Vitamin intake and colorectal cancer incidence and mortality: evidence from a large prospective cohort

Abstract

Emerging evidence suggests that vitamin intake may be associated with colorectal cancer (CRC) risk, yet prospective studies on CRC incidence and mortality remain limited. We therefore investigated the associations between vitamin intake and CRC incidence and mortality in a large cohort of US adults. We included 101,692 participants from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Vitamin intake (including dietary and supplement sources) was assessed using the Dietary History Questionnaire based on the USDA 1994–1996 survey and the University of Minnesota Nutrition Data System for Research. Prospective associations with CRC incidence and mortality were estimated using Cox proportional hazards regression models. Restricted cubic spline regression was applied to evaluate potential nonlinear relationships. Subgroup analyses were conducted to explore potential effect modifiers of CRC incidence and mortality. During 896,655 person-years of follow-up (mean 8.82 years), 1,085 participants were diagnosed with CRC, and 529 CRC deaths occurred during 1,533,506 person-years of follow-up (mean 15.08 years). In fully adjusted models, higher intakes of vitamin A (HR = 0.75, 95% CI: 0.60–0.93; P -trend = 0.005), vitamin B6 (HR = 0.74, 95% CI: 0.61–0.90; P -trend = 0.015), vitamin D (HR = 0.77, 95% CI: 0.64–0.93; P -trend = 0.022), and vitamin E (HR = 0.81, 95% CI: 0.68–0.97; P -trend = 0.008) were significantly associated with a lower incidence of CRC. In addition, higher intakes of vitamins A, B6, and C were significantly associated with reduced CRC mortality. No significant associations were observed for vitamin B12 with CRC incidence and mortality. Sensitivity and subgroup analyses supported the robustness of these findings. In conclusion, higher intake of vitamins A, B6, C, D, and E is associated with an decreased risk of CRC incidence and mortality. Appropriate vitamin intake may represent a modifiable factor for the primary prevention of CRC.