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What is Glucoraphanin?
Glucoraphanin is a natural molecule which is found in plant foods such as broccoli, cauliflower and mustard. Glucoraphanin is a precursor to the natural antioxidant sulforaphane. When digested, glucoraphanin is converted in sulforaphane by a gut-based enzyme called myrosinase. This process only happens when the plant molecules are damaged by chopping, cutting or chewing.
Glucoraphanin supplements contain extracted glucoraphanin combined with myrosinase. These supplements increase the precursor pool of glucoraphanin molecules for the synthesis of sulforaphane. Subsequently, sulforaphane levels are elevated.
Increased levels of sulforaphane have been linked to wide variety of health benefits. Many researchers now believe supplementing sulforaphane levels may be linked to reduced risk of various health conditions. These include:
- Cancer. Sulforaphane appears to have to have anti-cancer properties. In both cellular and animal studies, the molecule has been demonstrated to reduce the size and number of numerous types of cancer cell. It’s now believed by researchers that supplements which increase levels of sulforaphane may reduce the risk of cancer.
- Heart Disease. A number of studies now suggest that sulforaphane may support heart health. There are multiple way sulforaphane may help to reduce the risk of heart disease. Research indicates that sulforaphane can reduce inflammation. Inflammation is a known risk factor for the narrowing of arteries, one of the major players in heart disease. This reduction in inflammation likely reduces the risk of development heart disease. In rodent models, sulforaphane has also been shown to reduce blood pressure, another major risk factor for heart disease.
- Diabetes. One study investigated the effect of increased dietary sulforaphane in people with type-2 diabetes. People with type-2 diabetes transport sugar ineffective, meaning that stable blood sugar levels can be difficult to attain for these patients. Researchers found that sulforaphane reduced resting blood-sugar levels and improved markers of long-term blood sugar stability. These findings have also been replicated in animal studies.
- Skin protection. There are a few studies which suggest that sulforaphane may be able to protect skin against UV sun damage and associated skin cancers.
- Pain management. A number of studies have highlighted that sulforaphane supplementation (via glucoraphanin) may offer an effective treatment to a variety of types of pain.
The body-wide benefits of sulforaphane supplementation are clear. However, neuroscientists have become interested in the molecule due to some interesting studies which suggest sulforaphane may have a role in optimal brain health and function.
Brain Benefits and Mode of Action
Reduces Brain Inflammation and Trauma
A number of studies now suggest that glucoraphanin, and its downstream partner sulforaphane, can have a profoundly positive effect on brain health. Sulforaphane has been widely demonstrated to reduce brain inflammation in response to various pathogens. The compound also has the ability to reduce brain inflammation associated with neurodegenerative disorders.
Cellular studies have shown that sulforaphane can protect human neurons from non-prion mediated toxicity. Other researchers have demonstrated protective effects against brain damage in a rodent model of carbon monoxide poisoning.
Animal models have demonstrated that sulforaphane have potent anti-inflammatory and neuroprotective effects. In rodents, sulforaphane was able to reduce brain swelling after injury by ensure optimal function of the blood brain barrier. Sulforaphane also decreases levels of pro-inflammatory cytokines, and inhibits the overactivity of the inflammatory pathway NF-κB.
Another study showed the decreased inflammatory state as a result of sulforaphane was associated with improve cognitive function and enhanced working memory.
Glucoraphanin has also been shown to prevent the onset of characteristic cognitive deficits associated with rodent models of psychiatric disorders when administered through juvenile and adolescent periods. Supporting evidence comes from studies which have shown that sulforaphane can recover memory loss and cognitive function in rodent who have be subjected to chemically induce memory loss.
Mode of action: Sulforaphane has the ability to change the resting state of microglia, the resident immune cells of the brain. Microglial cells are responsible for immune responses and inflammatory states of the brain. Sulforaphane has been shown to change the resting state of microglial from a pro-inflammatory state, to an anti-inflammatory state. This may be one mechanism through which sulforaphane can reduce brain trauma and protect neurons.
Sulforaphane is also able to decrease levels of pro-inflammatory cytokines, and inhibiting the overactivity of the inflammatory pathway NF-κB. This confers a further reduction inflammation, protecting neurons again immune-related damage. Dysfunctional immune activity is intertwined with a variety of neurodegenerative and psychiatric disorders. Increases in glucoraphanin and sulforaphane can protect neurons via their powerful antioxidant and anti-inflammatory effect, but may also aid cognitive ability.
May Prevent Many Mental Health Conditions
Mounting research studies have begun to highlight that glucoraphanin, and its downstream partner sulforaphane, may provide an effect treatment and preventative measure for a variety of different mental health conditions.
- Depression and Anxiety
Sulforaphane may provide some mood stabilising properties which can help with disorders such as depression and anxiety.
Studies using chronic-stress models in rodents have shown the sulforaphane supplementation reversed symptoms of depression and anxiety. Researchers suggest that the mechanism underlying this involves inhibition various inflammatory responses, including that of the hypothalamic-pituitary-adrenal axis (HPA). The underlying mechanisms may also involve the dopaminergic system. Dopamine dysfunction is a key player in many mental health conditions, including depression. A number of studies have shown that sulforaphane can infer neuroprotection to dopaminergic neurons. Subsequently, these protective benefits may help to prevent conditions such as depression.
One of the core features of schizophrenia are a range of cognitive deficits, such as impairments in working memory, attention and social behaviours. Human studies in schizophrenia patients have reported that sulforaphane supplementation improved patient performance in cognitive learning-based tasks.
Methamphetamine and phencyclidine are two widely used laboratory models of schizophrenia. Administration of these drugs in rodents can be used to induce a schizophrenia-like phenotype. Behavioural effects in this model primarily include cognitive deficits and ‘negative’ symptoms (depression-like symptoms). By using these models in mice, researchers found that sulforaphane reduced the behavioural abnormalities which are associated with administration of methamphetamine and phencyclidine.
One of the major pathological features of Alzheimer’s disease are beta-amyloid plaques. The plaques surround cells and cause neuronal damage and cell loss. Studies have shown that sulforaphane rich foods, such as broccoli sprouts, can protect against beta-amyloid plaques, prevent inflammation and reduce cell death. Animal models have also shown that increased levels of sulforaphane can improve cognitive impairment in rodent models of Alzheimer’s disease.
The biological hallmark of Parkinson’s disease is the loss and damage of dopamine neurons in a brain region called the substantia nigra. Multiple animal studies have shown that increased levels of sulforaphane can improve the characteristic motor deficits which are associated with Parkinson’s disease. Moreover, sulforaphane appears to inhibit the loss of dopaminergic neurons.
Mode of action: A common feature across many of these research studies is the finding that sulforaphane often reduces cognitive impairments associated with various brain disorders. One cellular study found that sulforaphane increases expression of a critical neuronal growth factor, BDNF. The same study also found enhanced levels of key synaptic proteins, such as PSD-95, synaptophysin and MAP2. These are well-known markers of synaptic plasticity and strength.
This suggests that sulforaphane is able to modulate synaptic plasticity and remodelling through BDNF activity, which is one mechanism that could underlie the apparent cognitive benefits associated with the molecule.
How to Use
Glucoraphanin supplementation provides an excellent way to increase production of sulforaphane. In turn, these supplements increase the levels of sulforaphane to yield neuroprotective and, potentially, cognitive benefits.
Supplements can be taken orally and are well-tolerated and safe for use by most people. There aren’t generally any side-effects associated with increased sulforaphane levels. Some very mild side effects could include changes to bowel movements or gas.
Recommended Dose: 400µg daily
There is insufficient scientific research to provide a definitive recommendation on the most effect dose of glucoraphanin. However, most research and manufacturers suggest 400µg taken daily should provide health benefits.
Classification: Protection, Cognition
We’ve classified glucoraphanin as a robust neuroprotectant due to its body-wide antioxidant and anti-inflammatory effects. Glucoraphanin can help to support immune function in the brain and reduce inflammation, which makes it a perfect candidate for protecting against neurodegenerative illness. We’ve also classified glucoraphanin as a cognitive enhancer since it’s been shown to reverse cognitive deficits and decline in a number of animal models.
- Beibei Sun, Xiaohuan Zhang, Yanyan Yin, Hualei Sun, Huina Ge, Wenjie Li (2017) Effects of sulforaphane and vitamin E on cognitive disorder and oxidative damage in lead-exposed mice hippocampus at lactation. Journal of Trace Elements in Medicine and Biology, Volume 44, Pages 88-92, ISSN 0946-672X, https://doi.org/10.1016/j.jtemb.2017.06.004.
- Carrasco‐Pozo, C., Tan, K.N. and Borges, K. (2015), Sulforaphane is anticonvulsant and improves mitochondrial function. J. Neurochem., 135: 932-942. doi:10.1111/jnc.13361
- Chang Yu, Qi He, Jing Zheng, Ling Yu Li, Yang Hao Hou, Fang Zhou Song (2017) Sulforaphane improves outcomes and slows cerebral ischemic/reperfusion injury via inhibition of NLRP3 inflammasome activation in rats, International Immunopharmacology, Volume 45, Pages 74-78, ISSN 1567-5769, https://doi.org/10.1016/j.intimp.2017.01.034.
- Dash, P. K., Zhao, J., Orsi, S. A., Zhang, M., & Moore, A. N. (2009). Sulforaphane improves cognitive function administered following traumatic brain injury. Neuroscience letters, 460(2), 103–107. https://doi.org/10.1016/j.neulet.2009.04.028
- Hernández-Rabaza, V., Cabrera-Pastor, A., Taoro-González, L., Malaguarnera, M., Agustí, A., Llansola, M., & Felipo, V. (2016). Hyperammonemia induces glial activation, neuroinflammation and alters neurotransmitter receptors in hippocampus, impairing spatial learning: reversal by sulforaphane. Journal of neuroinflammation, 13, 41. https://doi.org/10.1186/s12974-016-0505-y
- Holloway, P. M., Gillespie, S., Becker, F., Vital, S. A., Nguyen, V., Alexander, J. S., Evans, P. C., & Gavins, F. (2016). Sulforaphane induces neurovascular protection against a systemic inflammatory challenge via both Nrf2-dependent and independent pathways. Vascular pharmacology, 85, 29–38. https://doi.org/10.1016/j.vph.2016.07.004
- Protective Effect of Sulforaphane against Dopaminergic Cell Death
- Ji Man Han, Yong Jin Lee, So Yeon Lee, Eun Mee Kim, Younghye Moon, Ha Won Kim and Onyou Hwang Protective Effect of Sulforaphane against Dopaminergic Cell Death Journal of Pharmacology and Experimental Therapeutics April 1, 2007, 321 (1) 249-256; DOI: https://doi.org/10.1124/jpet.106.110866
- Kim, J., Lee, S., Choi, B.‐R., Yang, H., Hwang, Y., Park, J. H. Y., LaFerla, F. M., Han, J.‐S., Lee, K. W., Kim, J., Mol. Nutr. Food Res. 2017, 1600194.
- Lucarini, E, Micheli, L, Trallori, E, et al. Effect of glucoraphanin and sulforaphane against chemotherapy‐induced neuropathic pain: Kv7 potassium channels modulation by H2S release in vivo. Phytotherapy Research. 2018; 32: 2226– 2234. https://doi.org/10.1002/ptr.6159
- Lynch, R., Diggins, E. L., Connors, S. L., Zimmerman, A. W., Singh, K., Liu, H., Talalay, P., & Fahey, J. W. (2017). Sulforaphane from Broccoli Reduces Symptoms of Autism: A Follow-up Case Series from a Randomized Double-blind Study. Global advances in health and medicine, 6, 2164957X17735826. https://doi.org/10.1177/2164957X17735826
- Ma, L. L., Xing, G. P., Yu, Y., Liang, H., Yu, T. X., Zheng, W. H., & Lai, T. B. (2015). Sulforaphane exerts neuroprotective effects via suppression of the inflammatory response in a rat model of focal cerebral ischemia. International journal of clinical and experimental medicine, 8(10), 17811–17817.
- Masci, A., Mattioli, R., Costantino, P., Baima, S., Morelli, G., Punzi, P., Giordano, C., Pinto, A., Donini, L. M., d’Erme, M., & Mosca, L. (2015). Neuroprotective Effect of Brassica oleracea Sprouts Crude Juice in a Cellular Model of Alzheimer’s Disease. Oxidative medicine and cellular longevity, 2015, 781938. https://doi.org/10.1155/2015/781938
- Matsuura, A., Ishima, T., Fujita, Y. et al. Dietary glucoraphanin prevents the onset of psychosis in the adult offspring after maternal immune activation. Sci Rep 8, 2158 (2018). https://doi.org/10.1038/s41598-018-20538-3
- Mas, S., Gassó, P., Trias, G., Bernardo, M. and Lafuente, A. (2012), Sulforaphane protects SK‐N‐SH cells against antipsychotic‐induced oxidative stress. Fundamental & Clinical Pharmacology, 26: 712-721. doi:10.1111/j.1472-8206.2011.00988.x
- Pu, Y, Qu, Y, Chang, L, et al. Dietary intake of glucoraphanin prevents the reduction of dopamine transporter in the mouse striatum after repeated administration of MPTP. Neuropsychopharmacol Rep. 2019; 39: 247– 251. https://doi.org/10.1002/npr2.12060
- Sandberg, M., Patil, J., D’Angelo, B., Weber, S. G., & Mallard, C. (2014). NRF2-regulation in brain health and disease: implication of cerebral inflammation. Neuropharmacology, 79, 298–306. https://doi.org/10.1016/j.neuropharm.2013.11.004
- Schachtele, S. J., Hu, S., & Lokensgard, J. R. (2012). Modulation of experimental herpes encephalitis-associated neurotoxicity through sulforaphane treatment. PloS one, 7(4), e36216. https://doi.org/10.1371/journal.pone.0036216
- Shiina, A., Kanahara, N., Sasaki, T., Oda, Y., Hashimoto, T., Hasegawa, T., Yoshida, T., Iyo, M., & Hashimoto, K. (2015). An Open Study of Sulforaphane-rich Broccoli Sprout Extract in Patients with Schizophrenia. Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology, 13(1), 62–67. https://doi.org/10.9758/cpn.2015.13.1.62
- Shirai, Y., Fujita, Y., Hashimoto, R., Ohi, K., Yamamori, H., Yasuda, Y., Ishima, T., Suganuma, H., Ushida, Y., Takeda, M., & Hashimoto, K. (2015). Dietary Intake of Sulforaphane-Rich Broccoli Sprout Extracts during Juvenile and Adolescence Can Prevent Phencyclidine-Induced Cognitive Deficits at Adulthood. PloS one, 10(6), e0127244. https://doi.org/10.1371/journal.pone.0127244
- Vauzour, D., Buonfiglio, M., Corona, G., Chirafisi, J., Vafeiadou, K., Angeloni, C., Hrelia, S., Hrelia, P. and Spencer, J.P.E. (2010), Sulforaphane protects cortical neurons against 5‐S‐cysteinyl‐dopamine‐induced toxicity through the activation of ERK1/2, Nrf‐2 and the upregulation of detoxification enzymes. Mol. Nutr. Food Res., 54: 532-542. doi:10.1002/mnfr.200900197
- Yao, W., Zhang, J. C., Ishima, T., Dong, C., Yang, C., Ren, Q., Ma, M., Han, M., Wu, J., Suganuma, H., Ushida, Y., Yamamoto, M., & Hashimoto, K. (2016). Role of Keap1-Nrf2 signaling in depression and dietary intake of glucoraphanin confers stress resilience in mice. Scientific reports, 6, 30659. https://doi.org/10.1038/srep30659
- Zhang, R., Miao, Q.-W., Zhu, C.-X., Zhao, Y., Liu, L., Yang, J., & An, L. (2015). Sulforaphane Ameliorates Neurobehavioral Deficits and Protects the Brain From Amyloid β Deposits and Peroxidation in Mice With Alzheimer-Like Lesions. American Journal of Alzheimer’s Disease & Other Dementiasr, 183–191. https://doi.org/10.1177/1533317514542645
- Zhang, R., Zhang, J., Fang, L., Li, X., Zhao, Y., Shi, W., & An, L. (2014). Neuroprotective effects of sulforaphane on cholinergic neurons in mice with Alzheimer’s disease-like lesions. International journal of molecular sciences, 15(8), 14396–14410. https://doi.org/10.3390/ijms150814396
- Zhou, Q., Chen, B., Wang, X., Wu, L., Yang, Y., Cheng, X., Hu, Z., Cai, X., Yang, J., Sun, X., Lu, W., Yan, H., Chen, J., Ye, J., Shen, J., & Cao, P. (2016). Sulforaphane protects against rotenone-induced neurotoxicity in vivo: Involvement of the mTOR, Nrf2, and autophagy pathways. Scientific reports, 6, 32206. https://doi.org/10.1038/srep32206
- Zhao, J., Moore, A.N., Clifton, G.L. and Dash, P.K. (2005), Sulforaphane enhances aquaporin‐4 expression and decreases cerebral edema following traumatic brain injury. J. Neurosci. Res., 82: 499-506. doi:10.1002/jnr.20649
- Xudong Zhao, Liting Wen, Min Dong, Xiaojie Lu (2016) Sulforaphane activates the cerebral vascular Nrf2–ARE pathway and suppresses inflammation to attenuate cerebral vasospasm in rat with subarachnoid hemorrhage, Brain Research, Volume 1653, Pages 1-7, ISSN 0006-8993, https://doi.org/10.1016/j.brainres.2016.09.035.