Development, implementation and evaluation of anxiety management program for women under gynecological surgery with spinal anesthesia: a participatory action research based on the PARIHS framework.

Opioid use disorder (OUD) remains a major public health crisis in the US (; ). Among the various health consequences of chronic opioid misuse are metabolic sequelae, including weight gain, inflammation, and sugar liking, but these effects remain relatively understudied and findings are widely inconsistent (). A clearer characterizing of the metabolic alterations associated with OUD is important for improving treatment strategies and long-term health outcomes in individuals with OUD. Several lines of evidence link active opioid use to weight loss. In preclinical rodent models, mice and rats receiving twice-daily injection of escalating does of morphine (; ) and rats given unlimited access to heroin self-administration () consumed less food and exhibited significantly lower body weight compared to saline-treated controls. In concordance with these findings, human observational studies also associated illicit use of opioid within the past 5-years () and past-year OUD diagnosis () with lower body mass index (BMI) and lower prevalence of obesity. In qualitive interview with individuals in recovery from substance use disorders, including OUD, participants recalled loss of appetite and rarely eating during active addiction, resulting in severe weight loss (). However, participants reported weight gain during recovery (). Furthermore, while opioid agonists methadone and buprenorphine are highly effective medications for OUD (MOUDs) (; ), their use have been associated with significant weight gain (; ; ). In addition to body weight, MOUDs also appear to influence other aspects of metabolic health. For example, patients treated with methadone have higher rates of metabolic syndrome compared to those treated with buprenorphine (), and longer methadone exposure was associated with poorer metabolic profiles (; ). OUD- and treatment-related increases in body weight, specifically visceral fat mass, may contribute to the elevated risk of metabolic dysfunction in OUD (). White adipose tissue, the predominant fat depot in the body, is an endocrine organ that secretes adipokines regulating various metabolic and inflammatory processes. Increased adiposity facilitates a phenotypic switch in white adipose tissue, promoting a chronic state of low-grade inflammation (; ). As such, several cross-sectional clinical studies have demonstrated correlations between abdominal adiposity and markers of inflammation, including C-reactive protein (CRP) and cumulative inflammation index (; ). These findings were corroborated by a genetic study showing that individuals with single-nucleotide polymorphisms in adiposity-related genes, and , exhibited higher body mass index (BMI) and CRP levels, suggesting a causal link between adiposity and inflammation (). Chronic inflammation, in turn, contributes to various forms of metabolic dysfunction. In healthy volunteers, experimentally induced inflammation using low-dose lipopolysaccharide triggered immediate elevations in inflammatory markers (e.g., CRP), altered gene expression related to insulin receptor signaling, and decreased insulin sensitivity within 24 hours (). Furthermore, inflammation appears to play a role in dyslipidemia. For example, polymorphisms in the gene have been linked to susceptibility to dyslipidemia (). Moreover, cross-sectional analyses have positively associated higher CRP levels with increased low-density lipoprotein cholesterol (LDL-C), total cholesterol (Total-C), and triglyceride levels, and with lower high-density lipoprotein cholesterol (HDL-C) levels ().