotoxicity .
Parkinson’s disease is characterized by selective loss of dopaminergic neurons in the substantia nigra of the brain. In animal models of Parkinson’s disease, sulforaphane improved deficits in motor coordination and inhibited dopaminergic neuronal loss [94, 95, 96, 97].
Abnormal production and aggregation of amyloid beta (Aβ) peptide are major factors implicated in the pathogenesis of Alzheimer’s disease (AD). Broccoli sprouts protected against Aβ-induced cell death, and sulforaphane inhibited Aβ-related inflammation [98, 99, 100].
Sulforaphane activated the protein degradation machinery that promotes huntingtin degradation and reduced huntingtin toxicity in mice .
Sulforaphane protected against seizures and elevated the seizure thresholds in mice .
Sulforaphane improved performance in a learning task in outpatients with schizophrenia .
Methamphetamine can induce psychosis in susceptible people. Sulforaphane weakened behavioral abnormalities in mice after administration of methamphetamine or phencyclidine, suggesting that it may help with schizophrenia .
Sulforaphane protected against antipsychotic-induced toxicity in dopaminergic neurons .
Sulforaphane weakened behavioral and neuropathological changes associated with methamphetamine exposure in mice. Pretreatment with sulforaphane weakened acute hyperlocomotion (increase in movement) in mice after a single administration of methamphetamine .
Also, the development of behavioral sensitization after repeated administrations of methamphetamine was significantly reduced by pretreatment with sulforaphane .
Sulforaphane may play a role in pain management, but human studies have not yet been conducted.
In mice, sulforaphane lessened pain, reduced pro-inflammatory cytokines, and increased anti-inflammatory cytokines. Sulforaphane blocked COX2 and iNOS in injured nerve cells, the 2 key enzymes implicated in inflammation and neuropathic pain .
In women, low levels of estrogen, such as during menopause or after an ovary removal surgery, can lead to reduced bone mass (osteoporosis). Researchers are currently investigating whether sulforaphane might help prevent bone loss.
Sulforaphane promoted bone formation and increased bone volume (∼20%) in both normal mice and mice without ovaries. Sulforaphane diminished bone resorption, thereby shifting the balance to a state favoring bone acquisition .
In mouse models of Duchenne muscular dystrophy, sulforaphane significantly increased muscle mass, muscle force (∼30%), and running distance. Sulforaphane also reduced muscle hypertrophy, heart muscle hypertrophy, and inflammation .
Sulforaphane may protect the kidneys from damaging chemicals, but this has only been studied in animals so far.
Chemotherapeutics, such as cisplatin, can be toxic to kidneys. In animals, sulforaphane prevented inflammation and kidney damage caused by cisplatin .
Researchers are investigating whether sulforaphane could prevent alcohol toxicity in people who are sensitive.
Many East Asians are highly intolerant to even modest alcohol consumption. These people accumulate acetaldehyde, the primary metabolite of alcohol, because of a genetic polymorphism in aldehyde dehydrogenase (ALDH2) that metabolizes acetaldehyde to nontoxic acetate. Sulforaphane upregulated ALDH2 by dietary means, thereby reducing acetaldehyde toxicity .
In mice, SFN dramatically increased tissue ALDH2 and doubled the rate of elimination of acetaldehyde after the administration of alcohol .
SFN activated human salivary aldehyde dehydrogenase (hsALDH) and increased its activity towards acetaldehyde .
Many more human trials will be required to determine whether these mechanisms play out in a living system.
When glucoraphanin (the precursor to sulforaphane) was administered to pregnant female rats, their offspring had lower blood pressure and less tissue inflammation in adulthood, regardless of their subsequent diet .
Oxidative stress due to excessive light exposure can exacerbate a variety of human retinal diseases by accelerating photoreceptor cell death (photoreceptors are cells that receive light and translate it into nerve impulses) .
SFN protected human retinal cells from UVA light-induced damage .
Sulforaphane treatment significantly decreased ischemia (reduced oxygen and blood flow), a condition that induces loss of retinal function in mice .
SFN protected human lens cells against oxidative stress and could potentially delay the onset of cataracts .
Also, SFN may help prevent complications after cataract surgery .
Fuchs endothelial corneal dystrophy (FECD) is a condition in which a deficiency in Nrf2 is observed. SFN significantly improved oxidative stress-induced cell death in FECD human cells .
Some researchers are investigating whether sulforaphane could improve healing and prevent excessive scarring. Sulforaphane inhibited cell growth and reduces collagen in keloids, a type of scar tissue .
In rats with bladder outlet obstruction, SFN treatment increased bladder capacity and bladder compliance. The potential implication for human health is unclear so far .
Hutchinson-Gilford progeria syndrome (HGPS) is a rare childhood premature aging disorder linked to mutations in the LMNA gene. Protein clearance and autophagy are impaired in HGPS cells. SFN stimulated protein clearance by autophagy and reversed cellular phenotypic changes, both of which are the hallmarks of HGPS .
Sulforaphane has not been studied in the context of HGPS itself, only its markers. Future animal studies and clinical trials will be needed.
Sulforaphane has shown promise for the prevention of recurrent prostate cancer and in some other clinical settings. For more, check out this post.
Sulforaphane is an organic compound abundant in cruciferous vegetables like kale, cabbage, and broccoli. The richest dietary source of sulforaphane is broccoli sprouts.
Sulforaphane has among the broadest potential pool of benefits of all dietary polyphenols, though much of the evidence for its benefits is limited to animal and cell research. In clinical studies, sulforaphane-rich vegetables have reduced cholesterol and blood sugar, prevented skin damage, improved symptoms of autism, protected against H. pylori, improved liver function, and prevented asthmatic reactions.