Prebiotic Treatment in People With Schizophrenia.

BACKGROUND: Preliminary evidence suggests that people with schizophrenia have decreased relative abundance of butyrate-producing bacteria in the gut microbiota. Butyrate plays a critical role in maintaining the integrity of the gut-blood barrier and has a number of anti-inflammatory effects. This proof-of-concept study was designed to assess whether the addition of the oligofructose-enriched inulin (OEI) prebiotic: Prebiotin could increase the production of butyrate. METHODS: Twenty-seven people who met the criteria for either Diagnostic and Statistical Manual of Mental Disorders, 5th Edition, schizophrenia or schizoaffective disorder were entered into a 10-day, double-blind, placebo-controlled, randomized clinical trial. The study was conducted on an inpatient unit to standardize the participant diet and environment. Participants were randomized to either OEI (4 g, 3 times a day) or a placebo (4 g of maltodextrin, 3 times a day). In order to assess the effect of OEI treatment on butyrate levels, participants underwent pretreatment and posttreatment OEI challenges. The primary outcome measure was relative change in postchallenge plasma butyrate levels after 10 days of OEI treatment. RESULTS: In both the intent-to-treat and completer analyses, OEI treatment was associated with a greater number of participants who met the OEI challenge responder criteria than those treated with placebo. OEI treatment was also associated with an increase in baseline butyrate levels (effect size for the group difference in the change of baseline butyrate levels was 0.58). CONCLUSIONS: We were able to demonstrate that treatment with the prebiotic OEI selectively increased the level of plasma butyrate in people with schizophrenia.Trial registration:ClinicalTrials.gov identifier NCT03617783.

Blinded Clinical Ratings of Social Media Data are Correlated with In-Person Clinical Ratings in Participants Diagnosed with Either Depression, Schizophrenia, or Healthy Controls.

This study investigates clinically valid signals about psychiatric symptoms in social media data, by rating severity of psychiatric symptoms in donated, de-identified Facebook posts and comparing to in-person clinical assessments. Participants with schizophrenia (N=8), depression (N=7), or who were healthy controls (N=8) also consented to the collection of their Facebook activity from three months before the in-person assessments to six weeks after this evaluation. Depressive symptoms were assessed in- person using the Montgomery-Åsberg Depression Rating Scale (MADRS), psychotic symptoms were assessed using the Brief Psychiatric Rating Scale (BPRS), and global functioning was assessed using the Community Assessment of Psychotic Experiences (CAPE-42). Independent raters (psychiatrists, non-psychiatrist mental health clinicians, and two staff members) rated depression, psychosis, and global functioning symptoms from the social media activity of deidentified participants. The correlations between in-person clinical ratings and blinded ratings based on social media data were evaluated. Significant correlations (and trends for significance in the mixed model controlling for multiple raters) were found for psychotic symptoms, global symptom ratings and depressive symptoms. Results like these, indicating the presence of clinically valid signal in social media, are an important step toward developing computational tools that could assist clinicians by providing additional data outside the context of clinical encounters.