Emerging evidence from the Nurses’ Health Study II (NHS II) suggests that high intake of ultraprocessed foods (UPFs) may contribute to the development of early-onset colorectal adenomas, highlighting a potentially modifiable dietary factor in the growing incidence of colorectal neoplasia among adults under 50.
The large, prospective cohort study evaluated 29,105 female nurses in the United States, born between 1947 and 1964, who underwent lower endoscopy before age 50. Over a median follow-up of 13 years, 1,189 cases of conventional adenomas and 1,598 serrated lesions were documented.
Participants with the highest quintile of UPF intake—defined using the NOVA classification system as industrially produced, ready-to-eat or ready-to-heat foods—had a 45% higher odds of developing conventional adenomas compared with those in the lowest quintile (multivariable-adjusted OR 1.45; 95% CI, 1.19–1.77). No significant association was observed for serrated lesions (OR 1.04; 95% CI, 0.89–1.22).
Higher UPF intake was associated with increased risk of early-onset colorectal conventional adenomas
The authors noted that “higher UPF intake was associated with increased risk of early-onset colorectal conventional adenomas.
“Our findings highlight the importance of diet in early-onset colorectal carcinogenesis and support dietary quality improvement as a strategy to mitigate the increasing burden of EOCRC.”
UPFs, which now account for approximately 60% of daily caloric intake in the US, are typically low in fibre, vitamins, and bioactive compounds, but high in refined starches, unhealthy fats, additives, and artificial sweeteners. These components may disrupt gut microbiota, increase intestinal inflammation, and contribute to colorectal carcinogenesis. In the NHS II cohort, UPFs contributed 34.8% of daily calories, with major sources including ultraprocessed breads, breakfast foods, sauces, condiments, and sweetened beverages.
The study controlled for multiple potential confounders, including age, BMI, type 2 diabetes, lifestyle factors, endoscopy frequency and indication, as well as dietary factors such as fibre, folate, calcium, vitamin D, and overall diet quality (AHEI-2010 score). Sensitivity analyses confirmed the robustness of the association, which remained consistent even when restricted to precursors diagnosed before age 45, preserving a relevant window for early-onset colorectal cancer (EOCRC) risk.
Interestingly, subgroup analyses did not identify a single UPF category responsible for the observed effect, suggesting a cumulative or synergistic impact of multiple processed food constituents on adenoma formation. The association was most pronounced for distal colon and rectal adenomas, aligning with known patterns of early-onset colorectal cancer.
While the study evaluated precursor lesions rather than invasive cancer due to limited EOCRC cases, findings provide clinically relevant insight into modifiable dietary exposures that may contribute to early colorectal tumorigenesis. The authors note that mechanisms such as microbiome disruption, proinflammatory signalling, and exposure to food-related genotoxins may disproportionately affect younger adults.
Given the rising incidence of EOCRC, clinicians may consider counselling patients—particularly younger adults—on limiting consumption of ultraprocessed foods. While causality cannot be definitively established from observational data, the study reinforces existing dietary guidance promoting whole foods, high fibre intake, and overall dietary quality as part of cancer prevention strategies.
Paper: Wang, C., et al. Ultraprocessed Food Consumption and Risk of Early-Onset Colorectal Cancer Precursors Among Women. JAMA Oncology. Published online November 13, 2025. doi:10.1001/jamaoncol.2025.4777
