CONCLUSIONS:
This result suggests that Sulforaphane has the potential to improve cognitive function in patients with schizophrenia.
A Shiina, N Kanahara, T Sasaki, Y Oda, T Hashimoto, T Hasegawa, T Yoshida, M Iyo and K Hashimoto,
Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology , Apr 30 2015
Schizophrenia is a mental disorder characterized by severe cognitive impairment. Accumulating evidence suggests a role for oxidative stress in the pathophysiology of schizophrenia. Sulforaphane (SFN) extracted from broccoli sprout is an agent with potent anti-oxidant and anti-inflammatory activity. In this study, we attempted to evaluate the effect of SFN on cognitive impairment in medicated patients with schizophrenia.We recruited a total of 10 outpatients with schizophrenia, all of whom gave informed consent. Participants took 3 tablets of SFN, consisting of 30 mg of SFN-glucosinolate per day, for 8 weeks. Clinical symptoms using the Positive and Negative Syndrome Scale (PANSS) and cognitive function using the Japanese version of CogState battery were evaluated at the beginning of the study and at week 8.A total of 7 patients completed the trial. The mean score in the Accuracy component of the One Card Learning Task increased significantly after the trial. However, we detected no other significant changes in participants.This result suggests that SFN has the potential to improve cognitive function in patients with schizophrenia.
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Well then, I’ll just have to get me some of that stuff now. I’m starting to think that there will be no end to what we can buy for this or that that is troubling us except the cure.
While on the dark side
Brought to you on behalf of all the broccoli growers of America. They can reach the multitudes just by simply advertising on any medium.
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Y Shirai, Y Fujita and K Hashimoto,
Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology , Aug 2012
Accumulating evidence suggests that oxidative stress plays a role in the pathophysiology of schizophrenia and that the potent antioxidants may be potential therapeutic drugs for schizophrenia. This study was undertaken to examine the effects of the potent antioxidant sulforaphane (SFN), found in cruciferous vegetables, on behavioral abnormalities (e.g., hyperlocomotion and prepulse inhibition [PPI] deficits) in mice after a single administration of the N-methyl-D-aspartate (NMDA)-receptor antagonist phencyclidine (PCP).Effects of SFN (3, 10, and 30 mg/kg, intraperitoneally [i.p.]) on hyperlocomotion and PPI deficits in the adult male ddY mice after administration of PCP (3.0 mg/kg, subcutaneously [s.c.]) were examined.Administration of SFN (30 mg/kg, intraperitoneally [i.p.]), but not low doses (3 and 10 mg/kg, i.p.), significantly attenuated hyperlocomotion in mice after PCP administration (3.0 mg/kg, subcutaneously [s.c.]). Furthermore, administration of SFN (3, 10, and 30 mg/kg, i.p.) attenuated the PPI deficits in mice after PCP administration (3.0 mg/kg, s.c.) in a dose-dependent manner.These results suggest that SFN has antipsychotic activity in an animal model of schizophrenia. Therefore, it is likely that SFN may be a potential therapeutic drug for schizophrenia.
There were only 4 pubmed articles with a search of the words Sulforaphane and schizophrenia.
While I completely agree that its good to be a little skeptical on new “treatments”, when the price is pretty cheap it seems like these things might be worth a try.
Here is a list of sources from Google’s shopping search engine.
Can someone please review the sources and see which ones have the greatest amount of Sulforaphane?
http://goo.gl/hcpQu6
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Well , I did just buy some broccoli and had some for lunch because I know I might be getting the real stuff that way. I like broccoli. I was just trying to be amusing to myself a bit. I tell myself jokes a lot during the day, although I’m not a clown, I don’t even like clowns.
Oh, and thanks firemonkey for the useful information you bring to this site.
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Man broccoli is the only vegetable I don’t like.
The average broccoli probably has very little sulforaphane. I think you need the high-sulforaphane extracts - at least that was what they studied here.
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Good points… and I would be cautious relative to “too much of a good thing may not be,” as that maxim applies all over the place in the world of mental health treatment.
firemonkey:
Sulforaphane
Related to this study above - another interesting study:
S Mas, P GassĂł, G Trias, M Bernardo and A Lafuente,
Fundamental & clinical pharmacology , Dec 2012
Adverse reactions to antipsychotic drugs (APs) have been attributed to oxidative stress. Sulforaphane (SF) is a potent antioxidant that protects against dopaminergic cell death. We examined the protective properties of SF against AP-induced oxidative stress in dopaminergic neuroblastoma cells. Human neuroblastoma SK-N-SH cells were treated with SF (0.5-5 ÎĽM), and 24 h later, haloperidol, risperidone or paliperidone (100 ÎĽM) was administered, either alone or in combination with dopamine (100 ÎĽM). To determine the antioxidant properties of SF, quinone oxidoreductase (NQO1) activity, glutathione S-transferase activity, and glutathione (GSH) levels were determined. Oxidative stress was measured by the increase in thiobarbituric acid reactive substances (TBARS) and in protein-bound quinones. Cell viability was also assessed. SF treatment increased GSH levels and induced NQO1 activity in SK-N-SH cells. Haloperidol was the only AP that increased TBARS when administered alone. When cells were cocultured with a drug in combination with dopamine, all three APs increased TBARS and protein-bound quinones and also induced neurotoxicity. In all the experimental conditions, 5 ÎĽM SF attenuated the accumulation of TBARS and protein-bound quinones and increased cell survival rates. Our results indicate that SF increases GSH levels and induces NQO1 activity and the removal of electrophilic quinones and radical oxygen species. Furthermore, SF could provide protective effects against AP-induced toxicity in dopaminergic cells.