Prior research has highlighted the significant roles of circulating retinol, retinol-binding protein 4 (RBP4), and apolipoprotein C (ApoC) in metabolic health. This study investigates the joint association of retinol and RBP4 with metabolic syndrome (MetS) and examines the potential mediating role of ApoCs in these relationships. This prospective study included 3,009 and 2,724 participants with baseline serum retinol and RBP4 data, respectively. Over a 9-year follow-up among 2,621 participants, 1,136, 127, 696, and 662 were categorized into MetS-free, recovered, incident MetS, and persistent MetS groups, respectively. Midway through the study, ApoC1-4 levels were measured in 2316 participants. Adjusted odds ratios (95% CIs) for the highest (vs. lowest) tertile of retinol and RBP4 levels were 3.63 (2.69-4.92) and 5.64 (4.05-7.92) for 9-year persistent MetS, respectively. The corresponding hazard ratios (95% CIs) were 1.67 (1.39-2.01) and 1.67(1.38, 2.03) for incident MetS, and 0.65 (0.41-1.03) and 0.44 (0.28, 0.70) for recovered MetS (all P-trends<.05). A synergistic association of retinol and RBP4 with MetS risk was observed for persistent MetS. Higher levels of retinol or RBP4 were associated with increased concentrations of ApoC1-4, which were linked to a greater risk of incident and persistent MetS. A newly developed composite score (ApoCS), derived from ApoC1-4 levels, explained 30.5% and 24.5% of the association between retinol or RBP4 and MetS, with ApoC2 and ApoC3 contributing predominantly to this connection. Our study identified notable positive correlations between serum retinol and RBP4 levels and MetS progression, explained by increases in circulating ApoC2 and ApoC3 within a Chinese cohort.

Research suggests associations between physical activity, sedentary behavior, sleep, and metabolic syndrome, but most has focused on healthy populations and individual behaviors. We investigated associations of 24-hr movement behavior compositions with cardiometabolic risk factors and metabolic syndrome in adults receiving rehabilitation for other health conditions.

 This cross-sectional study assessed 24-hr movement behaviors using thigh-worn accelerometers and metabolic outcomes via blood analyses in 145 adults attending outpatient rehabilitation. Regression models tested associations of five 24-hr time-use behaviors (time in bed, sedentary time, standing, light-intensity stepping, and moderate- to vigorous-intensity stepping) with cardiometabolic risk factors and metabolic syndrome severity score (a cumulative measure of risk derived from metabolic risk factors).

 Participants (64 [SD 12] years old; 52% women; 66% with metabolic syndrome, with 6 [SD 0.7] days of 24-hr data) spent 41% of a 24-hr day sedentary, 15% standing, 3% in light-intensity stepping, 2% in moderate- to vigorous-intensity stepping, and 38% in bed. Adjusted models indicated that a higher proportion of light-intensity stepping was associated with lower triglycerides, more time in bed was associated with a higher metabolic syndrome severity score, and more time stepping was associated with a lower metabolic syndrome severity score. There was no evidence of associations between the overall compositions and outcomes.

The consistently observed small proportions of physical activity, with lack of variation between participants, may not be sufficient to counteract the impact of high sedentary time on metabolic outcomes in adults attending outpatient rehabilitation.

 Future research may focus on exploring ways to increase light-intensity stepping in sedentary older adults with various health conditions.

Previous epidemiological studies have provided inconsistent findings regarding the association between metabolic syndrome (MetS) and risk of esophageal cancer.

We conducted a comprehensive literature search for prospective studies in MEDLINE and EMBASE databases through April 2024. Random-effects meta-analysis was used to calculate pooled hazard ratios (HR) with 95 % confidence intervals (CI) for the associations between MetS and risk of esophageal cancer by histological type. Between-study heterogeneity was assessed by Cochran's Q test and I2 statistics.

Among 8097 identified studies, six studies were included. MetS was associated with an increased risk of esophageal adenocarcinoma (pooled HR=1.24; 95 %CI, 1.07-1.42; Pheterogeneity=0.392, I2=3.8 %, N = 6), but not esophageal squamous cell carcinoma (HR=0.89; 95 % CI, 0.58-1.36; Pheterogeneity=0.040, I2=68.9 %, N = 3). An increased risk of esophageal adenocarcinoma was indicated for hyperglycemia (HR= 1.14; 95 % CI, 1.01-1.29; Pheterogeneity=0.693, I2=0.0 %, N = 3) and obesity (HR=1.50; 95 % CI, 1.24-1.82; Pheterogeneity=0.191, I2=34.5 %, N = 5), rather than the other components of MetS, i.e. hypertension or levels of triglyceride or high-density lipoprotein. Hypertension was associated with seemingly increased risk of esophageal squamous cell carcinoma (HR=1.39; 95 % CI, 0.93-2.09; Pheterogeneity=0.030, I2=71.4 %, N = 3), while obesity was associated with a decreased risk (HR=0.65; 95 % CI, 0.38-1.12; Pheterogeneity=0.009, I2=78.7 %, N = 3); no associations were observed for the other components of MetS with esophageal squamous cell carcinoma.

MetS, particularly hyperglycemia and obesity, may increase the risk of esophageal adenocarcinoma. MetS, by and large, may not influence the risk of esophageal squamous cell carcinoma.

Breast cancer (BC) is the primary cause of cancer-related deaths among women worldwide, with increasing evidence pointing to the effect of metabolic factors, particularly lipid levels, in its pathogenesis. In this research, Mendelian randomization (MR) was employed to explore the causality between four plasma lipid traits-total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C)-and the risk of BC. Additionally, we explored the potential mediating effects of coronary artery disease (CAD), total testosterone (TT) on these associations and possible mechanisms through bioinformatics analyses.

Data of genome-wide association study (GWAS) on lipids, CAD, TT and BC were obtained from public sources and websites as part of a genome-wide association research. The inference of causality was primarily assessed through the inverse variance weighting (IVW) approach, with supplementary tests for horizontal pleiotropy and heterogeneity. To verify the directionality of causal relationships, the MR Steiger test was applied. Additionally, reverse causality was evaluated by regarding BC as the exposure. To adjust for confounders, multivariate MR (MVMR) was performed, followed by a two-step mediation analysis to investigate the mediating roles of CAD in the lipid-BC association, and of TT in the CAD-BC relationship. The intersecting SNP (rs11556924) between causal pathways was established through a Venn diagram and its associated gene (Zinc Finger C3HC-Type Containing 1, ZC3HC1) was identified through the g:Profiler database. The expression of ZC3HC1 was further explored using the TIMER, GEPIA2 and HPA database. Finally, enrichment analyses of Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and protein-protein interactions (PPI) network analysis were conducted on ZC3HC1 and its related genes.

The random-effects IVW analysis yielded the following results: HDL-C on CAD (OR = 0.843, 95% CI 0.771-0.921, P < 0.001), CAD on BC (OR = 0.935, 95% CI 0.892-0.980, P = 0.005), HDL-C on BC (OR = 1.127, 95% CI 1.059-1.199, P < 0.001), CAD on TT (OR = 0.987, 95% CI 0.975-0.998, P = 0.020) and TT on BC (OR = 1.354, 95% CI 1.148-1.598, P < 0.001). The MR Steiger test results support the validity of the inferred causal direction (P < 0.001). There were no discernible causal relationships between BC and HDL-C/CAD according to reverse MR analysis (P > 0.05). Following MVMR adjustment, the causal effects of HDL-C, CAD, and TT on BC were still statistically significant (P < 0.05). Besides, the two-step mediation analysis indicated that CAD mediated 7.8% of the causal effect of HDL-C on BC, whereas TT mediated 6.1% of the causal effect between CAD and BC. The expression of ZC3HC1 showed no significant expression difference between normal and BC tissues (P > 0.05), which might indicate a carcinogenic effect independent of expression levels but driven by functional alterations induced by variants (C > T). Functional network analysis suggested that ZC3HC1 was associated with multiple signal pathways in cancers, such as PI3K-Akt and MAPK signal pathways.

From a genetic perspective, our study reveals that there is causality between HDL-C levels and BC risk, with CAD and TT acting as partial mediators in this relationship. Moreover, our study firstly establishes a potential link between CAD-associated SNP (rs11556924), the corresponding gene (ZC3HC1) functional dysregulation, and the initiation of BC. These findings shed light on the biological links between lipids and BC, potentially contributing to future prevention and treatment strategies.

Skin cancers are the third most common cancer worldwide, with incidence increasing. Metabolic syndrome (MetS) is a cluster of metabolic abnormalities strongly associated with the development of cardiovascular disease. More than one in five individuals have MetS, and it is linked with at least 14 different cancers. This study aimed to investigate whether MetS is a risk factor for skin cancer.

A prospective cohort study was conducted in the UK Biobank. The association between MetS and skin cancer was investigated using multivariable Poisson regression. To investigate causality, a two-sample Mendelian randomization (MR) study was conducted using summary-level genome-wide association study data from the UK Biobank (MetS) and FinnGen (skin cancer).

A total of 467,919 participants were included; 26.7% had MetS. Follow-up was for up to 10.8 years. MetS showed a moderately sized protective effect on basal-cell carcinoma, whereas the effect for squamous cell carcinoma and malignant melanoma crossed the null. Overall, MR found there was some weak evidence for increased odds of skin cancer in those with MetS [OR = 1.07 (95% confidence interval: 1.01, 1.14)].

The observational study identifies a moderately sized protective effect of MetS on basal-cell carcinoma with MR evidence suggesting a weak causal effect in the opposite direction.

This study has found little-to-no effect of MetS on skin cancer despite links between MetS and at least 14 other cancers.

Head and neck cancer (HNC) encompasses a heterogeneous group of malignancies originating in the oral cavity, pharynx, nasopharynx, larynx, paranasal sinuses, and salivary glands. Accumulating evidence indicates that metabolic syndrome (MetS) characterized by a constellation of conditions including central adiposity, hyperglycemia, dyslipidemia, hypertension, and insulin resistance, may significantly influence cancer pathogenesis and progression.

MetS has been epidemiologically linked to elevated risk for multiple malignancies through various metabolic mechanisms involving chronic systemic inflammation, insulin resistance, and dysregulated lipid metabolism. Especially in HNC, recent studies demonstrated that MetS and metabolic imbalance conditions may contribute to carcinogenesis, disease progression, and clinical outcomes, but the exact mechanisms behind the association between excess fat accumulation and HNC risk remain unclear. Considering previous studies, pharmacological agents targeting metabolic pathways, including biguanides (metformin), thiazolidinediones, sodium-glucose cotransporter-2 (SGLT-2) inhibitors, and HMG-CoA reductase inhibitors (statins) are being investigated for potential repurposing in cancer prevention and adjuvant therapy.

Here, we summarize the latest evidence on the relationship between MetS and HNC, highlighting the therapeutic potential of anti-diabetes drugs and anti-dyslipidemia drugs in ameliorating various pathological problems in HNC patients with MetS.

Conflicting evidence exists on the link between gout and cancer risk, with limited clarity on the impact of healthy lifestyle factors.

In the UK Biobank, 7,169 gout patients were matched with 21,507 non-gout controls (1:3 ratio) using propensity scores. Cox regression models assessed cancer risk associated with gout. Among 6,105 gout patients, cancer risk was further evaluated using an eight-factor Healthy Lifestyle Score (HLS) and a weighted HLS.

Gout was linked to a higher cancer incidence [HR (95% CI) = 1.075 (1.013-1.140)]. High HLS in gout patients correlated with a lower cancer risk [HR (95% CI) = 0.825 (0.717-0.948)], with the strongest protective effect observed in those aged ≥60. Sensitivity analyses confirmed these findings.

Gout patients have a higher risk of developing cancer, but a healthy lifestyle, particularly in those aged 60 and older, significantly reduces this risk. These findings highlight the importance of lifestyle interventions for cancer prevention in patients with gout.

The remnant cholesterol inflammatory index (RCII) is a novel metric that combines remnant cholesterol and high-sensitivity C-reactive protein, reflecting the metabolic and inflammatory risk. This study investigates the association between RCII and long-term risks of all-cause and cause-specific mortality in middle-aged and elderly populations in the US and China.

We analyzed data from the National Health and Nutrition Examination Survey (NHANES) and the China Health and Retirement Longitudinal Study (CHARLS), including 7,565 and 12,932 participants aged 45 years and older, respectively. The participants were categorized into quartiles based on natural log-transformed RCII (lnRCII) values. Kaplan-Meier survival analysis, Cox proportional hazards models, restricted cubic splines (RCS) and mediation analysis were used to examine the relationship between lnRCII and mortality outcomes, adjusting for potential covariates.

The mean age of the participants was 59.90 ± 10.44 years (NHANES) and 58.64 ± 9.78 years (CHARLS), with 53.28% and 52.50% female, respectively. Kaplan-Meier survival analysis showed that higher lnRCII quartiles (≥ 0.79 in NHANES, ≥ -0.13 in CHARLS) were significantly associated with increased all-cause mortality risk (p < 0.001). Each standard deviation (SD) increase in lnRCII corresponded to a higher risk of all-cause mortality, and the hazard ratios (HRs) and 95% confidence interval (CI) were 1.29 (95% CI: 1.21-1.36) in NHANES and 1.26 (95% CI: 1.15-1.38) in CHARLS. In NHANES, lnRCII was also associated with elevated risks of cardiovascular mortality (HR = 1.21, 95% CI: 1.08-1.35) and cancer mortality (HR = 1.30, 95% CI: 1.09-1.55). RCS analysis indicated a J-shaped relationship between lnRCII and both all-cause and cardiovascular mortality, and a linear association with cancer mortality. Mediation analysis showed that systolic blood pressure and fasting plasma glucose partially mediated these associations. Subgroup analyses suggested a stronger association between lnRCII and all-cause mortality in middle-aged US participants (p for interaction = 0.010).

Elevated RCII levels are significantly associated with increased all-cause mortality risk middle-aged and elderly populations in both the US and China. In the US population, RCII is also associated with increased risks of cardiovascular and cancer mortality. By integrating metabolic and inflammatory risk factors, RCII may serve as a valuable tool for mortality risk stratification and clinical decision-making.

Metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as non-alcoholic fatty liver disease (NAFLD), encompasses a spectrum of liver diseases characterized by hepatic steatosis, the presence of at least one cardiometabolic risk factor, and no other apparent cause. Metabolic syndrome (MetS) is a cluster of clinical conditions associated with increased risk of cardiovascular disease, type 2 diabetes, and overall morbidity and mortality. This narrative review summarizes the changes in the management of people with MetS and NAFLD/MASLD from screening to therapeutic strategies that have occurred in the last decades. Specifically, we underline the clinical importance of considering the different impacts of simple steatosis and advanced fibrosis and provide an up-to-date overview on non-invasive diagnostic tests (i.e., imaging and serum biomarkers), which now offer acceptable accuracy and are globally more accessible. Early detection of MetS and MASLD is a top priority as it allows for timely interventions, primarily through lifestyle modification. The liver and cardiovascular benefits of a global and multidimensional approach are not negligible. Therefore, a holistic approach to both conditions, MetS and related chronic liver disease, should be applied to improve overall health and longevity.

Metachronous gastric cancer (MGC) has gained increasing attention due to the preservation of the stomach during endoscopic resection for early gastric cancer (EGC).

This study aims to investigate the risk factors associated with MGC in the postoperative surveillance of endoscopic submucosal dissection (ESD).

A retrospective case-control study.

The retrospective study was conducted between January 1, 2014, and June 30, 2020, at the Affiliated Drum Tower Hospital of Nanjing University Medical School.

Several independent risk factors for developing MGC were identified as smoking history (hazard ratio (HR) 2.39, 95% confidence interval (CI) 1.25-4.58), metabolic dysfunction-associated steatotic liver disease (MASLD; HR 2.44, 95% CI 1.23-4.87), cerebrovascular disease (CD; HR 2.55, 95% CI 1.09-5.99), multiple lesions (HR 2.06, 95% CI 1.17-3.63), Helicobacter pylori infection status (eradicated vs negative: HR 1.42, 95% CI 0.60-3.39; persistent vs negative: HR 5.47, 95% CI 2.13-14.03), and atrophic gastritis (AG; moderate vs mild: HR 4.44, 95% CI 1.36-14.53; severe vs mild: HR 7.30, 95% CI 2.11-25.22). The established nomogram based on these risk factors demonstrated high accuracy both in the training and test sets, with concordance indexes of 0.787, 0.762, and 0.845 for the training set, and 0.764, 0.824, and 0.788 for the test set at 2, 3, and 5 years, respectively.

The risk factors for developing MGC after curative ESD for EGC were identified as smoking history, MASLD, CD, multiple lesions, H. pylori infection status, and AG. To reduce the risk of MGC, a healthy lifestyle, regular H. pylori testing, and annual endoscopic screening are recommended.

East Asian populations, which account for approximately 20% of the global population, have become central to the worldwide rise of metabolic diseases over the past few decades. The prevalence of metabolic disorders, including type 2 diabetes mellitus, hypertension and metabolic dysfunction-associated steatotic liver disease, has escalated sharply, contributing to a substantial burden of complications such as cardiovascular disease, chronic kidney disease, cancer and increased mortality. This concerning trend is primarily driven by a combination of genetic predisposition, unique fat distribution patterns and rapidly changing lifestyle factors, including urbanization and the adoption of Westernized dietary habits. Current advances in genomics, proteomics, metabolomics and microbiome research have provided new insights into the biological mechanisms that might contribute to the heightened susceptibility of East Asian populations to metabolic diseases. This Review synthesizes epidemiological data, risk factors and biomarkers to provide an overview of how metabolic diseases are reshaping public health in East Asia and offers insights into biological and societal drivers to guide effective, region-specific strategies.

This research seeks to explore the link between the oxidative balance score (OBS) and sarcopenia in American adults with Metabolic Syndrome (MetS) using data from a national, population-based survey.

The study included 3,625 participants diagnosed with Metabolic Syndrome, all aged 20 years and above, derived from NHANES datasets spanning 1999-2006 and 2011-2018. OBS evaluation was based on 16 dietary and 4 lifestyle elements. MetS diagnosis followed the NCEP-ATP III guidelines, while sarcopenia identification was based on FNIH standards. We employed multivariate logistic regression analyses to delve into the connections between OBS and sarcopenia within the MetS cohort.

Sarcopenia was found in 17.46% of the participants. In models adjusted for all variables, OBS, dietary OBS, and lifestyle OBS each showed a significant inverse relationship with sarcopenia among MetS individuals [OBS: OR = 0.959, 95%CI: (0.948, 0.982), P trend = 0.0005; dietary OBS: OR = 0.963, 95%CI: (0.939, 0.989), P trend = 0.0055; lifestyle OBS: OR = 0.860, 95%CI: (0.787, 0.939), P trend = 0.0011]. Higher scores in OBS were consistently linked with a decreased incidence of sarcopenia (all P for trend < 0.05). Restricted cubic spline analysis confirmed that these relationships were linear. The impact of age was significant, with OBS benefits only observed in those aged 40 and older.

Maintaining a diet and lifestyle rich in antioxidants is both independently and collectively linked with a lower occurrence of sarcopenia in individuals with MetS. These results bolster the proposition of developing OBS-centered preventive strategies for sarcopenia in MetS patients, particularly those aged 40 years and older.

Data regarding the connection between Fat Mass Index (FMI) and Metabolic Syndrome (MetS) in cancer survivors remain limited. This study aimed to assess the association between FMI and the likelihood of MetS among cancer survivors by conducting a population-based cross-sectional study. This cross-sectional study utilized data from the National Health and Nutrition Examination Survey (NHANES) to examine a sample of 799 adult cancer survivors, aged over 20 years old, spanning the years 1999-2006 and 2011-2018. MetS was defined according to the criteria established by the Adult Treatment Panel III of the National Cholesterol Education Program (NCEP). To explore the association between fat mass index FMI and the prevalence of MetS among cancer survivors, multivariate logistic regression analyses were conducted. Additionally, restricted cubic splines were used to assess both linear and nonlinear relationships between FMI and MetS. After adjusting for potential confounders, the logistic regression analysis of multistage weighted complex sampling data demonstrated that a higher FMI significantly increased the odds of developing MetS (odds ratio [OR] = 1.33, 95% confidence interval [CI]: 1.09-1.61, p = 0.01). This association remained robust when FMI was categorized into tertiles. Specifically, the adjusted ORs for MetS in the second and third tertiles were 4.80 (95% CI: 1.95-11.79) and 8.95 (95% CI: 2.51-31.94), respectively (p for trend = 0.001). Furthermore, our analysis indicated a significant nonlinear relationship between FMI and the likelihood of MetS (p < 0.0001). In this research, we discovered that an elevated FMI is significantly associated with a higher prevalence of MetS among cancer survivors in the U.S. adult population. These findings underscore the importance of managing body fat to prevent MetS in this group.

Evidence suggests a potential link between metabolic dysfunction and head and neck cancer (HNC). This study investigates the potential causal relationships between metabolic dysfunction and HNC using genetic data. While no significant causal associations were identified between metabolic indicators and HNC risk, the research revealed that inhibition of certain genes could reduce cancer risk. Specifically, inhibiting sodium/glucose cotransporter 2 (SLC5A2) was associated with a decreased risk of HNC and oropharyngeal cancer (OPC), while ATP-sensitive inward rectifier potassium channel 11 inhibition was linked to a reduced risk of oral cavity cancer. Additionally, inhibiting SLC5A1 and voltage-dependent L-type calcium channel subunit beta-2 showed a connection to lower OPC risk. These findings suggest that targeting these genes could offer promising therapeutic strategies for preventing and treating HNC, as well as improving both preoperative and postoperative management in affected patients.

Since many people die of either cancers or cardiovascular diseases worldwide, it is important to find the clinical pitfall that provokes cardiovascular diseases and cancer overall. Since metabolic syndrome (MetS) is largely linked to cardiovascular diseases, we have come to consider that MetS, even in its early state, may prime the occurrence of cancers overall. Indeed, the importance of MetS in causing pancreatic cancer has been proved using our large medical database. We analyzed Japanese healthcare and clinical data in 2005, who were followed up until 2020 and we examined the incidence of major cancers. At the enrollment, we examined the presence or absence of MetS judged by either Japanese criteria or NCEP/ATPIII. Of 2.7 million subjects without missing data, 102,930; 200,231; 237,420; 63,435; 76,172; and 2,422 subjects suffered lung, stomach, colon, liver and prostate cancer, respectively, and myelogenous leukemia during follow-up. MetS, defined by Japanese criteria, increased (p < 0.005 each) the incidence of cancer with a hazard ratio (HR) of 1.03-1.47 for lung, stomach, colon, liver, prostate cancers, and myelogenous leukemia. According to Japanese criteria, cancer incidence in the pre-stage MetS group was comparable to the MetS group. The results were almost identical when we defined MetS using NCEP ATP III. Taken together, we conclude that MetS is linked to majority of cancers.

The proportion of noodles in the Korean diet is increasing, but the effect of noodle intake on metabolic syndrome has not been sufficiently investigated. Therefore, we investigated noodle consumption and its relation to metabolic syndrome in Korean adults.

This study was conducted on 10,505 adults using the combined data of the 2012-2016 Korea National Health and Nutrition Examination Survey (KNHANES). Noodle intake was evaluated with a food frequency question-naire (FFQ) based on 112 food items. To compute odds ratios (ORs) and their 95% confidence intervals (CIs) controlled for confounders, multivariable logistic regression models were used.

Compared to people in the lowest levels of noodle intake, the OR of the metabolic syndrome of those in the highest levels was 1.48 (95% CI, 1.16-1.90; p-trend = 0.002). This positive association was also found for hypertriglyceridemia and abdominal obesity, which were metabolic syndrome components. Specifically, the odds of having hypertriglyceridemia were 38% (OR, 1.38; 95% CI, 1.14-1.66; p-trend < 0.001) higher for people with high noodle consumption compared to those with low noodle consumption in the overall population. The tendency for people who consume a lot of noodles to have raised odds of metabolic syndrome was observed when analyzed by the type of noodles.

This study suggested noodle intake was positively related to met-abolic syndrome and its components in Korean adults. Further clinical trials and prospective cohort studies are required to identify a causal relationship between noodle intake and metabolic syndrome in Koreans.

According to recent studies, prostate cancer (PCa) is strongly associated with metabolic syndrome (MetS). However, there has not been any bibliometric visual analysis of relevant papers. In order to acquire knowledge about research settings and possible future paths, a thorough bibliometric study of MetS-related PCa research was carried out.

From January 1, 2004 to December 31, 2023, original and review publications about MetS and PCa were retrieved from the Web of Science Core Collection (WOSCC) database. Analysis of co-authorship and co-occurrence was done using VOSviewer. To find the top terms with the greatest citation burst, CiteSpace was used.

There were 1,296 publications on PCa and MetS in all. The analysis showed that the number of yearly scientific papers in the sector was on the rise. The three most productive nations were China, Italy, and the USA. Most papers were published in the PLoS One, while most citations were obtained by the European Urology. The most influential author in terms of citations was Professor Smith MR, whereas the most prolific author was Professor Freedland SJ. Keyword analysis revealed that, apart from PCa and MetS, "obesity" was the most often used phrase, with "risk", "meta-analysis", and "inflammation" appearing as study subjects. Furthermore, "components" and "sex hormones" gained more and more attention.

The findings provide a thorough understanding of the larger context of this field of study. Future studies need to investigate PCa's metabolic processes and inflammatory mechanism. Furthermore, switching from observational research to meta-analysis offers the possibility of illness prediction and tailored therapies. These results may help researchers navigate the most recent advancements and influence the field's future paths.

Although metabolic syndrome (MetS) is associated with an increased risk of various cancers, the combined impact of MetS and healthy lifestyle factors (HLF) on cancer risk is unclear. This study aimed to investigate the independent and combined effects of MetS and HLF on the risk of 16 site-specific cancers in a large community-based cohort.

A total of 289,557 participants in the UK Biobank were analyzed. MetS was defined using a combination of metabolic factors, while HLF scores were evaluated based on lifestyle behaviors, such as smoking, alcohol consumption, physical activity, and diet. Cox proportional hazard models were used to investigate the relationship between MetS or HLF and cancer risk, adjusting for age, sex, ethnicity, education level, family history of cancer, and the Townsend Deprivation Index (TDI).

During a median follow-up of 11.69 years, 11,190 individuals developed cancer. MetS was associated with an increased risk of 9 cancers in men and 7 cancers in women. Compared with participants with unfavorable lifestyles, regardless of metabolic status, HLF was significantly associated with decreased risk of overall cancer (without MetS: HR: 0.812; 95% CI: 0.745-0.886 for intermediate lifestyle and HR: 0.757; 95% CI: 0.669-0.855 for favorable lifestyle; with MetS: HR: 0.702; 95% CI: 0.572-0.862 for favorable lifestyle) and oesophagus, stomach, liver, lung, bronchus, trachea cancers in men and of lung, bronchus, trachea cancers in women. Our analysis demonstrated that the protective association between HLF and reduced cancer risk was confined to subgroups without MetS. Specifically, this association was observed for cancers of the lip, oral cavity, pharynx, colon, rectum, pancreas, kidney, bladder, and lymphoid leukemia in men, and for overall cancer in women(HR: 0.917; 95% CI: 0.862-0.975 for intermediate lifestyle and HR: 0.875; 95% CI: 0.817-0.938 for favorable lifestyle).

MetS elevates risks for multiple cancers, while adopting a healthy lifestyle reduces risks of oesophagus, stomach, and lung, bronchus, trachea cancers in men and lung, bronchus, trachea cancer in women, regardless of metabolic status. However, MetS counteracts lifestyle-mediated protection against specific cancers-including lip, oral cavity, pharynx, colon, rectum, pancreas, kidney, and bladder cancers in men, as well as pancreas and breast cancers in women. These findings underscore the necessity to develop metabolic status-stratified management strategies and implement proactive prevention of MetS.

Metabolic syndrome (MS) is a complex metabolic disorder that is often closely associated with the development of chronic diseases such as cardiovascular disease and diabetes. This study aimed to explore the relationship between estimated glucose metabolic rate (eGDR) and MS. The correlation between eGDR levels and the prevalence of metabolic syndrome was analyzed here based on data from the National Health and Nutrition Examination Survey from 2005 to 2020. The study sample consisted of 63,131 adult participants, and the results showed that lower eGDR levels were significantly associated with a higher prevalence of metabolic syndrome. Further regression analyses showed that eGDR acted as a protective factor and that the risk of MS significantly decreased as its level increased. Subgroup analyses showed that this trend held across gender, age, and BMI categories, and that the protective effect of eGDR was weaker in the higher BMI group. Based on the nonlinear relationship between subjects' eGDR levels and MS prevalence, RCS analyses further confirmed a significant correlation between lower eGDR levels and increased risk of MS. In conclusion, the present study suggests that eGDR levels could serve as a potential biomarker for predicting metabolic syndrome, providing new perspectives for early screening and intervention of MS.

This large-scale, population-based cohort study examined the associations between metabolic syndrome and cholangiocarcinoma risk, including its intrahepatic and extrahepatic forms.

A total of 4,932,211 adults aged ≥40 years participated in a government-initiated health checkup program (2012-2017), which collected lifestyle data, anthropometric measurements, and biochemical tests. Follow-up continued until 2021, with data linkage to National Cancer and Death Registries to ascertain the occurrence of cholangiocarcinoma and obtain vital status information. Fine and Gray models accounted for competing risks. During 35,879,371 person-years of follow-up, 6117 cholangiocarcinoma cases were identified, with an incidence rate of 17.05 (95% CI: 15.90-18.20) per 100,000 person-years. Individuals with metabolic syndrome had significantly higher incidences of both intrahepatic and extrahepatic cholangiocarcinoma ( p <0.0001). The multivariate-adjusted HR for cholangiocarcinoma among those with metabolic syndrome was 1.20 (1.14-1.27). Stratification analyses by age, sex, liver enzyme levels, and comorbidities consistently demonstrated an increased cholangiocarcinoma risk among individuals with metabolic syndrome. A dose-response relationship was observed, with a higher number of metabolic components correlating with an elevated cholangiocarcinoma risk, even after accounting for all-cause mortality as a competing risk. The adjusted subdistribution HRs ranged from 1.16 (95% CI: 1.02-1.32) for individuals with one metabolic component to 1.67 (95% CI: 1.45-1.94) for those with five ( p for trend <0.0001).

The positive association between metabolic syndrome and cholangiocarcinoma risk suggests that managing metabolic risk factors might reduce the occurrence of both intrahepatic and extrahepatic cholangiocarcinoma.

The density of tumor-infiltrating lymphocytes (TILs) serves as a valuable indicator for predicting anti-tumor responses, but its broad impact across various types of cancers remains underexplored. We introduce TILScout, a pan-cancer deep-learning approach to compute patch-level TIL scores from whole slide images (WSIs). TILScout achieved accuracies of 0.9787 and 0.9628, and AUCs of 0.9988 and 0.9934 in classifying WSI patches into three categories-TIL-positive, TIL-negative, and other/necrotic-on validation and independent test sets, respectively, surpassing previous studies. The biological significance of TILScout-derived TIL scores across 28 cancers was validated through comprehensive functional and correlational analyses. A consistent decrease in TIL scores with an increase in cancer stage provides direct evidence that the lower TIL content may stimulate cancer progression. Additionally, TIL scores correlated with immune checkpoint gene expression and genomic variation in common cancer driver genes. Our comprehensive pan-cancer survey highlights the critical prognostic significance of TILs within the tumor microenvironment.

Circadian Syndrome (CircS) is a significant marker of metabolic imbalance and has been linked to various chronic diseases. However, its relationship with cancer risk remains underexplored. This research aims to explore the relationship between CircS and cancer, while also assessing the possible mediating role of the triglyceride glucose (TyG) index.

Baseline data from the 2011 China Health and Retirement Longitudinal Study (CHARLS) and follow-up data from 2015 were analyzed, including participants' sociodemographic characteristics, health behaviors, and metabolic indicators. Linear regression, mediation analysis, and logistic regression were employed to explore relationships between CircS, cancer risk, and the TyG index, with a dose-response analysis conducted on TyG index and cancer risk.

Among 7,864 middle-aged and elderly participants, CircS was significantly and positively associated with cancer risk (r = 0.17, P < 0.001). The TyG index showed a significant correlation with both CircS (r = 0.52, P < 0.001) and cancer (r = 0.15, P < 0.001). Mediation modeling indicated that the TyG index partially mediated the association between CircS and cancer, accounting for 23% of this relationship. Additionally, a significant nonlinear dose-response relationship was observed between the TyG index and cancer risk (Pnonlinear = 0.0024).

Circadian syndrome is associated with increased cancer risk, with the TyG index partially mediating this relationship.

Glucose is the main source of energy in human cells. Elevated levels of glucose are one of the most common metabolic disorders, and it has been shown to have a significant, mostly negative, effect on multiple chronic and acute diseases. Lung cancer remains one of the biggest challenges for treatment in modern medicine, with a high prevalence, incidence and mortality. Hyperglycemia is not uncommon in patients with lung cancer; however, it is usually overlooked. Patients with unregulated glycemia and lung cancer have been shown to have worse outcomes, reduced therapeutic effect and more complications during treatment. Studies have identified multiple molecular pathways common in both hyperglycemia and lung cancer; however, no clear correlation has been identified. By understanding these signaling pathways, we can influence the outcome therapeutically and thereby improve the survival of patients with lung cancer.

Single-nucleotide variants (SNVs) in regulatory DNA are linked to inherited cancer risk. Massively parallel reporter assays of 4,041 SNVs linked to 13 neoplasms comprising >90% of human malignancies were performed in pertinent primary human cell types and then integrated with matching chromatin accessibility, DNA looping and expression quantitative trait loci data to nominate 380 potentially regulatory SNVs and their putative target genes. The latter highlighted specific protein networks in lifetime cancer risk, including mitochondrial translation, DNA damage repair and Rho GTPase activity. A CRISPR knockout screen demonstrated that a subset of germline putative risk genes also enables the growth of established cancers. Editing one SNV, rs10411210 , showed that its risk allele increases rhophilin RHPN2 expression and stimulus-responsive RhoA activation, indicating that individual SNVs may upregulate cancer-linked pathways. These functional data are a resource for variant prioritization efforts and further interrogation of the mechanisms underlying inherited risk for cancer.

Triple-negative breast cancer (TNBC) has a poor prognosis. Pathological complete response (pCR) after neoadjuvant chemotherapy (NAC) is a prognostic factor. This study aimed to find predictors of efficacy.

A total of 266 TNBC patients treated with NAC were included. The relationship between MetS, S100A7/cPLA2 expression and clinicopathological features was investigated. The effect on pCR, clinical response, and disease-free survival (DFS) was observed. A cell co-culture model was established by the researchers to further assess the function of S100A7.

Correlation analysis revealed a strong association between the expressions of S100A7 and cPLA2, with both significantly higher in the MetS group compared to the non-MetS group. Logistic regression analysis indicated that MetS and S100A7/cPLA2 expressions were linked to pCR and clinical response. S100A7/cPLA2 served as an independent predictor of pCR, while cPLA2 was an independent predictor of clinical response. Survival analysis demonstrated that MetS and S100A7/cPLA2 were associated with an increased risk of disease progression. MP grading and clinical efficacy were independent predictors of DFS, with MetS and S100A7/cPLA2 expressions correlating with shortened DFS. In the co-culture model, S100A7 inhibited the NF-κB pathway, enhancing TNBC cell proliferation and invasion in the presence of macrophages, and promoting M2 macrophage polarization.

S100A7/cPLA2 expression predicts a low pCR rate in TNBC patients undergoing NAC and may serve as a potential mechanistic biomarker linking MetS with altered NAC efficacy in TNBC, warranting further investigation and intervention.

Metabolic syndrome (MetS) encompasses a collection of metabolic abnormalities. This study aims to determine which combination of MetS components has the highest mortality risk, and to investigate the causal relationships between MetS components and longevity.

Prospective analyses were conducted on 340,196 participants from the MJ cohort at baseline, and 121,936 participants had follow-up MetS information. We defined MetS according to the NCEP ATP III criteria. The study's outcomes included mortality from cardiovascular disease (CVD), cancer, and all causes combined. We employed Cox proportional hazard models to calculate hazard ratios (HRs) and 95% confidence intervals. Multivariable Mendelian randomization (MVMR) was employed to infer causality using the genetic data of MetS components and longevity.

Elevated blood pressure (BP) was the initial split for all-cause mortality, cancer mortality, and CVD mortality. Participants with MetS, especially those with elevated BP and elevated fasting plasma glucose (FPG), had higher mortality risks than those with other types of MetS. In the MJ cohort, participants with elevated BP and FPG (BG-type MetS) had a 44% (HR = 1.44, 95% CI = 1.37-1.51), 73% (HR = 1.73, 95% CI = 1.62-1.84), and 34% (HR = 1.34, 95% CI = 1.27-1.42) increased risk of all-cause mortality, cancer mortality, and CVD mortality, respectively, compared with non-BG-type MetS (12%, 24%, 5%). The highest mortality rate and mortality risk were observed in participants with BG-type MetS at baseline and follow-up (mortality rate/1000 person years = 9.73, 95% CI = 8.81-10.74; HR = 1.52, 95% CI = 1.35-1.72). SBP and FPG increases that were genetically proxied to a 1-standard deviation higher level decreased the probabilities of living to the 90th percentile age by 41% (OR = 0.59, 95% CI = 0.40-0.86) and 32% (OR = 0.68, 95% CI = 0.48-0.98) in MVMR, respectively.

Individuals with BG-type MetS are at a higher risk of death than those with other types of MetS. Therefore, these individuals should be targeted to improve MetS outcomes.

The American Heart Association (AHA) recently defined cardiovascular-kidney-metabolic (CKM) syndrome to better characterize the associations among cardiovascular, kidney, and metabolic diseases. Although about 9 in 10 United States adults have at least 1 risk factor for CKM syndrome, its prevalence in other populations is less understood. To fill this gap, we examined the prevalence of CKM syndrome in Korea and its association with demographic and socioeconomic status (SES).

Using data from the Korean National Health and Nutrition Examination Survey between 2011 and 2021, we calculated the prevalence of CKM syndrome across the following stages: stage 0 (no risk factors), stage 1 (excess or dysfunctional adiposity), stage 2 (other metabolic risk factors or chronic kidney disease), and stages 3-4 (subclinical/clinical cardiovascular diseases) among adults aged ≥20 years. Weighted analyses were used to estimate prevalence and 95% confidence intervals (CIs) for each CKM syndrome stage, stratified by age, gender, and SES factors.

Among 54,994 Korean adults, the prevalence of CKM syndrome was as follows: stage 0 (25.2%; 95% CI, 24.7 to 25.8), stage 1 (19.3%; 95% CI, 18.9 to 19.7), stage 2 (51.6%; 95% CI, 51.1 to 52.2), and stages 3-4 (3.9%; 95% CI, 3.7 to 4.0). The prevalence of stages 2 and 3-4 was higher in men than in women. In addition, stages 3-4 were more prevalent among rural residents and those with lower education or income.

About 3 out of 4 Koreans are at risk for CKM syndrome. These findings highlight that CKM syndrome is a global health problem and that interventions are urgently needed to prevent further progression.

Metabolic syndrome (MetS) is associated with increased cancer risk and poor cancer prognosis. The current study applied a mixed methods approach to better understand attitudes about making lifestyle changes and current dietary and physical activity behaviors among cancer patients with MetS at a cancer center and to explore the suitability of brief lifestyle questionnaires to help providers understand their patients' lifestyle attitudes and habits. Qualitative interviews were used to obtain patients' perspectives about lifestyle changes, and 3 quantitative questionnaires-the Readiness Ruler, Rate Your Plate, and the International Physical Activity Questionnaire-Short Form (IPAQ-SF)-were used to measure patients' readiness for lifestyle change, dietary habits, and physical activity levels, respectively. Nineteen patients participated in interviews, and 18 patients completed the questionnaires. Interview findings indicated that patients generally prioritized lifestyle changes over medication use, desired collaboration and coordination between multidisciplinary care teams and patient, and desired tailored interventions and practical implementation strategies to manage MetS. Questionnaire findings indicated that most patients agreed with the importance of lifestyle changes and expressed confidence in making them, reporting healthy food choices and high physical activity levels. A multidisciplinary approach tailored to patients' readiness, preferences, and constraints is recommended for effective MetS management in patients with cancer.

Body mass index (BMI) may misclassify obesity-related cancer (ORC) risk, as metabolic dysfunction can occur across BMI levels. We hypothesized that metabolic dysfunction at any BMI increases ORC risk compared with normal BMI without metabolic dysfunction. Postmenopausal women (n = 20,593) in the Women's Health Initiative with baseline metabolic dysfunction biomarkers [blood pressure, fasting triglycerides, high-density lipoprotein cholesterol, fasting glucose, homeostatic model assessment for insulin resistance (HOMA-IR), and high-sensitive C-reactive protein (hs-CRP)] were included. Metabolic phenotype (metabolically healthy normal weight, metabolically unhealthy normal weight, metabolically healthy overweight/obese, and metabolically unhealthy overweight/obese) was classified using four definitions of metabolic dysfunction: (i) Wildman criteria, (ii) National Cholesterol Education Program Adult Treatment Panel III, (iii) HOMA-IR, and (iv) hs-CRP. Multivariable Cox proportional hazards regression, with death as a competing risk, was used to assess the association between metabolic phenotype and ORC risk. After a median (IQR) follow-up duration of 21 (IQR, 15-22) years, 2,367 women developed an ORC. The risk of any ORC was elevated among metabolically unhealthy normal weight (HR = 1.12, 95% CI, 0.90-1.39), metabolically healthy overweight/obese (HR = 1.15, 95% CI, 1.00-1.32), and metabolically unhealthy overweight/obese (HR = 1.35, 95% CI, 1.18-1.54) individuals compared with metabolically healthy normal weight individuals using Wildman criteria. The results were similar using Adult Treatment Panel III criteria, hs-CRP alone, or HOMA-IR alone to define metabolic phenotype. Individuals with overweight or obesity with or without metabolic dysfunction were at higher risk of ORCs compared with metabolically healthy normal weight individuals. The magnitude of risk was greater among those with metabolic dysfunction, although the CIs of each category overlapped. Prevention Relevance: Recognizing metabolic dysfunction as a significant risk factor for ORCs underscores the importance of preventive measures targeting metabolic health improvement across all BMI categories.

This cross-sectional study aims to assess the associations between serum leptin, adiponectin, leptin-to-adiponectin ratio (L/A ratio), and metabolic syndrome (MS) and HOMA-IR in five African-origin populations: Ghana, South Africa, Jamaica, Seychelles, and US.

Clinical measures included serum glucose, insulin, adipokines, blood pressure and anthropometric measures. MS was determined using the Harmonized criteria. The final sample included 2087 adults.

After adjusting for age, sex, and fat mass, L/A ratio, unlike HOMA-IR, was significantly associated with MS across all sites (p < 0.001). Within sites, L/A ratio was only associated with MS and HOMA-IR in the US (p < 0.001) and South Africa (p < 0.01), respectively. Leptin was associated with MS in South Africa only (p < 0.05) but was significantly associated with HOMA-IR across all five sites and within the US (p < 0.05). Similarly, adiponectin was associated with HOMA-IR in South Africa (p < 0.05) and with MS across all five sites (p < 0.001) and within each site separately, except Ghana.

Our study suggests that individuals of the African diaspora in different geographical locations may differ in the determinants of MS. Future studies should investigate the determinants for the disparate relationships between MS, IS and adipokines across different African-origin populations.

Cancer stands as a leading cause of mortality and poses an escalating threat to global health. Epigenetic dysregulation is pivotal in the onset and advancement of cancer. Recent research on RNA 5-methylcytosine (m5C) methylation has underscored its significant role in cancer. RNA m5C methylation is a key component in gene expression regulation and is intricately linked to cancer development, offering valuable insights for cancer diagnosis, treatment, and prognosis. This review provides an in-depth examination of the three types of regulators associated with RNA m5C methylation and their biological functions. It further investigates the expression and impact of RNA m5C methylation and its regulators in cancer, focusing on their mechanisms in cancer progression and clinical relevance. The current research on inhibitors targeting RNA m5C methylation-related regulators remains underdeveloped, necessitating further exploration and discovery.

Intermittent fasting (IF) has proven to be a feasible dietary intervention for the wider population. The recent increase in IF clinical trials highlights its potential effects on health, including changes in body composition, cardiometabolic status, and aging. Although IF may have clinical applications in different populations, studies suggest there may be sex-specific responses in parameters such as body composition or glucose and lipid metabolism. Here, the existing literature on IF clinical trials is summarized, the application of IF in both disease prevention and management is discussed, and potential disparities in response to this type of diet between men and women are assessed. Moreover, the potential mechanisms that may be contributing to the sexually dimorphic response, such as age, body composition, tissue distribution, or sex hormones are investigated. This review underscores the need to further study these sex-specific responses to IF to define the most effective time frames and length of fasting periods for men and women. Tailoring IF to specific populations with a personalized approach may help achieve its full potential as a lifestyle intervention with clinical benefits.

The metabolic syndrome is a complex condition influenced by many factors including lifestyle. Recently, more and more studies explored the relationships between combined lifestyle factors (often measured as lifestyle scores/indices) and metabolic syndrome due to the co-occurrence of these factors. These scores/indices considered potential interactions among lifestyle factors, offering a more comprehensive understanding of their relationship with metabolic syndrome. However, no review/meta-analysis has been conducted to summarize existing evidence. Thus, this study aimed to synthesize the associations between lifestyle scores/indices and metabolic syndrome in cross-sectional and cohort studies.

A literature search was performed in Embase and Medline. Multivariable-adjusted estimates were synthesized using random-effects models. In research where higher scores indicated better health, we used original estimates directly. In studies where higher scores denoted poorer health, we first calculated the coefficients and standard errors based on original estimates. Afterward, we reversed coefficients' directions and recalculated new estimates. Thus, the pooled estimates compared the healthiest with the least-healthy lifestyles (the highest vs. lowest scores/indices). Subgroup analyses were conducted based on study design, region, baseline time, baseline age, sex, health status, metabolic syndrome diagnosis, and lifestyles' number. Sensitivity analyses were performed by including only high-quality studies and employing leave-one-out analyses.

Nineteen studies from 16 publications were included. Physical activity, diet, and smoking were the top three included lifestyle factors. Compared to participants with the least-healthy lifestyles, those with the healthiest lifestyles had a 43% lower metabolic syndrome risk (95% confidence interval = 0.41-0.73). In subgroup analyses, healthy lifestyle scores/indices were inversely associated with both metabolic syndrome prevalence in cross-sectional studies (Odds ratio = 0.62; 95% confidence interval = 0.51-0.73) and metabolic syndrome incidence in cohort studies (Odds ratio = 0.40; 95% confidence interval = 0.11-0.68). The inverse association was consistent in other subgroup and sensitivity analyses.

Adherence to a healthy lifestyle pattern was beneficial to metabolic syndrome prevention.

The Metformin and Dietary Restriction to Prevent Age-Related Morbid Events in People With Metabolic Syndrome (MeMeMe) trial tested whether 1,700 mg/day metformin (MET) with or without a Mediterranean diet (MedDiet) intervention could reduce the cumulative incidence of major noncommunicable diseases in people with metabolic syndrome.

A total of 1,442 participants were randomly assigned to one of four interventions: 1) MET (1,700 mg/day) plus MedDiet intervention (MET+MedDiet); 2) placebo plus MedDiet intervention; 3) MET (1,700 mg/day) alone; and 4) placebo alone. Participants were followed up for 3 years on average. The primary outcome was the cumulative incidence of major noncommunicable diseases (including type 2 diabetes, cardiovascular diseases, and cancer). Secondary outcomes were the incidence of type 2 diabetes and the changing prevalence of metabolic syndrome.

The crude incidence of the major noncommunicable diseases was 6.7 cases per 100 person-years in the MET+MedDiet group, 6.9 in the MET alone group, 13.3 in the placebo plus MedDiet group, and 11.3 in the placebo group. The differences were fully explained by the reduction of type 2 diabetes, which was 80% and 92% lower in the MET and MET+MedDiet groups, respectively, compared with placebo.

The use of 1,700 mg/day MET is effective to prevent diabetes in people selected on the basis of metabolic syndrome.

Evidence supports the benefits of concurrent training (CT), which combines endurance and resistance exercises, for enhancing health and physical fitness. Recently, low-volume, time-efficient exercise approaches such as low-volume high-intensity interval training (LOW-HIIT), whole-body electromyostimulation (WB-EMS), and single-set resistance training (1-RT) have gained popularity for their feasibility and efficacy in improving various health outcomes. This study investigated the effects of low-volume CT, focusing on (1) whether exercise order affects cardiometabolic health, inflammation, and fitness adaptations and (2) which combination, LOW-HIIT plus WB-EMS or LOW-HIIT plus 1-RT, yields better results.

Ninety-three obese metabolic syndrome (MetS) patients undergoing caloric restriction were randomly assigned to four groups performing the different low-volume CT protocols over 12 weeks. Outcomes included cardiometabolic, inflammatory, and fitness parameters.

In both combinations, no significant differences were found regarding exercise order. However, the pooled LOW-HIIT and 1-RT group achieved superior improvements in blood pressure, blood lipids, inflammation markers (CRP, hsCRP), the MetS severity score, and overall fitness compared to the LOW-HIIT and WB-EMS combination. Compared to previous studies using these modalities individually, LOW-HIIT plus 1-RT appeared to further reduce inflammation, whereas LOW-HIIT combined with WB-EMS was less effective for cardiometabolic health, potentially due to interference effects between modalities.

While LOW-HIIT plus WB-EMS appears to be a viable option for individuals unable to perform traditional resistance training, the findings suggest prioritizing LOW-HIIT plus 1-RT to maximize health outcomes. These findings highlight the importance of tailored exercise prescriptions and the need for further research into optimizing CT protocols for diverse populations.

Background: Metabolic syndrome (MetS) is a syndrome that comprises central obesity, increased serum triglyceride (TG) levels, decreased serum HDL cholesterol (HDL) levels, raised blood pressure (BP), and impaired glucose regulation, including prediabetic and diabetic glycaemic levels. Recently, the association with endometrial cancer (EC) has been described but it is unclear if the risk associated with MetS is higher than the individual effect of obesity alone. This study investigates the association between MetS components and differing MetS definitions on EC risk and compares the risk of MetS with the risk posed by obesity alone. It also analyses how MetS affects the risk of EC development in the pre- and post-menopausal subgroups. Methods: A prospective cohort study was undertaken using data from the UK biobank. Multivariable Cox proportional risk models with the time to diagnosis (years) were used to estimate the hazard ratio (HR) and 95% confidence interval (CI) of MetS and its components on the risk of EC. A subgroup analysis was also undertaken for pre- and post-menopausal participants. Kaplan-Meier (KM) was undertaken to assess the difference in the risk of EC development in differing BMI classes, and in pre- and post-menopausal subgroups. Results: A total of 177,005 females from the UK biobank were included in this study. Of those participants who developed EC (n = 1454), waist circumference > 80 cm, BMI > 30 kg/m2, hypertension > 130/80 mmHg, hyperlipidaemia and diabetes (HbA1C > 48 mmol/L were significant predictors of EC development, with waist circumference being the strongest predictor (HR = 2.21; 95% CI: 1.98-2.47, p < 0.001). Comparing the pre- and post-menopausal subgroup, hypertriglyceridaemia and diabetes were the strongest predictors of EC in the pre-menopausal subgroup (HR = 1.53; 95% CI: 1.18-1.99 and HR = 1.51; 95% CI: 1.08-2.12, p < 0.05, respectively). Raised waist circumference was not a significant independent predictor in the pre-menopausal subgroup. A KM curve analysis showed a clear distinction between those with and without MetS in the pre-menopausal group, suggesting a benefit of testing for MetS components in pre-menopausal women with obesity. Conclusions: Components of MetS, both independently and in combination, significantly increase the risk of EC. Screening those with obesity for MetS in their pre-menopausal years may help to identify those at the highest risk.

This study examines remaining life expectancy (RLE) after a cancer diagnosis, focusing on age, sex, cancer type, and metabolic syndrome (MS) components, using data from the SIDIAP database in Catalonia (2006-2017). RLE was analyzed for 13 cancer types, stratified by sex and MS components. The cohort study includes 183,364 individuals followed from diagnosis until death, transfer, or study end (December 2017). RLE at age 68 (median diagnosis age) was calculated based on MS components (0, 1, 2, and ≥ 3). Men aged 68 with 0 MS components had an RLE of 13.2 years, compared to 8.9 years for those with ≥ 3 MS. Women had an RLE of 15.9 years with 0 MS components versus 11.4 years with ≥ 3 MS. RLE varied by cancer type, with the highest RLE in men seen in prostate cancer and in women in non-Hodgkin lymphoma. The lowest RLE for both sexes was in pancreatic cancer. The largest differences between 0 and ≥ 3 MS components were observed in non-Hodgkin lymphoma and the smallest in pancreatic cancer. Increased MS components were associated with reduced RLE in at least 8 cancer types for men and 9 for women. Prevention strategies targeting MS components could increase RLE in cancer patients.

Cancer is a fatal disease with a high global prevalence and is associated with an increased incidence of metabolic disorders. This study aimed to develop a novel metabolic prognostic system to evaluate the overall metabolic disorder burden in cancer patients and its relationship with their prognosis. The patients in this study were enrolled from the Investigation on Nutrition Status and Clinical Outcome of Common Cancers (INSCOC) project. The least absolute shrinkage and selection operator (LASSO) analysis was used to screen for indicators of metabolic disorders. Cox regression analysis was used to evaluate the independent association between indicators of metabolic disorders and mortality in patients. The Kaplan-Meier method was used to evaluate the survival of patients with varying burdens of metabolic disorders. Finally, nomogram prognostic models and corresponding calculators were constructed and evaluated using the areas under the receiver operating characteristic curves (AUC), decision curve analysis (DCA), and calibration curves. Five of the 19 hematological indexes, including hemoglobin, neutrophils, direct bilirubin, albumin, and globulin, were selected as the evaluation indicators of metabolic disorder burden and independent risk factors for prognosis in cancer patients. Patients with a higher metabolic disorder burden had poorer survival rates. The AUC of the 1-year, 3-year, and 5-year overall survival of the prognostic nomogram was 0.678, 0.664, and 0.650, respectively. DCA and calibration curves indicated that the clinical benefit rate of metabolic disorder burden prognostic markers was high. Patients with a higher metabolic disorder burden had poorer survival rates. The nomogram and corresponding calculator can accurately evaluate the metabolic disorder burden and predict the prognosis of patients with cancer.