Study: Sulforaphan is promising for autism spectrum disorders

Study: Sulforaphan is promising for autism spectrum disorders
Reference
Singh K., Connors SL, Macklin EA, et al. Suloraphan treatment of autism spectrum disorders (ASD). Proc Natl ACAD SCI Us a. 2014; 111 (43): 15550-15555.
Design
placebo-controlled, double-blind, randomized study. The participants were given 50–150 μmol Sulforaphan from broccola sprouts per day. The dosage of Sulforaphan was dependent on the body weight: 50 μmol (1 capsule) for participants with a weight of 100 lb and less; 100 μmol (2 capsules) for participants between 101 lb and 199 lb; and 150 μmol (3 capsules) for participants over 90 kg. The placebo group received capsules without medication for the same dosage scheme and the same duration. The treatment period was 18 weeks, followed by 4 weeks without treatment.
participant
43 men aged 13 to 27 with medium to severe autism began the study. At the end of the study, the treatment group had 26 participants and the placebo group 14.
target parameter
follow-up reviews included the aberrant behavioral checklist (ABC), the social responsibility scale (SRS) and the clinical global improvement scale (cgi-i). The results were compared with initial reviews that were collected before the treatment.
important knowledge
participants who received Sulforaphan showed a significant improvement in the evaluation with ABC, SRS and CGI-i reviews compared to the initial value. A significantly greater improvement was shown by the participants of the treatment group after 4, 10 and 18 weeks for subscale irritability, lethargy, stereotypical and hyperactivity of the ABC and for subscale awareness, communication, motivation and mannerism of the SRS. Of which in the treatment group, 35 % showed these improvements in the SRS compared to 0 % in the placebo group, and 60 % of the treatment group showed improvements in the ABC compared to 20 % in the placebo group. The CGI-i analysis of the values after 18 weeks in the treatment group was 46 % (12 out of 26), 54 % (14 of 26) and 42 % (11 of 26) The participant in relation to social interaction strongly or very strongly improved, different behavior or verbal communication compared to 0 % (0 of 11; p = 0.007), 9 % (1 of 11; p = 0.014) and 0 % (0 of 11; p = 0.015) for those in the placebo group. After stopping the Sulforaphan treatment, all scales returned to the starting values.
practice implications
The treatment of autistic children can often be a challenging experience for both parents and the doctor. With the prevalence of autism in the United States, which reaches 1 of 68 children - an increase of 30 % compared to 2 years ago 1 and in the past ten years by 78 % 2 - the demand for effective therapies has been as high before. Currently the only treatments approved by the US Food and Drug Administration for the symptoms of Autism Risperidon and Aripiprazole are. Anxiety. 4.5 ironically, these are symptoms that can occur in children with autism, so that taking these medication can significantly increase the symptoms that are already available in autistic children.
Another theory of why Sulforaphan could benefit these children is activating the heat shock reaction. 13 This includes the high regulation of heat shock proteins in the brain, which is assumed that they improve communication between synapses during a fever. have shown. 15.16 This means that at least theoretically, the oppression of fever in children with autism may not be in the long term. It is also important to note that there is numerous evidence that the suppression of fever increases morbidity and mortality. 17 In terms of the currently currently to be checked, the majority (80 %) of the participants had a positive response to fever in the history. This is higher than the observed rate of "fever-responders" in the autistic population of 35 %. 18 If heat shock is actually the mechanism of the effect of Sulforaphan, this study has a distorted cohort with an overrepresentation of those who benefit from its use. Future Autism Research, which compares the results of the Sulforaphan administration in fever-responders with fever-non-responders, could result in a reliable predictor for the success of this treatment.
SULFORAPHAN fulfills several functions that address significant biochemical deviations that are routinely found in the autistic population, mainly by highly regulating genes that protect the body from oxidative stress, and those that control inflammation.
The side effects observed in the treatment group included weight gain and seizures. Some autistic children may have an increased intestinal permeability, 19 possibly as a result of a gastrointestinal inflammation (GI). In view of the fact that Sulforaphan could have an anti-inflammatory effect, weight gain may be the result of an improved nutrient absorption from the gastrointestinal tract and/or an improvement of the appetite by reducing abdominal complaint. Two participants suffered seizures during the study period. One attack occurred during the treatment period, the other several weeks after the end of the treatment. Both participants had a history of seizures. This may not be a major problem, since patients with autism have an already 3 to 22-fold increased risk of seizure.
for Sulforaphan is clearly necessary more research in the autistic population, in particular using reliable biomarkers for inflammation and oxidation that has been established in previous research. 21 This study only dealt with autism symptoms, and although it still gives insight into the potential of Sulforaph, the presence of Biomarker data to explain its effectiveness only expand the existing knowledge of natural and alternative therapies for autism.
Note from the editorial team: The product used in this study is currently not being sold. The researchers used a broccolism pross extract that was subjected to further treatment with myrosinase enzymes that were obtained from Daikon Rettich. It contained more Sulforaphan than the Sulforapanglucosinolate (SGS) products.
- autism and developmental disabilities monitoring network surveillance Year 2010 Principal Investigator. Prealence of autism spectrum disorders in children aged 8 years-Autism and Developmental Disabilities Monitoring Network, 11 locations, 2010. 2014; 63 (2): 1-24.
- surveillance network for autism and developmental disorders surveillance year 2008 Main investigator. Prevalence of autism spectrum disorders-network for monitoring autism and developmental disorders, 14 locations, USA, 2008. mmwr Morb Mortal Wkly Rep. 2012; 61 (3): 1-24.
- US Food and Drug Administration. Beware of false or misleading claims for the treatment of autism. Available: (link removed). Accessed on November 21, 2014.
- webmd. Ablify: side effects. Available around: (link removed). Accessed on November 21, 2014.
- webmd. Drugs and medication: risperidone. Available around: (link removed). Accessed on November 21, 2014.
- Oliveira G, Ataíde A, Marques C, et al. Epidemiology of the autism spectrum disorder in Portugal: prevalence, clinical characterization and illnesses. Dev Med Child Neurol. 2007; 49 (10): 726-733.
- Cassells C. Mitochondrial dysfunction can play a role in the etiology of autism spectrum disorders. Medical news from Medscape. April 15, 2008. Available at: (link away). Accessed on December 1, 2014.
- dl Vargas, C. NASCIMBENE, C. Krishnan, AW Zimmerman, CA Pardo. Neuroglia activation and neuroinflammation in the brain of patients with autism. Anna Neurol. 2005; 57 (1): 67-81.
- Connolly am, Chez Mg, Pestronk A, Arnold St, Mehta S, Deel RK. Serum autoantibodies against the brain in the Landau-Kleffner variant, autism and other neurological disorders. j Pediatr. 1999; 134 (5): 607-613.
- rose S., Frye Re., Slattery J., et al. Oxidative stress induces a mitochondrial dysfunction in a subgroup of autistic lymphoblastoid cell lines in a well-coordinated case control cohort. plus one. 2014; 9 (1): E85436.
- James SJ, Melnyk S, Jernigan S, et al. The metabolic endophenotype and related genotypes are associated with oxidative stress in children with autism. am j med Genet B Neuropsychiatr Genet. 2006; 141b (8): 947-956.
- Ming X, Stein TP, Brimacombe M, Johnson WG, Lambert GH, Wagner GC. Increased excretion of a lipid peroxidation biomarker in autism. prostaglandins leukot essent fatty acids. 2005; 73 (5): 379-384.
- gan n, wu yc, brunet m, et al. Sulforaphan activates the heat shock reaction and strengthens proteasoma activity by highly regulating HSP27. JBIOLCHEM. 2010; 285 (46): 35528-35536.
- Stetler Ra, Gan Y, Zhang W, et al. Heat shock proteins: cellular and molecular mechanisms in the central nervous system. Prog Neurobiol. 2010; 92 (2): 184-211.
- Mehler MF, Purpura dp. Autism, fever, epigenetics and the Locus Coeruleus. brain res rev. 2009; 59 (2): 388-392.
- Curran LK, Newschaffer CJ, Lee LC, et al. Behavior in connection with fever in children with autism spectrum disorders. Pediatrics. 2007; 120 (6): E1386-E1392.
- bryant Re, hood af, hood, ce, koenig mg. Factors that influence the mortality of gram -negative rod bacteremia. Arch Intern. 1971; 127 (1): 120-1281.
- Mooran D. Workshop report: Fever and autism. Available around: (link removed). Accessed on November 21, 2014.
- d’Eufemia P, Celli M, Finocchiaaro R, et al. Abnormal intestinal permeability in children with autism. Acta Paediatr. 1996; 85 (9): 1076-1079.
- Volkmar FR, Nelson DS. Slide disorders in autism. j am Acad Child Adolesc Psychiatry. 1990; 29 (1): 127-129.
- Bradstreet JJ, Smith S, Baral M, Rossignol there. Biomarker-guided interventions in clinically relevant diseases in connection with autism spectrum disorders and attention deficit hyperactivity disorder. Alter Med Rev. 2010; 15 (1): 15-32.