In 77,100 Norwegian women, processed food risk landed on one side of the colon

Norway has one of the highest colorectal cancer rates in the world [s1]. That makes it an informative place to test whether the degree of industrial processing in a diet — rather than its nutrient content — is associated with the disease.

A prospective analysis of the Norwegian Women and Cancer study, published in the British Journal of Nutrition on September 16, reports that it is, and that the association is concentrated in one anatomical location [s1].

What was analysed

The cohort comprised 77,100 women with 1,625 colorectal cancer cases and an average follow-up of 17.4 years [s1]. Dietary intake was collected using validated semi-quantitative food frequency questionnaires and categorised with the Nova classification system, which sorts foods by extent and purpose of processing [s1]. Multivariable Cox proportional hazards models estimated risk [s1].

Seventeen years of follow-up is long enough to matter for a cancer with a long latency, which is a genuine strength here — many ultra-processed food cohorts report on outcomes accruing over five to ten years.

The findings

Comparing the highest quartile of ultra-processed food intake with the lowest, and adjusting for all covariates including energy intake, total colorectal cancer risk was elevated: hazard ratio 1.24 (95% CI 1.04 to 1.49), with a test for trend at p = 0.02 [s1].

For right-sided colon cancer specifically, the association was substantially stronger: hazard ratio 1.58 (95% CI 1.19 to 2.09), with a test for trend at p < 0.001 [s1].

The authors state plainly that more research is needed to understand the associations between ultra-processed food, its subgroups, and cancer at different colorectal subsites [s1].

Why subsite is the interesting part

Right-sided and left-sided colorectal cancers differ in more than location. They differ in molecular profile, in the microbial environment they arise in, and in prognosis, and increasingly they are treated as related but distinct diseases. A dietary exposure that shows a stronger association on one side is therefore making a claim that can be tested mechanistically rather than just epidemiologically.

The right colon is where the gut microbiome is most metabolically active and where fermentation of what survives the small intestine occurs. If ultra-processing acts through emulsifiers, additives, or fibre structure altering that environment, a right-sided concentration is what one would predict.

That is a hypothesis, not a finding. The study reports the subsite difference; it does not investigate the mechanism [s1].

It is also worth noting that the subsite analysis was one of several the study performed. Splitting a cohort by tumour location multiplies comparisons, and the strongest estimate from a set of subgroup analyses is systematically biased upward. A hazard ratio of 1.58 with a lower bound of 1.19 [s1] is not a fragile result, but it should be read as the estimate most likely to shrink on replication.

The recurring limits of this literature

Food frequency questionnaires were built to estimate nutrients, not processing. Assigning Nova categories from FFQ responses requires judgment about what a reported item actually was, and the resulting misclassification affects every cohort in this field.

Diet was assessed at baseline for a cohort followed 17.4 years [s1]. Norwegian food supply and purchasing changed considerably over that period, and a single dietary measurement will misclassify some women's long-run exposure.

Confounding remains the central issue. Women who eat more ultra-processed food differ in smoking, physical activity, income, and screening participation — and colorectal cancer detection depends heavily on screening participation, which is not obviously independent of diet.

The cohort is women only [s1]. Colorectal cancer incidence and subsite distribution differ by sex, so this does not generalise to men.

The August 2025 American Heart Association science advisory on ultra-processed foods framed the core problem for the whole field: mechanisms remain unclear, and most ultra-processed foods overlap with foods already high in saturated fat, added sugars, and sodium [s2]. Its recommendation is to identify high-risk subgroups of ultra-processed foods rather than treat the Nova category as one exposure [s2]. That advice applies squarely here — this study reports an association with the category, not with any identified constituent.

What it adds

A long-follow-up prospective cohort in a high-incidence country, with a subsite-specific signal that gives mechanistic research something to aim at. That is a meaningful addition to a literature that the AHA advisory characterises as consistent in direction and unclear in mechanism [s2].

It is not evidence that changing processing while holding nutrients constant would change cancer risk. No cohort can show that.

What to watch

Whether the right-sided concentration replicates in other cohorts and in men; whether specific ultra-processed food subgroups or additives can be separated from the category as a whole; and whether controlled feeding studies find microbiome changes plausibly linking processing to colorectal carcinogenesis.

This article describes observational cohort research and is informational only. It is not medical advice and does not recommend any diet.

Sources

• [s1] Mols R, Huybrechts I, Skeie G, High consumption of ultra-processed food and risk of colorectal cancer: the Norwegian Women and Cancer cohort study, British Journal of Nutrition, 2025;134:497-506, published online 2025-09-16.
• [s2] Vadiveloo MK, Gardner CD, Bleich SN, Khandpur N, Lichtenstein AH, Otten JJ, Rebholz CM, Singleton CR, Vos MB, Wang S, et al., Ultraprocessed Foods and Their Association With Cardiometabolic Health: Evidence, Gaps, and Opportunities: A Science Advisory From the American Heart Association, Circulation, 2025;152:e245-e263, published 2025-08-08.