Xiaoqiang Liu

Glycemic control plays a crucial role in the outcomes of acute pancreatitis (AP), yet traditional glucose metrics have shown limited prognostic value. This study investigates the association between mean glucose area under the curve (AUC) and mortality outcomes in AP patients. We conducted a retrospective cohort study of 1085 intensive care unit patients with AP using data from the Medical Information Mart for Intensive Care IV database. Patients were stratified into tertiles based on mean glucose AUC. Multivariable Cox regression and restricted cubic spline analyses were employed to assess the relationship between mean glucose AUC and mortality outcomes. Predictive performance was quantified using receiver operating characteristic curve analysis, and robustness was further tested through comprehensive subgroup and sensitivity analyses. A higher mean glucose AUC was significantly associated with increased mortality risk. In the fully adjusted model, the hazard ratio for in-hospital mortality was 1.10 (95% confidence interval: 1.08–1.12; P < .001). Compared with the lowest tertile, patients in the highest tertile demonstrated an 11.12-fold increased mortality risk (95% confidence interval: 5.78–21.41; P < .001). Mean glucose AUC showed superior discriminative capacity for predicting in-hospital mortality (AUC = 0.783) compared with other glucose metrics. The association remained robust across various subgroups and sensitivity analyses. Mean glucose AUC serves as a powerful, independent predictor of in-hospital mortality in AP patients. This novel metric outperforms conventional glucose parameters in prognostic accuracy, suggesting its potential utility in clinical risk stratification and treatment optimization.

Objectives: Gastroesophageal reflux disease (GERD) is a common chronic digestive disorder, and diet is an important modifiable risk factor. The Dietary Index for Gut Microbiota (DI-GM) reflects dietary patterns considered favorable to the gut microbiota; however, the gut microbiome itself was not measured, and evidence on whether DI-GM is associated with GERD risk is limited. We aimed to evaluate the association between DI-GM and incident GERD and to explore potential intermediate pathways using mediation analysis and plasma proteomics. Methods: We included 133,915 UK Biobank participants free of GERD at baseline. DI-GM scores (range 0–14) were calculated from the Oxford WebQ 24-h dietary recall and grouped into four categories (0–3, 4, 5, ≥6). Incident GERD was identified from the UK Biobank first-occurrence records (ICD-10 K21). Cox proportional hazards regression was complemented by restricted cubic spline (RCS), subgroup, and Cox weighted quantile sum (WQS) analyses, counterfactual mediation analysis, integrated plasma proteomics (Olink Explore 3072), and a range of sensitivity analyses. Results: During a median follow-up of 13.6 years, 12,271 incident GERD cases occurred. In the fully adjusted model, each 1-point increase in DI-GM was associated with an approximately 4% lower hazard of GERD [hazard ratio (HR) 0.956, 95% CI 0.947–0.965; P < 0.001], and the highest DI-GM group (≥6) had a lower hazard than the lowest (0–3) (HR 0.812, 95% CI 0.774–0.851; P for trend < 0.001). RCS analysis showed a modest inverse dose–response relationship that was most apparent at higher DI-GM scores, and WQS analysis indicated that the association was driven by a few key components rather than shared equally across the index. BMI (proportion mediated 21.43%) and phenotypic age acceleration (7.53%) both significantly mediated the association (both P < 0.001). Integrated proteomic analysis identified 13 shared proteins; the nine positively associated with DI-GM and inversely associated with GERD showed exploratory enrichment in neurodevelopment- and cell-adhesion-related processes. Conclusions: Higher DI-GM was associated with a lower incidence of medically attended GERD, with mediation analysis suggesting that BMI and biological aging may partly account for this association. Exploratory proteomic analyses identified shared protein correlates, including adiposity-related and, tentatively, neurodevelopment- and cell-adhesion-related proteins; these are hypothesis-generating and require confirmation. Because the gut microbiome was not measured, the diet–microbiota link remains inferential, and these findings should be interpreted as associations rather than established mechanisms.

Obesity is linked to gut microbiota dysbiosis, and diet is a key determinant influencing the gut microbiome. This study examined the association between a newly proposed Dietary Index for Gut Microbiota (DI-GM) and obesity in the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2020. A total of 41,159 adults aged ≥ 20 years were included, with 15,327 individuals classified as obese (BMI ≥ 30 kg/m²) and 25,832 as living without obesity. DI-GM comprises 13 components deemed either beneficial or unfavorable to the gut microbiome, yielding a total score ranging from 0 to 13. Weighted logistic regression assessed the relationship between DI-GM (continuous and categorical) and obesity, adjusting for demographic and lifestyle factors plus comorbidities. Restricted cubic spline, stratified analyses, multiple imputation, and propensity score matching were also performed. Participants with obesity had a significantly lower mean DI-GM score than those without obesity (4.32 vs. 4.65, P < 0.001). Each 1-point increase in DI-GM was associated with 13% lower obesity odds (OR = 0.87, 95% CI: 0.85-0.88) in the crude model, remaining robust (OR = 0.88, 95% CI: 0.87-0.90, P < 0.001) after full adjustment. Higher DI-GM scores were linearly linked to lower odds of obesity, supported by multiple imputation and propensity score matching (P < 0.001). In this nationally representative U.S. population, a more microbiota-oriented diet, as proxied by higher DI-GM scores, was independently associated with lower odds of obesity. Prospective and randomized trials are warranted to verify causality and investigate underlying mechanisms.

Background: Portal vein diameter (PVD) is an important and objective marker of portal pressure and may be associated with the risk of recurrent esophagogastric variceal bleeding (EGVB) in patients with cirrhosis. However, the specific relationship between the two has not been clearly established. This study aims to investigate the association between PVD and the risk of recurrent EGVB in patients with cirrhosis. Methods: This study used a retrospective cohort design, including 1223 patients with cirrhosis discharged from Quanzhou First Hospital between January 2014 and December 2018. After applying inclusion and exclusion criteria, a total of 247 patients (179 males and 68 females) were included in the analysis. Portal vein diameter (PVD, in mm) was measured using standardized abdominal ultrasound or CT scans. EGVB events were confirmed by endoscopic diagnosis. The association between PVD and recurrent EGVB was assessed using a multivariate logistic regression model, adjusting for age, gender, etiology of cirrhosis, comorbidities, Child-Pugh classification, portal vein thrombosis (PVT), and laboratory indicators (such as platelet count, albumin, and coagulation function parameters). Stratified analyses and interaction tests were further conducted to verify the robustness of the results. Results: The incidence of recurrent EGVB increased significantly with an increase in PVD (trend test P =0.023). The multivariate-adjusted model showed that for every 1 mm increase in PVD, the risk of recurrent EGVB increased by 19% (HR=1.19, 95% CI: 1.01-1.40, P =0.039). Stratified analysis indicated that the risk was particularly significant when PVD>14 mm (adjusted HR=3.61, P =0.022). Subgroup analysis showed that, apart from an interaction between age and PVD (interaction P 0.05). Conclusions: An increased portal vein diameter is an independent risk factor for recurrent EGVB in patients with cirrhosis, with a particularly significant increase in risk when PVD>14 mm. Monitoring changes in PVD can provide an important basis for clinical identification of high-risk patients and optimization of portal hypertension management, thereby reducing the incidence of recurrent bleeding events.

Aging is closely linked to chronic diseases, and gut microbiota plays a significant role in this process. The Dietary Index for Gut Microbiota (DI-GM), a novel tool reflecting the potential impact of diet on gut microbiota diversity, has an unclear association with biological aging. This study aimed to evaluate the association between DI-GM and phenotypic age acceleration (PAA), revealing the potential regulatory effect of diet on aging. Data from 29,435 participants in NHANES 1999–2018 were analyzed using multivariable regression models to assess the association between DI-GM scores and PAA. Phenotypic age was estimated from 10 physiological indicators, with PAA defined as a positive age acceleration residual (ACR). DI-GM was constructed from 14 dietary components; higher scores indicate greater potential benefits to gut microbiota. Higher DI-GM scores were significantly associated with a lower risk of PAA. After adjusting for covariates, each 1-point increase in DI-GM was linked to a 7% reduction in PAA risk (OR = 0.93, 95% CI = 0.91–0.95, P < 0.001) and a decrease of 0.33 in ACR (β = -0.33, 95% CI = -0.39 to -0.26, P < 0.001). Subgroup and sensitivity analyses confirmed these findings. Higher DI-GM scores are significantly associated with reduced phenotypic age acceleration. Dietary improvements that promote gut microbiota health may effectively delay aging, providing scientific evidence for dietary interventions aimed at healthy aging.

Objective: The relationship between constipation and anxiety remains underexplored. This study investigates the association between constipation and anxiety in a representative sample of adults in the United States.Methods: A cross-sectional analysis was conducted using data from the National Health and Nutrition Examination Survey (NHANES) from 2007 to 2010, including 9,126 adults aged ≥20 years. Constipation and anxiety were assessed using standardized survey instruments. Multivariable logistic regression models were employed to calculate adjusted odds ratios (ORs), and subgroup and sensitivity analyses were performed to validate the findings. Additionally, Mendelian randomization (MR) was employed to assess the potential causal relationship between constipation and anxiety using genetic data from large GWAS datasets.Results: Of the 9,126 participants, 324 reported constipation (prevalence: 3.6%), and 2,424 reported anxiety (prevalence: 26.6%). Anxiety prevalence was significantly higher in individuals with constipation compared to those without (41.4% vs. 26.0%; P < 0.001). After adjusting for demographic, socioeconomic, lifestyle, and comorbid factors, constipation remained independently associated with anxiety (adjusted OR: 1.33, 95% CI: 1.02–1.73; P = 0.038). Subgroup analyses revealed no significant interactions. Sensitivity analyses, including multiple imputations, weighted analysis, and propensity score matching, corroborated the robustness of the results. MR analysis, however, revealed no significant causal association between constipation and anxiety.Conclusion: This study identifies a significant association between constipation and anxiety in a large, nationally representative cohort. While the association remains robust after adjusting for various factors, MR did not provide evidence for a causal relationship. Clinicians should consider evaluating and addressing anxiety symptoms as part of a comprehensive management strategy for patients presenting with constipation.

Objectives: The global prevalence of diabetes is continuously rising, and the gut microbiota is closely associated with it. The Dietary Index for Gut Microbiota (DI-GM) assesses the impact of diet on the microbiota, but its association with diabetes risk remains unclear. This study aims to investigate the association between DI-GM and the risk of diabetes and analyze the mediating roles of phenotypic age and body mass index (BMI).Methods: Utilizing data from the National Health and nutrition examination survey (NHANES) 1999–2018, we included 17,444 adults aged 20 years and older. DI-GM (score range: 0–13) was calculated based on dietary recall. Diabetes was diagnosed based on laboratory results and self-reported information. Multivariable logistic regression was used to analyze the association between DI-GM and diabetes, adjusting for relevant covariates. Mediation analysis evaluated the roles of phenotypic age and BMI.Results: After adjusting for confounders, higher DI-GM scores were significantly associated with a lower risk of diabetes (OR = 0.93, 95% CI = 0.90–0.96, p < 0.001). Compared to the group with DI-GM scores of 0–3, those with scores of 5 (OR = 0.76, 95% CI = 0.67–0.86) and ≥ 6 (OR = 0.77, 95% CI = 0.68–0.88) had significantly reduced diabetes risk. Phenotypic age and BMI accounted for 41.02 and 25.57% of the association between DI-GM and diabetes, respectively.Conclusion: Higher DI-GM scores are associated with a lower risk of diabetes, partially mediated through reduced phenotypic age and BMI.

Objective: This study investigates the association between phenotypic age acceleration (PAA) and all-cause and cause-specific mortality in obese individuals.Methods: Data were drawn from the National Health and Nutrition Examination Survey (NHANES) between 1999 and 2018, including 9,925 obese adults (BMI ≥ 30 kg/m²). PAA, defined as phenotypic age exceeding chronological age, was assessed using clinical biomarkers. Kaplan-Meier survival analysis and Cox proportional hazards models were used to assess the relationship between PAA and all-cause, cardiovascular, and cancer mortality, adjusting for covariates such as age, gender, race, lifestyle, and health status. Subgroup and sensitivity analyses were performed to ensure the robustness of the findings.Results: During a median follow-up of 10.6 years, 1,537 deaths were recorded, including 419 from cardiovascular disease and 357 from cancer. PAA was significantly associated with all-cause mortality (HR = 1.84, 95% CI: 1.64–2.06), cardiovascular mortality (HR = 1.86, 95% CI: 1.50–2.31), and cancer mortality (HR = 1.47, 95% CI: 1.17–1.85). These associations remained significant after adjusting for multiple variables, and sensitivity analyses confirmed the robustness of the results.Conclusion: PAA is an independent predictor of all-cause, cardiovascular, and cancer mortality in obese individuals. This study highlights the importance of PAA in mortality risk assessment and health management in the obese population.