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Objective: To determine whether statin medication in individuals with obesity, dyslipidemia, and metabolic syndrome affects their capacity to mobilize and oxidize fat during exercise. Methods: Twelve individuals with metabolic syndrome pedaled during 75 min at 54 ± 13% ...O2max (5.7 ± 0.5 metabolic equivalents) while taking statins (STATs) or after 96-hr statin withdrawal (PLAC) in a randomized double-blind fashion. Results: At rest, PLAC increased low-density lipoprotein cholesterol (i.e., STAT 2.55 ± 0.96 vs. PLAC 3.16 ± 0.76 mmol/L; p = .004) and total cholesterol blood levels (i.e., STAT 4.39 ± 1.16 vs. PLAC 4.98 ± 0.97 mmol/L; p = .008). At rest, fat oxidation (0.99 ± 0.34 vs. 0.76 ± 0.37 μmol⋅kg-1⋅min-1 for STAT vs. PLAC; p = .068) and the rates of plasma appearance of glucose and glycerol (i.e., Ra glucose-glycerol) were not affected by PLAC. After 70 min of exercise, fat oxidation was similar between trials (2.94 ± 1.56 vs. 3.06 ± 1.94 μmol⋅kg-1⋅min-1, STA vs. PLAC; p = .875). PLAC did not alter the rates of disappearance of glucose in plasma during exercise (i.e., 23.9 ± 6.9 vs. 24.5 ± 8.2 μmol⋅kg-1⋅min-1 for STAT vs. PLAC; p = .611) or the rate of plasma appearance of glycerol (i.e., 8.5 ± 1.9 vs. 7.9 ± 1.8 μmol⋅kg-1⋅min-1 for STAT vs. PLAC; p = .262). Conclusions: In patients with obesity, dyslipidemia, and metabolic syndrome, statins do not compromise their ability to mobilize and oxidize fat at rest or during prolonged, moderately intense exercise (i.e., equivalent to brisk walking). In these patients, the combination of statins and exercise could help to better manage their dyslipidemia. [ABSTRACT FROM AUTHOR]

Summary Background and Objectives Methods Results Conclusion This study aimed to examine the associations between breastfeeding duration and metabolic syndrome (MetS) in adolescents and to further investigate the role of birth weight for gestational age (GA) on these associations.A total of 10 275 participants aged 7 to 18 years were included applying multistage cluster random sampling from a Chinese national survey. Birth weight was classified into small for GA (SGA), appropriate for GA (AGA) and large for GA (LGA). Information was collected through a self‐administered questionnaire, physical examination and blood biochemical examination. Multivariable linear regression, logistic regression models, restricted cubic spline models were applied to assess the relationships of breastfeeding duration and MetS with different birth weight for GA.The prevalence of non‐breastfeeding, 0–5, 6–12 and >12 months groups were 16.2%, 23.1%, 42.5% and 18.2%, and the prevalence of SGA and LGA was 11.9% and 12.7%, respectively. Prolonged breastfeeding duration was associated with higher odds of MetS (β: 0.08, 95% CI: 0.03, 0.13), WC (β: 3.49, 95% CI: 2.82, 4.16) and SBP (β: 2.34, 95% CI: 1.80, 2.89). SGA and prolonged breastfeeding synergistically increased MetS risks, but LGA appeared to offset the adverse effects of prolonged breastfeeding.Prolonged breastfeeding may increase children's MetS risks. SGA synergies with prolonged breastfeeding increased MetS burden in children and adolescents, while LGA mitigated the risks. This reminds us that intensive attention should be paid to both early birth weight and subsequent living environment for children and adolescents' lifelong health. [ABSTRACT FROM AUTHOR]

Previous clinical studies on the anti-inflammatory effects of folic acid (FA) in patients with metabolic syndrome (MetS) have shown controversial results. This study aimed to synthesize the evidence on the effect of FA on inflammatory marker levels in MetS patients. We screened PubMed, Embase, Medline, and the Cochrane Library (from inception to March 2022) to identify relevant randomized controlled trials (RCTs). DerSimonian and Laird random effects were used to estimate the pooled weighted mean difference (WMD) with 95% confidence interval (CI). Funnel plot, Egger's test, and the Begg-Mazumdar correlation test was used to assess publication bias. Subgroup analysis, meta-regression and sensitivity analysis were performed to find out possible sources of between-study heterogeneity. Ten RCTs with a total of 511 participants were included. The analysis showed that FA reduced high sensitivity C-reactive protein (hs-CRP) (WMD, −0.94; 95% CI, −1.56 to −0.32; P = 0.00), interleukin-6 (IL-6) (WMD, −0.39; 95% CI, −0.51 to −0.28; P = 0.00), and tumor necrosis factor-alpha (TNF-α) (WMD, −1.28; 95% CI, −1.88 to −0.68; P = 0.00), but did not decrease the C-reactive protein (CRP) (WMD, 0.10; 95% CI, −0.13 to 0.33; P = 0.38). Sensitivity analysis, subgroup analysis, and meta-regression showed that the effect sizes remained stable. Our findings suggest that FA supplementation could reduce inflammatory markers, such as hs-CRP, IL-6, TNF-α in patients with MetS. This study is registered with PROSPERO (CRD42021223843). [ABSTRACT FROM AUTHOR]

Background: Metabolic syndrome (MetS) elevates cancer risk. However, a single MetS assessment does not fully reveal the long‐term association with cancer. Inflammation, alongside MetS, could synergistically expedite both the onset and advancement of cancer. This study aims to investigate MetS score trajectories and cancer risk in a large, prospective cohort study. Methods: The authors prospectively examined the relationship between MetS score trajectory patterns and new‐onset cancer in 44,115 participants. Latent mixture modeling was used to identify the MetS score trajectories. Cox proportional hazards regression models were used to evaluate the association between MetS score trajectory patterns and the risk of overall and site‐specific cancers. Results: Four MetS score trajectory patterns were identified: low‐stable (n = 4657), moderate‐low (n = 18,018), moderate‐high (n = 18,288), and elevated‐increasing (n = 3152). Compared to participants with a low‐stable trajectory pattern, the elevated‐increasing trajectory pattern was associated with an elevated risk of overall (hazard ratio [HR], 1.27; 95% confidence interval [CI], 1.04–1.55), breast (HR, 2.11; 95% CI, 1.04–4.34), endometrial (HR, 3.33; 95% CI, 1.16–6.77), kidney (HR, 4.52; 95% CI, 1.17–10.48), colorectal (HR, 2.54; 95% CI, 1.27–5.09), and liver (HR, 1.61; 95% CI, 1.09–4.57) cancers. Among participants with chronic inflammation (C‐reactive protein levels ≥3 mg/L), the elevated‐increasing trajectory pattern was significantly associated with subsequent breast, endometrial, colorectal, and liver cancers. Conclusions: Trajectories of MetS scores are associated with the occurrence of cancers, especially breast, endometrial, kidney, colorectal, and liver cancers, emphasizing the importance of long‐term monitoring and evaluation of MetS. Plain Language Summary: The association between long‐term elevated metabolic syndrome (MetS) scores and a heightened risk of various cancers is a pivotal finding of our study.Our research further indicates that individuals with MetS, particularly when coupled with chronic inflammation, are at an increased risk of cancer.We propose that sustained monitoring and management of MetS could be beneficial in reducing cancer risk. Metabolic syndrome (MetS) score trajectories have been linked to an increased risk of several cancers, including breast, endometrial, kidney, colorectal, and liver cancers. This highlights the critical need for long‐term monitoring and evaluation of MetS. [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma is one of the deadliest and fastest‐growing cancers. Among HCC etiologies, metabolic dysfunction‐associated fatty liver disease (MAFLD) has served as a major HCC driver due to its great potential for increasing cirrhosis. The obesogenic environment fosters a positive energy balance and results in a continuous rise of obesity and metabolic syndrome. However, it is difficult to understand how metabolic complications lead to the poor prognosis of liver diseases and which molecular mechanisms are underpinning MAFLD‐driven HCC development. Thus, suitable preclinical models that recapitulate human etiologies are essentially required. Numerous preclinical models have been created but not many mimicked anthropometric measures and the course of disease progression shown in the patients. Here we review the literature on adipose tissues, liver‐related HCC etiologies and recently discovered genetic mutation signatures found in MAFLD‐driven HCC patients. We also critically review current rodent models suggested for MAFLD‐driven HCC study. [ABSTRACT FROM AUTHOR]

Introduction/Aims Methods Results Discussion Spinal muscular atrophy (SMA) is a multisystem disorder. We assessed metabolic syndrome (MetS) prevalence in adults with SMA and its association with motor function, quality of life (QoL), fatigue, and depression.MetS was diagnosed using 2009 consensus criteria. Hammersmith Functional Motor Scale Expanded (HFMSE), Revised Upper Limb Module (RULM), Fatigue Severity Scale (FSS), Beck Depression Inventory (BDI), and 36‐Item Short Form Health Survey (SF‐36) were recorded and correlations between muscle function, depression, fatigue, QoL, and MetS were analyzed.We included 36 individuals (18 males; mean age: 38.7 ± 14.6 years). MetS was present in 25.0%. The most common component of MetS was central obesity (69.7%). Nearly half of the SMA individuals exhibited at least one abnormal lipid level result. Individuals with MetS more frequently were SMA type 3 (77.8% vs. 37.0%, p = .02) and had higher levels of fatigue (48.4 ± 6.7 vs. 39.5 ± 11.6, p = .03) than those without MetS. No associations of the presence of MetS with ambulatory status or HFMSE/RULM scores were observed. SMA individuals with MetS scored significantly lower in mental and social domains of QoL and total SF‐36 score (p = .04). We observed weak to moderate correlations between the presence of MetS and SMA type, presence of comorbidities, QoL, and fatigue.The frequency of MetS was modestly higher among adults with SMA than in the general population, particularly in SMA type 3. MetS was associated with reduced QoL and increased fatigue. Larger studies are needed to fully understand the significance of MetS in adults with SMA. [ABSTRACT FROM AUTHOR]

Metabolic Syndrome (MetS) represents a group of cardiovascular risk factors. This article aims to evaluate the accuracy of the tools of MetS diagnosis in Nursing professionals from Primary Health Care (PHC) in Bahia, Brazil. A cross-sectional study with a random sample selected according to essential health information for the diagnostic of MetS. For MetS diagnostic, we used EGIR, NCEP-ATPIII, AACE, IDF, Barbosa et al. (2006), and IDF/AHA/NHLBI (defined as gold standard) definition. Sensitivity, specificity, predictive values, and likelihood ratio were estimated for each diagnostic tool and compared with the gold standard. Kappa statistic was used to determine the agreement between the diagnostic methods. One thousand one hundred and eleven nursing professionals were included in this study. Sensitivity varied from 15% to 95.1%, and specificity varied between 99.5% and 100%. IDF and Barbosa et al. (2006) definitions were more sensitive (95.1% and 92.8%, respectively), and EGIR, NCEP, ATP III, and IDF showed 100% specificity. IDF and Barbosa et al. (2006) use suitable metabolic syndrome identification and confirmation criteria. The highest agreement was found in the definition of the IDF, Barbosa et al. (2006) and the NCEP ATP III. Defining metabolic syndrome with a higher diagnostic accuracy could contribute to the screening and the early identification of nursing professionals with cardiovascular disease risk factors, which provide opportunities for appropriate prevention and treatment. [ABSTRACT FROM AUTHOR]

Background: The study aimed to explore the relationship between low-density lipoprotein cholesterol (LDL-C) genetic variants and obstructive sleep apnea (OSA) and its complications, including cardiovascular diseases (CVD), insulin resistance (IR), and metabolic syndrome (MS). Method: 4329 individuals with suspected OSA who underwent a comprehensive assessment of anthropometric, biochemical, and polysomnography (PSG) data, along with 30 LDL-C single nucleotide polymorphisms (SNPs) were enrolled. The 10-year Framingham CVD risk score (FRS), IR and MS were evaluated for each subject. Linear regression and logistic regression were utilized to examine the correlations among these variables. Results: After the Benjamini-Hochberg correction, linear regression results indicated positive correlations between variants rs3741297 and rs629301 with FRS (β = 0.031, PBH=0.002; β = 0.026, PBH=0.015). Logistic regression revealed that rs3741297 increased MS risk among total subjects [OR = 1.67 (95% CI:1.369–2.038), PBH=1.32 × 10− 5] and increased IR risk in females [OR = 3.475 (95% CI:1.653–7.307), PBH=0.03]. In males, rs2642438 decreased MS risk [OR = 0.81 (95% CI:0.703–0.933), PBH=0.045]. Conclusions: The rs3741297 variant correlated with susceptibility to CVD, IR, and MS in the OSA population. OSA, CVD, IR and MS share a potentially common genetic background, which may promote precision medicine. Cinical trial registration: The study protocol was registered with the Chinese Clinical Trial Registry (ChiCTR1900025714). [ABSTRACT FROM AUTHOR]

Background: Although the association between mental disorder and metabolic syndrome as a bidirectional relationship has been demonstrated, there is little knowledge of the cumulative and individual effect of these conditions on peripartum mental health. This study aims to investigate the association between metabolic syndrome conditions (MetS-C) and maternal mental illness in the perinatal period, while exploring time to incident mental disorder diagnosis in postpartum women. Methods: This observational study identified perinatal women continuously enrolled 1 year prior to and 1 year post-delivery using Optum's de-identified Clinformatics® Data Mart Database (CDM) from 2014 to 2019 with MetS-C i.e. obesity, diabetes, high blood pressure, high triglycerides, or low HDL (1-year prior to delivery); perinatal comorbidities (9-months prior to and 4-month postpartum); and mental disorder (1-year prior to and 1-year post-delivery). Additionally, demographics and the number of days until mental disorder diagnosis were evaluated in this cohort. The analysis included descriptive statistics and multivariable logistic regression. MetS-C, perinatal comorbidities, and mental disorder were assessed using the International Classification of Diseases, Ninth, and Tenth Revision diagnosis codes. Results: 372,895 deliveries met inclusion/exclusion criteria. The prevalence of MetS-C was 13.43%. Multivariable logistic regression revealed prenatal prevalence (1.64, CI = 1.59–1.70) and postpartum incident (1.30, CI = 1.25–1.34) diagnosis of mental health disorder were significantly higher in those with at least one MetS-C. Further, the adjusted odds of having postpartum incident mental illness were 1.51 times higher (CI = 1.39–1.66) in those with 2 MetS-C and 2.12 times higher (CI = 1.21–4.01) in those with 3 or more MetS-C. Young women (under the age of 18 years) were more likely to have an incident mental health diagnosis as opposed to other age groups. Lastly, time from hospital discharge to incident mental disorder diagnosis revealed an average of 157 days (SD = 103 days). Conclusion: The risk of mental disorder (both prenatal and incident) has a significant association with MetS-C. An incremental relationship between incident mental illness diagnosis and the number of MetS-C, a significant association with younger mothers along with a relatively long period of diagnosis mental illness highlights the need for more screening and treatment during pregnancy and postpartum. [ABSTRACT FROM AUTHOR]

Objective Methods Results Conclusions This study investigated the effect of metabolic syndrome (MetS) on periodontal clinical parameters and salivary biomarkers' matrix metalloproteinase‐8 (MMP‐8) and myeloperoxidase (MPO) in patients with periodontitis.A total of 120 participants aged 25–55 were categorized into three groups: MetS with periodontitis (n = 40); systemically healthy with periodontitis (n = 40); and systemically and periodontally healthy controls (n = 40). Data collected included systemic parameters like waist circumference (WC), blood pressure (BP), high‐ and low‐density lipoproteins, triglycerides (TG), fasting blood sugar (FBS), and glycated hemoglobin (HbA1c). Periodontal parameters estimated included bleeding on probing score (BoP), full‐mouth plaque score (FMPS), periodontal probing depth (PPD), clinical attachment loss (CAL), and the number of missing teeth. Unstimulated whole saliva was analyzed via ELISA for active MMP‐8 (aMMP‐8), total MMP‐8 (tMMP‐8), and MPO.Participants with MetS and periodontitis exhibited significantly higher periodontal parameters, salivary aMMP‐8, and MPO (26.26 vs. 24.1 ng/mL and 13.53 vs. 11.55 ng/mL compared to systemically healthy periodontitis patients) (all p < 0.01). Positive correlations occurred between aMMP‐8 and WC, TG, and FBS (p < 0.01), and between MPO and WC, BP, and TG (p < 0.01).The positive associations between these biomarkers and metabolic parameters indicate their potential utility for monitoring cardiovascular and glycemic risk in patients with periodontal disease. [ABSTRACT FROM AUTHOR]

Background: Growing evidence shows that metabolic syndrome and frailty are significantly associated. Screening and assessing frailty in patients with metabolic syndrome is important to help improve their clinical outcomes and quality of life. Therefore, understanding the prevalence of frailty in patients with metabolic syndrome is the first critical step, however, the prevalence reported in the literature varies widely.Aim: To pool the overall prevalence of frailty among patients with metabolic syndrome.Design: Systematic review and meta-analysis.Methods: The Cochrane Library, PubMed, Web of Science, Embase, APA PsycINFO, Scopus, CINAHL Complete, CNKI, Wan Fang, SinoMed, and VIP databases were searched from the inception to March 6, 2024. Statistical analysis was performed using STATA15 software. The prevalence was pooled using the random-effects model. The sources of heterogeneity were investigated by using meta-regression and subgroup analyses.Results: A total of 22 original studies published between 2007 and 2023 were included in this systematic review and meta-analysis, involving 19,921 metabolic syndrome patients. The prevalence of frailty and pre-frailty among patients with metabolic syndrome was 20% (95% CI: 16% to 25%, I2 = 99.44%) and 45% (95% CI: 36% to 53%, I2 = 99.20%). Subgroup analyses revealed differences in prevalence by frailty instruments, geographic regions, study settings, publication years, study quality, study design, and different components of metabolic syndrome.Conclusions: This systematic review and meta-analysis showed the high prevalence of frailty and pre-frailty in patients with metabolic syndrome. In the future, more high-quality longitudinal studies and exploration of other potential demographic characteristics that may influence frailty are needed to understand more information on frailty in patients with metabolic syndrome. [ABSTRACT FROM AUTHOR]

Background: Metabolic syndrome (MetS) is a significant epidemiological problem worldwide. It is a pre-morbid, chronic and low-grade inflammatory disorder that precedes many chronic diseases. Wharton's jelly-derived mesenchymal stem cells (WJ-MSCs) could be used to treat MetS because they express high regenerative capacity, strong immunomodulatory properties and allogeneic biocompatibility. This study aims to investigate WJ-MSCs as a therapy against MetS in a rat model. Methods: Twenty-four animals were fed with high-fat high-fructose (HFHF) diet ad libitum. After 16 weeks, the animals were randomised into treatment groups (n = 8/group) and received a single intravenous administration of vehicle, that is, 3 × 106 cells/kg or 10 × 106 cells/kg of WJ-MSCs. A healthy animal group (n = 6) fed with a normal diet received the same vehicle as the control (CTRL). All animals were periodically assessed (every 4 weeks) for physical measurements, serum biochemistry, glucose tolerance test, cardiovascular function test and whole-body composition. Post-euthanasia, organs were weighed and processed for histopathology. Serum was collected for C-reactive protein and inflammatory cytokine assay. Results: The results between HFHF-treated groups and healthy or HFHF-CTRL did not achieve statistical significance (α = 0.05). The effects of WJ-MSCs were masked by the manifestation of different disease subclusters and continuous supplementation of HFHF diet. Based on secondary analysis, WJ-MSCs had major implications in improving cardiopulmonary morbidities. The lungs, liver and heart show significantly better histopathology in the WJ-MSC-treated groups than in the untreated CTRL group. The cells produced a dose-dependent effect (high dose lasted until week 8) in preventing further metabolic decay in MetS animals. Conclusions: The establishment of safety and therapeutic proof-of-concept encourages further studies by improving the current therapeutic model. [ABSTRACT FROM AUTHOR]

Background: Non-alcoholic fatty liver disease (NAFLD) and metabolic syndrome (MetS) are implicated in the aetiology of non-communicable diseases. Our study aimed to evaluate associations between NAFLD and MetS with overall and cause-specific mortality. Methods: We used dietary, lifestyle, anthropometric and metabolic biomarker data from a random subsample of 15,784 EPIC cohort participants. NAFLD was assessed using the fatty liver index (FLI) and MetS using the revised definition. Indices for metabolic dysfunction–associated fatty liver disease (MAFLD) were calculated. The individual associations of these indices with overall and cause-specific mortality were assessed using multivariable Cox proportional hazards models to estimate hazard ratios (HRs) and 95% confidence intervals (95%CIs). As a subobjective, risk associations with adaptations of new classifications of metabolic dysfunction–associated steatotic liver disease (MASLD) and metabolic and alcohol-related liver disease (MetALD) were also assessed. Results: Among the 15,784 sub-cohort participants, a total of 1997 deaths occurred (835 due to cancer, 520 to CVD, 642 to other causes) over a median 15.6 (IQR, 12.3–17.1) years of follow-up. Compared to an FLI < 30, FLI ≥ 60 was associated with increased risks of overall mortality (HR = 1.44, 95%CI = 1.27–1.63), and deaths from cancer (HR = 1.32, 95%CI = 1.09–1.60), CVD (HR = 2.06, 95% CI = 1.61–2.63) or other causes (HR = 1.21, 95%CI = 0.97–1.51). Mortality risk associations were also elevated for individuals with MAFLD compared to those without. Individuals with MetS were at increased risk of all mortality endpoints, except cancer-specific mortality. MASLD and MetALD were associated with higher risk of overall mortality. Conclusions: Our findings based on a prospective cohort suggest that individuals with hepatic steatosis or metabolic dysfunction have a higher overall and cause-specific mortality risk. [ABSTRACT FROM AUTHOR]

Metabolic syndrome (MetS) has a large clinical population nowadays, usually due to excessive energy intake and lack of exercise. During MetS, excess nutrients stress the mitochondria, resulting in relative hypoxia in tissues and organs, even when blood supply is not interrupted or reduced, making mitochondrial dysfunction a central pathogenesis of cardiovascular disease in the MetS. Sodium‐glucose cotransporter 2 inhibitors were designed as a hyperglycemic drug that acts on the renal tubules to block sugar reabsorption in primary urine. Recently they have been shown to have anti‐inflammatory and other protective effects on cardiomyocytes in MetS, and have also been recommended in the latest heart failure guidelines as a routine therapy. Among these inhibitors, empagliflozin shows better clinical promise due to less influence from glomerular filtration rate. This review focuses on the mitochondrial mechanisms of empagliflozin, which underlie the anti‐inflammatory and recover cellular functions in MetS cardiomyocytes, including stabilizing calcium concentration, mediating metabolic reprogramming, maintaining homeostasis of mitochondrial quantity and quality, stable mitochondrial DNA copy number, and repairing damaged mitochondrial DNA. [ABSTRACT FROM AUTHOR]

• Food insecure women are more likely to have metabolic syndrome than food secure women. • Very low food security was not associated with metabolic syndrome for men. • More research is needed to fully understand the role of gender in food insecurity and chronic disease. The primary objective of this study was to examine the association between food security status and metabolic syndrome (MetS) using a nationally representative dataset. We hypothesized that food insecurity would be associated with an increased odds of having MetS. This was a cross-sectional analysis of data from the 2005–2006 to 2015–2016 National Health and Nutrition Examination Survey data collection cycles. Food security was measured using the US Food Security Survey Module. Presence of MetS was determined using the National Cholesterol Education Program Adult Treatment Panel III criteria. The association between food insecurity and MetS was examined using logistic regression models stratified by sex and adjusted for poverty to income ratio, age, race, marital status, educational attainment, smoking status, and body mass index. After adjusting for covariates, men with marginal (odds ratio, 1.64; 95% confidence interval [CI], 1.22–2.20) and low (odds ratio, 1.33; 95% CI, 1.02–1.73) food security had a higher odds of having MetS than men with full food security; however, this association was lost among men with very low food security. For women, very low food security was associated with a 1.61 times greater odds of having MetS (95% CI, 1.16–2.25). These results suggest that food insecurity is generally associated with an increased prevalence of MetS for women, but not necessarily for men. These findings highlight the need to address rising food insecurity rates, while also highlighting the need for further research to fully elucidate the role of gender and sex in food insecurity and chronic disease. This secondary data analysis examined the association between food security and metabolic syndrome (MetS) using data from the National Health and Nutrition Examination Survey (NHANES) 2005–2016. The highest odds of MetS were found among women with very low food security and men with marginal food security. Very low food security was not associated with an increased odds of MetS for men, suggesting that there may be gender differences in how food security affects risk of chronic disease. [Display omitted] [ABSTRACT FROM AUTHOR]

Simple Summary: Although animal models have suggested that chronic stress can induce cancer, epidemiological findings have been inconsistent. One of the possible reasons for this inconsistency is the challenge to measure chronic stress. Recently, hair cortisol and its inactive form cortisone have shown to be a potential biomarker for chronic stress. Our study aims to investigate the relation between chronic biological stress, as measured by hair cortisol and hair cortisone, and cancer incidence, and adjust for other factors that can impact this relation such as metabolic syndrome components in a population-based cohort. While hair cortisone was related to cancer incidence when accounting for age as a confounder and gender as a moderator, we did not observe the association with hair cortisol. The involvement of metabolic syndrome components in the relation between chronic stress and cancer initiation was not found. Epidemiological results on the link between chronic stress and cancer initiation have been inconsistent. This study examined the relation between chronic biological stress, indicated as hair cortisol (HairF) and hair cortisone (HairE), and cancer incidence, adjusting for metabolic syndrome (MetS) components. We analyzed HairF and HairE samples from 6341 participants from the population-based cohort Lifelines in 2014. A linkage with the Dutch Nationwide Pathology Databank (Palga) provided the cancer incidence from 2015 to 2021. The association between dichotomized HairF and log-transformed HairE (LogHairE) and cancer incidence was estimated using Cox regression. MetS components were evaluated as confounders or moderators. Of the 2776 participants with known HairF levels and no cancer history, 238 developed cancer. The HairF level did not predict cancer incidence (HR: 0.993, 95%CI: 0.740–1.333). No confounders or moderators were identified. Among the 4699 participants with known HairE levels and no cancer history, 408 developed cancer. There was no association between LogHairE and cancer incidence (HR: 1.113, 95%CI: 0.738–1.678). When including age as a confounder and gender as a moderator, LogHairE was statistically significantly associated with cancer incidence (HR: 6.403, 95%CI: 1.110–36.92). In a population-based cohort, chronic biological stress, measured by HairE, was associated with cancer incidence, after controlling for age and gender. [ABSTRACT FROM AUTHOR]

Contemporary healthcare focuses on assessing the efficacy of dietary and exercise interventions in mitigating metabolic syndrome and its association with sleep apnea. Results demonstrate notable reductions in the HOMA Index and triglyceride levels among treated cohorts, indicating improved glycemic control and lipid profile. Additionally, intervention groups exhibit significant decreases in cholesterol levels, indicative of enhanced lipid profile. Marginal alterations in C-Reactive Protein imply limited impact on systemic inflammation, while consistent uric acid levels suggest potential autonomy from the interventions. Remarkable correlations between clinical parameters and sleep apnea risk underscore the pivotal role of lifestyle modifications in metabolic syndrome management, offering insights into underlying mechanisms. The aim of this study is to further investigate the underlying mechanisms behind the observed improvements in metabolic parameters following dietary and exercise interventions, with a specific focus on elucidating the relationship between these interventions and the risk of sleep apnea in individuals with metabolic syndrome. These findings elucidate the intricate interplay between metabolic risk factors and sleep apnea susceptibility, thereby informing therapeutic and preventive approaches for individuals with metabolic syndrome. [ABSTRACT FROM AUTHOR]

Rhamnan sulphate (RS) is a sulphated polysaccharide found in green algae such as Monostroma nitidum that exhibits various biological functions, including anticoagulant, antitumour, antiviral, and anti‐obesity properties. In our previous clinical trial, we demonstrated that RS intake improves constipation. However, no specific bacteria showed a significant (p <.05) change. Notably, these results were obtained after a short RS inoculation period of only 2 weeks. In the present study, to evaluate the long‐term effects of RS on the gut microbiota, we orally administered RS to BALB/c mice for 11 weeks, analyzed their blood biochemical data, and performed 16s rRNA‐sequencing. Oral administration of RS increased body weight with increased food intake, whereas plasma total cholesterol and fasting plasma glucose levels decreased. RS‐fed mice showed lower fasting insulin levels (p <.1) and decreased homeostatic model assessment for insulin resistance (HOMA‐IR, p <.0001), suggesting that RS improved insulin resistance. In the feces of mice, the amounts of acetic and propionic acids increased. In the gut microbiota, predictive metagenomic profiling using the phylogenetic investigation of communities by reconstruction of unobserved states (PICRUSt2) revealed functional alterations in Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathways in RS‐fed mice. Corresponding to the blood glucose‐lowering effect, the glycolysis and tricarboxylic acid (TCA) cycle pathways were activated. In addition, the Firmicutes/Bacteroides (F/B) ratio, which may be associated with various health outcomes, was also reduced. These results suggest that the blood glucose‐lowering effect, improvement in insulin resistance, and lipid‐lowering effect of RS may be due to changes in the intestinal microbiota. [ABSTRACT FROM AUTHOR]

Metabolic Syndrome (MetS) is a constellation of risk factors including abdominal obesity, high triglycerides, low HDL cholesterol (HDL‐C), elevated blood pressure, and elevated fasting glucose. In Spain, according to WHO criteria, the MetS prevalence is shown to be 32% in men and 29% in women. The role of dietary habits is one of the main therapeutic strategies for the management of MetS but the most effective dietary pattern has not been established yet. This study aimed to analyze the effect of on body composition, serum lipids, and MetS components of a high‐MUFA and high‐fiber diet (HMFD). A case–control study was performed considering 40 cohabiting women. Participants were randomly assigned to HMFD group or high mono‐unsaturated diet (HMD) group to receive one of the two proposed dietary interventions. All data (serum lipids, blood pressure, height, weight, body composition, and waist circumference) were collected fasting at baseline, 55, 98, and 132 days. The HMFD group showed higher decrease in waist circumference than in the HMD group. LDL‐C dropped in both groups. Triglycerides in the HMFD group dropped during the intervention, but once the intervention was over, they returned to baseline values. The mean systolic blood pressure was lower in HMFD group. A HMFD from a weekly consumption of processed meat (Torrezno de Soria) deeply fried in extra virgin olive oil in combination with vegetables logged in a Mediterranean diet can improve MetS risk factors in healthy overweight women. [ABSTRACT FROM AUTHOR]

Background: Acute myocardial infarction (AMI) and metabolic syndrome (MeS) are two major health problems worldwide. In recent years, MeS has been introduced as a significant risk factor for AMI. Objectives: To estimate the prevalence of MeS and its components among patients with AMI. Materials and methods: This was a cross-sectional study conducted at Al-Ramadi Teaching Hospital during a period from January to December 2022, including a total of 100 patients with AMI. The definition of MeS was established based on the criteria of the modified National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III). Results: The mean age of patients was 58.6 ± 7.1 (range: 41–81 years). Males represented 55% of the studied group. Clustering of MeS components among cases revealed that 57% had less than three components while 43% had 3 or more criteria for MeS diagnosis, giving a prevalence rate of 43% for MeS. Only 5 cases had none of these components. MeS was relatively more prevalent in younger age groups and females. The mean values of all components of MeS were significantly higher in the MeS group than in the non-MeS group (P-value < 0.05). Conclusion: MeS was an important risk factor for AMI. The study revealed a high prevalence of MeS among individuals with AMI and it was higher among women than men. [ABSTRACT FROM AUTHOR]

Aim: To analyse the relationships between muscular fitness (MF), fat mass (FM), fat- free mass (FFM) and its combined ratio with cardiometabolic risk (CMR) and whether the relationship between MF and CMR is mediated by body composition in schoolchildren. Methods: A cross-sectional study was conducted on schoolchildren from Cuenca, Spain, between September and November 2017. FM and FFM were estimated using bioimpedance analysis. The CMR index was calculated from triglycerides- HDL- c ratio, arterial pressure and fasting insulin. The MF index was assessed using handgrip and standing long jump tests. Analysis of covariance models assessed CMR index differences across the MF index and the FM/FFM ratio categories. Mediation analysis examined whether the MF index and the CMR index association were mediated by FM, FFM or FM/FFM ratio. Results: The analyses involved 485 schoolchildren aged 9-11 years (55.4% girls). Children with a higher MF index had a lower CMR index (p < 0.05). This association did not persist after controlling for FM/FFM. FM, FFM and FM/FFM ratio mediated the relationship between the MF index and the CMR index. Conclusion: Better levels of MF are associated with better cardiometabolic profile, but a healthy body composition is determinant to improve future health. [ABSTRACT FROM AUTHOR]

Polycystic ovary syndrome (PCOS) affects 6–20% of reproductive-aged women. It is associated with increased risks of metabolic syndrome, Type 2 diabetes, cardiovascular diseases, mood disorders, endometrial cancer and non-alcoholic fatty liver disease. Although various susceptibility loci have been identified through genetic studies, they account for ∼10% of PCOS heritability. Therefore, the etiology of PCOS remains unclear. This review explores the role of epigenetic changes and modifications in circadian clock genes as potential contributors to PCOS pathogenesis. Epigenetic alterations, such as DNA methylation, histone modifications, and non-coding RNA changes, have been described in diseases related to PCOS, such as diabetes, cardiovascular diseases, and obesity. Furthermore, several animal models have illustrated a link between prenatal exposure to androgens or anti-Müllerian hormone and PCOS-like phenotypes in subsequent generations, illustrating an epigenetic programming in PCOS. In humans, epigenetic changes have been reported in peripheral blood mononuclear cells (PBMC), adipose tissue, granulosa cells (GC), and liver from women with PCOS. The genome of women with PCOS is globally hypomethylated compared to healthy controls. However, specific hypomethylated or hypermethylated genes have been reported in the different tissues of these women. They are mainly involved in hormonal regulation and inflammatory pathways, as well as lipid and glucose metabolism. Additionally, sleep disorders are present in women with PCOS and disruptions in clock genes' expression patterns have been observed in their PBMC or GCs. While epigenetic changes hold promise as diagnostic biomarkers, the current challenge lies in distinguishing whether these changes are causes or consequences of PCOS. Targeting epigenetic modifications potentially opens avenues for precision medicine in PCOS, including lifestyle interventions and drug therapies. However, data are still lacking in large cohorts of well-characterized PCOS phenotypes. In conclusion, understanding the interplay between genetics, epigenetics, and circadian rhythms may provide valuable insights for early diagnosis and therapeutic strategies in PCOS in the future. [ABSTRACT FROM AUTHOR]

The aim of this study was to expand knowledge about endocrine disorders in individuals with Cornelia de Lange syndrome (CdLS), a rare developmental genetic disorder with anomalies in multiple organs and systems. Hormone levels, clinical scores, anthropometric measurements, and molecular analysis were assessed in 24 individuals with CdLS. Hyperprolactinemia was the most common endocrine disorder. Three patients showed subclinical hypothyroidism. Concerning the gonadotropic axis, mildly delayed puberty was observed, as well as genital anomalies, such as cryptorchidism. Despite short stature, levels of insulin-like growth factor 1 and insulin-like growth factor-binding protein 3 tended to be normal. Three prepubertal individuals without risk factors had higher than normal values for the homeostatic model assessment of insulin resistance (HOMA-IR) and for insulinemia, suggesting insulin resistance. Furthermore, two adults had elevated body mass indexes associated with HOMA-IR values over the cut-off values. CdLS may lead to dysregulation of the endocrine system, particularly in patients with high HOMA-IR values and insulinemia who are at risk of insulin resistance. Therefore, clinical follow-up with comprehensive hormonal assessment appears warranted in individuals with CdLS. [ABSTRACT FROM AUTHOR]

Intra-pancreatic fat deposition (IPFD) is suspected to be associated with various medical conditions. This study aimed to assess pancreatic fat content in lean and obese individuals, characterize obese individuals with and without IPFD, and explore the underlying mechanisms. Sixty-two obese individuals without diabetes and 35 lean controls underwent magnetic resonance imaging (MRI) using proton density fat fraction (PDFF) maps to evaluate pancreatic and hepatic fat content, and visceral adipose tissue (VAT) content. Pancreatic fibrosis was explored by T1 relaxation time and MR elastography (MRE) measurements. Associations between pancreatic fat, measures of obesity and metabolic syndrome were examined using uni- and multivariate regression analyses. Pancreatic PDFF was higher in obese than in lean controls (median 8.0%, interquartile range (6.1;13.3) % vs 2.6(1.7;3.9)%, p < 0.001). Obese individuals with IPFD (PDFF ≥6.2%) had higher waist circumference (114.0 ± 12.5 cm vs 105.2 ± 8.7 cm, p = 0.007) and VAT (224.9(142.1; 316.1) cm2 vs 168.2(103.4; 195.3) cm2, p < 0.001) than those without. In univariate analysis, pancreatic PDFF in obese individuals correlated with BMI (r = 0.27, p = 0.03), waist circumference (r = 0.44, p < 0.001), VAT (r = 0.37, p = 0.004), hepatic PDFF (r = 0.25, p = 0.046) and diastolic blood pressure (r = 0.32, p = 0.01). However, in multivariate analysis, only VAT was associated to pancreatic fat content. MRI measures of pancreatic fibrosis indicated no evident fibrosis in relation to increased pancreatic fat content. Pancreatic fat content was increased in obese individuals compared with lean controls and predominantly correlated with the amount of visceral adipose tissue. Pancreatic fat content was not clearly linked to measures of pancreatic fibrosis. [ABSTRACT FROM AUTHOR]

Objectives: Prevention of atherosclerotic cardiovascular disease (ASCVD) is important in individuals with metabolic syndrome components (MetS), and periodontitis may play an important role in this process. This study aims to evaluate the association between periodontitis and ASCVD in participants with the components of MetS, including obesity, dysglycemia, hypertension, and dyslipidemia. Materials and methods: This study conducted followed the MOOSE reporting guidelines and the PRISMA 2020 guidelines. EMBASE, MEDLINE, Web of Science, Cochrane Library, PubMed and OpenGrey were searched for observational studies about the linkage of periodontitis to ASCVD in people with MetS components up to April 9, 2023. Cohort, case-control and cross-sectional studies were included after study selection. Quality evaluation was carried out using the original and modified Newcastle-Ottawa Scale as appropriate. Random-effects model was employed for meta-analysis. Results: Nineteen studies were finally included in the quality analysis, and all of them were assessed as moderate to high quality. Meta-analyses among fifteen studies revealed that the participants with periodontitis were more likely to develop ASCVD in those who have dysglycemia (RR = 1.25, 95% CI = 1.13–1.37; p < 0.05), obesity (RR = 1.13, 95% CI = 1.02–1.24; p < 0.05), dyslipidemia (RR = 1.36, 95% CI = 1.13–1.65; p < 0.05), or hypertension (1.20, 95% CI = 1.05–1.36; p < 0.05). Conclusions: Periodontitis promotes the development of ASCVD in participants with one MetS component (obesity, dysglycemia, hypertension or dyslipidemia). Clinical relevance: In people with MetS components, periodontitis may contribute to the ASCVD incidence. [ABSTRACT FROM AUTHOR]

Grape pomace is the most important residual after wine making, and it is considered to be a very abundant source for the extraction of a wide range of polyphenols. These polyphenols exhibit a variety of bioactivities, such as antioxidant, anti-inflammatory, and anti-cancer. They are also beneficial in alleviating metabolic syndrome and regulating intestinal flora, etc. These health effects are most likely contributed by polyphenol metabolite, which are formed by the grape pomace phenolics after a complex metabolic process in vivo. Therefore, understanding the phenolic composition of grape pomace and its metabolism is the basis for an in-depth study of the biological activity of grape pomace polyphenols. In this paper, we first summarize the composition of phenolics in grape pomace, then review the recent studies on the metabolism of grape pomace phenolics, including changes in phenolics in the gastrointestinal tract, their pharmacokinetics in the systemic circulation, the tissue distribution of phenolic metabolites, and the beneficial effects of metabolites on intestinal health, and finally summarize the effects of human health status and dietary fiber on the metabolism of grape polyphenols. It is expected to provide help for the in-depth research on the metabolism and biological activity of grape pomace polyphenol extracts, and to provide theoretical support for the development and utilization of grape pomace. [ABSTRACT FROM AUTHOR]

This study examined the effects of pemafibrate, a selective peroxisome proliferator-activated receptor α agonist, on the serum biochemical parameters of male patients with coronary artery disease and metabolic syndrome (MetS). This was a post hoc analysis of a randomized, crossover study that treated hypertriglyceridemia with pemafibrate or bezafibrate for 24 weeks, followed by a crossover of another 24 weeks. Of the 60 patients enrolled in the study, 55 were male. Forty-one of 55 male patients were found to have MetS. In this sub-analysis, male patients with MetS (MetS group, n = 41) and those without MetS (non-MetS group, n = 14) were compared. The primary endpoint was a change in fasting serum triglyceride (TG) levels during pemafibrate therapy, and the secondary endpoints were changes in insulin resistance-related markers and liver function parameters. Serum TG levels significantly decreased (MetS group, from 266.6 to 148.0 mg/dL, p < 0.001; non-MetS group, from 203.9 to 97.6 mg/dL, p < 0.001); however, a percent change (%Change) was not significantly different between the groups (− 44.1% vs. − 51.6%, p = 0.084). Serum insulin levels and homeostasis model assessment of insulin resistance significantly decreased in the MetS group but not in the non-MetS group. %Change in liver enzyme levels was markedly decreased in the MetS group compared with that in the non-MetS group (alanine aminotransferase, − 25.1% vs. − 11.3%, p = 0.027; gamma-glutamyl transferase, − 45.8% vs. − 36.2%, p = 0.020). In conclusion, pemafibrate can effectively decrease TG levels in patients with MetS, and it may be a more efficient drug for improving insulin resistance and liver function in such patients. [ABSTRACT FROM AUTHOR]

This document is a correction notice for an article titled "Effect of Neo-Policaptil Gel Retard on Liver Fat Content and Fibrosis in Adults with Metabolic Syndrome and Type 2 Diabetes: A Non-invasive Approach to MAFLD." The correction includes revisions to formulas, interpretations, and terminology used in the original article. It also corrects errors in a table presenting general features of the two treatment groups. The document aims to provide accurate and updated information for researchers studying the effects of Neo-Policaptil Gel Retard on liver fat content and fibrosis in individuals with metabolic syndrome and type 2 diabetes. [Extracted from the article]

Summary: Laminitis associated with hyperinsulinaemia is a significant cause of morbidity and mortality in horses with equine metabolic syndrome. The diagnosis and management of hyperinsulinaemia are therefore critical to prevent the development of laminitis. This review article aims to help primary care clinicians manage patients with hyperinsulinaemia by providing an overview of diagnostics, management strategies and new therapies that are available. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Type 2 diabetes (T2D) increases the risk for major adverse liver outcomes (MALOs), including cirrhosis and its complications. Patients with T2D frequently have other traits of the metabolic syndrome (MetS). It remains uncertain whether there is a synergistic effect of accumulating MetS traits on future MALO risk. RESEARCH DESIGN AND METHODS: Patients with T2D without a history of liver disease were identified from national registers in Sweden from 1998 to 2021. MetS traits included hypertension, low HDL level, hypertriglyceridemia, obesity, and albuminuria, in addition to T2D. MALO events were identified based on administrative coding from national registers until 31 October 2022. Data were analyzed using Cox regression models. RESULTS: In total, 230,992 patients were identified (median age 64 years; 58% male), of whom 3,215 (1.39%) developed MALOs over a median follow-up of 9.9 years. Compared with patients with one MetS trait (only T2D) at baseline, those with more than one MetS trait had a higher rate of MALOs (adjusted hazard ratio [aHR] 2.33, 95% CI 1.53–3.54). The rate of MALOs increased progressively with increasing numbers of MetS traits at baseline (aHR 1.28 per added trait, 95% CI 1.23–1.33). During follow-up, patients who acquired additional MetS traits had a progressively higher rate of MALOs. The MetS trait with the largest association with incident MALOs was hypertension (aHR 2.06, 95% CI 1.57–2.71). CONCLUSIONS: Having or acquiring additional traits of MetS increase the rate of progression to MALOs in patients with T2D. These results could be used to inform screening initiatives for liver disease. [ABSTRACT FROM AUTHOR]

The influence of metabolic syndrome (MetS) on long-term prognosis of patients with myocardial infarction (MI), the most severe type of coronary artery disease, remains not fully determined. This systematic review and meta-analysis were conducted to investigate the association between MetS and long-term clinical outcomes of patients with MI. A systematic search of Medline, Web of Science, and Embase databases from inception to June 25, 2023, was conducted to obtain eligible studies. Only studies with follow-up duration for at least one year were considered. A random-effects model was utilized to pool the results, accounting for heterogeneity. Ten observational studies were included, which included 33 197 patients with MI. Among them, 17 244 (51.9%) were with MetS at baseline. During a follow-up duration of 12 to 48 months (mean: 22.5 months), patients with MetS were associated with higher incidence of major adverse cardiovascular events [risk ratio (RR): 1.35. 95% confidence interval (CI): 1.19 to 1.54, p<0.001; I2=64%] and all-cause deaths (RR: 1.34, 95% CI: 1.18 to 1.52, p<0.001; I2=23%), as compared to those without MetS at baseline. Subgroup analyses showed that the results were not significantly affected by study characteristics such as study country, design, type of MI, mean age of the patients, treatment with percutaneous coronary intervention, follow-up durations, or study quality scores (p for subgroup difference all>0.05). In patients with MI, MetS may be a risk factor of poor long-term prognosis. [ABSTRACT FROM AUTHOR]

Background: Nutritional status in pediatric patients undergoing heart transplantation (HT) is frequently a focus of clinical management and requires high resource utilization. Pre‐operative nutrition status has been shown to affect post‐operative mortality but no studies have been performed to assess how nutritional status may change and the risk of developing nutritional comorbidities long‐term in the post‐transplant period. Methods: A single‐center retrospective chart review of patients ≥2 years of age who underwent heart transplantation between 1/1/2005 and 4/30/2020 was performed. Patient data were collected at listing, time of transplant, 1‐year, and 3‐year follow‐up post‐transplant. Nutrition status was classified based on body mass index (BMI) percentile in the primary analysis. Alternative nutritional indices, namely the nutrition risk index (NRI), prognostic nutrition index (PNI), and BMI z‐score, were utilized in secondary analyses. Results: Of the 63 patients included, the proportion of patients with overweight/obese status increased from 21% at listing to 41% at 3‐year follow‐up. No underweight patients at listing became overweight/obese at follow‐up. Of patients who were overweight/obese at listing, 88% maintained that status at 3‐year follow‐up. Overweight/obese status at listing, 1‐year, and 3‐year post‐transplantation were significantly associated with developing metabolic syndrome. In comparison to the alternative nutritional indices, BMI percentile best predicted post‐transplant metabolic syndrome. Conclusions: The results suggest that pediatric patients who undergo heart transplantation are at risk of developing overweight/obesity and related nutritional sequelae (ie, metabolic syndrome). Improved surveillance and interventions targeted toward overweight/obese HT patients should be investigated to reduce the burden of associated comorbidities. [ABSTRACT FROM AUTHOR]

• Obesity is a state of increased adipose tissue, not body weight. • BMI inaccurately diagnoses obesity when compared to the determination of body fat%. • We propose a new classification system combining actual BF% and waist circumference. • This system allows to gradually estimating the cardiometabolic risk of the patients. The estimation of obesity-associated cardiometabolic risk does not usually take into account body composition or the distribution of adiposity. The aim of the present study was to assess the clinical usefulness of a novel obesity phenotyping system based on the combination of actual body fat percentage (BF%) and waist circumference (WC) according to the cardiometabolic risk estimation. A classification matrix combining BF% and WC as measures of both amount and distribution of adiposity establishing nine body phenotypes (3 BF% x 3 WC) was developed. Individuals were grouped in five different cardiometabolic risk phenotypes. We conducted a validation study in a large cohort of White subjects from both genders representing a wide range of ages and adiposity (n = 12,754; 65 % females, aged 18–88 years). The five risk groups using the matrix combination of BF% and WC exhibited a robust linear distribution regarding cardiometabolic risk, estimated by the Metabolic Syndrome Severity Score, showing a continuous increase between groups with significant differences (P < 0.001) among them, as well as in other cardiometabolic risk factors. An additional 24 % of patients at very high risk was detected with the new classification system proposed (P < 0.001) as compared to an equivalent matrix using BMI and WC instead of BF% and WC. A more detailed phenotyping should be a priority in the diagnosis and management of patients with obesity. Our classification system allows to gradually estimate the cardiometabolic risk according to BF% and WC, thus representing a novel and useful tool for both research and clinical practice. [Display omitted] [ABSTRACT FROM AUTHOR]

Summary: Mounting evidence shows that bisphenol A (BPA) is associated with metabolic risk factors. The aim of this study was to review related epidemiologic studies and conduct a meta‐analysis to quantitatively estimate the association between BPA and metabolic syndrome. Four electronic databases were systematically searched to identify suitable articles. A total of 47 published studies were finally included. Two studies involved metabolic syndrome. Of the 17, 17, 14, and 13 studies on the relationship between BPA with abdominal obesity, blood pressure, fasting plasma glucose, and dyslipidemia, 10, 6, 3, and 4 studies were included in the meta‐analysis, respectively. The results showed that the risk of abdominal obesity increased with the increase of BPA exposure, especially in the group with higher BPA exposure levels (Quartile 2 vs. Quartile 1, pooled OR = 1.16, 95%CI: 1.01, 1.33; Q3 vs. Q1, pooled OR = 1.31, 95%CI: 1.13, 1.51; Q4 vs. Q1, pooled OR = 1.40, 95%CI: 1.21, 1.61). However, there was no significant correlation between BPA exposure and metabolic syndrome components including hypertension, abnormal fasting plasma glucose, and dyslipidemia. The present study found that BPA exposure is significantly associated with a higher risk of abdominal obesity. However, the relationship between BPA with metabolic syndrome and its other components needs further longitudinal studies to verify. [ABSTRACT FROM AUTHOR]

Patients with affective and anxiety disorders are at risk of metabolic syndrome (MetS) and, consequently, cardiovascular disease and premature death. In this study, the course and treatment of MetS was investigated using longitudinal data from a naturalistic sample of affective- and anxiety-disordered outpatients (Monitoring Outcome of psychiatric PHARmacotherapy [MOPHAR]). Demographics, clinical characteristics, medication use, and MetS components were obtained for n = 2098 patients at baseline and, in a FU-subsample of n = 507 patients, after a median follow-up (FU) of 11 months. Furthermore, pharmacological treatment rates of MetS were investigated at baseline and FU. Finally, demographic and clinical determinants of change in MetS (component) scores were investigated. At baseline, 34.6 % of n = 2098 patients had MetS, 41.4 % of whom received treatment. Of patients with persisting MetS, 46.1 % received treatment for one (or more) MetS component(s) at baseline, and 56.6 % received treatment at FU. Treatment rates of solely elevated blood pressure and reduced HDL-cholesterol did significantly, but modestly, improve. Higher age, male sex, smoking behavior, low education, diabetes, and depressive versus anxiety disorder were predictors of worse outcome at FU on at least one MetS component. We did not have data on lifestyle interventions as a form of treatment, which might partly have explained the observed low pharmacotherapeutic treatment rates. MetS (components) show high persistence rates in affective- and anxiety-disordered patients, and are, despite adequate monitoring, undertreated over time. This indicates that adherence and implementation of monitoring protocols should be crucially improved in psychiatric outpatients in secondary care. • Metabolic syndrome's prevalence remains high in patients with mood/anxiety disorders. • Metabolic abnormalities persist, while treatment rates remain low. • Psychiatric and somatic care integration of cardiovascular risk assessment is needed. [ABSTRACT FROM AUTHOR]

Background: Metabolic syndrome (MetS), which can be induced or exacerbated by the current class of antipsychotic drugs, is highly prevalent in patients with schizophrenia and presents significant challenges to lifetime disease management. Supported by initial clinical results, trace amine‐associated receptor 1 (TAAR1) agonists have emerged as potential novel treatments for schizophrenia. Notably, non‐clinical studies have also shown weight‐lowering and glucoregulatory effects of TAAR1 agonists, including the investigational agent ulotaront. However, the translatability of these findings to humans has not been adequately assessed. Given that delayed gastric emptying (GE) was identified as a potential mechanism contributing to the metabolic benefits of TAAR1 agonists in rodents, the aim of this study was to evaluate the effect of ulotaront on GE in patients with schizophrenia and concurrent MetS with prediabetes. Methods: Patients with schizophrenia were randomized to receive a single oral dose of ulotaront (150 mg) and their previous antipsychotic (PA) in an open‐label, crossover, two‐sequence design (NCT05402111). Eligible participants fulfilled at least three of five MetS criteria and had prediabetes defined by elevated glycated haemoglobin (5.7‐6.4%) and/or fasting homeostatic model assessment of insulin resistance (i.e. ≥2.22). Following an overnight fast and 4 h post‐dose, participants ingested a 99mTc‐sulphur colloid radiolabelled egg meal (320 kcal, 30% fat). GE was measured by scintigraphy over 4 h. Endpoints included GE of solids half‐time (T1/2) and percentage gastric retention at 1, 2 and 4 h. Results: Thirty‐one adults were randomized and 27 completed the study. Ulotaront significantly delayed GE of solids [median GE T1/2 ulotaront at 139 min (119, 182) vs. the participant's PA of 124 min (109, 132), p =.006]. A significant increase in gastric retention was seen in the ulotaront versus the PA group at 1 h (80% vs. 75%, p =.015), 2 h (61% vs. 50%, p =.023) and 4 h (17% vs. 7%, p =.002) post‐meal. Conclusion: Ulotaront delayed the GE of solids in patients with schizophrenia and concurrent MetS with prediabetes. Additional studies are needed to assess whether treatment with TAAR1 agonists is associated with weight loss and glucoregulatory improvement. [ABSTRACT FROM AUTHOR]

Aims: To describe changes in homeostasis model assessment of insulin resistance index (HOMA‐IR) following testosterone therapy in men with hypogonadism and metabolic syndrome (MetS). Materials and Methods: A randomized, placebo‐controlled, double‐blind randomized controlled trial (RCT) comprising 184 men with MetS and hypogonadism (testosterone undecanoate [TU]: 113 men, placebo: 71 men) was conducted. This was followed by an open‐label phase in which all men were given TU. We focused on men who were not receiving antiglycaemic agents (TU: 81 men; placebo: 54 men) as these could affect HOMA‐IR. Inter‐group comparison of HOMA‐IR was restricted to the RCT (30 weeks), whilst intra‐group comparison was carried out on men provided TU during the RCT and open‐label phases (study cohort) and men given placebo during the RCT and then switched to TU during the open‐label phase (confirmatory cohort). Regression analysis was performed to identify factors associated with change in HOMA‐IR (∆HOMA‐IR). Results: The median HOMA‐IR was significantly reduced at almost every time point (after 18 weeks) compared to baseline in men receiving TU in both the study and confirmatory cohorts. There was a significant decrease in median values of fasting glucose (30 weeks: −2.1%; 138 weeks: −4.9%) and insulin (30 weeks: −10.5%; 138 weeks: −35.5%) after TU treatment. Placebo was not associated with significant ∆HOMA‐IR. The only consistent predictor of HOMA‐IR decrease following TU treatment was baseline HOMA‐IR (r2 ≥ 0.64). Conclusions: Baseline HOMA‐IR predicted ΔHOMA‐IR, with a greater percentage change in insulin than in fasting glucose. In men with MetS/type 2 diabetes (T2DM) not on antiglycaemic therapy, improvements in HOMA‐IR may be greater than suggested by change in fasting glucose. Our results suggest that hypogonadism screening be included in the management of men with MetS/T2DM. [ABSTRACT FROM AUTHOR]

Background: The role of diet choline in atherosclerotic cardiovascular disease (ASCVD) is uncertain. Findings from animal experiments are contradictory while there is a lack of clinical investigations. This study aimed to investigate the association between choline intake and ASCVD based on individuals from the National Health and Nutrition Examination Survey (NHANES) database. Methods: This cross-sectional study was conducted in 5525 individuals from the NHANES between 2011 and 2018. Participants were categorized into the ASCVD (n = 5015) and non-ASCVD (n = 510) groups. Univariable and multivariable-adjusted regression analyses were employed to investigate the relationship between diet choline and pertinent covariates. Logistic regression analysis and restricted cubic spline analysis were used to evaluate the association between choline intake and ASCVD. Results: ASCVD participants had higher choline intake compared to those without ASCVD. In the higher tertiles of choline intake, there was a greater proportion of males, married individuals, highly educated individuals, and those with increased physical activity, but a lower proportion of smokers and drinkers. In the higher tertiles of choline intake, a lower proportion of individuals had a history of congestive heart failure and stroke. After adjusting for age, gender, race, ethnicity, and physical activity, an inverse association between choline intake and heart disease, stroke, and ASCVD was found. A restricted cubic spline analysis showed a mirrored J-shaped relationship between choline and ASCVD, stroke and congestive heart failure in males. There was no association between dietary choline and metabolic syndrome. Conclusion: An inverse association was observed between choline intake and ASVCD among U.S. adults. Further large longitudinal studies are needed to test the causal relationship of choline and ASVCD. [ABSTRACT FROM AUTHOR]

Obesity, a burgeoning global health crisis, has tripled in prevalence over the past 45 years, necessitating innovative research methodologies. Adipocytes, which are responsible for energy storage, play a central role in obesity. However, most studies in this field rely on animal models or adipocyte monolayer cell cultures, which are limited in their ability to fully mimic the complex physiology of a living organism, or pose challenges in terms of cost, time consumption, and ethical considerations. These limitations prompt a shift towards alternative methodologies. In response, here we show a 3D in vitro model utilizing the 3T3-L1 cell line, aimed at faithfully replicating the metabolic intricacies of adipocytes in vivo. Using a workable cell line (3T3-L1), we produced adipocyte spheroids and differentiated them in presence and absence of TNF-α. Through a meticulous proteomic analysis, we compared the molecular profile of our adipose spheroids with that of adipose tissue from lean and obese C57BL/6J mice. This comparison demonstrated the model's efficacy in studying metabolic conditions, with TNF-α treated spheroids displaying a notable resemblance to obese white adipose tissue. Our findings underscore the model's simplicity, reproducibility, and cost-effectiveness, positioning it as a robust tool for authentically mimicking in vitro metabolic features of real adipose tissue. Notably, our model encapsulates key aspects of obesity, including insulin resistance and an obesity profile. This innovative approach has the potential to significantly impact the discovery of novel therapeutic interventions for metabolic syndrome and obesity. By providing a nuanced understanding of metabolic conditions, our 3D model stands as a transformative contribution to in vitro research, offering a pathway for the development of small molecules and biologics targeting these pervasive health issues in humans. [ABSTRACT FROM AUTHOR]

Background and objective: Non-alcoholic fatty liver disease (NAFLD) is primarily perceived as a condition prevalent among obese individuals. Its pathogenesis is closely intertwined with metabolic syndrome components. However, the association between insulin resistance and NAFLD in nonobese individuals remains ambiguous. Observational studies have scrutinized the prevalence of insulin resistance and metabolic syndrome in lean NAFLD patients. Materials and methods: This is an observational study, and NAFLD screening was carried out among inpatient and outpatient attendees at SRM Medical College's General Medicine Department. Out of 200 screened patients meeting inclusion and exclusion criteria, 80 were diagnosed with non-alcoholic fatty liver disease (NAFLD). The assessment of metabolic syndrome was performed using the NCEP-ATP III criteria, allowing for comparison between groups concerning insulin resistance and metabolic parameters. Results: Among NAFLD patients, those in the obese age group exhibited a higher prevalence of hypertension (57.8%; p < 0.001) and metabolic syndrome (75.6%; p < 0.0001). The lean NAFLD group showed elevated HOMA-IR levels (4.16) compared to obese NAFLD patients (2.92), with a significant statistical disparity (p < 0.0001). Additionally, the HSI value significantly increased in obese NAFLD patients (p < 0.00001). Conclusion: Insulin resistance, a key factor in metabolic syndrome, is prevalent in lean individuals with non-alcoholic fatty liver disease (NAFLD), playing a pivotal role in its development. This resistance, linked to metabolic syndrome, promotes hepatic triglyceride and fatty acid accumulation, leading to NAFLD. Moreover, insulin resistance correlates significantly with weight gain in NAFLD patients. [ABSTRACT FROM AUTHOR]

Background: Observational studies have reported that gut microbiota composition is associated with metabolic syndrome. However, the causal effect of gut microbiota on metabolic syndrome has yet to be confirmed. Methods: We performed a bidirectional Mendelian randomization study to investigate the causal effect between gut microbiota and metabolic syndrome in European population. Summary statistics of gut microbiota were from the largest available genome-wide association study meta-analysis (n = 13,266) conducted by the MiBioGen consortium. The summary statistics of outcome were obtained from the most comprehensive genome-wide association studies of metabolic syndrome (n = 291,107). The inverse-variance weighted method was applied as the primary method, and the robustness of the results was assessed by a series of sensitivity analyses. Results: In the primary causal estimates, Actinobacteria (OR = 0.935, 95% CI = 0.878–0.996, P = 0.037), Bifidobacteriales (OR = 0.928, 95% CI = 0.868–0.992, P = 0.028), Bifidobacteriaceae (OR = 0.928, 95% CI = 0.868–0.992, P = 0.028), Desulfovibrio (OR = 0.920, 95% CI = 0.869–0.975, P = 0.005), and RuminococcaceaeUCG010 (OR = 0.882, 95% CI = 0.803–0.969, P = 0.009) may be associated with a lower risk of metabolic syndrome, while Lachnospiraceae (OR = 1.130, 95% CI = 1.016–1.257, P = 0.025), Veillonellaceae (OR = 1.055, 95% CI = 1.004–1.108, P = 0.034) and Olsenella (OR = 1.046, 95% CI = 1.009–1.085, P = 0.015) may be linked to a higher risk for metabolic syndrome. Reverse MR analysis demonstrated that abundance of RuminococcaceaeUCG010 (OR = 0.938, 95% CI = 0.886–0.994, P = 0.030) may be downregulated by metabolic syndrome. Sensitivity analyses indicated no heterogeneity or horizontal pleiotropy. Conclusions: Our Mendelian randomization study provided causal relationship between specific gut microbiota and metabolic syndrome, which might provide new insights into the potential pathogenic mechanisms of gut microbiota in metabolic syndrome and the assignment of effective therapeutic strategies. [ABSTRACT FROM AUTHOR]

The association between Alzheimer's disease and metabolic disorders as significant risk factors is widely acknowledged. However, the intricate molecular mechanism intertwining these conditions remains elusive. To address this knowledge gap, we conducted a thorough investigation using a bioinformatics method to illuminate the molecular connections and pathways that provide novel perspectives on these disorders' pathological and clinical features. Microarray datasets (GSE5281, GSE122063) from the Gene Expression Omnibus (GEO) database facilitated the way to identify genes with differential expression in Alzheimer's disease (141 genes). Leveraging CoreMine, CTD, and Gene Card databases, we extracted genes associated with metabolic conditions, including hypertension, non-alcoholic fatty liver disease, and diabetes. Subsequent analysis uncovered overlapping genes implicated in metabolic conditions and Alzheimer's disease, revealing shared molecular links. We utilized String and HIPPIE databases to visualize these shared genes' protein-protein interactions (PPI) and constructed a PPI network using Cytoscape and MCODE plugin. SPP1, CD44, IGF1, and FLT1 were identified as crucial molecules in the main cluster of Alzheimer's disease and metabolic syndrome. Enrichment analysis by the DAVID dataset was employed and highlighted the SPP1 as a novel target, with its receptor CD44 playing a significant role in the inflammatory cascade and disruption of insulin signaling, contributing to the neurodegenerative aspects of Alzheimer's disease. ECM-receptor interactions, focal adhesion, and the PI3K/Akt pathways may all mediate these effects. Additionally, we investigated potential medications by repurposing the molecular links using the DGIdb database, revealing Tacrolimus and Calcitonin as promising candidates, particularly since they possess binding sites on the SPP1 molecule. In conclusion, our study unveils crucial molecular bridges between metabolic syndrome and AD, providing insights into their pathophysiology for therapeutic interventions. [ABSTRACT FROM AUTHOR]

Background: Metabolic syndrome (MetS) is associated to sleep duration. It is crucial to identify factors that disrupt sleep regulation. The study aimed to assess the indirect effect of risk factors related to MetS severity through sleep duration by utilizing a structural equation model (SEM). Methods: The study involving 3,935 adults from the baseline data of the Ravansar Non-Communicable Disease (RaNCD) cohort study. MetS severity scores were the outcome variables. SEM was employed to explore the relationships, utilizing IBM SPSS and AMOS version 23. Results: The mean MetS severity score was higher in women compared to men (0.25 vs. 0.16, P = 0.003). In men, socioeconomic status (SES) has a positive direct effect (β = 0.048) and a negative indirect effect (β=-0.006) on MetS severity. Increased physical activity is directly (β=-0.036) and indirectly (β=-0.093) associated with reducing MetS severity. Nap duration is directly linked to an increase (β = 0.072) but has an indirect effect (β=-0.008) in decreasing MetS severity. In women, SES has a direct (β=-0.020) and indirect (β=-0.001) inverse relationship with MetS severity. Increased physical activity is directly (β=-0.048) and indirectly (β=-0.036) associated with decreasing MetS severity in women. Nap duration is directly associated with an increase in MetS severity (β=-0.018) but indirectly contributes to its reduction (β=-0.002). Sleep duration not only directly affects MetS severity but is also influenced by age, SES, physical activity, obesity and nap duration. Conclusion: Physical activity, SES, and nap duration directly and indirectly effect the MetS severity. Sleep duration was recognized as a mediating variable that supports the indirect effects. [ABSTRACT FROM AUTHOR]

Metabolic syndrome (MetS), a cluster of metabolic abnormalities composed of central obesity, elevated blood pressure, glucose disturbances, hypercholesterolemia and dyslipidaemia, has increasingly become a public health problem in the 21st century worldwide. The dysfunction of telomeres, the repetitive DNA with highly conserved sequences (5′-TTAGGG-3′), is remarkably correlated with organismal aging, even suggesting a causal relationship with metabolic disorders. The health benefits of n-3 polyunsaturated fatty acids (PUFAs) in multiple disorders are associated with telomere length in evidence, which have recently drawn wide attention. However, functional targets and pathways for the associations of n-3 PUFAs and telomere with MetS remain scare. Few studies have summarized the role of n-3 PUFAs in DNA damage repair pathways, anti-inflammatory pathways, and redox balance, linking with telomere biology, and other potential telomere-related signaling pathways. This review aims to (i) elucidate how n-3 PUFAs ameliorate telomere attrition in the context of anti-oxidation and anti-inflammation; (ii) unravel the role of n-3 PUFAs in modulating telomere-related neuron dysfunction and regulating the neuro-endocrine-immunological network in MetS; (iii) epidemiologically implicate the associations of metabolic disorders and n-3 PUFAs with telomere length; and (iv) suggest promising biochemical approaches and advancing methodologies to overcome the inter-variation problem helpful for future research. [ABSTRACT FROM AUTHOR]

Background: Remnant cholesterol (RC) has been known as an important factor for the assessment of the metabolic syndrome (Mets) risk. However, the correlation between RC and hyperuricemia (HUA) in type 2 diabetes mellitus (T2DM) remains unclear. This study aims to explore the correlation between RC and HUA in patients with T2DM. Methods: A total of 2956 patients with T2DM admitted to the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University from 2020 to 2022 were included. The correlation between RC and HUA was evaluated with Spearman's correlation, multiple logistic regression, subgroup analyses, receiver operating characteristic (ROC) curves analyses and generalized smooth curve fitting. Total cholesterol (TC) < 5.18mmol/L was defined as normal TC. Results: RC was correlated with uric acid in patients with T2DM (Spearman's correlation coefficient = 0.279, P < 0.001). According to the multiple logistic regression analyses, there was an independent positive correlation between RC and HUA (OR = 1.63, 95%CI = 1.40, 1.90). In addition, a non-linear correlation between RC and HUA was identified. The area under the ROC curve (AUC) of RC (0.658, 95%CI = 0.635, 0.681) was the largest compared with those of low-density lipoprotein cholesterol (LDL-C), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C) and TC. Subgroup analyses showed a more significant positive correlation among females or normal TC groups. Conclusion: Elevated RC is correlated with HUA in patients with T2DM significantly and positively. RC is better in its predictability for HUA than that of conventional lipid indexes. [ABSTRACT FROM AUTHOR]

Metabolic syndrome (MetS) is a cluster of clinical syndromes that is closely associated with an elevated risk of developing atherosclerotic cardiovascular disease. In a series of animal experiments and clinical trials, crocus sativus and its component crocin have demonstrated promising hypoglycemic effects. However, there is currently insufficient evidence regarding their impact on cardiometabolic parameters. Our study aimed to assess the impact of Crocus sativus and crocin on glycemic control in individuals with metabolic syndrome and associated disorders, as well as their potential effects on improving cardiometabolic parameters. We searched Cochrane Library, PubMed, Embase, and Web of Science databases to ascertain the pertinent randomized controlled trials (RCTs) until December 30, 2023. Q-test and I2 statistics were utilized to evaluate heterogeneity among the included studies. Data were merged using a random-effects model and presented as (WMD) with a 95% confidence interval (CI). The current comprehensive review and meta-analysis, encompassing 13 RCTs involving a total of 840 patients diagnosed with metabolic syndrome and associated disorders, demonstrates that Crocus sativus was superior to placebo on Hemoglobin A1c(HbA1c) (WMD: -0.31;95% CI [-0.44,-0.19]. P = 0.002) and systolic blood pressure(SBP) (WMD:-7.49;95% CI [-11.67,-3.30]. P = 0.99) respectively. Moreover, Crocus sativus improved fasting blood glucose (FBG) (WMD:-7.25;95% CI [-11.82, -2.57]. P = 0.002) when used crocin and on other chronic diseases. Crocus sativus reduced the total cholesterol (TC) among the metabolic syndromepatients (WMD:-13.64;95%CI [-26.26, -1.03]. P = 0.03). We demonstrated that Crocus sativus exerts beneficial effects on glycemic control and cardiometabolic parameters in individuals with metabolic syndrome and related disorders. [ABSTRACT FROM AUTHOR]

Background Methods Results Conclusion Metabolic syndrome (MetS), a condition that includes several risk factors specific for cardiovascular disease, is commonly detected among patients with schizophrenia (SCZ). This study elucidated the factors contributing to the development and severity of MetS in first‐treatment drug‐naïve (FTDN) patients with SCZ.The study enrolled 668 individuals with FTDN SCZ, aged 18–49 years, who had no exposure to antipsychotic medications and been hospitalized between February 2017 and June 2022 at the largest psychiatric specialty institution in central China. Patient sociodemographic and general clinical data were collected, and their psychopathology scores and illness severity were assessed using the Positive and Negative Symptom Scale (PANSS) and Clinical Global Impression Scale–Severity of Illness (CGI‐SI), respectively. MetS score was calculated to determine the disease severity.The prevalence of MetS among this study population was 10.93%. Binary logistic regression analysis revealed onset age, female sex, total cholesterol, and red blood and white blood cell counts as risk factors for MetS, and deemed free tetraiodothyronine (FT4) and CGI‐SI score as protective factors. Multiple linear regression analysis result confirmed older SCZ onset age as a risk factor for elevated MetS score.This study determined the prevalence of MetS in patients with FTDN SCZ and revealed the factors that influence the occurrence and severity of the disease. These findings will allow development of specific prevention and treatment strategies in clinical practice. [ABSTRACT FROM AUTHOR]

Background: Heavy menstrual bleeding (HMB) is a common menstrual disorder associated with multiple risk factors of cardiovascular disease (CVD) in women. In addition, HMB is often present with irregular menstruation (IM) which is a risk factor for CVD outcomes. However, the relationship between HMB and CVD outcomes is unexplored in the presence or absence of IM. We determined the association of HMB with multiple CVD outcomes using a nationally representative sample of female hospitalizations in the US. Methods: All hospitalizations of females with HMB diagnosis and normal menstrual cycles from ages of 18 to 70 years were extracted from the National Inpatient Sample Database, 2017. The HMB was defined using the International Classification of Diseases (ICD)-10 for excessive and frequent menstruation bleeding and included any current or history of HMB diagnosis. Outcomes including major adverse cardiovascular events (MACE), coronary heart disease (CHD), stroke, heart failure (HF), atrial fibrillation (AF) or arrhythmia, myocardial infarction (MI), and diabetes (DM) were defined using ICD-10 codes. Adjusted logistic regression and prosperity scores-matched logistic regression analyses were conducted to summarize adjusted associations with an odds ratio (OR) and a 95% confidence interval (CI). Results: Among 2,430,851 hospitalizations, HMB was observed in 7762 (0.68%) females with age ≤ 40 years and 11,164 (0.86%) females with age > 40 years. Among hospitalizations with age ≤ 40 years, HMB was significantly associated with increased odds of CVD outcomes including MACE (OR = 1.61; 95% CI: 1.25, 2.08), CHD (OR = 1.72; 95% CI: 1.10, 2.71), stroke (OR = 1.95; 95% CI: 1.12, 3.40), HF (OR = 1.53; 95% CI: 1.15, 2.03), and AF/arrhythmia (OR = 1.84; 95% CI: 1.34, 2.54). These associations were confirmed in multiple sensitivity analyses. In contrast, HMB was not robustly associated with CVD events among hospitalizations of women with age > 40 years. HMB without IM was strongly associated with DM, HF, AF, and MACE outcomes while HMB with IM was strongly associated with CHD and AF outcomes in hospitalizations of young women. Conclusions: HMB is associated with CVD events among US hospitalizations of young women. A routine investigation and screening of menstrual disorders, especially HMB, is useful for CVD risk stratification and management in young women. [ABSTRACT FROM AUTHOR]