Is Sulforaphane the Key to Schizophrenia Treatment?

Sulforaphane, a natural compound found in broccoli sprouts (a.k.a Microgreens) and other cruciferous vegetables, is increasingly being viewed as a superfood. Unlike many of the other so-called superfoods available, sulforaphane actually has a growing body of promising research behind it, and the data continues to add up.

Recently, sulforaphane has been identified as a potential treatment for schizophrenia, a mental disorder that affects more than twenty-one million people globally. Could this simple natural compound have the potential to treat a serious neurological disorder, and what other benefits are being identified by researchers?

Current Schizophrenia Treatments Need Improvement

Schizophrenia can cause severe disruption to normal routines, relationships, and families. Patients suffering from the most severe cases can experience hallucinations, confused thinking, delusions, decreased motivation, and depression.

Symptoms typically appear gradually in early adulthood, and in many cases, they are never resolved. Antipsychotic drugs are typically prescribed for sufferers of schizophrenia. These don’t always offer a complete cure for patients and come with side effects like blurred vision, drowsiness, weight gain, and tremors.

Identifying a need for more effective schizophrenia treatments, researchers from the Johns Hopkins University [1] engaged in a series of studies to analyze the link between sulforaphane and chemical imbalances in the brain.

Glutamate and Its Relationship with the Brain

Researchers measured the brains of schizophrenic patients using magnetic resonance spectroscopy (MRS). It was discovered that patients who had experienced at least one episode of psychosis had lower levels of glutamate in the anterior cingulate cortex area of the brain. Levels were 4% below the expected average. This area of the brain is responsible for cognition and some aspects of social behavior.

Glutamate stimulates neuron activity in the brain, and it is linked to schizophrenia as well as depression.

Researchers also found that other areas of the brain had below average levels of glutathione, the substance of which glutamate is a component. Glutathione levels in psychosis patients were up to 8% lower than the expected average.

Learning that there’s a connection between glutamate and schizophrenia, researchers set out to create specific conditions in animal studies.

• By using a clinical drug called L-Buthionine sulfoximine in rodents, the researchers were able to block the process that turns glutamate into glutathione. As glutamate was used up rapidly, the rodent brains showed rapid neural activity, similar to the brains of schizophrenic patients.
• The researchers then reversed the process by using sulforaphane, the same compound that is found naturally in cruciferous vegetables. Sulforaphane causes glutamate to become stored in the form of glutathione. This gives the brain a ‘fuel tank’ to use glutamate when necessary. This slowed the speed of neural activity, resulting in conditions similar to people who don’t suffer from schizophrenia.

This research showed that sulforaphane could help to regulate glutamate in the brain by converting it to glutathione. The next step was to trial a sulforaphane supplement on human patients.

Using the Research for Human Trials

Nine healthy volunteers (five male and four female) were given two daily doses of a pure broccoli sprout extract over a period of seven days. After the seven days, brain measurements were taken to identify glutathione. It was found that the test subjects had an average of a 30% increase in glutathione levels.

The key to remember here is that glutathione contains glutamate in a stored state, effectively giving the brain a reserve. By storing glutamate rather than using it immediately, rapid neural activity is decreased, which could reduce the risk of developing psychosis and schizophrenia.

Sulforaphane was well tolerated in the test subjects, with only minor cases of gas or bloating reported as side effects.

More Mental Health Benefits from Sulforaphane

Ongoing research into sulforaphane is extremely promising, especially when considering the implications for schizophrenia sufferers. The compound could also have a role to play in treating depression and anxiety, conditions which are in many cases diagnosed along with schizophrenia.

There is strong evidence that suggests a link between inflammation and depression. Inflammatory processes can be caused by stress, physical violence, and nutritional deprivation.

Sulforaphane can stimulate the Nrf2 activator, which is associated with inflammation in the brain. A 2016 study recorded in the U.S. National Library of Medicine [2] found that even a single dose of sulforaphane can reduce inflammation and could be used as a future treatment or preventer of depression and anxiety.

Diet Could be a Key Factor in Maintaining Mental Health

Today, it is universally accepted that diet has a critical role to play in physical health. Adjustments to diet can help to control or prevent a range of conditions from heart disease to certain cancers. The same could eventually become true of mental health disorders. Sulforaphane is produced by combining two compounds found in Broccoli Microgreens (glucoraphanin & myrosinase) and is 100x more abundant than the adult plant. More and more people are beginning to realize the health benefits of microgreens. This has resulted in a diet shift that includes microgreens along with other healthy foods.

The growing body of research shows that there is a relationship between sulforaphane, schizophrenia, and depression. As studies continue, it’s very likely that sulforaphane could become a major component of widely used treatments.

Sources:

1. Broccoli Sprout Compound May Restore Brain Chemistry Imbalance Linked to Schizophrenia https://www.hopkinsmedicine.org/news/newsroom/news-releases/broccoli-sprout-compound-may-restore-brain-chemistry-imbalance-linked-to-schizophrenia
2. Prophylactic effects of sulforaphane on depression-like behavior and dendritic changes in mice after inflammation. https://www.ncbi.nlm.nih.gov/pubmed/27833054