The Lancet Diabetes & Endocrinology Commission recognizes clinical obesity as an independent disease, although its link to heart failure (HF) remains underexplored. The goal of this study was to evaluate the impact of clinical obesity on new-onset HF risk and subsequent all-cause mortality after the development of HF. Clinical obesity was defined based on body mass index, waist circumference, waist-to-hip ratio, waist-to-height ratio, and 10 clinical criteria. A total of 99,131 participants from the Kailuan Study cohort were classified into nonobese, preclinical obesity, and clinical obesity groups. A Cox proportional hazards model was applied to assess the association between clinical obesity and the risk of new-onset HF, and all-cause mortality was examined among those with HF. Over a median follow-up of 16.0 years, 3,280 participants developed HF, and there were 19,170 deaths from any cause. Compared with the nonobese group, clinical obesity was associated with a 63% higher risk of new-onset HF (adjusted [aHR]: 1.63; 95% CI: 1.49-1.77), with varying risks across HF subtypes. Within the clinical obesity group, HF risk increased with the number of clinical criteria: one (aHR: 1.50; 95% CI: 1.37-1.64), two (aHR: 1.91; 95% CI: 1.70-2.14), and three or more (aHR: 2.20; 95% CI: 1.80-2.68). However, clinical obesity was not associated with increased all-cause mortality after HF (aHR: 1.01; 95% CI: 0.90-1.15). These findings highlight clinical obesity as a risk factor for new-onset HF and all-cause mortality, driven both by excess weight and associated clinical conditions. Recognizing clinical obesity as an independent disease may support more effective HF prevention strategies.
Obesity and binge eating disorder (BED) are global health concerns that share overlapping neural mechanisms. These include alterations in the brain's reward and control systems leading to heightened sensitivity to food cues and impaired self-regulation, which underpin overeating. Identifying neuroimaging-based biomarkers that index these mechanisms could advance individualised treatments. This scoping review examined evidence on fMRI food cue reactivity as a potential approach for developing predictive and response biomarkers relevant to the treatment of obesity and BED. A systematic search of MEDLINE, Scopus, PsycINFO, and Embase (to July 2025) identified 57 eligible studies incorporating fMRI cue reactivity measures in the context of pharmacological, surgical, psychological, and lifestyle interventions. Of these, 7 reported predictive outcomes only (6 for adults with obesity and 1 for children and adolescents with obesity), 41 reported response outcomes only (36 for adults with obesity, 3 for children and adolescents with obesity and 2 for adults with binge eating), and 9 reported both predictive and response outcomes (8 for adults with obesity and 1 for adults with binge eating). Across paradigms and intervention modalities, there was consistent involvement of reward (striatum, insula, orbitofrontal and ventromedial prefrontal cortex) and cognitive control regions (dorsolateral and dorsomedial prefrontal cortex) as response outcomes from successful treatment. Reductions in reward-system reactivity following interventions were consistently associated with improved clinical outcomes, supporting the potential of fMRI food cue reactivity as a candidate biomarker of treatment response. However, this finding is highly skewed towards obesity, given the limited number of studies that report results for BED (3 studies). Furthermore, consistent evidence for reliable predictive biomarkers was also limited, likely due to methodological variability and small sample sizes. Overall, this review supports the potential of response outcomes from fMRI food cue reactivity as an indicator of treatment efficacy in obesity and highlights the limited evidence in BED. We also emphasise the need for further standardisation of paradigms and biomarker validation efforts.
To determine whether obesity is associated with an increased risk of pregnancy loss in patients undergoing autologous euploid frozen embryo transfer (FET). Retrospective cohort study. Patients with recorded body mass index (BMI) from nine clinical sites during January 2019 to December 2024 undergoing first, autologous, single, euploid FET were included. Other PGT indications were excluded. Patients were stratified into two groups; patients with obesity (BMI≥30.0kg/m2) and non-obese patients (BMI<30.0kg/m2). Primary outcome was biochemical pregnancy loss (bHCG>5mIU/ml without ultrasound evidence of pregnancy until bHCG <5mIU/ml) or clinical pregnancy loss (ultrasound evidence of at least an intrauterine gestational sac, which did not progress to live birth). Secondary outcomes included implantation, ectopic, clinical and ongoing pregnancy (8-9 weeks gestational age with cardiac activity) and live birth (neonate > 24 weeks gestational age). 14,990 patients were included: 11,179 non-obese and 3,811 with obesity. Compared to non-obese, patients with obesity were older. Parity, anti-mullerian hormone (AMH) and blastulation day were similar between groups. After adjustment, patients with obesity had a 19% increased risk of pregnancy loss (aRR 1.19, 95% CI 1.14-1.24, p<0.001) compared to non-obese. When stratified by BMI categories; class I (BMI 30.0-34.9 kg/m2), II (BMI 35.0-39.9 kg/m2) and III (BMI ≥40.0 kg/m2) obesities had 12%, 22% and 41% increased risk of pregnancy loss while underweight (BMI <18.0 kg/m2) and overweight (BMI 25.0-29.9 kg/m2) groups performed similarly to healthy weight (BMI 18.5-24.9 kg/m2). The predicted probability of pregnancy loss was lowest at a BMI of 25.3 kg/m2. While there was no difference in implantation (aRR 0.98, 95% CI 0.86-1.37, p=0.09), patients with obesity had lower chances of clinical (aRR 0.96, 95% CI 0.94-0.99, p=0.002) and ongoing pregnancy (aRR 0.94, 95% CI 0.92-0.96, p<0.001) and livebirth (aRR 0.92, 95% CI 0.91-0.94, p<0.001). Risk of pregnancy loss was attenuated in parous patients with obesity (aRR 0.90, 95% CI 0.79-1.02, p=0.09). When accounting for embryonic aneuploidy in the setting of euploid only transfers, patients with obesity had a 19% increased risk of early pregnancy loss compared to non-obese patients, with risk rising across BMIs and BMI categories.
Eating disorders (EDs) and obesity have traditionally been conceptualized as distinct entities, yet accumulating evidence points to overlapping vulnerabilities spanning genetic, neurobiological, behavioral and psychological domains. Shared risk factors suggest convergent mechanisms, particularly in impulse control, reward processing, emotion regulation and body-image representation. In this scenario, functional near-infrared spectroscopy (fNIRS) offers a clinically accessible tool to examine cortical activity, although findings remain dispersed across heterogeneous studies. A systematic search of PubMed, Scopus and Ovid Embase identified peer-reviewed fNIRS studies in individuals with anorexia nervosa, bulimia nervosa, binge eating disorder and obesity. Eligible studies included at least one clinical group, reported original data and applied fNIRS to assess cortical responses. From 990 records, 26 studies met inclusion criteria. Eighteen studies incorporated healthy controls, while eight investigated clinical samples only. Across case-control comparisons, consistent alteration emerged in the prefrontal cortex (PFC). Obesity and binge eating disorders were associated with attenuated PFC activation during inhibitory control, decision-making and food-related paradigms, whereas bulimia nervosa showed condition-dependent alterations linked to loss-of-control symptoms. Findings in anorexia nervosa were mixed, with reduced activation during executive tasks but heightened responses to socially or emotionally salient stimuli. Broader ED samples showed blunted frontal and temporal activation during verbal fluency. Evidence highlights the PFC as a transdiagnostic hub of altered activity in EDs and obesity, consistent with overlapping vulnerabilities. Disorder-specific profiles underscore context-dependent modulation. Standardized, large-scale studies are needed to clarify the utility of fNIRS in delineating common and distinct neural substrates across the ED-obesity spectrum.
Maternal obesity increases the risk of congenital anomalies and later-life metabolic disease in offspring. Still, underlying mechanisms remain unclear, particularly in extraembryonic lineages at the maternal-fetal interface, which remain poorly studied. We jointly profiled gene expression and chromatin accessibility in single nuclei from mouse embryos and extraembryonic tissues in a diet-induced obesity model at embryonic day 8.5, when multiple organogenesis programs are underway. This analysis generated an atlas of 36 cell lineages, including derivatives of all three germ layers and trophoblast populations. Lineage allocation was preserved in embryos from obese dams. However, transcription was widely dysregulated. Oxidative phosphorylation genes were broadly suppressed, and genes involved in hypoxia, cytoskeleton remodeling, and cell migration were enriched among upregulated pathways. Chromatin accessibility changed in a few lineages, most notably in extraembryonic visceral endoderm and parietal trophoblast giant cells. Differently accessible chromatin was enriched in binding motifs for retinoic acid receptors. Indeed, genes involved in retinol and lipoprotein transport were suppressed, and RNA in situ hybridization confirmed reduced expression of retinol transporters Ttr, Rbp4, and Stra6, and lipoprotein transporter Apoa1 in visceral yolk sac. Thus, obesity during pregnancy causes early transcriptional dysregulation that impairs retinoic acid and lipoprotein transport at the maternal-fetal interface, suggesting a mechanism through which maternal obesity could influence long-term developmental outcomes.
Public health systems face a major challenge because of the worldwide obesity epidemic. The number of obese individuals has increased dramatically and, even in Switzerland which may be considered a relatively "lean" country, the numbers are alarmingly high and have reached almost 50% of the adult population. There is an urgent need for effective, safe and widely-available therapeutic interventions worldwide. The development of analogues of physiological gut hormones has led to highly effective treatment options based on two incretins: glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP). Analogues of the pancreatic hormone amylin, next to the above incretins and glucagon, have yielded more promising body weight-lowering effects in preclinical and clinical studies, and several new amylin analogues are under development. Despite progress in anti-obesity pharmacotherapy, major challenges remain. Here, I discuss recent findings in the amylin field, including amylin's potential role in improving memory, and the characterisation of specific neurons and circuits involved in amylin signalling in the caudal hindbrain. This is followed by a more in-depth discussion of challenges linked to amylin pharmacotherapy, or anti-obesity pharmacotherapy in general. Three of these challenges are addressed, specifically: (1) What are the potential mechanisms of the muscle sparing effect of amylin-based weight loss drugs? (2) Is there improved weight loss effectiveness of amylin-based anti-obesity therapy in type 2 diabetes mellitus (T2D) patients compared with incretin-based approaches? (3) Can amylin analogues improve maintenance of reduced body weight after the weight loss phase because of their role as leptin sensitiser?
People with epilepsy (PWE), particularly Native Hawaiians and Pacific Islanders (NHPI), face significant cardiometabolic disparities. This study characterized the "triple burden" of obesity, diabetes, and tobacco use across White, Asian, and NHPI PWE in Hawaii and identified factors associated with seizure control. A retrospective chart review of 403 adult PWE (41.2% White, 24.1% Asian, 34.7% NHPI) was conducted at a Hawaii-based clinic. Multivariable logistic regression compared comorbidity profiles and identified factors associated with poor seizure control (breakthrough or drug-resistant). After adjustment, NHPI patients faced significantly higher odds of obesity (OR=2.03, 95% CI [1.26-3.28]), diabetes (OR=2.97, 95% CI [1.42-6.21]), and tobacco use (OR=1.89, 95% CI [1.06-3.34]) compared to White patients. Current tobacco use was the strongest factor associated with poor seizure control (OR=2.08, 95% CI [1.12-3.89], p = 0.021). Obesity (p = 0.149) and diabetes (p = 0.933) were not significantly associated with seizure outcomes. NHPI PWE face a disproportionate triple burden of cardiometabolic risks. While all are critical for health, tobacco use was the only factor independently associated with poor seizure control. These findings underscore the importance of culturally tailored smoking cessation programs to address risk as both a behavioral and cardiometabolic condition as a supportive intervention to improve neurologic outcomes in this population.
Children with congenital heart disease (CHD) are at increased baseline cardiovascular (CV) risk due to their structural heart disease and social determinants of health may further increase their CV risk. The Child Opportunity Index (COI) is a measure of neighborhood conditions and is associated with cardiometabolic risk in children. However, the impact of COI on children with CHD and associated cardiometabolic risk factors has not been well described. Patients aged 13-17 years with echocardiogram data between 2012 and 2019 were reviewed. COI scores were calculated using geolocation data. Patients were classified into state-normed COI groups into Very Low, Low, Moderate, High, and Very High opportunity groups. Prevalence of obesity, hypertension, and left ventricular hypertrophy (LVH) were determined. A total of 768 patients (mean age 15.49 ± 1.46 years, 57% male (437/768) were included. A high proportion of patients were in the Very Low and Low COI groups (37.5%). There were significant differences in obesity prevalence between COI groups (X2 = 18.52, df = 4, p < 0.001) with the Low group having the highest prevalence (26.4%). There was not a significant difference in hypertension prevalence between groups. There were significant differences in LVH prevalence between groups (X2 = 11.43, df = 4, p = 0.02) with the highest prevalence in the Low COI group (32.3%). Adolescents with CHD had significant differences in prevalence of obesity and LVH by COI with higher prevalence in the more adverse COI groups. This highlights the importance of considering SDoH when risk stratifying children with CHD.
Obesity is an established risk factor for invasive breast cancer; however, the specific molecular heterogeneity distinguishing invasive ductal carcinoma (IDC) from ductal carcinoma in situ (DCIS) within the obese tumor microenvironment is not well defined. In the current study, spatially resolved transcriptomics was utilized to profile the epithelial, stromal, and immune compartments of DCIS and IDC lesions stratified by host body mass index, categorized as non-obese (≤29.9 kg/m2) or obese (≥30 kg/m2). These analyses reveal that the transcriptional signatures defining the invasive state differ significantly across BMI categories. In non-obese patients, IDC lesions exhibited canonical profiles driven by proliferation and epithelial-to-mesenchymal transition, compared with DCIS. Conversely, the obese setting was characterized by a distinct "stress-adaptive" phenotype, enriched for metabolic adjustment, oxidative stress response, and inflammatory signaling. The epithelial component was accompanied by a fibro-inflammatory stromal signature and an immunosuppressive niche characterized by B cell depletion and M2 macrophage enrichment. Furthermore, SULF2, an extracellular endosulfatase involved in extracellular matrix organization and signaling, was consistently upregulated within the obese epithelium, providing a plausible link between metabolic stress and structural remodeling. Collectively, these data indicate obesity-associated differences consistent with an alternative invasive transcriptional program that is less dominated by classical proliferative drivers in this cohort. Consequently, standard prognostic markers may be context-dependent, highlighting the need to integrate metabolic health into precision risk stratification.
Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) represent a major advancement in obesity treatment, offering robust efficacy in weight loss and metabolic regulation. Beyond these effects, emerging evidence indicates that GLP-1 RAs also modulate appetite, reward sensitivity, and self-regulation, domains that intersect with behavioral and psychological functioning. This review adopts a biopsychosocial perspective to examine how GLP-1 RAs interact with eating behavior, mood, identity, and self-regulation, particularly in individuals with binge eating disorder (BED) or other psychiatric comorbidities. A clinical framework is proposed to integrate pharmacotherapy with lifestyle and psychological interventions. The temporary reduction in appetite and food reward may create a "low-drive window" in which behavioral strategies such as self-monitoring or stimulus control become more effective. However, high emotional eating, mood symptoms, or identity conflicts may moderate treatment response. Given the high prevalence of psychiatric comorbidities, structured screening using tools like the Patient Health Questionnaire-9 (PHQ-9) or Binge Eating Scale (BES) is recommended. A stepped-care approach from brief digital interventions to formal psychotherapy may help address varying support needs. Crucially, weight regain after discontinuation is common. The review discusses behavioral, psychological, and social mechanisms of relapse and highlights strategies for long-term stabilization. These include emotion regulation, body image work, and maintenance-focused behavioral interventions. GLP-1 RAs should therefore be seen not as standalone treatments but as facilitators of self-directed, sustainable change within integrated care models. Future research should define composite outcomes, explore digital tools for relapse prevention, and develop adaptive pathways tailored to individual psychological profiles.
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Binge Eating Disorder (BED) is prevalent among adults with overweight/obesity, yet its detection remains limited by the scarcity of validated tools for Spanish-speaking populations. This study aimed to culturally adapt and evaluate the psychometric properties of the Binge Eating Disorder Screener-7 (BEDS-7) in Chilean adults with overweight/obesity and recurrent binge-eating episodes. The BEDS-7 was translated, back-translated, reviewed by expert judges, and pilot tested to ensure linguistic and cultural adequacy. Content validity evaluation also led to the exploratory addition of two DSM-5-based items. In total, 1,497 adults were recruited; after applying eligibility criteria, 435 were retained. Participants completed the Spanish BEDS-7 and online measures. Content validity was evaluated through expert judgment, structural validity using confirmatory factor analysis and exploratory structural equation modeling, internal consistency using omega coefficients, measurement invariance using multigroup analyses across gender, BMI, and physical activity, and concurrent validity through associations with negative affect. Content validity analyses indicated adequate clarity, coherence, and relevance, although lower sufficiency supported the exploratory inclusion of two additional items. For the BEDS-7, a two-factor structure showed excellent fit (CFI = 0.995; TLI = 0.998; RMSEA = 0.014) and acceptable internal consistency (ω = 0.706), with factors labeled "loss of control" and "emotional distress." Measurement invariance was supported across gender, BMI, and physical activity groups, and negative affect was positively associated with both factors. The Spanish BEDS-7 demonstrated adequate psychometric properties for assessing binge-eating symptomatology in Chilean adults with overweight/obesity and recurrent binge-eating. This study provides novel evidence from Latin America and contributes to cross-cultural comparability. Future research should assess diagnostic accuracy and temporal stability. Binge-eating involves eating large amounts of food while feeling unable to stop. It is common among adults living with overweight or obesity, but many people are not identified early because very few short screening tools exist in Spanish. To help address this gap, we adapted the Binge Eating Disorder Screener-7 (BEDS-7) for use in Chile. Nearly 1,500 adults took part, and 435 met the criteria needed for the analysis. We first checked whether the questions were clear and meaningful for Chilean adults, which led to the addition of two items. We then examined how the questions grouped together and found two main areas: loss of control around eating and emotional distress related to eating. The questionnaire also worked in a similar way for people of different genders, different body-weight categories, and different levels of physical activity. These findings suggest that the Spanish BEDS-7 can be a useful tool for assessing binge-eating symptoms in Chilean adults with overweight or obesity and recurrent binge-eating.
Burkina Faso is experiencing a rapid nutritional transition, yet evidence on the double burden of malnutrition (DBM) at household and individual levels remains limited. This study aimed to estimate the national prevalence of DBMs and identify associated factors with a particular focus on the most common type of DBM. We used data from the 2021 Burkina Faso Demographic Health Survey, a nationally representative cross-sectional survey. The analysis included 4119 households with 5146 women of reproductive age (15-49 years) and 4114 mother-child pair. Eleven (11) potential combinations of maternal and child nutritional status indicators, defined according to WHO standards (anemia, stunting, wasting, underweight, and overweight/obesity) were assessed. Weighted descriptive and bivariate analyses were conducted to identify the most prevalent double burden of malnutrition (DBM) combination, which was selected as the primary outcome. Factors associated with this outcome were examined using multivariate logistic regression with four nested models incorporating household, maternal, and child level characteristics. Overall, 72% of children were affected by anemia, 23% by stunting, and 17% were in underweight condition. Among women, 53% were living with anemia, 17.9% with underweight, and 7.6% with obesity. The predominant DBM form was children with anemia combined with overweight/obesity in women, affecting 14.3% of households. The individual prevalence of anemia and overweight/obesity in women was 9.47%, while stunting paired with overweight in children affected 3.6% of households. Multivariate analysis identified several independent of the predominant form of DBM: region (aOR = 1.94, 95% CI = 1.09-3.45 for Sahel region vs. Boucle du Mouhoun), household wealth (aOR = 3.1, 95% CI = 1.74-5.53 for richest vs. poorest), place of residence (aOR = 0.6, 95% CI = 0.45-0.79 for rural vs. urban), women's age (aOR = 6.48, 95% CI = 2.53-16.61 for 35-39 years compared to 15-19), and women's occupation (aOR = 2.71, 95% CI = 1.5-4.87 for professional manager vs. not working). The most common DBM, child with anemia and maternal overweight/obese women affect more than one in seven households in Burkina Faso, with a higher risk in urban and wealthier settings. Integrated "double duty" interventions are urgently needed to address both mother with overweight/obesity and child with anemia while addressing the structural drivers of nutrition transition and broader social determinants of health.
Setmelanotide, a melanocortin 4 receptor (MC4R) agonist, is a promising pharmacological treatment option for people with rare monogenic obesity conditions affecting the leptin-melanocortin signaling pathway, including proprotein convertase subtilisin/kexin type 1 (PCSK1) gene mutations. It has been studied in people with homozygous mutations causing a complete deficiency of PCSK1. We report the first case of a 40-year-old female with a heterozygous PCSK1 N221D (c.661 A>G) variant mutation leading to severe early-onset treatment-resistant obesity with previous suboptimal response to bariatric surgery and conventional obesity medications, who achieved a total weight loss of 11.8% with setmelanotide treatment over the course of 3 months. Although her mutation confers a loss of 10% to 30% enzymatic function in in vitro studies, setmelanotide was highly effective in treating her obesity. It is also the first reported case of a cutaneous adverse effect of setmelanotide in the form of severe skin hyperpigmentation in a patient with a pathogenic PCSK1 variant. This case underscores the effectiveness and safety of setmelanotide in a heterozygous PCSK1 mutation.
Evidence suggests a significant link between migraine and metabolic syndrome,, especially in those with chronic or refractory migraine. Weight loss and exercise may effectively prevent migraine. Here, we review the evidence behind exercise and weight loss as migraine treatments. While metabolic syndrome and pain have long had a known association, only recently have strong studies demonstrated a higher risk of developing metabolic syndrome in people with migraine. Additionally, other sequelae of metabolic syndrome, obesity, hypertension, hypercoagulability, and diabetes also interplay with migraine. New medications like GLP-1 agonists may be a potential treatment for migraine as well as obesity. For patients with migraine, metabolic syndrome, and obesity, care should be taken when selecting prophylactic medications, favoring those without a propensity to induce weight gain. Additionally, there is strong evidence for weight loss and exercise for improving migraine outcomes.
This retrospective cohort study aimed to compare the effectiveness of glucagon-like peptide-1 receptor agonists (GLP-1RAs) versus metformin for preventing type 2 diabetes mellitus (T2DM), reducing mortality, and improving body mass index (BMI) in antipsychotic-treated patients with overweight /obesity. We used data from the TriNetX Global Collaborative Network. Adults (aged ≥18 years) with overweight or obesity, antipsychotic exposure, and no prior T2DM diagnosis were identified. After propensity score matching, patients initiating GLP-1RA therapy were compared with those initiating metformin. The primary outcome was incident T2DM occurring between 1 and 5 years after treatment initiation. Secondary outcomes included all-cause mortality and BMI change. Among 9939 eligible patients, 3115 matched pairs were included. The incidence of T2DM was significantly lower in the GLP-1RA group compared with the metformin group (1.96% vs 7.26%; hazard ratio [HR]=0.34; 95% CI, 0.26-0.46; p < 0.001). All-cause mortality was also reduced in the GLP-1RA group (0.32% vs 1.96%; HR, 0.25; 95% CI, 0.13-0.49; p < 0.001). Regarding BMI change, patients receiving GLP-1RA experienced greater weight reduction than those receiving metformin. The mean (standard deviation) change in BMI was -2.66 (8.51) kg/m² in the GLP-1 group versus -1.36 (8.63) kg/m² in the metformin group (p < 0.001). In conclusion, in this large real-world cohort of antipsychotic-treated patients with overweight or obesity, GLP-1RA therapy was associated with significantly lower risks of T2DM and mortality, and greater BMI reduction compared with metformin. These findings suggest that GLP-1RAs may offer a more favorable profile against antipsychotic-induced glucose dysregulation.
Self-rated health (SRH) is a widely used indicator of overall health and a robust predictor of morbidity and mortality. Although metabolic health and obesity are well-established determinants of SRH, most previous studies have examined these factors at the individual level. This study investigated how spousal metabolic phenotypes, defined by metabolic and weight status, are jointly associated with SRH among Korean adults. We analyzed nationally representative data from 1817 heterosexual couples. Participants were classified into four phenotypes: metabolically healthy normal weight (MHNW), metabolically healthy obesity (MHO), metabolically unhealthy normal weight (MUNW), and metabolically unhealthy obesity (MUO). We applied actor-partner interdependence models (APIM) and couple-level analyses to assess associations with worse SRH, adjusting for sociodemographic factors, health behaviors, perceived stress, and comorbidities. Among husbands, the MUNW phenotype was significantly associated with worse SRH, with marginal partner effects were observed when wives were MUNW. Among wives, both MUNW and MUO were significant predictors of worse SRH, whereas partner effects were not significant. At the couple level, husbands had higher odds of worse SRH across all non-MHNW couple combinations, whereas wives had higher odds only in discordant couples in which the wife was non-MHNW and the husband was MHNW. Sensitivity analyses among older couples confirmed these findings. These findings highlight gender-specific actor and partner effects and suggest that couple-level metabolic profiles may shape SRH, underscoring the importance of considering spousal metabolic status in its assessment.
Childhood obesity is common and associated with adverse health outcomes. Fetal programming via epigenetics is a potential mechanism underlying its pathogenesis. We conducted an epigenome-wide association study (EWAS) on cord blood DNA to identify DNA methylation sites that may mediate the association of maternal body mass index (BMI) with offspring adiposity using data from the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) Study and its follow-up study (HAPO FUS). HAPO was a prospective, multicenter, international observational study that recruited pregnant women between 2000 and 2006 for glucose tolerance testing; cord blood was collected at delivery and newborn anthropometrics were obtained. The HAPO FUS was conducted from 2013 to 2016, where the 10-14 year-old offspring underwent measures of body composition, anthropometrics, and a fasting glucose tolerance test. Eligibility for HAPO FUS included gestational age at delivery ≥ 37 weeks without major neonatal malformations. There were 3,243 samples with cord blood DNA methylation (cbDNAm) data; mean child age at follow-up was 11.5 years. The present study used cord blood DNA to conduct methylation profiling using the Infinium MethylationEPIC 850 K BeadChip. Linear regression models were used to test the association between maternal BMI and cbDNAm levels adjusting for population substructure, cell count, maternal and child co-variates; multiple testing was accounted for using Bonferroni correction. Mediation analysis tested if cbDNAm CpG sites that were associated (Bonferroni P < 0.05) with maternal BMI explained the known association between maternal BMI and child BMI. This analysis included 3,116 mother-child pairs, 48% White, 21% Asian, 19% Black, 12% Hispanic and < 1% other race/ethnicity self-identified by the mother; 36% of mothers and 28.3% of children had an overweight or obese BMI. Maternal BMI was associated with DNAm at 7 CpG sites following adjustment including: cg00579423, cg07138793, cg12188424, cg19345626, cg20020844, cg02988288 and cg26974062. The 2 CpG sites on the TXNIP gene have been identified in previous EWAS of glucose metabolism and diabetes. Cord blood DNA methylation at cg20020844 (SP6) demonstrated mediation of 1.2% of the association between maternal BMI and child BMI z-score. Exposure to maternal obesity in utero and subsequent differential methylation present at birth may contribute to the prenatal programing of childhood obesity.
To estimate the prevalence of overweight among school-aged children in Tunisia and to identify factors associated with overweight. We conducted a cross-sectional descriptive study between January and April 2025 among children aged 6-11 years attending a Maternal and Child Protection Center in Tunis. Anthropometric measurements were collected, and dietary intake was assessed using a 24-hour dietary recall. Body mass index (BMI) categories were defined according to International Obesity Task Force (IOTF) references. Sociodemographic, perinatal, behavioral, and nutritional variables were analyzed. Multivariable logistic regression was used to identify factors associated with overweight. A total of 225 children aged 6 to 11 years (mean age 9.18±1.73 years; 58% girls). The mean BMI was 18.05±3.6 kg/m². Based on French and IOTF growth references, 26.7% of participants were overweight, including 11.6% classified as obese, and 16.9% showed visceral fat excess. Multivariate analysis identified early adiposity rebound (OR=1.43; p<0.001), grade retention (OR=3.28; p=0.039), maternal obesity (OR=1.5; p=0.035), breastfeeding duration under 6 months (OR=2.61; p=0.003), introduction of cow's milk before 6 months (OR=1.78; p=0.003), hyperphagia (OR=2.03; p=0.001), snacking (OR=4.45; p=0.019), lack of physical activity (OR=4.02; p=0.019), low vitamin A intake (OR=1.02; p=0.029), and high sodium intake (OR=1.15; p=0.043) as independent factors associated with overweight. These findings highlight the importance of early identification and intervention on modifiable behaviors and dietary habits to reduce the burden of childhood overweight.
Dyslipidemia remains a major modifiable contributor to China's cardiovascular disease (CVD) burden, yet large-scale evidence on risk-stratified management gaps is lacking. In this nationwide study across 1,785 hospitals in 28 Chinese provinces, 604,250 outpatients with dyslipidemia were enrolled. We analyzed lipid levels, quantified control rate among treated population and rates of requiring lipid-lowering therapy (LLT) among untreated population across regions, socioeconomic status, and demographic groups. Total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) levels were higher among females, middle-aged individuals, and individuals with obesity. LDL-C levels were also higher among urban residents, while TC showed no significant urban-rural difference. Triglyceride (TG) levels were higher in males, middle-aged individuals, individuals with obesity, and rural residents. Among treated population, LDL-C/non-HDL-C control rates reached 95% in low-risk, 70-90% in moderate-risk, 40-50% in high-risk, and 5-15% in very-high-risk groups. Among untreated population, rates of requiring LLT reached about 20% in the low-risk group and over 70% in moderate- and high-risk groups. After adjusting for covariates, males, older individuals, smokers, patients with hypertension or type 2 diabetes mellitus, as well as those in rural and low-gross-domestic-product areas were associated with lower lipid control rates and higher treatment needs. Our findings highlight the urgent need for risk-stratified lipid management in primary care, improved access to LLT, and policies addressing regional and socioeconomic disparities to enhance lipid control and reduce CVD burden in China. Lessons from China can inform global strategies to improve lipid management and reduce the CVD burden.