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; Ptrend = .0099) and mortality due to this cancer (subdistribution hazard ratiotertile 3 vs 1 0.65; 95% confidence interval: 0.47, 0.89; Ptrend = .0108) in a linear dose–response manner (all Pnonlinearity > .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.

Liver is one of the organs with the highest injury rate, and in recent decades, the guidelines for the treatment of liver trauma have changed considerably. Now, there is a growing consensus that the most important step is diagnosis and depending upon the degree of severity, non-operative therapy is the main treatment method for hepatic trauma if conditions permit. For serious hepatic trauma patients such as those with hemodynamic instability, they should be operated upon as soon as possible. Regardless of the surgical options, doctors should control damage to patients and try to prevent complications. New therapies such as hepatic artery embolization and liver transplantation have been more and more used for the treatment of serious hepatic damage in clinics.

No epidemiological studies have been conducted to assess the association of dietary vitamin K intake with the risk of pancreatic cancer. We used prospective data from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial between 1993 and 2009 to fill this gap. A total of 101695 subjects were identified. Dietary intakes of phylloquinone (vitamin K1), menaquinones (vitamin K2), and dihydrophylloquinone (dihydrovitamin K1) were assessed with a food frequency questionnaire. Cox regression was applied to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). During a mean follow-up of 8.86 years (900744.57 person-years), 361 pancreatic cancer cases were documented. In the fully adjusted model, dietary intakes of phylloquinone (HRquartile 4 versus 1: 0.57; 95% CI: 0.39, 0.83; Ptrend=0.002) and dihydrophylloquinone (HRquartile 4 versus 1: 0.59; 95% CI: 0.41, 0.85; Ptrend=0.006), but not menaquinones (HRquartile 4 versus 1: 0.93; 95% CI: 0.65, 1.33; Ptrend=0.816), were found to be inversely associated with the risk of pancreatic cancer in a nonlinear dose–response manner (all Pnonlinearity<0.05), which were not modified by predefined stratification factors and remained in sensitivity analyses. In conclusion, dietary intakes of phylloquinone and dihydrophylloquinone, but not menaquinones, confer a reduced risk of pancreatic cancer. Future studies should confirm our findings.

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 95962 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 vs. the lowest quartiles of the overall low-carbohydrate-diet score was found to be associated with a reduced risk of pancreatic cancer (hazard ratioquartile 4 vs. 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 <65 years (Pinteraction=0.015). Similar results were obtained for animal and vegetable low-carbohydrate-diet scores. In conclusion, low-carbohydrate diets, regardless of the type of protein and fat, are associated with a lower risk of pancreatic cancer in the US population, suggesting that adherence to low-carbohydrate-diets may be beneficial for pancreatic cancer prevention. Future studies should validate our findings in other populations.