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Body mass index (BMI) on its own is a poor diagnostic and staging tool for obesity because it does not measure health status. The newly published Lancet Clinical Obesity Criteria (LCOC) for defining clinical obesity distinguish preclinical and clinical obesity based on organ or tissue dysfunction. The King's Obesity Staging System (KOSS) goes further and incorporates biomedical, psychosocial, and economic factors while offering a practical, holistic, and health domain-specific assessment of obesity's impact. This paper compares and maps the LCOC against the KOSS to highlight their complementary aspects, strengths, and potential for integration. By combining the LCOC philosophical framework with the practical patient-centred approach of the KOSS, we propose a unified model that enhances diagnostic ability and allows the clinician to track the impact of any obesity treatment. This integrated framework advances obesity management, addressing both medical, functional, and broader psychosocial challenges.

The field of reverse cardio-oncology examines how subclinical and overt cardiometabolic dysfunction-such as obesity-fuels breast cancer (BCa) risk and altered tumour biology through shared mechanisms such as chronic inflammation, hormonal dysregulation, and cellular senescence. Limitations of body mass index (BMI) have prompted the development of refined obesity phenotypes, including metabolically healthy vs unhealthy obesity and sarcopenic obesity that more accurately stratify BCa risk. Reverse cardio-oncology is conceptually distinguished from traditional cardio-oncology by focusing on how cardiometabolic impairment-even in the absence of manifest cardiovascular disease-increases BCa incidence and worsens prognosis. Within a common-soil framework, senescent adipose tissue is recognized as a key driver of breast tumour microenvironment remodelling through senescence-associated secretory phenotype (SASP), epigenetic reprogramming, and immunosenescence. Emerging translational strategies-including lifestyle modification, cardiometabolic therapies such as GLP-1 receptor agonists and SGLT2 inhibitors, and senolytic approaches-highlight opportunities to integrate cardiovascular and oncologic prevention and treatment in women with or at risk for BCa. Overall, this review synthesizes current knowledge on obesity's mechanistic links to BCa within a reverse cardio-oncology paradigm and provides a conceptual foundation for improved risk stratification and interdisciplinary clinical management.

Although various studies have linked environmental toxins, mumps infections, alcohol consumption, and abnormal body mass index (BMI) to impaired semen quality, the precise causes of infertility remain unclear. This study investigates the impact of BMI on oxidative stress markers in semen analysis among infertile men, illuminating the role of oxidative stress in cases of unexplained infertility. In this cross-sectional study, 280 patients exhibiting infertility symptoms were recruited. Comprehensive semen analysis was conducted, evaluating reactive oxygen species (ROS) levels, sperm plasma membrane lipid peroxidation via flow cytometry, total antioxidant capacity (TAC), and results from the sperm chromatin structure assay. Participants were categorized based on their BMI, facilitating comparisons between obese and non-obese individuals. Both BMI and age significantly influenced male fertility, particularly in obese individuals. Strong correlations were identified between elevated BMI, increased ROS levels, and decreased TAC. The obese infertile group exhibited substantially lower TAC compared to controls, highlighting obesity's detrimental effect on antioxidant defenses. Furthermore, significant reductions in sperm count, motility, and normal morphology were observed, alongside an increase in non-motile sperm. These outcomes demonstrate the complex relationship among oxidative stress, BMI, and fertility, emphasizing the necessity for targeted interventions addressing obesity's effects on reproductive health. This study underscores the importance of managing obesity and understanding its impact on oxidative stress as essential components in improving reproductive outcomes among affected men.

Inflammation is increasingly considered a vulnerability factor for deficits in reward motivation. It remains unclear if such motivational changes differ between acute and chronic low-grade inflammation. Given obesity's link to chronic low-grade inflammation, the present study a priori tested the effects of obesity and low-grade inflammation (elevated CRP concentrations), as well as acute inflammation (experimental immune challenge using lipopolysaccharide), on motivation for a monetary reward. Moreover, the wear-and-tear induced by chronic inflammation could amplify motivational changes induced by immune challenge. Thus, we also tested the a priori hypotheses that acute inflammation is associated with more strongly altered reward motivation for individuals with higher low-grade inflammation, and for obese than normal-weight individuals. Obese (n = 14) and normal-weight (n = 21) young adults, all without current or past history of medical or psychiatric conditions, were intravenously injected with a bacterial endotoxin (lipopolysaccharide, LPS [0.8 ng/kg body weight]) to trigger an acute inflammatory response, and placebo (saline) in a counterbalanced, randomized, crossover design. The Effort Expenditure for Reward Task (EEfRT) was administered 2 h following each injection to assess reward motivation. Blood was sampled pre- and post-injection to quantify concentrations of inflammatory proteins (interleukin [IL]-6 and C-reactive protein [CRP]). Obesity and higher low-grade inflammation (baseline CRP) were associated with overall reduced motivation to expend effort for reward in the placebo condition. Interactions with reward magnitude were observed, so that this effect occurred at smaller reward values, but not when reward values increased. However, these interaction effects were not significant in a posteriori sensitivity analyses. LPS-induced inflammatory responses (IL-6 concentrations during EEfRT) were associated with a weaker influence of reward magnitude on increasing effort. Unexpectedly, we did not detect the amplification effect of obesity and its associated low-grade inflammation on the ability of lipopolysaccharide to modulate reward motivation. Lipopolysaccharide-induced and low-grade inflammation may alter how effort is allocated towards reward: low-grade inflammation reduced the willingness to expend effort, while acute inflammation dampened reward sensitivity. This study offers a nuanced understanding of inflammatory processes underlying alterations in reward motivation.

Background Obesity and type 2 diabetes mellitus (T2DM) represent major and rapidly increasing public health burdens in Saudi Arabia. Metabolic (bariatric) surgery is an effective long-term intervention for obesity-related T2DM, while modern injectable pharmacotherapies, including glucagon-like peptide-1 receptor agonists, have become increasingly popular. However, public awareness and perceptions regarding these modalities remain insufficiently characterized in Saudi communities. Hence, this study aimed to assess public awareness, perceptions, misconceptions, and self-reported treatment preferences regarding metabolic (bariatric) surgery and injectable pharmacotherapies for obesity-related T2DM among adult residents of Jeddah, Saudi Arabia, using a perception-based cross-sectional survey. Methodology A community-based, descriptive, cross-sectional survey was conducted using an online, self-administered questionnaire distributed via social media platforms. The survey assessed sociodemographic characteristics, self-reported diabetes status, awareness and perceptions of obesity, metabolic (bariatric) surgery, and injectable pharmacotherapies, as well as stated treatment preferences. All outcomes reflect participant perceptions and were not intended to measure clinical knowledge or treatment effectiveness. Accordingly, type 2 diabetes status and related variables were self-reported and not verified through medical records. Descriptive statistics were used to summarize participant characteristics and awareness indicators. Chi-square tests were applied to explore exploratory associations between selected demographic variables and treatment preferences, with statistical significance set at a p-value <0.05. Results Participants demonstrated high awareness that obesity is a major modifiable risk factor for T2DM (74.6%). However, only 21.1% of participants recognized metabolic (bariatric) surgery as an effective metabolic intervention for diabetes improvement. Injectable therapies were preferred by 57.9% of participants, while 42.1% preferred surgical options. Misconceptions regarding indications, risks, and long-term outcomes were prevalent. Conclusions Although general awareness of obesity's metabolic impact was high, understanding of the therapeutic role of metabolic (bariatric) surgery for T2DM remained limited. Injectable therapies were more frequently preferred than surgical options; however, the present data do not allow definitive conclusions regarding the underlying drivers of these preferences. These findings highlight the need for structured public education initiatives to address misconceptions and improve metabolic literacy. The results reflect public perceptions rather than clinical decision-making or treatment effectiveness.

Given obesity's rising prevalence and its established role as an independent thromboembolic risk factor, potentially inducing a procoagulant state post-trauma, this study aimed to pinpoint key obesity-related factors influencing thromboembolic occurrences in this vulnerable patient group to guide interventions. This retrospective study analyzed a consecutive cohort of 1547 trauma patients age&#x2009;&#x2265;&#x2009;18 years with an Injury-Severity-Score (ISS)&#x2009;&#x2265;&#x2009;9 admitted to our level I trauma center between 01/2018 and 12/2024. Patients' data were extracted from electronic medical records. Exclusions included pregnancy, malignant/neurodegenerative disease, prior thromboembolism, and inconclusive documentation. Risk factors and influencing factors regarding obesity to suffer post-traumatic thromboembolism were evaluated. Older age, higher Body Mass Index (BMI), and greater Injury Severity Score (ISS) (p&#x2009;<&#x2009;0.05 for all) were identified as significant independent predictors, with BMI revealing the strongest effect (OR 1.077, p&#x2009;=&#x2009;0.001). In the obese cohort (BMI&#x2009;&#x2265;&#x2009;30), administration rates of tranexamic acid (TXA) and erythrocytes did not significantly differ between the TE and non-TE-groups (p&#x2009;>&#x2009;0.05). Hemoglobin levels were significantly lower in the TE group at 0, 24 and 48&#xa0;h post trauma (p&#x2009;<&#x2009;0.05), while International Normalized Ratio (INR) and Partial Thromboplastin Time (aPTT) did not significantly differ. Older patient age, higher BMI, and ISS are independent predictors of post-traumatic thromboembolism. Crucially, the administration of TXA and erythrocyte concentrates, essential for acute hemorrhage control, was not associated with an increased thromboembolic risk in the obese cohort. These findings support aggressive hemostatic resuscitation in high-risk obese patients.

Tamoxifen, a selective estrogen receptor modulator (SERM), is commonly prescribed in hormone receptor-positive breast cancer. While effective in reducing recurrence and mortality, tamoxifen is associated with weight gain in a significant proportion of patients. This weight gain complicates survivorship care, particularly given obesity's association with recurrence risk and all-cause mortality. Although lifestyle modification remains the standard of care for weight management, many breast cancer survivors struggle to achieve sufficient results with behavioral interventions alone. Current guidelines from oncology and obesity societies provide limited, nonspecific direction regarding pharmacologic weight management for tamoxifen-treated patients. Medication classes including GLP-1 receptor agonists, tirzepatide, phentermine-topiramate, bupropion-naltrexone, and orlistat are reviewed with attention to efficacy, safety, potential interactions, and tamoxifen-specific considerations. Practical monitoring strategies and prescribing considerations are provided to support oncology practitioners. This narrative review summarizes available evidence on tamoxifen-associated weight gain and outlines considerations for the use of anti-obesity medications in this population.

Childhood and adolescent obesity is a growing health concern with complex multifactorial origins, encompassing genetic, environmental, physiological, and psychosocial factors. In Greece, the prevalence of childhood obesity is among the highest in Europe, indicating an urgent need to understand its underlying mechanisms. Herein, we explore the genetic basis of obesity, focusing on both monogenic and polygenic factors, and how early life stressors contribute to obesity's onset and progression. Genetic predispositions, such as mutations in leptin-melanocortin pathways, and the role of epigenetic modifications influenced by environmental factors, are examined to understand obesity's complexity. Moreover, stress-related hormonal dysregulation impacts metabolic pathways, exacerbating weight gain and obesity-related complications. Through advanced algorithms like neural networks, decision trees, and clustering techniques, ML/AI approaches have demonstrated high accuracy in predicting obesity, identifying genetic markers, and analyzing interactions between genetic and lifestyle factors. These technologies hold promise for early detection, personalized interventions, and the development of targeted prevention strategies. The integration of ML/AI with genomic, epigenomic, and clinical data offers a comprehensive understanding of childhood obesity, paving the way for more effective management and treatment. This study contributes to a deeper understanding of the genetic and environmental factors in childhood obesity and highlights the potential of AI-driven approaches in addressing this critical public health challenge.

Frailty is an age-associated condition characterized by a state of vulnerability that compromises the quality of life and independence of older adults. To date, no studies have employed Mendelian randomization (MR) to investigate the causal relationship between obesity and frailty risk. Therefore, this study utilized a two-sample MR approach to elucidate the potential causal link between obesity and frailty. A two-sample MR analysis was conducted to assess the causal relationship between body mass index (BMI) or waist circumference and frailty. Independent genetic variants associated with obesity and frailty were selected as instrumental variables (IVs). MR analyses were primarily performed using inverse variance weighting, MR-Egger, weighted median, simple, and weighted models. In addition, the Mendelian Randomization Pleiotropy RESidual Sum and Outlier framework was applied to assess horizontal pleiotropy and to identify potential outlier variants. Through a rigorous and meticulous screening process, we identified 68 and 41 single nucleotide polymorphisms as IVs for BMI and waist circumference, respectively. Our analyses uncovered a significant positive causal association with frailty for both BMI (&#x3b2;&#x2005;=&#x2005;0.1283, SE&#x2005;=&#x2005;0.0255, P&#x2005;=&#x2005;5.2589e-07) and waist circumference (&#x3b2;&#x2005;=&#x2005;0.1340, SE&#x2005;=&#x2005;0.0357, P&#x2005;=&#x2005;.0001). Cochran Q-test indicated the presence of heterogeneity among the IV estimates attributable to individual variant effects in both analyses (Q&#x2005;=&#x2005;153.8575, P&#x2005;<&#x2005;8.753493e-09; Q&#x2005;=&#x2005;111.1552, P&#x2005;<&#x2005;7.432416e-09). Besides, no significant pleiotropy was detected for the association of BMI, waist circumference and with frailty (intercept&#x2005;=&#x2005;0.002609868, P&#x2005;=&#x2005;.2054007; intercept&#x2005;=&#x2005;0.003445858; P&#x2005;=&#x2005;.7968586). The Mendelian Randomization Pleiotropy RESidual Sum and Outlier analysis identified no outliers for either exposure, and thus no single nucleotide polymorphisms were excluded. This study substantiates the significant association between obesity and an elevated risk of frailty, thereby offering a robust theoretical foundation for policymakers to institute more stringent weight management strategies.

As the obesity epidemic expands, the alarming acceleration of youth obesity represents a critical global health concern. This timely analysis explores the underlying biological and socio-environmental drivers of childhood obesity and evaluates its role in the growing incidence of cardiometabolic disease. Moreover, this review aims to identify the limitations of existing preventive health systems and examine intervention strategies designed to mitigate the escalating burdens imposed by pediatric obesity. Contemporary research seeks to characterize distinct youth obesity phenotypes and to distinguish measurable markers of adiposity in early life that are implicated in the progression of cardiometabolic dysfunction. Recognizing the deficiencies of modern exercise education curricula, studies evaluating the implementation of school-based health interventions have demonstrated significant improvements in body composition and metabolic profiles among children and adolescents. The long-term health and societal consequences posed by rising pediatric obesity constitute one of the greatest population health challenges of our time. Future research should prioritize uncovering additional genetic and epigenetic determinants of youth obesity and emphasize the equitable delivery of early, accessible, and sustainable school-based health promotion programs to reverse the global trajectory of obesity-related cardiometabolic disease.

Obesity's metabolic heterogeneity is not fully captured by body mass index (BMI). Here we show that deep multi-omics phenotyping of 1,408 individuals defines a metabolome-informed obesity metric (metBMI) that captures adipose tissue-related dysfunction across organ systems. In an external cohort (n&#x2009;=&#x2009;466), metBMI explained 52% of BMI variance and more accurately reflected adiposity than other omics models. Individuals with higher-than-expected metBMI had 2-5-fold higher odds of fatty liver disease, diabetes, severe visceral fat accumulation and attenuation, insulin resistance, hyperinsulinemia and inflammation and, in bariatric surgery (n&#x2009;=&#x2009;75), achieved 30% less weight loss. This obesogenic signature aligned with reduced microbiome richness, altered ecology and functional potential. A 66-metabolite panel retained 38.6% explanatory power, with 90% covarying with the microbiome. Mediation analysis revealed a bidirectional, metabolite-centered host-microbiome axis, mediated by lipids, amino acids and diet-derived metabolites. These findings define an adipose-linked, microbiome-connected metabolic signature that outperforms BMI in stratifying cardiometabolic risk and guiding precision interventions.

Childhood obesity is a growing global concern linked to obstructive sleep apnea (OSA). Though adenotonsillar hypertrophy is a risk factor, obesity's independent role in prepubertal OSA severity is understudied. The aim of this study was&#xa0;to evaluate the association between obesity and the presence and severity of OSA in a cohort of prepubescent children referred for sleep-disordered breathing symptoms. We conducted a&#xa0;retrospective observational study of children referred to a pediatric sleep clinic. OSA was diagnosed using supervised nocturnal respiratory polygraphy and OSA severity was classified according to apnea-hypopnea index (AHI). BMI-z was calculated and categorized. A total of 645 children (17% obese, 13.2% overweight) were included with 70.9% having OSA. Obesity was significantly associated with severe OSA (OR&#x2009;=&#x2009;6.90; 95% CI 3.70-12.85; p&#x2009;<&#x2009;0.001), independent of tonsillar hypertrophy. A significant, dose-dependent correlation between BMI-z and AHI was observed across all age groups. In multivariate analysis, obesity was a significant predictor of severe OSA across all age strata: 1-2&#xa0;years (OR 5.55), 3-5&#xa0;years (OR 6.58), and&#x2009;&#x2265;&#x2009;6&#xa0;years (OR 6.11). Overweight status also conferred a significant risk (OR&#x2009;=&#x2009;4.82; 95% CI 2.39-9.73; p&#x2009;<&#x2009;0.001), particularly in the 3-5-year age group (OR 6.60) and in children with concurrent tonsillar hypertrophy. The predictive model for severe OSA achieved an AUC of 0.75. Obesity and overweight are associated with severe OSA in prepubertal children referred for sleep-disordered breathing symptoms. &#x2022; Obesity is a recognized risk factor for pediatric obstructive sleep apnea, but its specific influence on disease severity in prepubertal children remains incompletely defined. &#x2022; In a large cohort of prepubertal children referred for sleep-disordered breathing symptoms, obesity and overweightwere associated with severe OSA.

Obesity has risen to the forefront of global public health challenges, particularly due to its association with several chronic diseases. Its association with cancer has attracted significant research interest. The relationship between obesity and cancer is complex and profoundly influences tumorigenesis, cancer progression, metastasis, and therapeutic efficacy. This review provides the molecular basis of these interactions, elucidating how obesity triggers changes in the tumor microenvironment, disrupts metabolic pathways, and promotes inflammation. These factors facilitate cancer development and reduce the efficacy of treatments. By unraveling these mechanisms, we aim to identify therapeutic strategies that could mitigate obesity's detrimental effects on cancer outcomes and contribute to the development of more effective strategies for managing obesity-related cancers.

Pediatric obesity is increasing at an alarming rate, affecting over 381 million children worldwide and emerging as a critical public health issue. According to World Health Organization (WHO) 2016, 40% of adults are overweight and 13% are obese, highlighting obesity's persistence throughout life. Childhood obesity significantly heightens the risk of adult obesity and cardiovascular diseases (CVD) such as atherosclerosis and coronary artery disease, potentially leading to a global health crisis by 2050. Genetic predispositions identified through genome-wide association studies (GWAS) contribute to elevated body mass index (BMI), yet lifestyle factors reduced physical activity, prolonged screen time, and consumption of high-calorie, low-nutrient foods remain key drivers. This study aim is to explore the Real-world data (RWD) on childhood obesity from major countries, prevalence, risk factors, and cardiovascular consequences of pediatric obesity, evaluating public health initiatives, lifestyle interventions, and therapeutic strategies to address this growing concern. Data collected from PubMed, Scopus, and Springer databases reveal that childhood obesity is closely linked to hypertension, dysglycemia, dyslipidemia, and other cardiovascular disorders (heart attack, arrhythmias and stroke). The WHO Global Action Plan on Physical Activity 2018-2030 (GAPPA) emphasizes urgent preventive measures. Current management strategies include lifestyle modification, pharmacotherapy, and bariatric surgery. Glucagon-like peptide-1 (GLP-1) receptor agonists such as semaglutide and liraglutide are effective for weight management but commonly cause gastrointestinal adverse effects. The SURMOUNT-5 trial demonstrated superior weight-loss outcomes with tirzepatide, with a similar gastrointestinal safety profile. Emerging therapies including cagrilintide plus semaglutide, oral agents such as orforglipron and danuglipron, and the triagonist retatrutide may improve adherence and accessibility; however, these agents remain investigational and are currently under clinical evaluation. Despite promising advancements, gene therapy for pediatric obesity remains in the experimental phase. Overall, addressing childhood obesity requires multifaceted interventions combining public health initiatives, behavioral changes, and novel therapeutic strategies to mitigate cardiovascular risks and promote sustainable health outcomes.

Obesity's impact on breast cancer prognosis may depend on molecular subtype, yet there is limited research on premenopausal women with HR+HER2- breast cancer. In this study, we included 5,094 premenopausal women with HR+HER2- early-stage breast cancer who underwent radical surgery at 42 breast centers across China between 2016 and 2021. Patients were categorized into four BMI groups: underweight (UW), normal weight (NW), overweight (OW), and obese (OB). Using propensity score matching (PSM) to adjust for confounding factors, we compared disease-free survival (DFS) across BMI groups with Kaplan-Meier curves and performed multivariate Cox regression analysis to evaluate the effect of obesity on prognosis. Our results showed that obese patients had significantly worse DFS compared to those who were UW, NW, or OW (p&#x2009;=&#x2009;0.013). After adjusting for clinicopathologic factors and treatment, obesity remained an independent prognostic factor for DFS in premenopausal HR+/HER2- patients (p&#x2009;=&#x2009;0.043). After 1:1 PSM, OW/OB patients receiving selective estrogen receptor modulators (SERMs) alone had significantly worse DFS compared to UW/NW patients (p&#x2009;=&#x2009;0.022), whereas OW/OB patients treated with SERMs or aromatase inhibitors (AIs) in combination with ovarian function suppression (OFS) showed no significant difference in DFS from UW/NW patients. In addition, Restricted Cubic Splines (RCS) analysis demonstrated that the risk of recurrence increases with BMI in OW/OB patients. Collectively, these findings indicate that obesity may act as an independent adverse prognostic factor for DFS in premenopausal women with HR+/HER2-&#x2009;breast cancer. Importantly, our results also suggest that OFS may attenuate the detrimental effect of obesity in patients treated with SERMs.

Studies on Alarin, a newly identified orexigenic adipokine, have mainly focused on adults, while research investigating Alarin levels and its association with obesity in children remains limited. The aim of this study was to measure Alarin levels in children and adolescents with obesity and investigate their relationship with various metabolic parameters, as well as explore how these associations may differ by age group and gender. This prospective case-control study included 30 children with obesity (body mass index [BMI] standard deviation score [SDS]&#x2005;>&#x2005;+2) and 49 age- and gender-matched controls (BMI SDS between -1.9 and +1.9). Participants were recruited at the pediatric endocrinology outpatient clinic between April 2022 and April 2023. Clinical data, including chronological age, physical examination findings, and laboratory test results (alanine transaminase [ALT], aspartate transaminase [AST], total cholesterol, triglycerides, low-density lipoprotein cholesterol [LDL-C], high-density lipoprotein cholesterol [HDL-C], fasting blood glucose, and insulin levels), were collected from the hospital's information management system. The presence and severity of hepatosteatosis were assessed by abdominal ultrasound. Insulin resistance (IR) was determined using the HOMA-IR index, with a cutoff value of 2.5 for prepubertal patients and 3.16 for pubertal patients. The mean age of the participants was 11.6&#x2005;&#xb1;&#x2005;3.5 years (range: 4.5-17.7 years), with 58.2% (n&#x2005;=&#x2005;46) being female. Serum Alarin, LDL-C, &#x3b3;-glutamyl transferase (GGT), insulin, and HOMA-IR levels were significantly higher in the obesity group (P&#x2005;<&#x2005;.05). In the obese group, Alarin levels showed positive correlations with age, BMI SDS, fasting glucose, and presence of hepatic steatosis (P&#x2005;<&#x2005;.05). No significant correlations were found in the control group. The study found elevated Alarin levels in children and adolescents with obesity, similar to previous findings in adults. This suggests that Alarin may play a role in energy homeostasis and insulin resistance in childhood obesity. The results contribute to a deeper understanding of obesity's molecular mechanisms of obesity and may help to identify new therapeutic targets for preventing obesity-related complications and metabolic diseases.

Obese patients often show better short-term outcomes in cardiovascular disease, but the impact of severe obesity on acute myocardial infarction (AMI) outcomes is unclear. This study explored the relationship between severe obesity and in-hospital outcomes in AMI, with a focus on inflammation, as measured by high-sensitivity C-reactive protein (hs-CRP). We performed a retrospective analysis of 3887 AMI patients admitted to a tertiary cardiac center from 2010 to 2025. Patients were stratified by body mass index (BMI). The primary endpoint was a composite of in-hospital mortality, acute heart failure, and acute kidney injury. The primary endpoint incidence was similar across BMI groups up to BMI <35&#xa0;kg/m2, then significantly increased in patients with BMI &#x2265;35&#xa0;kg/m2 (20% vs. 31%; p&#xa0;=&#xa0;0.002). Severe obesity (BMI >35&#xa0;kg/m2; n&#xa0;=&#xa0;158) was associated with a two-fold increased risk of adverse outcomes (OR 2.21, 95%CI 1.04-2.97). After adjusting for admission hs-CRP, the predictive value of severe obesity was lost, while hs-CRP remained a strong independent predictor (OR 1.02, 95%CI 1.01-1.03 for every two-unit increase). Patients with severe obesity and elevated hs-CRP (&#x2265;2&#xa0;mg/dL) had the highest event rate (35%). Path analysis showed that 63% of severe obesity's effect on adverse outcomes was mediated by inflammation. Our findings show that severe obesity is a significant risk factor for adverse in-hospital outcomes in AMI, challenging the "obesity paradox." This increased risk is largely mediated by systemic inflammation.

Obesity, a global epidemic, drives coronary microvascular dysfunction (CMD), a precursor to cardiovascular disease, via gut microbiota dysbiosis. Clinical evidence shows a 47.7% reduction in coronary flow reserve among obese patients, highlighting obesity's pivotal role in CMD pathogenesis. This review elucidates molecular mechanisms linking obesity-induced dysbiosis to CMD, focusing on microbial metabolites: TMAO promotes lipid deposition and inflammation; reduced SCFAs impair endothelial function; bile acids modulate vascular tone via FXR/TGR5; LPS induces metabolic endotoxemia; BCAAs trigger insulin resistance; endogenous ethanol fosters oxidative stress; indole metabolites exert dual vascular effects; ImP and PAGln accelerate atherosclerosis and thrombosis; and H2S deficiency and elevated succinate exacerbate remodeling. The gut-heart axis amplifies CMD risk beyond traditional factors. Future multi-omics studies should identify biomarkers and develop targeted therapies, such as metabolite inhibitors and precision nutrition, to mitigate obesity-related CMD and improve outcomes. The Graphical Abstract is presented in Figure 1.[Figure: see text].

To examine the association between body mass index (BMI) category and history of stroke among current smokers, while assessing potential confounding, effect modification by age, and mediation by cardiovascular comorbidities. Data were analyzed from 53,939 current adult smokers participating in the 2021 Behavioral Risk Factor Surveillance System (BRFSS). Survey-weighted logistic regression estimated the association between BMI categories (underweight, normal, overweight, obese) and self-reported stroke history. The study assessed multicollinearity and adjusted for sociodemographic and health variables. Interaction terms were tested to evaluate effect modification by age, and exploratory decomposition analysis was used to assess mediation by conditions such as hypertension and diabetes. Stroke prevalence was highest among underweight smokers (6.3%). In adjusted models, the association between high BMI and stroke was attenuated or null. A significant interaction between BMI and age was identified; while younger underweight smokers showed lower stroke odds, older obese smokers exhibited odds ratios near or below 1.0 (such as ages 60-64: OR 0.70; 95% CI: 0.57-0.87), consistent with an "obesity paradox." Mediation analysis indicated that traditional cardiovascular risk factors did not mediate the relationship in underweight or overweight groups, with only partial mediation by hypertension and myocardial infarction observed in obese smokers. Among smokers, BMI is not consistently associated with increased stroke risk, and its impact is strongly modified by age. The findings suggest that the potent vascular toxicity of smoking may overwhelm or alter typical weight-related risk pathways, reinforcing smoking cessation as the primary preventive strategy.