Higher Ultraprocessed Food Intake Linked to Increased Risk of Early‑Onset Colorectal Adenomas in Women

Highlight

• In 29,105 women followed for 24 years, higher ultraprocessed food (UPF) intake was associated with greater odds of early‑onset conventional colorectal adenomas (highest vs lowest quintile AOR 1.45; 95% CI, 1.19–1.77).

• UPF intake (median 5.7 servings/day) explained a substantial portion of daily energy (≈35%) in this cohort; associations for serrated lesions were null.

• Associations persisted after adjustment for BMI, type 2 diabetes, fiber and micronutrients, and overall diet quality, suggesting an effect beyond traditional dietary risk factors.

Background

Colorectal cancer (CRC) incidence among adults younger than 50 years—so called early‑onset colorectal cancer (EOCRC)—has been increasing in many high‑income countries over the past several decades. This shift has prompted intensive research into lifestyle and environmental contributors that might explain the rising burden among younger adults. Diet is a leading candidate, and in parallel with temporal trends in EOCRC, intake of ultraprocessed foods (UPFs) has risen globally. UPFs are industrial formulations typically high in added sugars, refined starches, salt, and fats, and contain food substances not commonly used in culinary preparations (e.g., hydrogenated oils, flavor enhancers, emulsifiers). The NOVA classification system has been widely used to operationalize UPF intake in epidemiologic studies and public health recommendations.

Study design

This prospective analysis used data from the Nurses’ Health Study II (NHS II), a US cohort of female registered nurses established in 1989. The analytic sample included 29,105 participants who completed the 1991 baseline food‑frequency questionnaire (FFQ), underwent at least one lower endoscopy before age 50 after baseline, and had no prior colorectal polyps, inflammatory bowel disease, or cancer (other than nonmelanoma skin cancer) before the first endoscopy.

Dietary intake was assessed by FFQs every 4 years, and food items were classified by processing level using the NOVA system. UPF exposure was modeled as energy‑adjusted servings per day and categorized into quintiles. The primary outcomes were EOCRC precursors confirmed by medical records: conventional adenomas (tubular, tubulovillous, villous, and high‑grade dysplasia) and serrated lesions (hyperplastic polyps, sessile serrated lesions, traditional serrated adenomas). The follow‑up window spanned June 1, 1991, to June 1, 2015.

Multivariable logistic regression with generalized estimating equations accounted for clustering by participant (repeated endoscopies) and adjusted for age, race/ethnicity, family history of CRC, smoking, alcohol, physical activity, total energy, and other established or putative CRC risk factors. Additional models further adjusted for body mass index (BMI), prevalent type 2 diabetes, select dietary factors (fiber, folate, calcium, vitamin D), and an index of overall diet quality (Alternative Healthy Eating Index‑2010).

Key findings

Over 24 years of observation, the investigators documented 1,189 cases of early‑onset conventional adenomas and 1,598 serrated lesions among 29,105 women (mean age at baseline 45.2 years). Median UPF intake was 5.7 servings per day (IQR 4.5–7.4), accounting for approximately 34.8% of daily energy intake in the cohort.

Main adjusted results:

• Conventional adenomas: Women in the highest quintile of UPF intake had higher odds of early‑onset conventional adenomas compared with those in the lowest quintile (adjusted odds ratio [AOR] 1.45; 95% confidence interval [CI], 1.19–1.77; P for trend < .001). This association persisted after additional adjustment for BMI, type 2 diabetes, individual dietary components (fiber, folate, calcium, vitamin D), and the Alternative Healthy Eating Index‑2010 score.

• Serrated lesions: No significant association was observed between UPF intake and early‑onset serrated lesions (AOR highest vs lowest quintile 1.04; 95% CI, 0.89–1.22; P for trend = .48).

• Sensitivity analyses: Findings remained consistent in models excluding participants with a history of diabetes, when accounting for endoscopy frequency and indications, and when using alternative exposure metrics (e.g., percent energy from UPFs), indicating robustness to potential detection bias and measurement specification.

Effect sizes and clinical significance

The magnitude of the association—about a 45% higher odds of conventional adenomas for the highest UPF consumers—represents a meaningful relative increase at the population level, especially given the high prevalence of UPF intake in many countries. Conventional adenomas are established precursors of CRC; thus, factors that increase adenoma risk in younger adults may plausibly contribute to rising EOCRC incidence if exposure trends persist.

Expert commentary and interpretation

Interpretation of these findings should balance strengths and limitations. Strengths include the large prospective cohort with repeated dietary assessments, objective outcome confirmation through pathology reports, and rigorous adjustment for multiple confounders including measures of diet quality and metabolic risk. The use of the NOVA classification and repeated FFQs allows a longitudinal view of habitual UPF intake rather than cross‑sectional snapshots.

Biological plausibility

Several mechanisms could underpin an association between UPFs and colorectal tumorigenesis. UPFs tend to be energy‑dense, low in dietary fiber and micronutrients, and contribute to metabolic perturbations such as obesity and insulin resistance—established CRC risk factors. Beyond macronutrient composition, non‑nutritive ingredients prevalent in UPFs (e.g., additives, emulsifiers, artificial sweeteners, preservatives, high‑temperature processing by‑products) may alter gut barrier function, promote dysbiosis, or produce genotoxic compounds. Experimental models have demonstrated that certain emulsifiers can disturb the intestinal microbiome and promote low‑grade inflammation; some additives and contaminants formed during processing (e.g., acrylamide) are biologically plausible contributors to colorectal carcinogenesis.

Limitations and alternative explanations

Residual confounding is possible despite comprehensive adjustment. Participants in NHS II are health professionals with distinct health behaviors and demographic characteristics, and the cohort is predominantly White, potentially limiting generalizability. Measurement error in dietary assessment is inherent to FFQs, and misclassification of UPFs may occur—both random error and systematic biases could influence effect estimates. Detection bias is a potential concern because only participants who had at least one lower endoscopy before age 50 were included; however, investigators attempted to account for endoscopy frequency and indication. Reverse causation is unlikely given prospective ascertainment and exclusion of prevalent disease at baseline.

Context with prior evidence

This study complements a growing epidemiologic literature associating UPF intake with adverse health outcomes, including obesity, cardiometabolic disease, and some cancers. Broad cohort analyses have linked higher UPF consumption to overall cancer risk and to site‑specific cancers in some populations. The current report adds granularity by focusing on early‑onset colorectal neoplasia and by discriminating conventional adenomas from serrated lesions, suggesting specificity to classical adenoma‑carcinoma pathway lesions.

Clinical and public health implications

At the clinical level, these data support dietary counseling that emphasizes reduced consumption of ultraprocessed foods as part of CRC prevention strategies, particularly in younger adults and those with other risk factors. Public health implications are broader: given that UPFs constitute a large and growing share of energy intake in many countries, modest shifts in the food environment (e.g., reformulation, labeling, fiscal measures, policies limiting marketing to children) and in consumer behavior could translate into meaningful reductions in adenoma and ultimately CRC incidence over time.

Conclusion

The prospective analysis from the Nurses’ Health Study II shows that higher ultraprocessed food consumption is associated with an increased risk of early‑onset conventional colorectal adenomas among women, independent of BMI, diabetes, and overall diet quality. These findings strengthen the rationale for considering food processing—beyond nutrient composition—in cancer prevention strategies. Future research should seek to replicate findings in more diverse cohorts, clarify causal pathways (including additive‑ and processing‑specific effects), and evaluate whether reducing UPF exposure can lower adenoma incidence in intervention studies.

Funding and clinicaltrials.gov

The reported study authors listed funding sources in the original JAMA Oncology publication. The Nurses’ Health Study II is supported by grants from the National Institutes of Health and other sources (see original article for complete funding acknowledgements). This analysis is observational and not registered as a clinical trial.

Selected references

1. Wang C, Du M, Kim H, et al. Ultraprocessed Food Consumption and Risk of Early‑Onset Colorectal Cancer Precursors Among Women. JAMA Oncol. 2025 Nov 13. doi:10.1001/jamaoncol.2025.4777.

2. Monteiro CA, Cannon G, Lawrence M, et al. Ultra‑processed foods, diet quality, and public health. Public Health Nutr. 2019;22(5):936–941.

3. Siegel RL, Miller KD, Goding Sauer A, et al. Colorectal cancer statistics, 2020. CA Cancer J Clin. 2020;70(3):145–164.

Note: For a complete list of cohort methods, variable definitions, and funding details, readers should consult the original JAMA Oncology publication by Wang et al.