This study investigates the significant disparities between urban and rural areas in China, particularly in terms of health status, which are driven by economic inequality and the uneven distribution of healthcare resources. Chronic diseases are a major threat to the health of Chinese residents, and this study explores how these diseases contribute to the disparity in self-rated health between urban and rural populations. Using data from the 2021 Chinese General Social Survey, various data analysis methods, including descriptive, regression, and decomposition analyses, were employed. The results reveal substantial disparities in self-rated health between urban and rural residents, with chronic diseases playing a significant role in explaining these disparities. Approximately 39% of the urban-rural disparity in self-rated health can be explained by differences in chronic disease prevalence, with additional factors such as age, socio-economic status, social participation, and sleep quality also contributing. This study identified the correlation between chronic diseases and the disparity in self-rated health, and limitations may arise from the use of self-reported health and the complexity of urban-rural health disparities. The findings suggest that the urban-rural disparity in chronic diseases is the primary driver of the health disparity, and that policymakers should focus on improving health education, promoting chronic disease prevention and management, and emphasizing preventive healthcare in rural areas.

We aimed to examine the effect of continuous positive airway pressure on sleep quality and alcohol metabolism after alcohol consumption. Men (n = 53) aged ≥ 19 years with sleep disorders who regularly consumed an average of ≥ 1.0 g of alcohol/kg of bodyweight, were free of serious diseases (including liver disorders), and underwent polysomnography and continuous positive airway pressure titration between January 2016 and July 2021 were included. Participants drank a high dose of a traditional Korean liquor at a rate of 1.0 g/kg of bodyweight for 1 h. The main outcome measures included polysomnography results and blood and breath ethanol and acetaldehyde concentrations after alcohol consumption before and after sleep. Statistical analyses were performed using R software, version 4.0.5 (R Foundation, Vienna, Austria). Continuous positive airway pressure enhanced sleep quality after alcohol consumption, with oxygen significantly improving the metabolism of acetaldehyde over that of ethanol. Breath and blood sample analyses and polysomnography results revealed that continuous positive airway pressure improved sleep quality by reducing apnea-hypopnea index by 27.32 ± 24.87 (p < 0.001), increasing rapid eye movement sleep by 2.08 ± 6.74% (p < 0.05), and enhancing acetaldehyde breakdown by 21.2% (p < 0.001), while its effect on ethanol breakdown (4-5%) was not statistically significant. Continuous positive airway pressure is recommended after alcohol consumption for individuals with sleep apnea to enhance sleep quality.

Although macrophages and lipid metabolism significantly influence the progression of various cancers, their precise roles in pancreatic cancer (PC) remain unclear. This study focuses on identifying and validating biomarkers associated with macrophage-related genes (MRGs) and lipid metabolism-related genes (LMRGs), providing new targets and strategies for therapeutic intervention. This research utilized datasets from TCGA-PAAD, GSE62452, and GSE57495. Candidate genes were identified by overlapping differentially expressed genes with MRGs from WGCNA and LMRGs. Regression analyses were performed to pinpoint potential biomarkers and construct a risk model, which underwent evaluation. A nomogram was subsequently developed and validated. Additional analyses, including functional enrichment, somatic mutation profiling, immune landscape assessment, and RT-qPCR, were performed to investigate the underlying biological mechanisms in PC. The study identified ADH1A, ACACB, CD36, CERS4, PDE3B, ALOX5, and CRAT as biomarkers for PC. RT-qPCR results revealed reduced expression of ADH1A, ACACB, CD36, CERS4, PDE3B, and CRAT in tumor samples compared to adjacent tissues, whereas ALOX5 expression was significantly elevated in tumor samples. A risk model utilizing these biomarkers classified PC patients into high- and low-risk cohorts, with high-risk patients showing lower survival probabilities. Subsequently, risk score and N stage were identified as independent prognostic factors, leading to the development of a nomogram. Notably, both risk cohorts showed significant enrichment in the "cell cycle" pathway. Furthermore, TP53 mutations were prevalent in both high-risk (76%) and low-risk (50%) cohorts. Correlation analysis indicated that PVRL2 (an immunosuppressive factor), CD276 (an immunoactivator), and CCL20 (a chemotactic factor) had the highest positive correlation with the risk score. In this study, ADH1A, ACACB, CD36, CERS4, PDE3B, ALOX5, and CRAT were identified as biomarkers for PC, with their expression levels validated in clinical samples. These findings offered a potential theoretical foundation for developing targeted treatments for PC.

Alcohol-related liver disease (ALD) is a known contributor to non-hepatic cancers (NHC). We aimed to describe the incidence and predictors of NHC in patients with ALD.

The WALDO study is a multicenter cohort study of patients with histologically characterized ALD. Participants are followed from the time of liver biopsy and outcomes are captured from health records. The primary outcome was the incidence of the first NHC. Risk factors for NHC were presented as unadjusted and adjusted sub-distribution hazards (SDH) based on competing risk analysis. Statistical analyses were done in R.

691 patients were included. The median age was 51 years (IQR 43- 59), 427 (62 %) patients were male and 406 (59 %) had cirrhosis on biopsy. During a median follow-up of 4.7 years (IQR 1.2-9.5 years), 76 patients (11 %) with ALD developed NHC. The cumulative incidence of NHC in ALD was 2.4 % (1.4-3.9 %) over five years. The most common NHC was respiratory (18 cases, 23 % of NHC) followed by digestive tract (17 cases, 22 %) and cancers of the head and neck (13 cases, 17 %). On multivariable analysis, increasing age (SDH 1.04; CI 1.01-1.06; p = 0.011), previous smoking (SDH 3.65, CI 1.44-9.65; p = 0.006) and current smoking (SDH 3.14; CI 1.27-7.74; p = 0.013) were associated with a higher risk of NHC.

NHC is common and frequently fatal. However, NHC is an infrequent cause of morbidity or mortality in ALD compared to liver-related outcomes.

The incidence of lung adenocarcinoma (LAD) is increasing worldwide. Single-nucleotide polymorphisms in aldehyde dehydrogenase 2 family member gene ( ALDH2 ) rs671 and alcohol dehydrogenase 1B ( ADH1B ) rs1229984 are common and functionally important genetic variants to metabolize endogenous and exogenous aldehyde chemicals, related to cancer.

This is a case-control study. A total of 150 newly diagnosed LAD patients were from Kaohsiung Medical University Hospital, Taiwan, between 2019 and 2022. Two control groups, TWB-1 ( n  = 600) and TWB-2 ( n  = 29 683), were selected from Taiwan Biobank (TWB), and the case patients were frequency-matched with TWB-1 based on age category (30-60 or >60 years old), sex, and education levels. Logistic regression models were employed to analyze the association between two genetic variants and LAD risk.

A significant association was noted between ALDH2 and LAD risk. Those with ALDH2 rs671 *2/*2 in TWB-1 and TWB-2 controls had a 2.68-fold (95% CI = 1.43-4.99) and a 1.83-fold (95% CI = 1.07-3.11) increased risk of LAD, respectively, compared with those with ALDH2 rs671 *1/*1 or *1/*2 , after adjusting for covariates. This association was particularly pronounced in females. No overall significant association between ADH1B rs1229984 and LAD risk was observed.

The findings indicate a strong and robust risk association between ALDH2 rs671*2/*2 and LAD in the Taiwan population, particularly in Taiwanese female adults.

This study aims to establish a Bayesian network risk prediction model for gastric cancer using data mining methods. It explores both direct and indirect factors influencing the incidence of gastric cancer and reveals the interrelationships among these factors.

Data were collected from early cancer screenings conducted at the People's Hospital of Lincang between 2022 and 2023. Initial variable selection was performed using Least Absolute Shrinkage and Selection Operator (Lasso) and Sliding Windows Sequential Forward Selection (SWSFS), and the screened variables and demographic characteristics features were used as variables for constructing the Bayesian network (BN) model. Subsequently, the performance of the models was evaluated, and the optimal model was selected for network mapping and Bayesian inference using the best model.

The incidence rate of gastric cancer in this region's high-risk population was determined to be 7.09%. The BN model constructed from the set of variables consisting of Lasso's selection variables and demographic characteristics had better performance. A total of 12 variables were incorporated into the BN model to form a network structure consisting of 13 nodes and 18 edges. The model shows that age, gender, ethnicity, current address, upper gastrointestinal symptoms (nausea, acid reflux, vomiting), alcohol consumption, smoking, SGIM gastritis, and family history are important risk factors for gastric cancer development.

The Bayesian network model provides an intuitive framework for understanding the direct and indirect factors contributing to the early onset of gastric cancer, elucidating the interrelationships among these factors. Furthermore, the model demonstrates satisfactory predictive performance, which may facilitate the early detection of gastric cancer and enhance the levels of early diagnosis and treatment among high-risk populations.

Cancer-related fatigue is a common and distressing symptom experienced by cancer patients, which may persist from the time of diagnosis to the end of life. This fatigue negatively affects patients' physical, emotional, and cognitive well-being. Nutrition plays a key role in managing cancer-related fatigue, and recently, the Mediterranean diet has gained attention as a potential intervention. The present study uses data from the National Health and Nutrition Examination Survey (NHANES) to investigate the association between cancer-related fatigue and the Mediterranean diet.

Data from the NHANES 2017-2020.03 cycle were selected for this cross-sectional study. The Alternative Mediterranean Diet Adherence (AMED) score was used to evaluate the participants' adherence to the Mediterranean diet. AMED scores were calculated based on data from 24-h dietary recall interviews conducted on both day one and day two. Multiple linear regression modeling was used to explore the association between AMED scores and cancer-related fatigue, as well as the relationship between AMED scores and fatigue in the general population.

A total of 6,413 adults aged 20 years and older were included in the study, with 707 identified as cancer patients. There was a noteworthy inverse relationship found between AMED scores and fatigue, which was more pronounced in cancer patients: β = -0.121, 95% CI: -0.172, -0.071 (p < 0.001) in the unadjusted model. This correlation remained significant after adjusting for all variables in model 3: β = -0.074, 95% CI: -0.127, -0.021 (p = 0.007). A significant dose-dependent relationship was found when AMED scores were expressed in quartiles, with a more pronounced negative association as AMED increased across all models (p for trend <0.05). In the cancer population, the analysis of individual nutrients and fatigue revealed that alcohol was significantly negatively associated with cancer-related fatigue in all models, particularly in the unadjusted model: β = -0.710, 95% CI: -1.058, -0.362 (p < 0.001). Subgroup analyses indicated that diabetes, education level and type of cancer had a significant effect on the relationship between AMED and fatigue, with interaction p-values of 0.010, 0.023 and 0.049, respectively.

The present study suggests that higher adherence to the Mediterranean diet may contribute to reduce fatigue, especially in cancer patients; however, further research is necessary to validate this correlation.

Cancer and cardiovascular disease remain the leading causes of morbidity and mortality worldwide, and the two separate disease entities share several similarities and possible interactions. Patients with cancer may have underlying cardiovascular disease, which is often exacerbated by the stress of tumor growth or treatment. At the same time, cardiotoxicity induced by anti-cancer therapies or the malignant process itself can lead to new cardiovascular diseases. Efforts have been made to find a rational explanation for this phenomenon. As a classical tumor-promoting factor, we notice that SNAI2 simultaneously plays an important pathogenic role in cardiovascular diseases. Moreover, there are several striking parallels in the mechanisms of cancer and CVD, such as shared risk factors (e.g., smoking and diabetes), cellular phenotypic switching, and metabolic remodeling, all of which are mediated by SNAI2. This review aims to summarize SNAI2's role in the core mechanisms linking cancer and CVD, as well as explore therapeutic approaches targeting SNAI2 and also seeks to provide insights into the common mechanisms underlying both cancer and CVD.

Laryngeal cancer (LC), as a common head and neck tumor, significantly impacts the quality of life. Utilizing data from the 2021 Global Burden of Disease (GBD) study, we sought to delve deeply into the global LC burden experienced by individuals aged 55 and older from 1990 to 2021 at the global, regional, and national levels. This research encompassed three key indicators: incidence rate, mortality, and disability-adjusted life years (DALYs).

Based on the GBD 2021 database, we selected data from 204 countries and regions covering the period from 1990 to 2021 for individuals aged 55 and above. We analyzed LC's performance in terms of incidence, mortality, and DALYs, calculating the age-standardized rates and the mean average annual percent change (AAPC) at global, regional, and national levels. In our analysis of global trends, we carefully considered multiple variables including age, sex, and the socio-demographic index (SDI). Furthermore, we assessed potential risk factors for LC-associated DALYs and made prospective predictions for the possible scenario by 2035.

Globally, the age-standardized DALY rate of LC among adults aged 55 years and older has undergone significant changes. Specifically, this rate dropped sharply from 245.89 cases per 100,000 people in 1990 to 153.76 cases per 100,000 people in 2021, with an AAPC showing a decreasing trend of -2.916. Simultaneously, the age-standardized incidence rate and mortality rate also exhibited a similar downward trend. From a regional perspective, South Asia ranked highest in relevant indicators in 2021, reporting a death toll of 29,258.96, confirmed cases of 34,234.23, and DALYs related to LC reaching 709,622.00. In contrast, the figures in Oceania were the lowest, with only 26.23 deaths, 29.53 incident cases, and 609.09 DALYs. When divided according to the quintiles of the SDI, in 2021, the medium-high SDI led in incidence rates, while the low SDI ranked last. However, in terms of mortality and DALY rates, medium-low SDI topped the list, with high SDI being the lowest. In terms of gender differences, in 2021, the age-standardized DALY rate of LC in males was approximately 7.13 times that of females, with the former reaching 282.12 cases per 100,000 people and the latter only 39.59 cases per 100,000 people. Among all age groups, a notable decrease was observed in the age-specific incidence rate and DALY for adults aged 60-64 years, with AAPC values of -0.123 (95% CI: -0.130 to -0.116) and - 3.553 (95% CI: -3.620 to -3.486), respectively. Similarly, the mortality rate for adults aged 65-69 years also showed a significant decline, with an AAPC of -0.123 (95% CI: -0.127 to -0.118). Additionally, tobacco has been revealed as the most important risk factor affecting the mortality and DALY of LC in adults aged 55 years and older. Looking ahead, it is predicted that by 2035, the incidence rate, mortality rate, and DALY rate of LC among people over 55 years old will continue to decline.

Despite the current data and future predictions indicating a decline in the global age-standardized incidence rate, the absolute number of estimates continues to increase. Therefore, we advocate that cancer prevention strategies should place greater emphasis on vigorously addressing modifiable risk factors, particularly for the male population, which requires special attention and scientific intervention.

Alcohol is generally believed to be metabolized in the liver by alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), and to a much lesser extent cytochrome P450 2E1 (CYP2E1) and other enzymes. Recent studies suggest that gut also play important roles in the promotion of alcohol metabolism. ADH, ALDH, and CYP2E1 have several polymorphisms that markedly impact alcohol metabolism. These alcohol-metabolizing enzymes not only affect alcohol-associated liver disease (ALD), but may also modulate the pathogenesis of other liver diseases and cancer in the absence of alcohol consumption. In this review, we discuss alcohol metabolism and the roles of alcohol-metabolizing enzymes in the pathogenesis of ALD, metabolic dysfunction-associated steatotic liver disease, metabolic dysfunction and alcohol-associated liver disease, viral hepatitis, and liver cancer. We also discuss how alcohol-metabolizing enzymes may affect endogenous ethanol production, and how ethanol metabolism in the gut affects liver disease and cancer. Directions for future research on the roles of alcohol-metabolizing enzymes in liver disease and cancer are also elaborated.

To identify risk factors for Lymph Node Metastasis (LNM) in pT3-4 Laryngeal Squamous Cell Carcinoma (LSCC) patients with negative margins, and develop a nomogram to predict LNM risk.

872 patients were divided into training (2010-2014) and validation (2015-2016) cohorts. Univariate and multivariate analyses identified LNM risk factors. A nomogram incorporating significant factors was developed in the training cohort.

Smoking history, maximal tumor diameter ≥3.0 cm, depth of tumor invasion >1.0 cm, and supraglottic tumor location were significantly associated with LNM on multivariate analysis. A predictive nomogram incorporating these factors showed good discrimination (C-index > 0.7) in both cohorts. Patients were stratified into low, moderate and high-risk subgroups based on total risk scores.

A LNM risk prediction model and risk grouping system was established, which may aid treatment selection for pT3-4 LSCC patients. The model and algorithm could help optimize neck management for this high-risk patient population.

This study aimed to examine the correlation between smoking, alcohol drinking, and the prognosis of Nasopharyngeal Carcinoma (NPC).

Clinical data from 721 NPC cases treated at our hospital between January 2005 and December 2010 were collected. Information on smoking and drinking, including duration, daily quantity, and cumulative amount, was recorded and graded according to WHO standards. Statistical analysis was performed to assess the influence of smoking and alcohol drinking on NPC patient prognosis. After controlling for confounding factors, survival analysis compared the 5-year Progression-Free Survival rate (PFS) and Overall Survival rate (OS) among patients with varying degrees of smoking and drinking. The association between smoking, drinking, cumulative amount, and NPC patient prognosis was evaluated. Multivariate Cox regression analysis was then employed, considering patient demographic characteristics and clinical features, to comprehensively analyze prognostic influencing factors in NPC patients. Additionally, the multivariate Cox regression analysis was utilized to comprehensively examine the influencing factors of prognosis, taking into account the patients' basic demographic characteristics and clinical features. The findings revealed significant differences in the aforementioned rates.

(1) Analysis of PFS and OS differences in NPC patients considered smoking status, smoking duration, daily smoking quantity, and cumulative smoking amount. No significant influence of smoking on NPC patient PFS and OS within 5-years was observed (p > 0.05). (2) Non-drinkers with NPC exhibited higher 5-year PFS and OS rates compared to drinkers (p = 0.047, p = 0.026). Furthermore, non-drinkers and those with a drinking duration of less than 120 months or between 120-240 months showed higher 5-year PFS and OS rates than individuals with a drinking duration exceeding 240 months (p < 0.05). Similarly, non-drinkers and individuals consuming less than 50 g/day had higher 5-year PFS and OS rates compared to those consuming 50-100 g/day or more than 100 g/day (p < 0.05). Additionally, the 5-year PFS and OS rates were higher in the non-drinking and light drinking groups compared to the moderate and heavy drinking groups (p < 0.05). (3) A partial synergistic effect between smoking and alcohol drinking was observed in NPC. (4) Alcohol drinking emerged as an independent prognostic factor for NPC.

Alcohol drinking is a significant factor influencing the prognosis of nasopharyngeal carcinoma, with the adverse effects further amplified when combined with smoking.

Level 2.

This study aimed to explore the disparities in PD-1 and PD-L1 expression among oral squamous cell carcinomas (OSCCs) in individuals categorized as never-smokers/never-drinkers versus smokers/drinkers.

Immunohistochemical staining for PD-1 and PD-L1, along with PDCD1LG2/cen9 dual color probe analysis, was conducted on 130 OSCC specimens from both smoker/drinker and never-smoker/never-drinker cohorts. Associations between smoking/drinking status, clinicopathologic data, immunohistochemical antibody expression, fluorescence in situ hybridization, and survival outcomes were assessed.

OSCC in never-smokers/never-drinkers exhibited significantly elevated PD-1 expression (p = 0.003), increased PD-L1-TPS expression (p = 0.044), and elevated PD-L1-CPS expression (p < 0.001). High PD-L1-ICS expression was more prevalent in never-smokers (p = 0.042). Moreover, never-smokers and never-drinkers demonstrated augmented PD-L1 gene copy numbers (p = 0.081 and p = 0.054, respectively). Increased PD-L1 gene copy number, particularly amplification, correlated with PD-L1-TPS (p = 0.039 and p < 0.001). Conversely, PD-L1 gene copy loss was associated with negative PD-L1-CPS (p = 0.023). Notably, positive PD-L1-CPS was significantly linked with improved overall survival (p = 0.023).

OSCC arising in never-smokers/never-drinkers exhibit heightened PD-1/PD-L1 signaling, suggesting potential efficacy of immune checkpoint therapy in this subgroup of tumors.

Ireland has regulated for all packaged alcohol products to include a health warning that states that 'there is a link between alcohol and fatal cancers'. This warning is being opposed in the World Trade Organization by 12 member states who are raising that the warning is an unnecessary barrier to trade. The World Health Organization is supporting Ireland. Countries should not oppose Ireland's warning which is defensible from legal and public health perspectives.

While alcoholic beverage consumption increases cancer risk, red wine has been touted as a healthier option. To address this unexplored question, we conducted a meta-analysis to summarize evidence from observational studies.

A literature search of PubMed and EMBASE through December 2023 identified studies examining wine and cancer risk. A random-effects meta-analysis was performed to estimate relative risks (RRs) and 95% confidence intervals (CIs) for an association between wine intake and overall cancer risk.

A total of 20 cohort and 22 case-control studies were included. Wine intake was not associated with overall cancer risk (n = 95,923) when comparing the highest vs. lowest levels of consumption, with no differences observed by wine type (red: summary RR = 0.98 [95% CI = 0.87, 1.10], white: 1.00 [0.91, 1.10]; Pdifference = 0.74). However, white wine intake was significantly associated with an increased risk of cancer among women (white: 1.26 [1.05, 1.52], red: 0.91 [95% CI: 0.72, 1.16], Pdifference = 0.03) and in analyses restricted to cohort studies (white: 1.12 [1.03, 1.22], red: 1.02 [95% CI: 0.96, 1.09], Pdifference = 0.02). For individual cancer sites, there was a significant difference in associations between red and white wine intake only in skin cancer risk [6 studies, white: 1.22 (1.14, 1.30), red: 1.02 (0.95, 1.09); Pdifference = 0.0003].

We found no differences in the association between red or white wine consumption and overall cancer risk, challenging the common belief that red wine is healthier than white wine. Our significant results related to white wine intake in subgroup analyses warrant further investigation.

Obesity and alcohol consumption are established risk factors for colorectal cancer (CRC). Recently, a multisociety consensus group has introduced a new classification for steatotic liver disease (SLD), which encompasses metabolic dysfunction-associated steatotic liver disease (MASLD), MASLD and increased alcohol intake (MetALD), and alcohol-associated liver disease (ALD). However, the risk of developing CRC in each of these SLD subgroups is unknown. This nationwide cohort study investigated the risk of CRC in MASLD, MetALD, and ALD patients. The primary endpoint was the occurrence of CRC in each SLD subgroup.

We conducted a nationwide, population-based study that included 1,497,813 patients diagnosed with MASLD, MetALD, or ALD, alongside 4,885,536 individuals with no known liver disease as a comparison group. The primary outcome was the incidence of CRC and the risk of CRC was compared between MASLD, MetALD and ALD.

The 5- and 10-year cumulative CRC incidence rates were 0.22% and 0.48% for MASLD, 0.32% and 0.73% for MetALD, and 0.43% and 0.97% for ALD, and 0.15% and 0.31% for the comparison group, respectively. The cumulative incidence of CRC was highest for ALD and significantly greater than that for MetALD, MASLD, and the comparison group (both P < .001). Using the comparison group as the reference and adjusting for age, sex, smoking habit, number of colorectal examinations, diabetes mellitus, dyslipidemia, hypertension, and medication use, the adjusted hazard ratios for CRC were 1.73 (95% CI, 1.59-1.87) for ALD, 1.36 (95% CI, 1.28-1.45) for MetALD, and 1.28 (95% CI, 1.22-1.35) for MASLD.

The risk of CRC differs significantly among patients with SLD, with the highest incidence observed in those with ALD, followed by MetALD and MASLD.

Contamination of Cartagena Bay, Colombia with heavy metals such as mercury (Hg) and cadmium (Cd) presents a major environmental and public health concern, particularly for human communities residing on nearby islands and coastal areas. These populations face enhanced exposure risks owing to their traditional fishing practices and continuous interactions with polluted marine environments. This study aimed to evaluate the genotoxic effects of environmental exposure to Hg and Cd in populations from the island zone of the Cartagena district, Bolívar.

Ninety-four individuals from the four island communities (study group) and 30 individuals from the urban area of Cartagena (control group) participated in this study. The blood samples were collected to measure total mercury (T-Hg) and Cd concentrations, and a Buccal Micronucleus Cytome (BMCyt) assay was used to evaluate exposure effects.

Cadmiun levels in the blood of the study group were within the normal range and comparable to those of the control group (p > 0.05). However, the study group exhibited significantly higher T-Hg levels (7.34 μg/L) compared to the control group (2.01 μg/L), surpassing the accepted limit. Moreover, the study group showed a higher incidence of DNA damage and cell death biomarkers (p < 0.05). Additionally, significant correlations were observed between total blood Hg levels and the frequencies of micronuclei, karyorrhexis, and karyolysis.

These results suggest that island populations of Cartagena are exposed to high levels of Hg and exhibit genotoxic damage, indicating a problem that must be addressed.

Head and neck squamous cell carcinoma (HNSCC), one of the most common types of cancers occurring in the head and neck region, is often associated with high mortality rates due to its invasiveness and morbidity. The mainstream treatment methods in clinical settings, including surgery, chemotherapy, and radiotherapy, may cause poor overall survival rate and prognosis, with issues such as drug resistance, damage to adjacent healthy tissues, and potential recurrences. Other treatment approaches such as immunotherapy, photodynamic therapy (PDT), and photothermal therapy (PPT) also suffer from inefficient tumor targeting and suboptimal therapeutic outcomes. Early detection is vital for HNSCC patients, but it is always limited by insensitivity and confusing clinical manifestations. Hence, it is highly desirable to develop optimized therapeutic and diagnostic strategies. With the boom in nanomaterials, nanotechnology-conducted HNSCC therapy has attracted widespread attention. Nanoparticles (NPs) are distinguished by their unique morphology and superior physicochemical property, and some can exhibit direct antitumor activity, while others serve as promising candidates for drug delivery. In addition, NPs offer the potential for structural modification for drug delivery and tumor targeting, enabling specific delivery to tumor cells through conjugation with biomarker ligands and improving cargo biocompatibility. This work reviews current therapies and diagnosis methods for HNSCC, highlights the characteristics of the major NPs, surveys their uses and advantages in the treatment of HNSCC, and discusses the obstacles and prospects in clinical applications, aiming to enlighten future research directions for nanotechnology-based therapy for HNSCC.

Access to dental care may affect diagnosis of oral squamous cell carcinoma (OSCC). We tested whether the incidence rate of OSCC is higher in regions with less dental care access in the city of Chicago and state of Illinois.

Ecological cohort.

Population, outpatients, and inpatients.

We extracted 5-year averages of the state-wide county-level and city-level OSCC incidence rates from 2015 to 2019 from the Illinois Department of Public Health. Dental care access information was also collected for each county for the same period, as well as the percentage of people that had ≥1 visit to a dentist in the previous year in Chicago. Multivariate Poisson regression was used to investigate the relationship between county-level access to dental care (and city-level dentist visits) and OSCC incidence rate, controlling for confounders, with additional flexible semiparametric models for confirmatory sensitivity analysis.

In Illinois, higher 5-year incidence rate of OSCC was significantly associated with low access to dental care by county (IRR = 0.96, 95% CI 0.91, 0.98). Southern/southwestern counties had higher incidence rates of OSCC (15.5%-28.4%) and the lowest rates of dental care access (47.5%-69.2%) compared to northern counties (10.3%-15% and 55.4%-80.6%, respectively). In Chicago, people with more dentist visits had a reduced chance of being diagnosed with OSCC (IRR = 0.97, 95% CI 0.91, 0.99), consistent with state-wide analyses.

OSCC incidence rate is closely associated with poor local dental healthcare access in a major state and urban city. Increasing dental access could improve cancer outcomes via improved oral health and earlier detection.

High-risk strains of HPV are known to cause cervical cancer. Multiple clinical studies have emphasized that smoking and drinking are critical risk factors for cervical cancer and its high-grade precursors. In this study, we investigated if smoking and/or drinking augment the molecular mechanisms of cervical carcinogenesis and defined a potential therapeutic approach for their attenuation.

The impact of benzo[a]pyrene (B[a]P) and/or ethanol (EtOH) exposure on cervical cancer cells was assessed by measuring changes in their cell migration and invasion characteristics. Expression of HPV16 E6/E7, NF-κB, cytokines, and inflammation mediators was determined using qRT-PCR, immunoblotting, ELISA, luciferase reporter assay, and confocal microscopy. Herein, we used curcumin (Cur), and PLGA nanoparticle formulation of curcumin (PLGA-Cur) and determined effectiveness of free Cur and PLGA-Cur formulation on smoking and drinking activated NF-κB/IL-6 mediated inflammatory signaling pathways using in vitro cervical cancer models.

Treatments with B[a]P and/or EtOH altered the expression of HPV16 E6/E7 oncogenes and EMT markers in cervical cancer cells; it also enhanced migration and invasion. In addition, B[a]P and/or EtOH exposure promoted inflammation pathways through TNF-α and NF-κB signaling, leading to IL-6 upregulation and activation of VEGF. The molecular effects caused by B[a]P and/or EtOH exposure were effectively attenuated by curcumin (Cur)/PLGA-Cur treatment.

These data suggest a molecular link between smoking, drinking, and HPV infectivity in cervical carcinogenesis. In addition, attenuation of these effects by treatment with Cur/PLGA-Cur treatment, implies the role of curcumin in cervical cancer prevention and treatment.

Air pollution-related neoplasms are a major global public health issue and are one of the leading causes of death worldwide. Air pollution is one of the important risk factors of air pollution-related neoplasms and is associated with a variety of air pollution-related neoplasms.The primary objective of this study was to estimate the epidemiological patterns of death rates and disability-adjusted life years (DALYs) associated with air pollution-related neoplasms on a global scale, covering the period from 1990 to 2019. Furthermore, we aimed to predict the trends in these epidemiological patterns up to 2050. By achieving these goals, our study seeks to provide a comprehensive understanding of the potential causes underlying the observed disparities in neoplasm-related health outcomes, ultimately contributing to the development of effective strategies for addressing this major public health issue.

Based on data from the 2019 Global Burden of Disease (GBD) study, the indicators of the air pollution-related neoplasms disease burden was the numbers and age-standardized rates (ASR) of deaths and disability-adjusted life years (DALYs) from 1990 to 2019. First, we compared the burden of air pollution-related neoplasms and temporal trends by gender, age, socio-demographic index (SDI), region, and country. Furthermore, driving factors and improvement potential were evaluated using decomposition and frontier analysis. Finally, forecasting analyses of the changing trend in the burden of air pollution-related neoplasm up to 2050 was conducted based on time series forecasting models.

In 2019, air pollution-related neoplasms accounted for 387.45 million (95 % UI 288.04-490.06 million) deaths and 8951.97 million (95 % UI 6680.89-11342.60 million) DALYs globally. Deaths and DALYs demonstrated an upward trend from 1990 to 2019, while their ASR showed a downward trend. The disease burden and the decline degree of males were both significantly higher than that of females, and the high burden was mainly in the elderly groups. The middle SDI region possessed the highest burden with the most significant upward trend, while the high SDI region had the lowest burden with the most significant downward trend. Decomposition analyses represented that the increase in the overall deaths and DALYs of air pollution-related neoplasms was mainly driven by population growth. The predictive analyses expected that the deaths and DALYs of air pollution-related neoplasms will continue to rise, while their corresponding ASR will decrease by 2050.

The global burden of air pollution-related neoplasms remained high, and deaths and DALYs will be on upward trends up to 2050, with differences among genders, ages, SDI levels, GBD regions, and countries. It is essential to understand the air pollution-related neoplasm burden and contributing epidemiological factors for implementing effective and factor-tailored interventions to reduce the global burden.

Evidence of an association between trigeminal neuralgia (TN) and subsequent cancer risk remains sparse. The present study aimed to examine the association between TN and cancer risk in the Danish population.

A nationwide population-based cohort study using hospital diagnoses collected routinely and prospectively from Danish population-based registries in 1994-2022.

We identified 7846 individuals with a first-time diagnosis of TN. Within one year of diagnosis, we observed 193 cancer cases (standardized incidence rate (SIR) = 2.45, 95% confidence interval (CI) = 2.11-2.82). Absolute risk (AR) for all cancers within one year of TN diagnosis was 2.5% (95% CI = 2.2-2.9). Cancers of the head, neck and nervous system were most strongly associated with TN (AR 0.9% (95% CI = 0.7-1.1); SIR = 13.5 (95% CI = 10.5-17.0)) and the risk was persistently elevated one year after TN diagnosis. We observed 827 cancer diagnoses beyond one year after TN diagnosis, where smoking related cancers were associated with elevated cancer risk (SIR 1.13 = (95% CI = 0.98-1.29)).

TN was associated with an elevated risk of cancers of the head, neck and nervous system including site-specific cancers in the area. Our results suggest the potential importance of smoking related tumors in TN, either as a symptom, cause or shared risk factor.

While the number of publications on wine and health is steadily increasing, ranging from a molecular level to epidemiological studies, often with contradictory results, little attention has been given to a holistic approach to research, starting from the molecular level to arrive at pharmacological and medical conclusions. In this review, some unusual concepts are considered, such as the phytocomplex, the vehicle, and the Matrix effect. The concept of the phytocomplex is discussed, specifically the biological activities of Tyrosol, Hydroxytyrosol, and Resveratrol; indeed, the interactions among different molecules in herbal matrices provide a specific response. This is often markedly different from the response evoked by single constituents in the modulation of microbial populations in the gut, in intestinal stability and bioaccessibility, and, obviously, in inducing biological responses. Among the many alcoholic beverages which contain these molecules, wine has the most peculiar Matrix effect, which can heavily influence the bioavailability of the phytocomplex obtained by the fermentation processes that produce this beverage. Wine's Matrix effect plays an instrumental role in improving the beneficial compounds' bioavailability and/or in inhibiting alcohol metabolites' carcinogenicity. Underestimation of the wine Matrix effect could lead to deceiving results, as in the case of dealcoholized wine or wine-compound-based nutritional supplements; alternatively, this can occur in the emphasis of a single component's toxic activity, in this case, alcohol, ignoring the specific molecular-level protective action of other compounds (polyphenols) that are present in the same matrix. The dark side of the Matrix effect is also discussed. This review confirms the research recommendations made by the WHO Scientific Group, which suggests it is important "to investigate the possible protective effects of ingredients other than alcohol in alcoholic beverages", considering that most recent studies seem not only relevant but also capable of directing future research towards innovative points of view that have so far been too neglected.

This paper outlines the engagement process that was used to develop the Northwest Territories Alcohol Strategy, based on a recommendation by the developers of the Canadian Alcohol Policy Evaluation report, and how this informed the final actions in the strategy.

A literature review, four targeted engagement activities, and iterative validation by advisory groups and community and Indigenous leadership were used to evaluate, modify, or reject the original recommendations and develop the final actions that were included in the NWT Alcohol Strategy.

There are fourteen original CAPE recommendations, four of which had already been implemented in the Northwest Territories before the development of the strategy. On completion of the process, four recommendations had already been implemented in the NWT. Two recommendations were included in the strategy without changes, two were adapted for use in the strategy, and six were not included. One stand-alone alcohol policy measure was created and included.

Alcohol strategies are dependent on a variety of contextual factors. Developers need to take into consideration the unique geography, political climate, and cultural context of the region for which they are being developed, in order to produce a strategy that is applicable, acceptable, and feasible at the community level.

Cancer is a leading cause of death in the Americas. Colorectal cancer is the third most common cancer, while stomach cancer is the sixth most common cancer worldwide. Tobacco and alcohol consumption, unhealthy diet, physical inactivity and air pollution are risk factors for these cancers. This study aimed to identify the association between dietary patterns and gastric and colorectal cancer.

A multi-cluster ecological study, using as secondary sources two national databases, the HIGIA (High-Cost Account) and the ENSIN 2015 (National Survey of Nutritional Status of Colombia 2015), was carried out. The population consisted of 2585 people over 50 years of age, distributed in six regions of Colombia: Atlántica, Central, Oriental, Pacífica, Amazonía-Orinoquía, and Bogotá. Multiple linear regression was performed using R2 to measure goodness of fit to estimate the effect between colorectal cancer incidence rate/gastric cancer incidence rate and exposure factors.

A positive association was observed between colorectal cancer and non-compliance with the recommendation of vigorous physical activity (p = 0.00) and consumption of beverages/grilled food pattern (p = 0.001). Conversely, it decreased incidence by enjoying some specific health insurance and following a conservative dietary pattern (p = 0.05). Gastric cancer incidence was found to increase with age (p = 0.000), sex (p = 0.001), and consumption of the beverages/grilled food pattern (p = 0.006). However, being in the first wealth quartile decreased the incidence (p = 0.002).

There is evidence of an association between diet, physical activity and wealth quartile with colorectal and gastric cancer. This information should be considered for preventive interventions in the population.

Preclinical animal studies have suggested that myeloid cell-synthesized coagulation factor X dampens antitumor immunity and that rivaroxaban, a direct factor Xa inhibitor, can be used to promote tumor immunity. This study was aimed at assessing whether patients with atrial fibrillation taking direct factor Xa inhibitors have lower risk of cancer and cancer-related mortality than patients taking the direct thrombin inhibitor dabigatran.

This nationwide population-based cohort study in Denmark included adult patients with atrial fibrillation and without a history of cancer, who started taking a factor Xa inhibitor or dabigatran between 2011 and 2015. Data on medical history, outcomes, and drug use were acquired through Danish healthcare registries. The primary outcome was any cancer. Secondary outcomes were cancer-related mortality and all-cause mortality. Outcome events were assessed during 5 years of follow-up in an intention-to-treat analysis. The propensity score-based inverse probability of treatment weighting was used to compute cumulative incidence and subdistribution hazard ratios (SHRs) and corresponding 95% confidence intervals (CIs), with death as a competing event. Propensity scores were estimated using logistic regression and including in the model sex, age group at index date, comorbidities, and use of comedications. A total of 11,742 patients with atrial fibrillation starting a factor Xa inhibitor and 11,970 patients starting dabigatran were included. Mean age was 75.2 years (standard deviation [SD] 11.2) in the factor Xa cohort and 71.7 years (SD 11.1) in the dabigatran cohort. On the basis of the propensity score-weighted models, after 5 years of follow-up, no substantial difference in the cumulative incidence of cancer was observed between the factor Xa inhibitor (2,157/23,711; 9.11%, 95% CI [8.61%,9.63%]) and dabigatran (2,294/23,715; 9.68%, 95% CI [9.14%,10.25%]) groups (SHR 0.94, 95% CI [0.89,1.00], P value 0.0357). We observed no difference in cancer-related mortality (factor Xa inhibitors cohort 1,028/23,711; 4.33%, 95% CI [4.02%,4.68%]. Dabigatran cohort 1,001/23,715; 4.22%, 95% CI [3.83%,4.66%]; SHR 1.03, 95% CI [0.94,1.12]), but all-cause mortality was higher in the factor Xa inhibitor cohort (factor Xa inhibitors cohort 7,416/23,711; 31.31%, 95% CI [30.37%,32.29%]. Dabigatran cohort 6,531/23,715; 27.56%, 95% CI [26.69%,28.45%]; HR 1.17, 95% CI [1.13,1.21]). The main limitations of the study were the possibility of residual confounding and the short follow-up period.

In this population based cohort study, factor Xa inhibitor use was not associated with an overall lower incidence of cancer or cancer-related mortality when compared to dabigatran. We did observe an increase in all-cause mortality in the factor Xa inhibitor cohort.

Stanniocalcin 2 (STC2) is involved in many tumour types, but it remains unclear what its biological function is in laryngeal squamous cell carcinoma (LSCC). Therefore, we investigated STC2's expression, potential function, and prognostic significance of in LSCC. The expression and prognosis of STC2 in LSCC were described using the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases. In the TCGA database, the relationship between STC2 and immune infiltration, expression of immune cell chemokine and receptor genes, immune cell molecular marker genes, and epithelial‒mesenchymal transition (EMT) marker genes were analysed. The biological processes involved in STC2 and its expression-related genes were analysed comprehensively using bioinformatics. The single-gene ceRNA network of STC2 was constructed in the TCGA database. Finally, LSCC patients' tumour tissue STC2 expression was verified. STC2 silencing with the RNAi technique was used for the determination of cellular functions in a laryngeal cancer cell line. STC2 expression was higher in most tumours, including LSCC, than in normal tissues and was associated with poor prognosis. The relative proportions of naïve B, plasma, follicular helper T, and macrophage M0 cells in LSCC and normal samples differed significantly. STC2 expression correlated significantly positively with that of TGFB1 (biomarker of Tregs) and significantly negatively with that of D79A and CD19 (biomarkers of B cells). Furthermore, STC2 affected chemokine and receptor gene expression in immune cells. STC2 expression correlated with EMT marker gene expression in LSCC. STC2 was enriched in the PI3K/AKT signalling pathway, extracellular matrix (ECM) organisation, ECM-receptor interaction, and other tumour-related signalling pathways. STC2 was highly expressed in our clinical samples. N-cadherin and vimentin expression were decreased in the TU686 cell line after successful silencing of STC2, indicating that high STC2 expression may prompt LSCC cells to adopt a mesenchymal cell phenotype. STC2 silencing substantially reduced proliferation and migration in the TU686 cell line. STC2 may be a promising predictive biomarker for tumours, providing new approaches for LSCC diagnosis and treatment monitoring.

Previous studies reported that variations in dietary intake patterns substantially impact human health, specifically tumorigenesis. However, confounding factors in previous cohort studies have obscured the relationship between dietary differences and the risk of oral cancer (OC).

We developed an outcome dataset from genome-wide association studies (GWAS) data on three OCs within the GAME-ON project, using GWAS-META merging. We extracted 21 dietary exposures, including 10 dietary patterns, 6 vitamins, and 5 micronutrients, from the UK Biobank database, using the inverse variance weighting method as the primary statistical method. Sensitivity analysis was conducted to detect heterogeneity and pleiotropy. Serum metabolite concentrations were adjusted using multivariate Mendelian randomization.

Of the 10 analyzed dietary patterns, 8 showed no significant association with the risk of developing OC. Consumption of dark chocolate (inverse variance weighted [IVW]: Odds ratio (OR) = 0.786, 95% confidence interval [CI]: 0.622-0.993, p = 0.044) and sweet pepper exhibited an inverse relationship with OC risk (IVW: OR = 0.757, 95% CI: 0.574-0.997, p = 0.048). Reverse MR analysis revealed no reverse causality. Furthermore, no significant correlation was observed between the intake of 6 vitamins and 5 micronutrients and the risk of developing OC. After using multivariable MR to adjust for serum caffeine, linoleate, theophylline, and theobromine metabolism levels, consuming dark chocolate was unrelated to a decreased risk of OC. After adjusting each serum metabolite individually, the observed p-values deviated from the original values to varying degrees, indicating that the components of dark chocolate could have different effects. Among these components, theophylline demonstrated the most significant inhibitory effect.

This study demonstrated a causal relationship between the intake of dark chocolate and sweet peppers and a lower risk of OC. The components of dark chocolate could have different effects.

The rapid development of digital technology has radically changed people's lives. Simultaneously, as the population is rapidly aging, academic research is focusing on the use of Internet technology to improve middle-aged and older people's health, particularly owing to the popularity of mobile networks, which has further increased the population's accessibility to the Internet. However, related studies have not yet reached a consensus. Herein, empirical analysis of the influence of mobile Internet use on the subjective health and chronic disease status of individuals in their Middle Ages and above was conducted utilizing ordered logit, propensity score matching (PSM), and ordered probit models with data from the 2020 China Health and Retirement Longitudinal Study. The study aimed to provide a theoretical basis and reference for exploring technological advances to empower the development of a healthy Chinese population and to advance the process of healthy aging. The health of middle-aged and older adults mobile Internet users was greatly improved, according to our findings. Further, the use of mobile Internet by these persons resulted in improvements to both their self-assessed health and the state of their chronic diseases. As per the findings of the heterogeneity analysis, the impact of mobile Internet use was shown to be more pronounced on the well-being of middle-aged persons aged 45-60 years compared to those aged ≥ 60 years. Further, the endogeneity test revealed that the PSM model could better eliminate bias in sample selection. The results suggest that the estimates are more robust after eliminating endogeneity, and that failure to disentangle sample selectivity bias would overestimate not only the facilitating effect of mobile Internet use on the self-assessed health impacts of middle-aged and older adults, but also the ameliorating effect of mobile Internet use on the chronic diseases of middle-aged and older adults. The results of the mechanistic analysis suggest that social engagement is an important mediating mechanism between mobile Internet use and the health of middle-aged and older adults. This implies that mobile Internet use increases opportunities for social participation among middle-aged and older adults, thereby improving their health.

While DNA serves as the fundamental genetic blueprint for an organism, it is not a static entity. Gene expression, the process by which genetic information is utilized to create functional products like proteins, can be modulated by a diverse range of environmental factors. Epigenetic mechanisms, including DNA methylation, histone modification, and microRNAs, play a pivotal role in mediating the intricate interplay between the environment and gene expression. Intriguingly, alterations in the epigenome have the potential to be inherited across generations. Alcohol use disorder (AUD) poses significant health issues worldwide. Alcohol has the capability to induce changes in the epigenome, which can be inherited by offspring, thus impacting them even in the absence of direct alcohol exposure. This review delves into the impact of alcohol on the epigenome, examining how its effects vary based on factors such as the age of exposure (adolescence or adulthood), the duration of exposure (chronic or acute), and the specific sample collected (brain, blood, or sperm). The literature underscores that alcohol exposure can elicit diverse effects on the epigenome during different life stages. Furthermore, compelling evidence from human and animal studies demonstrates that alcohol induces alterations in epigenome content, affecting both the brain and blood. Notably, rodent studies suggest that these epigenetic changes can result in lasting phenotype alterations that extend across at least two generations. In conclusion, the comprehensive literature analysis supports the notion that alcohol exposure induces lasting epigenetic alterations, influencing the behavior and health of future generations. This knowledge emphasizes the significance of addressing the potential transgenerational effects of alcohol and highlights the importance of preventive measures to minimize the adverse impact on offspring.

The goal of this study is to look into the pharmacological mechanism of Bruceae Fructus in conjunction with GEO, network pharmacology, and in vitro assays for the treatment of laryngeal cancer to provide theoretical support for its therapeutic use. The active components and matching targets of Bruceae Fructus were retrieved from the TCMSP database, while genes linked with laryngeal cancer were obtained from the GEO, GeneCards, DisGeNET, and DrugBank databases. Besides, the components and targets were supplemented by literatures in PubMed database. Cytoscape software was used to create the active ingredients-target network diagram. The String database was used to build the PPI network. Following that, the core targets were subjected to GO enrichment and KEGG pathway analysis using the DAVID database. Finally, AutoDock was used to perform molecular docking between the core components and the core targets. To investigate the biological effects of beta-sitosterol, the viability of laryngeal cancer cells was assessed after beta-sitosterol therapy using the MTS technique. Following that, how beta-sitosterol affected colony formation after 14 days of culture of treated cells was researched. Flow cytometry was utilized to detect apoptosis to examine the influence of beta-sitosterol on laryngeal cancer cell apoptosis, and then detected mRNA and protein expression levels of 10 key genes by RT-qPCR and Western Blot assay. There were 1258 laryngeal cancer-related genes and 15 Bruceae Fructus components, with beta-sitosterol and luteolin serving as key components. Bruceae Fructus' primary targets against laryngeal cancer were IL6, JUN, TNF, IL2, IL4, IFNG, RELA, TP53, CDKN1A, and AKT1. GO enrichment yielded 41 CC, 78 MF, and 383 BP. Platinum drug resistance, the PI3K-Akt signaling pathway, the p53 signaling pathway, apoptosis, the HIF-1 signaling pathway, and 147 additional pathways have been added to KEGG. The results of molecular docking revealed that the core components had a high affinity for the core target. The results of the cell experiment indicate that beta-sitosterol suppressed Hep-2 cell activity in a concentration-dependent manner. Besides, beta-sitosterol has powerful antiproliferative properties in Hep-2 cells. Flow cytometry results showed that beta-sitosterol promoted laryngeal cancer cell apoptosis in a concentration-dependent manner. The results of RT-qPCR and Western Blot assay showed that the mRNA and protein expression levels of TP53, JUN, TNF-α, CDKN1A, and IL-2 were significantly up-regulated after beta-sitosterol treatment, while the mRNA and protein expression levels of RELA, AKT1, IL-6, IFNG, and IL-4 were significantly down-regulated. This study integrating GEO, network pharmacology, and in vitro assays investigated the probable mechanism of Bruceae Fructus' anti-laryngeal cancer activity, which can give a theoretical foundation for additional future animal experiments.

The concept of the exposome is the encompassing of all the environmental exposures, both exogenous and endogenous, across the life course. Many, if not all, of these exposures can result in the generation of reactive species, and/or the modulation of cellular processes, that can lead to a breadth of modifications of DNA, the nature of which may be used to infer their origin. Because of their role in cell function, such modifications have been associated with various major human diseases, including cancer, and so their assessment is crucial. Historically, most methods have been able to only measure one or a few DNA modifications at a time, limiting the information available. With the development of DNA adductomics, which aims to determine the totality of DNA modifications, a far more comprehensive picture of the DNA adduct burden can be gained. Importantly, DNA adductomics can facilitate a "top-down" investigative approach whereby patterns of adducts may be used to trace and identify the originating exposure source. This, together with other 'omic approaches, represents a major tool for unraveling the complexities of the exposome and hence allow a better a understanding of the environmental origins of disease.

Depression, anxiety and other psychosocial factors are hypothesized to be involved in cancer development. We examined whether psychosocial factors interact with or modify the effects of health behaviors, such as smoking and alcohol use, in relation to cancer incidence. Two-stage individual participant data meta-analyses were performed based on 22 cohorts of the PSYchosocial factors and CAncer (PSY-CA) study. We examined nine psychosocial factors (depression diagnosis, depression symptoms, anxiety diagnosis, anxiety symptoms, perceived social support, loss events, general distress, neuroticism, relationship status), seven health behaviors/behavior-related factors (smoking, alcohol use, physical activity, body mass index, sedentary behavior, sleep quality, sleep duration) and seven cancer outcomes (overall cancer, smoking-related, alcohol-related, breast, lung, prostate, colorectal). Effects of the psychosocial factor, health behavior and their product term on cancer incidence were estimated using Cox regression. We pooled cohort-specific estimates using multivariate random-effects meta-analyses. Additive and multiplicative interaction/effect modification was examined. This study involved 437,827 participants, 36,961 incident cancer diagnoses, and 4,749,481 person years of follow-up. Out of 744 combinations of psychosocial factors, health behaviors, and cancer outcomes, we found no evidence of interaction. Effect modification was found for some combinations, but there were no clear patterns for any particular factors or outcomes involved. In this first large study to systematically examine potential interaction and effect modification, we found no evidence for psychosocial factors to interact with or modify health behaviors in relation to cancer incidence. The behavioral risk profile for cancer incidence is similar in people with and without psychosocial stress.

Background The incidence of colorectal cancer (CRC) is increasing in developing countries. The factors contributing to the risk of CRC are not known in developing countries. Therefore, this study aimed to explore the role of a healthy lifestyle on CRC in the adult population in the Kurdistan Region of Iraq. Methodology In this case-control investigation, patients previously diagnosed with CRC were included as cases (n = 84) and the healthy adult population as healthy controls (n = 87). The patients were selected from the Gastroenterology Unit of Azadi Teaching Hospital and Emergency Teaching Hospital. The healthy controls were selected from the caregivers of patients who met the eligibility criteria. Results Individuals with a history of chronic disease (63.08% vs. 40.52%; p = 0.0043), a history of hypertension (71.74% vs. 40.80%; p = 0.0003), and a history of inflammatory bowel disease (IBD) (59.42% vs. 42.16%; p = 0.0267) had a significantly higher prevalence of CRC compared to healthy controls. CRC patients had significantly lower diet quality scores than healthy controls (36.27 vs. 37.83; p = 0.0002). The study showed that CRC patients had a significantly lower lifestyle index score compared to healthy controls (10.20 vs. 11.69; p = 0.0002). In addition, CRC patients had lower scores for diet (0.42 vs. 1.00; p < 0.0001), smoking (2.92 vs. 4.0; p < 0.0001), and physical activity (1.02 vs. 1.70; p < 0.0001) compared to healthy controls. However, CRC patients and healthy controls had similar alcohol index scores (5.0 vs. 530; p = 1.000) and body mass index (1.04 vs. 1.01; p = 0.8982). Conclusions This study showed that CRC was associated with having a history of bad diet quality and unhealthy lifestyles. In addition, a history of chronic diseases, hypertension, and IBD was associated with the risk of CRC.

Cancer of the head and neck is a confronting condition, as the disease and its treatments alter the appearance and function of body organs associated with physical appearance and identity. Many of the risk factors for head and neck cancers, including tobacco, alcohol, and human papilloma virus, can also have significant negative social and moral permutations. Language and action (discourse) plays an important role in constructing disease and illness and shape the way it is managed, both institutionally and socially. This research used a critical constructionist lens to investigate how the common discourses surrounding head and neck cancer are constructed within the healthcare context and how this influences patients and healthcare professionals' responses to the illness. Data were collected through semi-structured interviews, field noting, journaling and literature reviews. Analysis was guided by a three-dimensional approach to critical discourse analysis that investigated text, discursive practices, and social context. The overarching finding was that deviance dominates the common discourse and shapes head and neck cancer and responses to it. Deviance is channelled through metaphors, adjectives, descriptors, and collective nouns and is made overt through labelling, avoidance, blaming, shame, and categorization. Discourse is contextualized by a sociocultural understanding that when someone deviates from what is perceived as normal, they are devalued. Open dialogue and reflection on head and neck cancer discourse could enable better understanding of how people experience their condition and inform more supportive responses.

Head and neck cancer (HNC) is a prevalent and complex group of malignancies with increasing incidence globally. Alcohol dehydrogenases (ADHs) play a crucial role in alcohol metabolism, and their polymorphisms have been linked to HNC risk. This systematic review and meta-analysis aims to evaluate the association between ADH polymorphisms and susceptibility to HNCs, incorporating additional analyses and adding more studies to increase power and accuracy of the results.

Subgroup analysis, meta-regression analysis, and sensitivity analyses were conducted to explore potential differences within the data and assess the stability of pooled odds ratios (ORs). To mitigate the risk of false conclusions from meta-analyses, a trial sequential analysis was performed.

For ADH1B rs1229984, the pooled OR (95 % confidence interval (CI)) was 0.73 (0.65, 0.82), 0.42 (0.35, 0.50), 0.57 (0.44, 0.73), 0.56 (0.50, 0.62), and 0.80 (0.73, 0.88), as well as for ADH7 rs1573496, the pooled OR was 0.72 (0.62, 0.85), 0.36 (0.17, 0.74), 0.76 (0.64, 0.91), 0.80 (0.71, 0.91), and 0.38 (0.18, 0.78) with a p < 0.05 in all allelic, homozygous, heterozygous, recessive, and dominant models, respectively. However, no significant association was found between the ADH7 rs1154460 and rs284787 polymorphisms and the risk of HNC with pooled ORs of 1.11 (p = 0.19) and 1.09 (p = 0.24) for the recessive model, respectively. The ethnicities, tumor subsites, control sources, sample sizes, quality scores, and Hardy-Weinberg equilibrium statuses were confounding factors.

The ADH1B rs1229984 and ADH7 rs1573496 polymorphisms are significantly associated with a reduced risk of HNC.

This study aimed to investigate the relationship between drinking status and kidney stones occurrence among United States (US) adults who consume alcohol.

We conducted a cross-sectional analysis using data from the National Health and Nutrition Examination Survey (NHANES 2007-2018). Questionnaires yielded information on alcohol consumption and kidney health. Drinking status was categorized into four groups-former, mild, moderate, and heavy-based on alcohol consumption patterns. The aim was to explore the relationship between drinking status and the prevalence of kidney stones occurrence. For this analysis, we examined a group of individuals diagnosed with kidney stones. With survey weights applied, the total weight of the group was 185,690,415.

We used logistic regression to measure the relationship between drinking status and the likelihood of developing kidney stones. In a fully adjusted model, former drinkers were less likely to have previously experienced kidney stones (OR 0.762, 95% CI 0.595-0.977, P < 0.05). In subgroup analysis, heavy alcohol consumption was associated with a significantly reduced likelihood of kidney stones occurrence in various populations. The adjusted odds ratios (with 95% confidence intervals) of kidney stones risk for heavy alcohol consumption were 0.745 (0.566-0.981) for young individuals, 0.566 (0.342-0.939) for older individuals, 0.708 (0.510-0.981) for individuals of white race, 0.468 (0.269-0.817) for individuals with underweight/normal BMI, 0.192 (0.066-0.560) for widowed people, 0.538 (0.343-0.843) for smoking individuals, 0.749 (0.595-0.941) for individuals without a cancer history, and 0.724 (0.566-0.925) for individuals without a stroke history.

In US adults who consume alcohol, a negative linear relationship is apparent between drinking status and the prevalence of kidney stones, with heavy drinking showing a lower prevalence compared to former drinkers. However, the causal relationship between drinking status and kidney stones requires further investigation in future research endeavors.