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Proceedings of the National Academy of... Jan 2024Social anxiety disorder (SAD) is a crippling psychiatric disorder characterized by intense fear or anxiety in social situations and their avoidance. However, the...
Social anxiety disorder (SAD) is a crippling psychiatric disorder characterized by intense fear or anxiety in social situations and their avoidance. However, the underlying biology of SAD is unclear and better treatments are needed. Recently, the gut microbiota has emerged as a key regulator of both brain and behaviour, especially those related to social function. Moreover, increasing data supports a role for immune function and oxytocin signalling in social responses. To investigate whether the gut microbiota plays a causal role in modulating behaviours relevant to SAD, we transplanted the microbiota from SAD patients, which was identified by 16S rRNA sequencing to be of a differential composition compared to healthy controls, to mice. Although the mice that received the SAD microbiota had normal behaviours across a battery of tests designed to assess depression and general anxiety-like behaviours, they had a specific heightened sensitivity to social fear, a model of SAD. This distinct heightened social fear response was coupled with changes in central and peripheral immune function and oxytocin expression in the bed nucleus of the stria terminalis. This work demonstrates an interkingdom basis for social fear responses and posits the microbiome as a potential therapeutic target for SAD.
Topics: Humans; Animals; Mice; Phobia, Social; Gastrointestinal Microbiome; Oxytocin; RNA, Ribosomal, 16S; Fear; Anxiety
PubMed: 38147649
DOI: 10.1073/pnas.2308706120 -
Journal of Physiotherapy Jul 2023How much are the reductions in pain intensity and improvements in physical function from Pilates exercise mediated by changes in pain catastrophising and kinesiophobia? (Randomized Controlled Trial)
Randomized Controlled Trial
Pain catastrophising and kinesiophobia mediate pain and physical function improvements with Pilates exercise in chronic low back pain: a mediation analysis of a randomised controlled trial.
QUESTION
How much are the reductions in pain intensity and improvements in physical function from Pilates exercise mediated by changes in pain catastrophising and kinesiophobia?
DESIGN
This was a secondary causal mediation analysis of a four-arm randomised controlled trial testing Pilates exercise dosage (once, twice or thrice per week) against a booklet control.
PARTICIPANTS
Two hundred and fifty-five people with chronic low back pain.
DATA ANALYSIS
All analyses were conducted in R software (version 4.1.2) following a preregistered analysis plan. A directed acyclic graph was constructed to identify potential pre-treatment mediator-outcome confounders. For each mediator model, we estimated the intervention-mediator effect, the mediator-outcome effect, the total natural indirect effect (TNIE), the pure natural direct effect (PNDE), and the total effect (TE).
RESULTS
Pain catastrophising mediated the effect of Pilates exercise compared with control on the outcomes pain intensity (TNIE MD -0.21, 95% CI -0.47 to -0.03) and physical function (TNIE MD -0.64, 95% CI -1.20 to -0.18). Kinesiophobia mediated the effect of Pilates exercise compared with control on the outcomes pain intensity (TNIE MD -0.31, 95% CI -0.68 to -0.02) and physical function (TNIE MD -1.06, 95% CI -1.70 to -0.49). The proportion mediated by each mediator was moderate (21 to 55%).
CONCLUSION
Reductions in pain catastrophising and kinesiophobia partially mediated the pathway to improved pain intensity and physical function when using Pilates exercise for chronic low back pain. These psychological components may be important treatment targets for clinicians and researchers to consider when prescribing exercise for chronic low back pain.
Topics: Humans; Low Back Pain; Exercise Movement Techniques; Mediation Analysis; Chronic Pain; Kinesiophobia; Exercise Therapy
PubMed: 37277290
DOI: 10.1016/j.jphys.2023.05.008