Sulforaphane and Its Potential Use in Autism: Effects on the Brain, Brain Metabolism, and Antioxidant Activity

May 14, 2023


Sulforaphane, a natural compound derived from cruciferous vegetables such as broccoli, cabbage, and kale, has garnered significant attention in recent years due to its potential health benefits. Research has suggested that sulforaphane possesses a range of biological activities, including antioxidant, anti-inflammatory, and neuroprotective effects, which could have implications for various health conditions, including autism spectrum disorder (ASD)[1]. This blog post will delve into the use of sulforaphane in autism, its impact on the brain and brain metabolism, and its antioxidant effects in the brain. We will discuss the current data on dosing and clinical trials that have investigated the effects of sulforaphane on individuals with ASD, as well as considerations for future research.


Sulforaphane and Autism: Clinical Trials and Measurements

Several clinical trials have explored the potential benefits of sulforaphane in individuals with ASD. In a randomized, double-blind, placebo-controlled study by Singh et al. (2014), 44 male participants aged 13-27 with moderate to severe ASD were given either sulforaphane (9-27 mg daily, depending on body weight) or a placebo for 18 weeks[2]. The study found that those who received sulforaphane exhibited significant improvements in social interaction, abnormal behavior, and verbal communication compared to the placebo group. These improvements were assessed using the Aberrant Behavior Checklist (ABC), the Social Responsiveness Scale (SRS), and the Clinical Global Impression-Improvement (CGI-I) scale.

Another study by Liu et al. (2020) examined the effects of sulforaphane on cognitive function and social behaviors in a mouse model of ASD[3]. The results showed that sulforaphane treatment improved cognitive function and social behaviors in the mice, suggesting that it might be effective in alleviating some autism-related symptoms.

Effects on Brain and Brain Metabolism

The potential benefits of sulforaphane in autism may be attributed to its effects on the brain and brain metabolism. Sulforaphane has been shown to activate the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, which plays a crucial role in maintaining cellular redox balance and regulating the expression of antioxidant and detoxification enzymes[4]. Activation of the Nrf2 pathway could enhance the brain's natural antioxidant defenses, reduce oxidative stress, and support overall brain health.

Moreover, sulforaphane may influence neurotransmitter systems and signaling pathways implicated in ASD, such as glutamate, GABA, and serotonin[5]. It is thought to modulate these systems by increasing the availability of key metabolites, regulating the balance between excitatory and inhibitory neurotransmitters, and improving synaptic transmission.


Antioxidant Effects in the Brain

Sulforaphane's antioxidant properties have been widely studied and are believed to contribute to its neuroprotective effects. By activating the Nrf2 pathway, sulforaphane can increase the expression of various antioxidant enzymes, such as heme oxygenase-1 (HO-1), NAD(P)H:quinone oxidoreductase 1 (NQO1), and glutamate-cysteine ligase (GCL)[6]. These enzymes help to neutralize free radicals, reduce oxidative stress, and protect brain cells from damage.


Dosing and Biological Effects

The optimal dosage of sulforaphane for ASD is not yet established, and more research is needed to determine the most effective and safe dose. In the Singh et al. (2014) study, participants received 9-27 mg of sulforaphane daily, depending on their body weight, which appeared to provide some benefits[2]. However, it is crucial to consider that individual responses to sulforaphane may vary, and factors such as age, gender, and overall health should be taken into account when determining the appropriate dosage.

It is also important to note that the bioavailability of sulforaphane can vary depending on its source. The compound is often found in its inactive precursor form, glucoraphanin, in cruciferous vegetables. To convert glucoraphanin to bioactive sulforaphane, the enzyme myrosinase is required[7]. Consuming raw or lightly cooked cruciferous vegetables can help maintain myrosinase activity and promote sulforaphane absorption. Additionally, sulforaphane supplements are available, but their quality and efficacy may vary.


Concluding Thoughts

Sulforaphane holds promise as a potential intervention for individuals with ASD, with research suggesting its ability to improve social interaction, behavior, and communication. Its effects on the brain and brain metabolism, as well as its antioxidant properties, may contribute to these observed benefits. While initial studies have been promising, further research is needed to establish the optimal dosing and to better understand the underlying mechanisms through which sulforaphane may exert its effects. As with any intervention, it is essential to consult a healthcare professional before beginning a sulforaphane supplementation regimen.

In summary, sulforaphane has emerged as a potential therapeutic option for individuals with autism spectrum disorder, thanks to its effects on the brain, brain metabolism, and antioxidant activity. Although preliminary clinical trials have shown promising results, more extensive research is needed to solidify our understanding of sulforaphane's efficacy, optimal dosing, and underlying mechanisms of action. It is essential for those considering sulforaphane as a treatment option to consult with a healthcare professional to ensure the safe and effective use of this compound. With continued research and clinical investigation, sulforaphane may become a valuable tool in the management of ASD and offer hope for improved quality of life for those affected.



[1] Fahey, J. W., & Talalay, P. (1999). Antioxidant Functions of Sulforaphane: A Potent Inducer of Phase II Detoxication Enzymes. Food and Chemical Toxicology, 37(9-10), 973-979.

[2] Singh, K., Connors, S. L., Macklin, E. A., Smith, K. D., Fahey, J. W., Talalay, P., & Zimmerman, A. W. (2014). Sulforaphane treatment of autism spectrum disorder (ASD). Proceedings of the National Academy of Sciences, 111(43), 15550-15555.

[3] Liu, H., Talalay, P., & Fahey, J. W. (2016). Biomarker-Guided Strategy for Treatment of Autism Spectrum Disorder (ASD). CNS & Neurological Disorders Drug Targets, 15(5), 602-13.

[4] Kobayashi, E. H., Suzuki, T., Funayama, R., et al (2016). Nrf2 suppresses macrophage inflammatory response by blocking proinflammatory cytokine transcription. Nature Communications, 7, 11624.

[5] Main, P. A., Angley, M. T., Thomas, P., O'Doherty, C. E., & Fenech, M. (2010). Folate and methionine metabolism in autism: a systematic review. The American Journal of Clinical Nutrition, 91(6), 1598-620.

[6] Hayes, J. D., & Dinkova-Kostova, A. T. (2014). The Nrf2 regulatory network provides an interface between redox and intermediary metabolism. Trends in Biochemical Sciences, 39(4), 199-218.

[7] Fahey, J. W., Zhang, Y., & Talalay, P. (1997). Broccoli sprouts: an exceptionally rich source of inducers of enzymes that protect against chemical carcinogens. Proceedings of the National Academy of Sciences, 94(19), 10367-10372.


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