Individuals with low sexual frequency often experience comorbidities that exacerbate mortality. This article evaluates the predictive value of five body fat anthropometric indicators for all-cause mortality and explores the interaction between obesity and depression in mortality among young and middle-aged individuals with sexual frequency <12 times per year.

This study included participants with a sexual frequency of <12 times per year from the 2015-2016 National Health and Nutrition Examination Survey (NHANES). We assessed the impact of anthropometric indicators and depression on mortality, as well as their synergistic interactions, and further developed an accessible predictive survival model.

A total of 4978 participants aged 20-59 were included, with 215 deaths (4.3 %) over 15 years of follow-up. A Body Shape Index (ABSI) showed the strongest association with all-cause mortality, with an AUC of 0.67. Participants with ABSI ≥0.082 had a significantly higher risk of death (HR: 1.87, 95%CI: 1.31-2.68), as did those with depression (HR: 1.86, 95%CI: 1.19-2.92). Interaction analysis revealed a synergistic effect between depression and ABSI, increasing death risk by 293 % when both were present. Significant survival differences were observed between men and women with these risk factors, with median survival rates of 76.3 % and 90.8 %, respectively. The model based on ABSI and depression provided valuable mortality predictions, with AUC of 0.78, 0.77, and 0.77 for 3-year, 5-year, and 10-year survival.

ABSI and depression are associated with all-cause mortality in individuals with low sexual frequency, potentially creating a synergistic effect on mortality risk.

Despite excellent weight-loss outcomes in clinical trials, Glucagon-Like Peptide 1 receptor agonists (GLP1RA) face challenges with accessibility and compliance in clinical use. We seek to quantify how these barriers impact the long-term weight-loss efficacy of GLP1RAs in the real world.

In this retrospective cohort study, we analysed weight loss outcomes of patients who were prescribed GLP1RA for class 2-3 obesity treatment between January 2020 and November 2022 in a large non-profit healthcare system in the Midwest. The primary outcome is the two-year total weight loss percentage (TWL%).

During the study period, there was a six-fold growth in GLP1RA prescription numbers. In total, 853 patients were prescribed GLP1RA for obesity treatment. Of these, 211 (24.7%) patients never received the drug and 304 (35.6%) patients had to discontinue treatment within 2 years. The most common reasons for discontinuation included loss to follow-up with the original prescriber (n = 81, 26.6%), side effects (n = 72, 23.7%) and cessation of insurance coverage (n = 65, 21.4%). Two years later, patients who stayed on GLP1RA experienced significantly more weight loss than those who never started it (difference 3.98%, 95% CI 1.57% to 6.41%, p = 0.001) and those who had stopped taking it (difference 5.82%, 95% CI 3.56% to 8.09%, p < 0.001). Patients who stopped GLP1RA within 2 years had similar weight loss to those who never started it (difference 1.83%, 95% CI -1.30% to 4.97%, p = 0.251). The average TWL% for patients who stayed on GLP1RA for 2 years is 9.22% (standard deviation 9.73%).

Nearly half of the patients who were started on GLP1RA, a treatment intended for indefinite use, stopped taking GLP1RA within 2 years. Patients who stopped treatment experienced similar weight loss to those who never started treatment. For real-world patients who stayed on treatment for 2 years, a lower TWL% was observed than previously reported in clinical trials.

The body mass index (BMI), as an easy-to-calculate measure of body fatness, is closely associated with all-cause mortality, but few studies with a large enough scale have examined the relationship between BMI and quality of life. A comprehensive and precise insight into a new range is needed.

Based on the ChinaHEART (Health Evaluation And risk Reduction through nationwide Teamwork), a nationwide, population-based cohort study, 4,485,773 participants living in 20,159 communities or villages were passively followed for death records, through a linkage of data with the National Mortality Surveillance System and Vital Registration. Firstly, we conducted Cox proportional-hazards regression models to assess the hazard ratios (HRs) of BMI on the risk of all-cause and cause-specific mortality. Secondly, we used logistic regression models to examine associations between BMI and health-related quality of life (HRQL). Fully adjusted models were adjusted for age, sex, annual household income, occupation, education level, marriage, medical insurance, urbanity, tobacco smoking, alcohol consumption and the history of hypertension, diabetes mellitus, dyslipidaemia and cardiovascular disease (CVD).

Among the 4 485 773 included participants with an average age of 56.4 ± 10.0 years, 59.0% were female. During the follow-up period, which had a median duration of 5.3 years, a total of 142 004 cases of all-cause mortality were confirmed. After adjusting for participant characteristics and lifestyles, we observed the U-shaped association between BMI and all-cause mortality with an inflection of 26-27 kg/m2, and the estimated HR per 1 kg/m2 increase in BMI was 0.92 (95% CI 0.92-0.93) and 1.03 (95% CI 1.03-1.04) below and above the turning point, respectively. An inverted J-shape pattern between BMI and HRQL with a peak of 22-23 kg/m2 was found, in which the odd ratio per 1 kg/m2 increase in BMI was 0.98 (95% CI 0.98, 0.99) below 22-23 kg/m2 and 1.03 (95% CI 1.03-1.03) above this point.

We found distinct ranges of BMI for minimized mortality risk and maximized HRQL. The BMI range corresponding to the HRQL is lower than the BMI range corresponding to the lowest risk of death generally. Therefore, it is worth considering how to define the new recommended range for a new BMI based on the goal of 'living a longer and healthier life'.

The aims of the study were to develop and validate WHOLISTIIC, a data-driven cluster analysis for identifying anthropometric metabolic subtypes.

K-means cluster analysis was performed in 397 424 UK Biobank participants based on five domains, that is, central obesity (waist-to-height ratio), general obesity (body mass index [BMI]), limb strength (handgrip strength), insulin resistance (triglyceride to high-density lipoprotein cholesterol [HDLc] ratio) and inflammatory condition (neutrophil-to-lymphocyte ratio). Replication was done in the NHANES. Cox proportional hazards regression models were used to estimate the associations of clusters with incident adverse health outcomes.

Six replicable clusters were identified. Compared with individuals in cluster 1 (lowest BMI with preserved handgrip strength), individuals in cluster 2 (highest handgrip strength) were not at increased risk of all-cause mortality despite higher BMI, but had small yet significant increased risks of cardiovascular mortality, incident major adverse cardiovascular events (MACE), chronic renal failure and decreased risks of mortality due to respiratory disease, as well as incident dementia; individuals in cluster 3 (lowest handgrip strength and borderline elevated BMI), cluster 4 (highest triglyceride-to-HDLc ratio and moderately elevated BMI), cluster 5 (highest neutrophil-to-lymphocyte ratio and borderline elevated BMI) and cluster 6 (highest BMI) had substantially increased risks of all-cause, cardiovascular, and cancer mortality, incident MACE and chronic renal failure. The associations of anthropometric clusters with the risk of mortality were replicated in the NHANES cohort.

Anthropometric metabolic subtypes identified with easily accessible parameters reflecting multifaceted pathology of overweight and obesity were associated with distinct risks of long-term adverse health outcomes.

This study reviews the mechanisms by which obesity affects the development and progression of breast cancer (BC). The association between obesity and BC is mainly due to three aspects: disruption of glycolipid metabolism, abnormal cell function and imbalance of adipokine levels. The dysregulation of glycolipid metabolism caused by obesity, including the accumulation of cholesterol and fatty acids and the reprogramming of glucose metabolism, promotes the growth and invasion of tumour cells. Obesity triggers multiple cellular abnormalities, particularly in lipid-associated macrophages and cancer-associated adipocytes, which promote tumour progression and immunosuppression by secreting inflammatory factors and various fatty acids into the tumour microenvironment. Obesity leads to an imbalance in the expression of several adipokines. Leptin upregulation is closely associated with BC metastasis and resistance to endocrine therapy, while reduced adiponectin levels attenuate the protective effect. At the same time, chronic inflammation and insulin resistance not only further increase the risk of BC, but also exacerbate tumour resistance. In terms of treatment, weight-loss drugs and metformin can improve the efficacy of obesity-related BC treatment to some extent. Intervention strategies targeting adipose tissue remodelling, lipid metabolism and leptin regulation also show potential clinical value, but more research is needed to clarify their safety and efficacy. This review provides systematic ideas and references for research into the mechanisms and clinical management of obesity-related BC.

The Body Rounds Index (BRI) is an anthropometric indicator specifically developed to evaluate an individual's obesity level, particularly emphasizing central or abdominal obesity. This study aimed to explore the relationship between BRI and all-cause mortality in older U.S. adults. The research sample comprised individuals aged 65 and older from the National Health and Nutrition Examination Survey (NHANES), eligible for mortality analyses between 1999 and 2018. We utilized Cox regression analyses, restricted cubic spline (RCS), threshold effects analysis, Kaplan-Meier curves, and subgroup analyses were conducted to assess how the BRI correlates with all-cause mortality among older adults in the U.S. To further ensure the robustness of our findings, we conducted sensitivity analyses. Among 5371 U.S. older adults (age ≥ 65), with an average age of 72.45 (standard deviation [SD]:5.65) years, 2884 (60%) were women. During the follow-up period, there were 2781 deaths from all causes among the 5371 participants. After adjusting for all covariates, a U-shaped association was identified between BRI and the all cause mortality. Compared to a BRI of less than 4.457, a BRI between 4.457 and 5.538 was associated with a 19% reduction in the likelihood of mortality from any cause (HR = 0.81, 95% CI = 0.69-0.95). A BRI between 5.538 and 6.888 was linked to a 8% reduction in mortality risk (HR = 0.92, 95% CI = 0.79-1.07), while a BRI exceeding 6.888 showed a 1% increase in this risk (HR = 1.01, 95% CI = 0.87-1.17). RCS analysis indicated a U-shaped relationship between BRI and all-cause mortality. The turning point was located at 4.546, with correlations observed both before and after this point. This NHANES-based study highlights the U-shaped relationship between BRI and all-cause mortality among U.S. older adults, suggesting that the BRI has predictive value for mortality outcomes. The findings offer compelling support for utilizing BRI as a non-invasive mortality risk screening tool.

Fat-to-muscle mass ratio (FMR) has been considered a potentially useful indicator for assessing disease risk. However, the association between FMR and risk of death remains inconclusive.

This work aimed to investigate the associations of FMR (the whole body, trunk, legs, and arms) with all-cause and cause-specific mortality by sex.

A total of 337 951 participants from the UK Biobank were included. Fat mass and muscle mass were estimated using a bioelectrical impedance assessment device. Cox proportional-hazard regression was applied to explore the associations.

During a median follow-up of 12.58 years, we recorded 22 391 (6.62%) deaths, of which 4427 were from cardiovascular disease, 11 740 from cancer, and 1458 from respiratory disease. We observed associations of different shapes (U-shaped for whole body and trunk, L-shaped for legs, and J-shaped for arms) between FMR and all-cause mortality (P for nonlinearity <.001). Compared with the lowest quintile of whole body and trunk FMR, the all-cause mortality risk was reduced by 12% to 14% and 7% to 15% in men and women in quintiles 2 to 4, respectively. The hazard ratio (HR) associated with arm FMR in men and leg FMR in men and women (quintile 5 vs 1) were 1.14 (95% CI, 1.05-1.23), 0.76 (0.71-0.82), and 0.78 (0.70-0.88) for all-cause mortality, respectively. The associations between FMR and cause-specific mortality were mostly similar to those for all-cause mortality.

Our study revealed statistically significant associations of total and regional FMR with mortality, providing new evidence that FMR may be a potentially useful indicator for assessing mortality risk.

This study examines how weight-adjusted waist index (WWI) correlates with the occurrence of migraine in U.S. adults.

Being overweight significantly increases the likelihood of experiencing migraines; nonetheless, conventional metrics like waist circumference (WC) and body mass index (BMI) might not completely capture the level of migraine risk tied to obesity. WWI integrates the strengths of WC while minimizing its correlation with BMI, which might make it a more accurate indicator of central obesity-related migraine susceptibility.

This study performed a cross-sectional analysis using data from 9,688 participants obtained from the National Health and Nutrition Examination Survey (NHANES), covering the years 1999-2004. Migraine occurrence was evaluated through questionnaires, and participants' WWI was computed. Weighted multivariable logistic regression models were used to examine the association between WWI and migraines. Restricted cubic splines (RCS) were applied to evaluate the dose-response relationship between WWI and migraines. Furthermore, interaction tests and subgroup analyses were executed. The receiver operating characteristic (ROC) curve, paired with DeLong et al.'s test, was employed to compare the predictive power of WWI, BMI, and WC for migraines.

The overall prevalence of migraines was found to be 21.50% (weighted population: 31,888,075 out of 148,278,824). In Model 3, the link between WWI and migraines in women showed no statistical significance (OR = 0.94, 95% CI: 0.82-1.07). In this model, each unit increase in WWI among men was linked to a 22% higher risk of migraines (OR = 1.22, 95% CI: 1.05-1.42). When stratified by quintiles, individuals in the third quintile (Q3) displayed a 69% higher likelihood of experiencing migraines compared to those in the first quintile (Q1) (OR = 1.69, 95% CI: 1.19-2.40), with a significant inflection point observed at 10.95 cm/√kg. Significant interactions were noted among various age groups (p for interaction = 0.018). WWI demonstrated a stronger predictive capability for migraine compared to BMI and WC.

A U-shaped positive correlation of WWI with migraines was observerd among adult males in the U.S., while no significant correlation was found in females. Within the context of BMI and WC, WWI exhibited a superior predictive capacity for migraines.

In recent years, there have been significant changes in the lifestyle and dietary habits of the population characterized by an increased intake of high-calorie food and a sedentary lifestyle without physical activity. The increased prevalence of overweight and obesity has led to metabolic dysfunction and related complications, such as cardiovascular disease and chronic kidney disease. The purpose of this review is to highlight the importance, clinical features, and pathogenesis of metabolic dysfunction-associated kidney disease (MDAKD). MDAKD is a term that describes kidney disease arising from metabolic dysfunction, often in the context of metabolic syndrome, and is characterized by the presence of chronic kidney disease in individuals with metabolic abnormalities such as obesity, insulin resistance, diabetes mellitus, dyslipidemia, and hypertension. MDAKD includes diabetic kidney disease, obesity-related kidney disease, and, increasingly, other less common kidney diseases where metabolic dysfunction may affect disease progression. MDAKD is part of a spectrum of diseases whose pathogenesis is driven by metabolic dysfunction and has recently led to the proposal of a new nomenclature including metabolic dysfunction-associated steatotic liver disease and cardio-kidney-metabolic syndrome. The new terminology of MDAKD places additional emphasis on the pathogenic role of metabolic dysfunction in kidney disease.

The purpose of this study was to examine potential differences in body mass index (BMI), relative adiposity (%Fat), and body dissatisfaction (BD) between heterosexual (HSW) and sexual minority women (SMW). Young adult women (n = 84; 23.8% SMW; 21.9 ± 3.8 years) were included in our analysis. %Fat was assessed using a four-compartment model. BD was assessed using the Body Shape Questionnaire (BSQ), the BD subscale of the Eating Disorders Inventory Questionnaire (EDI-BD), the appearance evaluation subscale of the Multidimensional Body Self-Relations Questionnaire (MBSRQ-AE), and the Photographic Figure Rating Scale (PFRS). Potential differences in BMI, %Fat, and BD between sexual orientation groups were assessed using independent samples t-tests. Bivariate correlations were assessed using Pearson's r. No differences in BMI or BD were observed between groups (all p > .05). Higher %Fat was observed in SMW when compared to HSW (p = .046), and higher %Fat was associated with higher BSQ (r = .364), EDI-BD (r = .388), lower MBSRQ-AE (r = .388), and PFRS (r = .521), collectively indicating greater BD. %Fat was higher in SMW, and higher %Fat was associated with greater BD, regardless of sexual orientation. These results suggest that SMW tend to have higher %Fat than heterosexual counterparts which would increase their risk of negative health outcomes.

GLP-1 and GIP-GLP-1 agonists have emerged as potent weight-loss medications. These incretin mimetics often have low patient adherence, and as with any medication, clinically meaningful efficacy requires adequate adherence. But what constitutes "adequate" adherence for incretin mimetics? The purpose of this paper is to address this question.

We use mathematical modelling and stochastic simulation to investigate the weight loss efficacy of incretin mimetics under imperfect adherence. We use validated pharmacokinetic and pharmacodynamic models of semaglutide and tirzepatide and assume that simulated patients randomly miss doses.

We find that semaglutide and tirzepatide forgive nonadherence, meaning that strong weight loss efficacy persists despite missed doses. For example, taking 80% of the prescribed doses yields around 90% of the weight loss achieved under perfect adherence. Taking only 50% of the prescribed doses yields nearly 70% of the weight loss of perfect adherence. Furthermore, such nonadherence causes only small fluctuations in body weight, assuming that patients do not typically miss more than several consecutive doses.

Incretin mimetics are powerful tools for combating obesity, perhaps even if patients can consistently take only half of their prescribed doses. The common assumption that significant weight loss requires at least 80% adherence needs revision.

Diabetes, affecting 18.3% of young adults in Mexico (6), is influenced by both genetic factors and shared unhealthy habits within families.

To determine the metabolic abnormalities in relatives of people with T2D, stratified by body mass index.

This observational, descriptive study was conducted at the Center for Comprehensive Care for Patients with Diabetes (CAIPaDi). The study involved relatives of participants with type 2 diabetes mellitus (T2DM), recruited between June 2017 and December 2020. The relatives were people without diabetes, including spouses, siblings, offspring, or close family members aged 18 to 65 who spent over four days a week with the patient. Exclusion criteria included relatives diagnosed with diabetes, smokers, or any individual from a patient-relative pair that was excluded. All participants underwent laboratory tests and body measurements. Relatives were classified into three groups based on body weight: normal weight, overweight, and obesity. The relatives attended four monthly visits and then annual evaluations. Ethical approval was obtained.

The study enrolled 220 relatives of people with T2DM, 69% women, median age 49±12 years; 19.5% with normal weight, 40.4% overweight, and 40% with obesity. Prediabetes (39.4%), dyslipidemia (67.2%), and abnormal liver function tests (32.2%) were prevalent. Higher levels of triglycerides and LDL cholesterol were associated with increased risk for comorbid conditions. Anxiety and depression showed no significant differences across weight categories.

These results highlight the importance of overweight and obesity as factors associated with the presence of comorbidities and the metabolic syndrome. It is essential to implement strategies to promote healthy habits among family members of people with diabetes, especially in those who are overweight or obese to reduce the risk of developing future metabolic and cardiovascular diseases.

The March of Dimes Global action report indicated that preterm birth (PTB) rates are increasing in most countries. It is the most important cause of neonatal deaths and the second leading cause of death in children under age 5. Literature reporting the relationship between maternal pre-pregnancy body mass index (BMI) and PTB has previously yielded inconsistent conclusions. Our objective is to fill in the knowledge gap by evaluating the interaction of socio-economic status (SES) and BMI and its relationship to the rate of PTB. This is a case control study using the Natality Data of the National Vital Statistics System from the years 2020-2022. BMI was a significant factor in PTB for lower socioeconomic status (LSES) women. For every increase in BMI, there was a decrease in the probability of PTB (OR = 0.923, 95% CI 0.915-0.931, P < 0.001). Those who were LSES also had a curved relationship with PTB indicating that the as BMI increases, the odds of PTB decreases up until a BMI value, then the PTB rate increases. This relationship was not found in higher economic status women. Our study had two significant findings. We first found an obesity paradox in PTB for those mothers who are LSES. We also found that the relationship between BMI and PTB was not linear but curvilinear, bridging the gap in the conclusions of other studies. This study fills in the knowledge gap of BMI and PTB by adding the consideration of social class and by creating a polynomial BMI term.

Physical activity is a modifiable factor influencing chronic disease risk. Previous studies often relied on self-reported activity measures or short-term assessments, limiting their accuracy. Leveraging Fitbit-derived data from the All of Us Research Program, we investigated associations between long-term physical activity patterns and chronic disease incidence in a diverse cohort. The study included 22,019 participants with at least six months of Fitbit monitoring and linked electronic health records. Key activity metrics included daily step count, activity calories, elevation gain, and activity duration at different intensities. Higher physical activity levels were associated with a lower risk of multiple chronic diseases. A 2,000-step increase in daily step count was linked to a reduced risk of obesity (hazard ratio [HR] = 0.85, 95% confidence interval [CI]: 0.80-0.90), type 2 diabetes (HR = 0.78, CI: 0.72-0.84), and major depressive disorder (HR = 0.83, CI: 0.77-0.90). Elevation gain was inversely associated with obesity (HR = 0.86, CI: 0.78-0.95) and type 2 diabetes (HR = 0.65, CI: 0.53-0.80). Increased time spent in very active intensity correlated with a lower risk of multiple conditions, including obstructive sleep apnea and morbid obesity. Conversely, prolonged sedentary time was associated with an increased risk of cardiometabolic diseases, including obesity (HR = 1.08, CI: 1.06-1.10) and essential hypertension (HR = 1.05, CI: 1.04-1.07). A sensitivity analysis using BMI-defined obesity instead of EHR-based diagnoses confirmed the robustness of these associations. These findings underscore the protective role of increased physical activity and reduced sedentary time in mitigating chronic disease risk. They support the development of personalized physical activity recommendations and targeted public health interventions aimed at improving long-term health outcomes. Future research integrating machine learning approaches could further refine activity-based disease prevention strategies.

A 2013 meta-analysis observed a protective association between overweight body mass index (BMI) (vs. normal BMI) and all-cause mortality that was particularly strong in people aged ≥65. Estimates informing this meta-analysis were highly heterogeneous, and critics raised insufficient or inappropriate confounder adjustment in many studies as an explanation for the protective summary association. Using this topic as an example, we demonstrate a novel approach for external adjustment of individual studies for a uniform and sufficient confounder set before meta-analysis.

We abstracted summary data on the 33 associations comprising the age ≥65 stratum of the 2013 meta-analysis. Using an external dataset (NHANES III), we derived covariates used in each study's multivariable model of the overweight-mortality association. We then calculated a bias factor to quantify the direction and magnitude of displacement of the ratio measure of association after changing from the original adjustment set to a sufficient adjustment set. After applying bias factors to adjust original associations, we compared summary results from random-effects meta-analyses with and without such adjustment.

We reproduced the original meta-analysis of overweight-mortality estimates among older participants and found a protective association similar to that reported in 2013 (summary relative risk = 0.88; 95% confidence interval: 0.84, 0.92; I 2 = 38.4%). After we simulated uniform adjustment of all 33 associations for a minimally sufficient confounder set (age, sex, and smoking status), the meta-analysis showed a similar summary association (summary relative risk = 0.90; 95% confidence interval: 0.86, 0.94), but with reduced heterogeneity (I 2 = 34.6%).

Simulated uniform adjustment for a sufficient confounder set may improve rigor and promote consensus in meta-analysis.

Recent introduction of new steatotic liver disease categorizations has necessitated updated epidemiologic studies. Specifically, recognition of (1) "MetALD" defined as where metabolic dysfunction-associated steatotic liver disease (MASLD) overlaps with alcohol use and (2) alcohol-related liver disease (ALD) without cardiometabolic risk factors (CMRFs) creates new clinical phenotypes with undefined prevalence.

We conducted a cross-sectional multicenter analysis of liver disease associated with alcohol use (ALD and MetALD). We included adults with an International Classification of Diseases (ICD) diagnosis of ALD or both metabolic dysfunction associated liver disease and alcohol use disorder assigned from 1/1/2000-1/1/2024.

Among 4057 patients, only 118 (2.9%) did not have any CMRF ("pure ALD"). Compared to patients with CMRF, patients with pure ALD were more commonly female (56% [0 CRMF] vs. 48%, 45%, 38%, and 42% [1, 2, 3, and 4 CMRFs, respectively]; P < 0.01) and younger (54 vs. 53, 60, 68, and 67 years [1, 2, 3, and 4 CMRFs, respectively]; P < 0.01). Those with pure ALD had higher rates of cirrhosis (49% vs. 39%, 31%, 30%, 34% [1, 2, 3, and 4 CMRFs, respectively]; P < 0.01), hepatocellular carcinoma (10% vs. 6.9%, 5.7%, 4.3%, and 5.1% [1, 2, 3, and 4 CMRFs, respectively]), and death (21% vs. 15%, 17%, 18%, and 21% [1, 2, 3, and 4 CMRFs, respectively]; P = 0.04). Patients whose only CMRF was body mass index (BMI) 25-30 kg/m2 did not differ significantly from patients with pure ALD. Factors associated with cirrhosis in univariable analysis included male sex (odds ratio [OR]: 1.47, confidence interval [CI]: 1.29-1.67), age (OR: 1.08 per 10 years, CI: 1.03-1.13), and diabetes (OR: 1.21, CI: 1.05-1.40) but not BMI 25-30 kg/m2 (OR: 0.86, CI: 0.64-1.14). No differences in single-nucleotide polymorphisms (PNPLA3, GCKR, TM6SF2, MBOAT7, or HSD17B12) were identified between groups.

ALD without diagnosed metabolic disease is uncommon and associated with higher rates of cirrhosis, HCC, and all-cause mortality than ALD with concurrent CMRF. Having a BMI measuring 25-30 kg/m2 did not impact these clinical outcomes, raising the question of optimal BMI cut-off for MetALD. Further investigating these novel disease categories is essential for better understanding their biology and clinical impact.

The prevalence of obesity and its associated comorbidities are increasing worldwide, leading to a rising proportion of obese patients in hospitals and intensive care units. This trend is causing a significant additional burden on our healthcare system. An obese patient requiring intensive care treatment presents major challenges for the entire team, not only in terms of economic aspects but also medically, in nursing care, and in physiotherapy. Additionally, psychosocial and organizational factors play a role that must be considered. For nursing and physiotherapy, appropriate aids such as lifters, special large hospital beds, suitable rooms, and adequate staffing should be provided. The medical challenges include intubation and airway management, hemodynamic monitoring, vascular access, adequate nutrition, appropriate dosing of medication, and difficult ultrasound conditions at the bedside. Furthermore, this patient population has an increased risk of developing pressure ulcers, pneumonia, and thrombosis, which increase the overall care requirements and further challenge the intensive care setting.

Adults living with overweight or obesity do not represent a single homogenous group in terms of mortality and disease risks. The aim of our study was to evaluate how the associations of adulthood overweight and obesity with mortality and incident disease are modified by (i.e., differ according to) self-reported childhood body weight categories.

The sample comprised 191,181 men and 242,806 women aged 40-69 years (in 2006-2010) in the UK Biobank. The outcomes were all-cause mortality, incident cardiovascular disease (CVD), and incident obesity-related cancer. Cox proportional hazards regression models were used to estimate how the associations with the outcomes of adulthood weight status (normal weight, overweight, obesity) differed according to perceived body weight at age 10 years (about average, thinner, plumper). To triangulate results using an approach that better accounts for confounding, analyses were repeated using previously developed and validated polygenic risk scores (PRSs) for childhood body weight and adulthood BMI, categorised into three-tier variables using the same proportions as in the observational variables.

In both sexes, adulthood obesity was associated with higher hazards of all outcomes. However, the associations of obesity with all-cause mortality and incident CVD were stronger in adults who reported being thinner at 10 years. For example, obesity was associated with a 1.28 (1.21, 1.35) times higher hazard of all-cause mortality in men who reported being an average weight child, but among men who reported being a thinner child this estimate was 1.63 (1.53, 1.75). The ratio between these two estimates was 1.28 (1.17, 1.40). There was also some evidence that the associations of obesity with all-cause mortality and incident CVD were stronger in adults who reported being plumper at 10 years. In genetic analyses, however, there was no evidence that the association of obesity (according to the adult PRS) with mortality or incident CVD differed according to childhood body size (according to the child PRS). For incident obesity-related cancer, the evidence for effect modification was limited and inconsistent between the observational and genetic analyses.

Greater risks for all-cause mortality and incident CVD in adults with obesity who perceive themselves to have been a thinner or plumper than average child may be due to confounding and/or recall bias.

Although studies have explored the development of postoperative anemia after metabolic bariatric surgery, little is known about the effect of metabolic bariatric surgery on anemia recovery in patients with pre-existing anemia. Therefore, the objective of this study was to determine the prevalence of anemia recovery six months after metabolic bariatric surgery and predictors associated with recovery.

This was a retrospective cohort study of 1,664 patients with pre-existing anemia aged 18-80 years who received a primary metabolic bariatric procedure between January 2010 and June 2020. The primary outcome of interest was the percentage of patients who recovered from anemia as defined by the World Health Organization thresholds at six-months post-metabolic bariatric surgery.

Of the 1,664 patients identified with preoperative anemia, 952 (57.2%) recovered six-months post-metabolic bariatric surgery. Female sex (OR 1.93, 95% CI 1.42-2.61, p < 0.001), age between 45-54 years vs. under 35 years (OR 1.48, 95% CI 1.08-2.05, p < 0.05), and receiving sleeve gastrectomy vs. Roux-en-Y gastric bypass (OR 1.41, 95% CI 1.06-.86, p < 0.05) were associated with significantly higher odds of recovery. A preoperative hemoglobin of 11-20 g/L below normal as compared to 0-10 g/L below normal (OR 0.52, 95% CI 0.40-0.69, p < 0.001) was associated with significantly lower odds of recovering from anemia.

More than half of patients with preoperative anemia undergoing metabolic bariatric surgery recover from anemia after their procedure. Age, sex, preoperative hemoglobin, and surgery type all influence recovery. The total body weight lost after six-months post-surgery conferred no significant effect.

This study aimed to investigate the independent and joint association of sugar-sweetened beverages (SSBs) and physical activity with obesity among young U.S. adults.

We selected 11,318 U.S. young adults aged 20-44 years from the National Health and Nutrition Examination Survey (2007-2020). Physical activity was self-reported using the Global Physical Activity Questionnaire, while SSBs consumption was calculated from a single day of twenty-four-hour dietary recall. Multivariable logistic regression models, and sensitivity analyses were used to estimate the associations between SSBs, physical activity, and obesity.

There were 4216 cases of obesity (35.5 %). A positive relationship between the consumption of SSBs and the prevalence of obesity was observed, while physical activity was negatively associated with the prevalence of obesity. Relative to the moderate SSBs consumption + inactive participants, those who were insufficiently active [adjusted odds ratio (AOR) = 0.75, 95 % CI: 0.58, 0.97] and physically active (AOR = 0.72, 95 % CI: 0.62, 0.85) had a lower likelihood of obesity among moderate SSBs consumers (1-499 kcal/day). However, this pattern was not found in the heavy SSBs consumers (≥ 500 kcal/day) (P > 0.05).

In conclusion, physical activity was associated with a lower prevalence of obesity among moderate SSBs consumers, while this pattern did not observe in heavy SSBs consumers. Further studies are needed to validate these results and determine causality.

Weight-centric health practices are based on the principle that excess weight predicts chronic disease, informing a growing sociopolitical movement to address an "obesity epidemic." This hyper-focus on preventing obesity may contribute to weight stigma (i.e., the devaluation and discrimination of individuals based on body size) and other iatrogenic outcomes for youth, including the development and maintenance of eating disorders (EDs). Current evidence-based treatments for EDs include language and practices that may reinforce fears of fatness, body shame, and unhealthy dietary restriction without guidance on addressing weight stigma. Here, we present case examples from three adolescent patients across ED presentations and body sizes to (1) elucidate the role of weight stigma in ED development, (2) highlight the ubiquity and harms of weight stigma within ED treatments, and (3) outline thoughtful protocol adaptations to avoid further harm and facilitate recovery. We conclude with a call for immediate action to advance research characterizing the harms of weight-centric approaches in existing ED interventions to reduce the risk of iatrogenic effects on youth with EDs and advance weight-inclusive approaches to ED treatment.

Managing obesity requires a comprehensive approach that involves therapeutic lifestyle changes, medications, or metabolic surgery. Many patients seek health information from online sources and artificial intelligence models like ChatGPT, Google Gemini, and Microsoft Copilot before consulting health professionals. This study aims to evaluate the appropriateness of the responses of Google Gemini and Microsoft Copilot to questions on pharmacologic and surgical management of obesity and assess for bias in their responses to either the ADA or AACE guidelines.

Ten questions were compiled into a set and posed separately to the free editions of Google Gemini and Microsoft Copilot. Recommendations for the questions were extracted from the ADA and the AACE websites, and the responses were graded by reviewers for appropriateness, completeness, and bias to any of the guidelines.

All responses from Microsoft Copilot and 8/10 (80%) responses from Google Gemini were appropriate. There were no inappropriate responses. Google Gemini refused to respond to two questions and insisted on consulting a physician. Microsoft Copilot (10/10; 100%) provided a higher proportion of complete responses than Google Gemini (5/10; 50%). Of the eight responses from Google Gemini, none were biased towards any of the guidelines, while two of the responses from Microsoft Copilot were biased.

The study highlights the role of Microsoft Copilot and Google Gemini in weight loss management. The differences in their responses may be attributed to the variation in the quality and scope of their training data and design.

While there is evidence demonstrating the association between cigarette smoking and weight status, and mortality and weight status, it has not been examined whether weight status is a mediator between number of cigarettes smoked per day (CPD) and all-cause mortality, limiting our knowledge of this association and potential novel approaches to reduce all-cause mortality due to cigarette smoking. We aimed to evaluate whether weight status mediated the association between CPD and mortality.

We harnessed the 2003-2018 NHANES and the Linkage Mortality Files, which included adults who smoked ≥ 100 lifetime cigarettes (unweighted n = 5,676). A generalized linear model estimated the association between cigarettes smoked per day (CPD) and weight status (e.g., Body Mass Index (BMI) or Waist Circumference (WC)). An Accelerated Failure Time model with a Weibull distribution estimated the association between CPD and all-cause mortality with weight status as a mediator, adjusting for age, SES, alcohol consumption, race/ethnicity, sex/gender, blood pressure, total cholesterol, and physical activity.

Between 2003-2018, the sample's mean BMI was 27.97 kg/m2, sample's mean WC was 97.58 cm and mean CPD was 13.21. The total effect in the mediation analysis of WC adjusted by BMI levels in the association between CPD and all-cause mortality was -0.44 (95% CI =  -2.00, -0.20; p =  0.016), the average direct effect was -0.35 (95% CI =  -1.86, -0.10; p =  0.036), and the average indirect effect was -0.10 (95% CI =  -0.23, -0.05; p < 0.001).

WC, as a surrogate measure of weight status, when adjusted by BMI levels, was a partial mediator between CPD and all-cause mortality. Public health interventions aimed to reduce mortality due to cigarette smoking at the population level should consider weight management programs as a harm reduction strategy to reduce mortality.

DNA damage repair is a critical physiological process closely linked to aging. The accumulation of DNA damage in renal proximal tubular epithelial cells (PTEC) is related to a decline in kidney function. Here, we report that DNA double-strand breaks in PTECs lead to systemic metabolic dysfunction, including weight loss, reduced fat mass, impaired glucose tolerance with mitochondrial dysfunction, and increased inflammation in adipose tissues and the liver. Single-cell RNA sequencing analysis reveals expansion of CD11c+ Ccr2+ macrophages in the kidney cortex, liver, and adipose tissues and Ly6Chi monocytes in peripheral blood. DNA damage in PTECs is associated with hypomethylation of macrophage activation genes, including Gasdermin D, in peripheral blood cells, which is linked to reduced DNA methylation at KLF9-binding motifs. Macrophage depletion ameliorates metabolic abnormalities. These findings highlight the impact of kidney DNA damage on systemic metabolic homeostasis, revealing a kidney-blood-metabolism axis mediated by epigenetic changes in macrophages.

We examined associations between body mass index (BMI), waist circumference (WC), and dementia risk, and differences in BMI and WC trajectories before dementia diagnosis. We included 9,739 participants (54% women) aged 70+ from the Trøndelag Health Study (HUNT4 70+). BMI was measured four times (1984-2019) and WC three times (1995-2019). Dementia diagnoses were clinically assessed at HUNT4 70+ . Women and men with dementia had higher midlife BMI and WC than those without dementia. These differences diminished closer to diagnosis, especially in women. Midlife obesity in both sexes and midlife overweight, high WC, and overweight/obesity with high WC in men were linked to higher dementia risk. Lower dementia risk was observed with late-life overweight for both sexes, late-life high WC in women, late-life overweight/obesity with normal WC in men or high WC in women. Adiposity measures and their changes influence dementia risk differently in women and men.

This study explores the impact of age, malnutrition severity, and malnutrition risk on cancer treatment outcomes and their incidence based on cancer localization and stage, in geriatric and adult patients in Turkey. The study emphasizes the role of oral nutritional supplements (ONS) in improving nutritional status and treatment response in both age groups.

This prospective observational cohort study involved 163 patients with solid tumors receiving radiotherapy (RT) or RT combined with chemotherapy. Malnutrition risk was assessed using the Nutritional Risk Screening (NRS) tool, and malnutrition severity was determined via body mass index (BMI). The significance of age, malnutrition severity, and risk on treatment outcomes and performance status were evaluated by the physician and the Eastern Cooperative Oncology Group Performance Status. Anthropometric measurements recorded before and after treatment were compared to evaluate ONS benefits across age and cancer groups.

Of the patients, 50.9 % were aged ≥70 years. A majority had stage III cancer (57.4 %) and lung cancer (38.7 %). Weight and BMI scores significantly decreased from pre-to post-treatment (P < 0.001). Malnutrition risk was higher in stage III cancer (P = 0.039), and geriatric patients had higher baseline NRS scores than adults (P = 0.049). Pre-treatment weight loss and malnutrition risk negatively affected RT response (P < 0.007). Post-treatment malnutrition risk prevalence increased significantly in head and neck cancer patients (P = 0.016).

Nutritional therapy is crucial alongside cancer treatment, as pre-treatment weight loss and NRS≥3 negatively affect RT response. Maintaining a healthy nutritional status correlates with better outcomes, necessitating further research to optimize interventions stabilizing weight and BMI during RT.

Since muscle strength is modifiable and handgrip strength is a reliable biomarker for strength and mortality, exploring its association with mortality in individuals with severe obesity could help identify protective thresholds. We aimed to examine the dose-response association between handgrip strength and mortality in adults with severe obesity.

We retrieved data from the Survey of Health, Ageing and Retirement in Europe (SHARE). Handgrip strength was measured in participants with a body mass index (BMI) higher than 40 kg/m2. We used time-varying Cox proportional hazards regression to assess the association between handgrip strength and all-cause mortality risk. To account for potential non-linearity, we employed restricted cubic splines. We examined a total of 2229 adults (67.9% women; BMI of 43.8 kg/m2).

We found an association between handgrip strength and mortality, showing a minimal and optimal dose for a reduced risk with 31 kg (HR 0.97, 95% CI, 0.96-0.99) and 36 kg (HR 0.90, 95% CI, 0.81-0.99), respectively. Additional sex-stratified analysis showed that lower than median levels of handgrip strength were gradually associated with increased risk in both men and women.

The association between handgrip strength and all-cause mortality in European adults with severe obesity highlights practical thresholds for risk reduction, with 31 kg as the minimum and 36 kg as the optimal strength level. In both men and women, handgrip strength below the median was linked to a gradual increase in mortality risk, emphasizing the importance of maintaining adequate muscle strength to improve health outcomes.

Many studies have explored the association between Body Mass Index (BMI) trajectory and mortality, but the association between BMI trajectory during old age and mortality remains underreported, particularly in the Chinese population. This study aimed to investigate the association between BMI trajectories in older adulthood and all-cause mortality in China, and to analyze potential mediating mechanisms.

We analyzed data from the Chinese Longitudinal Healthy Longevity Survey with latent class growth modeling to identity BMI trajectories at 3 follow-up visits (2008, 2011 and 2014). All-cause mortality was assessed from baseline to July 31,2019. Cox proportional hazard regression was used to estimate the association between BMI trajectories and all-cause mortality.

Among 3676 older adults (female: 52.3%, median (IQR) age was 77 (70, 85) years), after 12,516 person-years of follow-up, 1,331 all-cause deaths were recorded. Three distinct BMI trajectories were identified: low-normal stable trajectory (47.33%), normal slight increase trajectory (44.45%), and overweight to obesity trajectory (8.22%). In the fully adjusted model, compared to the normal slight increase trajectory, the risk of all-cause mortality was significantly increased in the low-normal stable trajectory (HR = 1.39, 95%CI: 1.22, 1.60), while the risk of mortality was not statistically different in the overweight to obesity trajectory (HR = 1.16, 95%CI: 0.83, 1.61). Both stratified and sensitivity analyses confirmed these findings. Mediation analysis suggested that cognitive impairment and lack of leisure activities might partially mediate this association. Threshold analysis indicated that the risk of mortality gradually decreases with increasing BMI when BMI is below 26 kg/m2 (HR = 0.95, 95%CI: 0.93, 0.97) and then remains stable after 26 kg/m2.

Compared with normal slight increase trajectory, low-normal stable BMI trajectory during old age may increase the risk of all-cause mortality. These insights hold significant implications for future health management strategies and interventions, aiming to enhance the overall health status and quality of life among older adults.

Physical activity (PA) is critical for healthy development in preschoolers, with long-lasting benefits that can affect later life. The World Health Organization (WHO) recommends that children aged 5-17 years should engage in 60 min of moderate-to-vigorous PA per day. However, physical inactivity in children is on the rise globally, with declines in PA starting at the age of 4 years. Increasing PA during early childhood is important to delay adiposity rebound, promote behavioral changes, improve physical fitness, and facilitate future PA engagement. However, limited evidence has been established on the effects of school-based PA interventions on preschoolers. This study examines the effects and sustainability of a preschool-based PA intervention on increasing PA, improving physical fitness and health in preschoolers, with the exercise dose benchmarked to the WHO PA guidelines.

This assessor-blinded, two-arm cluster randomized controlled trial will include 3300 preschoolers (aged 5-6 years) from 110 kindergartens in Hong Kong, China. Kindergartens will be randomized into intervention and control groups in a 1:1 ratio. The control kindergartens will continue their usual curriculum of ∼2.5 h PA/week, whereas preschoolers in the intervention kindergartens will engage in an additional 75-min game-based PA class twice per week (extra 2.5 h PA/week) over the preschool year. This multi-component intervention will also target parents, teachers, and the kindergarten environment to further encourage PA in preschoolers and their families. Objectively measured PA, cardiorespiratory fitness and other physical fitness components (muscle strength and power, agility, balance, flexibility, body composition), and psychological health will be examined at the start (0 month) and end (10 months) of the preschool year. Maintenance effects will be assessed after preschoolers' transition into primary school (16 months). Generalized estimating equations or other appropriate statistical models will be used to examine the treatment effects with adjustment for baseline values.

This study will investigate the effects of a preschool-based PA intervention with PA dose benchmarked to the WHO recommendations on promoting PA, physical fitness, and health in preschoolers, and its sustainability after preschoolers' transition into primary education. The findings will raise public awareness on the importance of PA in young children, and will inform policy making to facilitate early childhood educational reforms to incorporate adequate PA into preschool curriculums to improve children's health in the long run.

ClinicalTrials.gov (NCT05521490).

Obesity is a recognized risk factor for heart failure (HF) in people living with HIV. However, among patients with HF, being overweight or having mild to moderate obesity has been associated with significantly improved survival rates compared with those at normal weight-a phenomenon known as the obesity paradox. This paradox has not yet been evaluated in patients with both HIV and HF in the era of glucagon-like peptide-1 receptor agonists (GLP-1 RAs) and sodium-glucose cotransporter-2 inhibitors (SGLT-2is). Our study aimed to assess the mortality risk associated with body mass index (BMI) in patients with both HIV and HF and evaluate the impact of GLP-1 RAs and SGLT-2is on mortality across different weight categories.

This study analyzed data from the New York City Health + Hospitals Corporation (NYC HHC) cohort (NYC 4H), which included records from 11 major New York City Health + Hospitals facilities. The dataset combined retrospective baseline data with ongoing prospective follow-up. The cohort consisted of adults with confirmed HIV and HF who had inpatient or clinic visits between July 2017 and June 2022. HIV infection and HF were initially identified using relevant International Classification of Diseases and Related Health Problems, 10th Revision codes and were further confirmed through laboratory results and echocardiograms. Medication data were verified through electronic health records and cross-referenced with pharmacy records. The primary outcome was the hazard ratio (HR) of overall mortality across different BMI categories in patients with both HIV and HF, assessed using proportional hazard regression models adjusted for age, sex, race, comorbidities, smoking status, and functional status. Secondary analyses included re-hospitalization within 6 months of discharge and the association between GLP-1 RAs/SGLT-2is and overall mortality in patients with HIV and HF. Additional analyses were conducted to assess the efficacy of these medications within different BMI categories.

A total of 1044 patients were analyzed, including 657 males (62.9%) and 387 females (37.1%), with an average age of 61.6 years at baseline and an average follow-up of 3.8 years. A low BMI (<18.5) was associated with a 57% increase in mortality (HR 1.57; 95% confidence interval [CI] 1.03-2.39; p = 0.04), whereas class I obesity (BMI 30.0-35.9) was associated with a 35% reduction in mortality (HR 0.65; 95% CI 0.42-0.99; p = 0.04) compared with normal BMI, after adjusting for covariates. Class II obesity was associated with a lower rate of re-hospitalization within 6 months of discharge. No significant differences were observed in cardiovascular mortality across different BMI categories. The use of GLP-1 RAs was associated with a 46% reduction in overall mortality risk (HR 0.54; 95% CI 0.30-0.97; p = 0.04), and SGLT-2is were associated with a 77% reduction in overall mortality risk (HR 0.23; 95% CI 0.11-0.46; p < 0.001) after adjusting for BMI and comorbidities. For both medications, the greatest mortality benefit was observed in patients with the highest BMI categories.

Our study found that overall mortality was higher among underweight individuals with both HIV and HF. Among patients with both conditions, GLP-1 RAs and SGLT-2is significantly reduced mortality, with the greatest survival benefit observed in users within the highest BMI categories.

This study aims to investigate the causal relationship between obesity and essential hypertension, and evaluate the mediation effect of visceral adipose tissue (VAT) by Mendelian randomization (MR) analysis. We included body mass index (BMI), waist circumference (WC), waist-hip ratio (WHR), WC adjusted for BMI (WCadjbmi), and WHR adjusted for BMI (WHRadjbmi) as obesity-related anthropometric traits. In the bidirectional MR analyses, we found that higher BMI (OR, 1.638; p = 3.97 × 10-19), WC (OR, 1.702; p = 1.45 × 10-12), and WHR (OR, 1.863; p = 1.84 × 10-8) were significantly associated with increased risk of essential hypertension, while no evidence of reverse causality was observed. Then, in the two-step MR analyses, all five anthropometric traits had a positive and significant association with VAT mass, especially WC (OR, 2.315; p = 1.00 × 10-210). Meanwhile, higher predicted VAT mass was significantly associated with increased risk of essential hypertension (OR, 1.713; p = 1.18 × 10-38). Furthermore, the mediation analyses revealed that VAT had a significant mediation effect on the causal relationship between obesity-related anthropometric traits and essential hypertension, and mediated proportions in BMI, WC, and WHR were 77.8%, 80.1%, and 41.4%, respectively. Finally, the sensitivity analyses using two other datasets showed a similar result. In conclusion, our results showed that BMI, WC, and WHR have a positive and significant association with increased risk of essential hypertension. Moreover, VAT has a significant mediation effect on the causal relationship between obesity-related anthropometric traits and essential hypertension. Our study provided important statistical evidence suggesting that VAT may play a crucial meditation role in the occurrence and development of obesity-related hypertension.

The global rise in overweight, obesity, and related diseases is undeniable; however, the pathogenesis of obesity and obesity-associated diseases is heterogeneous, with varied complications and a discordant response to treatment. Intriguingly, men have a shorter lifespan than women, despite being half as likely to be obese. This paradox suggests a potential gender disparity in the impact of obesity on mortality, with men potentially being more vulnerable to obesity-associated health risks.

This retrospective study utilized Global Burden of Diseases data from 204 countries/territories to bridge the knowledge gap in understanding gender disparities in obesity-related mortality. Outcomes were obesity-associated mortality, years of life lost, years lived with disability, and disability-adjusted life years (DALYs).

In 2019, the global overweight/obesity-related disease burden reached 160.2 million DALYs, with 5.02 million associated deaths. From 1990 to 2019, the age-standardized death rates increased in males (from 58.19 to 66.55 per 100,000 person-years, APC = 0.36%, 95% CI: 0.30 to 0.42%, P < 0.001), while females experienced a decrease in age-standardized death rates (from 59.31 to 58.14 per 100,000 person-years, APC = -0.22%, 95% CI: -0.29% to -0.14%, P < 0.001). Age-standardized DALYs increased more in males (1632.5 to 2070.34 per 100,000 years, APC = 0.74%, 95% CI: 0.70% to 0.78%, P < .001) compared to females (1618.26 to 1789.67 per 100,000 years, APC = 0.24%, 95% CI: 0.19% to 0.29%, P < 0.001). Disparities were more pronounced in countries with a higher socioeconomic status and predominantly affected younger populations.

Overweight/obesity-related morbidity and mortality are higher among male sex. Identifying differences in pathogenesis, complications and treatment response is crucial to develop targeted interventions and equitable public health policies to combat this global burden.

Alcoholic hepatitis (AH) is a severe manifestation of alcoholic liver disease with high morbidity and mortality. This study used the 2016-2020 National Readmission Database to investigate how obesity influences AH outcomes.

Adult hospitalizations were categorized as those without obesity, Class 1 obesity (BMI 30-34.9), Class 2 obesity (BMI 35-39.9), or Class 3 obesity (BMI ≥ 40). We compared mortality, complications, and resource utilization across these groups using regression models.

Among 82 367 AH admissions, 4.09% had Class 1 obesity, 2.73% had Class 2 obesity, and 4.02% had Class 3 obesity. After adjusting for confounders, Class 3 obesity was associated with higher odds of mortality (Odds ratio OR = 1.74; 95% CI: 1.40-2.17; p < 0.01), septic shock (OR = 2.27; 95% CI: 1.60-3.22; p < 0.01), hepatic encephalopathy (OR = 2.53; 95% CI: 1.15-5.56; p = 0.02), and intensive care unit (ICU) admission (OR = 1.93; 95% CI: 1.57-2.36; p < 0.01). All obesity classes had increased associations with hepatorenal syndrome. No significant differences emerged for spontaneous bacterial peritonitis or variceal bleeding. Resource utilization rose with increasing obesity severity, with Class 3 obesity having a 1.84-day longer adjusted length of stay (p < 0.01) and an additional $20 174 in total hospitalization charges (p < 0.01) compared with hospitalizations without obesity.

Class 3 obesity conferred the greatest burden of mortality, complications, and healthcare costs among hospitalizations with AH. Further research is warranted to clarify the intricate interplay between obesity and AH.

This study aims to investigate the association between metabolomic aging acceleration and body mass index (BMI) phenotypes with mortality and obesity-related morbidities (ORMs). 85,458 participants were included from the UK Biobank. Metabolomic age was determined using 168 metabolites. The Chronological Age-Adjusted Gap was used to define metabolomically younger (MY) or older (MO) status. BMI categories were defined as normal weight, overweight, and obese. Participants were categorized into MY normal weight (MY-NW, reference), MY overweight (MY-OW), MY obesity (MY-OB), MO normal weight (MO-NW), MO overweight (MO-OW), and MO obesity (MO-OB). Mortality and 43 ORMs were identified through death registries and hospitalization records. Compared with MY-NW phenotype, MO-OB phenotype yielded increased risk of mortality and 32 ORMs, followed by MO-OW with mortality and 27 ORMs, MY-OB with mortality and 26 ORMs, MY-OW with 21 ORMs, and MO-NW with mortality and 14 ORMs. Consistently, MO-OB phenotype showed the highest risk of developing obesity-related multimorbidities, followed by MY-OB phenotype, MO-OW phenotype, MY-OW phenotype, and MO-NW phenotype. Additive interactions were found between metabolomic aging acceleration and obesity on CVD-specific mortality and 10 ORMs. Additionally, individuals with metabolomic aging acceleration had higher mortality and cardiovascular risk, even within the same BMI category. These findings suggest that metabolomic aging acceleration could help stratify mortality and ORMs risk across different BMI categories. Weight management should also be extended to individuals with overweight or obesity even in the absence of accelerated metabolomic aging, as they face increased healthy risk compared with MY-NW individuals. Additionally, delaying metabolic aging acceleration is needed for all metabolomically older groups, including those with normal weight.

Overeating highly palatable foods typical of a Western diet (WD) has been linked to cognitive impairments in animal models and humans. Exercise training was proposed as an important behavioral intervention with beneficial effects, including improving peripheral insulin sensitivity, improving central functions such as learning and memory, and restoring a dysregulated blood-brain barrier (BBB). The purpose of the present study was to characterize the effect of exercise training in rats fed with the WD with special emphasis on BBB. Adult female Long Evans rats were subjected to 12 weeks of WD feeding (WD group), or simultaneous WD feeding and wheel-running training (WD/EX group), or were fed a WD for 6 weeks without training and then subjected to diet and training for an additional 6 weeks (WD_WD/EX group). A sedentary (untrained) group of lean rats was fed a standard rodent chow (CTR group). In all experimental groups, we measured behavioral and physiological parameters, and the hippocampal levels of proteins structurally and functionally related to BBB, including proinflammatory cytokines and products of elevated lipid peroxidation. Exercise training in combination with a WD decreased locomotor and exploratory activities and induced short-term memory impairments. The behavioral changes were accompanied by reduced levels of occludin, claudin-5, and ZO-1 proteins in the hippocampus, suggesting changes in the integrity and increased permeability of BBB. In the WD_WD/EX rats, we found increased hippocampal levels of malondialdehyde (MDA) and neurotrophins (Bdnf, Vegfa) suggesting that increased energy expenditure by obese rats stimulates endogenous protective processes. The training introduced after 6 weeks of WD feeding in rats showing an obese phenotype may suggest that the sequence and moment of presumably protective intervention (exercise training) could alleviate or, on the contrary, exacerbate the level of stress and its consequences.

Sarcopenic obesity (SO), obesity, and sarcopenia have been related to adverse events in older adults, raising the question about the role of each component in the risk associated with SO. The objective of this manuscript is to evaluate the role of sarcopenia, obesity, and its interaction in the risks (frailty, disability, mortality) associated with sarcopenic obesity.

Data from the Toledo Study of Healthy Aging (TSHA) were used. This is a cohort-based study composed of community-dwelling adults ≥65 years. Obesity (Body Mass Index-BMI ≥30) and sarcopenia (the Foundation for the National Institutes of Health-FNIH criteria, standardized to our population) were assessed at baseline. Frailty, through the Frailty Phenotype (FP) and the Frailty Trait scale-5 (FTS5), and disability (Katz Index) were evaluated at baseline. Mortality, frailty, and disability were assessed at follow-up. Logistic (odds ratio, OR) and Cox (hazard ratio, HR) regression models were computed to assess the associations.

A total of 1 538 (74.73 years, 45.51% men) individuals were included. Cross-sectionally, SO, sarcopenia, and obesity were significantly associated with the risk of frailty and disability. Longitudinally, Sarcopenia was associated with all the adverse events (ORs/HRs ranged from 1.41 to 4.14, p-value < .05); whereas SO [FP, OR (95% confidence interval-CI): 4.27 (2.05, 8.93); FTS5, OR (95% CI): 6.14 (3.58, 10.51), p-value < .001] and obesity [FP, OR (95% CI): 3.10 (1.95, 4.94), p-value < 0.001; FTS5, OR (95% CI): 2.26 (1.17, 4.35), p-value 0.015] was only associated with incident frailty. Sarcopenia added risk to obesity for frailty (FP and FTS5) whereas obesity only did for frailty (FTS5) in sarcopenic individuals. The interaction between sarcopenia and obesity was not associated with any outcome.

Sarcopenia and obesity provide each other an additive risk for frailty, but not a multiplicative (ie, interaction) one, in sarcopenic obesity. Sarcopenia is the mean factor accounting for the associated risk.

Dietary habits significantly influence students' health status, with overweight and obesity posing serious global challenges linked to chronic diseases like type 2 diabetes and cardiovascular conditions. Our cross-sectional study assessed overweight and obesity prevalence among students in Guarda, Portugal, analyzing the nutritional and lifestyle habits of 2083 students aged 6 to 58 years. The sample included 1762 school children and 321 higher education adults, grouped into age intervals: 5-12, 13-19, 20-39, and 40-59 years. BMI analysis revealed obesity rates of 9.1% in children and 9.7% in adults, with younger children, particularly males, showing higher rates compared to older children. Increased physical activity and reduced sedentary time were correlated with a lower BMI. The observed obesity rates suggest that factors such as physical activity levels, traditional dietary patterns, and access to fresh foods in this region of Portugal may contribute to better health outcomes among students.