Effects of Interventions Addressing School Environments or Educational Assets on Adolescent Sexual Health: Systematic Review and Meta-analysis.

CONTEXT: School-based interventions that aim to modify sexual health knowledge, attitudes and behaviors have mixed and often unsustained effects on adolescent sexual health outcomes. However, observational evidence suggests that broader school-related factors, such as school climate and academic attainment, can influence outcomes. METHODS: Nine databases were searched in July 2017 for randomized and quasi-experimental evaluations of interventions addressing school-level environment or student-level educational assets, to examine whether such interventions can promote young people's sexual health. Searches were limited to studies published since 1990 but were not restricted by language. Studies were assessed for risk of bias and synthesized narratively and meta-analytically. RESULTS: Searches yielded 11 evaluations, published from 1999 to 2016, of interventions related to school-level environment or student-level educational assets. Because of inconsistent reporting, the risk of bias was not clear for most studies, and meta-analysis was possible for only one outcome. The meta-analysis of three randomized trials provided some evidence that school-environment interventions may delay sexual debut (pooled odds ratio, 0.5). Narrative synthesis of the remaining outcomes found mixed results, but suggests that interventions addressing school-level environment may delay sexual debut and that those addressing student-level educational assets may reduce risk of pregnancy and STDs. CONCLUSIONS: Additional and more rigorous evidence is needed to assess the probability that interventions addressing school-related factors are effective and to provide better understanding of the mechanisms by which they may work to improve adolescent sexual health

Differential immune responses and microbiota profiles in children with autism spectrum disorders and co-morbid gastrointestinal symptoms

ObjectivesMany studies have reported the increased presence of gastrointestinal (GI) symptoms in children with autism spectrum disorders (ASD). Altered microbiome profiles, pro-inflammatory responses and impaired intestinal permeability have been observed in children with ASD and co-morbid GI symptoms, yet few studies have compared these findings to ASD children without GI issues or similarly aged typical developing children. The aim of this study was to determine whether there are biological signatures in terms of immune dysfunction and microbiota composition in children with ASD with GI symptoms.MethodsChildren were enrolled in one of four groups: ASD and GI symptoms of irregular bowel habits (ASDGI), children with ASD but without current or previous GI symptoms (ASDNoGI), typically developing children with GI symptoms (TDGI) and typically developing children without current or previous GI symptoms (TDNoGI). Peripheral blood mononuclear cells (PBMC) were isolated from the blood, stimulated and assessed for cytokine production, while stool samples were analyzed for microbial composition.ResultsFollowing Toll-Like receptor (TLR)-4 stimulation, the ASDGI group produced increased levels of mucosa-relevant cytokines including IL-5, IL-15 and IL-17 compared to ASDNoGI. The production of the regulatory cytokine TGFβ1 was decreased in the ASDGI group compared with both the ASDNoGI and TDNoGI groups. Analysis of the microbiome at the family level revealed differences in microbiome composition between ASD and TD children with GI symptoms; furthermore, a predictive metagenome functional content analysis revealed that pathways were differentially represented between ASD and TD subjects, independently of the presence of GI symptoms. The ASDGI also showed an over-representation of the gene encoding zonulin, a molecule regulating gut permeability, compared to the other groups.ConclusionsOverall our findings suggest that children with ASD who experience GI symptoms have an imbalance in their immune response, possibly influenced by or influencing metagenomic changes, and may have a propensity to impaired gut barrier function which may contribute to their symptoms and clinical outcome