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To reduce treatment-related side effects in low-risk prostate cancer (PCa), both focal therapy and deferred treatments, including active surveillance (AS) and watchful waiting (WW), are worth considering over radical prostatectomy (RP). Therefore, this study aimed to compare long-term survival outcomes between focal therapy and AS/WW. Data were obtained and analyzed from the Surveillance, Epidemiology, and End Results (SEER) database. Patients with low-risk PCa who received focal therapy or AS/WW from 2010 to 2016 were included. Focal therapy included cryotherapy and laser ablation. Multivariate Cox proportional hazards models were used to compare overall mortality (OM) and cancer-specific mortality (CSM) between AS/WW and focal therapy, and propensity score matching (PSM) was performed to reduce the influence of bias and unmeasured confounders. A total of 19 292 patients with low-risk PCa were included in this study. In multivariate Cox proportional hazards model analysis, the risk of OM was higher in patients receiving focal therapy than those receiving AS/WW (hazard ratio [HR] = 1.35, 95% confidence interval [CI]: 1.02-1.79, P = 0.037), whereas no significant difference was found in CSM (HR = 0.98, 95% CI: 0.23-4.11, P = 0.977). After PSM, the OM and CSM of focal therapy and AS/WW showed no significant differences (HR = 1.26, 95% CI: 0.92-1.74, P = 0.149; and HR = 1.26, 95% CI: 0.24-6.51, P = 0.782, respectively). For patients with low-risk PCa, focal therapy was no match for AS/WW in decreasing OM, suggesting that AS/WW could bring more overall survival benefits.

Background The impact of sodium intake on cardiovascular disease (CVD) health and mortality has been studied for decades, including the well-established association with blood pressure. However, non-linear patterns, dose–response associations, and sex differences in the relationship between sodium and potassium intakes and overall and cause-specific mortality remain to be elucidated and a comprehensive examination is lacking. Our study objective was to determine whether intake of sodium and potassium and the sodium–potassium ratio are associated with overall and cause-specific mortality in men and women. Methods We conducted a prospective analysis of 237,036 men and 179,068 women in the National Institutes of Health-AARP Diet and Health Study. Multivariable-adjusted Cox proportional hazard regression models were utilized to calculate hazard ratios. A systematic review and meta-analysis of cohort studies was also conducted. Results During 6,009,748 person-years of follow-up, there were 77,614 deaths, 49,297 among men and 28,317 among women. Adjusting for other risk factors, we found a significant positive association between higher sodium intake (≥ 2,000 mg/d) and increased overall and CVD mortality (overall mortality, fifth versus lowest quintile, men and women HRs = 1.06 and 1.10, P nonlinearity  < 0.0001; CVD mortality, fifth versus lowest quintile, HRs = 1.07 and 1.21, P nonlinearity  = 0.0002 and 0.01). Higher potassium intake and a lower sodium–potassium ratio were associated with a reduced mortality, with women showing stronger associations (overall mortality, fifth versus lowest quintile, HRs for potassium = 0.96 and 0.82, and HRs for the sodium–potassium ratio = 1.09 and 1.23, for men and women, respectively; P nonlinearity  < 0.05 and both P for interaction ≤ 0.0006). The overall mortality associations with intake of sodium, potassium and the sodium–potassium ratio were generally similar across population risk factor subgroups with the exception that the inverse potassium-mortality association was stronger in men with lower body mass index or fruit consumption (P interaction  < 0.0004). The updated meta-analysis of cohort studies based on 42 risk estimates, 2,085,904 participants, and 80,085 CVD events yielded very similar results (highest versus lowest sodium categories, pooled relative risk for CVD events = 1.13, 95% CI: 1.06–1.20; P nonlinearity  < 0.001). Conclusions Our study demonstrates significant positive associations between daily sodium intake (within the range of sodium intake between 2,000 and 7,500 mg/d), the sodium–potassium ratio, and risk of CVD and overall mortality, with women having stronger sodium–potassium ratio-mortality associations than men, and with the meta-analysis providing compelling support for the CVD associations. These data may suggest decreasing sodium intake and increasing potassium intake as means to improve health and longevity, and our data pointing to a sex difference in the potassium-mortality and sodium–potassium ratio-mortality relationships provide additional evidence relevant to current dietary guidelines for the general adult population. Systematic review registration PROSPERO Identifier: CRD42022331618.

Background The Correa’s cascade, encompassing chronic non-atrophic gastritis, atrophic gastritis, intestinal metaplasia, and dysplasia, represents the well-recognized pathway for the development of non-cardia gastric cancer. Population-based studies on all-cause and cause-specific mortalities among patients with gastric lesions in Correa’s cascade are scarce. Methods We compiled a cohort of 340 744 eligible patients who had undergone endoscopy with biopsy for non-malignant indications during the period 1979–2011, which was followed up until 2014. Standardized mortality ratios (SMRs) with 95% confidence intervals (CIs) provided estimation of the relative risk, using the general Swedish population as reference. Cox regression model was used to estimate hazard ratios (HRs) of death for internal comparison. Results A total of 306 117 patients were included in the final analysis, accumulating 3,049,009 person-years of follow-up. In total 106,625 deaths were observed during the study period. Compared to the general population, excess risks of overall mortality were noted in all subgroups, with SMRs ranging from 1.11 (95% CI 1.08–1.14) for the normal mucosa group to 1.54 (95% CI 1.46–1.62) for the dysplasia group. For cause-specific mortalities, mortality from gastric cancer gradually increased along Correa’s cascade, with excess risk rising from 105% for patients with chronic gastritis to more than 600% for the dysplasia group. These results were confirmed in the comparison with the normal mucosa group. For non-cancer conditions, increased death risks were noted for various diseases compared to the general population, especially among patients with more severe gastric precancerous lesions. But the results were confirmed only for “infectious diseases and parasitic diseases”, “respiratory system diseases”, and “digestive system disease”, when using the normal mucosa group as reference. Conclusions Increased mortality from gastric cancer suggests that early recognition and intervention of gastric precancerous lesions probably benefit the patients. Excess mortality due to non-cancer conditions should be interpreted with caution, and future studies are warranted.

Little is known about the association between dietary choline intake and mortality. We evaluated the link between choline consumption and overall as well as cause-specific mortality by using both individual data and pooling prospective studies by meta-analysis and systematic review. Furthermore, adjusted means of cardiometabolic risk factors across choline intake quartiles were calculated. Data from the National Health and Nutrition Examination Survey (1999–2010) were collected. Adjusted Cox regression was performed to determine the risk ratio (RR) and 95 % CI, as well as random-effects models and generic inverse variance methods to synthesise quantitative and pooling data, followed by a leave-one-out method for sensitivity analysis. After adjustments, we found that individuals consuming more choline had worse lipid profile and glucose homeostasis, but lower C-reactive protein levels ( P < 0·001 for all comparisons) with no significant differences in anthropometric parameters and blood pressure. Multivariable Cox regression models revealed that individuals in the highest quartile (Q4) of choline consumption had a greater risk of total (23 %), CVD (33 %) and stroke (30 %) mortality compared with the first quartile (Q1) ( P < 0·001 for all comparison). These results were confirmed in a meta-analysis, showing that choline intake was positively and significantly associated with overall (RR 1·12, 95 % CI 1·08, 1·17, I 2 = 2·9) and CVD (RR 1·28, 95 % CI 1·17, 1·39, I 2 = 9·6) mortality risk. In contrast, the positive association between choline consumption and stroke mortality became non-significant (RR 1·18, 95 % CI 0·97, 1·43, P = 0·092, I 2 = 1·1). Our findings shed light on the potential adverse effects of choline intake on selected cardiometabolic risk factors and mortality risk.

Background Overall mortality has been reported to be lower among individuals classified as overweight/obese when compared with their normal weight counterparts (“obesity paradox”) when obesity classification is based on the body mass index (BMI). One possible reason for this apparent paradox is that BMI is not a reliable measure of obesity-related risk as it does not differentiate fat mass from lean muscle mass or fat mass phenotypes. Waist circumference (WC), as a measure of central adiposity, may be a better indicator of obesity-related risk. We examined the association of overall mortality with BMI and with WC measures, including WC, waist-to-height ratio (WHtR) and waist-to-hip ratio (WHR). Methods Data from 3976 African American participants (551 deaths) in the Jackson Heart Study (JHS) were analyzed. Cox regression models were used to perform survival analysis. Obesity measures were analyzed as dichotomous (obese/non-obese) and continuous variables. Baseline covariates included age, sex and smoking status. Results Comparing obese to non-obese participants, adjusted hazard ratios (95% CI) for overall mortality were 1.14 (0.96, 1.35), 1.30 (1.07, 1.59), 1.02 (0.73, 1.41) and 1.45 (1.18, 1.79) when using BMI, WC, WHtR and WHR, respectively. For BMI, WC and WHtR, a J-shaped relationship was observed with overall mortality. For WHR, a monotonic increasing relationship was observed with overall mortality. Conclusions In the JHS, we found that obesity as defined by WC and WHR was associated with an increased risk of overall and CVD mortality, while obesity defined by BMI was associated only with an increased risk of CVD mortality. WHR was the only obesity measure that showed a monotonic increasing relationship with overall and CVD mortality.

Background and aims Controversy remains whether the mortality risk in people with fatty liver disease (FLD) including metabolic-(dysfunction) associated steatotic liver disease (MASLD) and metabolic-(dysfunction) associated fatty liver disease (MAFLD) is higher than observed in those without FLD. We aimed to determine the mortality rate and mortality rate ratio (MRR) for these FLDs. Methods The study population was a randomly selected cohort of community-dwelling adults in regional Victoria, Australia between 2001 and 2003 with sufficient data evaluable for Fatty Liver Index and determination on alcohol consumption. MASLD and MAFLD were diagnosed by established criteria. The primary outcome was overall mortality and main secondary outcome was major adverse liver outcomes (MALO) (i.e., decompensated liver disease, primary liver cancer and liver-related death). Non-fatal and fatal outcomes were captured via data linkage to hospital admission, cancer registry, and death registries. MRR was calculated with non-FLD participants as the comparator. Results 1444 (99.3%) and 1324 (91.1%) individuals from a total of 1454 were included in the final MAFLD and MASLD analyses. The median follow-up was 19.7 years (IQR 19.1–20.1) and there were 298 deaths. The MRR for MAFLD and MASLD was 1.39 (95% CI 1.10–1.76) and 1.25 (95% CI 0.96–1.61), respectively. MAFLD persisted as a risk factor for all-cause death on multivariable models correcting for lifestyle and socioeconomic variables, but not when adjusted for metabolic risk factors. MALOs were increased in MAFLD [incidence rate ratio (IRR) 3.03, 95% CI 1.22–8.18] and MASLD (IRR 2.80, 95% CI 1.05–7.90). Metabolic risk factors increased the risk of overall mortality and MALO, and cancer (34.3–34.6%) and cardiovascular disease (30.1–33.7%) were the most common cause of death in FLD. Conclusion In this population-based longitudinal study, MAFLD but not MASLD increases the risk of overall mortality, with metabolic syndrome components key risk factors increasing risk of death.

The number of cancer survivors is growing rapidly; however, specific lifestyle recommendations for these patients are still sparse, including dietary approaches. Thus, the aim of the present systematic review and meta-analysis was to examine the associations between adherence to diet-quality indices and dietary patterns on overall mortality, cancer-specific mortality, and cancer recurrence among cancer survivors. The literature search was conducted in PubMed and Web of Science between 18 May 2016 and 22 May 2022 with no language restrictions. Thirty-nine studies were included for quantitative analysis, providing data from 77,412 participants. Adherence to both diet-quality indices and a healthy/prudent dietary pattern was inversely associated with overall mortality (RR, 0.81; 95% CI, 0.77–0.86; RR, 0.80; 95% CI, 0.70–0.92, respectively) and with cancer-specific mortality (RR, 0.86; 95% CI, 0.79–0.94; RR, 0.79; 95% CI, 0.64–0.97, respectively). These associations could be observed following assessment of dietary patterns either pre- and/or postdiagnosis. For unhealthy/western dietary patterns, high adherence was associated with overall mortality (RR, 1.26; 95% CI, 1.08–1.47). Although the certainty of evidence was rated as low, we conclude that there are no reservations against high adherence to healthy dietary patterns or indices in cancer survivors.

•Paratuberculosis vaccination extends productive life of dairy cattle.•Paratuberculosis vaccination induces a reduced mortality non-specific effect (NSE)•This NSE fits the expected according to the trained immunity mechanism.•This inactivated vaccine has a positive effect on females.•Extended paratuberculosis vaccination could help reduce antibiotic use. Records of cattle vaccination against paratuberculosis (PTB) have been analyzed to determine whether or not non-specific effect (NSE) on overall mortality similar to that observed in BCG vaccinated humans occurs in animals. The results of a previously reported slaughterhouse study on PTB prevalence were used as a reference on the age incidence of advanced patent (clinical) epidemio-pathogenic forms. In the proper vaccine study, cows in 30 cattle farms in the Basque Country, Spain were followed-up for between 1 and 13 years. Vaccinated groups were composed by 1008 (592 right-censored) animals younger than 3 months treated as calves and by 3761 (3160 right-censored) vaccinated at any older age. Controls were 339 (157 right-censored) and 4592 (2213 right-censored) age matched animals, respectively. Individual last year presence in the annual testing was considered age at culling or death. A survival analysis was carried out according age at vaccination of vaccinated versus non-vaccinated animals. PTB age incidence in the slaughterhouse study was subtracted from the difference between vaccinated and non-vaccinated animals at the same age in order to estimate PTB-specific and non-specific effects. The maximum difference was observed at the 2–3 years interval with a 33.9% mortality reduction in the calf vaccinated group. This corresponded also with the maximum NSE that was 24.5% for a PTB incidence of 9.5%. Overall, vaccination afforded to calves a 26.5% yearly mortality protection, split between 11.1% PTB-specific and 15.4% NSE. These results support a NSE on total mortality associated with PTB vaccination that appeared to persist for up to 6–7 years. This confirms for the first time in an animal field study the innate immune system memory predicted by the recently proposed trained immunity theory. Contrasting the literature, no deleterious effects of killed vaccines on females were observed. Mortality reduction would offset vaccination costs and could improve livestock systems efficiency and potentially reduce antibiotic use. Clinical trial registered with Spanish Agency for Drugs and Sanitary products (AEMPS) as 11/012/ECV.

Metabolic dysfunction‐associated steatotic liver disease (MASLD) is a major cause of premature mortality, but data on sex differences in mortality remain limited. We compared the overall, nonliver‐related, and liver‐related mortality rates per 1000 person‐years in MASLD patients by sex. Propensity score matching (PSM) yielded 3579 pairs of females and males with balanced characteristics from a cohort of 8517 MASLD patients (53.1% female, 46.6% male) seen at Stanford University Medical Center (1995–2023). In the total PSM cohort, the overall (12.68 vs. 12.92), nonliver‐related (11.43 vs. 11.60), and liver‐related (1.25 vs. 1.32) mortality rates were similar between males and females. However, in age‐stratified analyses, females had higher overall (7.99 vs. 4.95, p = 0.02) and nonliver‐related (7.20 vs. 4.71, p = 0.05) mortality rates among younger (≤50 years) patients, with opposite direction among the older group with higher overall (21.40 vs. 16.51, p = 0.02) and nonliver‐related (19.02 vs. 14.80, p = 0.04) mortality rates in males. In Cox regression analyses, male sex was associated with lower risks of overall and nonliver‐related mortality (adjusted hazard ratio [aHR] 0.59 and 0.61) among patients ≤50 years, but with higher risks among those >50 years (aHR 1.32 and 1.30). Sex and age should be considered in the management strategies for people with MASLD. Data on the impact of sex for overall and cause‐specific mortality in patients with metabolic dysfunction‐associated steatotic liver disease (MASLD) is limited. Among older (>50 years) people with MASLD, males had about 40% higher risk of overall and nonliver related mortality, while the opposite was observed with females having about 30% higher risk among younger (≤50 years) people with MASLD. Significant sex differences exist in mortality risks of people with MASLD and should be taken into account in the management of MASLD.

Chocolate is a rich dietary source of various bioactive flavonoid compounds. Despite being one of the most popular foods worldwide, the association between chocolate consumption and long-term mortality remains unclear. The objective of this study is to determine the associations between chocolate consumption and long-term overall and cause-specific mortality, to evaluate dose–response and potential mediators, and to conduct an updated meta-analysis based on prospective cohort studies. We performed a prospective analysis in the Alpha-Tocopherol, Beta-Carotene cancer prevention (ATBC) Study with a total of 27,111 men who were recruited between 1985 and 1988 and followed through 2015. Exposure data of daily chocolate consumption was obtained from validated baseline food frequency questionnaire. Hazard ratios (HRs) and 30-year absolute risk differences (ARDs) including 95% confidence intervals (CI) for overall and cause-specific mortality were estimated using multivariable-adjusted Cox proportional hazards regression models. An updated meta-analysis of cohort studies was also conducted. During 482,807 person-years of follow-up, a total of 22,064 men died. The multivariable analyses showed a statistically significant inverse association between chocolate consumption and risk of overall mortality, with HRs of 0.91, 0.89, 0.89, and 0.88 for the increasing categories 2–5 as compared with those in the lowest category (Ptrend < 0.0001, and P for nonlinearity < 0.0001). We observed significantly lower mortality from cardiovascular disease (CVD), heart disease and cancer, representing 13%, 16% and 12% risk reductions for the highest compared to lowest chocolate category, respectively (all Ptrend ≤ 0.002; all P for nonlinearity < 0.0001). The inverse associations of chocolate consumption with risk of overall, CVD and heart disease mortality were generally consistent across cohort subgroups (e.g., body mass index and serum cholesterol). Mediation analysis showed that 4.3% of the inverse association of chocolate and overall mortality was mediated through reducing blood pressure. Within the updated meta-analysis of cohort studies (21 risk estimates, 908,390 participants and 65,407 events), greater consumption of chocolate (per 5 g/day) was associated with a lower risk of CVD incidence and mortality (pooled relative risk = 0.98, P value < 0.001; P for nonlinearity < 0.001). The predefined subgroup analyses generally revealed consistent inverse chocolate-CVD risk associations. In this prospective study, calorie-balanced greater consumption of chocolate was inversely associated with lower overall, CVD, heart disease and cancer mortality. The systematic review and meta-analysis provide support for the inverse chocolate-CVD association. Our findings may provide evidence to partially allay concerns regarding adverse health outcomes from low-to-moderate chocolate consumption.