Cortisol is a well-established biomarker of stress, assessed through salivary or blood samples, which are intrusive and time-consuming. Speech, influenced by physiological stress responses, offers a promising non-invasive, real-time alternative for stress detection. This study examined relationships between speech features, state anger, and salivary cortisol using a validated stress-induction paradigm.

Participants (N = 82) were assigned to cold (n = 43) or warm water (n = 39) groups. Saliva samples and speech recordings were collected before and 20 minutes after the Socially Evaluated Cold Pressor Test (SECPT), alongside State–Trait Anger Expression Inventory (STAXI) ratings. Acoustic features from frequency, energy, spectral, and temporal domains were analysed. Statistical analyses included Wilcoxon tests, correlations, linear mixed models (LMMs), and machine learning (ML) models, adjusting for covariates.

Post-intervention, the cold group showed significantly higher cortisol and state anger. Stress-related speech changes occurred across domains. Alpha ratio decreased and MFCC3 increased post-stress in the cold group, associated with cortisol and robust to sex and baseline levels. Cortisol–speech correlations were significant in the cold group, including sex-specific patterns. LMMs indicated baseline cortisol influenced feature changes, differing by sex. ML models modestly predicted SECPT group membership (AUC = 0.55) and showed moderate accuracy estimating cortisol and STAXI scores, with mean absolute errors corresponding to ∼ 24–38% and ∼16–28% of observed ranges, respectively.

This study demonstrates the potential of speech features as objective stress markers, revealing associations with cortisol and state anger. Speech analysis may offer a valuable, non-invasive tool for assessing stress responses, with notable sex differences in vocal biomarkers.

Extant literature indicated that glucagon-like peptide-1 (GLP-1) and glucagon-like peptide-1 receptor agonists (GLP-1 RAs) may potentially reduce risk of opioid overdose in persons with opioid use disorders (OUDs). Herein, we conducted a comprehensive synthesis of the effects of GLP-1 and GLP-1 RAs on OUDs.

We examined preclinical and clinical paradigms examining the effects of GLP-1 and GLP-1 RAs on OUD and OUD-associated behaviours (i.e. opioid self-administration, opioid-seeking behaviour). Relevant articles were retrieved from OVID (MedLine, Embase, AMED, PsychINFO, and JBI EBP Database), PubMed, and Web of Science from database inception to 1 May 2025. Primary studies (n = 10) examining the aforementioned effects associated with GLP-1 and GLP-1 RA administration were retrieved for analysis.

GLP-1 RAs (i.e. exenatide, liraglutide) reduced opioid-seeking behaviour (p < 0.05) and self-administration of opioid drugs (p < 0.05) in preclinical paradigms. In addition, results from human studies indicate that GLP-1 administration was associated with reducing the risk of opioid overdose in human studies (aIRR = 0.60, 95% CI [0.43, 0.83]).

GLP-1 RAs may affect opioid self-administration as well as the risk for overdose as evidenced by both preclinical and clinical data. There is a need for adequate well-controlled studies to determine whether GLP-1 RAs may provide clinically meaningful improvement and risk reduction in persons living with OUDs.