Testing the use of helminth worm ova in treating autism spectrum disorders
Eric Hollander, M.D., Ph.D.
Albert Einstein College of Medicine, Montefiore Medical Center
Many findings support links between the brain dysfunction seen in autism spectrum disorders (ASD), neuroinflammation and a dysregulated immune response. The ‘hygiene hypothesis’ of autoimmune illness and ASD suggests that a lack of favorable gut parasites results in activation of proinflammatory cytokines, leading to symptoms of autism. This association between immune dysfunction and ASD suggests that immunomodulatory interventions may be a therapeutic option for treating ASD.
Eric Hollander and his colleagues at the Albert Einstein College of Medicine in New York aim to test the neuroimmune response in children and adults with ASD to treatment with Trichuris suis ova (TSO). TSO is a helminth worm treatment that is a new therapeutic approach to ASD with minimal side effects. It has been studied with success in other autoimmune disorders, including Crohn's disease and inflammatory bowel disease. Pilot studies of people with ASD who are highly resistant to standard treatment have demonstrated marked improvement with TSO.
Hollander and his team plan to complete a 28-week double-blind crossover study in ten adults and children with ASD. The researchers plan to first study the adults to establish the safety and efficacy of the TSO treatment protocol. The participants will receive 12 weeks of placebo and 12 weeks of TSO treatment (2,500 ova ingested by capsule every two weeks), with a four-week washout period in between.
The researchers plan to assess the effect of TSO versus placebo using outcome measures of aggression and irritability, repetitive behaviors, global functioning, social behavior and social cognition. In addition, they may use exploratory biomarkers such as immunological assays to explore the relationships among baseline clinical features, immune measures and response to treatment. If the outcome is positive, this research will support the existence of an immune-inflammatory mechanism underlying the febrile response in ASD.
