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Background Ultra-processed foods have now become dominant in the global food system. Whether their consumption is associated with cardiovascular mortality remains controversial. Moreover, data on ultra-processed foods and cardiovascular outcomes are scarce in the US population. We aimed to examine the association of ultra-processed food consumption with cardiovascular mortality in a US population. Methods A population-based cohort of 91,891 participants was identified from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Dietary data were collected through a validated 137-item food frequency questionnaire. Ultra-processed foods were defined by the NOVA classification. Cox regression was used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for cardiovascular mortality. Restricted cubic spline regression was used to test nonlinearity. Subgroup analyses were conducted to identify the potential effect modifiers. Results After an average follow-up of 13.5 years (1,236,049.2 person-years), 5490 cardiovascular deaths were documented, including 3985 heart disease deaths and 1126 cerebrovascular deaths. In the fully adjusted model, participants in the highest vs. the lowest quintiles of ultra-processed food consumption had higher risks of death from cardiovascular disease (HRquintile 5 vs. 1, 1.50; 95% CI, 1.36–1.64) and heart disease (HRquintile 5 vs. 1, 1.68; 95% CI, 1.50–1.87) but not cerebrovascular disease (HRquintile 5 vs. 1, 0.94; 95% CI, 0.76–1.17). A nonlinear dose–response pattern was observed for overall cardiovascular and heart disease mortality (all Pnonlinearity Pinteraction Conclusions High consumption of ultra-processed foods is associated with increased risks of overall cardiovascular and heart disease mortality. These harmful associations may be more pronounced in women. Our findings need to be confirmed in other populations and settings.

Low-carbohydrate diets have become a popular approach for weight loss in recent years. However, whether low-carbohydrate diets are associated with the risk of pancreatic cancer remains to be elucidated. Hence, we examined the association of low-carbohydrate diets with the risk of pancreatic cancer in a US population. A population-based cohort of 95 962 individuals was identified. A low-carbohydrate-diet score was calculated to quantify adherence to this dietary pattern, with higher scores indicating greater adherence. Cox regression was used to calculate risk estimate for the association of the low-carbohydrate-diet score with the risk of pancreatic cancer. Subgroup analysis was used to identify the potential effect modifiers. After an average follow-up of 8.87 years (875856.9 person-years), we documented a total of 351 pancreatic cancer cases. In the fully adjusted model, the highest versus the lowest quartiles of the overall low-carbohydrate-diet score were found to be associated with a reduced risk of pancreatic cancer (hazard ratioquartile 4 versus 1: 0.61; 95% confidence interval: 0.45, 0.82; Ptrend < 0.001). Subgroup analysis found that the inverse association of low-carbohydrate diets with the risk of pancreatic cancer was more pronounced in individuals aged ≥65 years than in those aged

Background Whether adherence to the World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) cancer prevention recommendations is associated with a reduced risk of pancreatic cancer remains controversial. Additionally, no study has investigated this association in the US population. Hence, we investigated the association of adherence to the 2018 WCRF/AICR cancer prevention recommendations with pancreatic cancer incidence and mortality in a US population. Methods A population‐based cohort of 95 962 participants was identified. A score incorporating eight WCRF/AICR components was constructed to reflect adherence to the WCRF/AICR guidelines, with higher scores representing greater adherence to the guidelines. Cox and competing risk regression were used to calculate risk estimates for pancreatic cancer incidence and mortality, respectively. Restricted cubic spline functions were used to test nonlinearity. Results In the fully adjusted model, higher overall WCRF/AICR scores were shown to be associated with lower risks of developing pancreatic cancer (hazard ratiotertile 3 vs 1:0.67; 95% confidence interval: 0.49, 0.90; P trend = .0099) and mortality due to this cancer (subdistribution hazard ratiotertile 3 vs 1 0.65; 95% confidence interval: 0.47, 0.89; P trend = .0108) in a linear dose–response manner (all P nonlinearity > .05). The component “be physically active” was shown to be a key contributor to the observed associations. No association of the diet‐specific WCRF/AICR score with pancreatic incidence and mortality was found. Conclusions Adherence to the 2018 WCRF/AICR guidelines, especially “be physically active,” confers reduced risks of pancreatic cancer incidence and mortality in the US population; however, adherence to dietary components alone does not confer such beneficial effects., In this prospective study of 95962 American adults, we found that greater adherence to the 2018 WCRF/AICR recommendations was associated with lower risks of pancreatic cancer incidence and mortality. However, such beneficial effects were not found for adherence to diet‐specific recommendations alone.Importantly, the component “be physically active” was found to be a key driver of the observed associations.

We aimed to examine whether type 2 diabetes prevention diet, a dietary pattern previously developed for reducing type 2 diabetes risk, was associated with mortality in a US population. A population-based cohort of 86633 subjects was identified from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (study period: 1993 to 2015). Dietary information was collected with a food frequency questionnaire. A dietary diabetes risk reduction score was calculated to reflect adherence to this dietary pattern, with higher scores representing better adherence. Hazard ratios (HRs) and absolute risk differences (ARDs) in mortality rates per 10000 person-years were calculated. After a mean follow-up of 13.6 years, 17532 all-cause deaths were observed. The highest versus the lowest quintiles of dietary diabetes risk reduction score was associated with decreased risks of death from all causes (HRquintile 5 versus 1: 0.76; 95% CI: 0.72, 0.80; ARDquintile 5 versus 1: -81.94; 95% CI: -93.76, -71.12), cardiovascular disease (HRquintile 5 versus 1: 0.73; 95% CI: 0.66, 0.81; ARDquintile 5 versus 1: -17.82; 95% CI: -24.81, -11.30), and cancer (HRquintile 5 versus 1: 0.85; 95% CI: 0.78, 0.94; ARDquintile 5 versus 1: -9.92; 95%CI: -15.86, -3.59), which were modified by sex, smoking status, or alcohol consumption in subgroup analyses (all Pinteraction

Whether tenofovir disoproxil fumarate (TDF) is superior to entecavir in reducing hepatocellular carcinoma (HCC) risk among treatment-naive chronic hepatitis B (CHB) patients remains controversial. We aimed to clarify this controversy. Several databases, including PubMed and Embase, were retrieved through November 2020. Cohort studies comparing the effectiveness of TDF and entecavir in reducing HCC incidence among treatment-naive CHB patients were included if they reported multivariable-adjusted or propensity-score-matched risk estimates. A random-effects model was used to pool hazard ratios (HRs). Thirteen cohort studies, involving 4097 HCC cases and 80202 CHB patients, were included. Multivariable-adjusted meta-analysis revealed no significant difference in HCC incidence between TDF and entecavir groups (HR 0.86, 95% confidence interval 0.72-1.04), which was consistent with propensity-score-matched meta-analysis (HR 0.83, 95% confidence interval 0.66-1.03). Subgroup analysis showed that the observed similarity of TDF to entecavir for HCC prevention persisted in studies with follow-up length of ≥4 years but not in those with follow-up length of

Objective The association between high-density lipoprotein cholesterol (HDL-C) levels and mortality remains controversial. We aimed to investigate the potential dose–response associations between HDL-C levels and mortality from all causes, cardiovascular disease and cancer in the general population. Methods PubMed and Embase were searched through April 2019. Prospective cohort studies reporting risk estimates of HDL-C levels and mortality were included. Linear and non-linear dose–response analyses were conducted. A random-effects model was employed to calculate pooled hazard ratio. Results Thirty-seven studies, involving 3,524,505 participants and more than 612,027 deaths, were included. HDL-C level was found to be associated with mortality from all causes, cardiovascular disease and cancer in a J-shaped dose–response pattern, with the lowest risk observed at HDL-C levels of 54–58 mg/dL, 68–71 mg/dL and 64–68 mg/dL, respectively. Compared with HDL-C level of 56 mg/dL, the pooled hazard ratios for all-cause mortality were 1.03 (95% confidence interval (CI) 1.01, 1.05) and 1.10 (95% CI 1.09, 1.12) for each 10-mg/dL increase and decrease in HDL-C levels, respectively; furthermore, compared with the reference category, the pooled hazard ratios for all-cause mortality were 1.21 (95% CI 1.09, 1.36) and 1.36 (95% CI 1.21, 1.53) for the highest and the lowest categories of HDL-C levels, respectively. Similar results were obtained for cardiovascular and cancer mortality. Conclusions In the general population, HDL-C level is associated with mortality from all causes, cardiovascular disease and cancer in a J-shaped dose–response manner; both extremely high and low HDL-C levels are associated with an increased risk of mortality.

Supplemental Digital Content is available in the text., Major histocompatibility complex (MHC) class II regulatory genes play a paramount role in immune response that can exert a predominant influence on clinical outcome of Epstein–Barr virus infection consistently assumed as the main pathogenetic factor for nasopharyngeal carcinoma. To elucidate the relationship between allelic variants of MHC class II regulatory genes and susceptibility to nasopharyngeal carcinoma, a total of 28 polymorphic loci at MHC class II regulatory genes, involving CIITA, CREB1, RFX family genes (RFX5, RFXAP, and RFXANK), and NFY family genes (NFYA, NFYB, and NFYC), were genotyped by multiplex SNaPshot minisequencing in 137 patients with nasopharyngeal carcinoma and 107 healthy controls from the southern Chinese population. Allelic analysis disclosed that rs7404873, rs6498121, rs6498126, and rs56074043 shared correlations with nasopharyngeal carcinoma (Ptrend < 0.05). Further, rs6498126 on CIITA was independently associated with the risk of developing nasopharyngeal carcinoma (CC vs. GG, odds ratio: 7.386, 95% confidence interval: 1.934–28.207, Ptrend < 0.01). Conversely, rs7404873 on CIITA and rs56074043 on NFYB manifested epistatic interaction to decreased susceptibility of nasopharyngeal carcinoma (rs7404873, TT vs. GG, odds ratio: 0.256, 95% confidence interval: 0.088–0.740, Ptrend < 0.05; rs56074043, AA vs. AG, odds ratio: 0.341, 95% confidence interval: 0.129–0.900, Ptrend < 0.05). Additionally, bioinformatics analysis revealed that the three variants were transcriptional regulatory in function and might impact the expression of nearby genes. The findings suggested genetic variants on MHC class II regulatory genes contributed to nasopharyngeal carcinoma susceptibility and might provide new insights for screening high-risk population.

Background: Total antioxidant capacity (TAC) reflects an individual's overall antioxidant intake. We sought to clarify whether higher TAC is associated with lower risks of pancreatic cancer incidence and mortality in the U.S. general population. Methods: A total of 96,018 American adults were identified from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. A ferric-reducing ability of plasma score was used to reflect an individual's TAC intake from diet and/or supplements. Cox regression was used to calculate hazard ratios (HR) for pancreatic cancer incidence, and competing risk regression was used to calculate subdistribution HRs for pancreatic cancer mortality. Restricted cubic spline regression was used to test nonlinearity. Results: A total of 393 pancreatic cancer cases and 353 pancreatic cancer–related deaths were documented. Total (diet + supplements) TAC was found to be inversely associated with pancreatic cancer incidence (HR quartile 4 vs. quartile 1 = 0.53; 95% confidence interval, 0.39–0.72; Ptrend = 0.0002) and mortality (subdistribution HR quartile 4 vs. quartile 1 = 0.52; 95% confidence interval 0.38–0.72; Ptrend = 0.0003) in a nonlinear dose–response manner (all Pnonlinearity < 0.01). Similar results were observed for dietary TAC. No association of supplemental TAC with pancreatic cancer incidence and mortality was found. Conclusions: In the U.S. general population, dietary but not supplemental TAC level is inversely associated with risks of pancreatic cancer incidence and mortality in a nonlinear dose–response pattern. Impact: This is the first prospective study indicating that a diet rich in antioxidants may be beneficial in decreasing pancreatic cancer incidence and mortality.

Whether nonalcoholic fatty liver disease (NAFLD) is associated with an increased risk of mortality remains controversial. The present study aimed to clarify this issue. A systematic search of PubMed and Embase was conducted through October 2018. Studies providing risk estimates of NAFLD and mortality were included. A random-effects model was employed to calculate summary risk estimates. Subgroup analyses were performed to identify potential effect modifiers. Fourteen studies, involving 498501 subjects and 24234 deaths, were included. Patients with NAFLD were found to be at an elevated risk of all-cause mortality compared with those without [hazard ratio (HR) = 1.34; 95% confidence interval (CI) 1.17–1.54)]. The significantly positive association between NAFLD and all-cause mortality could not be modified by age, sex, follow-up duration, and adjustment for body mass index, diabetes, smoking or hypertension (all Pinteraction > 0.05), and remained in sensitivity analyses. No significant associations of NAFLD with CVD (HR = 1.13; 95% CI 0.92–1.38) and cancer (HR = 1.05; 95% CI 0.89–1.25) mortality were found. In conclusion, NAFLD is a predictor of increased all-cause mortality but not CVD and cancer mortality. These findings have important implications for decision making in public health and clinical practice, and highlight the urgency of developing effective treatments for NAFLD.

The fecal immunochemical test (FIT) and colonoscopy are the most commonly used strategies for colorectal cancer (CRC) screening worldwide. We aimed to compare their efficacy and cost-effectiveness in CRC screening in an average-risk population.PubMed, Embase, and National Health Services Economic Evaluation Database were searched. Risk ratio (RR) was used to evaluate the differences in detection rates of colorectal neoplasia between FIT and colonoscopy groups. A random-effects model was used to pool RRs. Incremental cost-effectiveness ratios (ICERs) were calculated to evaluate the cost-effectiveness of FIT versus colonoscopy.Six randomized controlled trials and 17 cost-effectiveness studies were included. The participation rate in the FIT group was higher than that in the colonoscopy group (41.6% vs 21.9%). In the intention-to-treat analysis, FIT had a detection rate of CRC comparable with colonoscopy (RR, .73; 95% confidence interval, .37-1.42) and lower detection rates of any adenoma and advanced adenoma than 1-time colonoscopy. Most included cost-effectiveness studies showed that annual (13/15) or biennial (5/6) FIT was cost-saving (ICER $0) or very cost-effective ($0 ICER ≤ $25000/quality-adjusted life-year) compared with colonoscopy every 10 years.FIT may be similar to 1-time colonoscopy in the detection rate of CRC, although it has lower detection rates of any adenoma and advanced adenoma than 1-time colonoscopy. Furthermore, annual or biennial FIT appears to be very cost-effective or cost-saving compared with colonoscopy every 10 years. These findings indicate, at least partly, that FIT is noninferior to colonoscopy in CRC screening in an average-risk population. Our findings should be treated with caution and need to be further confirmed.

BackgroundABO blood group has been associated with cardiovascular disease and cancer. However, whether ABO blood group is associated with nonalcoholic fatty liver disease (NAFLD) remains unknown. The present study aimed to clarify this issue.MethodsA hospital-based case-control study was performed in southwestern China. A total of 583 newly ultrasound-diagnosed NAFLD cases and 2068 controls were included. The adjusted odds ratios (ORs) and 95% confidence intervals (CIs) of developing NAFLD were calculated by multivariate logistic regression. A propensity score was developed for adjustment and matching.ResultsThe proportions of blood groups A, B, AB and O were 31%, 26%, 8% and 35%, respectively. Non-O blood groups were found to be significantly associated with an increased risk of NAFLD (the fully adjusted OR = 1.51, 95% CI: 1.19, 1.91); moreover, compared with blood group O, the fully adjusted ORs of developing NAFLD were 1.50 (95% CI: 1.13, 1.99) for blood group A, 1.59 (95% CI: 1.19, 2.14) for blood group B, and 1.37 (95% CI: 0.86, 2.18) for blood group AB. Similar results were obtained in both propensity-score-adjusted and propensity-score-matched analyses. No evidence of significant effect modification for the association of ABO blood group with the risk of NAFLD was found (all Pinteraction>0.05).ConclusionsNon-O blood groups are significantly associated with an increased risk of NAFLD. Our findings provide some epidemiological evidence for a possible role of ABO glycosyltransferase in the pathogenesis of NAFLD. However, these findings need to be validated by future studies.

The relation between hepatitis B virus (HBV) infection and fatty liver has been addressed by several observational studies, but their results remain controversial. To date, no study has precisely investigated the association of current and past HBV infection with the risk of nonalcoholic fatty liver disease (NAFLD) in the Chinese population. Therefore, we conducted a hospital-based case-control study in southwestern China to clarify this issue. A total of 631 newly ultrasound-diagnosed NAFLD cases and 2357 controls were selected from 123 243 consecutive patients admitted to a tertiary-care hospital between January 2015 and December 2016. Multivariate logistic regression was employed to calculate adjusted odds ratios (ORs) and 95% confidence intervals (CIs). A propensity score was developed for adjustment and matching. Subgroup analysis was conducted to identify potential effect modifiers. Current and past HBV infection had an overall prevalence of 9.7% and 55.2%, respectively. In the fully adjusted model, current HBV infection was associated with a decreased risk of NAFLD (OR 0.64; 95% CI 0.42-0.95). A similar inverse association was observed in both propensity-score-adjusted (OR 0.58; 95% CI 0.40-0.86) and propensity-score-matched analyses (OR 0.61; 95% CI 0.40-0.92).The inverse association was stronger in patients with hypertension than in those without (Pinteraction = .018).No significant association between past HBV infection and NAFLD risk was found. In conclusion, current but not past HBV infection is associated with a decreased risk of NAFLD in the Chinese population. The corresponding biological mechanisms remain to be elucidated.