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.
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.
Metabolic dysfunction-associated steatotic liver disease (MASLD) affects approximately 100 million individuals in the United States. Previous studies have reported a significant association between obesity and MASLD. The objective of our study was to examine the relationship between obesity and population-level trends in MASLD prevalence among US adults aged 20 years and older. We conducted a retrospective analysis of serial cross-sectional data from the National Health and Nutrition Examination Survey cycles (1999-2018). MASLD was defined using two criteria: (1) US Fatty Liver Index (USFLI) ≥30 or (2) cardiometabolic risk factors (≥1) with controlled attenuation parameter ≥288 dB/m (2017-2018 only). Temporal trends in the prevalence of MASLD and obesity were analyzed using logistic regression with the midpoint of a 2-year survey cycle as a continuous independent variable. Adjusted odds ratios (ORs) quantified obesity's association with MASLD trends, controlling for age, sex, race/ethnicity, and survey design variables. Among 17,824 participants, 36.62% were obese (body mass index ≥30 kg/m2) and 33.49% met MASLD criteria (USFLI ≥30). MASLD prevalence increased from 30.20% (95% confidence interval [CI] 26.57%-33.83%) in 1999-2000 to 38.64% (95% CI 35.47%-41.80%) in 2017-2018 mirroring rising obesity rates (30.26%-43.51%). MASLD prevalence varied significantly across different demographics, with the highest rates observed in older adults, males, and Mexican Americans. Obesity was associated with a 14.05-fold higher odds of MASLD (95% CI 12.62-15.65). MASLD prevalence trends closely parallel the obesity epidemic, with obesity strongly associated with MASLD risk. The differential prevalence rates among older adults, males, and Mexican Americans highlight the need for targeted prevention strategies, including obesity management.
The impact of obesity on brain health, spanning cerebrovascular disease, cognition, and neuroanatomy, remains incompletely understood. We conducted 2-sample Mendelian randomization to assess the causal effects of obesity traits on brain health outcomes. Potential biological pathways were explored using transcriptome-wide association study analyses. We further examined associations in the National Health and Nutrition Examination Survey using weighted, multivariable-adjusted logistic regression. Obesity measures included body mass index (BMI), waist circumference (WC), and waist-to-hip ratio (WHR). Outcomes comprised stroke, fluid intelligence, and brain image-derived phenotypes. Higher BMI (odds ratio [OR] = 1.18; 95% confidence interval [CI], 1.13-1.24; P = 8.99 × 10-12), WC (OR = 1.20; 95% CI, 1.09-1.31; P = 3.85 × 10-3), and WHR (OR = 1.23; 95% CI, 1.16-1.31; P = 9.19 × 10-11) were associated with increased stroke risk. BMI (β = -0.21; P = 8.62 × 10-6) and WHR (β = -0.33; P = 1.19 × 10-7) were linked to lower fluid intelligence scores. BMI showed causal effects on 7 brain image-derived phenotypes. Transcriptome-wide association study implicated pathways related to substrate metabolism, immune activation, and epigenetic regulation in mediating obesity's effects on brain health. In National Health and Nutrition Examination Survey, after adjustment for covariates, BMI (OR = 1.04; 95% CI, 1.02-1.06; P = 1.27 × 10-3), WC (OR = 1.01; 95% CI, 1.00-1.02; P = 9.58 × 10-3), and WHR (OR = 1.40; 95% CI, 1.08-1.81; P = 1.25 × 10-2) were positively associated with stroke risk. Obesity, particularly BMI, shows causal relationships with stroke risk, alterations in brain structure, and reduced cognitive performance. Mechanisms may involve metabolic, immune, and epigenetic pathways. These findings underscore the importance of obesity prevention and management to preserve brain health.
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 is a major global health issue, and current treatments targeting appetite suppression or fat absorption often have limited effectiveness and adverse side effects. Localized therapies with minimal systemic toxicity are needed to address obesity's underlying causes. We developed a photothermal therapy using intraperitoneally (IP) administered microwave-derived soybean lecithin-polypyrrole nanoparticles with a nano-pufferfish shape, responsive to near-infrared (NIR) light. This therapy directly targets adipose tissue to induce apoptosis, providing localized treatment with minimized side effects. Compared to untreated or NIR-only control groups, this method changed adipocyte metabolic activity. It also increased the expression of biomarkers, indicating activation of stress pathways that contribute to anti-obesity effects. This localized, adipose-targeted photothermal therapy significantly improves metabolism while minimizing systemic toxicity. It holds promise for long-term, self-administered obesity management, offering an effective, low-risk alternative to conventional treatments.
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 ≥ 18 years with an Injury-Severity-Score (ISS) ≥ 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 < 0.05 for all) were identified as significant independent predictors, with BMI revealing the strongest effect (OR 1.077, p = 0.001). In the obese cohort (BMI ≥ 30), administration rates of tranexamic acid (TXA) and erythrocytes did not significantly differ between the TE and non-TE-groups (p > 0.05). Hemoglobin levels were significantly lower in the TE group at 0, 24 and 48 h post trauma (p < 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.
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.
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.
This study explored the relationship between age at first childbirth and hypertension-diabetes comorbidity (HDC) risk in postmenopausal women, focusing on whether obesity metrics (BMI, waist-to-hip ratio, and lipid accumulation product) mediate this association. Data were extracted from the baseline survey of the China Multi-Ethnic Cohort study. The association between age at first childbirth and HDC was examined via logistic regression analysis. Then, the effect of obesity on the association between age at first childbirth and hypertension was determined via mediation analysis. Furthermore, subgroup analyses were conducted, followed by multivariable logistic regression modeling to assess the primary association. Included in this cross-sectional study were 5,741 postmenopausal women, with an average age at first childbirth of 23.56 years and current age of 59.44 years. The prevalence of hypertension-diabetes comorbidity (HDC) was 7.5% (429/5,741). Age at first childbirth was significantly associated with HDC prevalence (OR=0.737; 95% CI: 0.579-0.940). After adjustment, women who first gave birth at 21-25 (OR=0.739), 26-30 (OR=0.591), and >30 (OR=0.417) had lower HDC prevalence than those who first gave birth at ≤20 years. BMI, waist-to-hip ratio, and lipid accumulation product mediated this association, with mediation proportions of 29.42%, 18.97%, and 21.52%, respectively. In postmenopausal women of minority Chinese descent, age at first childbirth is significantly associated with HDC. Obesity mediates the effect of age at first childbirth on the development of the HDC.
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 (β = 0.1283, SE = 0.0255, P = 5.2589e-07) and waist circumference (β = 0.1340, SE = 0.0357, P = .0001). Cochran Q-test indicated the presence of heterogeneity among the IV estimates attributable to individual variant effects in both analyses (Q = 153.8575, P < 8.753493e-09; Q = 111.1552, P < 7.432416e-09). Besides, no significant pleiotropy was detected for the association of BMI, waist circumference and with frailty (intercept = 0.002609868, P = .2054007; intercept = 0.003445858; P = .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.
Despite limitations in using BMI to assess obesity, little is known about central obesity's role in pregnancy and postpartum cardiometabolic conditions. We investigated associations of central obesity with perinatal cardiometabolic conditions, independently and jointly with BMI. We examined associations of early pregnancy central obesity measures (waist circumference, waist-to-hip ratio, waist-to-height ratio, and body roundness index) with gestational diabetes mellitus, hypertensive disorders of pregnancy, postpartum prediabetes/diabetes, and postpartum chronic hypertension using modified Poisson (prenatal outcomes) and Cox (postpartum outcomes) regression. Among the 3,055 individuals in the study, there was a dose-response relationship between increasing central obesity and all outcomes, even after adjusting for BMI. Among individuals with healthy prepregnancy BMI, central obesity was associated with a higher risk of gestational diabetes mellitus (relative risks 1.92-2.42), postpartum prediabetes/diabetes (hazard ratios [HRs] 1.50-2.16), and postpartum chronic hypertension (HRs 2.04-3.63). Early pregnancy central obesity measures may enhance perinatal cardiometabolic risk assessment, helping identify at-risk individuals who could be missed using BMI alone.
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 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 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 = 6.90; 95% CI 3.70-12.85; p < 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 years (OR 5.55), 3-5 years (OR 6.58), and ≥ 6 years (OR 6.11). Overweight status also conferred a significant risk (OR = 4.82; 95% CI 2.39-9.73; p < 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. • Obesity is a recognized risk factor for pediatric obstructive sleep apnea, but its specific influence on disease severity in prepubertal children remains incompletely defined. • In a large cohort of prepubertal children referred for sleep-disordered breathing symptoms, obesity and overweightwere associated with severe OSA.
While GWAS (genome-wide association studies) have identified over 1000 obesity-associated loci, their functional impact on gene expression remains unclear. Moreover, many studies have not fully captured the genetic architecture of obesity in high-risk populations or considered the complexity of adiposity beyond traditional measures. To address these gaps, this study explores the genetic and transcriptomic pathways of obesity using diverse obesity phenotypes in a high-risk population. We analyzed genomic and whole-blood transcriptomic data from the CCHC (Cameron County Hispanic Cohort), performing GWAS on 13 obesity-related traits. Differential expression analysis was conducted for genes near GWAS-identified single nucleotide polymorphisms (P<5×10-6) followed by expression quantitative trait loci mapping and GWAS-expression quantitative trait loci colocalization. GWAS identified 486 trait associations, including 6 genome-wide significant (P<5×10-8) loci, with 3 novel signals linked to abdominal subcutaneous adipose tissue, body fat percentage, and waist circumference. Among 3024 genes near these loci, 60 showed differential expression. Further expression quantitative trait loci analysis suggested 2 single nucleotide polymorphism-gene-trait relationships: rs543314376-MAPK11, associated with subcutaneous adipose tissue volume in females, and rs963018484-PER1, linked to body mass index in females. Both genes play key roles in obesity-related pathways, including inflammation and circadian rhythm regulation. This integrative genomic-transcriptomic analysis uncovers 2 novel candidate genes for obesity and underscores the critical need for involving all populations and comprehensive adiposity measures in obesity research. By expanding beyond body mass index in a Hispanic/Latino population, we move closer to a deeper and more inclusive understanding of obesity's genetic architecture.
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.
Obesity represents a significant public health and economic challenge across Europe, driving an increased chronic disease burden and increased hospital utilisation. Despite this impact, cross-national evidence quantifying obesity’s hospitalisation burden remains sparse, and there is only a limited understanding of the potential cost savings achievable through obesity prevalence reduction. We analysed European Health Interview Survey (EHIS) Wave 3 (2019) data, encompassing adults aged 18 years and older across eight countries (Belgium, the Netherlands, Germany, Luxembourg, Spain, Italy, Portugal and Denmark). Our primary outcome was the number of hospital nights in the preceding 12 months. We employed negative binomial regression models with zero-inflated specifications to estimate the associations between hospitalisation and body mass index (BMI), alongside sociodemographic, health and lifestyle factors. Simulations were used to project the impacts of a 1% obesity prevalence reduction on hospital expenditures. Compared to normal weight, obesity and underweight were strongly associated with increased hospital nights (IRR = 1.19 and 1.92, respectively), while pre-obesity showed no such association. Hospitalisation increased markedly with age, whereas higher education and income provided protective effects in this regard, reducing stays by 7% and 8%, respectively. Hypertension, diabetes and depressive symptoms substantially elevated hospital utilisation, while physical activity reduced it by 28%. Regional variation emerged, with Southern and Northern Europe reporting lower rates than Western Europe. A 1% obesity prevalence reduction would yield €4.27 billion in annual savings, representing 1.71% of combined hospital budgets. Obesity and underweight significantly increase hospitalisation across Europe, placing substantial strain on health systems. Preventive strategies that promote healthy weight, physical activity and mental health could markedly reduce hospital demand and generate major economic savings. Even modest reductions in obesity prevalence offer strong health and fiscal benefits, underscoring the importance of sustained investment in prevention-focused public health policies intended to increase equity and healthcare sustainability across European countries. The online version contains supplementary material available at 10.1186/s12889-026-26705-w.
Body mass index (BMI) is commonly used to estimate obesity prevalence; however, reliance on BMI alone can lead to an incomplete understanding of obesity's impact on health. In line with the 2025 recommendations of the Lancet Diabetes & Endocrinology Commission, this study combines population-level measures of excess adiposity with indicators of physiological dysfunction and activity limitation across eight body system domains to characterize clinical and preclinical obesity among Canadian adults. Measured and self-reported data from the 2016 to 2019 Canadian Health Measures Survey were used to define excess adiposity as measured BMI in the obese range plus elevated waist circumference. A three-tier system was used to capture progressive obesity-related impairment. At each tier, clinical obesity was defined by excess adiposity and indicators of impairment in one or more domains (Tier 1), two or more domains (Tier 2), or three or more domains (Tier 3). Preclinical obesity at each tier was characterized by excess adiposity with fewer indicators of impairment than the corresponding clinical thresholds. Prevalence estimates for these indicators and characterizations of obesity were calculated by sex and age group. Just over one in four Canadian adults had excess adiposity. Prevalence of physiological dysfunction and activity limitation indicators varied across domains and sex and age groups. Clinical and preclinical obesity prevalences were 19% and 8% at Tier 1, 12% and 15% at Tier 2, and 7% and 20% at Tier 3, respectively. Preclinical obesity - especially at tiers 1 and 2 - was more common in younger adults and females. Younger adults and females with excess adiposity were less likely to present with obesity-related physiological dysfunction or activity limitation, indicating early stage impairment and highlighting opportunities for targeted prevention. Integrating measures of impairment when assessing obesity can refine population surveillance efforts.
Obesity is a complex, chronic disease influenced by genetic, environmental, behavioral, and psychosocial factors. While lifestyle modification remains the foundation of treatment, it is often insufficient for sustained weight loss and cardiometabolic risk reduction. The rising prevalence of obesity and its link to comorbidities such as type 2 diabetes, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease necessitate a comprehensive, multidisciplinary approach to care. To correlate the pathophysiology of adiposopathic atherogenic dyslipidemia with the need for patient-centered, team-based management strategies that improve long-term outcomes. This review describes the structure and function of interdisciplinary obesity care teams, highlighting the roles of lipid specialists, physicians, advanced practice providers, clinical pharmacists, registered dietitians, behavioral health professionals, and exercise specialists. The use of shared care plans, case reviews, electronic health record tools, and emerging technologies such as nutrigenetic testing is explored. Multidisciplinary care improves outcomes by addressing obesity's complexity, supporting adherence to evidence-based therapies, and reducing barriers to treatment. Challenges such as payer-related prior authorization delays and the social stigma of obesity remain obstacles to engagement and long-term success, underscoring the need for scalable, collaborative care models. Team-based, proactive, and individualized care is essential for effective obesity management. Health systems that invest in interdisciplinary approaches are better positioned to reduce the clinical, psychological, and economic burden of obesity and its complications.
This study investigates whether obesity mediates the relationship between sleep duration and depressive symptoms, aiming to provide evidence for obesity's mediating effect and inform public health interventions. Data from 23,190 adults in the National Health and Nutrition Examination Survey (NHANES) 2007-2018 were analyzed. Generalized linear regression models assessed the associations between sleep duration, obesity indicators [body mass index (BMI), waist circumference (WC), and body roundness index (BRI)], and depressive symptoms. Mediation analysis explored the mediating role of obesity, with subgroup analysis across gender, age, and race. Sleep duration was significantly negatively associated with BMI, WC, and BRI (all P < 0.001), and these obesity indicators were positively associated with depressive symptoms (all P < 0.001). Mediation analysis showed that obesity partially mediated the relationship between sleep duration and depressive symptoms, with slightly stronger effects observed in individuals with diabetes. Obesity, assessed by BMI, WC, and BRI, showed a modest, partial mediating role in the association between sleep duration and depressive symptoms, with exploratory evidence of larger indirect effects among individuals with diabetes.