Obesity, a chronic disease characterized by excessive adipose tissue accumulation, represents a critical global health challenge with profound metabolic, inflammatory, and oncogenic implications. To provide a multidisciplinary perspective, this narrative review integrates current literature examining metabolic, immunological, and oncological evidence to outline obesity as a multisystem disorder. Chronic inflammation is examined as a central mediator linking excessive adiposity to insulin resistance, type 2 diabetes, and cancer development, specifically detailing how adipose tissue dysfunction, altered adipokine profiles, and immune cell infiltration drive systemic pathogenesis. Emerging insights into the molecular mechanisms of tumor progression in a metabolically altered environment are highlighted, emphasizing the roles of hyperinsulinemia and dysregulated adipokines like leptin and adiponectin. In addition, the review explores innovative therapeutic strategies for obesity-related cancer, including the use of metformin and therapies targeting insulin-like growth factor 1 receptor and colony-stimulating factor 1 receptor pathways. It also discusses the therapeutic promise of white adipose tissue browning through inductors such as menthol and capsinoids to enhance metabolic homeostasis. Furthermore, hormonal and neural dysregulation of appetite control are addressed. Novel pharmacological treatments targeting appetite, such as glucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide receptor agonists, as well as neuromodulation techniques are discussed as promising avenues for personalized and effective interventions. This comprehensive understanding of obesity's complex nature is crucial for developing novel, integrated approaches to complement traditional diet and exercise 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.
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.
Obesity's impact on postoperative outcomes in abdominoplasty remains poorly defined despite its rising prevalence. This study evaluates the effect of obesity on 30-day postoperative complications to inform risk assessment and management. Investigate the effect of obesity on 30-day postoperative complications following abdominoplasty. We analyzed data from the American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP) for patients who underwent abdominoplasty between 2008 and 2022. Patients were categorized into obese (BMI ≥ 30 kg/m2) and non-obese (BMI < 30 kg/m2) groups. Univariate and multivariate analyses were performed to compare 30-day postoperative complication rates between the groups. A total of 1,778 patients were included; 618 (34.8%) had obesity (mean BMI 35.2 ± 5.0 kg/m2) and 1,160 (65.2%) did not (mean BMI 25.2 ± 2.9, p < 0.001). Average age of patients with obesity (45.0 ± 10.4 years) was comparable to those without (45.8 ± 11.4, p > 0.99). Postoperative complications occurred in 107 cases (6.0%), with a significantly higher incidence in patients with obesity (8.9% vs. 4.5%, p = 0.002). Deep vein thrombosis (DVT) occurred more frequently among patients with obesity (1.3% vs. 0.1%, p = 0.04). Obesity was associated with significantly increased overall complications (OR 1.79, p = 0.01), surgical complications (OR 1.68, p = 0.046), superficial wound infections (OR 2.23, p = 0.02), and unplanned readmissions (OR 2.75, p = 0.01). Obesity is an independent risk factor for complications following abdominoplasty. Optimized preoperative screening, potentially including DVT prophylaxis for patients with obesity, and tailored perioperative care are essential to improving outcomes in this population. Evidence-based guidelines are needed to enhance surgical safety for obese patients. This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .
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.
Identifying and prioritizing modifiable risk factors is crucial for the primary prevention of hypertension. However, large-scale data on the population attributable fraction (PAF) for a comprehensive range of modifiable risk factors for incident hypertension in the Japanese population have been scarce. This study analyzed 1,069,948 participants (median age 56, 43.7% men) without a history of hypertension from the DeSC database. Using Cox proportional hazards models, we evaluated the association between modifiable risk factors (obesity, diabetes mellitus, dyslipidemia, smoking, habitual alcohol consumption, physical inactivity, and sleep disorders) and incident hypertension to calculate their PAFs. Over a median follow-up of 3.64 years, 116,690 new hypertension diagnoses were recorded. Obesity had the highest PAF at 6.36%, followed by sleep disorder (4.11%), current smoking (3.39%), dyslipidemia (2.74%), habitual alcohol consumption (2.10%), physical inactivity (1.93%), and diabetes mellitus (1.55%). The PAF of obesity for incident hypertension decreased with age, from 15.10% among individuals aged <40 years to 7.93% among those aged 40-64 years and 3.70% among those aged ≥65 years. Similarly, obesity's PAF was higher in men (7.93%) than in women (5.02%). The total PAF for all evaluated modifiable risk factors showed a more pronounced contribution among younger adults and men. In conclusion, this research reveals that obesity is the largest modifiable contributor to incident hypertension in the Japanese population. Furthermore, the impact of modifiable risk factors for hypertension is more significant in younger adults and men. These findings offer valuable insights for developing effective public health policies aimed at preventing hypertension.
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'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 = 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 = 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.
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.
Fasting hyperinsulinaemia is a key feature of obesity and is implicated in diabetes progression. However, the following aspects of insulin secretion remain unclear: (1) which index of obesity is most important; (2) what is the shape of the dose-response curve between obesity and insulin secretion; (3) what physiological mechanisms sustain insulin hypersecretion; (4) what are the underlying causes; and (5) whether sex-related differences exist. We analysed data from 1250 healthy participants (547 men, 703 women) of the EGIR-RISC cohort followed up for 3.5 years, with age 30-60 years and BMI 18.5-40.0 kg/m2. Assessments included body composition, insulin secretion, beta cell function modelling from an OGTT and clamp-derived insulin sensitivity. Endogenous glucose production (EGP) was measured in a subset of 368 participants. Multivariable regression models and stratifications for BMI, body fat per cent, WHR and fat mass were applied to evaluate the effect of obesity on insulin secretion and beta cell function. The impact of obesity on fasting insulin secretion (FIS) was continuous across the full spectrum of BMI and WHR values and was greater in men than women. Among adiposity indices, fat mass (standardised β coefficient [Stβ] 0.27, p<0.0001) and waist circumference (Stβ 0.21, p<0.0001) were the strongest predictors of FIS. Insulin secretion increased 2.4-fold across BMI deciles, and adiposity-associated insulin hypersecretion appeared to be driven by the combination of hyperglycaemia and an increase in a specific beta cell function variable (insulin secretion rate at 5 mmol/l glucose [ISR@5]). In the follow-up cohort, weight gain (mean ± SD ∆ weight=+5.1 ± 3.8 kg) was associated with an increase in FIS and fasting glucose (+0.20 ± 0.63 mmol/l, p<0.03), whereas weight loss (-4.7 ± 2.8 kg) led to a reduction in FIS and fasting glucose (+0.06 ± 0.55 mmol/l, p<0.006). ISR@5 declined in both weight losers and those with stable weight (-0.17 ± 1.9 and -0.16 ± 1.0 U/h, respectively; p<0.002 for both) but not in weight gainers (-0.06 ± 1.1 U/h). Peripheral insulin resistance, plasma NEFA and leptin accounted for only part of obesity's effect on insulin secretion. Subset analysis of fasting and clamp EGP data suggested a rightwards shift in the dose-response curve across fat mass quintiles, indicating progressive hepatic glucose overproduction despite a preserved hepatic insulin response. The effect of body mass on insulin secretion is continuous, more pronounced in men, driven by fat mass and waist, sustained by hyperglycaemia and by an upregulation of beta cell insulin secretion and is only partially explained by typical hormonal and metabolic consequences of obesity. We suggest that hepatic glucose overproduction contributes to the fasting hyperinsulinaemia observed in individuals with obesity.
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] > +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 ± 3.5 years (range: 4.5-17.7 years), with 58.2% (n = 46) being female. Serum Alarin, LDL-C, γ-glutamyl transferase (GGT), insulin, and HOMA-IR levels were significantly higher in the obesity group (P < .05). In the obese group, Alarin levels showed positive correlations with age, BMI SDS, fasting glucose, and presence of hepatic steatosis (P < .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.
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.
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.
Obesity is a major risk factor for knee osteoarthritis, frequently requiring total knee arthroplasty (TKA). Although TKA improves mobility and reduces pain, obesity's influence on postoperative activity and gait metrics remains unclear. This study investigated the impact of body mass index (BMI) on daily activity following TKA. A prospective cohort study included 152 patients undergoing unilateral TKA, stratified into normal-weight (BMI: 18.5 to 25), overweight (BMI: 25.0 to 30), obese (30.0 to 40), and morbidly obese (BMI > 40) groups. Objective metrics-step count, standing hours, gait speed, steadiness, and 6-min walk test (6MWT)-were recorded preoperatively and at six weeks, six months, and 12 months postoperatively using watches. Multivariable regression analyses controlled for age and sex. Morbidly obese patients had significantly lower preoperative step counts (2,104 ± 1,622 versus 4,893 ± 2,977; P = 0.017). Postoperatively, all groups showed improvements in step count, gait speed, and steadiness, but morbidly obese patients maintained lower activity metrics. At 12 months, morbidly obese patients' step counts (2,255 ± 1,639) were significantly lower than normal-weight patients (7,262 ± 3,141; P = 0.011). Improvements in step count, gait speed, standing hours, and patient-reported outcomes (Knee Injury and Osteoarthritis Outcome Score, Joint Replacement [KOOS, JR], and EuroQol Five-Dimensional Questionnaire [EQ-5D]) occurred across BMI groups, without significant intergroup differences. Regression analyses identified higher BMI as associated with reduced postoperative activity at 12 months (P < 0.05), although the small size of the morbidly obese subgroup limits the strength of conclusions for this category. Higher BMI was associated with lower postoperative daily activity following TKA. Despite lower absolute activity levels in higher BMI groups, the magnitude of improvement from baseline was similar across all BMI categories. Prehabilitation and tailored rehabilitation programs targeting obese individuals' specific needs may optimize recovery and enhance postoperative physical activity.
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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.
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.
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 kg/m2, then significantly increased in patients with BMI ≥35 kg/m2 (20% vs. 31%; p = 0.002). Severe obesity (BMI >35 kg/m2; n = 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 (≥2 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.
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.
Offspring asthma has emerged as a significant yet underexplored consequence of maternal obesity. This review synthesizes evidence from human and animal studies linking maternal obesity to increased asthma risk in offspring. We examine potential mechanisms, including impaired fetal lung development, epigenetic modifications, microbiome alterations, and metabolic dysregulation. A dedicated section focuses on the novel role of insulin signaling in the developmental programming of airway hyperresponsiveness, as insulin resistance-and the resulting hyperinsulinemia-is common in offspring of obese mothers. By integrating current findings and identifying key research gaps, this review outlines future directions to advance understanding and mitigation of maternal obesity's impact on offspring respiratory health.