Search Results (121)

The present article is an opinion piece mainly based on selected articles in the field of sarcopenia, with possible relevance for pregnancy. Sarcopenia has gained increasing interest in recent years, since it has emerged that sarcopenia may determine significant health consequences, with related substantial health care expenditure. In particular, some studies suggested that sarcopenia may cause increased risk for several diseases, such as type 2 diabetes, obesity, and major cardiovascular events. On the other hand, some studies have reported that the association between sarcopenia and these diseases may be bidirectional. In particular, this holds for type 2 diabetes, because sarcopenia and type 2 diabetes share many etiological and pathogenetic factors, such as insulin resistance, oxidative stress, low-grade chronic inflammation, and adiposity. It is also worth noting that some studies have shown a non-negligible sarcopenia prevalence even in people below 40 years of age, and therefore of reproductive age. Taken together, the above considerations support the hypothesis that sarcopenia may be present in women with gestational diabetes (GDM), which shares common traits with type 2 diabetes. Notably, we hypothesize that sarcopenia may exacerbate GDM-related complications and may influence maternal–fetal outcomes, such as preterm birth or cesarean delivery. Additionally, since pregnancy often presents with insulin resistance independently of any comorbidity, it is plausible that sarcopenia may be present during pregnancy even in cases of normal glycemia. However, there is a lack of data about sarcopenia prevalence in pregnancy and its potential impact on outcomes. Therefore, future studies addressing these aspects are advisable. Full article

Background/Objectives: Obesity, a major risk factor for cardiometabolic traits, is influenced by both genetic and environmental factors. Genetic studies have identified multiple single-nucleotide polymorphisms (SNPs) associated with obesity and related traits. This study aimed to examine the association between genetic risk score (GRS) and obesity-associated traits, while incorporating SNPs with established gene–diet interactions to explore their potential role in precision nutrition (PN) strategies. Methods: A total of 4279 participants were stratified into low- and intermediate-/high-GRS groups based on 18 SNPs linked to obesity and cardiometabolic traits. This study followed a case–control design, where cases included individuals with overweight/obesity, T2DM-positive (+), or CVD-positive (+) individuals and controls, which comprised individuals free of these traits. Logistic regression area under the curve (AUC) models were used to assess the predictive power of the GRS and traditional risk factors on BMI, T2DM and CVD. Results: Individuals in the intermediate-/high-GRS group had higher odds of being overweight or obese (OR = 1.23, CI: 1.03–1.48, p = 0.02), presenting as T2DM+ (OR = 1.56, CI: 1.03–2.49, p = 0.03) and exhibiting CVD-related traits (OR = 1.56, CI: 1.25–1.95, p < 0.0001), compared to the low-GRS group. The GRS was the second most predictive factor after age for BMI (AUC = 0.515; 95% CI: 0.462–0.538). The GRS also demonstrated a predictive power of 0.528 (95% CI: 0.508–0.564) for CVD and 0.548 (95% CI: 0.440–0.605) for T2DM. Conclusions: This study supports the potential utility of the GRS in assessing obesity and cardiometabolic risk, while emphasizing the potential of PN approaches in modulating genetic susceptibility. Incorporating gene–diet interactions provides actionable insights for personalized dietary strategies. Future research should integrate multiple gene–diet and gene–gene interactions to enhance risk prediction and targeted interventions. Full article

Objectives: This study aimed to explore the mediating effects of iron homeostasis biomarkers linking central obesity with metabolic dysfunction-associated steatotic liver disease (MASLD) and primary liver cancer (PLC) via Mendelian randomization (MR) analysis. Methods: Two-sample bidirectional MR, multivariable MR, and mediation analyses were used to investigate the causal associations among obesity-related traits, iron homeostasis biomarkers, MASLD, and PLC. For the discovery and replication analyses, GWAS summary data for iron homeostasis biomarkers, MASLD, and PLC were extracted from two datasets, and the combined effects were pooled to corroborate the conclusions. Results: BMI and waist circumference were associated with a risk of MASLD in their combined effects (OR = 1.83, 95% CI = 1.33–2.52 for BMI; OR = 1.98, 95% CI = 1.63–2.41 for waist circumference). Waist circumference but not BMI had significant causal effects on the risk of PLC in the discovery dataset (OR = 1.71, 95% CI = 1.01–2.89 for BMI; OR = 2.72, 95% CI = 1.37–5.39 for waist circumference). In both of the iron homeostasis datasets, genetically predicted increased ferritin was associated with increased risk of MASLD by multivariable MR. We only observed that genetic liability to increased ferritin was associated with increased risk of PLC in iron homeostasis dataset 1 after adjusting for waist circumference. By two-step MR analysis, we found that genetic liability to ferritin mediated 3.34% (95% CI: 0.17–8.08%) of waist circumference effects on MASLD risk and 18.84% (95% CI: 3.01–40.51%) of its effects on PLC risk. Conclusions: Waist circumference and iron homeostasis biomarkers were causally associated with increased risks of MASLD and PLC. Central obesity may contribute to the development of MASLD and PLC by increasing ferritin levels. Full article

Background: Growth differentiation factor 15 (GDF-15), a member of the transforming growth factor-β (TGF-β) superfamily, is upregulated under cellular stress conditions and has emerged as a potential biomarker for metabolic disorders. However, its expression in relation to diabetes and obesity across different demographic groups remains understudied. This study investigated the association between plasma GDF-15 levels, diabetes mellitus, and obesity in individuals of varying ages, ethnicities, and genders. Methods: In a cross-sectional study, plasma GDF-15 concentrations were measured in 2083 participants enrolled in the Kuwait Diabetes Epidemiology Program (KDEP). The dataset included anthropometric, clinical, biochemical, and glycemic markers. Multivariate regression analysis was used to examine associations between GDF-15 levels and metabolic phenotypes. Results: Mean plasma GDF-15 levels were significantly higher in males than females (580.6 vs. 519.3 ng/L, p < 0.001), and in participants >50 years compared to those <50 years (781.4 vs. 563.4 ng/L, p < 0.001). Arab participants had higher GDF-15 levels than South and Southeast Asians (597.0 vs. 514.9 and 509.9 ng/L, respectively; p < 0.001). Positive correlations were found with BMI, waist and hip circumferences, blood pressure, insulin, and triglycerides; negative correlations were observed with HDL cholesterol. Median regression indicated that elevated GDF-15 levels were independently and significantly associated with male gender, older age, obesity, diabetes, and insulin resistance. Adjusted median regression indicated that male gender (β = 30.1, 95%CI: 11.7, 48.5), older age (β = 9.4, 95%CI: 8.0, 10.7), and insulin resistance (β = 7.73, 95%CI: 1.47, 14.0) indicated a significant positive association with GDF-15. South Asian participants (β= −41.7, 95%CI: −67.2, −16.2) had significantly but Southeast Asian participants (β= −23.3, 95%CI: −49.2, 2.56) had marginally significantly lower GDF-15 levels compared to participants of Arab ethnicity. Conclusions: Higher GDF-15 levels are associated with age, male gender, Arab ethnicity, obesity, and diabetic traits. These findings support the potential role of GDF-15 as a biomarker for metabolic disorders, particularly in high-risk demographic subgroups. Full article

Insulin resistance (IR) is a key mechanism underlying type 2 diabetes mellitus and is closely associated with obesity. Although numerous genome-wide association studies (GWASs) have identified variants that influence IR-related traits, it remains unclear whether the genetic architecture of IR differs according to obesity status. We conducted a stratified GWAS of the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) in 8906 Korean individuals from the Korean Genome and Epidemiology Study. Participants were categorized into a normal-weight group (Body Mass Index (BMI) ≤ 23 kg/m²) and an overweight or obese group (BMI > 23 kg/m²), and the GWAS was performed separately within each group. No significant genome-wide variants were identified in the normal-weight group; however, seven loci showed suggestive associations. In contrast, in the overweight and obese group, two loci, rs662799 in Apolipoprotein A5 (APOA5) and rs671 in Aldehyde Dehydrogenase 2 (ALDH2), showed genome-wide significance, with seven loci showing suggestive associations. The risk allele of rs662799 was associated with increased HOMA-IR values, with a stronger effect observed in the overweight and obese group. This finding aligns with the known role of APOA5 in triglyceride metabolism, suggesting that a higher BMI may exacerbate its effect on IR. These results highlight obesity-specific genetic susceptibility to IR and the need to consider obesity status in genetic studies of metabolic traits. Full article

Background/Objectives: There is scientific evidence showing that body- and/or body weight-related blaming, guilting, and shaming continue to be both promoted and tolerated in many societal contexts, including schools and healthcare settings. A deeply ingrained belief still prevails among many individuals that inducing these negative emotions can serve as a motivator for children and adolescents to engage in obesity treatment. Therefore, the aim of this systematic review is to examine these emotions (blame, guilt, shame) in relation to body weight and their impact on psychological functioning within the pediatric population affected by overweight and obesity. Methods: Articles were searched up using PubMed and Web of Science in June 2023 and March 2025. The search was conducted without limiting the years of publication. The inclusion criteria included the following: (1) pediatric samples, (2) full text available, and (3) original research articles. Articles were excluded if they were editorials, letters, replies from authors, review articles, and articles without a full text. Results: The initial search returned 199 results. A total of 16 articles were included in the study. Analysis of the collected records revealed associations between body- or weight-related blame, guilt, and shame and various aspects of psychological functioning in the pediatric population such as (a) interpersonal context (e.g., social stigma, bullying, teasing history, social connectedness, weight-related language used by parents in conversations with children and adolescents; (b) intrapsychic context—relationship with eating and food (e.g., binge eating, dietary restraint, emotional eating, and the risk of developing eating disorders); (c) intrapsychic context—self-perception (e.g., self-esteem, feelings of worthlessness, self-compassion, self-efficacy, perceived control); (d) intrapsychic context—emotional functioning (e.g., emotional distress, anxiety, depression, emotion regulation strategies); and (e) intrapsychic context—additional psychological factors (e.g., mindfulness, quality of life, willingness to seek help, and motivation for both help-seeking and sustaining successful lifestyle changes). Conclusions: Understanding the dynamics of body- and/or weight-related blame, guilt, and shame among children and adolescents with overweight and obesity is essential for developing effective support systems that enhance their well-being and psychological resilience in both the prevention and treatment of obesity. Further research is needed to explore the relationships between body- and weight-related blame, guilt, and shame and psychological functioning in pediatric populations with overweight and obesity, including the dynamics of child–parent–healthcare provider interactions, the context of parenting skills and attitudes that support the child during obesity treatment, the long-term consequences of body- and weight-related blame, guilt, and shame, the relationship between healthcare providers’ tendencies to engage in body- and weight-related shaming or blaming and their communication skills and mental well-being (e.g., levels of professional burnout, emotion regulation skills, and personality traits), as well as the influence of social media on body- and weight-related shame, guilt, and blame. Full article

Introduction: Obesity is a global health problem requiring effective interventions to achieve weight loss and maintain it in the long term. A major challenge for clinicians is weight regain (WR), defined as progressive weight gain following successful weight loss. WR is affected by multiple factors, including psychological traits linked to specific brain alterations. Understanding these mechanisms is crucial in developing strategies to prevent WR and to ensure effective weight control. Objectives: This narrative review aims to gather current findings on the psychological and neurobiological determinants of WR and to discuss the interplay between these factors. Methods: A literature search was conducted on PubMed, Medline, and Web of Science for English-language studies published between December 1990 and November 2024. Results: WR is driven by interconnected psychological and neurobiological factors that influence eating behavior and the regulation of body weight. Certain personality traits and emotional patterns are associated with specific changes in brain activity, which together affect vulnerability to WR. Although distinct mechanisms can be identified, the complexity of homeostatic and nonhomeostatic appetite control suggests that no single factor predominates. Conclusions: This review highlights the dynamic interplay between psychological and neurobiological predictors of WR. However, due to the narrative nature of this review, the focus on selected determinants, and the limited quality and size of the available studies, further research is needed to comprehensively understand causality and to improve relapse prevention strategies. Full article

Background and Objectives: Pre-eclampsia (PE) is a serious pregnancy complication defined by the onset of hypertension and multi-organ dysfunction occurring after 20 weeks of gestation. Studies have indicated the correlation between diabetes mellitus (DM) and PE, but the causal relationship remains unclear. Materials and Methods: The two-sample Mendelian randomization (MR) approach, including the inverse variance weighted random effects (IVW-RE) model and the traditional sensitivity model, was employed to assess the causal effects of pre-pregnancy type 1 diabetes (T1D) and type 2 diabetes (T2D) on PE using summary-level data obtained from genome-wide association studies. Additionally, diabetes-related factors, such as glycated hemoglobin (HbA1c) levels, fasting insulin levels, and body mass index (BMI), were evaluated for their potential causal effects on the risk of PE. Pleiotropy-robust and multivariable Mendelian randomization (MVMR) methods were further used because of the intricate associations among the traits. Insulin and metformin use was also assessed for their causal role in PE risk. Results: Our findings show that genetically predicted T1D (OR = 1.06, 95% CI: 1.03–1.09, p < 0.001), T2D (OR = 1.09, 95% CI: 1.04–1.14, p < 0.001), and BMI (OR = 1.64, 95% CI 1.49 to 1.80, p < 0.001) had causal effects on the incidence of PE, while the effects of HbA1c (OR = 0.77, 95% CI 0.59 to 1.02, p = 0.064) and fasting insulin levels (OR = 1.35, 95% CI 0.89 to 2.05, p = 0.153) on the occurrence of PE were not significant. The results were verified by MVMR analysis. Additionally, insulin use increased the risk of pre-eclampsia (OR = 1.11, 95% CI 1.05–1.17, p < 0.001). Conclusions: Our findings demonstrate a causal relationship between pre-pregnancy diabetes (DM) and obesity and the risk of PE from a genetic epidemiological perspective. Adverse maternal factors, including DM and obesity prior to pregnancy, should be considered in mechanistic studies of PE. In addition, comprehensive interventions for risk factors such as pre-pregnancy DM and obesity should be emphasized in clinical practice. Full article

In the domain of swine production, body weight (BW) and average daily gain (ADG) are recognized as the primary performance indicators. Nevertheless, the genetic architecture of ADG and BW in Dongliao black (DLB) pigs remains to be fully elucidated. In this study, we performed a genome-wide association analysis of BW, ADG, and body mass index (BMI) in 358 DLB pigs of different days of age. The genome-wide association study (GWAS) showed the following: (1) The most significant single nucleotide polymorphism (SNP) detected for BW was on Sus scrofa chromosome (SSC) 11:100,808 (p-value = 1.16 × 10⁻⁶) that was also the most significant SNP for ADG. (2) The most significant SNP associated with BMI was SSC17:51,463,521 (p-value = 5.16 × 10⁻⁸). (3) SNPs SSC10:6,523,844 and SSC17:23,852,682 were identified in both BW and ADG. A meta-analysis was conducted on BW at different days and demonstrated SSC5:39,028,335 (p-value = 8.37 × 10⁻⁶) which was not identified in the results of each single trait. The regions of two SNPs (SSC11:100,808, SSC4:10,703,277) exhibited considerable influence on both BW and ADG and the related regions were selected for linkage disequilibrium (LD) analyses that exhibited a notable linkage. In addition, several genes were identified that are associated with obesity and play roles in lipid metabolism, including MACROD2, PHLPP2, CYP2E1, and STT3B. Full article

Introduction: Autism and ADHD shape behaviours related to food, exercise, and body image, potentially influencing obesity treatment outcomes, as seen in eating disorder research. Resultantly, autistic and ADHD patients with obesity may have distinct experiences and differences compared to non-autistic and non-ADHD patients. This review maps existing literature on autism and ADHD in adults with obesity. Methods: Following PRISMA guidelines, six databases (Embase, MEDLINE, PsycINFO, Web of Science, CENTRAL, and Scopus) were searched for studies on autism and/or ADHD (diagnosed, probable, or traits) in adults with obesity. Screening and data extraction were conducted twice independently for each record. Results: Thirty-one studies were included, with 1,027,773 participants. Two case reports described successful use of weight loss drugs in autistic people with obesity. Eight prevalence studies suggested ADHD is overrepresented in obesity, regardless of binge eating status. Nineteen studies examined clinical profiles: ADHD patients had lower socioeconomic status, poorer health-related quality of life, increased impulsivity, cognitive inflexibility, and neuroticism, alongside lower agreeableness, conscientiousness, self-directedness, and cooperativeness. ADHD patients also exhibited higher psychopathology, problematic alcohol use, and disordered eating. Eight studies assessed treatment responses, noting poorer outcomes from behavioural programs and obesity pharmacotherapy, but similar post-surgical weight outcomes, despite increased complications. Two studies considered ADHD-specific treatment adaptions, one reporting a successful trial of ADHD medication for weight loss and the other reporting on switching to transdermal ADHD medications after bariatric surgery. Conclusions: This review underscores the need for more research on autism and obesity. For ADHD, findings suggest frequent co-occurrence with obesity, but lived experiences and tailored interventions remain underexplored. Full article

Chronic liver diseases, such as those encountered with obesity, chronic/abusive alcohol consumption or viral infections, represent not only major public health concerns with limited therapeutic options but also important risk factors for the onset of hepatocellular carcinoma (HCC). Deciphering the molecular traits underlying these disorders is of high interest for designing new and effective treatments. The tristetraprolin (TTP) family members are of particular importance given their ability to control the expression of a wide range of genes involved in metabolism, inflammation and carcinogenesis at the post-transcriptional level. This regulation can occur within small cytoplasmic granules, namely, processing bodies (P-bodies), where the mRNA degradation occurs. Increasing evidence indicates that TTP family members and P-bodies are involved in the development of chronic liver diseases and cancers. In this review, we discuss the role of this regulatory mechanism in metabolic-dysfunction-associated steatotic liver disease (MASLD), alcohol-related liver disease (ALD), hepatic viral infections and HCC. Full article

Background/Objectives: Binge eating (BE) is associated with physical and psychological consequences, such as obesity and reduced quality of life. The relationship between binge eating and childhood experiences of interpersonal trauma has been explored, yet few studies focus on the processes that may explain this association. In this regard, some personality traits and maladaptive cognitive-emotional regulation may help explain this relationship, as they have been associated, respectively, with BE and childhood interpersonal trauma. The purpose of this study is to explore the complex processes that link childhood interpersonal trauma and BE in a French-Canadian clinical adult population with obesity (BMI ≥ 30 kg/m²). Methods: This cross-sectional study included 148 participants aged 21 to 72, predominantly women of White ethnic background with a university degree, who were seeking treatment for eating or weight-related issues. They completed self-report questionnaires assessing maltreatment and bullying, BE, maladaptive cognitive-emotional regulation, and personality. Two multiple mediation models were tested to examine the indirect effects of personality and maladaptive regulation in the relationship between bullying and BE, as well as between maltreatment and BE. Results: The results revealed a significant indirect relationship between maltreatment and binge eating (BE), with personality traits and maladaptive cognitive-emotional regulation partially explaining this association. No direct effect was found for bullying, but a significant total indirect effect indicated that personality traits and maladaptive cognitive-emotional regulation play a mediating role in the relationship between bullying and BE. Finaly, self-directedness was found as a unique and significant contributor in both mediation models. Conclusions: This study draws attention to the multiple contributing factors in the relationship between interpersonal trauma and BE in adults with obesity. Further research is needed to gain a deeper understanding of the role of personality and maladaptive cognitive-emotional regulation in this relationship by focusing on individuals’ experiences. Full article

Background: Myocardial infarction (MI) can range from mild to severe cardiovascular events and typically develops through complex interactions between genetic and lifestyle factors. Objectives: We aimed to understand the genetic predisposition associated with MI through genetic correlation, colocalization analysis, and cells’ gene expression values to develop more effective prevention and treatment strategies to reduce its burden. Methods: A polygenic risk score (PRS) was employed to estimate the genetic risk for MI and to analyze the dietary interactions with PRS that affect MI risk in adults over 45 years (n = 58,701). Genetic correlation (rg) between MI and metabolic syndrome-related traits was estimated with linkage disequilibrium score regression. Single-cell RNA sequencing (scRNA-seq) analysis was performed to investigate cellular heterogeneity in MI-associated genes. Results: Ten significant genetic variants associated with MI risk were related to cardiac, immune, and brain functions. A high PRS was associated with a threefold increase in MI risk (OR: 3.074, 95% CI: 2.354–4.014, p < 0.001). This increased the risk of MI plus obesity, hyperglycemia, dyslipidemia, and hypertension by about twofold after adjusting for MI-related covariates (p < 0.001). The PRS interacted with moderate fat intake (>15 energy percent), alcohol consumption (<30 g/day), and non-smoking, reducing MI risk in participants with a high PRS. MI was negatively correlated with the consumption of olive oil, sesame oil, and perilla oil used for cooking (rg = −0.364). MI risk was associated with storkhead box 1 (STOX1) and vacuolar protein sorting-associated protein 26A (VPS26A) in atrial and ventricular cardiomyocytes and fibroblasts. Conclusions: This study identified novel genetic variants and gene expression patterns associated with MI risk, influenced by their interaction with fat and alcohol intake, and smoking status. Our findings provide insights for developing personalized prevention and treatment strategies targeting this complex clinical presentation of MI. Full article

Background: Metabolic inflammation (MI), long COVID (LC) and systemic lupus erythematosus (SLE) share some metabolic common manifestations and inflammatory pathophysiological similarities. Health-related quality of life (HRQoL) and metabolic age are indicators of health status. The “METAINFLAMMATION-CM Y2020/BIO-6600” project, a prospective controlled study, aimed to identify differential diagnostic tools and clinical features among three inflammatory conditions by comparing obesity status (low BMI vs. high BMI). Methods: A total of 272 adults of both Caucasian and Hispanic descent, diagnosed with MI, LC or SLE, and a range of BMI, were recruited. Clinical and phenotypic traits were measured to analyze body composition, metabolic and inflammatory markers, HRQoL data, metabolic age and lifestyle habits using a 3 × 2 (disease × BMI) factorial design. Results: Some inflammatory related variables, such as fibrinogen, RDW (red cell blood distribution width), ESR (erythrocyte sedimentation rate) and NLR (neutrophil/lymphocyte ratio), showed effect modifications depending on the BMI and disease type. In relation to HRQoL, the Physical Component Summary (PCS12) showed no relevant changes, while the Mental Component Summary (MCS12) showed a significant effect modification according to the disease type and BMI (p < 0.05). Furthermore, a significant interaction was identified between the disease type and BMI in relation to metabolic age (p = 0.02). Conclusions: Assessing the impact of BMI on these three inflammatory diseases may help to prevent clinical complications and to design personalized treatments, especially for patients with SLE, who have a worse prognosis with an increased BMI compared to the other two inflammatory diseases. Full article

Background and Objectives: Age at menarche is related to various biological and socioeconomic factors in childhood. The aim of the study was to examine the association of age at menarche with general and abdominal obesity in young women. Materials and Methods: A transversal anthropometric survey was conducted with 102 females from 21 to 25 years of age. The surveyed traits included height, weight, waist circumference (WC) and hip circumference (HC). General obesity was assessed using the body mass index (BMI) and abdominal obesity by WC, waist-to-hip ratio (WHR) and waist-to-height ratio (WHtR). A retrospective method was used for collecting age at menarche data. Results: The average age at menarche is 12.80 years. Early menarcheal age (<12 years) is detected in 25.5% of young females, while late onset of menarche (>14 years) is recorded for 20.6% of subjects. Early menarche age subjects exhibit significantly higher BMI, WC and WHtR in comparison with their late menarche age peers. There is a significant negative correlation between BMI, WC and WHtR values and menarcheal age. Late age at menarche is associated with higher probability of underweight status (BMI < 18.5 and/or WHtR < 0.4). Conclusions: Age at menarche has a negative correlation with general and abdominal obesity. Young women with early age at menarche show statistically higher values of BMI, WC and WHtR, while those with late menarcheal age show greater susceptibility to becoming underweight. Full article